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EDITED BY 


H. BRYANT, 


M.D., 


J. 


AND 
STEWARD, 





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LONDON: 


MDCCCCV. 


FRINTED BY ASH AND CO., LIMITED, 


42, SOUTHWARK STREET, BOROUGH, LONDON, В.Е. 


CONTENTS. 


PAGE. 


I. Coarctation of the Aorta, as illustrated by cases from 
the Post-Mortem Records of Guy’s Hospital from 
1826—1902. By Jonn Fawcert, M.D. ... 9 1 


II. Traumatic Subdural Hemorrhage. An Attempt at 
a Systematic Study based on the examination of 
Seventy-two Collected Cases. By W. H. Bowen, 
M.S. . js i bs is " sv 01 


III. The Behaviour of Leucocytes under the influence of 
Certain Bacterial and other Substances. By 
Tuomas Epwanp НоһмЕв, M.D. (Thesis for the 
M.D. Cambridge). ... is 2 ha ... 155 


IV. A Case of Subdiaphragmatic and Hepatic Abscess 
Consecutive to Mediterranean Fever. „Ву J. W. 
Н. Eyre; Mb. iud: бот, м;р. as .. 207 


V. Growths of Abe: : 4295: atid, Атпай, By OWEN 


RICHARDS, MB. „B-b. . Me me side ow (217 


VI. A Case of о ЕМ Ву G. Т. 
WRENCH, M.B., and J. Н. Bryant, M.D.... .. 888 


VII. A Collection of Cases in which the Operation of 
Excision of the Hip-joint has been performed for 
Disease of the Joint. By А. Б. Тномрвом, M.B., 
Ch.B., F.R.C.8., Surgical Registrar D .. 847 


176106 


iv. Contents. 


VIII. Notes from the Actinotherapeutic Department at 
Guy's. A Year's Experience. Ву G. SIcHEL 


Specimens recently added to the Pathological 
Museum. By Lauriston E. Ssaw, M.D., SIR 
CooPER PERRY, M.D., and Јонх Fawcett, M.D. 


List of Gentlemen Educated at Guy’s Hospital who 
have passed the Examinations of the several 
Universities, Colleges, etc., in the year 1903 


Medallists and Prizemen for 1904 

The Physical Society 

Clinical Appointments held during the year 1903 
Dental Appointments held during the year 1903 
Medical and Surgical Staff, 1904 

Lecturers and Demonstrators 


The Staff of the Dental School, 1904 


„з > t". ¿“> 
کک‎ wa lap ET. „е 


cS o£ owe oe $99. x 


PAGE. 


865 


385 


- 401 


408 
410 
410 
416 
418 
419 


421 





LIST OF ILLUSTRATIONS. 


PLATES. 
TO FACE 
Mr. Owen RICHARDS. PAGE 
Illustrating his Paper on Growths of the Kidney and 
Adrenals. Figs. I. and II. T i .. 242 
Figs. ПІ. and IV. ... ies .. 247 
Figs. V. and VI. s i .. 6 
Mr. G. SICHEL. PAGE 
Illustrating his Paper on Notes from the Actinothera- 
peutic Department at Guy's. Figs. I. and II. ... 3€7 
Figs. III. and IV. 3/1 
Figs. V. and VI. 313 
Figs.VIl.and VIII. 375 
Figs. IX. and X. 381 
CHARTS. 
PAGE 
Dr. THomas Epwarp HOLMES. 
Illustrating his Paper on The Behaviour of Leucocytes 
under the Influence of Certain Bacterial and 
other Substances ... P 7 ee .. 184 
Drs. J. W. Н. Eyre and J. FAWCETT. 
Illustrating their Paper on A Case of Subdiaphragm- 
atic and Hepatic Abscess Consecutive to Mediter- 
ranean Fever ... s Ua gi 209-212 


Drs. С. T. WRENCH and J. Н. BRYANT. 
Illustrating their Paper on А Case of Severe Hamo- 
cytolysis ... n M he T ... 490989 











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NOTICE. 


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Reports can be had at very reduced prices on application to the 
Editors. 


LIST OF SUBSCRIBERS. 


(Subscribers are requested to notify to the Editors any change of address.) 


Aberdeen Medico-Chirurgical Society, The Library, Medical Hall, 
29, King Street, Aberdeen 

Aberdeen University Library, Marischal College, Aberdeen 

Adams, E. H., Guy’s Hospital 

Adams, Matthew A., Trinity House, Maidstone 

Adeney, E. L., M.D., J.P., Howard Lodge, Mount Sion, Tun- 
bridge Wells 

Aikin, C. Edmund, Llandrillo, Corwin, North Wales 

Aikins, M. H., M.D., Burnhamthorpe, Ontario, Canada 

Alexander, К. B., M.B., Cambridge, East London, S. Africa, 
Cape Colony 

Alexander, S. R., M.D., Gatefield House, Faversham 

Allan, A. P., M.D., B.S., Abbotsford, 74, Croham Road, South 
Croydon 

Allen, R. William, M.A., Guy’s Hospital. 

Allport, A., 28a, Moorgate Street, Е.С. 

Alston, W. E., B. A., M.D., B.C., 22, Bentinck Street, Cavendish 
Square, W. 

Anderson, C. T., Cape Town, South Africa 

Anderson, K., Evesleigh, Banwell, Somerset 

Anderton, J. E., Thornfield, New Mills, Derbyshire 

Ashby, E., 58, Bootham, York 

Ashwin, R. H., M.D., High Street, Market-Weighton, East Yorks 

Assheton, R., M. A., Grantchester, Cambridge 

Atkins, Е. р., Chalk Pit House, Sutton, Surrey 

Atkinson, T. ` Reuell, M.D., Cardigan House, Chadwell Heath, 
Essex 

Audland, W. E., 5, Oxford Street, Wellingborough. 


Badcock, G. Wallace, Lulworth, Rushey Green, Catford, S.E. 
Badcock, J. H., 140, Harley Street, W. 

Baines, J. C., Etonhurst, Malvern 

Balderston, R., M.B., 30, Park Road, Forest Hill, S.E. 
Baldwin, F. B. J udge, Draycott House, Bodicote, Banbury 
Ball, J. A., M.D., Stradbroke, Eye, Suffolk 

Ball, W. C., B.A., 96, Gower Street, W.C. 

Barrs, A. G., M.D., 254, Park Square, Leeds 

Bartholomew, A. A., 31, West Hill, Wandsworth, S.W. 


x. Inst of Subscribers. 


Bartlett, B. P., Bourton, Dorset 

Bartlett, G. N., Guy's Hospital. 

Bartlett, H., M. D., C.M., 150, Norwood Road, West Norwood 

Barton, J. Kingston, 14, Ashburn Place, Courtfield Road, S.W. 

Batchelor, F. C., M.D., A. M. P. Buildings, Prince's Street, 
Dunedin, New Zealand 

Batchelor, F. S., Moray Place, Dunedin, New Zealand 

Beale, E. Clifford, M.A., M.B., 23, Upper Berkeley Street, Portman 

. Square, W. 

Bealey, Adam, M.D., Felsham Lodge, Hollington Park, 
St. Leonards-on-Sea 

Bearblock, Staff Surgeon W. J., R.N., H.M.S. Hawke, c/o 
Admiralty, S.W. 

Beard, F., M.B., The Crossways, South End, Croydon 

Beddard, A. P., M.A., M.D., B.C., 44, Seymour Street, Portman 
Square, W. 

Bedford, G. H., Harbottle, Rothbury, Northumberland 

Beley, G., Wandsworth Infirmary, St. John’s Hill, Wandsworth, 
S.W. 

. Bell, Arthur H., Maritzburg, Natal. 

Bell, H. T. S., Murwillumbah, N.S.W., Australia. 

Bennett, H., Builth, Breconshire 

Berry, H. Poole, M.B., The Priory, Grantham 

Bett, Fleet Surgeon W., R.N., H.M.S. Russell, Home Fleet. 

Biggs, T. Strange, West Coombe, Hassocks, Sussex 

Bird, Tom, M.A., 59a, Brook Street, W. 

Birdwood, R. A., M.A., M.D., Park Hospital, Hither Green, 
Lewisham, S.B. 

Bisshopp, Francis R. B., M.A., M.D., B.C., Parham House, 
Tunbridge Wells 

Black, G., M.B., 50, Cazenove Road, Stamford Hill, N. 

Black, K., Dhu House, South Road, Wandsworth Common, S.W. 

Blasson, Thomas, Billingborough, near Folkingham, Lincolnshire 

Blatherwick, H., Forward Lawn, Dulwich, S.E. 

Bligh, W., M.D., B.S., Minley, Caterham Valley 

Bolus, H. B., B.A., M.B., B.C., Haddon, Beckenham, Kent 

Bolus, P. R., M.B., 10, Stoke Newington Common, N. 

Booker, С. W., The Mount, Withey, Surrey 

Booth, E. H., M.D., 1, Cambridge Road, Hove, Brighton 

Bosworth, John Routledge, Sutton, Surrey 

Bowden, G. H., Roseneath, Reigate, Surrey 

Bowen, O., Mere Lodge, Everton, Liverpool 

Bowen, W. H., M.B., Guy’s Hospital 

Bowes, J., East Hill House, East Street, Herne Bay 

Box, W. F., M.B., Guy’s Hospital 

Boycott, A. E., M.A., M.D., B.Ch., B.Sc., Guy’s Hospital 

Brailey, W. A., M.A., M.D., 11, Old Burlington Street, W. 

Brayne, R. E., Guy’s Hospital 


List of Subscribers. xi. 


Bredin, R., M.B., Valparaiso, Chili 

Brenton, W. H., 44, Cobourg Street, Plymouth 

Brereton, F. S., M.D., 3, Queen's Road, Southport 

Bridger, J. Dell, Surrey Dispensary, Dover Road, S.E. 

British Medical Journal, The, 429, Strand, W.C. 

British Medical Association Library, 429, Strand, W.C. 

Brock, E. H., M.D., 21, Streatham Hill, S.W. 

Brockwell, J. B. C., 42, The Parade, Walton-on-Naze 

Brogden, В. W., M.B., B.S., 12, Lower Brook Street, Ipswich 

Bromley, J. B., Castle Hedingham, Essex 

Brookhouse, C. T., J.P., M.D., 19, Wickham Road, Brockley, S.E. 

Brooks, B., Sonning, near Reading 

Brown, G. Minter, Griqua Town, near Kimberley, Cape Colony 

Brown, T. E. Burton, C.I. E., M.D., 185, Willesden Lane, N.W. 

Browne, R. H. J., Fleet Surgeon, R.N., H.M. Albion, China 

Station 

Brussels, Académie Royale de Médecine de Belgique, Palais des 
. Académies (per the Secretary) 

Bryant, J. H., M.D., 8, Mansfield Street, Portland Place, W. 

Bryant, Thomas, M.Ch., 27, Grosvenor Street, W. 

Bryden, F. W. A., The Priory, Godalming 

Bryden, R. J., 21, Harmer Street, Gravesend 

Burghard, F. F., M.S., 86, Harley Street, W. 

Burt, A., 143, Uxbridge Road, W. 

Burton, Herbert C., Lee Park Lodge, Blackheath, S.E. 

Burton-Brown, F. H., M.A., M.B., B.Ch., Guy's Hospital 

Butcher, Н. О. F., Ware, Hertfordshire 

Butler, H. R. C., Oaklands, Abbey Road, Torquay 

Butler, J. A., M.B., B.S., Hillside, Widford, Ware, Herts 


Cadel, N. P., Foxlease, Camberley, Surrey 

Caldecott, C., M.B., B.S., Earlswood Asylum, Redhill, Surrey 

Cameron, J., Melrose House, Stockton-on-Tees 

Campbell, H. J., M.D., 36, Manningham Lane, Bradford, Yorks 

Campkin, P. S., 40, Curzon Street, Mayfair, W. 

Camps, P. W. L., M.B., White House, Teddington 

Canning, H. A. E., 11, King's Terrace, Southsea 

Carden, W. A., Frazerburg, Cape Colony 

Cardiff Medical Society (per A. P. Fiddian, M.B., 23, The Walk, 
Cardiff) 

Carey, Francis, M.D., Villa Carey, Grange Road, Guernsey 

Carling, W., B.A., M.B., B.C., 40, Highland Road, Southsea 

Carlisle, G., Guy’s Hospital 

Carpmael, С. E., M.B., B.S., 17, Half Moon Lane, Herne 
Hill, S.B. 

Carter, H. H., M.B., Guy's Hospital 

Carrell, С. N. P., 34, The Drive, Шога. 

Cazenove, W. R., Beechurst, Long Sutton, Lincolnshire 


xii. List of Subscribers. 


Charles, H. E., 82, St. Helen's Road, Swansea 

Childe, Major L. F., M.B., Malabar Hill, Bombay 

Churchward, A., M.D., 206, Selhurst Road, South Norwood 

Clague, J., Crofton, Castletown, Isle of Man 

Clapham, Crochley, M.D., The Gables, Mayfield, Sussex 

Clark, A. W., La Roche, Onslow Gardens, Wallington, Surrey 

Clarke, Henry, H. M. Prison, Wakefield, Yorkshire 

Claxton, E. I., M.A., M.B., B.C., 111, Great Mersey Street, 
Liverpool 

Cleveland, A. J., M.D., 8, Thorpe Mansions, Norwich 

Clogg, A. H., 15, Central Hill, Upper Norwood, S.E. 

Clowes, N. B., 45, London Road, Reading 

Cobb, W. E. S., 12, Drakefield Road, Upper Tooting, S.W. 

Cock, F. W., M.D., M.S., 1, Porchester Houses, Porchester 
Square, W. 

Cock, J., 17, Morton Crescent, Exmouth, Devon 

Cock, W., 147, Queen's Road, Peckham, S.E. 

Cogan, Lee F., 51, Sheep Street, Northampton 

Colclough, W. F., M.A., M.D., B.C., Bainton House, Sherborne, 
Dorset 

Cole, P. P., St. John's Hospital, Lewisham, S.E. 

Cole, W. H., 8, Beech House Road, Croydon 

сш Е. J., M.D., B.S., 60, Spencer Place, Roundhay Road, 
Leeds 

Coleman, J. J., M.B., Wellington House, Bridlington, Yorks 

Collet, Augustus H., B.A., Ashurst Lodge, Worthing, Sussex 

Collier, H. W., M.B., B.S., Murillo House, High Road, Lee, S.E. 

Collington, F. A., 28, Much Park Street, Coventry 

Collins, H. W., Langford, near Bristol 

Collins, M. A., M.B., B.S., Heath Asylum, Bexley, Kent 

Constant, F. C., 15, Queen's Street, Cheapside, E.C. 

Cooke, T. A. B., New Milford, Pembrokeshire 

Cooper, H., M. A., M.D., B. Ch., Fownhope, Ewell Road, Surbiton 

Copland, J. В., Banks Terrace, ' Sheerness 

Coplans, M., M. D., 14, Lower Bridge Street, Canterbury 

Copley, S., Innes Road, Stamford Hill, Durban, Natal 

Counsell, H. E., 27, Banbury Road, Oxford 

Cox, J. H., 232, Alfreton Road, Nottingham 

Craig, M., M.A., M.D., B.C., Bethlem Hospital, S.E. 

Creasy, R., Windlesham, Surrey 

Cregeen, J. Nelson, 21, Prince's Avenue, Liverpool 

Cressy, A. Z. C., Wallington, Surrey 

Crew, John, J.P., Higham Ferrars, Northamptonshire 

Cross, F. G., Montpelier, Cranes Park, Surbiton 

Croydon Medical Reading Society (per Dr. E. Hulse Willock, 113, 
London Road, Croydon) 

Cruickshank, J. D., The Lodge, Chingford 


List of Subscribers. xiii. 


Cuff, H. E., M.D., North-Eastern Fever Hospital, St. Ann’s 
Road, South Tottenham 

Cuff, R., J.P., C.C., M.B., 1, The Crescent, Scarborough 

Currie, Andrew S., M.D., 81, Queen's Road, Brownswood Park, N. 

Currie, O. J.. M. B., 18, Longmarket Street, Maritzburg, Natal, 
South Africa 

Curtis, F., Lyndens, Redhill, Surrey 


Dadd, J. W., B.A., Guy’s Hospital 

Daldy, A. M., M.D., B.S., 25, Claremont Road, Surbiton 

Dalton, B. N., M.D., Selhurst Road, South Norwood, S.E. 

Daniell, George Williamson, Blandford, Dorsetshire 

Davies, F. W. S., 21, Newport Road, Cardiff 

Davies, W. T. F., D.S.O., M.D., B.S., Post Office Box 1750, 
J ohannesburg, Transvaal 

Davies-Colley, H., B.A., M.B., B.C., 42, Borough, Pulborough, 
Sussex 

Davy, Henry, M.D., Southernhay House, Exeter 

Dawson, W. J. O., Portarlington, College Place, Southampton 

Day, T. M., Harlow, Essex 

Deane, E., Greenham Villa, Caversham, Reading 

Delbruck, R. E., B.A., M.B., B.C., 18, Buckingham Gate, S.W. 

Denham, N., 29, Albemarle Road, Beckenham, Kent 

Denman, R., Port Victoria, Mahé, Seychelles 

Derriman, W. E., Cerne Abbas, Dorset 

Desprez, Н. S., Shoreham, Sevenoaks 

Dobson, Т. H. B., M.D., Knott End, Windermere 

Dodd, A. H., 49, Church Road, Hove, Brighton 

Dowsett, E. B., 1, Gloucester Street, Portman Square, W. 

Drake, G. H., 35, Old Elvet, Durham 

Drew, Н. W., Eastgate, East Croydon 

Du Boulay, H. H., 2, Royal Terrace, Weymouth 

Du Buisson, E. W., Hereford 

Duffett, H. A., Withy Holt, Sidcup 

Dundee Medical Library, c/o Dr. G. A. Pirie, 48, Tay Strect, 

, Dundee 

Dunn, L. A., M.S., 51, Devonshire Street, W. 

Dupigny, J. Elford, 7, Streatham Hill, S.W. 

Duran, Carlos, and Nunez, Daniel, San José, Costa Rica, Central 
America 

Durham, F., M.B., 52, Brook Street, W. 

Durham, H. Е., М. A., M.B., B. C., Physiological Laboratory, 
Cambridge 


Eager, Reginald, M.D., Northwoods Asylum, Frampton Cotterell, 
near Bristol 

Eason, H. L., M.D., M.S., The College, Guy’s Hospital 

Eastes, George, M.B., 35, Gloucester Terrace, Hyde Park, W. 


xiv. Inst of Subscribers. 


Eastes, G. Leslie, M.B., B.Sc., 62, Queen Anne Street, S.W. 

Eastes, T., M.D., 18, Manor Road, Folkestone 

Eccles, H. D., Kawa Kawa, New Zealand 

Edridge, Ray, Guy's Hospital 

Edwards, C., 104, Shooters Hill Road, Blackheath, S.E. 

Edwards, C. D., B.A., M.B., B.C. Alton Lodge, Woodford 
Green, Essex 

Edwards, F. H., M.D., Camberwell House, Peckham Road, S.E. 

Edwards, O., 34, Etnam Street, Leominster 

Elcum, Lieutenant-Colonel, D., M.D., 92, Gloucester Street, 
Warwick Square, W. 

Elliott, С. C., M.D., B.S., Sea Point, Cape Town, South Africa 

Ellis, G. G., 49, Sandgate Road, Folkestone 

Elphinstone, R., Forest House, Silverstone, Towcester, North- 
amptonshire 

Emms, A. Wilson, J.P., M.D., Belgrave, Leicester 

English, D. C., M.D., Post Office Box 87, New Brunswick, New 
Jersey, U. S. America 

Ensor, C. A., Tisbury, Salisbury 

Evans, Alfred H., Sutton Coldfield, Warwickshire 

Evans, G., M.B., Heath Asylum, Bexley, Kent 

Evans, J. H., Broomfield, Crosby Road North, Waterloo, Liverpool 

Evans, J., M. B., B.S., Shoreditch Infirmary, Hoxton Street, N. 

Evans, J. R., Cartref, ‘Narberth, Pembroke 

Evershed, A. R. F., 49, Knollys Road, Streatham, S.W. 

Every-Clayton, L. Е. V., M.D., B.S., Rosslyn, Clevedon, Somerset 

Evison, F. A., March, Cambridgshire 

Ewart, J. H., Eastney, Devonshire Place, Eastbourne 

Eyre, J. W. H., M.D., M.S., Guy's Hospital 


Fagge, C. H., M.S., 22, St. Thomas's Street, S.E. 

Fagge, R. H., High Street, Melton Mowbray 

Farrant, E., 52, High Street, Wellington, Somerset 

Faulks, E., Heath Asylum, Bexley, Kent 

Fawcett, J., M.D., B.S., 66, Wimpole Street, W. 

Fawsett, F. W., M.B., 228, Fore Street, Upper Edmonton, N. 

Fawsitt, Thomas, 46, Union Street West, Oldham 

Felton, R., M.B., Guy's Hospital 

Fenn, C. D., Park House, Diss, Norfolk 

Field, Ernest, M.D., 8, Belmont, Bath 

Fisher, Theo., M.D., Harley Lodge, Clifton Down, Clifton, Bristol 

Fisher, W. H., M.A., M.B., B.C., Oak Street, Fakenham, 
Norfolk 

Fleury, Captain C. M., R.A.M.C., Station Hospital, Bulford 
Camp, Salisbury Plain, Wilts 

Floyd, S. G., M.D., B.S., Lister House, Grays, Essex 

Forman, E. Baxter, M.D., 11, Bramham Gardens, South Ken- 
sington, S.W, 





List of Subseribers. XV. 


Forsyth, D., M.D., 6, St. Thomas's Street, S.E. 

Fortescue-Brickdale, J. M., M.A., M.D., B.Ch., 52, Pembroke 
Road, Clifton, Bristol 

Forty, D. H., Edbrook, Wotton-under-Edge, Gloucestershire 

Foster, C. M., M.D., 1101, Yonge Street, Toronto, Canada 

Fox, H. ui Croker, M.B., Knole Lodge, Knyveton Road, Bourne- 
mout 

Fox, H. J., 38, Prince of Wales Road, Norwich 

Fox, J. A., Tregea House, Penzance 

Francis, J. S., 2, Cambridge Street, Hyde Park Square, W. 

Fraser, J. A., Western Lodge, Romford, Essex 

Frazer, E. E., M.D., B.S., Helena House, Great Union Road, 
Jerse 

French, Н. S., B.A., М.В., B.Ch., 26, St. Thomas’s Street, S.E. 

Fripp, Sir Alfred, C.B., C.V.O., M.S., 19, Portland Place, W. 

Fry, A. Cradock, B.A., M.B., Priory House, Wellesley Road, 
Colchester 

Fry, J. Farrant, 18, Dane Road, St. Leonard’s-on-Sea 

Fuller, Courtenay J., 88, Nightingale Place, Woolwich 


Gaitskell, Н. A., M.A., M.D., B.C., Shannleigh, Burgess Hill, 
Sussex 

Galabin, A. L., M.A., M.D., 49, Wimpole Street, W. 

Galton, J. H., M.D., Chunam, 14, Sylvan Road, Norwood, S.E. 

Gardiner, J. N., B.A., M.D., B.C., Dunmow, Essex 

Garner, W. L., B.A., M.B., B.C., The Limes, Ampthill, Beds. 

Garrard, W. A., Chatham House, Rotherham, Yorkshire 

Gater, A. W., Black House, West End, Southampton 

Gibson, F. G., M.A., M.D., Papanui Road, St. Abans, Christ- 
church, New Zealand 

Gibson, J. H., 1, Lansdown Road, Cargate, Aldershot 

Gilford, H., 205, King’s Road, Reading 

Gill, J. McD., M.D., 18, College Street, Hyde Park, Sydney, 
New South Wales 

Gillibrand, F. J., M.A., M.B., B.C., 21, Albert Road, Southport 

Gillingham, A., 485, High Road, Chiswick 

Glanville, L. S. H., M.B., Guy's Hospital 

Glenn, C. H., B.A., M.B., B.C., 18, Barclay Road, Croydon 

Glover, J. A., M.B., West Malling, Kent 

Goadby, K. W., 21, New Cavendish Street, Cavendish Square, W. 

Goble, F. G., Guy’s Hospital 


Godson, A. H., B.A., M.B., B.C., 63, Union Street West, Oldham 

Godson, F. A., 7, Station Road, Cheadle Hulme, near Stockport 

Godson, J. H., B.A., M.B., B.C., Bank House, Cheadle, Cheshire 

Golding-Bird, C. H., M.B., 12, Queen Anne Street, Cavendish 
Square, W. 

Goodall, E. W., M.D., Homerton Fever Hospital, N. 


M.D. 
Goodhart, J. F., M.D., 25, Portland Place, W. 


xvi. List of Subscribers. 


Gosse, H. W., Eccleshall, Staffordshire 

Graham, G. H., M.D., 14, Old Cavendish Street, W. 
Granger, E. B., Little Milton, Tetsworth, Oxon 

Greaves, B. H., Amersham, Bucks | 

Green, A., M.B., Burlington Street, Chesterfield, Derbyshire 
Green, A. W., 4, Wardrobe Place, St. Paul’s Churchyard, E.C. 
Greenwood, E. Climson, 19, St. John’s Wood Park, N.W. 
Griffen, W. E., Melville Hall, Ryde, Isle of Wight 

Grove, W. Reginald, B.A., M.B., B.C., St. Ives, Hunts 
Growse, W., B.A., Dudley House, Kenilworth 

Gruggen, W., 7, Grosvenor Road, Watford 

Guy's Hospital Library (Two Copies) 

Guy's Hospital Museum (c/o Curator) 

Gwynn, S. T., M.D., St. Mary's House, Whitchurch, Salop 


Habershon, S. H., M.D., 88, Harley Street, Cavendish Square, W. 

Hall, F. W., M.D., M.S., 18, College Street, Hyde Park, Sydney, 
New South Wales 

Hall, Surgeon R. W. B., H.M.S. Bramble, China Station 

Hamilton, G., Guy's Hospital 

Hammond, J. A. B., M.B., Carlyon, Shanklin, Isle of Wight 

Hancock, W. I., 19, Harley Street, W. 

Handley, W. S., M.D., M.S., 51, Devonshire Street, W. 

Hardenberg, E. F. H., M.B., Duffield House, Upton Road, 
Watford | 

Hardenberg, E. J. F., Annesley, Fairlop Road, Leytonstone, N.E. 

Hardy, G. F., Guy’s Hospital 

Hare, Major E. С., c/o King, Hamilton & Co., Calcutta 

Harnett, C. J., M.D., The Limes, Hawley Street, Margate 

Harries, T. D., Grosvenor House, Aberystwith 

Harris, Е. B., 1, Holy Innocents’ Road, Tottenham Lane, 
Hornsey, N. 

Harris, J., M.D., B.S., 291, Elizabeth Street, Hyde Park, Sydney, 
New South Wales 

Harris, R., M.B., 18, Duke Street, Southport 

Harris, W. J., M.A., M.D., B.C., 37, Bell Street, Shaftesbury 

Harrison, W. W., 115, Ditchling Road, Brighton 

Harsant, J. G., M.D., The Hive, Exeter Road, Bournemouth 

Harsant, W. H., Tower House, Pembroke Road, Clifton, 
Bristol 

Harvey, J. S. S., M.D., 1, Astwood Road, Cromwell Road, South 
Kensington, S.W. 

Hawkins, H., Broxbourne, Herts 

Hayward, John W., Whitstable, Kent 

He F., M.B., B.S., 1, Bouquet Street, Cape Town, South 

rica 
Heatherley, F., M.B., B.S., Endellion, New Ferry, Cheshire 
Henderson, E. E., 12, Kensington Square, S.W. 











List of Subscribers. xvii. 


Henson, W. J., Elmsett Hall, Wedmore, Weston-super-Mare 
Hetley, Henry, M.D., Beaufort House, Church Road, Norwood, 
S.E. 


Hewetson, Captain H., R.A.M.C., Measham Vicarage, Atherstone 

Hickman, H. V., M.B., Overton House, Wanstead, N.E. 

Hicks, H. T., 4, St. Thomas’s Street, S.E. 

Hicks, R. G., 126, High Street, Ramsgate 

. Higgens, C., 52, Brook Street, W. 

Hilbers, H., 49, Montpelier Road, Brighton 

Hillier, H. N., 19, Waterloo Place, Leamington Spa 

Hills, A. Phillips, Carlton House, Prince of Wales Road, Batter- 
sea Park, S.W. 

Hinchliff, C. J., 211, Selhurst Road, South Norwood 

Hind, Wheelton, M.D., Roxeth House, Stoke-on-Trent 

Hindle, F. T., Hill Croft, Askerne, Doncaster 

Hitchins, F. C., St. Austell, Cornwall 

Hogarth, B. W., M.D., B.S., 11, Erving Terrace, Morecambe 

Hogg, R. Bowen, Timaru, Canterbury, New Zealand 

Holloway, S. F., Holmwood, Bedford Park, W. 

Holman, Sir Constantine, M.D., J.P., 26, Gloucester Place, 
Portman Square, W. 

Holman, F. K., M.D., Galeston, Eton Avenue, South Hampstead, 
N.W. 

Holman, H. J., 1, Hardwick Road, Eastbourne 

Holmes, T., M.B., B.S., Guy’s Hospital 

Holmes, T. E., M.A., M.B., B.C., Rosendal, Redland Road, Bristol 

Hood, Donald W. C., C.V.O., M.D., 43, Green Street, Park Lane, 
W 


Hooper, H. P., Linda, Poole Road, Bournemouth 

Hopkins, C. L., B.A., M.B., B.C., Kent County Asylum, Barming 
Heath, Maidstone 

Hopson, M. F., 30, Thurlow Road, Rosslyn Hill, Hampstead, N.W. 

Horrocks, P., M.D., 45, Brook Street, W. ; 

Horsley, H., 60, London Road, Croydon 

Howard, J. A., M.D., 40, Harold Road, Upper Norwood, S.E. 

Howard, R., M.A., M.B., B.Ch., Universities Mission, Lake 
Nyassa, Central Africa 

Howard, Wilfred, New Buckenham, Norfolk 

Howe, J. D., Deepdale House, Burrow Road, Preston 

Howell, J., M.B., B.S., 7, Imperial Square, Cheltenham 

Howell, J. B., 86, North Side, Wandsworth Common, S.W. 

Howell, T. A. I., 18, Upper Richmond Road, Putney, S.W. 

Howse, Sir Henry, M.S., 59, Brook Street, W. 

Hudson, A. B., Vine House, Cobham, Surrey 

Hugill, George F., M.D., 197, High Road, Balham, S.W. 

Hull Medical Society, c/o Dr. J. McNidder, Duncallan House, 
Hull 


VOL. LiX. 2 


švili. List of Subscribers. 


Huntley, E., M.B., B.S., Friar Street, Sudbury, Suffolk 
Hutchinson, F. E., Belgrave, Leicester 


Ince, Lieut.-Colonel John, M.D., Montague House, Swanley, Kent 
Ingram, P. C. P., Guy's Hospital. 
Iredell, C. E., Guy's Hospital 


Jackson, P. J., 216, Great Dover Street, S.E. 
Jackson, T. L., B.A., M.B., B.C., The Beeches, Cheadle, Man- 


chester 
Jackson, T. S., c/o C. E. Burkinyoung, Esq., 54, Carter Lane, 
E.C 


Jacobson, T. B., Sleaford, Lincolnshire 

Jacobson, W. H. A., M.A., M.Ch., Lordine Court, Ewhurst, 
Hawkhurst, Sussex 

Jalland, W. H., D.L., J.P., St. Leonard's House, York 

Jaynes, V. A., 157, Jamaica Road, S.E. 

Jephcott, C., M.A., M.B., B.C., 2, The Northgate, Chester 

Jimenez, R. San José, Costa Rica, Central America 

Jones,.B., M.D., Leigh, Lancashire 

Jones, F. "Felix, Llanfyllin, near Oswestry 

Jones, G. H. West, Southgate, Eckington, Derbyshire 

Jones, H. J., 30, Lillie Road, West Brompton, W. 

Jones, H. Stanley, M.B., The Butts, Brentford 

Jones, J. Edwards, D.L..J.P., M.D., Bryn-y-ffynon, Dolgelly . 
North Wales | 

Jones, Robert, 11, Nelson Street, Liverpool 

Jones, S. H., Hazelwood Lodge, London Road, Enfield 

Jones, W. Makeig, M.D., Beaumont, Torquay 

J oslen, H., St. Ann’s Bay, Jamaica, WAL. 

Judson, Т. В., 44, Mill Lane, West Derby, Liverpool 


Keates, Н. C., M.B., Lieutenant, I. M. S., Peshawur Road, 
Rawal Pindee, Punjab, India 

Keele, S., 8, Highbury Place, N. 

Kelsey, Staff Surgeon A. E., R.N., Parkgate, Reigate, Surrey 

Kemp, G. L., M.D., Worksop, Notts 

Kendall, G., Battle, Sussex 

Kendall, Walter B., Greenheys, King’s Wear, Devon 

Ker, Hugh Richard, Tintern, 2, Balham Hill, S.W. 

Key, M. Aston, B. ‘A, M. B., B.C., 67, Victoria Road North 
Southsea 

Kidd, W. A., M.D., B.S., 12, Montpelier Row, Blackheath, S.E. 

King, T. W., M.D., Purbrook, Dorking 

Kinsey-Morgan, A., M.D., Hilleote, Richmond Hill, Bournemouth - 

Knaggs, R. Lawford, M.A., M.D., M.C., 27, Park Square, Leeds 

Knowles, C. H., Casamajor Road, Egmore, Madras, India 


- Inst of Subscribers. xix. 


Lacey, E. E., c/o Dr. Thomas, I. Petersplatz, 4, Vienna 

Lacey, W. J. M., Clyde House, 6, Ware Road, Hertford 

Lamb, W. H., M.B., 23, Palace Court, Bayswater Hill, W. 

Lambert, A. L., 98, Montpelier Road, Brighton | 

Lancaster, H. F., M.D., 154, Westbourne Terrace W. 

Lancereaux, E., M.D., 44, Rue de la Bienfaisance, Paris 

Lancet, The, 423, Strand, W.C. | 

Landon, E. E. B., Bradbourn House, Acton, W. 

Lane, W. Arbuthnot, M.S., 21, Cavendish Square, W. 

Langdale, H. M., Ulverston House, Uckfield, Sussex 

Lansdale, W., M.D., 44, Trinity Square, S.E. | 

Lansdown, R. G. P., M.D., B.S., 39, Oakfield Road, Clifton, Bristol 

Larkin, F. G., Grove Park, Lee, Kent 

Larking, A. E., M.D., 4, London Street, Folkestone 

Lavers, N., M.D., Mount Zeehan, Canterbury 

Leader, H., M.B., 279, Glossop Road, Sheffield 

Leckie, M., Guy's Hospital | 

Leeds School of Medicine Library (per the Secretary of Yorkshire 
College, Leeds) 

Leeming, A., M.B., Guy's Hospital 

Leigh, W. W., J.P., Treharris, R.S.O., South Wales 

Lidderdale, F. J., M.B., B.C., Grove Hospital, Tooting, S.W. 

Lipscomb, E. H., M.B., St. Alban’s, Herts — 

Lipscomb, E. R. S., Starcross, Exeter 

Lister, T. D., M.D., B.S., 50, Brook Street, W. 

Lloyd, M., M.D., Vale Villa, Llanarthney, R.S.O., Wales 

Lockwood, J. P., Faringdon, Berkshire 

Lockyer, G. E., The Cottage, Amesbury, Wilts. 

Long, D. S., B.A., M.D., B.C., 71, Micklegate, York 

Loosely, W. H., 14, Stratford Place, Oxford Street, W. 

Loud, F., Albion House, Lewes 

Louisson, M. G., M.B., Guy's Hospital 

Love, À. E. B., Richmond Villa, Bournemouth 

Loveday, W. D., Becket House, Wantage, Berks 

Lueas, H., Huntingdon 

Lucas, R. Clement, B.S., 50, Wimpole Street, W. 

Luce, R. H., B.A., M.B., B.C., 42, Friargate, Derby 

Luscombe, T. B., Cromer House, Teddington 


McCarthy, J., McC., M.D., St. George's, Wellington, Salop 

MeGavin, L. H., 6, Mansfield Street, Cavendish Square, W 

MeGill University Medical Library, Montreal, Canada 

MacLehose, Messrs. James & Sons, 61, St. Vincent Street, 
Glasgow, (2 copies) 

MacIlwaine, S. W., 26, Westmoreland Road, Bromley, Kent 

Mackern, George, M.D., Calle Maipu, 445, Buenos Ayres 

Maggs, W. A., 14, Upper Wimpole Street, W. 

Magowan, P. D. F., Guy's Hospital 


хх. | Inst of Subscribers. 


Maisey, C. T. B., The Wilderness, Witham, Essex 

Maisey, F. T., Charlbury, Oxon 

Makepeace, A. J., Hertford Chambers, Hertford Street, Coventry 

Malcolm, J. D., M.B., C.M., 13, Portman Street, Portman 
Square, W. 

Mallam, W. P., 169, Uxbridge Road, Shepherd’s Bush, W. 

Manby, Sir Alan, M.V.O., M.D., East Rudham, Norfolk 

Manley, J. H. H., M.A., M. D., 20, New Street, West Bromwich 

Mann, H. C. C., М. В., Guy’ 8 Hospital 

Manning, Т, Davys, M. B., B.S., Hoddesdon, Herts 

Mansell, E. R., 44, Wellington Square, Hastings 

Manser, F., The Priory, Church Road, Tunbridge Wells 

March, E. G., M.D., 41, Castle Street, Reading | 

Marriott, Hyde, B. Sc., M.B. , The Limes, Hall Street, Stockport 

Marriott, O., c/o Dr. Rennie, Hong Kong, China 

Marshall, R. P., 143, Grange Road, S.E. 

Marshall, W. L. W., Vernon House, New North Road, Hudders- 
field 

Martin, Albert, M.D., Ingestre Street, Wellington, New Zealand 

Martin, F. J. H., Perim, Arabia 

Martin, James P., Slope of the Bank, Box, Wilts 

Mason, W. Inglis, J.P., Sudbury, Suffolk 

Matcham, Alfred, 116, St. George's Road, Southwark, S.E. 

Mathews, H. Dewe, 39, Brook Street, Grosvenor Square, W. 

Maurice, H., 65, St. John’s Terrace, West Brighton 

Mayston, R. W., M.D., 58, Pier Road, Erith 

Meachen, G. N., M.D., B. S., 27, New Cavendish Siteet: W. 

Meek, J. W., M. D., 329, Norwood Road, Herne Hill 

Mesquita, 8. В. de, M.D., B.S., 1, Highbury New Park, N. 

Metcalfe, G. H., Clare, Suffolk 

Meyer, Major C. H. L., M.D., The Ridge, Malabar Hill, Bombay 

Meyrick-Jones, H. M., M. D., B.S., Overbury, Charlton Kings, 
Cheltenham 

Michael, C. E., M.A., M.B., B.C., Trelawne, Crystal Palace Park 
Road, S.E. 

Millbank-Smith, H. J. M., Broadwater Villa, Broadwater Road, 
Worthing 

Milligan, R. A., M.D., Ardmae, Northampton 

Mills, C., P.O. Box 112, Kroonstadt, O.R.C., South Africa 

Milsom, E. H., M.B., B. S., Guy’s Hospital 

Milton, W. T., M.B., M.S., Southernhay, Westmount Road, 
Eltham, Kent 

Moffatt, H. A., B.A., Somerset Hospital, Cape Town 

Moll, О. С. Н. L., Rosemount, Edwards Road, Whitley Bay, 
N orthumberland 

Moore, A. M., Holland Road, Weihai Weymouth 

Moore, W. H., 18, Church Street, Kidderminster 


Inst of Subscribers. xxi. 


Morgan, J., J.P., Mount Hazel, Pontryd-y-Groes, R.S8.O., 
Aberystwith 

Morgan, T., Garnant, R.S.O., Carmarthenshire, S. Wales 

Morice, C. G. F., M.D., Greymouth, New Zealand 

Morres, Е., Guy’s Hospital 

Morse, T. H., 41, All Saints’ Green, Norwich 

Moss, E., M.D., B.S., 6, King Street, Wrexham 

Mothersole, В. D., M.D., M.S., 44, St. George's Terrace, Bolton 

Mugford, S. A., 135, Kennington Park Road, S.E. 

Muir, B., Guy's Hospital 

Mullins, R. С., M.A., M.B., B.Ch, West Hill, Grahamstown, 
Cape Colony, South Africa . 

Munden, C., Ilminster, Somerset 

Munro, D. J., M.B., B.S., 56, Aere Lane, Brixton, S.W. 

Munro, H. A., B.A., M.B., B.Ch., Lulworth, Rushey Green, 
Catford 

Muriel, G. B., B.A., M.B., B.C., 109, Scotch Street, Whitehaven 

Murphy, Sir Shirley, 9, Bentinck Terrace, Regent’s Park, N.W. 

Musgrove, E. H.. 55, High Street, Merthyr Tydvil 

Muspratt, C. D., M.D., B.S., Tantallon, Madeira Road, Bourne- 
mouth 

Mutch, R. 8., M.D., De Montfort House, Streatham, S.W. 


Naish, G., Beechcroft, Normandy Street, Alton, Hants 

Nash, W. G., Welford, Rugby 

Nason, J. J., M.B., Church, House, Stratford-on-Avon 

Neale, B. G., Cromhall, near Falfield, R.S.O., Glosters 

Newland-Pedley. Е., 82, Devonshire Place, W. 

Newnham, W. Н. C., M.B., Chandos Villa, 134, Queen's Road, 
Clifton, Bristol 

Nicholson, J. W., Red Hall, Gainsborough 

Nicholson, T. M., M.A., Elm Tree Lodge, Harehills Lane, Leeds 

Norburn, A. E., M.D., Kidbrooke Lodge, Oldfield Park, Bath 

Norman, A., 35, Coleherne Road, Earl's Court, S.W. 

Northampton General Infirmary Library (per the House Surgeon) 

Norton, E. L., Guy's Hospital 


O'Brien, A. B., Guy's Hospital 

Odgers, P. N. Blake, B.A., M.B., M.Ch., South Devon Hospital, 
Plymouth 

Oddy, A. E., 5, Duchess Street, W. 

Ogle, C. J., 1, Cavendish Place, W. 

Oldham, C. J., 38, Brunswick Square, Brighton 

Oldham, Montagu W., M.D., 56, West Gate, Mansfield 

Oram, R. R. W., Cremyll, Bolingbroke Grove, Wandsworth 
Common, S.W. 

Ormond, A. W., The College, Guy's Hospital 

Osborn, A. G., M.B., Clifton House, Sheet Street, Windsor 


xxii. List of Subscribers. 


Pakes, A. E. H., B.Sc., District Surgeon, Belfast, Transvaal 

Pakes, W. C. C., Government Laboratories, Hospital Street, 
P.O. Box 1080, Johannesburg, South Africa 

. Paliologus, A. L., 14, Beckenbam Road, Beckenham, Kent 

Palmer, A. E., 103, Ashby Road, Loughborough, Leicestershire 

Palmer, J. Irwin, 47, Queen Anne Street, W. 

Palmer, P. H. Hayes, 8, Cumberland Mansions, West Hamp- 
stead, N.W. 

Pantin, C. S., M.D., B.S., 1, Albert Terrace, Douglas, Isle of Man 

Paramore, Richard, M.D., 2, Gordon Square, W.C. 

Parfitt, J. B., Farleigh House, King’s Road, Reading 

Park, W. C. C., 1, Ardgowan Gardens, Hither Green Lane, S.E. 

Parke, C. J., St. Kilda, Breakspears Road, Brockley, S.E. 

Parker, W. G., M.B., Earlsmead, Brentford 

Parry, R., M.B., Ty Newydd, Carnarvon 

Partridge, A. A. H., M.A., M.D., B.Ch., St. Germans, Grove 
Road, Sutton, Surrey 

Paul, Frank T., 38, Rodney Street, Liverpool 

Pavy, F. W., M.D., 35, Grosvenor Street, W. 

Payne, J. Lewin, 44, Devonshire Street, W. 

Peake, W. H., M.D., B.S., 1, Platt’s Lane, Finchley Road, 
Hampstead, N.W. 

Peal, P. A., M.B., Highbury Grove, Highbury, N. 

Pearce, F. J., 59, Queen Anne Street, W. 

Pearse, A. S. J., M.A., M.B., B.C., 110, Cathedral Road, Cardiff 

Pedley, S. E., The Terrace, 18, Peckham Road, Camberwell 

Pegge, Charles, Baglan House Asylum, Britton Ferry, Gla- 
morganshire 

Pembrey, M. S., M.A., M.D., B.Ch., Guy's Hospital 

Pendlebury, J. P., Knowles House, Ormskirk 

Pendred, V., M.D., Greville House, Buckingham 

Penfold, F. W.H., Rainham, Kent 

Pennell, G. H., M.D., English Club, 77, Calle S. Martin, Buenos 
Ayres, Argentina 

Pennington, S. A. B. C. C., Carter House, Argyll Road, West 
Ealing, S.W. 

Penny, E., M.D., The Hermitage, Marlborough 

Percival, G. H., M.B., 66, Abingdon Street, Northampton 

Perkins, H. B., Highfield, Barking, Essex 

Perry, C. E., M.D., 1, Castle Hill Avenue, Folkestone 

Perry, Sir Cooper, M.A., M.D., Superintendent's House, Guy's 
Hospital 

Peters, E. A., B.A., M.D., B.C., 52, Wimpole Street, W. 

Philipps, A. E., 50, Epple Road, Fulham, S.W. 

Phillipps, W. A., M.D., 18, John Street, Berkeley Square, W. 

Phillips, F. B. Willmer, M.A., M.D., B.Sc., 7, Harpur Place, 
Bedford 

Pigeon, H. W., M.A., M.C., 6, Albion Street, Hull 


List of Subscribers. xxiii. 


Piggot, A. P., County Asylum, Newport, Isle of Wight 

Pike, Douglas R., B.A,, M. B., B. Ch., 3, Cromwell Crescent, 
Kensington, S.W. 

Pike, N. H., M.B., Heckmondwikė, Yorks 

Pilkington, F. W., Kencott House, Lechlade, Glos. 

Pillin, H. L., 33, George Street, Hanover Square, W. 

Pinching, Charles J. W., 76, New Road, Gravesend 

Pinching, C. J., B.A., 76, New Road, Gravesend 

Pinder, G., M.D., B.C., 29, Cedar Street, Southport 

Pitt, G. Newton, M.A., M.D., 15, Portland Place, W. 

Plimmer, H. G., 28, St. John’s Wood Road, N.W. 

Plummer, W. E., Wenchow, Shanghai, China 

Poland, John, 2, Mansfield Street, Cavendish Square, W. 

Pollard, C., M.D., 23, Foregate Street, Worcester 

Pollard, G. S., Midsomer Norton, Somerset 

Poole, T. B., M.D., B.S., Campions, Harlow, Essex 

Poolman, A. E., B.A., 10, Weymouth Street, Portland Place, W. 

Portsmouth Medical Library (c/o Dr. F. Lord, 16, Landport 
Terrace, Southsea) 

Prall, S. L., 19, Elgin Mansions, Maida Vale, W. 

Price, A. E., М.р. M.S., Thanet Lodge, Bromley, Kent 

Price, John A. P., M.D., 124, Castle Street, Reading 

Price-Jones, C., M.B., 7, Claremont Road, Surbiton 

Prince, P. C., Egremont, Reigate 

Pryn, Fleet Surgeon W. W., R.N., Royal Hospital, Greenwich, 
S.E. | 


Puzey, Chauncy, 71, Rodney Street, Liverpool 
Pye-Smith, C. D., M.B., Guy’s Hospital | 
Pye-Smith, Р. H., B.A., M.D., 48, Brook Street, W. 
Pye-Smith, R. J., 450, Glossop Road, Sheffield 


Rake, H. V., “ St. Ives," Fordingbridge, Salisbury 

Ramsden, W., M.A., M.D., B.Ch., Pembroke College, Oxford 

Ramskill, Josiah, 29, Meadow Lane, Leeds 

Randall, Philip N., M.B., Aldermary, Rodway Road, Bromley, 
Kent 

Ransford, L. U., Peakville, Anerley Hill, Upper Norwood, S.E. 

Ransford, T. D., 6, Queen's Square, Bath 

Ransford, W. R., Somerville House, Forest Road, West, 
Nottingham 

Rawlings, J. Adams, Bryn Awel, Sketty, Glam. 

Ray, Edward Reynolds, 15a, Upper Brook Street, W. 

Rayson, H. K., M.D., 86, Osmaston Road, Derby 

Recordon, R. B., 1, Duncombe Place, York. 

Reeves, А., 6, Streatham Hill, S. W. 

Reeves, J. K., 66, Upper Tulse Hill, S.W. 

Reid, A., M. B. | B. S., The Cranes, Tooting, S.W. 

Reid, E., 200, St. Helen' s Road, Swansea 


xxiv. . Dist of Subscribers. 


Reinold, A. W., M.A., 9, Vanbrugh Park, Blackheath 

Reinhold, C. J., Clovelly, Park Road, West Dulwich, S.E. 

Rendall, W., Maiden Newton, Dorset 

Reynolds, B. Gore, “ Silverhowe," College Park, N.W. 

Reynolds, W. P., 128, Stamford Hill, N. 

Richards, D. H., Guy's Hospital 

Richards, Owen W., M.A., M.B., B.Ch., 27, Lancaster Gate, W. 

Richardson, T. A., Park House, Coombe Martin 

Richardson, W. S., M.D., "*Melbury," Christchurch Road, 
Bournemouth 

Richmond, B. A., M.B., B.S., B.Sc., 28, Lower Road, Rother- 
hithe, S.E. 

Ricketts, T. F., M.D., B.Sc., Hospital Ships, Long Reach, 
Dartford, Kent | 

Rix, В., 2, Mount Ephraim Road, Tunbridge Wells 

Roberts, Astley C., Badlesmere, Eastbourne 

Roberts, C. Gordon, M.A., M.B., B.C., Halstead, Essex 

Roberts, H. J., Pen-y-groes, North Wales 

Roberts, Н. W., 3, Breakspear’s Road, St. John’s, S.E. 

Roberts, J. Lloyd, B.A., M.D., B.S., B.Sc., 68, Rodney Street, 
Liverpool 

Roberts, R. J., M.A., M.B., B.C., 71, The Neuk, Whitehall 
Park, N. 

Roberts, W. O., County Asylum, Lancaster 

a C. H., M.B., B.S., Longmarket Street, Maritzburg, 
Nata 

Robertson, W. I., M.D., St. Annes, Thurlow Park Road, West 
Dulwich 

Robinson, F. W., M.D., New North Road, Huddersfield 

Robinson, W. E., B.A., M.B., B. Ch., The White House, Sonning, 
Berks. 

Robinson, J. F., Offerton, Beddington, Surrey 

Robson, E. Sheddon, J.P., B.A., 3, North Bailey, Durham 

Rodman, G. Hook, M.D., Sheen Gate House, Sheen Lane, East 
Sheen, S.W. 

Roots, W. H., Canbury House, Kingston-on-Thames 

Roper, A., M.D., Colby, Lewisham Hill, S.E. 

- Routh, C. F., M.D., Purbeck House, Clarence Parade, Southsea 

Rouw, R. Wynne, 7, Wimpole Street, W. 

Rowell, G., 6, Cavendish Place, Cavendish Square, W. 

Rowland, E. W. S., 315, Oxford Road, Reading 

Rowland, F. W., M.D., B.S., 6, Waterloo Place, Brighton 

Rowland, W. J., B.A., M.B., B.S., 5, St. George’s Road, 
Brighton 

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List of Subscribers. | XXV. 


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xxvi. List of Subscribers. 


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List of Subscribers. xxvii. 


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xxviii. Inst of Subscribers. 


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List of Subscribers. xxix. 


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COARCTATION OF THE AORTA 


AS ILLUSTRATED BY CASES FROM THE 
POST-MORTEM RECORDS OF GUYS HOSPITAL 
FROM 1826—1902. 


By JOHN FAWOETT, M.D. 


In the work connected with re-cataloguing the museum I have 
recently met with several specimens of the condition which 
gives the title to this paper, and as the lesion is a rare and 
interesting one I have collected together the cases from our 
records. Some of them, to which reference will be made, have 
already been published in the transactions of various societies 
The rarity of the lesion is evidenced by the fact that there are 
only eighteen cases of coarctation of aorta out of some 22,316 
autopsies performed since 1826. The abstracts of the cases form 
an appendix to the paper. 


Site and form of strictwre.—The site of the lesion is variously 
described in the reports, but coincides with that noted by 
Peacock (') and others, viz., at or near to the point where the 
ductus arteriosus joins the descending aorta. The subjoined 
table gives an analysis of the shape and degree of stenosis as 
detailed in the reports :— 


VOL. LIX. дА 


Coarctation of the Aorta. 













































































To the left side of the left | A well-marked contraction. 





| (No note of.) 


SIZE AND FORM OF CONTRACTION. 





** Very marked." 








Lumen admitted a fine probe 
only. Cone-like. 





— 


Complete occlusion, Cone-like. 


— — ——— —— | ———M ——MÀÀMÀ M А. 


Lumen admitted & fine probe 
only. 








Lumen measures g inch in 
diameter. 

Lumen measures 4 inch in 
diameter or less. 

Admitted No. 8-10 catheter. 
Sudden annular stricture. 

Admitted No. 6-8 catheter. 


“Conical in shape from left 
carotid artery onwards, and 
then became closely con- 
stricted.” 





Lumen admitted an ordinary 
probe. Gradually narrowed 
into a conical shape. 

* Tight narrow band more than 

4 the circumference of the 

vessel.” 








‘“ Narrowing much and con- 
tracting to a probe fissure.” 


Opposite abnormal point of | A ridge-like narrowing. 


meeen ———— а A N € meman 


Lumen less than 4 inch 
diameter. 














— 


SITE. 

CasE 1) Immediately above the ductus 
arteriosus. 

CASE 2 | (Exact position not stated.) 

Case З | Immediately below the ductus 
arteriosus. 

CASE 4| Just beyond left subclavian. 
CasE 5| Lowest branchial arch beyond 
left subclavian. 

CasE 6 | 1 inch below left subclavian. 

CASE 7| At or just before the ductus 
arteriosus. 

Case 8! Just beyond the ductus 
arteriosus. 

Case 9| At site of ductus arteriosus. 

CasE 10 | Opposite or slightly above left 
subclavian. Just above | 
ductus arteriosus. 

CasE 11| (Exact site not stated.) 

CasE 12 CA didge:like: 
origin of right subclavian, | 
which was situated below 
the left subclavian. 

CASE 13 
subclavian. 

CasE 14 | ** Below the pit of the duct." 
? Arteriosus. 

CasE 15 | Immediately to the right of 
the ductus arteriosus. 

CasE 16| Near the former opening of 
the ductus arteriosus. 

Case 17 





clavian. 
— 





CasE 18 | Beyond ductus arteriosus. 


1 inch beyond the left sub- | Sudden annular constriction about 


one line in breadth. 


Decidedly small aorta. 


Coarctation of the Aorta. 3 


It will be seen in the table that in only one case (No. 3) was the 
aorta completely obliterated, while in the others the lumen varied 
from half an inch in diameter to one which would admit the 
passage of a fine probe only. The narrowing is seen to take the 
form either of an abrupt annular constriction, or of a gradual 
diminution in size in the form of a cone. 

The proportion of examples of occlusion is, in this series, much 
smaller than in Peacock’s original collection of cases, among which 
ten out of forty showed complete obliteration of the canal. Lee 
Dickinson and Fenton (*) state that out of one hundred and five 
cases there were fourteen examples of complete occlusion of the 
vessel. | 

Condition of ductus arieriosus.—lt is stated by most writers 
on this subject that the duct is closed in the larger number of 
cases, but the present series does not support that statement. In 
nine out of the eighteen cases this point is not referred to, but 
in six of the remaining nine the duct was found to be open. 

Condition of the heart and its valves, and of the aorta :— 

(i.) Heart.—In twelve cases the heart was enlarged, with a 
general increase in size in seven, viz. (Nos. 2, 9, 10, 11, 12, 16 
and 17). In two cases (Nos. 7 and 15) the left ventricle was 
chiefly affected, and in one case (No. 8) the right ventricle. In 
two others (Nos. 13 and 14) the right side was apparently 
alone involved ; in No. 18, there were several malformations 
present and no doubt the right side of the heart had had most 
of the work to do during life, the left side being small, the aorta 
narrow and its walls small and thin. In No. 14, the details of 
the autopsy are too meagre to allow any conclusion to the drawn 
as to the cause of the enlargement of the right side. 

On reference to the cases it may be seen that in several of 
them the increase in size was considerable, e.g. :— 


Case 2 T x е weight, 23 ounces. 
x 8 es t s j 17 , 
" 10 eee " 18 " 


In three cases (Nos. 3, 5 and 6) there was no marked 
enlargement of the heart, although in Nos. 3 and 6, it was 
probably somewhat larger than normal. ln the remaining three 


4 Coarctation of the Aorta. 


cases the associated congenital malformations and consequent 
early death, are such as to exclude them from consideration. 

From the above analysis it is clear that the block in 
the aorta has led to a dilatation and hypertrophy of the heart 
such as might result from obstruction at the aortic orifice. 
Peacock found the same result, the heart being uniformly and 
considerably enlarged in eighteen out of forty cases, while in 
ten others there was a moderate increase in size affecting chiefly 
the left ventricle. In only two cases of his series is the heart 
stated to have been quite healthy. These results have been 
confirmed by later observers, thus showing that, in a large 
proportion of the cases, coarctation of the aorta does give rise 
to enlargement of the heart. 

(ii.) Valves.—The constant strain to which the aortic valves 
are subjected leads in the majority of cases to a chronic inflam- 
matory change, with the result that the valves become thickened, 
or adherent, or the orifice stenosed. For example, in no less 
than ten cases (Nos. 3,7, 8, 9, 10,11, 12, 14, 15 and 17) were 
the aortic valves affected, and in six of them the mitral valve 
showed a similar change. In only three cases (Nos. 2, 5 and 6) 
were the valves apparently healthy. In one case (No. 16) 
there is no note of the condition of the valves, and in another 
(No. 18) the aortic valves were thin and ill developed, the main 
portion of the work of the heart having been performed by 
the right ventricle. 

The cases (Nos. 1, 4 and 18) are omitted from consideration 
in this connection on account of the many congenital malforma- 
tions which existed. 

(ii.) Aorta.—The aorta on the proximal side of the stricture 
has been described as dilated in most cases, e.g., in 
Peacock’s series, out of the twenty-nine cases in which the 
condition of the vessel is mentioned, it was found to be of natural 
size and free from disease in three only. In the present series 
the aorta was little affected, for in only four of the eighteen 
cases (Nos. 8, 12, 14 and 16) is there any record of a dilatation of 
that vessel. The degree of dilatation, too, can only have been 
slight, for the terms used in describing it in the reports are 


Coarctation of the Aorta. 5 


"full large," ‘little dilated,” ‘dilated to end of arch," and 
'" wide in ascending part," respectively. 

Again, in many of the previously recorded cases the ео оп 
the proximal side is ‘described as being thickened and athero- 
matous, but in the ‘‘Guy’s’’ series this does not appear to 
have been во, in that it was only noted in five cases (Nos. 2, 3 
9, 6 and 10). In cases Nos. 7 and 8, Dr. Goodhart suggested 
that the reason for this part of the aorta being so little damaged 
was that the tension in the vessel was less on account of the 
chronic endocarditis present. In this connection it is interesting 
to note that in Cases Nos. 2, 5 and 6 the valves were healthy, 
while in Nos. 8 and 10 aortic stenosis was present. 

On the distal side of the stricture the aorta has been noticed 
to either rapidly dilate so as to become larger than usual, and 
then to gradually lessen in size again, or to remain small through- 
out. The coats also are sometimes thinner than normal and 
aneurysmal dilatations may be present. In the present series 
there is no mention of a dilatation of the aorta immediately below 
the stricture, but in three cases an aneurysm was present. 

In Case No. 5, death was due to the rupture of a small 
aneurysm on the proximal side of the obstruction. In Case 
No. 7, the aorta is described as having cracked over a patch of 
atheroma below the constriction, and given rise to a dissecting 
aneurysm in an early stage of development. In Case No. 14, 
a larger saccular aneurysm arose from the ascending portion of 
the aorta. 

In Cases Nos. 3, 7, 8, 9, 10, 12 and 18, the descending aorta 
was small, and in Nos. 10 and 13, the description is such as to 
indicate that this portion of the vessel was narrow throughout. 
In only three cases was the wall of the vessel thin, viz., in Nos. 
3 and 8 below the constriction, and in No. 17 above it. There 
is no note as to the size of the aorta in Cases Nos. 2, 5, 6, 
14, 15 and 16. 

As the lumen of the main trunk of the aorta-is more or less 
obstructed in the different cases, so in order to maintain an 
adequate circulation through the body the blood must pass 
through other channels which, as a result, become enlarged. : 


VOL. LIX. 3 


6 Coarctation of the Aorta. 


The anastomotic connections have been shown to be chiefly 
through some of the branches of the subclavian artery with 
branches arising from the aorta below the site of constriction. 
These vessels are the transverse cervical and the posterior scapular 
branches of the thyroid axis; the subscapular, the superior inter- 
costal, the aortic intercostals, the internal mammary and its 
branches, in particular the superior epigastric in its anastomoses 
with the deep epigastric branch of the external iliac artery. 


In this collection of cases the collateral circulation has been 
only imperfectly dealt with, but in Cases Nos. 2, 3, 7, 8, 9, 11, 
13 and 17, the following vessels were found enlarged and in 
some cases tortuous, viz., the large vessels from the arch, the 
scapular, the superior intercostal, the internal mammary and 
the iliac arteries. The anastomoses are well shown in a specimen 
taken from the dissecting room and preserved in the museum; 
it was fully described by Dr. Hale White (°). The subject was 
a man æt. 46 years, thought during life to have heart disease 
only. 

In all the cases of the “ Guy's" series in which the collateral 
circulation was well developed it may be seen (v. Table p. 2) 
that. the constriction was considerable and was associated either 
with enlargement of the heart, or changes in the aortic valves, 
or both. 

Associated malformations.—In eight out of the eighteen cases 
various congenital malformations were present. They were most 
numerous in Cases Nos. 1, 4 and 18, the coarctation of the aorta 
having in consequence no special bearing on the clinical history 
of the cases. 

In Case No. 1, the heart was much enlarged, especially the 
right ventricle, the ductus arteriosus was patent, the septum of 
the ventricles imperfect, and the mitral orifice stenosed. The 
stomach, intestines, pancreas and spleen were transposed and 
the right kidney was situated much lower down than normal. 


In Case No. 4, the foramen ovale and ductus arteriosus were 
patent, the ventricular septum was imperfect, the two carotids 
and the left subclavian arteries arose directly from the aorta, 


Coarctation of the Aorta. 7 


but the right subclavian artery could not be found. There was 
no direct communication between the right auricle and ventricle. 

In Case No. 18, the aorta and pulmonary artery were transposed 
and in addition to other peculiarities, the septum between the 
auricles, ав well as that of the ventricles, was perforated. 

In Case No. 9, the mitral valves were malformed, the muscle 
columns being absent, and at the intermembranous septum a 
pouch projected into the right ventricle. 

In Case No. 10, a miniature additional valve was present in 
the aorta just above the valves. 

In Case No. 12, four vessels arose from the aorta, viz., the 
right and left carotid, the left and right subclavian arteries, 
in the order named from right to left. The right subclavian 
artery arose from the posterior part of the descending portion of 
the arch, crossed the vertebral column behind the cesophagus, 
and so passed onwards to its usual destination. | 

In Case No. 18, the foramen ovale was patent, and posterior 
to it the septum was deficient. The right pulmonary veins 
opened into the right auricle. The aorta was narrow and its 
valves thin. 

In Case No. 15, the anterior portion of the falx cerebri was 
wanting. The left kidney was only half the usual size, while 
the right was twice as large as normal. A large branch from 
the middle of the basilar artery ran into the cavernous sinus. 

The large proportion of associated congenital malformations 
is referred to by many previous writers as a frequent accompani- 
ment oi coarctation of the aorta, and the present series of cases 
fully confirms the statement. 

Age and sex.—Peacock states that the cases are met with most 
frequently during the active period of adult life. This is borne 
out by the ‘‘Guy’s”’ series, for out of the eighteen cases, twelve, 
or 66 per cent., were between the ages of twenty-one and 
fifty years at the time of death. The youngest of the whole 
number was sixteen hours and the oldest sixty-four years. In 
Peacock’s series the relation of males to females was nearly 
four to one, but in the present series they are almost equally 


8 Coarctation of the Aorta. 


divided, viz., nine males to eight females, the sex in one case not 
being stated. 

Clinical features and diagnosis.—This collection of cases may 
be divided up clinically into three groups :— 

1. Those with physical signs indicative of some cardiac 
lesion. 

2. Those without any symptoms of a cardiac lesion, or of 
a lesion cf the circulatory system. 

3. Those who died early and in whom there were many 
congenital malformations present. 

Group 1, contains the cases of most interest from the clinical 
side, and includes Cases Nos. 2, 3, 7, 8, 9, 10 and 16. 

(In Cases Nos. 12, 13, 14 and 15, no clinical history was available; 
but in No. 12, in association with the enlargement of the heart, 
it was noticed at the autopsy that there was oedema of the legs 
and scrotum.) 

In not one of the cases, however, were any physical signs 
detected during life affording a clue to the actual condition which 
existed, e.g.— 

Case No. 2; was thought to be suffering from a chronic 
interstitial nephritis. | 

Case No. 8; the diagnosis was that of mitral stenosis and 
regurgitation, in addition to disease of the aortic valves. 

Case No. 7; the symptoms suggested a renal origin rather 
than a cardiac one. 

Cases Nos. 8, 9 and 16, were apparently in the last stage of 
chronic heart disease. | 

Case No. 10; the bruits heard were not typical of any particular. 
lesion, but Mr. Wilkinson King thought that they indicated the 
presence of a patent ductus arteriosus. 

In Group 2 (including Cases Nos. 5, 6, 11, and 17), death 
ensued from various causes. 

Case No. 5; sudden death from rupture of a small aneurysm 
on the proximal side of the obstruction. 

Case No. 6; death resulted from an epithelioma of the tongue, 
with dysphagia and bronchitis. 


Coarctation of the Aorta. 9 


Case No. 11; death occurred from cerebral hemorrhage. 

Case No. 17; death resulted from acute pericarditis and jaundice 
associated with an impacted gall-stone. | 

In Group 3 (including Cases Nos. 1, 4 and 18), death was the 
result, either directly or indirectly, of the various malformations 
which existed. 

From the above analysis it is seen that some of the cases 
remained latent throughout, while in others the patients were 
thought to be the subjects of a chronic heart lesion. In a few 
recorded instances a correct diagnosis has been arrived at by the 
discovery of enlarged and tortuous vessels on the trunk, in 
particular of the epigastric, the posterior scapular, and internal 
mammary arteries. Thus, although the disease is so rare, yet a 
diagnosis would be quite possible in the presence of a well 
developed collateral circulation. 

. Other signs to which attention has been drawn by previous 
observers are: 

(i) Purring sensation felt in the varicose vessels; a bruit 
heard over them. | 

(ii.) The pulse in the abdominal aorta or in the lower extrem- 
ities, may be feeble, slow, or delayed. | 

(ш.) Special cardiac murmurs, e.g., a systolic bruit on the left 
side behind, in the region of the fourth dorsal vertebra, and 
transmitted downwards between it and the left scapula. 

(iv.) Dilatation of the arch of the aorta, which may be felt in 
the suprasternal notcb. 

Ajtiology.—In that the stenosis or obliteration of the aorta in 
these cases is always situated at or about the same place, and 
that the coats of the aorta are not necessarily diseased, previous 
writers have, for the most part, regarded the lesion as due to a 
developmental defect. Peacock is of this opinion and points to 
the large proportion of associated congenital malformations 
which he says, ‘‘ would scarcely be met with in an equal number 
of cases of any form of accidental disease.” This latter point is 
well exemplified in the present series (vide Associated Malform- 
ations). 


10 Coarctation of the Aorta. 


The actual method of production is somewhat doubtful, but 
the most commonly accepted explanation is, that it is due to the 
defective development of the portions of the branchial arches 
which go to form the aorta, between the left subclavian artery 
and the ductus arteriosus, this part of the vessel not expanding 
and developing in the usual way. | 

In the cases in which the ductus arteriosus remains patent the 
narrowing of the aorta must have been sufficient at birth to pro- 
duce some obstruction to the blood-flow into the descending aorta, 
and so some of it reached that vessel through the ductus arteriosus. 
In those cases in which the ductus arteriosus is closed, the 
obstruction of the aorta at birth cannot have been very great, 
but what probably happens in these cases is that the affected 
portion of the vessel does not expand with the growth of the 
body generally, and so an obstruction is gradually produced. 
This latter process, as Peacock observes, is very favourable to the 
development of a well-marked collateral circulation, and when 
this is complete the aortic constriction will be no longer kept 
expanded by the blood passing through it, but will contract 
and may ultimately result in a complete occlusion of the aorta at 
the narrowed part. | 

The other theories that have been put forward are :— 

(i.) That the obstruction of the vessel is due to organisation 
of a thrombus formed during the closure of the ductus 
arteriosus, the process spreading on to the aorta. 

(i) That the stenosis is the result of an extension of the 
process, by means of which the ductus arteriosus is 
closed, into the aorta. 

Peacock points out that in relation to theory (i.), the process 
of obliteration of the duct does not depend upon closure by a 
thrombus, but by a gradual thickening and contraction of its 
coats, commencing at the aortic extremity. With regard to 
theory (ii. he also says that the explanation suggested is 
insufficient to account for those cases in which the ductus 
arteriosus remains patent, and also that it would not coincide 
with the path of closure of the ducts which commences at its 
aortic and not at its pulmonary extremity. 


Coarctation of the Aorta. 11 


In the Cases Nos. 7 and 8, Dr. Goodhart (*) suggests that 
the coarctation is the result of a chronic inflammatory change 
connected with the closure of the ductus arteriosus. The ductus 
arteriosus was very thick in both of these cases, and in the second 
case there was a considerable amount of fibrous tissue around it. 
In most of the cases recorded there is, however, little or no 
evidence of inflammatory change, and it would appear possible 
that the thickening noted in these two cases may have been the 
result of a somewhat excessive proliferation of the tissues of 
the vessel wall during the process of closure of the duct, or 
during the progressive narrowing of the aorta, following the 
establishment of the collateral circulation. 


REFERENCES. 


1. Peacock, British and Foreign Medico-Chirurgical Review, vol. xxv.» 
1860, p. 467. 

. Lee Dickinson and Fenton, Lancet, October 27th, 1900. 

. Hale White, W., Trans. Patholog. Soc., vol. xxxvi., 1885. 

. Goodhart, J. F., Trans. Patholog. Soc., vol. xxvi., 1875. 

. Wilks, S., Trans. Patholog. Soc., vol. x., 1859. 

. Babington, W., Trans. Patholog. Soc., vol. i., 1847. 

. Quincke, Diseases of Arteries, Ziemssen’s Cyclopedia, vol. vi., p. 473. 


“Im Ct i» бо b 


12 ` Appendix of Cases. 


APPENDIX OF CASES. 


In each case the reference in brackets at the head of the 
report applies to the post-mortem records of Guy's Hospital. 


In abstracting the cases, the words used by the reporter in 
describing the cases have, as far as possible, been adhered to, 
even though many of the terms are not now in use. 


Case 1 (see Insp., 1901, No. 375).—Grace S., et. 5 months, was admitted 
under Dr. Hale White for cough and difficulty in breathing of six weeks' 
duration. The child had previously suffered from  measles, bronchitis, 
diarrhoea and vomiting. On admission, respiration was very rapid, and 
there were signs of a general bronchitis. A systolic bruit was heard in the 
pulmonary area. There was no cyanosis nor anasarca. Autopsy: The heart 
was enlarged. The ventricles were hypertrophied, especially the right. Dr. 
Bryant states that the heart was quite double the size of that of a seven 
months’ child he had examined the same afternoon. A very marked coarcta- 
tion of the aorta was present, immediately above the point of junction of the 
ductus arteriosus. The ductus arteriosus was patent. There was a com- 
munication between the two ventricles, both at the upper and the lower 
part of the septum. The mitral valve was thickened and stenosed, and the 
chorde tendinee also thickened. The left auricle was hypertrophied, and 
the right auricle very large. The aortic and pulmonary valves were healthy. 
The stomach, intestines, pancreas and spleen were transposed, the spleen 
being situated beneath the right lobe of the liver. The right kidney was much 
lower than normal, being on & level with the prominence of the sacrum. 
There was a diffuse broncho-pneumonia with collapse distributed over the 
posterior third of both lower lobes. 


CasE 2 (see Insp., 1899, No. 142).— Thomas M., set. 45, was admitted under 
Dr. Pye-Smith for dyspncea and cedema of the lower extremities. He was 
said to have had ‘‘rheumatic gout’’ seven years before, which confined him to 
bed for two months. He, however, recovered from this except for & slight cough 
and palpitation. In October, 1897, he is stated to have been treated by a 
doctor for an enlarged heart, and in October, 1898, he was admitted into Guy’s 
Hospital with effusion into the right pleura. The arteries were caltareous, the 
left ven'ricle was hypertrophied. After returning to work in January, 1899, 
the ‘‘heart’’ symptoms became more marked, and were associated with 
palpitation, and cedema of the legs. There was a history of venereal disease. 
On admission, he was orthopneic, the pulse-rate could not be counted, and 
there was an apical systolic bruit. The patient died quite suddenly while 
sitting in front of the fire. Autopsy: The heart weighed 23 ounces. The 
auricles were dilated and the ventricles both dilated and hypertrophied. The 


Appendix of Cases. 13 


aortic valves were competent, but their edges, perhaps, were a little 
thickened. All the other valves were healthy. The pulmonary artery was 
large and its wall hypertrophied. Aorta: The ascending portion of the arch 
was atheromatous, large, hard, calcareous plates being present. There was 
а very marked narrowing of the aorta, so as only to just admit a fine probe. 
(There is no note as to the exact position of the construction nor as to whether 
the ductus arteriosus was patent or not.) Enlargement, atheroma and tor- 
tuosity of the scapular arteries was present, the vessels being as big as & 
normal radial. The spleen was small—24 ounces. The kidneys contained 
some infarcts. The liver, which was ‘‘ nutmegged,'"' showed some slight scarring 
and puckering on its upper surface. The pleure were thickened and adhesions 
were present. The lungs were cadematous and part of the right lung was 
carnified. The branches of the pulmonary artery were thickened, dilated 
and atheromatous. 


. CASE 3 (see Insp., 1899, No. 441).—Eliza S., æt. circa 45, was admitted 
under Dr. Horrocks for pregnancy associated with heart disease. She had 
born eight live children, the last confinement having taken place a year 
previously. On admission, the patient was very dyspnoeic, and had bronchitis 
and albuminuria. The physical signs were thought to indicate disease 
of both the aortic &nd mitral valves. The day following admission labour was 
induced as the patient's condition was critical. She did not improve after 
this, but during the next fortnight the cedema of the lega increased, and she 
lapsed into & semi-comatose condition, with twitchings of the hands and face 
and incontinence of urine and feces. Autopsy: The heart was very little, if 
any, larger than normal. The aortic valves were thickened and irregular, &nd 
the orifice stenosed, two of the valves having coalesced. The neighbouring 
portion of the aorta was atheromatous. Attached to the ventricular aspect of 
one of the cusps was an organised pyramidal-shaped mass of fibrin 2:25 centi- 
metres in length. All the other valves were normal. The aorta was com- 
pletely occluded immediately below the point of junction of the ductus 
arteriosus with the aorta. Above the occlusion the left subclavian and common 
carotid were seen to be dilated, and as large as the innominate artery, the 
subclavian artery being the largest of them all. From the origin of the left 
subclavian the aorta gradually contracted, being conical in shape, down to the 
occluded part. Below this the thoracic aorta was diminished in size by about 
one half, the abdominal aorta was still smaller, and the coats, although thin, 
were healthy in appearance. The ductus arteriosus was patent The lungs 
were indurated, the liver was ‘‘ nutmegged,’’.the spleen firm, and the kidneys 
tough and congested. 





‚ CASE 4 (see Insp., 1893, No. 100).—A female child, æt. 16 hours, admitted 
under Mr. Davies-Colley, with a ventral hernia, which contained a large part 
of the small intestine. The sac was opened, the intestine returned and the 
opening closed with sutures. The child became cyanosed and convulsed, and 
died the same evening. Autopsy: Tho heart was broader than normal, the 
right side being thicker than the left. The right ventricle was small, 
the left auricle very large, at least six times the volume of the right. The 
foramen ovale was patent. There was no direct communication between the 
right auricle and ventricle. The septum ventriculorum was imperfect, and the 
left ventricle was small and contracted. The pulmonary and mitral valves 


14 Appendix of Cases. 


were rather thickened, and minute vegetations were present upon them. 
The aorta arose as usual by а large trunk from which sprung the two 
carotid arteries and the left subclavian artery, but Dr. Pitt, who made the 
autopsy, was unable to find the right subclavian artery. Just beyond the 
origin of the left subclavian artery the vessel was contracted so as only to 
admit a fine probe, and beyond this again the aorta was dilated. 


CasE 5 (see Insp., 1886, No. 75).—Emily M., et. 41, was admitted under 
Dr. Pavy for pain in the back between the scapule. The heart and lung sounds 
were normal. Shortly after admission the house-physician was called to see 
the patient and found her in a collapsed and pulseless condition. She died 
two hours later. She was a book-felder, and the report states that there was 
some reason to suspect a toper. Autopsy: Опе and a quarter pints of blood 
were found in the left pleura; the whole mediastinum was infiltrated with 
blood together with the connective tissue at the root of the neck and base of 
the heart. One ounce, or more, of liquid blood was present in the pericardium. 
Dr. Goodhart, who made the post-mortem examination, states that ‘‘ the 
aorta was rather atheromatous, especially about the distal half of the trans- 
verse arch, and the situation of the lowest branchial arch, beyond the left 
subclavian was obviously more than usually contracted. It did not approach 
any extreme degree of coarctation, being three-eights of an inch in diameter, 
and it could not have caused any obstruction for the heart only weighed six 
ounces. Nor was the aorta at all dilated.” The valves were healthy. About 
half an inch on the proximal side of the contraction, below and to the left of 
the left subclavian artery there was а round opening, which Dr. Goodhart 
thought was most probably a small aneurysm of the aorta, and that this had 
ruptured and formed a dissecting aneurysm tearing across the thoracic inter- 
costals and oesophageal branches in its course. From this opening as far as 
the coeliac axis the blood had dissected downwards, apparently in the external 
coat, but in some places the wall between the proper channel and the new 
one was so thin that it was almost through again into the normal channel. 
The abdominal aorta was extensively diseased, as were also the coronary 
arteries of the heart and the iliac arteries. The celiac axis and other 
abdominal vessels were all thick and soft, also the arteries of the neck. 


CASE 6 (see Insp., 1885, No. 201).—Geo. Y., æt. 64, was admitted under 
Dr. Pye-Smith for an epithelioma of the tongue involving the larynx. He 
had had dysphagia for three months. On admission, he was dyspneeic, and 
respiration was of a wheezy character. Death ensued shortly afterwards, 
being preceded by delirium at night. There is no record of any cardiac 
lesion, nor of the patient having suffered from any symptoms indicative of heart 
disease. Autopsy: The heart weighed 11 ounces and was normal. In the 
descending portion of the aorta, an inch from the left subclavian artery, the 
vessel was stenosed, measuring at this point half an inch in diameter or 
rather less. The three trunks from the arch were atheromatous, and in the 
abdominal aorta there was a similar degeneration, with calcareous deposits. 
The cerebral arteries were thickened and the main branches of the abdominal 
aorta showed atheromatous degeneration. The lungs were very emphysema- 
tous, the tubes dilated, and the branches of the pulmonary artery thickened. 
The pleura was thickened, and there were secondary deposits of growth on 
this membrane as well as in the bronchial and cervical glands and in the liver. 


Appendix of Cases. 15 


CasE 7 (see Insp., 1875, No. 87, and Trans. Pathological Soc., vol. xxvi., 
1875).—James M., æt. 27, was admitted under Dr. Wilks for dropsy and 
deficient respiratory murmur at the base of the right lung. His occupation 
had been that of & carpenter. Nine weeks previously his face and eyelids 
had become swollen, and his urine scanty and black. The cardiac impulse 
was situated an inch outside and below the nipple. A loud apical systolic 
bruit was audible, traceable towards the axilla and up into the 
aortic area, and described as post-diastolic in rhythm. After admission it 
disappeared from the front of the chest. There was one-third of albumen 
present in the urine. Death was gradual, being due to exhaustion associated 
with a restless delirium. Autopsy: There was moderate cedema of the legs 
and much ascites. The right pleura was full of fluid, and the left contained 
some fluid, as well as recent lymph on the surface. The heart weighed 
fourteen and a half ounces, the left ventricle being extremely hypertrophied. 
Its cavity contained a small amount of ante-mortem coagulum. The mitral 
valve was thick and rather small, with recent vegetations on the auricular 
surface. The two anterior cusps of the aortic valve were adherent, and from 
the angle of adhesion sprang a tough fibrinous mass the size of a pea. The 
posterior cusp was somewhat thickened. The aorta above the constriction 
was rather thick and of full calibre, though not remarkably dilated. At the 
point of junction of the ductus arteriosus the vessel was suddenly constricted 
as if & cord had been tied round it, the lumen of this portion being the 
size of a No. 8 or 10 gum elastic catheter. Below the constriction the vessel 
had cracked over an atheromatous patch about two-thirds of an inch in length. 
The breach of surface was situated at the closed end of the ductus arteriosus, 
and an early dissecting aneurysm had formed between it and the left branch 
of the pulmonary artery. The branches of the thyroid axis were all large, 
especially the superior intercostal. The internal mammary was also large, 
and the anastomoses between the epigastric arteries were well marked and the 
vessels tortuous. The ductus arteriosus was closed. There was a chronic 
tubal nephritis present, and infarctions of the spleen. 


CasE 8 (see Insp., 1875, No. 122, and Trans. Pathological Soc., vol. xxvi., 
1875).—William McH., et. 37, was admitted under Dr. Wilks. About six or 
seven years before he had had an attack of bronchitis lasting six or seven 
weeks. Three years ago he had had gonorrhea and a swollen testicle. At 
Christmas, 1874, he became ill, with increasing weakness, and from the first 
some swelling of the abdomen. There was a month’s history of swelling of 
the legs and face. Ten days before admission he developed a right hemi- 
plegia. On admission, there was slight swelling of both ankles and the legs 
and chest were cedematous; the face was yellowish and the capillaries on the 
cheeks congested. There was some paresis of the tongue on the right side 
and a sensation of numbness. The chest was narrow and there was cdema 
of the bases of the lungs. The area of precordial dulness was large; the 
cardiac impulse was situated two inches below and half an inch external to 
the nipple. Heart's action irregular and quick, and sounds muffled. An 
apical systolic bruit was heard and а doubtful pericardial rub. The liver and 
spleen were enlarged. The urine contained about three-quarters albumen. 
The patient had some hemoptysis, the quantity of albumen in the urine 
increased, and he sank delirious. Autopsy: The heart weighed about seven- 
teen ounces. It was much hypertrophied, especially the right side. The left 


16 Р Appendix of Cases. 


ventricle was also thick, but not to anything like the extent of the right side, 
but its cavity was considerably dilated. The endocardium was throughout 
white and thick. The edges of the aortic valves were thickened so as to cause 
much incompetence, and the mitral valve was thick and rather small, only 
admitting two fingers. The aorta began to contract opposite the left carotid 
artery, and then narrowed. Just beyond the closed orifice of the ductus 
arteriosus it was closely constricted as by a cord, and the lumen of the vessel 
would only allow of a No. 6 or 8 gum elastic catheter being passed through it. 
Beyond this the artery again dilated to its full size, though towards the end 
of the thoracic aorta it was diminished. The abdominal aorta and the iliac 
arteries were also rather small. The ascending aorta was ‘full large,” but 
healthy. Beyond the constriction the coats of the vessel were thin and on 
the concave aspect white and cicatricial looking. The great vessels were all 
thick and large. The superior intercostal and internal mammary arteries 
were about twice the normal size, the former being especially tortuous. The 
epigastric arteries were not particularly large. The ductus arteriosus was 
closed, and there was a good deal of fibrous tissue around it. The liver was 
nutmegged, and the kidneys congested and tough. 


CasE 9 (see Insp., 1858, No. 161, and Trans. Pathological Soc., vol. x., 
1859).—James D., æt. 22, was admitted under Dr. Rees. He had had good 
health until puberty but after that time was only able to do light work at the 
docks. Later on he joined tbe militia but had to leave the service as the 
work was too severe for him. He then again went to the docks and continued 
at his work until two weeks before admission to the hospital and six weeks 
before his death. On admission, he was very dyspneic and the legs were 
cedematous. The heart was enlarged, ani its action tumultuous. No bruit 
was heard. He was thought to be suffering from cardiac disease, although 
its nature was not very clear, but it was said to be more like disease of the 
arch of the aorta. These symptoms increased until death. Autopsy: The 
heart was much enlarged but its normal shape maintained, the hypertrophy 
of the right side being proportional to that of the left. Two of the aortic 
valves had coalesced. The mitral curtains and cords were malformed. The 
right papillary muscle was scarcely present and the cords spread out. On 
the left side the muscle column was wanting. At the intermembranous 
septum a pouch projected into the right ventricle. The arch of the aorta 
was of the usual size but then gradually narrowed, having a conical shape. 
Immediately beneath the left subclavian artery the aorta became constricted, 
so as only to allow the passage of an ordinary probe, the opening being 
rounded and having slightly projecting edges. Below this the aorta was 
rather small and its wall thinner than usual, and the iliac arteries also, but 
after receiving the epigastric branches they became suddenly larger. The 
large trunks from the arch were all larger than normal, and the vessels from 
the subclavian much increased in size. The thoracic vessels, the superior 
intercostal, and the intercostal arteries lower down were all much enlarged. 





CASE 10 (see Trans. Pathological Soc., vol. i., 1847).—The patient, a female, 
æt. 34, was admitted in January, 1847, under Dr. Barlow. She was of 
phlegmatic temperament and stunted development. The face was pale, puffy, 
and abundantly streaked with capillary veins. Аб six or seven years of age 
she had suffered from palpitation, shortness of breath, occasional sickness 


Appendix of Cases. 17 


and swelling of the legs and ankles. She was subjected to cough and 
expectorated a good deal, the sputa being occasionally streaked with blood. 
At fourteen years of age the patient went to live in the country, and after 
that remained in apparently good health until twenty years of age, when the 
previous symptoms recurred. In 1846 the patient was in Guy’s under Dr. 
Addison for the same symptoms and went out in three weeks relieved, but 
since her discharge she had gradually become worse again. On admission, 
the symptoms present were of the same nature as those above-mentioned. 
The chest was narrow and very prominent. There was cedema of the legs 
and ankles. The heart’s action was forcible and irregular. Two loud 
“sawing” murmurs were audible over the precordial area, most marked over 
the third and fourth sterno-costal articulation on either side. The patient 
became gradually weaker and died three months after admission. She was 
said to have been a seven months’ child. Mr. Wilkinson King had diagnosed 
the presence of a patent ductus arteriosus. Autopsy : The heart was enlarged 
and, with the blood-vessels attached to it, weighed eighteen ounces. Both 
ventricles were dilated and the walls thickened. The aortic orifice was 
stenosed measuring two and six-tenths inches. Large, bony and cretaceous 
vegetations, the size ofa filbert nut, were attached to one of the anterior 
aortic cusps, and there was an aneurysmal bulging of this valve. The 
adjacent cusps were perforated, and there were fibrinous vegetations on one 
of them, and also a few small vegetations on the mitral valve. Within the 
aorta, a quarter of an inch above the valves a miniature fourth valve was 
present. The aorta was narrow throughout, and there was much atheroma 
everywhere. Immediately opposite, or perhaps slightly above, the origin of 
the left subclavian artery there was a tight narrow band, more than one- 
third the circumference of the vessel, very much narrowing its calibre. 
Immediately beyond this band was a circular opening, the remains of the 
ductus arteriosus, surrounded by small vegetations, leading into the pul- 
monary artery. 


Case 11 (see Insp., vol. 34, p. 7).—Martha W., et. 17, was admitted in 
1845 under Dr. Babington. The history of the case states that about three 
weeks before her death she had fainted in chapel, and during the day retched 
several times. The retching continued for some days, and was associated 
with vomiting and pain in the head. Later she passed into a dejected condi- 
tion and remained speechless until her death, which took place about half an 
hour after a fainting fit accompanied by vomiting, similar to that above 
described. She was much emaciated. Autopsy: The report states that the 
heart was ‘‘ almost а man's," the left valves being **coarse." The arch of the 
aorta was ‘‘smallish and strong, narrowing much and contracting to a probe 
fissure, then at once fairly dilating." The ductus arteriosus admitted a 
bristle. The mammary epigastric and first intercostal arteries were very 
large and thin. Some blood was extravasated over the anterior half of the 
brain, with a layer of clot below. There was a hemorrhage in the anterior 
end of each hemisphere, the right, the size of a walnut, the left, the larger, 
had ruptured into the ventricle. 


CASE 12 (see Insp., vol. 35, р. 12).— William T., æt. 26, was admitted in 
1847 under Dr. Rees. There is no clinical account of the case in the post- 
mortem records. Autopsy: The pericardium was adherent everywhere, but. 


18 Appendix of Cases. 


although the adhesions were of old standing, yet they were easily broken 
down with the finger. The heart was hypertrophied and dilated. The aortic 
valves were opaque, thick, and the edges rounded and fissured. ‘Che mitral 
valve was very thick, the edges being rounded, and the chorde tendines 
enlarged, opaque and rigid. The tricuspid valve was thicker and more opaque 
than usual. Four vessels arose from the aortic arch, viz. (1), the right carotid ; 
(2) the left carotid; (3) the left subclavian; (4) the right subclavian, which 
after coming off from the posterior portion of the descending part of the arch 
crossed the vertebral column behind the cesophagus and trachea, and so on 
to its destination. At the point of origin of the right subclavian artery 
the aorta presented internally a ridge, and was also slightly contracted. 
The arch of the aorta was a little dilated, but below the ridge it appeared of 
smaller diameter than usual. There was cedema of the lower extremities 
and scrotum, and blood-tinged serum in the abdominal cavity. 


CASE 13 (see Insp., vol. 33, р. 16).—A woman, whose age is not stated, 
was admitted in 1844. There is no clinical history of the case. Autopsy: 
** The extremities of both hands and feet were of a leaden hue, suggesting the 
blue disease." The skeleton was deformed and the spine slightly curved. 
The heart occupied a median position in the chest, the right side, which was 
exceedingly dilated and hypertrophied, forming the apex and extending about 
an inch beyond the left ventricle. The left side of the heart was small. 
Two vene cave entered as usual the right auricle, and also all the right 
pulmonary veins. The foramen ovale was patent, and posterior to it the 
septum was deficient over an area the size of half-a-crown. The aorta was 
narrow, &nd its valves small and thin. A well-marked contraction was 
present to the left side of the left subclavian artery, and below that the aorta 
was again somewhat increased in size, but still unusually small and gradually 
diminishing down to the common iliac arteries. There was some atheroma 
in places. Neither the internal mammary nor intercostal arteries presented 
any obvious enlargement. The pulmonary artery, its aperture and branches 
were enormously dilated. 


Case 14 (see Insp., vol. 32, p. 45).—Eliza W., et. 40, was admitted in 1842 
under Mr. Cooper. Thére is no clinical history of the case in the post-mortem 
report. Autopsy: A saccular aneurysm, the size of a small adult heart, was 
found springing from the ascending aorta on the right side. It had caused 
some erosion of the ribs. The aorta was dilated to the end of the arch, where 
there was ‘‘a slight narrowing beyond the pit of the duct, a partial thickish 
ridge." Just beyond there was a dilatation. The aortic valves were a little 
contracted, the right ventricle was rather large and thick, and the pulmonary 
artery large. 


CasE 15 (see Insp., vol. 31, p. 111).— Stephen $., st. 21, was admitted 
in 1841 under Dr. Addison. There is no clinical history of the case in the 
post-mortem report. Autopsy: The left auricle is described as being wider 
than the right and “ thick and opaque within.” The left ventricle was ‘‘ very 
large and thick," and the mitral valve a little opaque. The aortic orifice 
presented only two valves and was wide. The ductus arteriosus was patent 
and wider than a goose quill, and immediately to the right of it the aorta 
was contracted to less than half an inch in diameter. Just beyond this on 


Appendix of Cases. 19 


the convexity was an incipient aneurysm, a circular patch as large as a penny, 
of inflammatory softening and yielding of all the coats. The anterior part of 
the falx cerebri was deficient. A large artery ran from the middle of the 
basilar artery into the right cavernous sinus. 


CASE 16 (see Insp., vol. 19, р. 78).—John B., æt. 33, was admitted in 1834 
under Dr. Back. He was & big stout man, and was said to have been ill 
about three months. The history of his case states that he came into the 
hospital with manifest over-action of the heart and serious symptoms of chest 
obstruction. The bruit de scie was extreme. The patient quickly sank and 
died in a comatose condition. Autopsy: The legs were slightly cedematous. 
The heart was quite twice the natural size, all its cavities seeming equally 
affected, being dilated and hypertrophied. The pulmonary artery was very 
wide. АП the valves were probably incompetent from widening of the cavities. 
The aorta was wide in its ascending portion, and there was a slight constric- 
tion near the former opening of the ductus arteriosus. (No further particulars 
are recorded in the post-mortem report.) 

CasE 17 (see Insp., vol. 18, p. 19).—James H., æt. 38, was admitted in 
1834 under Mr. Key, suffering from jaundice due to an impacted gall-stone. 
Autopsy: The body was that of a moderately fat man and was slightly 
jaundiced. The heart was of good size, the left ventricle being somewhat 
hypertrophied. The mitral and aortic valves were thickened. There was a 
sudden annular constriction of the aorta of little more than a line in breadth, 
and situated about one inch beyond the left subclavian artery. The contracted 
orifice would not admit the little finger; it was somewhat indurated, and 
external to it were some large and indurated glands. The aorta was narrow 
and thin above the constriction, and below thickened and atheromatous. The 
abdominal aorta and the iliac arteries were of natural size; the intercostal 
arteries were large. 


Case 18 (see Insp., vol. 15, p. 1, and Drawing 41 (12), also Monthly Journal 
of Medical Science, 1844, vol. iv., p. 32).— The description of the specimen 
was written in 1839 by Mr. Wilkinson King. It came from a child et. 249, 
years, who was said to have always been thin and to have never been able to 
walk. The child died suddenly. Description of specimen: The aorta and 
pulmonary artery were transposed, and the septum of auricles and ventricles 
perforated. The right auricle was dilated and hypertrophied, and the fossa ' 
ovalis large and cribriform, having apertures in it the size of a common black 
lead pencil. The right ventricle was large and strong. The left auricle was 
of moderate size and received only two veins. The left ventricle was small. 
The ductus arteriosus was closed, but beyond this the aorta appeared decidedly 
smallish. 


TRAUMATIC SUBDURAL 
HAEMORRHAGE. 


AN ATTEMPT AT A SYSTEMATIC STUDY 
BASED ON THE EXAMINATION OF SEVENTY- 
TWO COLLECTED CASES. 


By W. Н. BOWEN, M.S. 


© Cee Ce 


My attention was first directed to the subject of extravasation 
of blood beneath the dura mater in the latter part of tbe year 
1902, when as house-surgeon to Mr. C. J. Symonds, I worked 
under thàt surgeon, and .had the care of his beds in his absence. 
The case which I shall give in full below, was admitted soon 
after I first took on the appointment of house-surgeon, and it 
was whilst endeavouring to find out some description of the 
signs, symptoms, etc., of the condition, that I discovered how 
httle systematic study of the subject had been made. Unable 
at that time to go further into the matter, I left the subject, 
but towards the latter half of the year 1908, having time to spare, 
I thought it could be spent at least profitably in looking up the 
literature on the subject. Mr. Jacobson's well-known paper on 
Middle Meningeal Hemorrhage, has put cerebral compression 
by blood-clot in almost all its aspects, whilst the numerous 
papers and lectures on injuries to the brain and skull have made 
a heterogeneous collection of cases unnecessary. The following 
are therefore a few points in favour of considering the form of 
head injury about which I write. In the first place, I may 


VOL. LIX. 4 


29 Traumatic Subdural Hemorrhage. 


say that in the English language I could find no systematic 
consideration of compression of the brain by blood which is 
situated beneath the dura mater and yet is not intracerebral, and 
even in the few cases in which reference is made to the subject, 
and conclusions drawn, especially with regard to symptoms and 
diagnosis, these conclusions, having been based upon but a few 
cases (one case alone being usually given), are, if not erroneous, 
at least unreliable. Again, a systematic study of the subject, 
based on a large number of cases, has brought into prominence 
one or two points which are scarcely recognised, and certainly 
not emphasised in text-books, one being the very long lucid 
interval which may be present, another that consciousness may 
never be lost, and a third, into which I shall go more fully when 
dealing with treatment, that the blood may be mixed with a 
watery fluid which is either serum or cerebro-spinal fluid. As 
an additional reason for this paper, I may say that the detailed 
study of the signs and symptoms in a large number of cases of 
traumatic cerebral compression, in the way that I have arranged 
them in this paper, has seldom been made; whilst the fre- 
quency with which the diagnosis has been an open question or 
wrong, would seem to show that the subject is ore that would 
repay investigation. 

I am greatly indebted to Mr. Symonds for permission to 
report the following case. It was the study of this case which 
first aroused my interest in the subject, and led to those 
investigations with which this paper deals. The report is a 
copy of notes I made at the time :— 

“J. J., is a man said to be 40 years of age, but looking older, 
а seaman and a Swede, but speaking English well. On October 
10th, 1902, whilst working in the Surrey Commercial Docks on 
his ship he fell down the hatch, was picked up unconscious, and 
brought up by à dock policeman who knew nothing about him, 
and, his ship sailing next day, his friends were never seen. 

** When admitted, he was unconscious, with rather stertorous 


breathing. He had been in this condition since the accident, 


There had been no sickness, no hemorrhage from ears, nose, or 
mouth. Two scalp wounds were present, one on the right side 


Traumatic Subdural Hemorrhage. 23 


of the middle line of the head, over the right parietal bone 
running obliquely forwards and outwards, and two and a half 
inches long, the lower is three inches long and is directed more 
transversely just below the occipital protuberance. The upper 
one shows that the occipito-frontalis is not torn, the lower has a 
small area of bare bone exposed. The edges of the wound are 
clean cut. "There is very little hemorrhage. The wounds were 
most thoroughly scrubbed with an antiseptic lotion, the head 
being as fixed as possible. The patient was sufficiently roused 
by this cleansing to endeavour to resist and muttered to himself. 
A little iodoform was sprinkled on the wound. Iodoform gauze 
was applied with blue wool, and the patient at once sent into 
the ward. An ice-bag was applied to his head and Calomel 
grs. 5 was given. He recovered somewhat a few hours after he 
came in. His stertorous breathing gave way to normal respira- 
tions. His pupils were from the first equal and reacted to light. 
He had no sign of paralysis. 

“ Left quiet, with light nourishment (first, milk for about two 
days, then farinaceous diet, and later fish) he made apparently a 
very good recovery, his head being less painful day by day. 
There can, however, be very little doubt, looking back upon his 
recovery, that it was far from perfect. No special feature can 
perhaps be pointed to as marking him out as still in danger, 
but there remained an air of languor, a feebleness in movement 
and a failure to respond quickly, which on retrospection we are 
bound to consider as due to persistence of some cerebral lesion. 
It is perhaps with greater emphasis that we can lay stress upon 
this point, when we remember that he was a seaman, used 
probably to climbing rigging and to quickly obeying orders. 

“On October 21st, the patient was out in the open air and 
apparently recovered; he smoked his pipe, and conversed with 
his fellows, but there was always the indefinite feebleness. On 
the few occasions on which his eyes were examined, the pupils 
were equal and reacted to light. He had no paralysis. 


On October 23rd, he should have gone out to a convalescent 
home, but as there was a little bare bone at the bottom of the 


24 Traumatic Subdural Hemorrhage. 


lower wound which had not quite healed, it was decided to let 
him remain in another week. 

“On October 25th, the patient seemed to be ill; he had a 
severe headache, did not take his food, seemed inclined to sleep 
the whole time, and his pulse rate became slow. The wounds 
were carefully examined; the upper one had quite healed, the 
lower one was still open with a bit of bare bone at the bottom 
of it, but it was quite clean. The eyes showed the pupils to be 
equal and reacting to light and accommodation. There were 
no paresis or paralysis. Tongue a little furred ; no sickness. 

'* On October 28th, as he seemed to be sinking into a condition 
of coma, it being very hard to rouse him at all, it was decided 
to trephine him over the area of bare bone. It was thought that 
an extradural abscess might be present. The centre of the area 
of bare bone was used for the pin of the trephine. Chloroform 
was given. The dura mater was found normal. It was opened, 
and a little serum escaped, otherwise all was normal. The 
opening in the dura mater was not stitched up, but the skin 
wound (an incision transverse to the original cut, thus making 
the wound crucial, was made) was sewn up with salmon gut and 
the patient put back to bed. The temperature had been normal 
the whole course of the illness. The operation made practically 
no difference to his condition, but during the next couple of days 
he developed paresis on the left side, with rigidity on the right. 
This affected the upper extremities much more than the lower. 
The change was gradual, the grip of the left hand growing less 
and less until ultimately it disappeared, so that whereas on 
shouting at him he would give a feeble grasp with the right 
hand, he gave none with the left, even on putting one’s hand 
into his and squeezing it. The right upper limb in what appeared 
to be his position of rest occupied the position seen after hemi- 
plegia, i.e., the elbow flexed somewhat beyond the right angle, 
the forearm pronated, the wrist and fingers flexed, but he could 
and would move all his limbs at times, and at times one found 
him supporting his head with his right arm as he lay on his 
right side. He always lay on his right side with his head turned 
to the right. This was practically the condition found on 


Traumatic Subdural Hemorrhage. 25 


October 31st. The right pupil was a little larger than the left, 
and Dr. Eason, who saw him, stated that he had commencing 
optic neuritis on both sides. No sickness. He was taking food 
very badly. The coma was certainly deepening but he still put out 
his tongue a little if repeatedly shouted at. No facial paralysis. 
Mr. Symonds decided that he should be trephined on the right 
side of the skull over the temporal region. Chloroform was 
again administered. A flap was turned down and a circle of 
bone removed with a one inch trephine, dura mater exposed 
appearing bluish in colour. This was incised, and immediately 
some thick dark blood escaped, followed by a quantity of bloody 
serum. The condition within the dura mater was then examined, 
and it was found that over the whole of the right Rolandic 
and frontal regions, the brain was compressed by this fluid, 
which welled out under some pressure. The anesthetist noted 
that after the fluid was let out the pupils reacted to light. They 
had not done so before operation whilst the anesthetic was being 
administered. The patient was put very lightly under the 
anesthetic. The flap was punctured at its centre, and a rubber 
drainage tube put through into the cavity left between the 
depressed brain and the dura mater. Dressing put over with 
‘plenty of blue wool. . The pulse was 70 when the patient was 
removed to bed. 

“The operation was about 4.30 p.m., at 10.30 p.m. the follow- 
ing was his condition: Pulse 64, regular; no sickness; right side 
being rigid and practically the same as before operation, left side 
very limp, and practically the same as before operation; pupils 
equal and react to light. Very dull and apathetic. Tongue put 
out on demand. Right plantar reflex flexor, left extensor. 
Knee-jerks present on both sides. Ankle clonus on both sides. 
He moves both legs. 

“Оп November 1st, he was still very dull but certainly improved. 
Pulse 60 to 64. Both arms rather rigid, but right much more 
than left. Incapable of grasping with left hand. Had two slight 
convulsive attacks in the morning about 9.30 and what appeared 
to be an attack of syncope at 11 a.m. (pulse scarcely to be felt ; 
loss of colour; pupils equal). The wound was dressed and the 


26 Traumatic Subdural Hemorrhage. 


trephine opening very gently irrigated with normal saline 
solution. There was not much discharge from the wound. 

“On November 2nd, pupils equal and react to light. The 
temperature is down; no sickness, very drowsy still, puts tongue 
out when told to. White fur on dorsum of tongue. Pulse 64, 
regular; wound quite healthy. Rigidity of right arm, paresis of 
left. Capable of getting cut of bed and he then uses all his 
limbs. The evacuations are passed under him (this has been so 

since October 25th), no facial paralysis. 

. “On November 3rd, when the patient was seen this 
morning he had his eyes open and was lying on the left side. 
He put his tongue out, and paresis seemed to have disappeared 
from left side. The grasp-of either hand was feeble. Tempera- 
ture normal, pulse 66. He had several convulsive twitchings of 
the mouth during the day. As they were only noticed when he 
lay on the right side, it was thought that they might be due to 
pressure from the drainage tube on the face area; with this idea 
the tube was shortened, but during the night he had three other 
attacks, and these were present when the patient was on his left 
side as well as on his right. He was restless in the evening and 
tried to get out of bed. 

“On November 4th, he was sitting up in bed with eyes open 
when seen this morning, but he still has very imperfect muttering 
speech, which prevents one getting proper replies to questions. 
No sickness, temperature normal, feeble grasp with both hands. 
Pulse regular, 64. At 10 p.m. patient was quite quiet, pulse 80, 
temperature 98°, respiration 20. At 10.30 p.m. patient had a fit. 
There were violent twitchings of face and eyes, also left arm . 
and leg, and slight frothing at mouth. The fit was followed by 
marked blowing in and out of cheeks. Its duration was two 
minutes. The patient was rather blue during the fit, but there 
was no sign of collapse afterwards. At 11 p.m. there was a 
similar fit, but slightly shorter in duration. At 12.20 on the 
5th there was a similar fit, but more violent and longer and 
accompanied by slight twitchings of right arm. Pulse 80. At 
1.15 a.m., 2.30 a.m., 3.30 a.m., 5 a.m. and 7 a.m. fits occurred. 
He had his last fit, a severe one, affecting the whole of the left 


Traumatic Subdural Hemorrhage. 27 


side of the body, later on during the morning of the Sth. 
Dr. Eason stated that the optic neuritis was more pronounced 
than when seen before. | 
_ “On November 6th there were no fits and no paralyses, but it 
was noticeable that the pulse was very irregular in rate and force. 
On the 7th he asked for everything he wanted, and words being 
as distinct as before the relapse. Said he had no pain and no 
headache. The tongue was moist and clean. The drainage tube 
which had been put down level with the dura mater was taken 
out to-day. 

“On November 11th the pulse was regular as regards fre- 
quency but irregular in force. 

“From this time the patient never went back, but his recovery 
was very slow. His movements were slow and hesitating for a 
long time, and he had no desire to converse, although he could 
speak quite well. On the other hand, he had no headache, took 
his food well, and had a normal pulse, temperature and respira- 
tion. When he was discharged to a convalescent home on 
January 8th, 1908, he was practically perfectly recovered in all 
respects, save for slightly delayed cerebration. He had memory 
for past events but not for recent ones connected with the 
accident and convalescence. When he returned from the 
convalescent home at the end of three weeks he was, as far as it 
was possible to say, quite recovered, and Dr. Eason, who 
examined his eyes, said it was impossible, from the condition 
then present, to say that optic neuritis had ever been present." 

Such is the history of this case, and before passing on toa 
. Systematic study of subdural hemorrhage, the result of injury, I 
would call attention more particularly to the long lucid interval, 
the absence of any signs of cerebral laceration, or of fractured 
skull, the difficulties in making a diagnosis, the correct conditions 
only being found at the second operation, the appearances found 
at the operation, especially the bluish colour of the dura mater, 
which enclosed blood clot and bloody fluid with marked compres- 
sion of the brain, the presence of optic neuritis, and the delayed 
convalescence but ultimate recovery. These matters will each be 
considered more fully later. 


28 Traumatic Subdural Hemorrhage. 


I had originally intended to base this paper entirely upon the 
cases reported in the surgical reports of Guy’s Hospital, kept in 
the surgical registrar’s room, and with this end in view went 
carefully through these reports for thirty years, viz., 1870 to 
1900, supplementing them wherever possible by the post-mortem 
records, but for more than one reason I found that this was not 
sufficient. In the first place, the reports only supplied one case 
eimilar to the above, and ending in recovery, and in the second 
place, I quickly found many side problems came into the question. 
These required investigation, necessitating reference to many 
books, and it was whilst consulting these references that I first 
found some of the best and most typical examples of cases 
coming under class A, and led me finally to refer to that 
encyclopedia of medical reference, the Index Catalogue of the 
Surgeon-General's office of the United States Army. A biblio- 
graphy will be given at the end of this paper, but I may say that 
I consulted the Transactions of the Medico-Chirurgical, the 
Pathological, the Clinical, and Medical Societies from their 
commencement up to the year 1902, the Reports of Guy's, St. 
Thomas's, St. Bartholomew's, Westminster, and King's College 
Hospitals, up to the year 1902, Brain, American Journal of 
Medical Sciences, the Journal of the American Medical Associa- 
tion, the Medical Record, and the Boston Medical and Surgical 
Journal, in addition to the many British medical journals and 
papers. By this means a total of seventy-two cases of subdural 
hemorrhage, the result of injury, was found. These have been 
divided into two groups of cases under class A and class B; the 
former may be described as cases of practically pure compression 
by blood clot, there being no reason to suspect that laceration, or 
even contusion, were present in any of the cases; the latter, 
class B, on the other hand, have been grouped together because 
in these cases the compression had been complicated by the 
presence of laceration, very pronounced contusion or severe 
general concussion which has considerably influenced the course 
| of the cases, and must, in most cases at least, be looked upon as 

the real cause of the fatal termination which followed. Extra- 
dural hemorrhage is associated with the subdural hemorrhage in 


Traumatic Subdural Hemorrhage. 29 


five cases (see under Condition of the Brain), all five coming under 
class B. 

A few words may here be appropriately written upon the 
value of the word “subdural” as opposed to ‘‘ subarachnoid " 
or “‘intermeningeal” or “subpial,’’ etc. Phelps, in his work 
“Traumatic Injuries of the Brain," р. 44, says, ‘If the prefix 
epidural is invariably used to. characterise a hemorrhage which 
separates the dura from the cranial wall, “pial” to characterize 
a hemorrhage into that membrane from rupture of its vessels, 
and ‘‘cortical’’ to characterise a hemorrhage upon the surface 
of the brain from laceration of its substance, both the source and 
location of the hemorrhage will be expressed in a single word 
with accuracy and conciseness, and the description of cases much 
shortened and facilitated." . Despite this, however, and whilst 
not for one moment discussing its accuracy as far as it goes, І 
hold that the word “pial” does not sufficiently describe those 
eases including, I believe, the majority of cases of extensive 
hemorrhage belonging to class A, in which the blood is situated 
in the so-called “cavity ” of the arachnoid, t.e., the subdural 
space. Again, cases are reported where blood is situated both 
supra- and sub-arachnoid and supra- and sub-pial (see cases 
18, 25, 26 and 64), and also cases where the exact position and 
origin of the blood is difficult to make out. Hence I have 
adhered to the word subdural, as embracing all cases, and as 
being used commonly in reference to both suppuration and 
hemorrhage beneath the dura mater. There is, of course, the 
objection to subdural that it includes intracerebral hemorrhage, 
but at the same time the special term of cerebral hemorrhage is 
so universally given to this form of hemorrhage as cerebral 
abscess to intracerebral suppuration, that the expression subdural 
is invariably looked upon as also equivalent to extra cerebral. 

It is my intention, before passing on to the signs and symptoms, 
diagnosis, prognosis and treatment of traumatic subdural 
hemorrhage, to consider somewhat fully the etiology of subdural 
hemorrhage, both traumatic and non-traumatic. It is important 
to consider the latter class of cases, often described as 
‘hematoma, of the dura mater,” or “meningeal hemorrhage,” or 


30 Traumatic Subdural Hemorrhage. 


when of more remote occurrence and becoming organised, 
passing under the name of Pachymeningitis Interna Hamor- 
rhagica, because in these cases one expects to find those 
conditions present which tend to idiopathic hemorrhage, and in 
which therefore but very slight injury would be sufficient to lead 
to extravasation of blood, whereas in a healthy body such an 
injury would have no such effect.. The earliest consideration of 
this question that I found was Prescott Hewett’s grouping in his 
paper read before the Medico-Chirurgical Society and published 
in vol. 28 (1845) of the Transactions of the Society “ On extrav- 
asation of blood into the cavity of the Arachnoid." This writer 
divided the etiological factors into two groups, the first all ** those 
leading to a decided determination of blood to the head by what- 
soever cause produced," and the second those leading to and 
associated with arterial degeneration. Two other classifications 
of the causes of subdural hemorrhage were found, one in the 
Journal of the American Medical Association for January 26th, 
1901, where the subject is considered in an editorial article, and 
also the case No. 67 reported (class B) and the other which really 
deals with the etiology of Pachymeningitis Interna Heemorrhagica 
in the Gazette des Hospitaux, Saturday, March 13th, 1897. 
“Les Méningites Cerebrales Hamorrhagiques," by Dr. F. de 
Grandmaison. | EP 

From these three sources and the many cases of idiopathic 
and traumatic cases singly reported in the Journals and Transac- 
tions, I have come to the conclusion that the following is the 
best classification which I can make. | 


A. CONDITIONS LEADING TO A DECIDED DETER- 
MINATION OF BLOOD TO THE HEAD BY 
WHATSOEVER CAUSE PRODUCED (P. Hewett). 


This group included— 
1. ALCOHOLISM. 
Grandmaison (vide supra) points out that alcohol predisposes 
in two ways :— 
1. By its sclerosing property. 
2. By the congestion it brings about. 


. Traumatic Subdural Hemorrhage. 31 


With regard to the former, I would call attention to the case 
reported by Dr. R. Van Santvoord, and referred to when dealing 
with prognosis (p. 114). 

The latter is important, since despite the proverb that 
< Providence watches over a drunken man,” hospital experience 
shows that he is particularly liable to injury, and the injury 
being very often to the skull acts indirectly upon a congested 
brain. | 

I have classified the seventy-two cases with a view to their 
bearing upon this subject, and the following is the result :— 

In class A, out of the thirty-six cases reported, there is some 
alcoholic history in nine, and of these five died. Of these nine 
cases, in only three is it definitely stated that the man was 
drunk when the accident occurred, and of these three, two 
recovered and one died. In only one case does it say that the 
man was а total abstainer, and he died (case No. 3). 

In class B (also thirty-six cases) there was some alcoholic 
history present in eight cases, and of these seven died. In the 
other twenty-eight cases, there is no record of any history of 
alcoholism, and no post-mortem evidence, if a post-mortem was 
made. Of the eight cases in which an alcoholic history was 
present, in three the patient was undoubtedly drunk when the 
accident happened, and in two he was probably drunk. In all 
these cases the patients died. 

It is scarcely necessary to refer to the unsatisfactory nature 
of the above evidence, the absence of negative history in the 
reports is noteworthy in the majority of cases, and the known 
difficulty in getting a reliable history from hospital patients, 
makes a negative history often of doubtful value when obtained. 
The absence of any report upon the condition of the liver in 
the post-mortem examinations made in cases coming under 
class B, also nullifies the value of the cases when considering 
this question. 

2. Acute DISEASES. 

This class of case is placed here owing to the liability to 
cerebral hyperemia. Cases of the occurrence of subdural 
hemorrhage with anthrax are reported (British Medical Journal, 


32 Traumatic Subdural Hemorrhage. 


July 20th, 1901, and Soc. Med. des Hosp., 2 Mars, 1894), and 
with erysipelas (M. Lancereaux referred to by Grandmaison). 
These cases have no bearing on traumatic subdural hemorrhage, 
and are in the form of diffuse hemorrhage (thin yen in the 
subarachnoid space. 


3. GREAT ANXIETY OF MIND (Prescott Hewett). 


I find no case reported, but in connection with this class of 
case, the following case is interesting. It is reported in the 
Gazette des Hospitaux (Paris), 1884, lvii., p. 531, by M. Maheut, 
under the title of ** Heamorrhagie dans les Meninges Cerebrales 
chez une jeune fille de treize ans." The case briefly stated is 
as follows :— 

A girl, thirteen years of age, witnessing a quarrel between her 
mother and father (April 21st) was extremely frightened. The 
same night she was agitated, and vomited. Next day at 10 a.m. 
she lost consciousness, convulsions ‘(convulsions eclamptiques) 
followed. She was taken to the Hôtel Dieu. Later she had 
general paralysis, pupils dilated, and not reacting to light. Pulse 
120. Temperature subnormal. Ice was applied to the shaved 
head, calomel given, and artificial feeding resorted to. She died 
April 27th-28th at night, remaining practically the same until 
the end. 

Post-mortem.—On opening the skull the dura mater was seen 
to be slightly adherent over the convex part of the hemisphere, 
with a tinge of red beneath it. Beneath this membrane was a 
coagulum thick enough to conceal the cerebral convolutions. 
The deposit of blood was between the arachnoid and pia mater 
from the anterior extremity to the junction of the middle and 
posterior thirds. The blood was adherent to the membranes and 
difficult to free. The pia mater was intimately attached to the 
superficial parts of the brain, which showed on section a most 
pronouncedly injected state. The right hemisphere was feebly 
injected. The ventricles contained much yellow serous fluid 
without a trace of blood. The other organs were normal. 

The case is extremely interesting on account of the age of the 
patient, the absence of any visceral lesions, and the cause which 


Traumatic Subdural Hemorrhage. 33 


led to the cerebral hyperemia, and it would seem to attach 
additional significance to the importance of quiet and freedom of 
worry during convalescence and even subsequent lifetime of 
those who have once suffered from subdural hemorrhage. 


4. 


Another interesting case which is not without a significance of 
its own is recorded in the post-mortem reports of Guy’s Hospital 
(No. 230), for the year 1872. The patient, in the Eye wards 
under Mr. Bader, was being anaesthetised preliminary to operation. 
He struggled violently, became blue, tlic pulse ceased, and he 
died. At the subsequent post-mortem cxamination the sinuses 
were full of dark blood. There was blood on the surfaces of both 
hemispheres into the pia mater, and the vessels of the membrane 
were also very turgid. The brain weighed fifty-two ounces; 
puncta vasculosa were dark and very evident, otherwise normal. 
Internally viscera congested, otherwise normal. 

` The significance of such a case when the operative treatment 
is considered becomes obvious. It is noticeable that chloroform 
alone was used and that there is no mention of any visceral 
lesion. It is also to be remembered that many cases of traumatic 
subdural hemorrhage, especially those coming under class А, | 
are operated on during the lucid interval. 


5. THROMBOSIS, OR OBSTRUCTION OF THE LONGITUDINAL SINUS. 


As regards thrombosis, under the title of “ Саѕеѕ from Sir 
Dyce Duckworth’s Wards,” by F. E. A. Colby, published in 
vol. xxviii. of the St. Bartholomew’s Reports, is a case of throm- 
bosis of the superior longitudinal sinus. At the post-mortem 
examination congenital heart disease was found, with thrombosis 
of the superior longitudinal sinus, rupture of à vein of the pia 
mater from distension, and subarachnoid hemorrhage. 

In reference to obstruction of the superior longitudinal sinus, 
I may refer those interested in the subject to the New York 
Medical Journal for January 24th, 1885, p. 104, where the 
question of meningeal hemorrhage in the new-born, associated 
with difficult. labour, is discussed, and to the Semaine Medicale, 


4 


94 Traumatic Subdural Hemorrhage. 


1890, 10, p. 408, where M. Kundrat explains hemorrhages in 
newly-born children as being due to the displacement of the 
parietal bones during labour, compression of the longitudinal 
sinus, regurgitation of blood towards the veins of the convexity 
and rupture of these veins. On the other hand, Cushing, in the 
Mütter Lecture for 1901, entitled, ‘‘Some experimental and 
Clinical observations concerning states of increased intracranial 
tension," the general methods of the experiments performed and 
conclusions which they led to, being published in the American 
Journal of Medical Sciences for September, 1902, states that the 
arrangements of the veins opening into the superior longitudinal 
sinus allows of a valve-like action preventing regurgitation of 
blood from the sinus into the veins. It is proved by the fact 
that injection into the sinus will not pass back into the veins. 
His experiments were made on dogs, and he also states that 
“contrary to the general belief, the longitudinal sinus, in the 
dog at any rate, may be completely collapsed by an increase of 
intracranial tension. With reference to the effects of compres- 
sion, the following sentences are important. “If the distension 
of the bag is further increased the intracranial tension in its 
vicinity finally reaches that’ of capillary pressure, at which time 
the convolutions of the brain, not only in the neighbourhood of the 
foreign body, but if the process is still further advanced, even in 
remote parts of the hemisphere abruptly lose their rosy colour and 
become blanched, the veins meanwhile remain filed with dark 
blood, whose means of escape seems to have been cut off, as it 
were, at both ends. Now, such a condition of anemia of the 
hemispheres may be brought about, in the dog at all events, 
with but little evidence of the so-called major symptoms of 
compression." Hence it appears that although regurgitation 
does not take place from the sinus, yet the blood is unable to 
pass from the pial veins into the sinus; engorgement results, 
and should the vein be torn, the venous congestion would lead to 
excessive extravasation of blood; the intracranial tension is 
further raised, and in fact a vicious circle is formed. 

In discussing the origin of the blood, however, it will be found 
that I have arrived at the conclusion that a venous origin must 


Traumatic Subdural Hemorrhage. 35 


be very rare, owing to the fact that compression means forcing 
the blood from the brain, which is almost synonymous to a 
greater pressure of blocd in the veins than in the arteries, if the 
source be looked upon as venous. This is impossible as far as 
we know, but that some other factor is introduced is shown by 
case 20, where there is every reason to believe that the lateral 
sinus was the only source of blood, and yet compression was 
present and the description of the post-mortem examination says 
that there were several ounces of blood in the middle fossa. 
The cases recorded of extradural hemorrhage, from rupture of 
the lateral sinus, point in the same direction. It almost looks as 
though clinical experience and experimental pathology were at 
variance. 


6. PorsoNiNG By Opium (Prescott Hewett). 


7. ACTIVITY IN OVER-HEATED Room (Journ. Amer. 
Med. Assoc.). 

I can find no cases reported of either of these conditions. 
Prescott Hewett states that he bas seen subdural hemorrhage 
due to the former, and looking upon it as probably due to venous 
congestion secondary to respiratory failure, I have put it here. 


B. CONDITIONS ASSOCIATED WITH ATROPHY OF 
THE BRAIN. 


This group of cases included (a) the cases of subdural hæmor- 
rhage occurring in the insane, the hemorrhage being secondary 
to loss of support of the vessels owing to cerebral atrophy. In 
the Transactions of the Pathological Society, vol. xlvi., is a paper 
entitled, * Some gross lesions in the Brains of Lunatics, with 
remarks upon the frequency with which the two sides of the 
brain are affected," by Cecil F. Beadles. The writer gives a table 
showing the vascular lesions met with in three thousand three 
hundred consecutive brains examined. In the Journal of 
Mental Science for January, 1888, is a paper entitled “On 
Hemorrhages and False Membranes within the cerebral Sub- 
dural space occurring in the insane (including the so-called 


36 Traumatic Subdural Hemorrhage. 


Pachy-Meningitis),” by Joseph Wigglesworth, M.D. Lond. 
The paper is based on four hundred unselected post-mortem 
examinations. Dr. Wigglesworth’s conclusions are given on 
p. 523 of that Journal, that coming under No. 5 is as follows: 
* Whilst in the great majority of cases traumatism may be 
confidently excluded, there seems reason for believing that under 
favourable predisposing conditions a slight injury may start a 
hemorrhage which may prove fatal." In the seventy-two cases 
reported at the end of this paper there is no reason to suppose 
that any primary degenerative change in the brain existed in any 
of them. It is noticeable, however, that in the case reported 
by Taylor and Ballance (Lancet, August 29th, 1908) to which I 
shall refer when discussing prognosis, the family history shows a 
clear tendency to mental instability; the mother ccmmitted 
suicide, one sister was in an asylum, and an aunt had been 
temporarily insane. 

b. The cases associated with wasting diseases, such as plithisis, 
have no bearing on our subject beyond the possibility that 
patients suffering from such conditions are more liable to 
subdural hemorrhage from slight violence. 


C. THOSE CONDITIONS LEADING TO, OR ASSOCIATED 
WITH, DEGENHRATIVE CHANGES IN THE 
BLOOD VESSELS. 


a. Atheroma and aneurysm. 


Subdural hemorrhage due to rupture of aneurysms is not at 
all uncommon. Two cases are reported in vol. xxviii. of the 
St. Bartholomew's Hospital Reports in the paper to which I 
have made reference before. In these cases the aneurysms 
involved in the one case the left sylvian artery, in the other the 
anterior communieating artery. In the post-mortem reports of 
Guy's Hospital for the year 1870 (No. 23) there is recorded 
subdural hemorrhage due to ruptured aneurysm of the middle 
cerebral artery in à man who was brought in dead. That 


investigation would reveal many other similar cases I have no 
doubt. | | 


Traumatic Subdural Hemorrhage. 37 


With reference to the association of subdural hemorrhage and 
atheroma, it. would seem right to conclude that in the presence 
of the latter comparatively slight violence would lead to the 
former. Now, if this were so, we might expect more particularly 
those cases coming under class A to suffer from this form of 
arterial degeneration, for there can be little doubt, from a con- 
sideration of the two groups of cases, that whereas those coming 
under class B were due in most cases to the severest forms of 
violence, accompanied by fractures of the skull and severe 
injury to the brain, those coming under class A were the result 
of slighter violence if we take into consideration the absence of 
fractures or cerebral injury. Unfortunately, no records have 
‘been made of the condition of the vessels as regards tension or 
other points which might have thrown light upon the matter’ in 
those cases which recovered, numbering ла -two out of the 
thirty-six collected. 


Of the fourteen cases which died the following is an abstract :— 


The condition of the vessels is mentioned in nine. In two cases 
they were “healthy” and ‘no signs of atheroma.” These were 
in patients aged eighteen and forty-three respectively (cases 12 
and 5). In ease 12 the injury was a blow on the head whilst 
fighting. In case 5 it was a severe blow from the hook on the 
pulley of a crane. 

In one the arch of the aorta was atheromatous and dilated, 
the patient was sixty years of age and the kidneys were cystic 
and granular (case 15). The patient fell twelve feet, pitching 
on his head. i 

In two cases there was slight atheroma in the commencement 
of the aorta. The ages of these patients were thirty-one and 
twenty respectively. In the former the kidneys were affected 
(case 16); in the latter they were normal (case 17). In the former 
(ease 16) the accident was that the patient fell whilst walking, 
striking his head against the kerb, but he had a lucid interval 
of twelve days. In case 17 the man received blows whilst 
` boxing, none of which were particularly.hard. He passed into 
-a state of coma at once, and died two hours after admission. | 


VOL. LIX. 5 


58 Traumatic Subdural Hemorrhage. 


In one case the aortic valves were very atheromatous (case 31). 
The patient was aged 80. The accident was a fall downstairs, 
but it is only right to mention that the woman felt giddy before 
she fell. 


The other three cases are Nos. 4,18 and 19. Incase 4, the vessels 
of the base of the brain ‘‘have some thickening and are opaque.” 
Kidneys affected ; age forty-eight. The woman was said to have 
fallen whilst drunk. In case 13, the subependymal vessels were 
fatty here and there; age thirty-five. This man was struck 
twice on the head by another man and died almost immediately 
after the blows. In case 19, the “ walls of the blood-vessels of 
the brain seem degenerated.” The man was aged forty-three. 
He suffered from old syphilis and was a hard drinker. He fell 
off a waggon, striking his head against the kerb. 


Hence, in nine cases in which the vessels are mentioned, in 
seven they were diseased to a greater or lesser extent, and 
although no very decided opinion is to be ventured on such a 
small number of cases, it may be stated that the evidence points 
to a greater predisposition to extravasation in those the subject 
of arterial decay. At the same time, attention may be called 
to cases 18 and 36, where the hemorrhage occurred in young 
boys as a result of comparatively slight violence. A comparison 
with the occurrence of idiopathic cerebral hemorrhage, however, 
reveals that even here there are marked exceptions to the ex- 
planation of their origin in arterial decay. The three following 
cases will show the weakness of dogmatising. In the Lancet, for 
December 22nd, 1883, p. 1083, Dr. Walter Fergus records a 
case of death from cerebral hemorrhage in a boy of sixteen 
years. Inthe British Medical Journal for 1897, Vol. i., p. 834, 
there is a report of a meeting of the Pathological Society of 
Manchester, at which Dr. Lea showed the brain from a girl 
twelve years of age, who died of idiopathic cerebral hemorrhage. 
' The family history was good, no history of syphilis, no disease 
of viscera found, and the vessels were healthy. It may have 
been possibly due to rupture of a vein of the choroid plexus.” 
And again, in the British Medical Journal for 1889, Vol. ii., p. 


Traumatic Subdural Hemorrhage. 39 


719, Dr. William Collier describes a case of death from cerebral 
hemorrhage in a girl six and a half years of age. 

At this point it will not be inappropriate to discuss the age 
of the patients, since if atheroma be at all a strong factor in 
the etiology of traumatic subdural hemorrhage on the line of 
argument laid down above, it would rather be expected that the 
average age of the patients belonging to class A would approach 
that at which arterial decay begins to become common, viz., 
over fifty years of age, whereas the cases coming under class B, 
one would expect the average age to be under fifty, since such 
accidents would be most likely to occur in adult men in active 
employment. The following are the facts :— 

` Class A. — 
The youngest patient was one and a half years (case 29). 
The oldest patient was eighty years (case 62). 
The average age calculated from the thirty cases in which 
the age is given is thirty-nine years ten months. 


In six cases no record of the age is given, but of these, all 
were adults saye one, which was a boy. 


Of the thirty cases in which the age is mentioned, there 


were— 
From 1 to 10 years of age... 2 cases. 
" 11 „ 20 " 3 
» 21 , 80 ý o v 
» 3l , 40 " 6 , 
„ 41 , 950 ; 4 X 
» Ol , 60 Р 6 , 
, 01 , 70 i 3 ж 
„ (1 , 80 Й T€ l1 
(The numbers in age are inclusive.) 
Class B. 


The average age calculated from the thirty-three cases in 
which age is given is— 
97 years and 8 months. 
The youngest is eighteen (case 59). 


The oldest is sixty-four (case 12). 


40 Traumatic Subdural Hemorrhage. 


It will be noticed that cases coming under class B bear out the 
argument that they should occur in men under fifty years of age. 
The average age calculated from the cases is that of activity and 
hard work. On the other hand, although the average of patients 
in class A is above that of class B, yet it is so slight as to be 
practically negligible, and is also the age of activity and hard 
work as opposed to that of arterial decay. Thus, the consideration 
of the age alone points to arterial degeneration playing no part 
in the occurrence of this form of injury. 

The following considerations, however, have led me to retain 
my opinion on arterial decay as a predisposing factor :— 

Firstly, the amount of evidence put forward when considering 
the presence of arterial decay in the cases coming under class A. 

Secondly, the fact that people over fifty years of age are less 
liable to injury than those under fifty. Thus, of the thirty-three 
cases belonging to class B only six were over fifty years of age. 
These belong to the groups of cases in which the accident is 
received during the time they are employed in actively following 
some occupation. 

And thirdly, that the cases belonging to class A, are taken 
from those reported in various Medical Journals, the majority of 
which are recoveries (twenty-two out of thirty-six), and as the 
prognosis for such conditions is better the younger the patient 
(speaking broadly, and referring chiefly to the point of above or 
below fifty years of age) the conclusions derived from them inay 
not be an index of the true facts when taken alone. 

b. -Arterio-Sclerosis.—I have taken the condition found in the 
kidney at post-mortem examinations as an indication of the 
presence of any general degeneration of the arterial system. 
The few results of the examination of the urine which have 
been made I have considered under the Signs and Symptoms 
(q.v.). The following are the facts which have been gathered on 
the present subject :— 

Class .4.—Of the cases which died. 

In one there was no post-mortem examination, and in one the 
brain only was examined ; of the other twelve cases, the kidneys 
were abnormal in three, viz., case 4, where the right kidney was 


Traumatic Subdural Hemorrhage. 41 


atrophied and contained two cysts; the left was hypertrophied, 
weighing twelve ounces, also fatty and motiled; capsule 
adherent. 

Case 15. Kidneys “© cystic and granular." 

Case 16. Large, and capsule in places adherent. Beyond 
swelling of the cortex, probably from slight infiltration, there was 
no evidence of disease. 

It will be noticed that there was some arterial degeneration 
in all these cases. 

The kidneys were normal in three cases, whilst their condition 
is not described in five cases. In the single remaining case, the 


viscera are described as “ not healthy’ 

Class B. 

Of the twenty-five cases in which a post-mortem examination 
was made, the kidneys are only referred to in seven cases. 

In five cases the kidneys were normal, and in two cases 
abnormal; of the latter, in case 48, the left kidney was small 
and puckered, the right kidney was large with one scar. In 
case 55 the kidneys were granular. 

It is impossible to draw any conclusions from the above data, 
but it is probable that the same significance may be attached to 
arterio-sclerosis as to atheroma. The systematic examination 
of all the viscera at post-mortem examinations made on cases of 
head injuries, especially such as come under class A, would 
throw more light upon the matter. 

c. Escape of blood externally in case of intracerebral hæmor- 
rhage (Journ. of American Med. Assoc.). Cases of this nature 
undoubtedly occur. Case No. 70 I take to belong to this group. 
The following case, admitted under Mr. Lucas, December 24th, 
1889 (Report No. 380), is probably of the same class of case : — 

H. C., aged 35, was riding on the box-seat of an omnibus when 
the latter collided with a cab. The patient fell off on to the 
pavement. On admission, he had profuse bleeding from the left 
ear, was unconscious but beginning to come round. The pupils 
reacted to light. There was slight bleeding from one nostril. 
No albumen or sugar in the urine. He was very sick soon after 


42 Traumatic Subdural Hemorrhage. 


admission, later he became very violent, and was removed to 
the strong room, where he had to be strapped down.  'fem- 
perature 100.2». On the 28th (four days after admission), he 
was quieter, complained of swimming sensations in the head, 
and also of pain which was chiefly on the right side of the head. 
Temperature 99:6?, pulse 86, and respiration 30. Improvement 
followed, his pulse, temperature, and respiration being normal 
on December 31st, but on January 1st, he became decidedly 
worse. There was an internal squint of the left eye, left facial 
paralysis; when spoken to loudly he answers in a rational 
manner: on the 4th, he was much better again; on the 5th, 
he bit the end off the thermometer, swallowed the mercury, and 
was violently purged in consequence. On the 6th, pulse 120, 
temperature 103°, respiration 38. Hedied on the 8th, at 10 a.m., 
becoming very irritable, with rapid pulse and respiration. Tem- 
perature 108-7?, and deviation of eyes to the left, pupil of right 
eye contracted, left dilated. At the post-mortem examination 
there was bruising of right frontal and temporo-sphenoidal lobes 
and subdural hemorrhage over right side of the brain. In the 
right temporo-sphenoidal lobe there was a cavity containing 
semi-fluid blood, not communicating with the ventricle, but with 
the subdural collection of blood by a small aperture. There 
was no fractured base. 

In the American Journal of Med. Sciences, vol. 118, there is 
reference to a case reported by Borsuk and Witzel in the Archiv. 
fiir. Klin. Chir., 1897, Band liv. Heft I., of haemorrhage into the 
white substance of the brain, followed by aphasia, hemiparesis, 
and Jacksonian epilepsy which was cured by surgical interference, 
and although there is no suggestion that the blood had broken 
through externally in this case, there is every reason to suppose 
that this would have happened. 

The probability is that in these cases the layer of brain which 
lies between the area of hemorrhage and the pia mater either 
gradually softens and so gives way, allowing the blood to escape 
externally, or as the result of some straining or other cause of 
rise of arterial tension, an additional extravasation of blood is 
able to break down this layer. It will be noted that in case 70 


Traumatic Subdural Hemorrhage. 43 


the patient was the subject of some form of chronic nephritis. 
We shall refer to the matter again under Prognosis. 


D. TENDENCY TO HAEMORRHAGE (“ Hemorrhagic 
Diseases,” Journ. American Med. Assoc.), 


This has no bearing on traumatic, subdural hemorrhage beyond 
the possibility of liability to hemorrhage with slight injuries. 
The collected cases supply no evidence of such predisposing 
causes.’ 

E. TRAUMA. 


The etiological factors arranged under A, B, C and D are 
merely predisposing causes if they act at all, for this paper only 
attempts to deal with injury as the cause of subdural hsemor- 
rhage, and beyond the importance of recognisable lesions being 
present and leading to spontaneous extravasation and, as stated 
at the commencement, being therefore liable to predispose to 
rupture of vessels if slight violence be applied, no further con- 
sideration of non-traumatic subdural hemorrhage will be given. 
In passing on to a systematic study of subdural hemorrhage 
based on the cases reported at the end of this paper, it is well 
that I should refer to two classes of cases which I shall leave 
unconsidered, since in neither can death be in any way attributed 
to compression of the brain, although in both a varying amount 
of subdural hemorrhage is present. These two groups are, 
firstly, those cases where usually from a fall on the occiput or 
vertex, laceration of the frontal or temporo-sphenoidal lobes, or 
both together, follows, associated with some hemorrhage from 
vessels of the injured brain. No compression symptoms are 
present, and the blood extravasated has no bearing upon the 
prognosis or treatment. It is this last sentence which definitely 
excludes them from class B. These cases are clinically identical 
with cases of laceration of the brain. The second group of cases 

1 Cases of Spontaneous Hemorrhage associated with Ansmia, are quoted 
by Sir Samuel Wilks (Guy's Hospital Reports, 3 s., vol. v.), by Dr. W. Р. 
Herringham in vol. xlvi. of Pathological Society's Transactions (Splenic 


Anemia), and by Dr. G. A. Sutherland in Brain, vol. xvii. (On Hematoma 
of the Dura Mater associated with Scurvy in Children). 


44 Traumatic Subdural Hemorrhage. 


are those of very severe concussion with a thin layer of blood 
overlying the brain at one or more parts. There is marked con- 
gestion of the whole of the brain substance with ali the 
pathological signs of severe concussion. The patients clinically 
correspond to this condition and the blood extravasated is ina 
thin layer, causing practically no compression, although some 
signs of cerebral irritation may be present, or the blood may be 
in the form of a general infiltration of the subarachnoid space. 

The following points will now be discussed :— 

1, The nature of the injury. 

2. The site of hemorrhage with regard to the position of the 
head injury, t.e., whether the extravasation of blood is 
below the seat of injury or opposite to it (contre-coup). 

3. Presence or absence of fractured base, together with a 
consideration of the thickness of the skull in cases 
belonging to class A. 

4. Condition of the brain. 


1. THE NATCRE OF THE INJURY. 


It is difficult to say from a written description of an accident 
what its real severity was, but there can be no doubt that the 
violence of the injury in the cases belonging to class A was much 
less than that in class B. A reference below to the presence of 
fracture of the base of the skull and the presence of laceration 
or contusion, will also bear this out. At the same time it is 
doubtful whether in any of the reported cases the violence was 
as slight as in those cases of meningeal hemorrhage reported by 
Erichsen and quoted by Mr. Jacobson. It is noticeable, however, 
that the slightest forms of violence recorded were much the 
same аз in Erichsen’s cases, where the patients slipped while 
going downstairs, striking the head against a wall. | 

In the simplest forms of violence coming under class А, the 
injury was in the form of blows received whilst boxing or in 
anger, and are to be found in cases 12, 13, 17 and 20. In case 
12 the man was admitted conscious eleven days after the injury, 
and died the same night, apparently from a large secondary 


Traumatic Subdural Hemoirhage. 45 


hemorrhage on the top of a small primary one. In case 13 the 
man was struck twice on the head, apparently in anger, and died 
immediately afterwards. The blows in cases 17 and 20 were 
received whilst boxing. In neither cases were the blows severe 
or fractures of the skull present, in both unconsciousness super- 
vened almost immediately and persisted until death. The 
absence of any primary unconsciousness or external wound in 
many cases coming under class A also shows that comparatively 
slight violence may cause extravasation. In class B, as might be 
expected, the injuries were always severe. 


2. THE SITE OF HEMORRHAGE WITH REGARD TO 
"THE POSITION OF THE HEAD INJURY, i.e. 
WHETHER THE EXTRAVASATION OF BLOOD 
IS BELOW THE SEAT OF INJURY OR OPPOSITE 
TO IT (CONTRE-COUP). 


The following is an analysis of the collected cases :— 


Class A. Class B. 
(a) Injury to one side of skull, hemor- 4 cases. 8 cases. 


rhage on the opposite side, t.e., 
` extravasation of blood by contre- 
coup. 
(b) Injury not quite corresponding to 3 , 3 
opposite point, but for practical 
purposes the extravasation of 
blood is by contre-coup. 
(c) Injury over occipital region, extra- 3 , 4 
vasation of blood over a motor 
region. 
(d) Injury and extravasation definitely 8 , 14 , 
on the same side. 
(е) No record to be obtained of relation- 14 
ship between injury and site of 
clot. 


f 5 „ 


Class A.—Of the* remaining four cases, in one the injury was 
on one side and the extravasation of blood was on both sides (case 


46 Traumatic Subdural Hemorrhage. 


`» 


34). In two, the extravasation was probably on the same side 
as the injury, and in the last case the lateral sinus was ruptured 
by a blow on the same side of the jaw. 

Class B.—Of the two remaining cases :—In one there were 
injuries on both sides of the head but unilateral hemorrhage, and 
in the other there was blood subdurally on both sides. 

It will thus be seen that the extravasation of blood may be on 
the same side as the injury or on the opposite side. The fact 
that a blow on the occiput may lead to compression of a motor 
region by extravasated blood must also be noticed. 


3. THE PRESENCE OF FRACTURED BASE WITH THE 
QUESTION OF THICKNESS OF THE SKULL. 


Of the fourteen cases belonging to class A which died, fractured 
base was not present in a single one. Of the twenty-two which 
recovered, in two there were clinical signs of fractured base, viz., 
in cases Nos. 29 and 34. In the former there was bleeding from 
the right ear, and at operation the subdural hæmorrhage was on 
the left side and due to rupture of the middle meningeal artery. 
In the second case which is reported by Guthrie, it is said that 
the patient bled from the ears, eyes, nose, and mouth. The man 
had bilateral subdural hemorrhage. 

In class B, only six patients recovered, and of these one only 
(case 69) had signs of fractured base. In this case there was 
bleeding from the right ear. It occurred outside the hospital 
after the accident and also on the second day in the hospital. 
The patient, it is said, was unconscious for eight hours after the 
injury, and then had a lucid interval up to the time of operation. 
At the operation, no fracture of the skull was found, but there 
was some laceration of the brain. 

Of the thirty cases which died :— There was evidence of 
fractured base during life or at the subsequent post-mortem 
examination in twenty cases (of these, there was external evidence, 
shown by blood from the ears, nose, or stomach, or subcon- 
junctival hemorrhage, in ten cases; of these the fractures were 
confirmed at a subsequent post-mortem examination in six, 


Traumatic Subdural Hemorrhage. 47 


whilst in four no post-mortem examination was made. There 
was no external evidenee of fractured base but post-mortem 
showed it to be present in ten cases). There was no evidence 
of fractured. base during life, and no post-mortem examination 
was made in one case. There was no evidence of fractured base 
during life, and at the post-mortem examination it was proved 
to be absent in nine cases. 

From the above it will be seen that in class A fractured base 
is rare, in class B it is common, being present in two-thirds of 
all the case which died. This but bears out the recognised facts 
that the evil prognostic significance of fractured base depends 
upon the concomitant injury to the brain, and on this account 
it is of the same evil import in cases of compression as in cases 
unassociated with compression. The risks of septic infection 
of the clot, if on the same side as the fractured base, must not be 
lost sight of (vide cases 34 and 46).? 

As regards the question of thickness of the skull, it can be 
settled with in a few words. The question that seemed to me 
worth considering was, whether in those cases belonging to 
class A where fracture is not commonly found, the thickness of 
the skull might account for this, and a blow which in the average 
thickness of a skull would fracture it, in these cases is sufficient 
to rupture vessels but not enough to fracture the bone owing to 
its inordinate thickness. 

A reference to the cases shows that observations upon the 
bone are very seldom made, and even where they are the thick- 
ness of a bone is a relative measurement. Where the thickness 
is given, it would be important to know whether the bone is 
thicker at that spot than in a normal skull, for a skull might 
have an abnormally thin squamo-occipital and yet as regards the 
thickness of the bone, it might be greater than that of some 
parts of the lateral region (see Mr. Jacobson’s paper on Middle 
Meningeal Hemorrhage, with plates). Other points, such as the 
density of the cancellous tissue of the diplo, the proximity of 
sutures and the elasticity of the bone must necessarily enter into 


3 Possibly occurring in Guthrie's Case of Bilateral Subdural Hemorrhage 
where one side suppurated. 


48 Traumatic Subdural Hemorrhage. 


the question. It is noticeable that under class A are classified 
those cases in which laceration and contusion of the brain are 
inappreciable, and hence we should imagine the violence to have 
been comparatively slight, and, as pointed out above, it certainly 
is much less than is found in cases coming under class B, and the 
probability is that in most cases at least it is not the conditions 
of the bone, so much as those of the blood-vessels, which are the 
important factors in producing extravasation without fractures. 
The cases coming under class A, in which thickness of the bone 
is mentioned, are Nos. 11 and 21, but the details are very meagre ; 
on the other hand, that the thickness of the skull may be of 
some significance is shown by cases 47 and 59, belonging to 
class B. It is in reference to the latter case that Mr. Jonathan 
Hutchinson says, ‘‘It seemed probable in this case the great 
strength of the calvaria had permitted the reception of a very 
severe blow or fall, without fracture, and that ín consequence 
blood-vessels had been ruptured at various places, and the lateral 
sinus given way." There is one lesson to be learnt from these 
cases, which is, that even if the bone be exposed and no signs of 
fracture detected, it does not follow that there is no extravasation 
beneath the bone. 


4. THE CONDITION OF THE BRAIN. 


As has been mentioned above, the division into classes A and 
B has been decided upon the condition of the brain. In class A 
there is every reason to believe from the clinical or post-mortem 
evidence that the brain had not been seriously damaged by the 
injury, and that if the compressing blood had been removed, 
recovery would have followed. In class B, on the other hand, 
in most cases the compression by the extravasated blood has been 
of secondary importance compared with the concomitant injury 
to the brain. Of the cases belonging to this class, which 
recovered, in four there was definite laceration found at th 
operation, but the patient survived this; in one (case 67) there is 
no mention of the condition of the brain found at operation, but 
the fact that some mental or motor impairment remained, points 


Traumatic Subdural Hemorrhage. 49 


to some.cerebral lesion, and the last case (No. 64) which 
recovered, the patient was operated on for compound depressed 
fracture, and although no mention of laceration is made, I 
thought from the nature of the case it was best placed under 
class B. | 

The following is a brief summary of the condition of the brain 
in eases of class B :— 

a. Marked laceration of the brain was present in fifteen cases. 
Of these fifteen cases, twelve are from the evidence found at the 
post-mortem examination, and three are from the observations 
made during the operation. In twelve of these fifteen cases the 
frontal or temporo-sphenoidal lobes (anterior extremities) were 
lacerated separately or together. In two cases the motor region 
was lacerated, in one opposite the anterior and middle fossa, and 
in the other it was found at operation beneath’ the blood clot. In 
one the position of the laceration is not stated. 


In addition to these fifteen cases in which laceration was 
present, there were three others (viz., cases Nos. 54, 69 and 70) 
in which some laceration was present. 


(In case 54 there was a ''lacerated hole one-third of an inch 
deep and one inch in diameter over the second and third temporo- 
sphenoidal convolutions traversed by a vein which was the 
probable source of hemorrhage. In case 69 there was perhaps 
a slight. cortical laceration of motor region beneath the clot.” 
The patient recovefed. In case 70, * Hole in posterior part of left 
Superior temporal gyrus, into which a probe could be passed one 
and a half inches into gyrus at junction of middle and posterior 
partof convolution." This patient recovered but he suffered from 
albuminuria and granular casts, and I am inclined to look upon 
the case as one primarily of hemorrhage into the brain which 
then broke through extra-cerebrally). 

b. Contusion of the brain (local bruising) was present in seven 
cases. In four of these seven cases the frontal or temporo- 
sphenoidal lobes were the parts bruised. In three the position of 
the bruising is not mentioned, but from what the report says it is 
probably over the motor area in two of these. 


50 Traumatic Subdural Hemorrhage. 


с. Of the remaining eleven cases belonging to class В. In four, 
no post-mortem examination was made. In three of these extra- 
dural hemorrhage was present in addition to the subdural. In 
three there was general concussion (in case 59 this was associated 
with pontine hemorrhage). In two cases the patients recovered 
(vide cases 64 and 67 above), and in two cases which ended in 
death there is reason to believe that there was some injury to 
the brain from the presence of delirium. 

Reference will again be made to these points in discussing 
prognosis. We have now to pass on to a consideration of the 
origin of the blood in these cases. I shall commence by giving 
a list of the possible sources and then proceed to a consideration 
of each individually. The possible sources are :— 

a. The main arteries entering the skull, viz., the internal 
carotid arteries, and the vertebral arteries of either side. The 
basilar artery may be considered under this head. 

b. The meningeal vessels. 

c. The sinuses of the dura mater. 

d. The vessels of the pia mater and the continuation of these 
which run across the subarachnoid space (the veins pass chiefly 
into the longitudinal sinus, the arteries are branches of the 
internal carotid and vertebral arteries but are considered separately 
here for convenience). 

e. The cerebral vessels. 

At the outset I may point out one difficulty in deciding upon 
the origin of the blood in cases coming under class A, the only 
group which presents difficulty, and that is that at operation in 
most cases, the clot is turned out, no bleeding point is found, 
and as the patient recovers no further investigation is possible ; 
not only is this so, but in cases which die, in some cases a most 
careful post-mortem examination has failed to give any exact 
localisation of the source of the hemorrhage. Mr. Henry Morris 
(Lancet, November 11th, 1882), drew attention to this, for he 
says, '* If there be no fracture of the skull, no injury to the dura 
mater, no tear in the visceral arachnoid, no bruising or laceration 
of the brain, it is impossible to say whence the effused blood 
is derived.” 


Traumatic Subdural Hemorrhage. 51 


a. With regard to the origin of the blood from the main arteries 
entering the skull. This is extremely rare, I have no record of 
the clot being due to this cause in any of the seventy-two 
collected cases, and nowhere can I find reported a case of rupture 
of the vertebral or basilar artery due to trauma; on the other 
hand, I have found two cases reported of rupture of the internal 
carotid artery, with subdural hemorrhage, but, as was to be 
expected, both were fatal. 

In the year 1876, James F., 17 years old, was admitted under 
Mr. Bryant. He had fallen from a wharf on to the deck of a 
ship, a distance of twenty feet. He had bruising of head and 
swelling of eyelids. He spoke a little after admission but soon 
became comatose. Pulse 102, gradually rose to170. Respiration 
failed and pulse beat for two and a half a minutes after the last 
breath. The left,side was thought to be paralysed. Не lived 
three and a half hours. At the post-mortem examination (No. 68 
for 1876) a fracture of the vertex extended into the base and 
passing across the left carotid foramen ruptured the artery, leading 
to extravasation of blood all through the arachnoid over the 
cerebellum. The left anterior lobe was torn through and the 
ventricle full of blood. 

Another case is reported in the Lancet, October 24th, 1894, 
p. 912, “Case of Fracture of Base of the Skull, Rupture of the 
Internal Carotid Artery, Necropsy." Under the care of Dr. J. 
W. Stenhouse (Leith Hospital). Hemorrhage was subdural over 
the right side of the cerebrum, and the whole of the anterior 
and middle fossa of the skull base. The patient lived almost four 
days after the accident. It occurred in a woman, aged 70, 
a chronic alcoholic. The right internal carotid artery was 
ruptured and a clot the size of a pea was found in the pons. 
Such cases are undoubtedly rare.’ 

b. The meningeal vessels. This practically resolves itself into 
an investigation on the position of the blood in cases of rupture 

3 Mr. L. B. Rawlings, in his recent Hunterian Lectures on ‘‘ Fractures of the 
Skull" (Lecture No. 2, abstracted in the Lancet of April 16th, 1904), reports 
two cases of rupture of the Internal Carotid Artery, within the Skull, both 


leading to immediate death, the blood escaping externally along the line of 
fracture. 


52 Traumatic Subdural Hemorrhage. 


of the middle meningeal artery within the skull. This is usually 
extradural, and in most cases is associated with a fissured 
fracture of the skull, which is the cause of the tear in the artery. 
The artery is torn in the groove on the bone whilst the dura 
mater remains intact. If, however, the dura mater is torn at the 
same time as the artery, the blood will be subdural rather than 
extradural, since it is far easier to separate the arachnoid from 
the dura mater than the dura mater from the bone. At the same 
time we should expect a small amount of blood to be between 
the dura mater and the bone since, as shown by the experiments 
of Sir Charles Bell, a small area of dura mater is separated from 
the bone at the site of the external blow. Cases No. 50 and 66 
in Mr. Jacobson’s papers were of this nature. 

Of the cases upon which this paper 1з founded, No. 29 was also 
of this kind, and Mr. Mansell Moullin thought that, in the case 
he reported (No. 5 at the end), the source of the blood was the 
middle meningeal artery. That is to say, that of the seventy-two 
cases reported in this paper, one was definitely due to rupture 
of the middle meningeal artery, and one was probably due to 
this cause. I found one other case reported. This was in the 
King's College Hospital Reports, vol. ii. p. 185. Тһе patient 
was admitted under Mr. Barrow on October 13th and died 
October 16th. The sternum, right clavicle, and six right upper 
ribs were fractured, and the second to the fifth on the left side. 
At the post-mortem the kidneys were granular and the heart 
atheromatous. His age was sixty-eight. It seems justifiable 
to conclude that although subdural hemorrhage may be due to 
rupture of the middle meningeal artery, such an origin is rare. 

c. The sinuses of the dura mater. Of the seventy-two cases 
collected, the source of the hemorrhage was undoubtedly a sinus 
(lateral) in one (No. 20). In this case the blood filled the sub- 
dural space on both sides of the brain, and spread down to the 
vital centres. In one case the lateral sinus was ruptured and the 
brain also lacerated (No. 43) in one case (No. 59), the source of 
hemorrhage may have been the lateral sinus. In considering 
case No. 20 it is interesting to note what Sir B. Brodie wrote in 
1828. In a paper on “ Pathological and Surgical Observations 


Traumatic Subdural Hemorrhage. 53 


relating to Injuries of the Brain," published in vol. xiv., p. 237, 
of the Pathological Society's Transactions, he says, “ Wounds 
of the sinuses sometimes bleed profusely where there is a 
free opening in the bone made by accident or operation 
through which the blood can readily escape. But a very slight 
pressure is adequate to the suppression of this, as well as of 
other venous hemorrhages, and I have never known an instance 
in which there was such a collection of blood as was capable of 
interfering with the functions of the brain, between the dura mater 
and the bone, or between the dura mater and the brain, in conse- 
quence of a wounded sinus." The common situation of blood 
due to rupture of a sinus of the dura mater is between the bone 
and dura mater. I refer the reader to a paper published in the 
Annals of Surgery for 1901, entitled, * Wounds of the venous 
Sinuses of the Brain," an analysis of seventy cases, by Henry R. 
Wharton, M.D. In this paper I found that subdural hemorrhage 
was undoubtedly present in seven of these cases. In three of 
these the dura mater was torn clean through and in four it was 
only torn on its visceral side, i.e., the inner layer of dura mater 
which limited the sinus was torn through, whilst the outer layer 
remained intact. On the other hand, there are only eight cases 
in which the blood from the sinus was definitely extradural. In 
“ Revue de Chirurgie," September 10th, 1899, is a paper by MM. 
Gangolphe and Piery, on lesions of the lateral sinus based on 
eight cases, including one of their own. ‘They consider that tho 
clot is usually extradural, but frequently there coexists a 
hemorrhage into the arachnoid cavity.‘ 


d. The vessels of the pia mater and the continuations of these 
which run across the subarachnoid space. Of the eight cases 
out of the seventy-two cases reported, in which the source of 


4 Mr. L. B. Rawlings, in his recent Hunterian Lectures on ‘‘ Fractures of 
the Skull" (Lecture 2, abstracted in the Lancet of April 16th, 1904), comes 
to the conclusion that the blood extravasated from a sinus as the result of 
its rupture is ‘‘ mainly intradural." 

For Cases of Extradural Hemorrhage due to Rupture of a Sinus,” see 
vol. i. of the Pathological Society’s Transactions, pp. 183 and 186, also 
vol. x., p. 167. Cases 76 and 77 in Mr. Jacobson's paper are also examples of 
extradural hemorrhage due to rupture of a sinus. 


VOL. LIX. | 6 


54 Traumatic Subdural Hemorrhage. 


the extravasated blood is given, in five it is said to come from a 
vein or artery of the pia mater, but the most powerful evidence 
in favour of this origin of the blood is that in those cases in 
class A where post-mortem examinations have been made, in the 
majority of cases no rupture of a meningeal artery or sinus has 
been discovered, laceration of the brain is entirely absent, and 
the pia mater itself is usually intact. In these cases I think it 
is right to conclude the source of the blood is a vessel in the 
subarachnoid space. 

We are compelled, unfortunately, to fall back upon negative 
evidence and the problem as to whether the blood is usually 
arterial or venous in origin seems to me, in the absence of data 
to rely upon, to be beyond even venturing an opinion. The 
following, however, may be considered :— | 

(1) The condition of the clot. This is described as black, 
dark, or venous, if it is mentioned at all (eight cases out of thirty- 
six belonging to class A). This points to a venous origin, but 
the explanation may be the same as that put forward by Mr. 
Jacobson in his paper (see pp. 161 and 162, Guy's Hospital 
Reports, 3 s., vol. xxviii., 1885). 

(2) If the rupture of the vessel be due to its stretching when a 
violent movement is given to the brain inside the skull, the 
arteries having more elastic tissue than the veins, would be less 
likely to give way as a result of the stretching. 

(3) Against a venous origin is the long lucid interval which 
may be present. It is almost inconceivable that a vein can start 
to bleed three weeks after its original rupture, and whereas in 
the case of an artery a late hemorrhage is capable of explanation 
on the supposition that an aneurysm has formed at the injured 
site perhaps associated with loss of support owing to destruction 
of the brain in the neighbourhood either from laceration or, in 
the case of contusion, from thrombosis of the vessels, no such 
explanation is possible in connection with late extravasation 
from a vein. 

(4) Against a venous hemorrhage also is the fact that to get 
the marked compression of the brain which is often present, we 
have to suppose that the extravasated blood forces the blood 


Traumatic Subdural Hemorrhage. | 55 


out of the arteries of the corresponding hemisphere: in other 
words, the venous blood-pressure is capable of becoming greater 
than the arterial. This is against all known facts, and on the 
contrary, Cushing has shown (Mütter Lect. vide supra) that 
the blood-pressure is raised in order to overcome the compressing 
agent and ‘‘ the centres are again nourished,” and so on if the 
intracranial tension be again raised until the arterial pressure 
be forced two to three times above its normal level. This, how- 
ever, as Dr. Cushing points out later, depends upon the integrity 
of the vascular control of the great splanchnic field, t.e., to say 
that, in severe shock where this vascular control is lost, this 
compensatory rise in blood-pressure would not occur. But it 
is to be remembered that it is during ‘‘shock” that extravasation 
is usually deferred, and only as the patient rallies that the 
compressing blood flows out of the wounded vessel, t.e., that 
nature brings into play the compensatory mechanism at the same 
time that the evil begins to act. On the other hand, it will be 
seen that Cushing’s experiments point to the possible formation 
of a vicious circle if the blood be extravasated from an artery, 
for the pressure of the clot which leads to stoppage of the 
hemorrhage is also compressing the brain. The vasomotor 
centre is brought into play and the arterial blood-pressure 
raised. This may dislodge any clot from the wounded artery, 
starting a fresh pouring out of blood which continues until once 
more the clot compresses, once more the vasomotor centre acts, 
and so on. 


I venture the opinion, recognising, however, that the evidence 
I have put forward is purely negative, that the compressing 
blood is derived in most of the cases coming under class A, and 
those unassociated with laceration coming under class B, from 
the vessels of the pia mater and those running in the sub- 
arachnoid space. Further, from the experimental work of 
Dr. Cushing, I am inclined to look upon the blood as in most 
cases arterial or both venous and arterial in origin and rarely 
venous alone. In a small proportion of cases the blood is 
derived from the corresponding middle meningeal artery or one 
of the sinuses of the dura mater. · 


56 Traumatic Subdural Hemorrhage. 


е. The cerebral vessels. By these I refer to the vessels 
supplying the grey and white matter of the hemispheres and in 
cases Of laceration of the brain associated with subdural hemor- 
rhage, the most probable source of the blood is the ruptured 
arteries and veins. 


THE SIGNS AND SYMPTOMS. 

I propose to discuss these under the following headings, viz., 
Lucidity, Condition of the Pupils, Respiration and Pulse, the Tem- 
perature, Condition of the Limbs, Sickness, Delirium, Condition 
of the Urine, the Optic Discs. Although these signs and symp- 
toms are thus grouped together it does not mean that they are all 
to be relied upon as leading to a diagnosis of subdural hemorrhage, 
but merely that they are all worthy of consideration in dealing 
with head injuries, and an analysis of the presence or absence 
of such in the collected cases may at least tend to show whether 
any importance is to be attached to a particular sign or symptom. 


« LUCIDITY?” AND ‘ LATENCY." 


The lucid interval is so universally recognised that no 
further words are needed to describe it, but there is-a con- 
dition to which I propose to give the words ‘‘latent interval” 
concerning which a few words of explanation are necessary. 
It is а well recognised fact that compression of the brain may 
occur without loss of consciousness but recognised by the 
appearance of paralysis, rigidity, or fits. In describing case 
10 (q. v), Dr. Kiliani mentions a ''free interval" of twenty- 
one days which refers to the fact that the signs of compression 
of the brain did not occur for twenty-one days after the 
original accident. When I first gave the words ‘‘latent interval" 
to this interval which elapses between the original injury and the 
onset of symptoms of compression, unassociated with loss of 
consciousness, I had not seen Dr. Kiliani's case and had, in fact, 
habituated myself to the word latent as separate from lucid, 
hence my reasons for keeping to the word. That it is necessary 
that some such word should be used distinguishing between the 
onset of signs or symptoms unassociated with loss of conscious- 
ness and that of unconsciousness, becomes obvious when an 


Traumatic Subdural Hemorrhage. 57 


analysis of the reported cases is made. The one other question 
which arises is to decide where the latent interval ends. Does 
the onset of headache mean the termination of a latent interval ? 
The safest position to take up, it seems to me, is to say that the 
latent interval ends when definite objective symptoms pointing 
to compression set in. Thus, with the onset of aphasia, paralysis, 
rigidity affecting one side and passing on to paralysis, fits, or a 
Hutchinson pupil, the latent interval terminates. In case No. 1 
the latent interval of fourteen days terminated when “һе 
developed a squint and soon became totally blind, began to 
lose power of speech and stammered a good deal." In case 23 
the man lost consciousness suddenly a week after the accident 
and on recovering was ''more or less speechless." In this case 
I have considered the latent interval as ending with the onset of 
the unconsciousness owing to the recovery of consciousness soon 
after and its persistence to operation. It is probable in this case 
that the loss of consciousness was due either to sudden addition 
of a large amount of blood to a small primary clot, or to a sudden 
primary hemorrhage. The early recovery of consciousness must 
be looked upon as due to some power of compensation on the 
part of the brain. In cases 6 and 25, and several others where 
the latent intervals ended with the onset of fits accompanied by 
loss of consciousness, but where between the fits the patients 
were quite sensible again, I have not looked upon the loss of 
consciousness with each fit as ending a lucid interval as opposed 
to a latent one. The matter may be briefly stated as follows :— 
The lucid interval ends when the patient merges into a state of 
unconsciousness which is only relieved by operation. 


The following is an abstract of the conditions found in the 
seventy-two cases analysed :— 
In class A.— 
a. There was a “latent” or “lucid” interval present in thirty 
cases. Of these eleven died and nineteen recovered. 


b. Of the remaining six cases in which no latent or lucid 
interval was present, three died and three recovered. (Of the 
three that died one was brought in dead, the injury was a blow 


ГА 


58 Traumatic Subdural Hemorrhage. 


with the fist. The other two were almost identical injuries, 
viz., blows received whilst boxing). 





a. Of the thirty cases in which a lucid or latent interval 
was present— 

A latent interval was present in fourteen cases. 

(In five of these the latent interval was terminated by the 
onset of fits, and during the fits the patient was unconscious. 
Consciousness was present between the fits.) 

A lucid interval was present in thirteen cases. 

(Of these thirteen cases, in one case, No. 4, the return to 
consciousness was brief and scarcely complete, whilst in 
case 12 the lucid interval was ended by death). 

Of the remaining three cases, two had latent intervals 
which ended, but the lucid intervals still persisted for 
some days, finally ending in coma. In case 33, sudden 
hemorrhage led to death on the ninth day without any 
previous warning. 

As regards the length of time the intervals lasted, the 
following may be noted :— 





Latent intervals :—* 
The longest is in case 10 where twenty-seven days 
elapsed. 
The interval is under twenty-four hours in two cases. 





The interval is over twenty-four hours and under seven 
days in eight cases. 

The interval is over seven days and under fourteen 
days in one case. 

The interval is fourteen days or more in three cases. 

Lucid intervals : — 

The longest is in case 21 where it is three weeks. 

The interval is under twenty-four hours in seven cases. 

The interval is twenty-four hours or more but under 
seven days in two cases. 

The interval is seven days or more and under fourteen 
days in two cases. 

The interval is fourteen days or over in two cases. 


Traumatic Subdural Hemorrhage. 59 


Of the other three cases— 

In case 11 the latent interval ended on the second day 
after the accident, and the lucid interval persisted for another 
seven days ending on the ninth day. 

In case 24 the latent interval ended on the twenty-fourth 
day, the lucid interval on the twenty-seventh day. 

Case 33 is described above. 

In class B.— 
a. A lucid or latent interval was present. in thirty cases. Of 
these twenty-four died and six recovered. 
b. No lucid or latent interval was present in six cases. All 
these died. 
Of group (a). 
A definite lucid interval was present in nineteen cases. 

(In case 60 the lucid interval was very brief. In case 62 it 
is to be noted that the patient lost much blood from a scalp 
wound, and the lucid interval lasted six days. 

In case 68 the patient was twice bled immediately after 
the accident and remained conscious for three days when 
hemorrhage suddenly came on and he died). 

A definite latent interval was only present in one case 
(No. 72), but cases 51, 63 and 67 also had an indefinite 
latent interval. 

Thus, in case 51 the patient was noisy and delirious after 
admission until the onset of fits. During the fits he was 
unconscious, but after the fits he could be made to answer 
questions. | 

In case 68 the patient had primary unconsciousness, from 
which he recovered. Two days later he became delirious 

and then aphasic. At the time that aphasia is first 
mentioned it is also said that the patient was almost 
comatose. Five days later fits set in. Не still remained 
aphasic but conscious up to the operation, which was per- 
formed two days after the onset of fits. At the operation 
laceration of the brain was found beneath the clot. The 
patient recovered. 


60 


Traumatic Subdural Hemorrhage. 


In case 67, there was a period of primary unconscious- 
ness followed by delirium and excitement. No paralyses 
present. Morphia being given to induce sleep, twitching 
which ultimately became general convulsions, set in during 
sleep. 

The remaining seven cases come under neither of the 
above headings and a brief abstract is given of each below. 

In case 43, thera was no definite lucid interval present, 
but on admission the patient could be roused. Early coma 
get in. . 

In саве 48, injury December 30th. Delirious and wander- 
ing from December 21st to 31st. Coma January 1st. Death 
January 3rd. 

In case 55, unconsciousness for two days, then brief 
return to consciousness followed by coma again. 

In case 58, primary unconsciousness (21st). State of con- 
cussion from the 22nd to the 24th, then half comatose 
condition till death on the 24th of the following month. 

In case, 64 primary unconsciousness. Lucid interval 
followed and the man was operated upon during the lucid 
interval for compound depressed fracture of the skull. 

In case 69, primary unconsciousness for eight hours, then 
patient recovered consciousness, but was aphasic and 
remained so up to the time of operation. In this case it 
will be noticed that there was no latent interval but a lucid 
interval which only ended with the anesthetic. 

In case 72, irritable stupor gave way to violence, which 
was later succeeded by coma. | 

It will be noted that in the majority of these cases 3 there 
was some approach to a lucid interval. 

b. As regards the cases where no lucid interval was 
present, they may be considered as the most severe form of 
injury. They were all operated on save No. 61, but none of 
them derived much benefit from the operation. Fractured 
base was present in all those where a post-mortem examina- 
tion was made, and in those in which no such examination 
was made there were signs during life pointing to fractured 


base. In two of the cases the blood was both extradural and 
subdural. 








Traumatic Subdural Hemorrhage. 61 


To sum up, it will be seen that the cases bear out the importance 
of a lucid interval in diagnosing traumatic extravasation of blood. 
The significance of this interval of lucidity has hitherto been 
emphasised in relation to extradural hemorrhage but the above 
analysis shows that it has an equal importance when considering 
subdural heemorrhage. As regards the presence of a latent 
interval, it may be asked why is it not present in cases of 
extradural hemorrhage? I think the reply to this question is 
that the latent and lucid intervals end at practically the same 
time in this variety of blood extravasation. The latent interval 
is noticeable and important in cases of subdural hemorrhage, in 
the first place, because it lasts such a long time; and, in the 
second place, because in a large number of cases the lucid interval 
persists up to the time of operation when anesthesia is produced. 
This is so in all the cases classed under latent interval above, in 
not one of these was the lucid interval ended when the patients 
were prepared for operation, but in all the latent interval was 
ended by the onset of aphasia, fits, or paralyses, and thereby the 
diagnosis of compression of the brain made in most cases. On 
the other hand, in the analysis of the cases given above where 
the patient is described as having had a lucid interval it means 
that no aphasic, paralytic, convulsive or other objective symptoms 
preceded the onset of coma. An exception, however, to this may 
be granted in the case 29, where focal symptoms were present 
before consciousness was fully lost. In a study of the cases 
of subdural hemorrhage as distinguished from extradural extra- 
vasation, two points are to be emphasised. They are probably 
more valuable from a diagnostic point of view than any others 
and may be looked upon as the most important which an 
analysis of the cases has elucidated; the first is the presence of 
a distinct latent interval as opposed to a lucid one, and the 
second is the long period of time which may elapse before 
the onset of any symptoms of compression of the brain in these 
cases, t.2., the long interval of time which may elapse between the 
injury and the termination of the latent or lucid intervals. Before 
leaving this subject, I propose to discuss briefly two further points. 
Firstly, the reason for a latent period in one case and a lucid 


62 Ттаиталс Subdural Hemorrhage. 


period in another; and secondly, any explanations which can be 
given of the very long latent and lucid intervals which may 
occur. For a consideration of factors tending to cause bleeding 
and also the medico-legal importance of the lucid interval I refer 
the reader to Mr. Jacobson’s paper (vide supra) pp. 260-264. 

Experimental pathology shows that coma depends upon the 
anæmia of the brain resulting from the compression. This being 
so, we should expect the difference between those cases in which 
coma sets in without any objective symptoms preceding it and 
those in which objective symptoms associated with consciousness 
are present to depend upon the amount of the compressing force 
as a measure of the amount of blood forced from the cerebral 
vessels and leading to anæmia. 

In the thirteen cases in which a latent interval was present, in 
seven the compressing blood, or blood and fluid, was small in 
amount. On the other hand, in four it was large. In one of 
these (case 10) it is reported as one and a quarter inches thick 
and practically covering the entire left hemisphere. Yet in this 
case the man never lost consciousness. It is possible that in 
the cases where the clot is extensive the brain may be atrophic 
and hence a considerable amount of clot be present without 
any marked compression. Failing this explanation, we must 
conclude that coma does not depend entirely upon the amount of 
the compressing agent, or if it does, in cases where the compress- 
ing agent is large, this has been gradually produced and allowed 
the brain to compensate. This power of compensation is rather 
suggested by case 10, referred to above. Here the accident was 
on May 5th. The patient had some prodromal symptoms on the 
20th, on the 22nd he had * violent frontal headache," on the 
26th “ whilst walking from bed to table became dizzy and almost 
fell. This sensation passed away in a few minutes. Became 
weaker and unable to walk." On June Ist ‘slight hesitancy of 
speech" began, increasing till the time of admission, about June 
7th. If the prodromal symptoms on May 20th be looked upon 
as the first onset of hemorrhage and the maximum be looked 
upon as reached cn June 7th, it means that blood was gradually 
poured out for eighteen days. There is no mention of any 











Traumatic Subdural Hemorrhage. 63 


appearance of the clot found at the operation, and suggesting 
that one part was older than another. The brain was very 
definitely compressed. 

In cases with slow onset of hemorrhage and gradual extra- 
vasation the explanation of absence of coma may be the same 
as in some cases of cerebral tumour, t.e., that a corresponding 
atrophy of the brain occurs and allows the new growth (in this 
case blood) to take its place. (Allbutt’s System of Medicine, 
vol. vii, р. 269, * Experimental Pathology of the Cerebral 
Circulation.” By L. Hill.) 

Turning to the question of why a latent or lucid interval 
should be present, many explanations have been given. A 
gradual hemorrhage, as mentioned above, has been given as 
explanation. Prescott Hewett, writing in vol. xxviii. of the 
Medico-Chirurgical Society's Transactions (1845), p. 81, says, 
‘Connected with these extravasations there is, however, one 
remarkable circumstance which having been already observed in 
several cases ought not, I think, to pass unnoticed. I allude to 
an intermission in the symptoms either of coma or even of 
paralysis. This intermission occurs under different circum- 
stances; it may be dependent upon an interruption in the 
pouring out of the blood, during which the brain gets accustomed 
to the pressure and recovers its functions, until a further extra- 
vasation takes place. If carefully examined the extravasated 
blood will, in these cases, be found of different hues.” He then 
proceeds to discuss the occurrence of intermissions also when 
the blood organizes and becomes enclosed to form a cyst. 

Sir Benjamin Brodie, in describing the case reported at the end 
(No. 68), discusses the possibility of ‘‘secondary hemorrhage ” 
occurring in the cavity of the cranium and concludes that, 
although rare, this case is an example of it. He explains its 
infrequency by the ‘strictly antiphlogistic regimen usually 
pursued for a considerable time after the occurrence of the 
accident ” (Transactions of Medico-Chirurgical Society, vol. xiv.). 
It is probable that reference is here made merely to what we 
should now call reactionary hemorrhage, t.e., bleeding coming on 
after a lapse of twenty-four hours. Since no sepsis was present 


64 Traumatic Subdural Hemorrhage. 


and no ligature used our present knowledge ascribes this 
“ secondary hemorrhage ’’ to sudden forcible action of the heart, 
increased arterial tension, or pathological conditions of the walls 
of the vessels. 

In discussing the case described by him in the Journ. Amer. 
Medical Assoc., vol. viii. (reported as No. 22 at the end), Dr. 
Armstrong says, “pathologically the case is still obscure and the 
comprehensive term of intermeningeal hematoma was adopted 
as most closely covering the condition as evidenced. Agnew 
(Surg., vol. i., p. 287) explains the condition as ‘‘a vascular 
paralysis so modifying the vital properties of the walls of the 
blood-vessels of the brain as to favour the free escape of their 
liquid contents." Considering the fluid character of the blood, 
and that, had the hemorrhage been from a ruptured vein or 
artery, clot should have been present, this explanation is worthy 
of attention.” A comparison with other cases, of which Mr. 
Butlin’s is the best example, leads me to the opinion that, 
however ingenious the above idea may be, the more probable 
explanation is the effusion of serum round a small clot. The 
explanation of the late onset of symptoms may be explained by 
a recent collection of serum round an old clot which was not 
itself of sufficient size to cause compression symptoms. Even 
allowing the presence of such a “ vascular paralysis" of which 
I do not know the counterpart in other injuries, save where 
inflammatory changes follow, its late onset seems difficult to 
explain. 

Dr. Bremer, in considering the reason for the late onset of 
symptoms in the case which he and Dr. Carson published 
(No. 23 at the end) and in which he says the clot was old, 
suggests as & reason for the late onset of symptoms that the 
gradual hemorrhage on the cortex had no effect at first but 
slight pressure. This irritates the vessels at the base and leads 
to afflux of blood through the lenticulo-striate artery. The 
cortex then becomes compressed between the clot on the surface 
and the increased flow through the basal ganglia. 


5 Compare with Cushing on raising of blood-pressure to overcome resistance 
of compressing agent referred to on p. 55, 








Traumatic Subdural Hemorrhage. — 65 


In reporting the case which is No. 24 of the series, Mr. Hulke 
writes of “ the hypothesis of hemorrhage in this situation through 
bursting of a vessel consequent upon cerebral congestion as a 
late excessive reactionary effect." 

It seems probable that in the majority of cases the late 
onset of symptoms means late onset of hemorrhage, but it is a 
dificult matter at any time to say what the age of a collection 
of blood, within the skull, may be. It is to be noticed that of 
the ten cases belonging to class A, in which the latent or lucid 
interval is greater than seven days, in only three (Nos. 12, 22 
and 24), is there reason to look upon the cloti as old, and in two 
of these the compressing agent is “dark brown blood and fluid ” 
in one (No. 22), and “ brown flocculent fluid in another (No. 24). 
Reference to a paper entitled ‘‘Tumours containing fluid blood" 
by the late Mr. Morrant Baker, published in vol. i. of St. 
Bartholomew's Hospital Reports, may be referred to as throwing 
some light upon the possibility of so-called fluid blood being 
found long after its first extravasation and might possibly be 
brought forward to explain the presence of uncoagulated blood in 
some of these cases. He proves that in some cases fluid having 
every appearance of normal non-coagulated blood may be found 
in cysts of very old standing in which there can be no doubt that 
the extravasation is of old date. He then proceeds on experi- 
mental lines to show the reason for this, and on p. 218 writes, 
“the fluid is not simply uncoagulated blood but a mixture of 
serum (derived probably not only from extravasated blood but 
secreted also by surrounding parts) with blood cells, diffused 
colouring matter and disintegrated fibrine." In the cases under 
consideration, however, this explanation may be neglected for 
these reasons, firstly, that in the cases of long latent or lucid 
intervals clotted blood has usually been found, that in the cases 
of fluid blood being found it is extremely improbable that the 
above explanation is sufficient to account for it, since the 
changes leading to its formation, as pointed out in the above 
paper, in the series of experiments made, take many months; 
and lastly, that cases such as Nos. 22 and 24 are probably 
to be explained by a small clot and exudation of serum about 


66 Traumatic Subdural Hemorrhage. 


it, as pointed out by Mr. Butlm. For reference I have given 
a table showing the condition of the blood extravasation and. 
the length of the latent or lucid interval in the ten cases in 
which this exceeded seven days. 


TABLE OF REFERENCE 


to Condition of Extravasated Blood found where the length of 
latent or lucid interval was over seven days. 
No. of Length of 


Case Condition of extravasated blood. latent or lucid 
. interval. 











1 Small blood-clot and some dark coloured blood 14 days. 
which slowly welled up 


2 Dark semi-fluid clot was removed. Cerebral 14 days. 
pulsations now recommenced causing more 
clot to collect 


3 Clot 1j inches thick covering practically the 27 days. 
entire left hemisphere 


11 Black clotted blood exuded with each pulsation 2-9 days. 


12 Blood fluid, or in the form of loose coagula. 11 days. 
From reading the report it seems probable 
that there was an old part of the clot be- 
coming organised and a more or less recent 
part in addition 


16 * Blood" ... T TN vas val з 12 days. 
21 “Clot” (microscopically showed ‘‘ softening ’’) 21 days. 


22 A hypodermic needle drew forth dark blood 22 days. 
‘fluid’? pressed out in larger quantity. 
(This “fluid”? under the microscope con- 
sisted of ‘‘brown colored serum and color- 
less red blood corpuscles ’’ 


23 Clot extending in all directions. On raising 7 days. 
the dura mater semi-liquid blood forced itself 
through the superficial layer of the clot 
and reached 2-3 feet in height. 


24 Brown ‘‘flocculent fluid ” sie саг s 24-27 days. 


It is of course possible that some cases may be explained by 
the rupture of aneurysmal dilatations of vessels which were 
damaged, but not opened at the time of injury. Very strongly 
against this is the fact that no post-mortem examinations 


Traumatic Subdural Hemorrhage. 67 


describe aneurysmal dilatations on vessels some days after injury 
either in the case of extravasation of the blood or laceration of 
the brain. It is useless to discuss the matter further, from what- 
ever point of view the problem is approached it seems insoluble 
but it at least points to a moral and emphasizes the importance 
of careful post-mortem examination. In leaving this part of the 
subject it may also be pointed out that in some cases of early 
onset of coma also, we are compelled to conclude that factors 
are introduced which are outside our grasp, thus in the case 
reported by Mr. Mansell Moullin (No. 5) the man who was not 
stunned by the blow worked as a stevedore for four hours after 
the accident. To say that it took four hours for the shock to 
pass away and the heart and vessels to recover from any 
temporary depression seems absurd. 

It seems probable on anatomical lines that a subdural hemor- 
rhage is more likely to slow increase covering a long period of 
time, since whereas in the case of extradural hemorrhage the 
blood has both to compress the brain and also separate the 
adhesions of the dura mater to the wall of the skull, a subdural 
hemorrhage has practically only the former to do. 


THE PUvupPILs. 
The following is an analysis of the conditions found in the 
seventy-two cases reported :— 
The pupils are not mentioned in ... n .. 26 cases. 
It is mentioned that they are equal and reacting in 10 , 
There was slight inequality of the pupils passing to 
а normal condition in  .. "E. m 
There was some abnormality of the "T in e. dd y 
a. There was unilateral dilatation of the pupils in 7 , 
(But in only four of these was there a definite 
Hutchinson pupil.) 
b. There was bilateral dilatation in с : 9 , 
(But of these in one case the pupils ае. 
later and in опе the dilatation was only 
present during the fits (case 26). 
c. There was no case of definite unilateral 
contraction ... үе с T ex dE 


68 Traumatic Subdural Hemorrhage. 


d. There was bilateral contraction in  ... ... Û савез. 
(In one case it was pin-point and in this case 
unfortunately no post-mortem examination 
was made. In one case itis said that the 
one pupil responded to light and the other 
did not). 

e. The pupils are described as unequal in xe 0575 

f. Of the remaining four cases :— 

In case 66 the pupils were fixed and unequal. 

In case 40 they were normal in size but non-reacting. 

In case 53 a small local fracture of the middle fossa 
with hemorrhage probably accounted for the various 
changes the one pupil underwent. 

In case 45 the pupils varied. The right was greater 
than the left at first, then the left greater than the 
right, and finally the left was widely dilated and 
neither reacted. 

The division into class A and class B shows the following :— 
Of the twenty-six cases in which the pupils are not 
mentioned— 
18 belong to class A; and 
8 belong to class B. 
It is probable that in the majority of these cases the 
pupils were equal and reacting. 
Of the ten cases in which the pupils are equal and 


reacting— 
6 belong to class A; and 


4 belong to class B. 
Of the three cases where practically no change is 


present— 
2 belong to class A; and 


1 belongs to class B. 
Of the thirty-three cases in which some pupillary change 
is present— 
9 belong to class A; and 
24 belong to class B. 
The typical Hutchinson pupil was only present in one of 
all the thirty-six cases coming under class A. 


Traumatic Subdural Hemorrhage, 69 


With regard to the mortality :— 
Of the twenty-six cases in which the pupils are not 


mentioned— 
16 recovered, and 


10 died. 
Of the ten cases in which there was no change— 
5 recovered, and 
9 died. JE 

Of the three cases in which there was practically no 

change— 

| 1 recovered, and 

2 died. 
Of the thirty-three cases in which an abnormality of 
pupils was present— 
6 recovered, and 
27 died. 
Of the four cases of definite Hutchinson pupil all died. 
Further examination of these four cases is as follows :— 

In ease 16, the pupil change occurred with onset of coma 
twelve days after admission. No operation was performed. 
The post-mortem examination states that the clot extended 
into the anterior fossa. 

In case 52, botb extra- and subdural hemorrhage were 
present. Most of the extradural hainorrhage had escaped 
through a fissure of the skull. After the operation it is 
stated that the right pupil was a shade larger than the left 
and that both reacted to light. 

In case 60, an operation was performed but the dura 
mater was not opened. No extradural hemorrhage was 
present. There is no mention of blood extending to the base 
of the brain. 

In case 65, the pupil change came on twenty-four hours 
after admission. The patient was trephined, but died twelve 
hours later. 

The following conclusions may be added :— 
That of the cases in which the pupil is mentioned, abnormalities 
were present in 72 per cent. The real percentage, however, is 


VOL. LIX: T 


70 Traumatic Subdural Hemorrhage. 


probably much lower, since the probability is that of the twenty- 
seven cases in which no mention is made of the pupils they were 
normal in the majority. ` 

The abnormality of the pupils points to a bad prognosis, whilst 
a Hutchinson pupil is of particularly evil significance. 

That the Hutchinson pupil is comparatively rare. 

That the abnormality (inequality) of the pupils associated 

with simple concussion is to be distinguished from the abnor- 

` malities both as regards size and reaction to light occurring in 
cases of compression and associated with focal symptoms. 


THE PULSE. 


Class A.— 
a. There is no record of rate or character in .. 15 cases. 
b. Of the remaining twenty-one cases, there is a 
pulse rate of under 65 in "M 52 uen. 6 , 


(Of these six, the slowing of the pulse was associated with 
coma in two cases, viz., case 1], in which the pulse rate 
was 60, and case 17, in which it was 50. The former 
recovered after operation; the latter was not operated on 
and died.) 

In the other four cases the patients were conscious at the time 
the pulse rate was recorded. It is necessary to go more care- 
fully into these four cases :— 

In case 23, there were signs of compression shown by 
paresis at the time that the pulse was slowed to 43. After 
operation, at which a large clot was evacuated, the pulse 
rose to 86. | 

In case 24, the patient was admitted with a pulse rate of 
50 (very compressible) a fortnight after the injury, and at 
this time he had no focal symptoms. Signs of paralysis 
occurred on the fifth day in hospital, and, when on the 
seventh day he became comatose, the pulse rate was 70 
(temperature 98°). Three to four ounces of brown flocculent 
fluid were removed from beneath the dura mater. 

In case 29, the pulse rate of 64 on admission, soon after 
the injury, was indubitably due to shock, the patient at this 
time having no signs of compression. When these set in 


Traumatic Subdural Hemorrhage. 71 


nearly twenty hours later commencing with hemiparesis 
the pulse was 86, full and bounding. 

Case 83 was anomalous. The hemorrhage probably came 
on suddenly and was almost immediately fatal. The pulse 
rate was recorded on the day before his death, when no signs 
of compression were present. It was then 60. 

This being so, we are, on the evidence supplied by our cases, 

compelled to acknowledge that in only two was there slowing of 
the pulse due to the compression and associated with coma, and 
in two others the pulse was slowed, the patient having focal 
symptoms but being quite conscious. In one of these last two, 
as the signs of compression increased and the patient passed into 
coma, the pulse rate increased from 50 to 70 per minute. 
. In two cases the pulse is described as slow and full. In the 
one it later ran up to 125 before the patient died, no operation 
being performed; in the other the patient recovered after 
operation, and, although the rate is not mentioned, the case may 
be perhaps added to the above as compression leading to slow- 
ing of the pulse. 

The pulse rate was 100 or more in seven cases. 


(Of these seven cases, six were comatose when the pulse 
rate was taken and of these, three were having fits, the pulse 
rates in these cases being respectively 160, 123 and 100.) 

In one case the pulse was 70 on admission and became 
more and more rapid before death. 

The pulse rate was between 65 and 100 in seven cases. 
Class B.— 
a. There is no record of the rate or character in eight cases. 
b. Of the remaining twenty-eight cases :— 
Frequency per minute of less than 65 in ten cases. 

(Of these ten cases, in four the slowing of the pulse must 
be put down to shock. Thus :— 

In case 40, the pulse was 58 and temperature 97? imme- 
diately after a severe injury. 

In case 43, the pulse was 50 and the temperature 97° on 
admission. 


72 Traumatic Subdural Hemorrhage. 


In case 49, the pulse was 50 and feeble immediately after 
the accident, and there is evary reason to believe that here 
also the slowing of the pulse rate was one of the signs of 
severe shock. The pulse later ran up to 180. 

In the other six cases the slowing is probably due to the com- 
pression by blood clot or concomitant injury to the brain. It is 
necessary to consider these further :— 

In case 48, the pulse was 58 when the patient became 
comatose, eleven days after the injury. The pulse rate 
reached 120 after the operation, at which two to three ounces 
of blood were removed. At the post-mortem examination 
contusion of the brain was found. 

In case 52, extradural hemorrhage was present in addition 
to subdural, the pulse rate was 51 (full), with coma. Post- 
mortem, laceration of the brain. 

In case 53, the pulse was 40, laboured, and associated with 
Cheyne-Stokes’ respiration half an hour after admission. 
Next day it was 60, rather small. This day the man was 
operated on and the day after his pulse rose to 96. Next 
day the pulse rate fell to 40, Cheyne-Stokes’ respiration super- 
vened and he died. Post-mortem, smashing of the anterior 
part of the right side of brain. 

In case 56, the pulse rate was 54 on the fourth day after 
the accident. Post-mortem, bruising of brain and subdural 
hemorrhage. 

In case 63, the pulse was full and slow, 60 on admission, 
and though increasing in rate a little was still slow and full 
three days later. Recovery followed operation, at which clot 
was removed and laceration of hrain found. 

In case 71, the pulse was 60 and full one hour after 
admission. Clot was removed but patient died two hours 
afterwards, and at the post-mortem examination numerous 
small hemorrhages throughout both hemispheres were found. 

In one case the pulse is described as slow and regular on 
admission but later rose to 90 when paralysis was present. 

Frequency per minute of 100 or more in gix cases. 





Traumatic Subdural Hemorrhage. 73 


(All these patients died. In four of them bruising was 
found post-mortem without laceration. In one, laceration 
was present, whilst in the remaining case (54) although a 
small lacerated hole was found in the temporo-sphenoidal 
lobe beneath the clot it was thought that had the clot been 
removed the patient would have recovered.) 

The frequency per minute between 65 and 100. Eleven cases. 

(It is to be noted that in case 59, where the pulse was 72 
and laboured, on admission the man had had a definite lucid 
interval, and at the post-mortem examination the brain was 
compressed by five ounces of blood subdurally and numerous 
ecchymoses were found in various parts of the brain. 

Irregularity of the pulse :— 

This is only mentioned once in class A, viz., in case 20. In 
this case from other signs and as shown at the post-mortem, 
blood had gravitated down around the medulla. 

In class B, irregularity is mentioned three times (cases 45, 46 
and 54). These all died. One of these cases (No. 54) it will be 
noted is the case mentioned above. 

It will be remembered that in Mr. Symond’s case the pulse 
was slowed with the onset of coma. This slowing in rate 
persisted urtil the time of operation. About a week after the 
operation irregularity of the pulse set in and lasted for some days. 

As a summary of the above we may venture the following 
opinions :— 

That whereas those cases coming under class A are to be looked 
upon as pure compression unassociated with concussion, con- 
tusion, or laceration, as far as this is possible after such violence, 
the fact that slowing of the pulse occurred in only four out of 
the thirty-six cases is against any significance being &ttached 
to the absence of slowing of the pulse in suspected compression*, 

That if a pulse rate of between 65 and 100 be looked upon 
as & normal rate then in 37 per cent. of all the cases in which 
the pulse rate is mentioned (belonging to both A and B) the rate 


6 In his paper, “ One hundred Cases of Cerebral Tumour,” published in 
the Guy's Hospital Reports for 1885-1886, Dr. Hale White calls attention to 
the infrequency of slowing of the pulse in cases of tumour of the brain. 


74 Traumatic Subdural Hemorrhage. 


is normal, but it was normal in a greater percentage of cases 
belonging to class B than belonging to class A. If, however, the 
pulse rate be looked: upon as normal in those cases in class A, in 
which no mention of the rate is made, and it is probable that this 
is 80, it would raise the percentage of cases belonging to class A 
in which a normal pulse rate is present to 60 per cent. 

That of the cases coming under class B, in which contusion 
aud laceration were present in only 16 per cent., is the pulse rate 
over 100 (t.e. six out of thirty-six). 

That irregularity is of evil import, probably pointing to either 
severe laceration of the brain or gravitation of the blood to the 
region of the pons and medulla. 


THE TEMPERATURE. 
Class A.— 


Of the fourteen cases which died :— 

In five no record of the temperature was given. 

In one the only mention is that the surface of the body 
was cool (17). 

In one it is said that he ''evidently had considerable 
pyrexia ’’ (12). 

In one case on the eighth day the temperature was 97°, 
on the ninth day the patient died, probably from a sudden 
large hemorrhage (33). 

In the six remaining cases there was some rise of temperature :— 

In one it is said that with coma the temperature was 
slightly elevated. 

In one the temperature was above normal from the first, 
and rose until at death it was 106°4°. At the post-mortem 
there was blood round the medulla (20). 

In the other four there is a period of subnormal, normal, 
or slightly normal temperature followed by pronounced fever 
before death. Of these, in case 2 there was a period of 
sixteen days’ apyrexia; operation was then performed and 
the temperature afterwards rose to 101° between operation 
and death (no post-mortem made). In case 3 there was a 
period of eight days’ normal temperature preceding operation, 


Traumatic Subdural Hemorrhage. 75 


a period of twelve days’ apyrexia followed, after which the 
temperature rose to 104? at death (compression by clot at 
post-mortem). 

In ease 5 the temperature was normal till the evening 
before death (period of ten days) when it went up to 1099, 
(post-mortem: compression by clot ; trephining on the wrong 
side). 

Of the twenty-two cases which recovered :— 

In nine there is no record of the temperature. 

In one (No. 14) the only mention is that two weeks after 
operation the temperature fell to normal. 

In the other twelve the temperature is stated to have been over 
98-4? at some period of the illness :— 

In two of these it is practically normal, being 99? and 98:6? 
(on admission). 

In one (No. 29) the temperature was 97:5? on admission 
(shock), but after the operation temperature rose to 110°F. 
during the night but immediately fell and gradually came 
down to normal. 

Of the remaining nine cases there was fever prior to 
operation :— 

In five of these cases the patient had convulsions (6, 18, 
21, 23, 28) associated with the pyrexia and possibly 
accounting for it, although in case No. 18 the fever was also 
present before the onset of fits and apparently but little 
affected by their onset. | 

In one case there was some fever present but the tempera- 
ture fell to normal later and the day after this fall fits set in. 

In the three other cases (10, 22 and 34) no fits were 
present, in the last one (34) the fever, associated with 
delirium, preceded the second operation, at which a suppu- 
rating clot was found. 

In four cases it is definitely stated that operation was followed 
by a normal temperature. These all recovered. 
In four cases there was some fever following operation. 


These all recovered. 


76 Traumatic Subdural Hemorrhage. 


In four cases the temperature reached 104° or over during 
the course of the illness (6, 21, 27 and 29). These all recovered 
and are as follows :— | 

In сазе 6, the temperature on admission, six days after 
the injury, was 102°. This followed multiple fits for which 
he was admitted and which he continued to have up to time 
of operation. Four hours after operation temperature 105? 
and for four days varied from 101:4? to 104?. No fits after 
operation. 

In case 21, the patient was admitted after a fit and had 
convulsions up to time of operation. The clot was removed 
at operation. It was said on the microscopical examination 
to be “breaking down." . The temperature rose from 102° 
to 105° during stay in hospital preceding operation. Opera- 
tion on twenty-second day. Four hours after operation 
temperature was 103°, on the twenty-fourth day it was 104° 
On the twenty-sixth it was 99°. 

In case 27, the temperature was 104° two days before. 
onset of fits and normal the day preceding the onset of fits. 
No other record. 

Case 29 has been referred to above. 

Convulsions were present in fifteen cases :— 

In eight of these there is no record of the temperature. 

In three others no relationship between the fits and tem- 
perature is to be made out. 

In four there was fever associated with the fits. 


Class B.— 
In fourteen cases there is no mention of the temperature. Of 
the twenty-two other cases :— 
There was a temperature of over 104?F. in three cascs. 
These all died. 
In case 38, temperature rose to 107° before death. 
In ease 52, temperature rose to 104:6? before death. 
And in case 66, temperature rose to 107° before death. 
In ten cases temperatures from 99° to 104° are reported. Of 
these :— 


Traumatic Subdural Hemorrhage. 11 


In one it is between 99° and 100° (died). 

In three it is between 100° and 102° (two lived, one died). 

In four it is between 102° and 103? (all died). 

And in two it is between 103° and 104° (one lived and one 
died). 

In three fever was present but its degree not stated (45, 58 
and 61). 

No fever was present when the temperature was recorded in 
three cases :— 

In two of these only one reference to the temperature is 
made, and in the other one there are two references. These 
references are, however, important, as will be seen from the 
cases. 

In case 50, the accident was on the 10th. On the 15th 
the temperature was 98°6°. Death on the 17th. (Post- 
mortem, pulping of frontal and temporo-sphenoidal convo- 
lutions). . 

In case 54, accident on 5th. On 12th, temperature 98.4°. 
Died on 16th. (Post-mortem: No injury to general surface 
of brain but shallow local laceration of brain, one inch by 
one-third of an inch). 

In ease 56, accident 7th, admission 9th, died 19th. Tem- 
perature on 10th, 98:4, on 11th, right axilla, 95:82, left axilla 
97°8°. (Post-mortem: Superficial bruising of under surface 
of middle and anterior lobes). 

With regard to the occurrence of pyrexia in association with 
laceration or contusion of the brain the following may be поќе]. 
In all the cases of lacerated brain where the temperature is 


recorded after admission there is some pyrexia, save in three, 
viz., 54, 55 and 61. 


In case 61, there was a gradual rise, followed by a subse- 
quent fall before death. Definite laceration was present at 
post-mortem examination. 


In case 54, mentioned above, the laceration is extremely 


local and probably not to be classed with that usually 
described, whilst in case 55 it was superficial. 


78 Traumatic Subdural Hemorrhage. 


In the cases complicated with contusion the temperature is 
mentioned in five, and of these some pyrexia was present in four. 
In one case, 56, mentioned above, fever is absent as far as 
recorded temperatures go. 

In all the three cases where the temperature was over 104° 
before death all had cerebral laceration at the post-mortem 
examination. 


A reference to the various conditions found in the analysis of 
the temperature given above will be a sufficient reason for not 
drawing conclusions, and beyond merely epitomising the facts as 
follows, we shall discuss the matter no further. 


That in what appears as the simplest varieties of compression 
a marked rise in température may occur and may even proceed 
to hyperpyrexia shortly before a fatal termination.’ 


That the presence of a mild degree of pyrexia is not of evil 
significance, since it occurred in 75 per cent. of the cases in which 
a report of the temperature was given in the cases of recovery 
belonging to class À. 


That pyrexia may follow operation and yet the patient recover. 
(It ssems probable that in these cases the fever persists from the 
first, but that should it set in on the third day it has the usual 
sinister meaning). 

That in those cases where on айай or on their being seen 
soon after the injury the temperature is subnormal from shock 
but afterwards continuously rises to hyperpyrexia, the prognosis 


7 Attention may be here called to Lecture III., on ‘‘ Some points relating 
to Injuries to the Head,” delivered by Mr. Battle before the Royal College of 
Surgeons of England, and reported in the British Medical Journal, vol. ii., 
p. 141, where the relationship between compression of the brain and pyrexia 
is considered. He refers to three cases quoted by Mr. Jacobson in his paper 
on Middle Meningeal Hemorrhage in which the temperature rose, and all 
had some laceration. Не also refers to two or three where the temperature 
rose after operation. Passing on to Dr. Weisman’s cases, he refers to twelve 
of these in which pyrexia was present: in six of these, one recovered, and no 
post-mortem examination was made on the other five; in the six others in 
which a post-mortem examination was made, contusion of the brain was 
found in four, one had a temperature over 102° before operation and died 
of pneumonia, and in the last the temperature rose to over 106° without any 
apparent contusion of the brain. 


Traumatic Subdural Hemorrhage. 19 


is very bad and may even be said to be hopeless, since severe 
laceration of the brain substance is present. 


RESPIRATION. 
Class A.— 


There is no mention of the rate or character of the breathing 
in fifteen cases; of the remaining twenty-one cases— 

In seven it is mentioned that there was stertor with coma. 
In one of these (17) it is also described as interrupted, and 
the patient died two hours later ‘‘ asphyxiated.” 

In seven it is described as normal, or from the account 
there is every reason to believe that it is normal. In none 
of these cases was coma present. 

In the remaining seven cases various conditions were 
present. | 

These are in cases 4, 6, 11, 18, 20, 21 and 31, and must be 
considered a little more fully :— 

In case 4, the accident was on the 28th at 6.30 p.m. At 
9 p.m. on the 29th there was Cheyne-Stokes’ respiration, 
pulse feeble, 160, and the woman had been having fits for 
twenty-four hours. Her husband said that she suffered from 
epileptic fits and was a heavy drinker. At the post-mortem 
examination there was a little blood in the middle fossa by 
gravitation from a clot of two ounces over the left hemisphere. 
There was no blood round the pons or medulla nor was there 
blood intracerebrally. The kidneys were diseased, and the 
vessels at the base thickened and opaque but not aneurysmal. 
In this case the Cheyne-Stokes’ character of the respiration 
may have been due to the renal disease. It may be noticed 
that Cushing, in his Mütter lecture, looked upon Cheyne- 
Stokes’ respiration and the Traube Hering waves as due to 
the straining of the vaso-motor centre to overcome the 
conditions tending to produce bulbar anemia. This almost 
certainly is the explanation in case 20 reported below, but I 
do not consider it as a probable explanation of this case. 

In case 6, there was cyanosis with the fits, otherwise 
normal. 


80 


Traumatic Subdural Hemorrhage. 


In case 11, loud and stertorous, with convulsions, other- 
wise normal. 

In case 18, there is no mention save that the diaphragm 
worked spasmodically with the later fits. 

In case 20, there was first stertor. Later a tendency to 
Cheyne-Stokes’ respiration followed again by stertor. At the 
post-mortem examination blood was found to have gravitated 
around the medulla. 

In case 21, the rate only is mentioned. 

In case 31, the respirations ceased when the patient had a 
fit and when this was ended several deep breaths were taken. 
Class B.— 


There is no mention of rate or character of the breathing in six 


cases. Of the remaining thirty cases :— 


In twenty stertor is mentioned as being associated with 
coma. 

In one it is thirty to thirty-five, forcible, with coma. 

In one case (60) it is definitely said that there was no 
stertor when coma was present. In this case the patient 
had been bled before Mr. Hutchinson saw him, and his face 
is described as pale and pulse rapid and feeble. The lucid 
interval was very short. _ 

Cheyne-Stokes’ respiration is mentioned as being present 
in two cases (Nos. 53 and 67). 

In case 53, the patient first had stertor with coma, later 
there came Cheyne-Stokes’ respiration. After operation, at 
which а quantity of blood was removed, the respiration was 
again stertorous. The Cheyne-Stokes’ character recurred 
again before death. At the post-mortem examination there 
was a fracture of the vault and a small local fracture in the 
middle fossa at the left side. No hemorrhage about medulla 
or pons. The anterior part of the brain on the right side 
was smashed. Organs healthy. 

In case 67, the respiration was Cheyne-Stokes in character 
before operation. The skull was trephined, a large flat 
blood clot, found over the right motor area, removed, and 
recovery followed. 


The other references to the respiration are unimportant. 


Traumatic Subdural Hemorrhage. 81 


CONDITIONS OF THE LIMBS, 
Including the presence or absence of aphasia. 


I have thought it best to arrange the signs present under the 
headings given below. The division into class A and class B is 
adhered to. 

Class A.— 

a. Aphasia was present in eight cases (1, 7, 10, 11, 18, 23, 28 
and 30). In all these cases the aphasia was associated with some 
change in the condition of the limbs, paresis, paralysis or con- 
vulsions. 

b. Paresis or paralysis unassociated with convulsions occurred 
in eleven cases. Of these :— 

Consciousness was present in ... ... 6 (1,8, 7, 10, 
22, 23). 
Five were hemiplegic and one monoplegic (arm). 
Consciousness passing into coma was 
present in iud -— sèi — .. 2 (24 and 29). 
(Both were cases of hemiplegia.) 
Unconsciousness throughout was only 
present in ps ids E T ... 2 (5 and 34). 
(Hemiplegia was present in one, no record is given in the 
other case.) 
A condition of semi-coma with the obscure 
paralytic symptoms was present in the other 
case (32). 

c. Convulsions unassociated with paresis or paralysis were 
present in nine cases :— 

These were Jacksonian in type in... .. 2 (18 and 36). 
Unconsciousness during the fits with con- 

sciousness in between the fits was present in 3 (26, 27, 28). 
Convulsions, at first, Jacksonian in type 

but later associated with unconsciousness 

were present in m T ids .. 1 (19). 
Complete unconsciousness was present 

both during and between the fits in... ... 3 (4, 8, 21). 


82 Traumatic Subdural Hemorrhage. 


d. Paralysis or paresis associated with convulsions was present 
in seven cases :— 
The convulsions preceded the paresis or 


paralysis іп ... i i im ... 2 (4 and 31). 
The convulsions followed the appearance 
of paresis or paralysis in... i .. 2 (11 and 30). 


(In one of these the fits were Jacksonian in type.) 

The paresis preceded the convulsions and 
the paralysis followed in... 2 .. 1 (14). 

No statement as to the precedence of onset 
of convulsions, or paresis or paralysis is 
made in... s E $us - .. 2 (6 and 25). 

e. There is no mention of any paralysis, rigidity, or fits in five 
cases (2, 9, 13, 33 and 35), 

f. There are four other cases unclassified, viz., Nos. 15, 16, 17 
and 20. 

In case 15, there were twitchings of the muscles of the face 
and left upper extremity when the patient was in coma just 
before operation. At the post-mortem examination a large 
coagulum was found compressing the brain. No mention 
is made of any laceration. Atheroma of the aorta and 
granular kidneys were present. 

In case 16, there were very slight twitchings of both upper 
limbs when the patient was in coma on 26th. At the post- 
mortem examination blood was found compressing the left 
side of the brain. 

In ease 17, the limbs were powerless and flaccid from 
admission till death, there being no spasm at any time. At 
the autopsy, a quantity of soft blood-clot was found over the 
left middle cerebral lobe with very small ecchymoses beneath 
the pia mater on the same side. 

In ease 20, there was rigidity of all the limbs, with spasm. 
At the post-mortem examination blood was present over the 
whole brain and had gravitated down to the pons and 
medulla. 

It will be noticed that all these four patients died. 


Traumatic Subdural Hemorrhage. 83 


Class B.— 

a. Aphasia was present in two cases (63 and 69). Both re- 
covered after operation. The one was associated with Jacksonian 
epilepsy, the other with right facial paralysis and paresis of the 
right upper limb. 

Dysphasia was present in one case (64). This was a case of 
compound depressed fracture which came in with left-sided 
paralysis of the tongue, possibly the cause of the difficulty in 
speaking. The man recovered after operation. 

In case 70, the patient suffered from inability to name objects, 
following convulsions, which occurred a week after the accident. 
He recovered after operation. | 

It will be noticed that the above cases include four out of the 
six cases of recovery in class B. | 

b. Paresis or paralysis unassociated with convulsions occurred 
in ten cases :— 

Of these hemiplegia was present in six (45, 47, 55, 60, 62, 
65). 

err in two (61 and 69). 

Diplegia in one (both arms seem paralysed) (53). 

And general paralysis in one (72). 

In case 48, not included above, there was slight unilateral 
facial paralysis but uo difference in tonicity of limbs. 

c. Convulsions were present in ten cases :— 

In one of these cases the type was Jacksonian and 
associated with aphasia (63). 

In four there was some paresis or paralysis between the 
convulsions (46, 51, 54, 56). 

In one case there was rigidity of the right arm between 
the fits (67). 

In all save one (57) the convulsions, though usually starting 
in one definite part, spread to the whole of the body. In this 
one case they were unilateral. 

d. Rigidity is mentioned as being present in five cases (88, 39, 
44, 52 and 66) :— 

In four of these the rigidity was general, and in one of 
these it was preceded by clonic movements and associated 
with double facial paralysis. 


84 Traumatic Subdural Hemorrhage. 


In the remaining case (44) the left arm is described as 
twitching, and the left leg as rigid. 

e. General twitchings are mentioned in one case (40). In this 
case there was pronounced extradural and subdural hemorrhage 
with severe laceration of the brain. 

f. There is no record of the condition of the limbs in three 
cases (55, 59 and 68). 

g. Four cases caunot be classified as above. 

In two of these (42 and 43) there was no paralysis or 
rigidity before the onset of coma. In one (49) the limbs 
were flaccid on admission, but about two hours later power 
in the left arm was regained. Coma the whole time. In 
the remaining case there were clonic contractions at short 
intervals of the right arm and leg and sometimes of the left 
arm, with persistent tendency of the face to turn to 
the left side (case 71). Post-mortem, general concussion 
was found. 

All these four cases died. 


VoMITING. 

It seemed to me that it would be worth while making an 
analysis of the cases in which vomiting was present and those 
cases in which it was absent, in order to see if any connection 
between vomiting and compression might be suggested. Unfor- 
tunately there is no reliable evidence, since in only five of 
the cases belonging to class A was vomiting noted as being 
present, whilst the negative evidence is not given. It is probable, 
however, that in the majority of the cases in which no reference 
to sickness was made, none was present. Of the five cases in 
which the patients vomited, one died, and in this case the 
patient was only sick when on the eve of an attack of delirium 
tremens. Again, in class В, reference is only made to the 
occurrence of vomiting in eleven of the thirty-six cases, and 
in four of these the vomited matter was pure or mixed blood 
and associated with fractured base. No importance, of course, 
can be attached to this small amount of evidence, but I am 
of the opinion that vomiting and this form of brain compres- 
sion have but little relationship. Of the evidence forthcoming 


Traumatic Subdural Hemorrhage. 85 


above in most cases the sickness occurred before or immediately 
after arrival at the hospital and probably denoted recovery from 
the primary concussion. It is noticeable that in those cases with 
a long latent or lucid interval the patient did not suffer from 
vomiting during this interval. 


DELIRIUM.® 
This symptom has a threefold importance. In the first place, 


it may lead to the onset of hemorrhage owing to restlessness or - 
violence of movements, or increase the extravasation of blood if 
this be already present. Secondly, it may be an important sign 
of coexistent brain lesion, and lastly, it may point to acute or 
chronic alcoholism (drunkenness on admission or delirium 
tremens later.) 


The following is an abstract of the cases :— 
Class A.— 
No mention of delirium in eight cases. 


No delirium present or every reason to believe that none 
was present in thirteen cases. 

Of these, there was no lucid or latent interval in three, 
there was an alcoholic history in five; eight lived and five. 
died. 

Delirium was stated to be present in thirteen cases :— 

Of these eight lived and five died. One of the five that 

died was & case of delirium tremens, the only one reported, 
In addition the following cases (all of which recovered) may 
be specially mentioned :— 

Case 14, the delirium followed washing out of the stomach, 
and was followed by the onset of paralysis. 

Case 21, delirium was present iu the intervals between the 
fits. 

Case 25, it followed operation. 

Case 27, mentions that three days after the accident he 
was feverish (104°) and delirious. This was two days before 
the onset of fits. 

8 The presence of restlessness, constantly tossing about in bed, with total 
disregard for surroundings, at the same time muttering indistinctly or shout- 


ing loudly, violent movements, efforts to get out of bed, etc., are looked upon 
ав reasons for considering the patients delirious. 


VOL. LIX. 8 


86 Traumatic Subdural Hemorrhage. 


Case 34, the delirium was present after the first operation. 
At the second operation a glassful of dark red foetid matter 
was evacuated. 

Of the two remaining cases, 11 and 13, in the former the 
patient was restless and frequently moaned before passing 
into coma, whilst the latter was brought in dead. 

` Class B.— 

a. Cases in which it cannot be said that delirium was present 
or absent, 10. | 

6. Cases in which no lucid interval was present, 6. 

c. Cases in which there is no reason to believe that any delirium 
was present (64 and 69), 2. 

Case 64 was a case of compound depressed fracture of 
the skull for which the patient was trephined immediately 
after admission. 

Case 69, the patient was conscious up to the time of the 
operation after eight hours’ primary unconsciousness. 

Both of these patients recovered. 

Case 70 probably belongs to this group also. 


9 In looking through the cases coming under this class, it is rather difficult 
to decide how to arrange them in order that a fair idea may be obtained 
as to the presence or absence of delirium. The trouble is that in many cases, 
from what I have seen, delirium as shown by mere restlessness in bed, with 
incoherent talking or muttering, may be overlooked by those who have charge 
of the case owing to their leaving the patient to be washed and looked after 
by the nursing staff. By the time they again come to the patient in these 
cases it will be found in a large number that they will have become stupid, 
the early indication of passing into coma. Again, my own observations lead 
me to the conclusion that cases of compression associated with laceration 
may give no signs of delirium until the primary concussion has to a great 
extent passed off, and in many of these cases as the signs of concussion pass 
away the signs of compression set in. What I think is often found is that 
the patient is admitted unconscious; he starts to ‘‘come round," perhaps 
becomes a little restless, objects to examination, wants to lie still and almost 
immediately after this begins to pass into coma, the result of compression. 
When I first abstracted the cases coming under Class B, I found a large pro- 
portion in which there is no delirium mentioned, and no reason to believe 
that any was present, but a more careful examination showed me that in 
most of these cases the absence of reference to delirium was more probably 
to be explained by the absence of continuous observation and a definite 
active lucidity in between the primary unconsciousness and coma from com- 
pression. This contention will be borne out, I think, by reference to ten 


cases—37, 39, 42, 47, 52, 56, 59, 60, 66 and 71—and hence the heading (a) 
which refers to these cases. 


Traumatic Subdural Hemorrhage. 87 


d. Delirium was definitely present in 13 cases. 

In six of these there is a history of alcoholism, either 
from friends of the patient, or the patient was admitted 
drunk. In two of these six cases the delirium was probably 
that of delirium tremens. 

е. In the remaining four cases (45, 55, 65 and 68) a short 
period of restlessness, incoherent talking, or condition allied to 
delirium was present. 


THE URINE. 

The reason the presence in, or absence from, the urine of 
albumen was considered, was with the view of considering the 
possibility of traumatic subdural hemorrhage leading to the 
presence of albuminuria without renal or cardiac disease or 
intracerebral hemorrhage. 

The condition of the urine is only mentioned nine times in the 
cases coming under Class A. In six of these albumen was absent, 
whilst in three it was present; these were cases 6, 16 and 20. 

In case 6, there was a dense cloud of albumen present on 
admission, when the patient was having fits at intervals of one to 
five minutes, his temperature being 102° and pulse rate 100. 
There is no record of the condition of the urine following 
operation. | 

In case 16, the man had a large quantity of albumen in the 
urne when he passed into coma twelve days after admission. 
Nine days before the onset of coma there was no albuminuria. 
No operation was performed, and the patient died. The post- 
mortem record states that the kidneys were large and capsules 
adherent in places. Beyond swelling of the cortex, probably 
“from slight infiltration," there was no evidence of disease. 

In case 21, the patient was admitted after a fit in the street, 
and on admission the urine was 1020 with a slight amount of 
albumen, no casts, no sugar. He had frequent fits up to the 
time of operation, and temperature on admission was 102°, 
reaching 105° before operation. He recovered. 

The paucity of the information probably points to infrequency 
of albuminuria, and it is to be noticed that of the three cases 
in which albumen was present, two may possibly be explained 


88 Traumatic Subdural Hemorrhage. 


by the presence of convulsions, probably leading to elevation of 
blood-pressure and some increase of temperature, whilst in the 
third case, the albuminuria may have been the result of kidney 
disease. 

Of the cases coming under Class B, the condition of the urine 
is mentioned in ten cases, and of these albuminuria was present in 
four. In one of these (case 39) there was traumatic intracerebral 
hemorrhage unassociated with fracture of the skull. No disease 
of the kidneys or heart was found at the autopsy, and a lucid 
interval preceded the onset of coma. In the second case (67) 
fits occurred, and albumen was found in the urine. The patient 
was operated on, the clot removed, and recovery followed, but 
some motor and mental impairment remained. 

In case 69, there was a faint trace of albumen found in a man 
aged 39; urine alkaline, with specific gravity of 1035. At opera- 
_ tion, a slight cortical laceration was found. Recovery ensued. 

In case 70, the man was the subject of some form of chronic 
nephritis, and it is interesting to notice that recovery followed 
operation. 

These cases, again, neither prove nor disprove, but attention 
may be particularly called to the fact that subdural haemorrhage 
may be associated with the presence of albuminuria, and although 
the one cannot, from our facts, be said to be due to the other, 
and although the occurrence of the two together is not beyond 
the possibility of being due to coincidence, yet the fact that the 
two have been associated together in the same person, and yet 
recovery follow the removal of the clot, must not be lost sight of 
when considering diagnosis or prognosis. It may further be said 
that if multiple fits have occurred, the two cases coming under 
Class A and quoted above, point to their being a possible cause 


of albuminuria. 
Optic NEURITIS. 


It will have been noticed in reading the report of Mr. Symond’s 
case, given at the beginning of this paper, that optic neuritis 
was: found to be present, but cleared up perfectly after operation. 
It seemed to me worth while to find out what references were 
made to the optic discs in the cases reported. An examination 


Traumatic Subdural Hemorrhage. 89 


of the cases coming under Class A shows that in two cases the 
discs were normal (7 and 10) in one other the “ ophthalmic 
examination is negative " (17), whilst in case 22 there was double 
optic neuritis which was of a higher grade on the side of the clot. 
In this case the accident was at the end of February, the 
examination on the 28th April, and the man was conscious up to 
the time of operation (May 1st). These are the only references 
to the optic discs made in cases belonging to Class A. In Class B 
the optic discs are mentioned three times, viz., in cases 50, 52 
and 70. In case 50 Mr. Lane found double optic neuritis on the 
sixth day after injury; the patient died next day. At the post- 
mortem examination there was found extra- and subdural hæmor- 
rhage associated with severe laceration of the brain. In case 52 
both discs were found ‘‘completely blurred over” three days 
after the accident. Here, also, in addition to the clot there was 
severe laceration. In the third case (No. 70) the ‘slight chok- 
ing" of the right optic disc may have been due to the nephritis 
present. The importance of the possibility of optic neuritis 
occurring in cases of subdural hemorrhage is, it seems to me, 
that as the late onset of symptoms of compression may lead to a 
diagnosis of intracranial suppuration or possibly tumour, it is of 
some importance to remember that optic neuritis does not settle 
the diagnosis in favour of pus being present. Careful examina- 
tion of the optic discs in cases of compression by blood would 
probably show that changes in the discs are not at all uncommon 
in accidents associated with this complication. Its explanation 
probably lies in the venous stasis brought about by the compress- 
ing blood, as pointed out by Cushing (Mütter Lecture for 1902).? 
It must not be lost sight of, however, that optic neuritis may be 
found associated with concussion or with fractured base when no 
hemorrhage is present (see Lecture II. of Battle’s Lectures 
before the Royal College of Surgeons on “ Some points relating 
to Injuries to the Нега”). 


10 Attention may also be called to Dr. Fleming’s paper in the British 
Medical Journal, February 21st, 1908, vol. i., p. 409, “ Retinal Hemorrhages 
as a diagnostic feature in fracture of the base of the skull and in subarach- 
noid hemorrhage.’’ 


90 Traumatic Subdural Hemorrhage. 


DIAGNOSIS. 

In discussing the differential diagnosis of traumatic subdural 
hemorrhage, it is not my intention to inquire into the causes of 
coma, but to briefly refer to those conditions which have been 
seriously discussed when the diagnosis has proved difficult. These 
are extradural hemorrhage, intracranial suppuration, uremia, 
idiopathic epilepsy, cerebral hemorrhage and meningeal apoplexy. 

With regard to extradural hemorrhage, the following words 
from Mr. Jacobson’s paper on Middle Meningeal Hemorrhage, 
(p. 295), written when considering the differential diagnosis 
between extradural hemorrhage and hemorrhage into the cavity 
of the arachnoid may be advisedly quoted—‘‘ While the diagnosis 
between these two extravasations must remain for the present 
very difficult, if not impossible, the treatment must be the 
same,’ etc. The writer then justly points out that the diagnosis 
is usually made when the crown of bone having been removed 
by the trephine, ‘‘ the condition of the dura mater will very likely 
point to the presence of blood beneath it.” This is all that is 
really necessary to say upon the differential diagnosis of these 
conditions. They have these points in common, that there is 
blood compressing the brain, that if relief to the compression is 
not given the patients will most probably die, and the relief in 
both cases is afforded by the operation of trephining. With the 
present day antiseptic methods there is no need to vary the 
prognosis as the dura mater is opened or not. It is probable 
that in the case of a latent or lucid interval of over a week the 
diagnosis will cease to lie between the position of the blood with 
regard to the dura mater, whether it be external or internal to it, 
but will more probably raise the question of whether the com- 
pressing agent is blood or pus. At the same time the two 
following cases found in the Surgical Reports of Guy’s Hospital 
would point to the late onset of signs or symptoms in some cases 
of extradural hemorrhage also. 

G. C., 164 years of age, admitted under Sir Henry Howse in 
1888 (Report 220). His history was a kick on the right side of 
the head and shoulder on June 4th. He was admitted to a 
hospital from which he walked out on June 11th, but was 


Traumatic Subdural Hemorrhage. 91 


obliged to return next day. Не left this hospital again on June 
22nd and was admitted into Guy’s Hospital the same day at 
6 p.m., when he had double optic neuritis, retracted head, 
twitchings in the left arm, opisthotonos, pain in the head, photo- 
phobia, deafness of right ear and continuous crying. Mr. Howse 
trephined him in the afternoon of the 26th and a clot was removed 
from between the dura mater and the bone. The report does 
not mention the amount of the clot. The patient recovered after 
a long convalescence. 

In 1878, there was admitted under Mr. Cooper Foster (Report 
No. 271) a man of 30. The accident was on December 2nd, and, 
save for a series of fits on the 6th and 7th, in which the con- 
vulsions were general, he had no more symptoms pointing to 
compression. No operation was performed and the man 
ultimately died December 18th. At the post-mortem examina- 
tion a rather thick cake of black clot was found extradurally on 
the left side, with considerable bruising of the brain. The pulse 
was slow from admission on the 2nd until the 7th, but on the 
13th it was 100. | 

With regard to the diagnosis between this form of subdural 
hemorrhage and uremia, the question will be specially raised in 
those cases where convulsions follow the injury after the lapse of 
a long lucid interval. What was said about the albuminuria 
possibly resulting from the fits must not be forgotten. The 
spread of the fits from some definite part of the body is in 
favour of compression but the points upon which the diagnosis 
will be made will be multiple and the pros and cons weighed 
carefully before any opinion can be finally given. Mr. Henry 
Morris’s case (No. 16) was treated as though the coma was 
uremic in origin and the case may be cited as an example of the 
extreme difficulty which may be found in arriving at a diagnosis 
in anomalous cases. Beyond the coma it may be said that there 
was no sign or symptom pointing to compression, save a 
Hutchinson’s pupil. Attention may also be called to the fact 
that therapeutic treatment (pilocarpine, hot air bath, and calomel) 
led to marked improvement. It was when reporting this case 
that Mr. Morris wrote, ‘‘ They give rise to no symptoms which 


92 Traumatic Subdural Hemorrhage. 


are pathognomonic or which even suggest with any definiteness 
their presence. The symptoms of coma and paralysis which 
they excite may be delayed for an indefinite period and are liable 
to intermissions dependent on recurrence of the hemorrhage, or 
in old cases upon the more or less rapid absorption and effusion 
of the cyst fluid. Even when immediate symptoms of compres- 
sion occur neither the nature of the accident, nor the character 
of the injury to the head affords any clue whatever to the exact 
locality of the blood." 


Another example of difficulty in diagnosis is in the case 
reported by Raymond Johnson and Risien Russell (abstracted as 
case 6), and I cannot do better than repeat their own words 
when reporting the case. They wrote, ‘‘In the consideration of 
the nature of the case two possibilities may here be mentioned, 
The first, which was not, however, seriously entertained, was 
that the convulsions were urgmic in origin, for the urine 
contained a dense cloud of albumen. The second possibility 
which called for more careful consideration was that the case was 
one of idiopathic epilepsy brought out by a traumatism in an 
alcoholic subject with a strong predisposition to the disease, for 
we learned that the patient's father had died of epilepsy and that 
a brother was subject to epileptic fits. In this connection it may 
be noted that, although the fits almost invariably commenced on 
the left side, the first movement was commonly the turning of 
the head and eyes to that side, & mode of commencement that 
is too common in idiopathic epilepsy to be regarded as of much 
value in the diagnosis of a gross lesion of the brain. 


* Many fits, however, began by twitching of the left side of the 
face, and others by movements of the left hand, and this fact, 
taken in association with the weakness of the left arm, which 
was observed between the fits, the exaggeration of the left knee- 
jerk, and the presence of the extensor response on the same side, 
was regarded as indicating the existence of a definite irritation of 
the right cerebral hemisphere. The evidence at our disposal did 
not seem to justify the diagnosis of a focal lesion, in that the fits 
did not constantly begin in the same region, whilst all the other 


Traumatic Subdural Hemorrhage. 93 


phenomena observed could be as well accounted for by a general 
disturbance of the right hemisphere as by a limited lesion. 

"In the consideration of the nature of the lesion it may he 
remarked that, had the onset of the symptoms followed rapidly 
upon the injury, no hesitation would have been felt in regarding 
them as the result of an extravasation of blood over the right 
hemisphere caused by the blow on the opposite side of the head, 
the position of which was indicated by a small superficial scalp 
wound near the left parietal eminence. It was possible to 
explain the late onset of the convulsions by regarding them as 
the result of a simple non-inflammatory cedema spreading around 
a contusion or hemorrhagic focus in the cerebral substance; but 
the chief difficulty in accepting this explanation consisted in the 
absence of any sensory or motor phenomena during the six days 
preceding the onset of symptoms. Notwithstanding, therefore, 
the absence of any satisfactory source of infection, we were 
forced to the conclusion that the lesion was probably inflam- 
matory in nature—in fact, a meningitis.”’ 

In Mr. Symonds’ case a diagnosis of probably extradural pus 
associated with infective osteo-myelitis of the bare bone seen at 
the bottom of the occipital wound was made, and with this idea 
the patient was trephined here at the first operation, Nancrede 
in discussing the diagnosis between compression by blood and 
pus, wrote :-—““ A differential diagnosis can, under the most 
favourable circumstances, be only probable and in most cases 
impossible." It is also to be noticed that Sir William Stokes 
puts a long latent period as one of the points in diagnosis of 
traumatic subdural abscess (‘‘ Operative and Clinical Surgery," 
p. 200), and passes on to say that the condition associated with 
pus production may be apyrexial. These statements and cases 
are the best means of showing that the differential diagnosis 
may prove extremely difficult in many cases. The correctness 
or incorrectness of the diagnosis between the presence of an 
intracranial collection of pus or blood is not such a serious 
matter as that between compression by blood and uremia or 
idiopathic epilepsy, since, whether pus or blood be looked upon 
as leading to the compression, the only relief will be by trephining. 


94 Traumatic Subdural Hemorrhage. 


The diagnosis between traumatic subdural hemorrhage and 
the so-called meningeal apoplexy and idiopathic cerebral hemorr- 
hage may also be noted as extremely difficult at times. 


The following cases reported by Mr. J. Wood with the title of 
“ Meningeal Apoplexy’’ in Vol. xiii. of the Transactions of the 
Pathological Society (p. 1) will show how such difficulties occur. 


The man was found insensible (3 a.m. November 3rd), with no 
movements on the right side. On the left side the limbs moved 
on sprinkling the face with water. The mouth was not 
perceptibly drawn to either side. No reflex movements on 
tickling foot or leg of right side. Right pupil largely dilated; 
left, if anything, contracted. No movements of right eyelid, but 
friends said that he partly opened the left. 

November 4th. Coma the same. Stertorous breathing, 
flapping of cheeks. Died 2.30 p.m. 

The history was that he was an intemperate man, that he was 
intoxicated on the night previous to being first seen, but was able 
to walk. On arrival home, he threw himself on the bed and 
complained of headache. He finally went to sleep (or became 
insensible), not showing any signs of consciousness from that 
time until his death. 

Post-mortem: No marks of violence. Large clot in the 
cavity of the arachnoid on the right side covering the middle and 
posterior lobes. Surface of brain compressed. Clot extended to 
the base in the middle fossa and as far as the optic nerve, 
also covering the tentorium. Membranes healthy save for a patch 
of bright crimson colour on the inner surface of the dura mater, 
opposite the position of the largest portion of the clot. Effusion 
of lymph in this situation and an appearance of ulceration. The 
brain itself afforded no appearance of disease save that the veins 
were full of blood. The age was not given.” 


п As an example of the difficulty in diagnosis between traumatic subdural 
hemorrhage and idiopathic cerebral hemorrhage, reference may be made to 
a case reported by Sir John Ericksen in his ‘‘ Science and Art of Surgery,” 
vol. i., 10th edition, рр. 767—768. In this case symptoms of compression 
set in a fortnight after injury. The man was treated antiphlogistically but 
died in three days. At the autopsy there was fracture of the base of the left 
side and subdural hemorrhage on the right side. 


Traumatic Subdural Hemorrhage. 95 


It is almost impossible in many of the cases to decide with 
any certainty upon the diagnosis when some conflicting piece of 
evidence comes forward, but in leaving these brief notes upon the 
difficulties of diagnosis, after again emphasising the fact that 
most of these cases have been treated as extradural middle 
meningeal hemorrhage in the past, and will probably be so 
diagnosed in many cases in the future, the following may be 
stated as the most valuable signs of the lesion being due to 
compression by blood. The first of these is the presence of a 
scalp wound or bruise, recent or remote. The importance of the 
presence of an old scalp wound may be emphasised by such a 
case as that reported as number 21 (abstract of cases at the end 
of the paper). Here the man suddenly fell in the street, was 
taken to a hospital, where he remained entirely unconscious 
without any history, save that given by a scar, which was judged 
to be from three to six weeks old. He was trephined over the 
situation of this probable evidence of a previous accident and 
removal of a large clot resulted in recovery. In these cases 
where the onset of symptoms is so late the examination of the 
scalp in cases showing compression symptoms is especially 
valuable. The second important point to rely upon is the 
presence of a lucid interval. The importance of this symptom 
needs no discussion, but I think that attention may be called to 
one point, and that is that the length of the lucid interval may 
have some prognostic importance, in that the longer the interval 
lasts the better the chance of recovery for the patient at 
operation. It seems to me that, broadly speaking, this condition 
is borne out by an examination of the cases. This is to be 
looked upon as very far from a dogmatic statement, and whilst I 
hold that it will, on the whole, probably hold true, I do not lose 
sight of such cases as No. 83, reported at the end, where sudden 
death from a large extravasation occurred on the ninth day. 
Lastly, of all the other signs and symptoms given it is probable 
that the most important are the presence of a fractured base and 
pupillary changes, especially a Hutchinson pupil, which, however, 
must be looked upon as rarely occurring. At the same time it 
must be recollected that in the cases belonging to class А, in 


96 Traumatic Subdural Hemorrhage. 


which the diagnosis proves most difficult, fracture of the base of 
the skull is rarely present and pupil changes are not common. 


TREATMENT. 

‘‘Trephine and trephine early" was the dictum of Mr. 
Jacobson in reference to the treatment of middle meningeal 
hemorrhage, and this is the summary of the treatment of sub- 
dural hemorrhage. In the presence of symptoms it is the only 
treatment which affords relief, yet a number of cases having 
died without the performance of operation makes it worth while 
to consider the cases more carefully from this point of view, after 
which the conditions found at operation, and the principles of 
treatment dealing with the removal of the compressing blood, 
etc., will be considered. 

Of the thirty-six cases coming under class A, no operation at 
all was performed in ten; in one (15) an incision was made down 
to the bone over the position of the injury, but as no fracture 
was found the trephine was not used; whilst in one case (5) the 
dura mater was exposed it did not pulsate, an incision was made 
into it, when the brain immediately bulged and began to pulsate, 
no clot, however, being found. The patient died, and at the 
subsequent posi-mortem examination the clot was found on the 
opposite side. This case will be referred to again later. The 
ten cases in which no operation was performed were cases 4, 12, 
13, 16, 17, 19, 20, 31, 32 and 38. The reasons for operation not 
being performed in these cases are briefly stated as follows :— 
Fits, thought to be epileptic, a history of epilepsy being obtained 
(4); ahsence of symptoms up to practically the time of death 
(12 and 33); death immediately following blows, the man being 
brought into the hospital dead (13); late onset of symptoms with 
no reliable signs, a diagnosis of uremia being probably made 
(16); early death with no very reliable symptoms (17); a diagnosis 
of blood extending down to and compressing the vital centres 
and hence a belief in the uselessness of any operation (20), 
indefinite history of accident and great probability of idiopathie 
cerebral hemorrhage (31 and 82). 

Of the thirty-six cases coming under class B, no operation was 
performed in ten (39, 50, 54, 55, 56, 58, 59, 61, 62 and 68). In 


Traumatic Subdural Hemorrhage. 97 


the majority the explanation of witbholding the trephine probably 
is that severe laceration or contusion was diagnosed. 

The question of where to trephine will depend upon, first the 
situation of the blood as shown by the position of the paralysis, 
the site of onset of the fits, if such can be determined, or the 
side of a Hutchinson pupil should such be present. In the 
second place, the position of the injury to the scalp or cranial 
bones will have to be considered in many cases where definite 
localising symptoms are not present. The references to the 
occurrence of the hemorrhage beneath the position of the scalp 
wound or fractured skull, or its preséuce at the corresponding 
point on the opposite side of the skull (2.е., at position of contre- 
coup) are important; whilst the few facts relative to the condition 
of the skull bones may also be considered, and ainong these 
particularly the fact that in many of the cases belonging to 
class A no fracture of the skull has been present at all. As 
before stated, the probability is that in many cases the patients 
will be trephined with the diagnosis of extradural haemorrhages, 
the crown of the bone will be removed, and no clot being found 
the possibility of the blood being subdural will have to be taken 
into consideration. What are the points upon which this is 
decided? They are two in number, (1) the non-pulsation of 
the membrane, and (2) its colour. I have made an analysis of 
the conditions present in the seventy-two cases collected with a 
view to the reliability of these signs. The following is a table 
of the results :— 

Class A.— 

a. No mention of either colour or pulsation in thirteen 
cases. | 

b. No mention of colour but no pulsation present, or the 
dura mater is described as bulging out on removal of the 
crown of bone in five cases. 

c. The dura mater is described as ‘‘ brownish blue," 
“rather black," “ bluish,’’ ‘blood seems under," '*dark 
colour,” “ greenish hue,” “ dark cloudy ” in thirteen cases. 

(Of these thirteen cases there is absence of pulsation or 
presence of bulging of the dura mater in nine, in one the 


98 Traumatic Subdural Hemorrhage. 


fontanelle was bulging, whilst in one case where no operation 
was performed the dura mater was described at the post-mortem 
examination as ‘ flaccid " (No. 12). 

d. Of the remaining five cases—In case 5, mentioned 
above, the dura mater was exposed, did not bulge into tke 
wound, was incised; the brain bulged and at once began to 
pulsate. At the post-mortem the clot was found on the 
opposite side. 

In case ll, it is said the dura mater seemed normal, but a 
point of increased resistance was found in the lower third. 
After an incision here black clotted blood immediately exuded 
with each pulsation. 

In case 24, the dura mater was healthy, free, but no pulsation. 
On incision brown flocculent fluid came away. 

In case 25, the dura mater was healthy. It was opened and a 
clot found no bigger than a finger-nail. Serum around the clot 
produced compression. 

In case 29, the blood lay within the torn dura mater. The 
middle meningeal artery was the source of hemorrhage. 

It will be noticed that pulsation of the dura mater is not 
stated to be present in a single case, and that it is definitely 
stated to be absent, or the dura mater bulging in fifteen out of 
the thirty-six cases. 

Class B.— 

There is no mention of the dura mater either as regards 
colouration or pulsation in twenty cases. (Of these twenty cases, 
in ten no operation at all was performed; in one the skull was 
trephined on the wrong side; in two of them ‘ fluid” and “ red 
serum " came out under pressure.) 

Of the remaining sixteen cases— n twelve the dura mater 
is described as bulging, tense or non-pulsating. 

In one ease (44) extradural blood was removed in quantity and 
the dura mater was exposed, barely pulsating, tense and dark.” 


12 Note in this case the presence of a quantity of extradural clot. It is 
possible that the ‘‘ barely pulsating’’ may have been a slight immediate 
response to the removal of this extradural clot. 


Traumatic Subdural Hemorrhage. 99 


In two cases ‘‘ fluid was thought to be under the dura mater.” 
No reasons are assigned for this belief. 


In the remaining case (60) the patient was trephined with the 
diagnosis of right middle meningeal hemorrhage. No blood 
being found extradurally, nothing more was done. At the 
autopsy one and a half ounces of blood was found extravasated 
into the arachnoid on the side on which the trephine had been 
employed. 

Of the same sixteen cases—In only five is there any mention 
of the colour of the dura mater. In four of these it was “ dark,” 
“blackish,” “ black mass beneath," and ‘‘ somewhat yellowish 
opaque.” 

In the other case it appeared white, and in this case there was 
a small clot with a quantity of clear fluid surrounding it and 
compressing the brain. 

Case 35 (reported by Guthrie) is interesting reading when con- 
sidering the intracranial tension produced by subdural hemorrhage 
and its effect upon the pulsation of the dura mater. The man, 
a grenadier, after a lucid interval, fell into coma and was 
trepanned, but no extradural clot being found nothing further 
was done. 

“ Five or six hours after the operation he spoke and answered 
some questions, took some nourishment, but relapsed shortly 
afterwards into a similar state of stupefaction. On removing the 
ürst dressing the cause of evil was made manifest, the dura mater 
had risen up into the opening made by the trepan and was above 
the level of the bone, which had given some relief to the com- 
pressed parts and had probably been the cause of the temporary 
amelioration which had taken place." The dura mater was 
opened, blood evacuated, and the man recovered. It is after 
recounting this case that Mr. Guthrie goes on to say, ‘‘ I consider 
this tense elevation and the absence of pulsation to be positive 
signs of there being a fluid beneath requiring an incision into the 
dura mater for its evacuation. It is a point, scarcely, if at all, 
noticed in English surgery, although much insisted upon in 
France.” That the tenseness and non-pulsation of the dura 
mater are far more valuable than the colour will be emphasised 


100 Traumatic Subdural Hemorrhage. 


by the fact that if colour be relied upon, two conditions at least 
may lead to error, one being that the compressing agent is not 
always blood, but may be blood and serum, or serum alone, 
when there will be practically no discolouration notwithstanding 
the presence of pronounced compression; the other, that a thin 
layer of blood over the surface of the brain, associated with 
severe coptusion yet incapable of compression, may cause dis- 
colouration, and this may also appear to be present when 
merely caused by the very distended veins on the surface of the 
brain pressed against the membrane. Of course, in the cases of 
subdural hemorrhage the cause of the tense dura mater is the 
excessive intradural tension which will also be present in cases 
of tumour, abscess, oedema, or large intracerebral hemorrhage. 

Before leaving the subject of tenseness of the dura mater 
reference may be made to the line of treatment to be followed 
when the dura mater is exposed, opened, and yet no compressing 
blood or fluid of any kind can be found. In these cases the 
brain usually bulges through and begins pulsating. Of course it | 
is possible the diagnosis is wrong and that a collection of pus 
may be present intracerebrally, but two possibilities must 
always be kept in view, the one being that the exact situation 
of the blood has not been found, and that another trephine hole 
may be necessary. Under these circumstances the relationship 
of the trephine opening to the brain and the motor phenomena 
present have rapidly to be considered, and the introduction of a 
curved director into the arachnoid cavity for the purpose of 
examining the neighbouring areas will probably prove satis- 
factory. The other possibility is that the paralysis and lesion 
may be on the same side. A sufficient number of such cases 
have now been reported to make it always worth while con- 
sidering such a possibility. I will refer to four cases in which 
the paralysis and lesion were on the same side. Mr. Mansell 
Moullin’s case (5) is one. Another was reported by Dr. Dawbarn 
(Transactions of the New York Surgical Society). 

The patient had a blow on the right side of the head. During 
the following week he became more and more irritable. Then 
partial left hemiplegia and left facial paralysis developed. Two 


Traumatic Subdural Hemorrhage. 101 


discs of bone were removed from the site of injury and nothing 
found. The patient died two days later. At the autopsy a large 
blood clot was found over the left motor area, between the dura 
and the skull. Examination showed subsequently that it was 
one of those very rare cases where motor fibres had not crossed. 

In the Lancet for May 26th, 1894, p. 1302, is reported a case 
by Мг. G. E. Turgnam, “Fracture of the Skull, paralysis on the 
same side as the lesion." 

The case was one of depressed fracture, in a girl, aged 5. 

The last case to which I shall refer is reported in the Wein. 
Klin. Rundsch (abstracted in the Journal of the American Medical 
Association, December 4th, 1897, p. 1188, “ Subdural hematoma 
with uncrossed motor nerve tracts." ‘After a fall, dangerous 
symptoms developed, all indicating a subdural hematoma on the 
left side. Trephined on the left side without any result. As a 
fatal termination was imminent trephining was performed on the 
right side and a hematoma found. Recovery was prompt and 
complete, demonstrating the existence of uncrossed nerve 
tracts.” 

It seems worth while from the above recorded cases to suggest 
that when the clot cannot be found on the one side after a 
careful search, the opposite side of the skull should be trephined 
and a careful search be made for it there. 

Inreading through the reported casesit will be found that the com- 
pressing agent in some cases was not only blood, either as coagulum 
or fluid, but in addition some clearer fluid was present. In some 
cases this “fluid” was quite clear, surrounding a small clot, as in 
Mr. Butlin’s case (25), in others it was tinted red by the blood 
present and is then described as “red serum," such as was 
present in Mr. Symonds’ case. My attention was first called to 
the importance of deciding what the explanation of this “ serous 
fluid" was by Mr. Symonds, who remarked upon it when it was 
removed at operation. For a long time, beyond Mr. Butlin’s 
case and his explanation of it and the fact that such fluid was 
present also in cases, 22, 24, 26, and 30 belonging to class A, 
and cases 37, 40, 41, 42, 45 and 46 belonging to class B, I could 
find no reference to the probable source and nature of this fluid. 


VOL. LIX. 9 


102 Traumatic Subdural Hemorrhage. 


Mr. Butlin explained its origin in the case he reported as: 
probably being derived as an effusion, serous in origin, the result 
of the irritation set up by the presence of the clot. In the 
American Journal of the Medical Sciences, vol. 116 (1898), 
however, I found a paper entitled, ‘‘ Subarachnoid serous exuda- 
tion productive of pressure symptoms after head injuries,” by 
George L. Walton, M.D., in which the presence of a clear serous 
fluid without blood or injury to the brain is described as a cause 
of cerebral compression. His words are as follows: ‘It not 
unfrequently happens in these cases that trephining over the 
area indicated by the paralysis shows negative results beyond 
revealing a tensely bulging dura, incising of which is followed by 
a free flow or rather gush of clear fluid, the brain beneath 
presenting no laceration or other abnormality beyond perhaps 
oedema.” Dr. Walton then cites two cases; in one, а boy, aged 
16, pronounced focal symptoms came on immediately after an 
injury, in fact the writer says, ‘‘The case up to this time had 
appeared very suggestive of middle meningeal hemorrhage.” 
Improvement, however, steadily took place and the boy 
recovered perfectly without any surgical interference. His second 
case, occurring in a child three and a half years old, was similar. 
He then quotes another case in which operation was per- 
formed and this condition found. After giving diagnostic 
suggestions he draws a series of conclusions of which an abstract 
is as follows. That the condition can occur directly at the site 
of injury or contre coup, with or without cedema of the brain 
substance ; that meningeal hemorrhage may be simulated; that 
the condition is not compensatory but represents ineffectual 
efforts to relieve tension; that the lesion is self-limiting ; and, 
finally, that paralysis following a blow on the head is not a 
reason for immediate operation. 

In looking through the surgical reports of Guy's Hospital, I 
have found several cases reported where operation for compres- 
sion has been performed, clear serous fluid escaped, and the 
patient recovered. The following is an example :— 

Year 1878. Report 464, Mr. Davies-Colley.—Charles F., 
æt. 38, fell twenty to thirty feet. Picked up unconscious, 


Traumatic Subdural Hemorrhage. 108 


brought up to the hospital and admitted October 6th. Remained 
unconscious until the 9th, when he developed fits on the right 
side. Trephined and a subdural collection of cerebro-spinal 
fluid found on the left side. No injury to the brain.. The dura 
mater was not sewn up nor the bone replaced. Flap sewn up. 
From 11th to 14th had fits. On the 15th consciousness returned. 
(Urine 1020, no albumen.) Paralysis which had been present 
on the right side is said to have passed off on the 16th, but a 
little paralysis of the left side of the face remains. On October 
20th the stitches were taken out, the wound healing by first 
intention, and the man went out soon after. 


The next case is one of recovery without operation :— 

Year 1881, report 216, Mr. Bryant.— This is the report of a 
girl, Eliz. C., 12 years old, who fell backwards down four steps 
on to the back of her head. She lay for a few seconds then got 
up, walked upstairs, and again became unconscious. She was 
admitted on June 20th, and was sick three times within twelve 
hours of coming in. She recovered perfectly without operation 
and was discharged on July 3rd. 


This last case may be compared with one given by Guthrie. 


P. T., 24, was struck on March 16th, 1837, by a musket-ball, 
on the frontal bone, which it fractured but did not penetrate. 
Walked into the ward from the field of battle, some two miles 
distant, and conversed intelligibly for some time to his comrades. 
Much hemorrhage had taken place. Towards evening he 
became comatose; pulse slow, weak; surface pale and cold. 
Mercury, jalap and some pulv. ipecac. were given at 9 p.m. 
Noted that a small arterial branch had bled very freely, by 
which the symptoms have been relieved. On the 22nd, the 
pulse was 52, sluggish. He made a perfect recovery. 


In this case the loss of blood probably had much to do with 
the recovery, since all the available fluid was, in all probability, 
immediately taken up by the vessels. This idea receives support 
from the case reported by Le Drans, and quoted by Guthrie 
with the above case.  (Guthrie's ‘‘Injuries of the Head," 
p. 97.) 


104 Traumatic Subdural Hemorrhage. 


A case in which a diagnosis of ruptured middle meningeal 
artery was made was reported by Mr. Legg in the Clinical 
Journal, December 30th, 1903, p. 176, “ Head Injuries." 

In the New York Medical Journal, April 7th, 1894, p. 434, is 
a case reported of ‘‘ Brain Cyst, the result of injury, causing 
aphasia, hemiplegia, etc. Evacuation; complete recovery," by 
C. H. Mayo, M.D. 

O. S., female, 11 years, thrown from a waggon, June 30th, 
1893. Picked up unconscious, bleeding freely from the nose, 
and while being carried into the house had a severe vomiting 
spell. There was a small scalp-wound and extensive bruising. She 
remained unconscious for six weeks; afterwards she began to 
notice things with her eyes. She had right hemiplegia, and on 
the fifth day after admission she had twenty-five convulsions, 
and these were continued for a week, becoming less frequent 
each day. On August 18th she was trephined over the left 
fissure of Rolando; four ounces of clear fluid was removed 
subdurally and the left Rolandic area was found to have been 
depressed one inch from the skull. 

This case would seem to suggest that the self-limiting power 
of the effusion is not absolute. 

A case of extradural clot in a thin layer with clear fluid 
subdurally is reported by Mr. A. E. Maylard. The case was 
brought before the Glasgow Medico-Chirurgical Society on 
November the 1st, 1895, and is reported in the Glasgow Medical 
Journal, February, 1896. It occurred in a girl of nine years old. 

The effusion may occur without trauma. Two such cases are 
reported. Опе in the Lancet, September 22nd, 1900, ‘‘ Trephin- 
ing and Drainage in an apparently moribund case of Status 
Epilepticus: Recovery." (Under the care of Dr. W. Alexander, 
notes of the case by Dr. W. T. D. Allen, Sen. Resd. Med. Off.) 

This was a woman, æt. 36, admitted July 4th, 1900, in a semi- 
conscious state, suffering from very severe epileptiform convul- 
sions. From the previous history the patient appeared to have 
been in good health until the previous February, except for 
occasional attacks of articular rheumatism. She had been very 
much addicted to drink, and in February had been taken into 


Traumatic Subdural Hemorrhage. 105 


custody for this cause, and it is stated that the policeman then 
struck her on the head with his bâton. The head became 
swollen and she was treated in the prison hospital. After two 
weeks in prison she was removed to the workhouse, where she 
had an epileptiform fit which lasted fifteen minutes. The con- 
vulsions involved the limbs on both sides of the body and the 
patient was in a rather stupid condition for a day and a half 
after the fit; she made a gradual recovery in ten days. She had 
never had a tit of any kind previous to this time. During the 
next four months she was in fair health, save for a pain in her 
head, which was at times very severe. On July 1st, convulsions 
began again and continued at very short intervals for four days 
until she was taken to the workhouse hospital. On admission 
she was semi-conscious ; she had over forty fits in twenty hours. 
These began with twitchings of the muscles of the lower part of 
the face on the right side, which then spread to the right hand, 
arm, and leg. Corneal reflex was absent and the eyes directed 
to the right. Each fit lasted three to four minutes. On July 
5th the patient appeared moribund and was trephined by Dr. 
Alexander over the upper motor area on the left side. The 
dura mater bulged into the opening on removal of the bone 
and was opened. The cerebral veins were much enlarged and 
lay bathed in a layer of fluid a quarter of an inch thick. The fluid 
was held in the meshes of the arachnoid and pia mater, and 
when the meshes were pricked the fluid ran away in a clear 
sparkling stream ; a gauze drain was used. After the operation, 
the patient had several fits and these continued for three days 
but gradually diminished in frequency and severity. Since then 
there has been no return of the convulsions or headache. 

Of course, in this case it is possible that the whole trouble 
dated from the injury and that the symptoms varied as the 
fluid “ ebbed or flowed.” The other case is reported in the 
B. M. J., October 17th, 1896, vol. ii., p. 114. It is the first of 
"Two cases of Jacksonian epilepsy treated by operation," by 
Albert E. Morison. 

Subdural collection of straw-coloured fluid, but without any 
history of accident at all: Operation: Recovery. 


106 Traumatic Subdural Hemorrhage. 


From the above cases it would seem that in cases of subdural 
hemorrhage the compressing force of the blood extravasated 
may be added to by the exudation of a serous fluid probably 
derived from the lymphatics. The irritation of the brain 
by blood-clot seems to be sufficient reason for this fluid 
being extravasated in some cases, but that other factors are 
introduced is certain from the cases quoted above. The date of 
the extravasation also seems variable; thus, in cases 22 and 24 
there was a latent interval of twenty-two and twenty-four days 
respectively, and at operation brown serum was removed in each 
case. In these cases it seems probable that there was & small 
clot, much as in Mr. Butlin's case, but for some reason which for 
the present seems inexplicable, the serous exudation did not 
occur until the clot was undergoing degenerative changes, as 
shown by the.brown colour. In case 24 the latent interval 
lasted up to the twenty-fourth day, but the lucid interval up to 
the twenty-seventh day, when the patient lapsed into coma. 
This is the only case coming under class À where coma super- 
vened as a result of such exudation. In the other three cases— 
Nos. 25, 26 and 80—there were latent intervals respectively of 
four, six and two days. 


There is very little more to be said upon the compressing 
blood. In the cases of marked hematoma it will lie in the 
cavity of the arachnoid,” and will be exposed immediately the 
dura mater is incised. The probable reason for this is that as a 
result of the injury the delicate arachnoid is torn at the site of 
injury and extravasation, and even were this not so it seems 
probable that the force of the extravasated blood would cause it 
to break through into the loose cavity of the arachnoid (which, 
though only a potential space is capable of becoming a very 
large actual one) rather than constantly breaking down the 


13 Sir Prescott Hewett speaks of extravasations of blood into the cavity of 
the arachnoid. Mr. Henry Morris reported his case as hemorrhage into the 
cavity of the arachnoid. Mr. Jacobson, in his paper referred to above, 
differentiates between extradural middle meningeal hemorrhage and 
hemorrhage into the arachnoid cavity. Ihe cavity of the arachnoid is thus 
generally recognised as the situation of the blood. 








Traumatic Subdural Hemorrhage. 107 


meshes of the subarachnoid space. The following is an analysis 
of the amount of the compressing blood or blood serum :— 
Class A.— 

The amount present is mentioned in ten cases :— 

The greatest amount present was four ounces (case 12). 
The least amount present was half an ounce (case 18). 

The average amount present in nine cases was two and one- 
third ounces approximately. 

In the tenth case twenty-five grammes were present. 

The thickness of the clot is mentioned in three cases (10, 5 
and 19), where it was respectively one and a quarter inch, three- 
quarters of an inch and one-sixth of an inch thick. In this last 
case the man had a definite lucid interval and focal symptoms. 
He was not trephined only because of the disadvantages of his 
position. 

Class B.— 

The amount is only mentioned seven times. 

The greatest amount present was five ounces (case 59). 
The least amount present was one ounce (case 14). 

The thickness was mentioned on three occasions, when two 
and a half inches, one inch and half an inch were given. 

The case in which the clot was two and a half inches thick 
had a lucid interval of at least twelve hours (case 65). 

There is & case, however, reported by Sir B. Brodie in a 
paper to the Medico-Chirurgical Society (Transations, pp. 347- 
348), in which the compressing blood measured eight ounces. 
The case is not classed in the seventy-two reported cases owing 
to the want of detail. The woman had a lucid interval of one 
hour. No operation was performed, the condition being found 
post-mortem. 

One other point requires mention, which is the possible 
presence of two strata of blood, one of which may be removed 
and the other left, giving some relief which may only prove 
temporary. The best example of this is the case reported by 
Mr. Edmund Owen (case 18). Here at the first operation a large 
clot was most thoroughly removed from the cavity of the 
arachnoid. After the operation a quiet night supervened but 


108 ` Traumatic Subdural Hemorrhage. 


further progress was stayed by the onset of severe convulsions 
which led to the wound being reopened two days after the first 
operation; the arachnoid membrane was incised and some clot 
removed from the subarachnoid space. Gradual complete 
recovery followed. 

In case 64 also there were two layers of clot. 

The method of removing the clot will vary with the operation 
and the conditions present. Various methods have been employed 
by different operators. In case 1 a blunt spoon was used; in 
case 10 a finger and spoon; in case 27 the little finger and the 
scoop end of a director. 

There is an interesting case reported in the Journal of the 
American Medical Association, vol. xxiii, p. 952, by Dr. J. B. 
Hamilton, in which the method of removing the blood showed 
great ingenuity. 

Sister A., et. 20, strong and healthy. Struck on the head just 
posterior to the right Rolandic fissure by a staple or hook, on 
June 18th. There was great pain, but no wound. Severe head- 
ache followed which never disappeared. Vision in the right eye 
gradually failed and she became totally blind in that eye. Deaf 
ness in the right ear began almost immediately after the accident 
and continued. "There was no motor paralysis, no loss of sense of 
smell or taste. "Vision and hearing apparently normal on the left 
side. Trephining November 15th. The dura mater was healthy ; 
it was incised and a silver wire loop passed downwards and 
forwards towards the optic commissure. On withdrawal, a firm 
round coagulum about 3 cms. in length was found attached to 
the wire. The dura mater was sutured and the bone replaced, 
the wound being closed. Complete recovery followed. 

Irrigation was stated to be employed in five cases. These were 
18, 28, 42, 47, 69. Various fluids have been used, including 
boracic lotion, lysol, carbolised water and salt solution. 

In the cases belonging to class A, it seems that the hemorrhage 
is not difficult to stop, there seldom being any recurrence of the 
bleeding when the clot is removed, but in the cases belonging 
to class B severe and even dangerous recurrence of the bleeding 
may take place. This was so in cases 43, 44, 46, 47, 64 and 66. 


Traumatic Subdural Hemorrhage. 109 


In case 48, the blood coming from lower down in the subdural 
space seems to have been impossible to arrest, even by packing 
with gauze. The dressings were repeatedly soaked through with 
blood, and so great was the loss that the patient was infused 
just before death." | 

In most of the cases of severe hemorrhage a plug of gauze 
seems to have controlled it. In cases where severe persistent 
bleeding comes from low down its origin is probably from the 
lateral sinus. In case 71, a bleeding cerebral artery was tied and 
in case 40 a bleeding cerebral vein. 

Lastly, the advisability of drainage will have to be considered. 
An analysis of the seventy-two cases is as follows :— 

Class A.— 

In the first place, it is to be noticed that of the fourteen cases 
which died, eleven had no operation at all; in one the operation 
was performed on the side opposite to the collection of blood and 
had no bearing on the result; of the two remaining cases, in one 
drainage was employed and in one the dura mater was sutured 
and the bone replaced. 

Of the twenty-two cases which recovered :— 

Drainage was definitely employed in ten. 
A tube was used in three. 

Gauze was used in two. 

Horsehair was used in two. 

The nature of the drain is not mentioned in 2; whilst in the 
remaining case the space was drained with a strip of gutta 
percha, the bone being replaced. 

No drainage at all was used in one case (No. 1). In No. 6 also 
no drainage was probably used, the divided dura turned into 
position, the scalp incision sutured, the bone not replaced. 

Two cases came in in the pre-antiseptic days and in these the 
dura mater was only punctured. 

In case 18, some form of drainage was probably employed down 
to the dura mater, which was sutured. 

In case 26, the dura mater was stitched, but the bone not 
replaced ** because of bulging.” 


и Unfortunately no post-mortem examination was made. 


110 Traumatic Subdural Hemorrhage. 


There is no reference to the method of suturing or dressing in 
SIX Cases. 

It may be noticed that in case 28 ‘‘the wound was lightly 
packed with gauze and allowed to granulate." It might be 
thought that by this method there would be a risk of anchoring 
the surface of the brain to the bone round the trephine opening, 
it is therefore interesting to note that he made a perfect recovery, 
and three months after his discharge was working in a colliery 
where he had been for some weeks, and was doing perfectly 
well.” 

Class B.— 

Of the six cases which recovered, in five drainage was used, 
and in the other there is no mention as to whether it was used 
or not. 

Of the other thirty cases — 


There was no operation in 242 “ ; . 10 
The dura mater was not opened after Керн in... 1 
There is no mention whether drainage was or was not 
used іп ... ' T -— xe O 
Drainage was definitely saployedt i us "S .. 10 
No drainage was employed in  ... ae uve. d 


These last three patients were Nos. 46, 47 und 66. 

In case 46, the dura mater was stitched, the bone replaced, and 
the flap sutured in position. This was on January 25th. On 
the 10th day of February grave symptoms set in, the patient 
having done very well for the previous sixteen days. The wound 
was opened up and a cerebral abscess found. Death followed. 
There was no autopsy. A fracture of the base was undoubtedly 
present. 

In ease 47, the wound in the dura mater was closed, the bone 
being replaced in pieces, and the skin sewn up with a gauze 
drain. Death occurred three days later, and at the post-mortem 
examination a re-accumulation of blood was found. 

In case 66, “as the bleeding came from some inaccessible 
source, the wound was sewn up and the man sent to bed. At 


15 The fact that only three months had elapsed makes the value of this 
statement practically negative from a prognostic point of view. 


Traumatic Subdural Hemorrhage 111 


the post-mortem examination, the subarachnoid space over the 
hemispheres was practically filled with blood.” 

It will thus be noted that of the two cases where it was 
considered satisfactory to do without drainage (viz., 46 and 47), 
in the one, had it not been for the accidental complication, there 
is every reason to believe that a. satisfactory result would have 
followed, whilst in the other there can be little doubt that lack 
of drainage at least hastened a fatal result. 

It would seem safe to close the wound entirely when all clot 
has been removed, no recurrence of bleeding has taken place, 
and expansion of the brain has followed, but no rules can be 
finally laid down, and every case will probably be treated from 
the special conditions found. 


PROGNOSIS. 


The importance of compression by blood seems to depend 
upon three points— the first, the rapidity with which the blood is 
poured out; the second, the amount of blood so poured out; and 
the third its position. The importance of the rapidity with 
which the blood is poured out is shown by cases such as 
Nos. 17 and 38, where the patient dies almost at once. Such 
cases may show a much smaller amount of blood extravasated 
than in many which recover after operation, but the rapid 
extravasation would appear to lead to sudden paralysis of the 
vital centres in the medulla, probably from the sudden trans- 
mission of the compressing force. That the amount of blood 
poured out is another important factor is again undoubted, and 
this acts by the transmission of the pressure to the vasomotor 
and respiratory centres in the medulla, whilst the importance 
of the position is that the nearer the clot is to the base the 
greater its effect upon these vital centres. Sir B. Brodie, with 
reference to the importance of the position of the clot, said, 
“There is reason to believe that pressure is on the whole more 
dangerous when it affects the lower part of the brain than when 
it affects the upper part.” 

The division of the seventy-two cases under consideration into 
classes A and B is a prognostic one. The former are pure 


112 Traumatic Subdural Hemorrhage. 

compression, and being such, the relief of the compression 
should mean recovery; the latter are associated with severe 
cerebral injuries, and, although the compressing blood may be 
removed, in most cases early death will usually follow, owing to 
the severe concomitant injury to the brain. In class A, of the 
thirty-six cases recorded, twenty-two recovered and fourteen 
died. The reasons for death occurring in these cases has been 
set forward briefly when considering treatment. It will be 
noticed that a bad prognosis would have been given in the 
majority. In class B, numbering also thirty-six cases, only six 
recovered. In these cases the laceration or contusion of the 
brain most probably accounted for the fatal result. Of the total 
seventy-two cases collected, therefore, twenty-eight recovered and 
forty-four died, ?.e., thirty-nine per cent. of recoveries. This 
compares well with the eight recoveries out of the seventy cases 
reported by Mr. Jacobson of extradural hemorrhage from 
rupture of the middle meningeal artery, t.e., 11:5 per cent. of 
recoveries. 

It must be mentioned, however, that Mr. Jacobson goes on to 
say that five other recoveries are reported. But no statistics 
will prove of any real avail in giving a prognosis in cases of 
compression by blood clot in individual cases. What has to be 
considered on such occasions are the signs and symptoms of 
the case under consideration, and it is possible that no sign or 
symptom is so valuable in leading to a good prognosis as a 
definite active lucid interval, during which the patient has 
appeared comparatively well and acted as an intelligent indi- 
vidual, whereas no prospect will appear more hopeless than that 
where no lucid interval at all has been present, or if it has been 
present, has been brief and associated with a nervous irritability 
and irresponsibility, which bodes ill, pointing as it does to severe 
brain injury. 

In people advancing in age hemorrhage into the brain sub- 
stance may occur in association with the subdural extravasation. 
Dr. Goodhart mentions such a case in his paper (case 32) on 
* Meningeal Hemorrhage,” published in vol. xxi. of the Guy's 
Hospital Reports. 


Traumatic Subdural Hemorrhage. 118 


. A man, set. 68, slipped on a step and fell a short distance, 

striking the left temple. Short lucid interval followed. He had 
slow breathing and slow pulse. Pupils could not be observed. 
At the autopsy, there was two ounces of blood in the left sub- 
dural space, and hemorrhage into the corpus stratum and 
septum lucidum on the opposite side. 


A case of subdural hemorrhage, associated with pontine 
hemorrhage, was admitted under Mr. Durham in May, 1891 
(Report 341). | 

Mary A., æt. 51.—She had brought up a large quantity of 
blood six months before. She drank freely. She was found 
at the bottom of ‘fourteen steps perfectly unconscious, and 
with stertorous breathing. She remained the same all night, 
save for some slight bleeding from the nose and mouth, and was 
sent up and admitted next morning. The right pupil was 
dilated, the left contracted, neither reacted to light. Pulse 60, 
irregular. The right arm was slightly stronger than the left. 
Paresis of the right side of the face. There was some bogginess 
over the left parietal. She was trephined over the left side but 
nothing found. At the subsequent post-mortem examination, 
there was two and & half ounces of clot subdurally on the right 
side, and several small perivascular hemorrhages into the pons. 
Extensive bruising of the brain was present but no fracture of 
the skull. 

A somewhat similar case was under Mr. Davies Colley's cars 
in 1889 (Report 307). 

An unknown man was knocked down by a van and admitted 
to the hospital. He was unconscious and with a slow pulse on 
admission. А small scalp wound above the occipital protuber- 
ance was present. After he had been in a few minutes the pulse 
fell to 40, the pupils became unequal, the left contracted and 
right dilated ; some rigidity was present on the left side, including 
the facial muscles. No strabismus was present. He was 
trephined over the scalp wound, but the exposed membranes found 
to be healthy. At the autopsy, he had an ounce of blood sub- 
durally, bruising of the brain, and multiple hemorrhage into the 
pons. 


114 Traumatic Subdural Hemorrhage. 


In cases where the subdural hemorrhage is probably due to 
a cerebral hemorrhage breaking through externally, a very 
guarded prognosis will be given, even though the patient may 
survive (as in case 70) and in those cases where there is found 
thickening of the meninges, associated or not with hemorrhage 
(the so-called pachymeningitis interna hzemorrhagica) the patient, 
though he recover, will always be liable to serious trouble 
following slight injury. In the Medical Record for April 30th, 
1898, p. 115, Dr. R. Van Santvoord reports & case of subdural 
hemorrhage found at post-mortem examination where there was 
* general congestion of the meninges with thickening of the pia,” 
concerning which he says, “this man evidently had a chronic 
alcoholic meningitis before his injury. The essential factor in his 
case was apparently a traumatic exacerbation of this disease.” 
In the American Journal of the Medical Sciences, vol. 109, pp. 
404-406, there is a case of ‘‘ Localised hemorrhage beneath the 
pla mater, over the upper third of the Rolandic area, due to a fall 
on the head." By Dr. J. J. Putnam. 

The patient was a lady, aged 72, who fell down some steps. 
She was not fully stunned and with assistance walked into the 
house and upstairs. She was seen by Dr. С. Р. Putnam and 
then appeared in a good general condition, but had bruising of 
the scalp. For twenty-four hours she did well, after which 
spasms, followed by paresis and ultimately paralysis set in. 
Two days later coma was present. Death took place ten days 
after the accident. At the autopsy, there was no fracture of the 
skull but subdural hemorrhage on the right side of the skull, 
especially posteriorly. Microscopic examination showed the 
existence of an old vascular false membrane. It was from these 
vessels that the subdural hemorrhage had occurred. 

In the Transactions of the Clinical Society, vol. xxv., pp. 
157-160, is reported a case of *'Pachymeniugitis Interna 
Hemorrhagica treated by trephining." By Mr. Stanley Boyd. 

An innkeeper, 40 years of age, accustomed to live freely, fell 
on March 31st, 1891. Bruising of the scalp with a somewhat 
dazed condition, was found soon after. For the next fortnight 
he suffered from headache and remained in bed. He went back 


Traumatic Subdural Hemorrhage. 115 


to work on April 21st. Two months later, about June 18th, 
headache and paresis set in. When seen by Dr. Mitchell Bruce 
on the 22nd the discs were normal. Right sided paresis developed 
into paralysis, and on the 28th he was comatose, the pulse was 
quick and full. A diagnosis of abscess on the right arm area 
was made and the patient trephined on the left side. The dura 
was bulging and motionless. A flap of the dura mater was 
turned down. It was adherent on the deep surface but stripped 
off easily, leaving exposed a slightly bulging, motionless, greyish- 
yellow surface. This required a distinct amount of force to send 
the knife through it. When opened four ounces of dark red 
clear fluid escaped. ‘‘ Evidently a cystic clot had been opened.” 
A drainage tube was left in the cavity. Recovery was slow. Mr. 
Boyd suggests that the slow recovery of consciousness may 
perhaps have been due to rigidity of the cyst wall, preventing 
expansion of the brain. There was no albumen or sugar in the 
urine before operation. He went to the seaside on August 15th, 
and in May of next year was very well. 

This case is particularly interesting in that a long latent 
interval was present, during which time, from the condition of 
the clot, the blood was present in the cranium. It is extremely 
probable that the case reported by Taylor and Ballance passed 
through the stage found here before finally becoming the typical 
cyst removed at operation. 16 had originally been my intention 
io deal fully with the remote history of cases of subdural 
hemorrhage, which pass on to organisation of the clot and the 
formation of cysts, but this paper has already reached a length 
to which, in the first place, it had no pretensions, so that beyond 
giving a list of the reported cases which I have found, I shall 
dwell no more on the subject. There are three other points of 
some importance to be considered, however, before leaving 
prognosis, viz. :— 

1. The question of perfect recovery from paresis or 
paralysis. 

2. The relationship of traumatic subdural hemorrhage to 
traumatic epilepsy ; and 

3. The relationship between traumatic subdural hemorr- 
hage and insanity. 


116 Traumatic Subdural Hemorrhage. 


1. With regard to the persistence of paresis or paralysis after 
operation and removal of the clot, it may depend upon either 
the damage produced by continuous pressure or the result of 
laceration of the brain. The following facts have a bearing 
upon the subject. In case 10, the operation was performed 
thirty-six days after the injury (but only twenty-one days after 
the onset of symptoms) with perfect recovery. In the case 
reported on page 104, where compression of the brain had been 
present probably for six weeks, and where, after removal of the 
cerebro-spinal fluid, the brain in the Rolandic region was over 
one inch from the skull, the mother wrote five months later to 
say that the child plays about with other children, and she 
considers her perfectly recovered. In vol. xviii., p. 379, of the 
Transactions of the Medical Society is the report of a case where 
hemiplegia followed injury two years before. At operation, a 
cyst of the arachnoid was removed, after which freedom of 
movement in the hitherto rigid limbs followed. From these 
cases it would appear that as long as the brain surface is 
uninjured, a very long period of compression may occur, and yet 
if it be relieved perfect recovery follow. 

On the other hand, it will be seen that in the case reported by 
Dr. McBurney some paresis persisted. This may be considered 
with the case reported by Dr. Hale White, published in ethe 
Pathological Society's transactions (vol. xxviii.) —* Old meningeal 
hemorrhage with softening and secondary descending degenera- 
tion." 

Mary G., et. 36. Seven years ago fell down whilst skating. 
Eighteen months ago the right arm and leg gradually became 
weak and she completely lost the use of these limbs, but after 
four months could walk again with assistance. She gradually 
sank and died from a fecal fistula in connection with an old 
femoral hernia. Autopsy.—Cranial bones and cerebral arteries 
normal. Left side over ascending frontal and ascending parietal 
convolutions, back part of a little of the first and third frontal 
and posterior third of second frontal was some soft yellowish- 
white material, evidently very old blood clot. The grey matter 
corresponding to this area was gone, there being a distinct 


Traumatic Subdural Hemorrhage. 117 


depression in the brain substance filled up by the above material. 
The white substance beneath was little altered. No distinct 
degeneration could be seen in the internal capsule or pons, but 
the pyramidal tract in the medulla and the crossed and direct 
tracts in the cord were decidedly grey and translucent and hard; 
the lateral columns on the affected side were certainly the 
smaller. The kidneys were granular. 

In both these last two cases some laceration of the brain may 
have been present, and I think from the reported cases that it is 
justifiable to say that, if at the time of operation the brain is not 
lacerated, if the patient recover, his or her paresis or paralysis 
should entirely disappear. In the event of some laceration 
associated with paresis or paralysis being present, and especially 
if the paresis or paralysis has persisted for a long time, some 
permanent damage may remain. 

With regard to the relationship of traumatic subdural hemor- 
rhage to traumatic epilepsy and insanity, from the reported cases 
and opinions 16 seems very improbable that this form of 
hemorrhage leads to persistent fits or ultimate insanity. In the 
case of fits occurring as the result of pressure by clot, it seems 
almost certain that when they occur they progress rapidly and 
lead to early operation, very often a diagnosis of some purulent 
collection within the skull! being made; whilst it is a truth, I 
think, that the hemorrhage found subdurally in lunatic asylum 
autopsies is not the cause of the insanity but is the result of the 
atrophy of the brain associated with the mental change. I 
would draw especial attention on this point to Dr. Wiggles- 
worth’s paper on “ Hemorrhages and False Membranes within 
the cerebral subdural space occurring in the insane (including the 
so-called Pachymeningitis).’’”” i / 


16 See Walsham ''On Trephining the Skull in Traumatic Epilepsy," 
St. Bartholomew’s Hospital Reports, Vol. xix. 

11 See also Vol. xliii. of the Pathological Society's Transactions. ‘‘ Sub- 
dural Hemorrhage,” by E. T. Wynne, M.B., also Dr. Newton Pitt's paper 
“ Double Subdural Cysts of Hemorrhagic Origin,’’ in the same volume. In 
the forty-sixth volume of the same Society’s Transactions is a paper by Dr. 
C. F. Beadles on ‘‘ Some Gross Lesions in the Brains of Lunatics, etc." 
See also '* Brain," Vol. xv., ‘‘The Traumatic Factor in Mental Disease," 
by Dr. W. J. Mickle. 


VOL. LIX. 10 


118 Traumatic Subdural Hemorrhage. 


Finally, on the uncertainty of the future history of any case 
of head injury, I may quote a sentence from Gross’ System of 
Surgery (1882)—“ The prognosis of wounds of the brain and its 
membranes is too variable to admit of general specification. 
While in some cases, indeed in a great many, the slightest injury 
causes death, in others, attended with excessive shock and the 
loss of a large quantity of blood and cerebral matter, the most 
prompt and satisfactory recovery occurs.” 

In conclusion, I would thank the surgeons of Guy’s Hospital 
for permission to publish the twenty-four hitherto unrecorded 
cases which are derived from the Surgical Reports of Guy’s 
Hospital. These twenty-four cases number a third of the total 
cases upon which this paper is based. 

To Мт. Jacobson and Mr. Symonds, surgeons of Guy’s 
Hospital, I owe a special debt of gratitude. Were it not for 
their assistance and advice this paper would, even if written, 
never have approached the completeness which it ultimately 
endeavoured to realise. To anyone reading it, the numerous 
references to Mr. Jacobson’s paper on “On Middle Meningeal 
Hemorrhage,” are a sufficient indication of my indebtedness to 
this work, but I may say that this is only a small part of a 
greater series of obligations, the extent of which I alone can 
realise and which I take this opportunity of very ‘gratefully 
acknowledging. 





Abstract of Cases. 119 


ABSTRACT OF CASES. 


CLASS A. 


No. 1.—Mr. Golding-Bird and Mr. Dunn. Guy’s Hospital Surgical Reports, 
1901. Report No. 586.—Walter A., æt. 24, was knocked down (November 
1st) by an engine towards which his back was turned. He was rendered 
unconscious and brought up at once to the hospital. On admission, he was 
unconscious; there were three scalp wounds, two over the vertex, and one in 
the occipital region. There had been very little blood lost, and all bleeding 
had ceased. The tenth rib was broken, and there was a large oval bruise on 
the back. The wounds were cleansed and stitched up, gauze drains being 
used, no anesthetic being necessary. On November 2nd, the wounds were 
healthy, but he had severe headache and was sick during the morning. He 
got up after tea, but was glad to get to bed again.. On the 4th, he still 
complained of severe pain in the frontal region, and slept badly. On the 5th, 
the headache still persisted; the wounds were quite healthy, On November 
6th, there is a note saying he did not complain of any pain and was discharged. 
The man was readmitted to the strong-room on November 16th, 4.е., ten 
days after his discharge. The history was that since leaving the hospital he 
had done no work, had spent most of his time indoors, complaining of aching 
pains in the back of his head, and had been restless, very irritable and unable 
to sleep. He took food well, but the bowels were constipated. Three days 
before readmission the pains in the head became much worse and the patient 
excessively irritable. On the day previous to readmission he developed a 
squint and soon became totally blind, began to lose the power of speech and 
stammered. At times the right arm was paralytic, and at times rigid. 
There was no vomiting. On readmission the man was excessively restless, 
but inclined to be drowsy. Pulse 76. Respiration 20. Temperature 99°. 
Aphasia was marked, and movement of the right arm impaired. It is said 
that although the patient could see objects presented to him he did not 
appear to recognise them. Hearing was apparently normal. He was seen 
by Mr. Dunn and Dr. Fawcett, who diagnosed a clot pressing on the arm 
area and decided to trephine at once. Operation: A.C.E. mixture being 
administered, the dura mater was exposed and seemed dark brownish-blue in 
colour. It was incised and reflected exposing a small blood clot and some 
dark-coloured blood which slowly welled up. This was carefully removed 
with the aid of a blunt spoon. The piece of trephined bone was replaced and 
the skin sutured continuously. November 17th: Patient appears much 
better this morning. Temperature 98. Pulse 80. Respiration 16. Delirious 
during the night, and this morning complains of headache, but he speaks 
quite well, although slightly indistinctly, Movement in the right arm 
appears quite normal, There is no sickness. Urine slightly alkaline, sp. gr. 


-_ 


120 Traumatic Subdural Hemorrhage. 


1022, no albumen, pus or sugar. On November 29th, when he was 
discharged, he seemed perfectly recovered, having full power of movement in 
the right arm and free speech. 


No. 2.—Mr. Jacobson. Guy's Hospital Surgical Reports, 1901. Report 
No. 566.— Thomas M., set. 62, was pushing a trolley up a raised platform 
(December 9th, 1901) when he fell & distance of three feet to the ground, 
striking the right side of his head against a stone. On admission, he was 
unconscious, with a scalp wound above the right ear. Pulse regular, fairly 
full and strong. Temperature 99°. Right pupil smaller than left. Conscious- 
ness was present next day, but the pupils were still unequal. On the 12th, 
he was restless and trying to pull his bandages off, but from this time up till 
the 24th he steadily improved. From the 24th to 28th he gradually became 
comatose, and on this last date his breathing becoming stertorous and his 
condition critical, it was decided to operate. No anesthetic was administered. 
A flap being turned down in the right temporal region, the skull was trephined 
and the dura exposed nonpulsating. Incision of the membrane exposed а 
quantity of dark semi-fluid clot, which was removed. Cerebral pulsation now 
recommenced, causing more of the clot to collect. A gauze drain was inserted. 
The patient died at 9.10 p.m. on the 30th, remaining unconscious till the end. 





No. 9.— Mr. Davies-Colley. Guy's Hospital Surgical Reports, 1898. 
Report 341.—John F., et. 56, fell from a railway platform and struck the 
back of his head on a dummy capstan (July 2nd). He did not lose conscious- 
ness, and after having a scalp wound dressed was sent home. Next day he 
could not use the left arm or left leg. This paralysis persisted until his 
admission into the hospital on July 8th. On admission, there was bare bone 
exposed at the bottom of a wound in the occipital region. There was 
paralysis of the left lower limb, and paresis of the left upper. No loss of 
sensation. No facial paralysis. Pupils equal and react. Answers questions 
intelligently. Pulse 80, regular, rather easily compressible. Temperature 
99°2°. Respiration 18. The patient remained much the same, but his rest- 
lessness required the administration of soporifics at night until the 19th, 
when, as he was growing weaker, and no improvement had taken place in his 
paralysis, it was decided to operate. The trephine was applied over the 
middle of the ascending frontal convolution. The dura mater appeared black. 
Blood was exposed subdurally and removed. The bone being replaced, the 
wound was sutured. From the time of completion of the operation he made 
no improvement, required sleeping draughts for his restlessness and insomnia, 
and becoming weaker and weaker he ultimately died on August 5th. At the 
autopsy, only the hrain was examined. A clot was found with a depression 
in the brain a short distance in front of the upper part of the fissure of 
Rolando. 


No. 4.—Mr. Bryant. Guy's Hospital Surgical Reports, 1885. Report No. 
274.—Jessie S., et. 48, found insensible and bleeding, by the police. Said to 
have fallen whilst drunk (November 28th). On admission, she was insensible, 
and could not be roused. Pupils equal, moderately dilated and not reacting 
tolight. Deep scalp wound over right side of heal two inches loug, with 
exposure of bone. Pulse rapid and feeble. Four hours after admission 
she had afit. Some weakness of right side of face and right arm noticed. 





Abstract of Cases. 121 


Epileptiform convulsions now occurred frequently, affecting the left side at 
first, but later becoming bilateral. 'lhe fits were kept in check with bromides. 
On the 29th she could be roused, and answered her name. The fits persisted 
all day save when restrained by bromides. The pulse increased in rate, and 
she died on the 30th, at 5.30 a.m., Cheyne-Stokes’ respiration occurring 
towards the last. Her husband said she suffered from epileptic fits, and was 
aheavy drinker. At the autopsy, no fracture of the skull could be found; 
there was no extradural hemorrhage. Middle meningeal artery uninjured. 
Over the left temporo-parietal part of the brain compression had been 
produced by two ounces of blood, situated beneath the dura mater. The clot 
was easily removed, and no laceration of the brain discovered. There was no 
intracerebral heemorrhage. The vessels of the base showed some thickening, 
and rather opaque appearance. They were also distinctly pouched in one or 
two situations. Heart normal. Liver fatty. Right kidney atrophied, and 
contained two cysts. Left kidney hypertrophied, weighing twelve ounc’s, 
also fatty and moftled, with adherent capsule in places. 


No. 5.—Mr. Mansell Moullin. Clinical Society’s Transactions, vol. xxvii. 
“Traumatic arachnoid hemorrhage with symptoms on the same side as the 
lesion’? (November 10th, 1893).—T. C., а stevedore, set. 43, had a violent blow 
on the side of the head with the hook of a crane at 10 &.m. Did not lose con- 
sciousness and continued his work until nearly 1 p.m., when he felt faint, and 
quickly became unconscious. On admission, the breathing was deep and 
noisy. Pulse 70, full and regular. Temperature 99°. Weakness of right face 
muscles, rigidity of right limbs. Pupils evenly contracted, but after exposure 
the right pupil dilated more than the left. The right side of the skull was 
exposed in the hope that a fissured fracture might be found extending round 
to the left side from the site of injury, but none was found. Next day there 
was some improvement, and towards evening he recovered consciousness. No 
increase in paralysis. For the next two or three days there was no material 
change, then delirium at night, coming on at intervals, set in. Nine days 
after the accident, as coma was deepening and the breathing becoming more 
and more stertorous, the left side of the cranium was explored. The dura 
mater did not bulge on exposure. It was incised. The brain bulged at once 
and began to pulsate. Bone replaced. Death occurred twenty-four hours 
later, the temperature rising from normal to 109° just before death. 
Autopsy: no trace of fracture. No extradural hemorrhage. “Under the 
dura on the right side, between it and the arachnoid, was a large black clot 
covering the greater part of that hemisphere. Nearly three-quarters of an 
inch thick over the lower end of the fissure of Rolando, and from there it 
thinned off in all directions, but it reached nearly to the falx above, on to 
the occipital lobe behind, and to the clinoid process below." The brain was 
cupped, but uninjured. There was no atheroma. There were strong reasons 
for believing that the source of the blood was the middle meningeal artery. 


. No. 6. —Mr. Raymond Johnson and Dr. Risien Russell. Clinical Society’s 
Transactions, vol. xxxiv., case 26.  ''Traumatic subdural hemorrhage 
occasioning convulsions on the 6th day after injury, and successfully treated 
by operation (May 24th, 1901). —Frederic W., æt. 23, admitted to University 
College Hospital early in the morning of October 23rd, 1900, suffering from 


122 Traumatic Subdural Hemorrhage. 


frequently recurring epileptiform convulsions affecting chiefly the left side of 
the body. On October 17th he had fallen down some steps whilst drunk, and 
being picked up unconscious had been put to bed. Next morning he walked 
to a medical man and had a scalp wound dressed. He complained of head- 
ache and feeling shaken. Не did no work, but kept free from any definite 
symptoms until the night of October 22nd at 10 p.m., when fits set in. On 
admission to hospital, he was bathed in perspiration. Pulse 100. Temperature 
102°. Each fit lasted two to four minutes, and the intervals between the fits 
varied from one to five minutes. The onset of a fit was marked by his 
turning head and eyes to the left, or by twitching of the left side of the face. 
The left side and right leg, and occasionally the right arm, were affected. 
The spasms were clonic. In the intervals he was sufficiently conscious to 
answer questions. Pupils equal, medium size and reacted. No facial 
paralysis. Left arm weaker than right. Chloroform was administered to stop 
convulsions. Bromide and chloral also administered. The urine contained a 
dense cloud of albumen. Ursmia and idiopathic epilepsy were both seriously 
considered, but meningitis was finally considered to be present (for discussion 
of diagnosis see under diagnosis in text, pp. 92 & 93). Operation was decided on. 
The skull being opened, the dura mater bulged and had a bluish tint as though 
blood was beneath it. On incising this membrane, two to three drams of 
blood escaped. The brain appeared perfectly normal. The dura mater was 
sutured, the bone not replaced. There were no fits after operation, but it was 
nearly a month before the left arm completely recovered. The temperature 
rose to 105° four hours after operation, and for four days it varied between 
101:4? and 104°. The patient passed through a mild attack of delirium 
tremens. 


No. 7.—Professor McBurney. Brain, vol. xiv., p. 284.—A physician, et. 
40. Thrown from his carriage August 17th, 1889. Slightly stunned by the 
fall, but with no wound, and able to assist his wife. For several hours he 
seemed only suffering from bruises and did some professional work. In the 
course of the evening, however, he became delirious, then stupid, and, for the 
next three days, lay in a semi-comatose condition. On the morning after the 
injury he was found hemiplegic on the right side, and aphasic. When after a 
week his consciousness had fully returned, it appeared that the aphasia was 
purely motor. He came under the care of Professor McBurney at the 
Roosevelt Hospital in December, nearly four months after the accident. He 
then had partial right hemiplegia with motor aphasia, was mentally unstable, 
and the left pupil was one-third larger than the right. There was no facial 
paralysis, and the optic discs on examination were quite normal. Professor 
McBurney came to the conclusion that a vein had ruptured and slow hemor- 
rhage occurred over the left hemisphere at the posterior part of the third 
frontal convolution and over the anterior central convolution in its middle 
third. On December 13th, he trephined the skull over this region; the dura 
mater did not pulsate. On opening ıt the pia was found very edematous and 
discoloured, and the surface of the brain separated from the dura by a space 
of half an inch in depth and did not pulsate. Blood clot was seen lying 
beneath the pia mater. The clot was removed. Drainage with tubes was 
employed for a week. Two months after operation he walked with a cane. 
The return of speech was slow but continuous. Fifteen months after opera- 
tion paralysis of the right hand remained. This was thought to be due to 
permanent nutritive changes in the arm area, 





Abstract of Cases. 128 


No. 8.—Mr. T. Chevalier. Medical and Physical Journal, vol. viii., p. 
505 (1802).—A baby, 14 years old, fell out of the servant’s arms at 10 o'clock 
in the forenoon and struck its head violently against the head of a door, 
Taken up senseless. After remaining comatose for one and a half hours, the 
infant went into convulsions. After these had continued for two hours Mr. 
Chevalier was called in. There were no external marks of injury on the scalp 
but the fontanelle was distended, and a bleeding vessel under the dura mater 
was diagnosed. An angular incision, through the fontanelle, was made on 
the right side, since the limbs on the left side were much more violently 
convulsed than those on the right. Blood was seen under the dura mater, 
which was punctured. The blood spurted out one foot: three to four ounces 
at least were discharged. It appeared venous. All spasms ceased in three- 
quarters of an hour, and the baby made a perfect recovery. 


No. 9.—Mr. Ogle. From B. Brodie’s Paper in the Medico-Chirurgical 
Transactions, vol. xiv.—A woman, whose age is not given, had fallen down 
into a cellar from the street head foremost. Picked up comatose. Shaving 
of the head was ordered.. There was no wound of the scalp, but she flinched 
when pressure was made on a spot near the anterior superior angle of one of 
the parietal bones. An incision was made here, but no fracture discovered. 
Bone being removed with a trephine, the dura mater of a dark colour rose 
into the opening nearly as high as the external surface of the cranium. The 
dura mater was punctured with a lancet. Blood spurted out to a height of 
some feet. The woman who till that moment had remained totally insensible 
regained consciousness and spoke, describing the accident. She recovered 
without any untoward symptoms. 


No. 10.—Dr. Otto G. T. Kiliani. Annals of Surgery, 1901, 33, p. 325.— 
A man, age not stated, admitted to the German Hospital on June 6th, 1900, 
with a bistory that on May 5th he was struck by a falling brick (forty feet) 
which, as he wore & Derby hat at the time, neither caused & wound or 
produced unconsciousness. He was dazed for a short time. On May 21st he 
was seized with violent frontal headache. On the 26th, he became dizzy and 
nearly fell whilst walking. On June 1st hesitancy of speech set in. On 
admission to hospital he was somewhat somnolent, becoming slightly restless 
when aroused. Slight spastic paresis of right arm and hand, and to a less 
extent of right leg. Ataxia in both arms. Partial motor aphasia. No facial 
paralysis. Optic discs normal. Temperature 98° to 100°. Pulse ranging from 
68 to 92 (mostly 64 to 68). Respiration 12 to 24. June 11th (thirty-six days 
after injury), anesthetic administered and a flap turned down on the left side 
of the skull. Dura mater exposed, after removal of bone, nonpulsating and 
with large tensely-filled veins of a dark colour shining through. Incision into 
dura mater and evacuation of the clot, which was an inch and a quarter thick, 
covering practically the entire left hemisphere. Pia mater and convolutions 
normal. The wound was drained with a tube. A perfect recovery followed, 
and on August 19th he is stated to be perfectly well and attends to business. 

(Dr. Kiliani also refers to a case reported by Hahn, Ein Bertrag zur 
Chirurgie des Gehirns; Centralblatt für Chirurgie, 1896, 6; Deutsche 
Medinische Wochenschrift 14-16 ; Subdural large hematoma without fracture. 
Trephining. Recovery.] 


124 Traumatic Subdural Hemorrhage. 


No. 11.—Drs. Russell and Pinkertog. British Medical Journal, i., 1895, 
p. 1818.—J. H., a healthy, wiry man of 67, was thrown from his tricycle on 
March 8rd, 1894. He was not stunned but had wounds which bled freely. 
On March 4th, when first seen, he had vomited all that he had taken. On 
the 5th aphasia set in with paresis of right arm. At 11 p.m. on the 6th 
convulsions set in, affecting the whole body. Three such convulsions were 
noted. On the 8th and 9th his condition was improved, and he was con- 
scious, but from the 10th to 12th he gradually got worse, became first 
lethargic and restless and finally comatose. Pulse 60, full. An operation was 
performed on March 13th. After two trephine openings had been madea 
point of **increased resistance” was found. The dura mater was incised 
here and black clotted blood exuded with each pulsation. This was removed 
and the cavity drained. The man moved the right arm a little immediately 
after the operation. The aphasia began to improve on the fifth day. Advance- 
ment was slow until the eleventh day and then rapid, so that by the twenty- 
fifth day he could speak fairly well. 


No. 19.—Dr, Barlow, (quoted by Sir Samuel Wilks in his paper оп 
** Sanguineous meningeal effusions : spontaneous and from injury ’’).—A. G., 
et. 18, admitted into Guy's Hospital under Dr. Barlow on July 17th, 1856, 
and died next morning. He received a blow on the head whilst fighting in a 
barge on July 6th. He did not suffer much in consequence, and continued 
his employment during the next ten days, but on the 17th he had headache, 
and it is said that he evidently had considerable pyrexia on admission. 
Post-mortem (Report No. 187 for 1856): There were no external signs of 
injury to the head and no fracture of the skull. On the right side the dura 
mater was flaccid and purple. Four ounces of blood, either fluid or in the 
form of loose coagulum, were present subdurally on this side. The blood 
compressed the right side of the brain and had extended to the base, 
compressing the Pons Varolii. The left hemisphere was unaffected. There 
was no cerebral laceration, or source of hemorrhage found. No laceration 
of sinuses or meningeal arteries. An examination of the clot seemed to show 
that there was an old part becoming organised, and & more or less recent 
hemorrhage in addition. All the internal organs were healthy. 


No. 18.—Dr. Goodhart. Guy's Hospital Reports, vol. xxi. From paper 
on ** Meningeal Hemorrhage.’’ (Case 31.)—James R., about 35. Struck by 
another man twice on the head. Brought into the hospital dead. At the 
post-mortem examination there was slight ecchymosis in the upper part of 
the right temporal muscle. No fracture of the skull. About the brain in the 
arachnoid and subarachnoid space there was a quantity of blood which had 
gravitated to the base. The subependymal arteries were fatty here and there. 
Many recent small extravasations into the lungs. 


No. 14, —From the St. Bartholomew’s Reports. Cases from Mr. Walsham's 
Wards. (No. 1922. Kenton.)—Man, et. 37, admitted unconscious. He had 
been knocked down by a cab the day before, the wheel, it was said, having 
passed over his neck. The man was very drunk, and was washed out in the 
surgery. Soon became noisy and delirious and eventually drowsy, whilst 
paresis of the left side of the face, the left arm, and to a less extent of the 


Abstract of Cases. 125 


left leg set in. During the night a fit (thirty seconds) occurred, followed by 
general twichings and afterwards a complete paralysis of the left face and 
arm, and increasing weakness of the left leg. Trephining over the right 
motor area was performed 12.30 p.m. No extradural blood was present, but 
on incising the dura mater a large quantity of blood escaped. The patient 
slowly recovered consciousness, and in two weeks the paralysis had disap- 
peared and the temperature fallen to normal. From this time he gradually 
recovered, and left the hospital quite well. 


No. 15.—From the St. George’s Hospital Reports (1875). Cases from Mr. 
Holmes’ Wards. No. 467.—John T., set. 60, fell twelve feet, pitching on his 
head. Admitted shortly afterwards with slight concussion, from which he 
was easily aroused, Starred wound over right frontal eminence, but without 
exposure of bone. Twenty-four hours after admission he gradually lost 
consciousness and became restless. Twitchings in the muscles of the face 
and the left upper extremity followed. Within three-quarters of an hour of 
the onset of these symptoms the wound in the forehead was enlarged and the 
bone examined. No fracture was detected. Twitchings with unconsciousness 
continued, the patient dying quietly fifty hours after admission. The 
breathing became stertorous half an hour before death. At the autopsy, a 
large, recent coagulum was found on the right side of the brain, in the cavity 
of the arachnoid, also slight extravasation of blood in the neighbourhood of 
the veins of Galen. The first part of the aorta was atheromatous and dilated, 
the kidneys granular and cystic. 


No. 16.—Mr. Henry Morris. Lancet, November 11th, 1882.—James J., 
æt. 81, was admitted into the Middlesex Hospital, December 14th, 1881. For 
& fortnight before admission he had been living in a dissipated condition at 
Brighton, and on his return to London, had fallen heavily, striking the back 
of his head against the kerbstone. Being picked up half unconscious, he was 
first taken to a police station, but subsequently to the hospital. On 
admission, he smelt strongly of drink, and was in & muddled state, with a 
small scalp wound slightly to the left of the occipital protuberance. The 
periosteum was not exposed. Pupils equal and reacting. Respiration and 
pulse normal. No signs of any fracture of the skull. Stupidity put down to 
alcohol, and passed off in several hours. For the next three days the only 
abnormal feature of his case were complaint of headache and double vision. 
He then passed through an attack of delirium tremens, from which he had 
recovered on December 22nd, when he seemed quite well though weak. On 
December 25th he went to church, but complained of feeling drowsy and 
having pain in his back. During the night the nurse on duty noticed how 
restless he was, and next morning (26th) it was found impossible to wake him. 
At 10 a.m. he was found to be in coma, with the right pupil widely dilated 
and the left very contracted ; neither responded to light, and the conjunctive 
were insensitive. Pulse 100, small and jerky. There was very slight 
twitchings of both upper limbs, but no paralysis at all. A sample of urine 
(which had been free from albumen on the 17th) was found to contain a lot 
of albumen. Temperature 101:6?. There was no cedema round the scalp 
wound, but a little purulent discharge from it. He was treated with pilocar- 
pine and calomel, and on the 27th seemed better, answering when spoken to, 


126 Traumatic Subdural Hemorrhage. 


but the pupils remained unequal. The urine was still highly charged with 
albumen, so that a hot-air bath and jalap were ordered. On December 28th 
and 29th, he was much the same, the albumen, however, being half what it 
was. Later his breathing became more stertorous, and he could neither speak 
nor swallow. At 9 p.m. оп the 29th his temperature rose to 104°2°, and at 
3.10 a.m. on the 30th the man died. At the post-mortem examination made 
by Dr. Fowler, there was no fracture of the skull. The right half of the 
dura mater covering the brain appeared somewhat distended. Blood was 
found spread out beneath it. This was most abundant over the frontal lobe 
and in the anterior fossa, but there was also a considerable quantity beneath 
the parietal eminence, and over the occipital convolutions. The blood was of 
a mahogany tint, the coagula being soft and adherent to the under surface 
of the arachnoid. The source of the blood could not be found. There was 
a small clot on the left side immediately below the wound. There were some 
spots of atheroma in the aorta, the lungs were emphysematous, the kidneys 
were large and the capsule in places adherent, but beyond swelling of the 
cortex, probably from slight infiltration, there was no evidence of disease. 


No. 17.—Reported by Mr. Leopold Hudson, in the Lancet of March 8th, 
1890. The case was under Mr. George Lawson.—J. W., male, æt. 20, single. 
The patient, whilst boxing, was noticed to become suddenly weak, but con- 
tinued to box for a few seconds, when he fell back across the ropes. Не did 
not strike his head as he fell, but when picked up he was quite insensible. 
As he did not recover consciousness &t the end of half an hour, he was taken 
to the Middlesex Hospital and admitted. No particularly hard blows had 
been given. On admission, he was comatose, the pulse was 50, full, the 
respiration stertorous and interrupted, the pupils fixed and dilated, surface of 
the body cool, the extremities powerless and flaccid. The urine (by catheter) 
contained no albumen. An ophthalmoscopic examination was negative. The 
patient lived for two hours after admission. No spasm was observed at any 
time. At the autopsy (made by Dr. Sidney Martin) a little dried blood was 
found in the anterior nares. A subcutaneous ecchymosis was present below 
and to the outer side of the left eye. No fracture of the cranial bones was 
present. No injury to the dura mater or meningeal arteries was present. On 
opening the dura mater there was found over the middle lobe of the left 
cerebral hemisphere a quantity of soft blood clot depressing the subjacent 
convolutions. It appeared to be derived from the arachnoid. There were 
three very small ecchymoses. beneath the pia mater on the left side. No 
laceration of the brain was present. With the exception of slight atheroma 
in the commencement of the aorta the viscera were normal. 


No. 18.—Mr. Edmund Owen. British Medical Journal, 1888, vol. ii. 
p. 817.— Wm. MacC., 9 years old, was brought to St. Mary's Hospital on 
May 8th, stunned by a fall from a cart. He vomited profusely, turned his 
head from the light, and when asked questions said ‘‘go away." Pupils 
equal and reacted. No fracture could be detected. Тһе movements of the 
limbs were perfect, but he was very drowsy. Next day he was restless, 
muttering and jumping out of bed. Temperature 101°. Five days after 
admission Jacksonian epilepsy set in, affecting in the first place the right 
facial and suprahyoid muscles, and later the muscles of the right hand, 





Abstract of Cases. 127 


causing clenching of the fist. The evening temperature was 101°8°. During 
the next day he had slight fits, but towards evening a most severe one 
affecting, in addition to the muscles previously mentioned, the diaphragm and 
right sterno-mastoid. The boy was aphasic, but conscious. On May 15th 
at 4 p.m. ether was administered and the skull opened. The dura mater 
presented a somewhat greenish hue and bulged. On incising it a quantity of 
dark fluid blood escaped. The total blood removed was thought to amount to 
half an ounce. It lay over the lower part of the left motor area. The space 
under the dura mater was irrigated with warm carbolised water, and the dura 
sutured. On the 16th and 17th, the fits recurring, further extravasation was 
diagnosed. On re-operating a small quantity of black fluid blood was removed 
from the subarachnoid space, which had not previously been opened. He 
was discharged cured on June 15th. 


No. 19.—Dr. J. S. Horsley. Medical News (Philadelphia), November 3rd, 
1894.—A. B., coloured, aged 48, the subject of chronic syphilis and a hard 
drinker, but with no previous history of epileptic fits or cerebral lesion, fell 
off a waggon on August 6th, 1894, striking the left parietal eminence against 
the kerbstone. A wound, one to one and a half inches long, not reaching bone, 
was formed. He got up, and seemed to have a slight convulsion of his left 
arm. After some attention he was sent home (4.30 p.m.). At this time 
he was quite conscious. Half an hour later a doctor was sent for and found 
the man having general convulsions. He gave morphine and atropine, and 
the spasms became localised to the left arm, At 6.30 p.m. the man was 
completely unconscious, with stertorous breathing, a full slow pulse, and 
slightly elevated temperature. Four hours later he was much worse, with 
shallow respirations, slightly dilated pupils, and a weak pulse with a rate of a 
hundred and twenty-five per minute. There was spasm of the left arm. 
The head and eyes were rotated to the left. He died at 12.30 p.m., 
no operation being performed on account of his adverse surroundings. 
Post-mortem: No fracture. Subdurally on the outer side of the right 
temporo-sphenoidal lobe was an irregularly-shaped clot. The source of 
hemorrhage was an artery between the middle and inferior temporo-sphenoidal 
convolutions. The clot was about two inches at its broadest diameter, one 
inch at its widest, and one-sixth of an inch at its thickest point. The walls of 
the blood vessels seemed degenerated. 


No. 20.—From the Boston Medical and Surgical Journal, vol. cxxx., 
p.201. (1894.)—A. H. L., a tall athletic student, 19 years of age, was struck 
in a friendly sparring bout on the left jaw. Large gloves were used. The 
patient, after commenting on the excellence of the blow, said he felt queer, 
put both hands to his head, jumped up and down several times, reached out 
his hands for the wall, staggered, and fell unconscious. This was at 5 p.m. 
on February 13th. Consciousness was not recovered, breathing became 
stertorous, pupils first dilated then contracted. Within four hours rigidity 
had appeared in all four extremities, preceded by restlessness. At one a.m. on 
February 14th a consultation was held as to the advisability of operation. 
At this time all four extremities were in a condition of rigid contraction. 
There were in addition clonic movements of the right hand. Eyes turned 
somewhat to the left but without strabismus, Both pupils large and 


128 Traumatic Subdural Hemorrhage. 


only slightly reacting to light. Breathing heavy, abdominal, and with a 
tendency to Cheyne-Stokes’ respiration. Tendency to lateral nystagmus. 
No priapism. Pulse 96, strong, full. Temperature 1019. No signs of 
fractured base. The signs of pressure on the pons and medulla were con- 
sidered to contraindicate operation. On the 15th the rigidity entirely 
disappeared leaving all the extremities paralysed. Temperature 102°. 
Respiration 30, stertorous. The patient gradually failed and died quietly at 
3.50 p.m. on the 18th. Temperature in afternoon 106°. At the autopsy 
there were no signs of external injury. The surface of the brain was covered 
with extravasated blood beneath the dura mater. The extravasation was 
most marked over the occipital lobes and on the left side. The blood was 
blackish in colour and of & tarry consistency. On removing the brain the 
middle fossa on the left side was found to contain several ounces of the same 
black tarry blood, which also extended into the vertebral canal. There wasa 
small rent in the lateral sinus near the outer margin of the temporal bone. 
About this rent for a short distance the dura mater was dissected up. There 
was no fracture of the skull, and no extravasation of blood into the brain. 





No. 21.—Dr. F. L. Wells. Medical Record (New York), vol. xli. (1892).— 
The patient, a German, æt. about 23, was walking along the street when he 
was suddenly seen to fall and become convulsed. These convulsions ceased 
before the arrival of the ambulance, but were described as being of his face 
and all his extremities, associated with frothing at the mouth and blueness 
of the face. On admission to hospital he was entirely unconscious, tongue 
bitten, and no evidence of injury save a scar on the left side of the head 
anterior to and a little above the ear. It was judged to be three to six weeks 
old. Both pupils were dilated, but reacted to light. Temperature 102°. 
Respiration 30. Pulse 120. No paralysis.. Urine of specific gravity 1020, 
with a slight amount of albumen present, no casts and no sugar. Convulsions 
occurred at intervals of a half to two hours, were general, and lasted one to 
two minutes. In the intervals between the fits the patient was completely 
unconscious, delirious, and with difficulty kept in bed. He was frequently 
given morphine sulphate hypodermically. Towards evening the temperature 
rose to 104°. Next day, August 21st, the temperature was 103°, the 
pulse rate 110, and the respirations 26. The convulsions were carefully 
noted and were found to begin in the muscles of the right eye or right 
corner of the mouth. They advanced then to the right arm and leg, 
and then became general. The advance was so rapid, however, as to make 
them appear general from the first. The evening temperature was 105°. It 
was followed by sweating. The convulsions became more severe and more 
frequent. During the night following the convulsions were nearly constant. 
It was decided to operate. Before operation the temperature was 105°, pulse 
123, and respiration 22. At the operation a flap was turned back including 
the scar. The periosteum was found more firmly adherent than is natural. 
No evidence of fracture could be detected, and no elevation or depression 
existed. Theskull was trephined at about the centre of the motor area. The 
circle of bone was removed with great difficulty, the dura mater being 80 
adherent as to tear away pieces of the bone. The bone itself was three 
sixteenths of an inch thick, and perhaps a little more vascular than normal. 
No depression of the inner table was found, but the dura mater was dark in 


Abstract of Cases. 129 


colour and nonpulsating. A crucial incision was made in the tense membrane 
when blood clot immediately protruded. The incision was then enlarged and 
a handful of clotted blood removed which was covering the motor area of the 
face, arm and leg; the largest part being over the face centre. Microscopical 
examination showed the clot to be undergoing softening and a transformation 
into pus. The pia mater was seen to be very much reddened and inflamed. 
The brain itself was greatly compressed but not softened. The cavity was 
cleansed with biniodide, 1 in 20,000, and iodoform gauze used for drainage, 
the bone not being replaced. The patient, on coming round from the ether, 
spoke the first rational words since admission, asking for a drink of water. 
Temperature at night (four hours after operation) 103°. During the night 
following and the 28rd several general convulsions occurred. On the 26th, the 
temperature fell to 99°, and kept at about that level until his recovery. He 
gradually recovered and gave the following histcry: That he was struck on 
the head three weeks before admission to the hospital, the scar found on 
admission being due to the cut then received. He had never been troubled 
by the injury until a fortnight after the blow, when severe headache set in, 
and for a few days before admission he noticed that the right arm and leg 
were not as strong as usual. He was discharged September 23rd. 


No. 22.—Dr. S. T. Armstrong. Journal of the American Medical Associa- 
tion, June 18th, 1887, vol. viii.—George J., æt. 53, a shoemaker, was, on 
February 27th, struck on the left forehead by a brick. An irregular lacerated 
wound about half an inch above the outer edge of the eyebrow was caused, 
The man was rendered unconscious for a short time. Не was seen by Dr. 
Armstrong next morning, who treated his wound. He walked half a mile to 
have the required dressings, and was discharged with the wound healed on 
March 14th. On April 24th (i.e., six weeks after his first discharge) he 
consulted Dr. Armstrong again for a roaring in the head which had persisted 
since the injury, and on April 18th he noticed that there was a tendency of 
the right foot to drag slightly. On the 19th, whilst eating breakfast, his 
head had fallen forward on the table, and the right arm and leg seemed 
paralysed. Since this date the right foot dragged a little more and he would 
notice an occasional loss of control over the right arm and leg. On examina- 
tion, arcus senilis was noticed ; the pupils were small and responded well to 
light; tongue and face not paralysed; pulse 70, tense and regular; arteries 
rigid; muscular power of the hands equal, but in walking he drags the 
right foot slightly. On the 26th, the paralysis of the right lower extremity 
was more pronounced, and on the 28th paresis of the right arm set in. The 
dises were found, by Dr. J. L. Minor, to be the seat of double optic neuritis 
(of а lower grade on the right side). An internal purulent inflammation was 
diagnosed, and on May 1st, chloroform having been given, the skull was 
trephined. The dura mater was exposed, dark and nonpulsating. A 
hypordermic needle introduced withdrew dark-brown blood. The dura mater 
being opened the pulsations of the brain pressed fluid out which on examina- 
tion consisted of brown-coloured serum and colourless red blood corpuscles. 
Four strands of disinfected horse-hair were used as drains. A perfect and 
uninterrupted recovery followed. 


130 Traumatic Subdural Hemorrhage. 


No. 23.—Drs. Bremer and Carson. International Journal of Medical 
Sciences. New Series. Vol. ciii., p. 184.— H. T. K., 21 years old, a healthy 
well-built youth, had become intoxicated, two weeks before being веер, апі 
fallen between the joists of a new building. This he stated subsequent to his 
recovery. Save for a headache and occasional vomiting no evil results 
remained. A week later, whilst out walking, he suddenly became unconscious 
and fell. He was assisted home, and, undressing himself, went to bed. 
Dysphasia was found to be present, and the pulse slow and laborious. It was 
also noted that in the afternoon, when his temperature was 101°, he was 
more or less speechless, whereas in the morning when free from fever his 
dysphasia was less marked. He was first seen by Dr. Bremer thirteen days 
after the injury. The patient's condition then was quite rational, no injury 
to the head ; motor aphasia of the ataxic variety was present combined with 
agraphia, paraphasia and paragraphia. Paresis almost amounting to paralysis 
. of the right side of the face and tongue. All the limbs moved equally well. 
Sensation, muscular sense, and sense of temperature and pain were dulled on 
the right side. Next day, the grip of the right hand being weaker than the 
left, and the pulse having fallen to 43, Dr. Carson operated. Under the dura 
mater was found semi-liquid and clotted blood which extended as high as the 
longitudinal sinus above, and to the base below. A horse-hair drain was 
used. He was discharged May 18th. 


No. 24.— Mr. Hulke. Lancet, 1883, vol. ii., p. 814.— The patient, æt. 60, 
an Irish day labourer, was admitted October 21st, 1881. He had had an 
injury fourteen days before and complained of darting pains passing through 
his head from a slightly ecchymosed lump in the right temple. His mind 
was quite clear. The accident was that a falling ladder, twenty-five feet 
long, struck him a glancing blow on the right temple, stunning him for a few 
moments. On the third day after the accident he had to give up work on 
&ccount of severe headache. "There was effusion of blood into the eyelids 
after the accident, but none into the conjunctive. On admission, he walked 
feebly into the ward, but no paralysis or loss of sensibility were present, the 
temperature was normal, the pulse 50, very compressible. On the fourth 
day in hospital he wandered in his mind. On the fifth day, paralysis of the 
right arm and leg occurred. His wife refused to allow him to be operated 
on. On the seventh day he was practically comatose with pulse rate of 70 
and temperature 98:6?. On the eleventh day spastic rigidity of the left arm 
was first observed and this arm also occasionally twitched. An operation 
was now performed. The dura mater when exposed was healthy but bulged 
tensely and was non-pulsating. Three to four ounces of a brown flocculent 
fluid were evacuated. He made a steady recovery from the time of operation. 


No. 25.—Mr. Butlin. Medical Press and Circular, vol. cxi., p. 357 (1895). 
—A man, 55 years of age, was hanging up paper on September 4th when he 
slipped and fell, striking his head against the corner of the mantelpiece. 
When admitted to the hospital he appeared badly shaken, there was bruising 
of the back part of the head in the middle-line. He had not lost consciousness. 
Next day there was some drowsiness and irritability. He remained like this 
until September 8th, when without any warning he was heard to cry out and 
the sister found him in a fit. He had seventeen fits before Mr. Butlin 





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Abstract of Cases. 181 


arrived. In the fits he turned the head and eyes to the left, then the left 
upper limb became flexed, followed by the left leg and the extremities of the 
other side in that order. The rigidity was succeeded by clonic spasms which 
affected the left side of the face first, afterwards spreading to the limbs in the 
same order as the rigidity. He was conscious between the fits, but some 
paresis of the left side of the face and left upper extremity remained. 
Operation being decided upon, he was trephined at the junction of the 
middle and lower part of the fissure of Rolando. No sign of fracture was 
present, but beneath the dura mater was a clot no bigger than a finger-nail. 
This blood was not quite fresh, having evidently formed some days before. 
The arachnoid corresponding to the clot was somewhat raised from the pia 
mater by a collection of clear fluid. This serum was collected just over the 
fissure of Rolando, and it produced a depression of brain substance into 
which the finger could be put. It was drained with a strip of gutta-percha, 
the bone being put back. After the operation there were no more fits, but 
he was violent, excited and restless, complaining in his lucid intervals of 
headache. He required a male nurse until October 22nd, but ultimately 
recovered perfectly, as far as could be seen. 





No. 26.—Mr. Cant. Lancet, 1891, vol. i., p. 542. Reported by Dr. Brock. 
—C. C., 34 years of age, a carter, was kicked on the right cheek and temple 
by a horse on September 25th. He was unconscious for some minutes after 
the injury, and then walked to the hospital. No fracture could be made out. 
He refused admission, so was dressed outside up to October 1st. On this 
day he had two fits for the first time in his life, and was admitted into the 
Lincoln County Hospital. On admission, he was perfectly conscious, and 
with no abnormal signs to be found. Urine 1015; no albumen present. He 
had eleven fits between the time of admission and 11 a.m. next morning. 
These fits began as a twitching of the left side of the mouth, followed by 
twichings of the hand and protrusion of the tongue to the right. During 
this time the right side and both legs were unaffected, but he now turned 
over on his back clenching his hands and drawing them up whilst the legs 
were extended stiffly, the eyes closed and the teeth clenched, the back being 
so arched that he rested on his head and his heels. This condition of 
opisthotonus lasted for a few seconds and then suddenly relaxed; at the same 
time he gave & loud cry and struck the bed violently several times, not rapidly 
but at intervals of five Seconds drawing up his hands and arching his back, 
and then after a pause violently extending the arms whilst the back relaxed. 
The attack lasted four minutes. Immediately before he recovered he sighed 
deeply, turned on his right side, and put his right hand to his right temple, 
regaining consciousness perfectly in the course of a minute. The pupils were 
widely dilated, and he did not pass urine during the attack. Before a fit 
came on he had pain at the site of injury, which passed round his head, and 
he then lost consciousness. He continued having fits and getting weaker. 
The fits were longer and less violent, but the tongue was often bitten. On 
November 10th he was trephined over the right temporal region. No fracture 
of the skull was found, but on removing bone the dura mater bulged into the 
wound, and on opening it а quantity of yellowish fluid was found beneath 
the arachnoid and two small blood clots beneath the pia mater, which were 
removed. He was discharged December 22nd in perfect health and spirits, 
there having been no return of fits of any kind. 


132 Traumatic Subdural Hemorrhage. 


No 27.—Dr. I. G. Modlin. British Medical Journal, 1902, vol. ii., р. 704.— 
W. 8., æt. 37, was admitted into the Monkwearmouth and Southwick Hospital 
on June 14th, with thefollowing history. He had been drinking pretty heavily 
during the first week of the month. On the evening of June 9th he fell down, 
but no importance was attached to this fact. On the 10th he rested, and 
slept for the greater part of the day, on the 11th he went to work in a ship 
yard as usual, on the 12th he awoke in a feverish condition, with pains all 
over the body, was delirious, and with & temperature of 104?. He was 
prescribed for, and on the 18th was much better, the pain gone, and no 
delirium or fever present. At 2 p.m. on June 14th, fits set in suddenly. At 
first they were infrequent and slight, but as they increased in frequency and 
severity, he was sent to the hospital at 9.45 p.m. On admission, fits were 
recurring every two minutes. In the intervals between them the man was 
semi-conscious, and could answer questions. The face was flushed, the pupils 
dilated and fixed, the pulse slow and full. There was a slight indistinct 
bruise over the left parietal bone. The fits began as a blinking of the left 
eyelid, the muscles of the left side of the face were then affected, followed by 
the right side of the face. The movements then began in the fingers and toes 
of the left side, passing thence to the whole limbs. The right extremities 
were finally involved, though not as much as on the left side, It was decided 
to operate. On removing a crown of bone, a large clot was seen under the 
dura mater, no pulsation of the brain being evident. The membranes were 
incised, and clot found to extend round as far as could be felt. As much as 
possible was removed with the little finger and the scoop end of a director. A 
small drainage tube was employed. Another fit occurred a quarter of an hour 
after his return to bed, and nine more at gradually increasing intervals for the 
next five and a half hours, after which the man made an uninterrupted 
recovery. 


No. 28.—Messrs. R. H. Cowan and E. H. Monks. Lancet, 1899, vol. ii., 
p. 1441.—A man of 55, was admitted to the Royal Albert Edward Infirmary, 
Wigan, on September 23rd, 1896. Four days previously he had fallen down- 
stairs, and the day before admission had been seized with fits. On admission, 
he was conscious but aphasic, and his temperature was 100°. During the 
twelve hours following admission he had four attacks, each more severe than 
the one before. During the attacks the patient was unconscious, and the 
muscles of the right side of the face and right arm were in & condition of 
clonic spasm lasting several minutes. The only evidence of injury was 4 
small bruise on the right side of the occiput, which was evidently superficial. 
He was trephined over the centres for the right arm and right side of the face. 
The dura mater bulged on removal of the bone. On incising the membranea 
large blood clot presented. The clot was broken up, and washed away with 
boracic lotion. The wound was lightly packed with iodoform gauze and 
allowed to granulate up. Twitchings ceased entirely after operation. He 
spoke distinctly on the third day. He was discharged on November 7th, and 
in the February following he had been working as а collier for some weeks, 
and was quite well. 


No. 29.—Dr. Charles L. Scudder. Medical Record, June 18th, 1898, 
p. 876.—M. A. B., a spinster, æt. 69, was brought to the Massachusetts 
General Hospital at about 10.30 p.m. She had fallen one and a half hours 


Abstract of Cases. 133 


previously, having been struck by a coasting sled. On examination, she did 
not know of the accident which had befallen her, or why she was at the 
hospital. She spoke coherently, but was suffering from slight shock. Pulse 
rate 64, respirations 16, temperature 97:5°. Bleeding from the right ear, and 
blood coming from the nostrils. No visible external injury, and no paralysis. 
The pupils were equal, contracted, and reacted to light. The patient was 
talkative, but not restless. During the night, however, she was restless, only 
sleeping two or three hours, and she vomited two or three times. At 3 p.m. 
the next afternoon the pupils were equal and reacting, she understood what 
was said to her, but did not speak coherently or distinctly. There was almost 
complete paralysis of the right arm, and paresis of the right leg. „Pulse 85, 
fulland bounding. No para'ysis of face. At 4.30 p.m. the symptoms were 
considerably intensified, the breathing laboured and stertorous, and there were 
right hemiplegia and facial paralysis. Bleeding from the right ear continued 
to a slight extent all day. Middle meningeal hemorrhage was diagnosed, and 
at 6.15 p.m. ether being given, the left middle meningeal artery was exposed. 
The blood was found within the dura mater, which was lacerated, The clot 
was temporo-parietal. The vessel was tied, and a drain, reaching to the dura, 
inserted. Ths temperature rose to 110° F. during the night, but fell immedi- 
ately, and gradually came down to normal. The paralysis began to clear up 
on the 6th day from the leg, and the 10th day from the arm. The 30th day 
she walked alone, and left the hospital. 


No. 80.—R. Lépine. Revue de Médicin, vol. xvi., 1896.—A man, 29 years 
of age, very intelligent, but an incorrigible drunkard, and subject to epileptic 
fits, fell downstairs on June 21st, 1889, and was rendered unconscious. Two 
days later he was brought up to the Hotel de Dieu (de Lyon). On admission 
coma was absolute, but no signs of external injury were present, and no 
discharge from the ears or the nose. In two days the coma gradually 
disappeared, but aphasia remained. In addition, slight paralysis of the face 
and right extremities was present, whilst the tongue deviated to the right. 
After this, epileptic fits, Jacksonian in type set in, always starting with 
twitching of the right labial commissure, immediately followed by convulsions 
affecting the right extremities. Ten days after the fall, as there was no 
improvement, Dr. Jaboulay trephined over the lower part of the left Rolandic 
area. At the moment that the dura mater was incised, there spouted out 
about twenty-five grammes of a brownish red liquid. Antiseptic dressings 
were applied. After this the aphasia and paralysis gradually cleared up. The 
patient left the hospital in December. Later he had some slight attacks of 
epilepsy, but these have not prevented him from working in a dyeing manu- 
factory, and they have not recurred. 


No. 31.—Dr. Hughlings Jackson. London Hospital Lectures and Reports, 
vol. iv., 1867, p. 352.—Mrs. S., et. 80. On Saturday, February 9th, she was 
standing on the top of a short flight of stairs when she felt stupid and 
remembered nothing further until she found herself at the bottom of the 
stairs. On being picked up she said she was not much hurt, and went up 
another flight of stairs, being seen by another neighbour who thought she 
looked dazed. She lay on her bed, but later undressed and went to bed. 
On February 10th she seemed comfortable, and spoke well. On the 11th she 


VOL. LIX. 11 


134 Traumatic Subdural Hemorrhage. 


was found on the floor insensible, having, it was supposed, got out of bed to 
make water. She was seen this day by Dr. Hughlings Jackson with Dr. 
Roberts. She was still insensible, and for four hours (ending 8.30 a.m.) had 
had a series of fits. In each fit the right side of the face had been affected, 
It was said that both arms were affected. At 10.30 a.m., the hour she was 
examined, she took no notice of what was said to her. Occasionally she 
opens her eyes, and sometimes moves her left hand to her head. Continually 
moans. Once only she moved her right hand for a very little distance. She 
drew up both her legs and kept them up. Eyes were closed and there was a 
deviation to the left. The pupils were unequal and small, but not abnormally 
so. Pulse 96. Respiration 36, with each expiration was a moan. On the 
13th she was still insensible. Pulse 100. Respiration 34; по stertor. The 
right arm was apparently paralysed. Her mouth was constantly moving and 
she moaned. During the night she had had constant fits. In these the 
working of the mouth increased, the right cheek and right orbicularis 
palpebrarum twitched, the jaws moved together, the head and eyes turned to 
the right a trifle more than in the interval, the respiration ceased, but the 
thorax and abdomen seemed to jerk alittle. When the fit ended several 
deep breaths were taken. The arm in most attacks was unaffected, but in 
two others there was a very little jerky movement in it. February 14th, she 
had been in fits nearly the whole night, the right arm being now involved 
but the leg never moved. During the evening the respirations were 48 per 
minute and were very shallow, she had fewer fits and died. She only spoke 
four times during this period of unconsciousness. Three times she called а 
daughter's name (Isabella) and once replied ‘‘ Yes ’’ to a question (relatives' 
testimony). At the post-mortem: There was much blood under the dura 
mater, on the left side only, from front to back of the hemisphere and at the 
base. The bulk of it was pressing on the frontal convolutions. The blood 
was above the arachnoid. About half-way up the fissure of Rolando was an 
opening in the arachnoid blocked by a piece of clot, and through this it was 
believed the blood had come. The heart was soft and small, the valves 
competent, but the aortic ones very atheromatous. The kidneys were healthy. 


No. 32.—Dr. Harrington Sainsbury. Pathological Society's Transactions, 
vol. xxxviii.—J. M., a woman, 42 years of age, was admitted to the Royal 
Free Hospital under Dr. Samuel West on December 1st, 1886. On admission, 
she was in a semi-comatose condition which persisted more or less till death 
on January 2nd, 1887. Obscure paralytic symptoms were present, referable 
chiefly to the right side. The woman was a drinker and had recently drunk 
heavily. She was reported to have fallen four days before admission. There 
was bruising over the right hip-bone. No albumen in the urine, At the 
autopsy, there was blood-clot covering the fronto-parietal region of the right 
hemisphere and extending into the anterior and middle fosse of the right 
side. The dura mater was rather firmly adherent to it in some places. The 
clot was placenta-shaped. No source of hemorrhage was discovered. The 
dura mater over the left side of the brain was perfectly healthy. 


No. 33.—Dr. D. G. Denton. Lancet, 1898, vol.i., p. 690 (Report of Meeting 
of ZEsculapian Society).—An alcoholic man received a blow two inches above 
the left ear. He was picked up at once unconscious. On the second day 


Abstract of Cases. 135 


with return to consciousness headache was complained of. On the eighth 
day the pulse-rate was 60, the temperature 97°. He died suddenly on the 
ninth day. At the autopsy a blood-clot weighing one and a half ounces was 
found adherent to the brain. The viscera were not healthy. 


No. 34.— Dr. Molleson. Journal de Médicin, Août, 1766, Paris (reported 
by Guthrie in ‘‘ Injuries of the Head,” p. 65).—A young man received a blow 
on the right parietal bone, which wounded the integuments without causing 
fracture. Coma, with paralysis, followed, and he bled from ears, eyes, nose 
and mouth.  Trephined over the right parietal bone, dura mater opened, and 
blood escaped. Тһе patient was relieved. Five days later he complained o 
pain on the left parietal bone, which was soon followed by fever and delirium. 
Bone exposed on this side and a fissured fracture tound. Trephined, and dura 
mater opened, from under which a glassful of dark red fetid matter was 
evacuated. The patient recovered. 





No. 35.— Dr. Petit (from Guthrie's “Injuries of the Head,” р. 125).—A 
grenadier, struck on the side of the head by the splinter of a shell was knocked 
down on the glacis, but on being carried away soon recovered his senses. He 
had scarcely arrived &t the hospital when he fell into a state of stupefaction. 
He was again bled, and a tumour which had formed over the temporal muscle 
was laid open. The bone beneath was not fractured, neither was the perios- 
teum detached. As the symptoms of pressure persisted the trepan was 
applied, but no extravasation was discovered underneath. Five or six hours 
after the operation he spoke and answered some questions, took some nourish- 
ment, but relapsed shortly afterwards into a similar state of stupefaction. On 
removing the first dressing, the cause of evil was made manifest. The dura 
mater had risen into the opening made by the trepan, and was above the 
level of the bone, which had given some relief to the compressed parts, and 
had probably been the cause of the temporary amelioration which had taken 
place. The dura mater was opened by a crucial incision, and two table- 
spoonfuls of half fluid, half coagulated blood were evacuated. His stupefaction 
csased two hours afterwards, and he recovered so as to be removed with the 
other wounded who were nearly cured. (Originally reported by Dr. J. L. 
Petit in his work ‘‘ Des plaies de la Tete dans le Traité des Maladies Chirur- 
gicales," Paris, 1730). 


No. 36.—Dr. (now Sir) William McEwen. British Medical Journal, 1888, 
vol. ii., p. 305. —A boy had fallen six days previously, causing some slight 
braising about the face and head, and accompanied by а shade of mental 
obscuration. Forty-eight hours after the injury he appeared so well that his 
parents wanted to let him get out of bed. On the sixth day, however, a series 
of convulsions seized him. Twitchings began in the left side of the face and 
gradually involved the left arm, and subsequently the left leg, during which 
consciousness was preserved.  Paresis of these parts remained, though sensa- 
tion was unimpaired. On the following day the convulsions persisted, finally 
becoming general, with loss of consciousness. When the head was shaved for 
operation, a scarcely perceptible irregularity was detected in the cranial vault 
near the coronal suture. The skull was exposed, with a fissure running across 
the coronal suture. Trephined. The dura mater had a dark colour, and on 
openirg gave vent to two ounces of fluid and coagulated blood contained in the 
subdural cavity. Patient made an uninterrupted, typical afebrile recovery. 


136 Traumatic Subdural Hemorrhage. 


CLASS B. 


No. 37.—Mr. Golding-Bird. Guy’s Hospital Surgical Reports, 1902. No. 
74.—A. 8. W., 32 years of age, fell out of a train and was admitted into Guy’s 
Hospital on January 24th with a compound depressed fracture of the skull. 
He was quite conscious on admission, but half an hour later became drowsy, 
and in four hours was unconscious, with stertorous breathing. Pulse 94. 
Respirations 42. He was trephined at the seat of fracture and the bone 
elevated. Extradurally there were two ounces of dark blood. As the dura 
bulged, a small hole was made into it ; cerebro-spinal fluid spurted out toa 
height of six inches. At first clear, it was later mixed with blood. The 
patient’s conjunctive were blood shot and dark, and it was thought that the 
base of the skull was fractured. Death occurred nine hours after the 
operation, and thirteen hours after the injury. No post-mortem record is to 
be obtained. 





No. 88.— Sir Henry Howse. Guy's Hospital Surgical Reports, 
1901. No. 522.—A. G. H., а waterside labourer, 30 years old, was knocked 
down by a heavy van in the Old Kent Road. On admission, there were two 
scalp wounds, both extending to bone. He was unconscious and remained 
so till death. There was no bleeding from the ncse, ears or mouth, but he 
vomited blood. Pulse 42, feeble. Respiration 28, stertorous. Temperature 
95°, The pupils were normal and reacted to light, but afterwards alternately 
contracted and dilated. Later still, the right eye became widely dilated and 
remained so, whilst the left eye had an internal strabismus. Arms and legs 
rigid. No involuntary passage of urine or fæces. He was trephined some 
hours after admission, first on the left side where no blood was found, 
afterwards on the right side where subdurally blood was found. He died five 
hours after operation, the temperature rising to 107° before death. At the 
post-mortem examination a transverse fracture of the occipital bone with 

laceration of the brain was found. 


No. 39.—Mr. Golding-Bird. Guy's Hospital Surgical Reports, 1901. No. 
195.—A. H., set. 50, admitted March 24th, 1901. An iron plate had fallen 
on his head whilst at work. He walked home and went to bed. Some hours 
later he fell into a comatose condition, and was brought up to the hospital on 
an ambulance. On admission, his pulse-rate was 98, and in character it was 
full and easily compressible. The temperature was 99°4°, but higher in the 
right axilla than in the left. Respiration 30 to 35, somewhat forcible. Ina 
semi-conscious condition with an irregular, bleeding scalp wound in the 
occipital region, not reaching to bone. He was able to move his limbs, but 
there was considerable rigidity in the limbs of both sides, more in the left 
than the right. Both knees were stiffly semi-flexed, and observed to twitch 
once or twice. Left pupil larger than right. On the 25th, he was much the 
same. On the 26th, he was worse, and at 1.30 p.m. spasmodic twitchings of 
the face, almost entirely confined to the right side, and of the right hand, set 
in. These attacks recurred every five to fifteen minutes. At 6 p.m. Cheyne- 
Stokes' respiration set in. He died at 1.30 a.m. on the 27th. At the autopsy 
the whole of the left side of the cerebrum was covered with subdural 
hemorrhage. The anterior pole of the frontal lobe was severely lacerated. 


Abstract of Cases. 137 


Small amount of subdural hemorrhage on the right side also. On cutting 
open the brain а large blood-clot was found in the anterior horn of the 
lateral ventricle (left), which communicated through the lacerated anterior 
frontal lobe with the subdural hemorrhage. No fracture of the skull. No 
indication of arterial disease at base of the brain. Kidneys, heart, liver 
and spleen normal. 


No. 40.—Sir Henry Howse. Guy's Hospital Surgical Reports, 
1900. No. 171.—G. H. D., a labourer, æt. 19, was struck on the head by a 
passing express train, and picked up unconscious. He was brought up to the 
hospital from Norwood Junction. On admission, his pulse rate was 58, his 
temperature 97:8?. He was unconscious and bleeding from wounds in the 
right temporal region which exposed bone. Bleeding from the nose and 
hematemesis. Pupils equal and moderately dilated, reacting to light on the 
left side, but very slightly on the right. Knee-jerks exaggerated in both 
limbs. Later twitchings set in in the fingers, then the arms and legs, and 
finally over the whole body. Decided to trephine. Right temporal region 
exposed, found fractured. A large clot was found between the dura mater and 
the skull. This was removed. The dura mater was then punctured, letting 
out a large quantity of dark coloured blood which kept welling out of a 
ruptured cerebral vein, which was therefore tied. The brain was pulped in 
this region. The patient died the same evening at 9 p.m. without recovering 
consciousness. No post-mortem examination. 


No. 41.—Mr. Golding-Bird. Guy’s Hospital Surgical Reports, 1900. No. 
621.— Joseph D., æt. 86, an occasional drinker, fell downstairs on December 
23rd, and was thought to have injured his head. He was put to bed, no 
symptoms being noticed by his friends. On the 24th, curious movements of 
the eyeballs were noticed by his landlord, and that he was not in complete 
possession of his faculties. He was brought up to the hospital by two men, 
being able to walk with their assistance. He was told to come up each day 
if he should not get well. On the evening of the 24th and the morning of the 
25th, he suffered from delusions. On the 26th and 27th, he was brought to 
the hospital, and was thought by his friends to be more delirious. On the 
28th, bleeding from one ear was noticed, and towards midnight he began to 
have fits which recurred at intervals of a quarter to half an hour. These fits 
started in the left hand, spread to the limb, the left side, and finally involved 
the right side. He was admitted to the hospital at 8 a.m. on the 29th. On 
admission, pulse 136. Temperature 101°8°. ^ Respirations 92, stertorous. 
Quite unconscious. A strong, muscular, well nourished man. Incontinence 
of urine and feces. Nystagmus in both eyes. Fits at intervals of a quarter 
to half an hour. There was sweating, and the temperature was higher in the 
left axilla than in the right. Locally there was bruising in the right parietal 
region, and some dried up blood in the external auditory meatus. The fits 
becoming more violent, operation was decided upon, and at 11.30 a.m. a flap 
was turned down in the right temporal region. A fracture along a line 
passing backwards over the right ear was found. A large amount of partially 
dried up blood clot was present above the dura mater. On its removal blood 
welled up from below, and was thought to come from the lateral sinus. Fluid 
was thought to be under the dura mater, and on incising this membrane fluid 


138 Traumatic Subdural Hemorrhage. 


came out under a high pressure. A small incision was made into the pia 
mater, and the brain substance found to be infiltrated with blood. During 
the r. st of the day there was no return to consciousness. On the 30th, there 
were signs of returning consciousness in the early morning, but at 9 a.m. fits 
set in again much as before, and although the wound was opened up and the 
subdural space drained the fits persisted, and he died at 5.30 p.m. At the 
autopsy, fracture of the base on the right side was found, with ecchymoses over 
the whole surface of the brain, and extensive subdural hemorrhage over the 
right temporo-sphenoidal lobe. 


No. 42.— Sir Henry Howse. Guy's Hospital Surgical Reports, 
1899. Мо. 112.—James R., æt. 45, a brewers’ carman; was admitted at 8 a.m. 
on the 2nd of October, 1899, shortly after falling from his dray on to his head. 
He was unconscious for a quarter of an hour after the accident. On admis- 
sion, he was dazed, but not alcoholic, the pupils were equal and dilated and 
there were no paralyses. There was a severe bruise at the top of the head 
with the skin slightly broken; no bleeding from ear, nose, etc. Seemed 
rather better when admitted into the ward, and helped to take off his clothes. 
Pulse 80. Temperature 97:87. During the night he was quiet except for one 
occasion when he tried to get out of bed. At 8 a.m. next morning he became 
с matose, with stertorous breathing. Pulse 120. Temperature 102:6?. Mr. 
Jacobson saw the patient and decided to operate. The skull was trephined. 
The dura mater was first punctured with a needle, when clear serum came 
away. Later blood clot was removed subdurally. The patient never came 
round from the coma, and died about an hour after the completion of the 
operation. The temperature before death was 104:8?. At the autopsy, there 
was extensive subdural clot along the left side of the brain, the left frontal 
lobe was lacerated at the base, and the base of the skull was fractured on the 
left side over the bend of the lateral sinus. 


No. 43.—Mr. Lucas. Guy's Hospital Surgical Reports, 1889. No. 274.— 
Edwin G., æt. 31, fell downstairs, and was picked up unconscious. On admission 
to the hospital he could be roused, but was occasionally violent. Both pupils 
were equal and contracted, and reacted normally. No signs of fractured base 
no paralysis or rigidity. Pulse 50, full. Temperature 97?. "There was swell- 
ing across the back of the head and over the right eye. Became suddenly 
comatose, the pulse went up to 72, the left pupil became larger than the right 
and did not react to light, the limbs were all flaccid and the breathing 
 Stertorous. Operation being decided upon, а flap was turned down in the 
left temporal region. A fissured fracture of the skull was found. The skull 
was trephined and the dura mater exposed, tense and bulging. On incising 
it, a lot of clot was found and removed. The brain below was seen to be 
lacerated, and the whole vault of the cranium appeared to be loose. The 
patient died four hours after the operation. Atthe post-mortem examination 
a longitudinal fracture through the base with rupture of the lateral sinus was 
found. Subdural blood clot with laceration of the temporo-sphenoidal lobe. 


No. 44.—Mr. Lueas. Guy’s Hospital Surgical Reports, 1899. No. 705.— 
William B., et. 43, was admitted at 6.30 p.m., on December 1st, 1899. He had 
fallen 15 feet head downwards, and a heavy door had fallen on him. He was 


Abstract of Cases. 139 


. picked up unconscious. On admission, he was unconscious with stertorous 
breathing. Blood came profusely from both nostrils, especially the right. 
The left arm was twitching, the left leg rigid. The pupils were contracted 
to the size of pin-points. There was a compound depressed fracture affecting 
the right parietal bone. The patient was taken to the theatre, and A.C.E., 
followed by ether, given. Extensive fracturing of the skull was found, and 
extradural blood clot was removed in quantity. The dura mater was then 
found tense, barely pulsating, and dark in colour. Beneath it a large clot 
was found compressing the Rolandic area. The clot was removed, and 
hemorrhage controlled by a plug of gauze low down in the subdural space. 
The dressings repeatedly became soaked through and had to be changed. The 
patient was infused just before he died. No post-mortem examination was 
made. 


No. 45.—Mr. Golding-Bird. Guy's Hospital Surgical Reports, 1899. No. 
427.— Phoebe G., æt. 59, a heavy drinker, fell a distance of 16 feet from a window 
to the pavement. Нег head struck the ground first. She was picked up 
unconscious and bleeding from the left ear. Two hours later she was brought 
up to the hospital, having vomited twice on the way up. On admission, she 
was unconscious, with a large bruise half-way down and just anterior to the 
left parieto-occipital suture. Pulse 72, soft, irregular.  Respirations 28, 
stertorous. The right pupil larger than the left, both reacting to light. She 
regained consciousness in an hour, becoming irritable and restless, and soon 
falling into a state of drowsiness. At 10 p.m., when it was decided to operate, 
she was unconscious, with very stertorous breathing, and the pupils were 
uneven, the left being widely dilated, and neither of them reacting to light. 
The skull was trephined over the region of the left middle meningeal artery. 
The dura mater was found tense and non-pulsating. The membrane was 
incised, when some serum and then a quantity of blood clot were removed. 
Drainage with gauze was used. The patient was obviously relieved by the 
operation, but the coma persisted, and she died four hours after the operation. 
No post-mortem examination was allowed by the coroner. | 


Ко. 46.—Mr. Davies-Colley. Guy’s Hospital Surgical Reports, 1898. No. 
70.—Mary L., æt. 64, fell downstairs and struck her head. She was unccn- 
scious when picked up, but when a friend returned with a doctor she was 
conscious again and had vomited. She was sent up to the hospital and 
admitted on the 22nd January. On admission, she was conscious and 
answered questions well. There was bleeding from the mouth and left ear, 
and she vomited blood. Pupils equal, breathing easy. The pulse was 96 
and rather irregular. The right cheek was puffing slightly with expiration, 
otherwise there was no paralysis or rigidity. Next day she was much the 
same. On the 24th the patient was unconscious, there was a bruise immedi- 
ately in front of the mastoid process, and extending upwards towards the 
temporal ridge. On pressing this bruise the left arm moved, the right arm 
remaining still. Twitching of the left side of the face was marked. The right 

side of the face was apparently paralysed save for the corrugator supercilii 
muscle. The right eye was fixed, insensitive, pupil contracted but reacted very 
Slightly to light. The right eye was quite sensitive and reacted to light, but 
the pupil was contracted. Legs both drawn up on pressure on the bruise on 


140. Traumatic Subdural Hemorrhage. 


the head. On the 25th, there was no change, whilst towards evening fits set in, 
confined for the most part to the right side of the body and head. These 
started in the chin and spread in order to face, arm and leg. The eyes were 
directed on each occasion to the side on which the fit occurred. She was 
trephined over the left lower Rolandic area. Extradural hemorrhage was 
found. The dura mater was opened, and a large quantity of blood and serum 
escaped. The brain was much depressed, but pulsating. The blood was 
thought to come from the middle meningeal artery, but pressure on the artery 
did not arrest the bleeding. The hemorrhage was stopped with pads, the 
dura mater stitched with catgut, the trephine bone replaced, and the wound 
sutured. Next day the patient was much better, she could use the right arm 
freely, and the facial paralysis was less marked. Her condition was quite 
satisfactory up to February 10th, when she became irritable and refused food. 
On the 12th the wound was opened, the dura mater incised, and a large 
abscess found in the left hemisphere. She died next day. 


No. 47.—Mr. Davies-Colley. Guy's Hospital Surgical Reports, 1898. No. 
427.—Dave S., 55 years of age, was brought to the hospital on September 5th 
with a bruise and small scalp wound at the back of the head. He was very 
drunk, and the cause of his injury was never discovered. He was admitted 
to the surgery at 1.30 p.m. and detained till 5 p.m. He several times tried to 
escape, and finally before being discharged in charge of the police at 5 p.m., 
he was washed out. At 10.30 p.m. the police brought him back and he was 
admitted to Cornelius ward. At this time he was quite comatose, with the 
right arm and leg pardlysed. Pupils both dilated and not reacting to light. 
Pulse 80, full and strong. Respiration stertorous. No facial paralysis. An 
hour after admission he was operatcd upon. Chloroform was given, and the 
left Rolandic area exposed. The skull was very thick, and while removing 
the piece of bone with the elevator it broke across quite easily near the centre. 
Very little force was used, and it was considered that there must have been a 
pre-existing fracture there. The line of fracture was nearly parallel to the 
zygoma. No extradural hemorrhage was present. On opening the dura 
mater a large blood clot was exposed to view and removed. The clot hada 
diameter of four inches, and its removal was followed by severe hemorrhage. 
The wound was temporarily packed, and then irrigated with warm boracic 
lotion. The wound in the dura mater was sewn up, the bone replaced in 
pieces, the skin sewn up, a gauze drain being inserted. Next day he was much 
better, and the improvement continued until 4.30 p.m. on the 7th, when he 
suddenly became worse. Improvement again followed, but he ultimately 
died at 11.25 p.m. on the 8th. Atthe autopsy а large clot was found between 
the dura mater and the brain, whilst the brain itself was extensively bruised. 
There was no fracture of the skull, no laceration of the lateral sinus, and по 
sign of rupture of middle meningeal artery. 


No. 48.—Mr. Durham. Guy's Hospital Surgical Reports, 1894. Мо. 3.— 
Edward B., st. 42, lighterman, was admitted into Cornelius ward on 
December 20th, 1893. He fell backwards whilst going upstairs in an alcoholic 
condition. On admission, he had stertorous breathing, pupils contracted and 
insensitive to light, pulse regular, urine 1,020, no albumen. There was à 
hematoma over the parietal and occipital bones of the right side. The 


Abstract of Cases. 141 


muscular resistance was fairly good when the arms were raised. On the 21st 
he was drowsy, but could be roused. For the next week he was semi-conscious, 
restless, and at times noisy. On the 28th he was moved up to the strong 
room (pulse 74), and apparently passed through an attack of delirium tremens. 
On the 31st he was somnolent, but could be awakened (temperature 97°, 
pulse 74). On January 156 he was comatose. At 11 a.m. the pupils were 
equal, as also the tone of the muscles on the two sides. At 2 p.m. the left 
pupil was larger than the right, there was slight facial paresis on the left side, 
breathing stertorous. Pulse 58. Operation was performed at 2.30 p.m. The 
dura mater was found bulging and not pulsating. On incising it, there came 
a gush of dark-brownish blood. About two or three ounces of blood came away 
altogether. The opening in the dura mater was left open for drainage, but no 
tube used. There was some improvement after operation, but the coma 
persisted, and the patient died shortly after 12 a.m. on the 3rd. At the 
autopsy blood was found covering the right and left frontal lobes beneath the 
dura mater, the poles of the frontal and temporo-sphenoidal lobes were 
contused more on the left side than the right. There was a fracture of the 


posterior fossa. The left kidney was small and puckered, the right large, with 
one scar. 


No. 49.— Sir Henry Howse. Guy’s Hospital Surgical Reports, 1891. 
No. 289.—John M., æt. 36, fell from the side of a dock into a moored 
barge, a distance of about twenty feet, and was admitted to Guy’s at 11.80 
p.m. on January 28th. On admission he was unconscious, wholly paralysed, 
bleeding from both ears and both nares; respirations slow and shallow ; pulse 
about 50, feeble. At 2 a.m. on the 29th he recovered the use of the left arm. 
Trephined at 9.30 a.m. in the left temporal region. The brain was found 
congested, but no clot present. He died two hours later, with stertorous 
respiration and pupils dilated and fixed. At the post-mortem examination, 
there was a large effusion into the right temporal muscle. There was a large 
temporo-parietal subdural clot half an inch thick on the right side. The blood 
came from the vessels of the pia mater. The brain was severely bruised, and 
there were severe fractures of the skull. 





No. 50.—Mr. Durham. Guy’s Hospital Surgical Reports, 1890. No. 297. 
—Walter B., æt. 28, fell from the dickey of his van on to his head on July 
10th and was brought up to the hospital. On admission he was excitable. 
There was a scalp wound over the lambdoid suture exposing periosteum. The 
pupils were equal and reacted. No paralysis. No sigus of fractured base. He 
was alcoholic, and soon after admission was removed to the strong-room on 
account of his noisy behaviour. He was brought back to the ward on the 11th, 
at 2 p.m. On the 13th he was quiet and knew his friends. (His mother stated 
that he was a heavy drinker and had had a severe blow on his head before.) 
On the 14th he had fits. He had had three slight ones involving the left side 
of the face during the night. At 9 a.m. he had one which spread to the left 
arm and leg and then the right arm and leg. He remained unconscious, with 
stertorous breathing between the attacks, The fits recurred at intervals of 
one and a half to two minutes. On the 15th the fits were less. He had had 
two during the night but less violent than before. Temperature 98:6. On 
the 16th, he was unconscious, with stertorous breathing. Mr. Lane 


142 Traumatic Subdural Hemorrhage. 


examined the eyes with the ophthalmoscope and found double optic neuritis. 
He remained the same till 7 a.m. on the 17th, when he seemed to have a 
choking fit and died suddenly. At the autopsy there was a V-shaped fracture, 
with limbs horizontal, in the right occipito-temporal region. There was 
blood both internal and external to the dura mater. The former amounted 
to one and a half ounces. There was extensive pulping of the orbital convo- 
lution, and the pole of the temporo-sphenoidal lobe on the right side. The 
left side of the brain was normal. The heart was healthy, the kidneys large 
and tough but otherwise normal; the Jiver weighed seventy-three ounces. 


No. 51.—Mr. Durham. Guy's Hospital Surgical Reports, 1890. No. 326. 
—Henry T., æt. 32, was knocked from the seat of his van to the road, the 
result of a collision with an omnibus. On admission (October 3rd), he was 
irritable, would not keep quiet, and seemed under the influence of drink. 
He vomited a lot. There was bleeding from the left ear, but no scalp 
wound or hematoma. He was noisy, and tried to get out of bed the following 
night, necessitating his being strapped down. Temperature 101:2°. No 
albuminuria. On the 5th he was transferred to the strong-room. On the 6th 
he had a fit at 6.30 p.m., and had twenty-three up to 8 a.m. on the 7th. -The 
fits start with deviation of the head and eyes to the left, then twichings began 
in the left eyelid and spread to the whole of the left side not affecting the 
right. During the fit both pupils contracted. Between the fits he was conscious 
. and had left hemiplegia. Temperature 100:4°. He was given chloroform and 
trephined in the right temporal region. The dura mater was exposed tense, 
and on incising fluid squirted out four inches high. Blood clot was present 
and removed. Ор the 9th he was conscious: the hemiplegia had cleared up, 
but the facial paralysis on the left side persisted. On the 10th he appeared 
well, answering questions and speaking intelligently. On the lith bad 
symptoms set in, and on the 12th he died, the temperature reaching 104° 
before death. At the post-mortem examination there was diffuse meningitis. 
There was bruising of the right temporo-sphenoidal lobe. There were fractures 
of the middle and posterior fosse of the skull. 


No. 52.—Sir Henry Howse. Guy’s Hospital Surgical Reports, 1890. 
No. 276.—Alfred N., æt. 60, was knocked down by a cab on November 
7th. Не was able to walk int» the surgery at about 6 p.m. The pulse was 
rapid, and he had a wound at the back of the head, not, however, exposing 
the bone. At 8 p.m. his breathing had become stertorous, the right pupil 
was dilated and fixed, the left being normal; all the limbs were rigid: the 
` pulse was 51 and full. He was trephined over the right middle meningeal 
artery. A fissured fracture of the skull was found and through it most of the 
blood from a rupture of the middle meningeal artery had escaped into the 
tissues of the scalp. The dura mater being opened, the front part of the brain 
was found lacerated, and there was a temporo-parietal clot. Next day he 
answered when spoken to; the right pupil was a shade larger than the left, 
and both react to light; there were no unilateral symptoms. On the 9th he 
seemed to be progressing favourably, but on the 10th, at 10.30 a.m., the 
temperature was 104°6°; at 2.15 the respirations were stertorous (48), the 
pulse 160, and the temperature 104:9°, The optic discs were completely 
blurred over. He died at 3.30 in the afternoon, At the post-mortem, 


| 
| 


Abstract of Cases. 143 


the fracture found at operation extended to the occipital bone, but there was 
no fracture of the base. About one ounce of blood was found internal to the 
dura mater, and a small quantity of blood superficial to the dura mater. No 
meningitis. The right temporo-sphenoidal lobe was lacerated and soft. No 
atheroma, of vessels ; kidneys normal and heart fatty. 


No. 53.—Mr. Davies-Colley. Guy’s Hospital Surgical Reports, 1888.— 
John B., æt. 35, fell downstairs on to his head, and was admitted into Guy's 
Hospital at 11 p.m., on March 11th, 1888. On admission, he was comatose, 
with stertorous breathing. The pupils were unequal, the left being contracted. 
Over the right parietal bone at its posterior part was a Jarge bruise. At 
11.30 p.m. Cheyne-Stokes breathing was present; the pulse was 40, labouring, 
the respirations 38 ; the left pupil dilated. At 12 midnight the left pupil had 
contracted again. On the morning of the 12th the coma still persisted ; the 
respirations were 30 per minute, sometimes almost Cheyne-Stokes like in 
character and sometimes stertorous ; pulse 60, rather small; left pupil con- 
tracted. When seen by Mr. Davies-Colley at 1.45 p.m. the left pupil was 
more dilated, but still & goed deal smaller than the right. Marked Cheyne- 
Stokes respiration was present. Trephined over fore part of right temporal 
region. On opening the dura mater some dark fluid blood at first came out, 
then black clot. Mr. Davies-Colley passed a finger between the dura mater 
and the brain till it rested on the dura mater covering the lesser wing of the 
sphenoid. On withdrawing the finger, more clot came out and some broken- 
down brain matter. The patient improved for a time after the operation, but 
died with Cheyne-Stokes respiration and pulse-rate of 40 at 2 a.m. on the 18th. 
At the post-mortem examination there was an extensive fissured fracture of 
the vertex, and a small localised fracture of the left middle fossa at the base. 
The fore part of the right frontal lobe was pulped. The viscera were healthy. 


No. 54.—Sir Henry Howse. Guy's Hospital Surgical Reports, 1887. No. 
224.—Henry Brown, et. 25, was thrown from his waggon on to his head 
on February 5th. He walked home and became drowsy. On February 
Tth he was admitted to Guy's Hospital in an unconscious condition 
(11.15 p.m.). On admission, he became restless when irritated, but did not 
speak. His movements are confined to the left side of the body. Pulse 80, 
irregular; pupi's equal, active and moderately dilated; right facial paresis. 
No bruising of head found and no signs of fractured base. At 3.80 a.m. on 
the 8th he had a fit beginning with vertical oscillation of the eyes and move- 
ments of the left arm. These increased, spreading to the mouth and face 
and then to the legs. The fits continued during the day and the next night 
became increasingly frequent and involved the whole body as clonic move- 
ments. At 10a.m. on the 9th he was quiet, but now had paralysis of the 
left arm and paresis of the left leg. The left eye became inflamed, appar- 
ently from exposure, owing to the orbicularis palpebrarum not acting. At 
8.80 he spoke, asking for a drink, which he took. On the 10th he seemed 
better, the left hemiplegia had disappeared, but he was restless and tried to get 
out of bed. On the 12th he had recovered his senses largely, attempting to 
protrude his tongue and whistle when asked to. Pupils equal; internal 
strabismus of. left eye. Pulse feeble. Temperature 984°. Can move his 
arm and legs perfectly. After this he became restless again and relapsed into 


144 Traumatic Subdural Hemorrhage. 


а condition of coma, finally dying at 9.15 p.m. on February 16th. At the 
autopsy, about 8 ounces of clot and brown-coloured blood were removed from 
beneath the dura mater on the right side. Тһе clot was temporo-parietal 
chiefly, but extended forwards somewhat. The general surface of the brain 
was uninjured, but there was an area about one inch in diameter over the 
second and third right temporal convolutions where the arachnoid and pia 
mater enclosed a hemorrhage, and with a depression due to destruction of 
brain substance which was traversed by a fair-sized vein, which was probably 
lacerated and the origin of the blood. The brain was quite healthy, and the 
post-mortem report (No 45, 1887) says, “It appears probable thut had the 
clot been removed he would have recovered.’’ Viscera healthy. 








No, 55.—Mr. Bryant. Guy’s Hospital Surgical Reports, 1884. No. 279.— 
Thomas C., æt. 56, was kicked in the abdomen by a horse, and, falling on 
some stones, struck the right side of his head. He was rendered unconscious, 
and was still in the same condition when admitted into Guy’s Hospital at 
1.40 a.m. on September 6th. A wound was present in the occipito-parietal 
region which did not expose bone. The pulse was slow, regular, the breathing 
stertorous, and the pupils contracted, the left more so than the right. Both 
arms were rigid, the legs slightly so. At 10.15 there was paresis of the right 
side of the face, right hemiplegia and divergent strabismus. On the 7th he 
remained much the same, but the breathing was quieter. On the 8th he was 
noisy, recognised his wife and asked for a drink. On the 9th he was becoming 
cyanosed. Pulse-rate 90. Respirations 60. Не died on the morning of the 
10th, the right hemiplegia remaining till the end. At the autopsy there was 
a fracture of the right side of the skull, bifurcating in the middle fossa. 
Subdural hemorrhage over left side of brain with superficial laceration. The 
heart was normal, the vessels good, the kidneys granular. Liver very tough. 
Testicles healthy. . 





No. 56.— Mr. Durham. Guy's Hospital Surgical Reports, 1878. No. 324. 
— William G., æt. 25, was thrown out of a cart and pitched on his head two 
days before admission. He was picked up insensible and carried home. 
After some time he regained partial consciousness and was admitted into 
hospital like this on January 9th. It was said that he had been very sick 
and vomited up some blood. On admission, he was semi-conscious and could 
scarcely be roused, complained of headache, and had both pupils dilated, 
the right more than the left. There was slight paresis on the left side of the 
body, but no facial paralysis. Small scalp wound in the occipital region. On 
the 10th he remained much the same. Temperature 98:4?. Respirations 16. 
Pulse 56. On the 11th he appeared to be better, putting his tongue out and 
moving his arms and legs when requested. Slight facial paralysis on the left 
side. At 9 p.m. he had two fits and another at 9.20. After this last one he 
remained unconscious. The fits resembled epileptic fits, the movements 
beginning on the right side. The fits continued to increase in frequency, and 
he died suddenly after the fortieth. At the post-mortem examination, a thin 
layer of blood clot covered the anterior part of the left hemisphere and 
frontal lobe of the right side. The brain was bruised extensively but super- 
ficially on the under surface of the middle and anterior lobes. There was à 
fracture of the middle fossa. 


Abstract of Cases. 145 


No. 57.—Mr. H. W. Allingham. Clinical Society’s Transactions, vol. xxii. 
—Nathaniel C., æt. 40, admitted into the Great Northern Hospital, December 
7th, 1888. He had fallen in getting off a tram-car, but did not remember the 
circumstance himself. Found to be somewhat concussed and complained of 
pain in the left shoulder, but nothing objective was to be seen there. No 
external signs of injury to the head were found. Given a draught of chloral 
and bromide and slept well. Next day he was rather drowsy, with pains in 
the right side of the head. The pupils were equal and reacted to light. 
December 11th, remained in the same drowsy state ; irritable when disturbed 
or examined ; at times rather light headed. Highest temperature yet 100:6? 
on December 9th. No paralysis; pupils normal; no vomiting; no albuminuria. 
On the 13th, at 6 am., convulsions set in. They began in the muscles 
of the left side of the face and affected the left limbs. Right pupil larger 
than left. Stertorous breathing. Fits recurred at frequent intervals. Mr. 
Allingham decided to operate. Posterior branch of middle meningeal artery 
exposed. A dark mass appeared beneath the dura mater, which did not 
pulsate ; it proved to be a large black clot of blood which was removed leaving 
a large cavity extending almost as far as the finger could reach. This was 
irrigated with carbolised lotion till all clot had been washed away. The 
brain seemed a good deal lacerated over the right frontal lobe. Drainage 
tubes, two in number, were inserted. The man made a good recovery, and 
there is an additional note that on July 1st he was quite well and suffering 
no inconvenience at all. 

No. 58.—Mr. Cock. (Reported by Sir Samuel Wilks in vol. v. Guy’s 
Hospital Reports.)—A. W., æt. 25, was thrown down іп a scuffle and struck 
his head on the pavement on October 21st. He was picked up insensible, 
taken to a neighbouring hospital, where his wound was dressed. He was 
then sent home. On the 22nd he was in a ha!f-stupid state and had what 
was thought to be an epileptic fit. Another of these fits occurred on the 23rd. 
On the 24th he was sent to Guy’s Hospital, where he appeared to be in a state 
resembling concussion and with a scalp wound on the left side behind. In 
the evening he was restless, with delirium. On the 25th he was quiet all day. 
That night, however, he had another epileptic fit which left him in an almost 
maniacal condition, from which he sank into a half-comatose state, occa- 
sionally screaming out. The pupils became contracted at the last, and the 
sphincters paralysed. He died November 15th. At the autopsy, there was 
no injury to the bone. On the right side there was a subdural collection of 
blood one inch thick. It existed more on the anterior and lateral parts towards 
the base. The clot was dull red in colour, and in some parts yellow, showing 
age. At two portions of the base yellow clot was distinctly adherent to the 

brain, and, on removing it the latter was found to be bruised and soft. ** Thus 
it is tolerably clear that the hemorrhage was from some ruptured vein of the 
pia mater at this spot." None of the large arteries or venous sinuses were 
found injured. No inflammatory products were found in any part of the 
brain. 


No. 59.—Mr. Jonathan Hutchinson, Senr. Clinical Lectures and Reports 
(London Hospital), vol. iv., p. 10.—A sailor, 35 years of age, fell in the street, 
and was brought up to the London Hospital, where a scalp wound was dressed. 
It was 10 a.m. when he entered the surgery. He was discharged after the 


146 Traumatic Subdural Hemorrhage. 


dressing of his wound, and at 5.30 p.m. he was again brought up to the 
hospital, this time by the police, who had found him insensible. On admission, 
he was unconscious and had stertorous breathing, the pulse was 72, laboured, 
the left pupil was larger than the right, but neither much dilated and neither 
reacting to light. The eyes diverged a little. There was a considerable bruise 
of the left eyelid, and on the occiput of the same side a considerable laceration. 
Mr. Hutchinson decided to trephine in an hour’s time, but the man died 
before his return. At the autopsy the skull was found exceedingly thick and 
dense. Subdurally over the left hemisphere was a thick clot which weighed 
about five ounces, and extended to the base of the brain. A thin adherent 
film covered the whole of the opposite hemisphere, occupying the arachnoid 
cavity. There was по fracture of the skull, and no rupture of the middle 
meningeal artery. In the middle of the pons varolii were four or five well- 
marked circumscribed blood clots, from the size of a pea to & pin’s head. 


No. 60.—Mr. Jonathan Hutchinson, Senr. Ibid., p. 49 (quoted in Mr. 
Jacobson's paper ‘‘On Middle Meningeal Hsemorrhage," under differential 
diagnosis).—4A man fell from a hay cart in October, 1867. When admitted he 
had a cut on the occiput, with an irregularity in the bone near it. There was 
also & bruise on the right side of the head. He told his name an4 put out his 
tongue on admission, but soon afterwards became unconscious. He had left 
hemiplegia and left facial paralysis. The right pupil was widely dilated and 
not reacting, the left was normal. There was no stertor. He had been bled 
before Mr. Hutchinson saw him, probably causing the rapid and feeble condi- 
tion of the pulse. There was a large extravasation of blood over the right 
temporal region. The diagnosis of ruptured middle meningeal artery having 
been made, the dura mater was exposed, but no extradural clot found. Atthe 
post-mortem examination, there was an extensive fracture of tne occipital bone 
and posterior part of the parietal. A laceration of the outer surface of the 
right hemisphere was present near its middle, with much extravasation into 
the arachnoid. There was severe concussion of the whole brain. 


No. 61.—Mr. George Cowell, Westminster Hospital Reports, vol. iv.—A 
man, about 45 years of age, was taken by the police to the surgery at 8.30 
p.m. on October 1st in an unconscious condition. The police said that whilst 
intoxicated he had been knocked down by a cab. On admission, he was 
breathing slowly and heavily and could not be roused. When seen next 
morning by Mr. Cowell he was unconscious and breathing heavily. He could 
not be roused. There were slight abrasions on the head and face. No signs 
of fractured base and no vomiting. The jaws were somewhat rigidly fixed. 
The pupils were contracted, the left more than the right. Loss of power in 
the left arm with rigidity in right. There was very little difference between 
the legs, if anything the left was more rigid than the right. Both legs were 
slowly moved on tickling the soles. Complete retention of urine was present. 
Temperature 92°. Pulse 72. Respiration 24. The patient's symptoms 
gradually increased, the paralysis of the left arm became more marked on 
the morning of the 4th, and left facial paralysis showed itself. The uncons- 
ciousness deepened and the stertor became more marked. He died sixty-seven 
hours after admission. The temperature chart showed a gradual rise and 
subsequent fall. At the autopsy there was fracture of the base, On dividing 





Abstract of Cases. 147 


the dura mater a considerable layer of black clot was found covering the 
anterior part of the brain. The anterior part of the right frontal lobe was 
found lacerated and soft. The viscera were healthy. 


No. 62.— St. George's Hospital Reports, vol. x., No. 1325.—D. M., a man 
of 48, was admitted to St. George’s Hospital on August 9th. He had fallen 
downstairs whilst drunk and alighted on the back of his head. Ор admission, 
he was insensible and almost moribund from the loss of blood from two scalp 
wounds in the occipital region, which exposed bone freely. Stimulants being 
given, he revived. On August 10th to 12th he seems to have bordered on, if 
not actually suffered from, delirium tremens. On the 16th the scalp was 
incised for cellulitis, the temperature was 99°, the pulse 72. During the next 
three days there was some improvement. On August 21st there was rather 
less restlessness. Pulse 140. Temperature 103:4?. Complete right hemi- 
plegia and coma. Death followed. At the post-mortem examination there 
was a fracture of the middle fossa on the right side. Over the left side of the 
brain there were 2% of dark fluid and membranous coagulum. The under 
surface of the left frontal lobe was much bruised. 


No. 63.—Drs. Homans and Walton. Boston Medical and Surgical Journal, 
vol. 124.— J. M., æt. 28, a waiter, was admitted into the Massachusetts 
Hospital after having been thrown from a horse and supposed to have struck 
his head against the cobble stones. On admission, temperature 98:2?. Pulse 
60. There was a hematoma, with abrasion of the scalp, at & point corres- 
ponding to about the middle of the suture between the right parietal and 
occipital bones. The right pupil was dilated on admission. When seen by 
Dr. George Eliot, within two minutes of admission, consciousness was 
returning, the pupils were normal, the pulse slow and full. The hematoma 
was opened under cocaine but no fracture found. No paralysis. On the 
third day, May 15th, after admission he was delirious in the evening and 
trying to get out of bed. Temperature 103°. On the 16th he was almost 
comatose and aphasic. On the 21st the temperature had gradually come 
down to normal. The pulse was a little faster though still full and slow. 
Aphasic. Early in the morning of this day spasmodic twitchings of the right 
side of the face were noticed, and the right side of the mouth was drawn down. 
These recurred during the day. At 10 p.m. the same day convulsive move- 
ments appeared in the muscles of the left side of the face, and the right eyelid 
was kept closed whilst the left side was twitching. He seemed conscious 
though unable to speak. On the 10th day from admissson, he had convulsive 
twitchings of the side of the face, increasing in frequency towards the evening; 
they commenced at the angle of the mouth. ‘There was paresis of the right 
side of the face in between the attacks. The man was conscious, but aphasic. 
Üperation was decided on. Before operation the convulsions had spread first 
lo the right arm, then t» the right side of the body, and finally to the whole 
body. Ether being given, trephining was performed just anterior to the lower 
part of the fissure of Rolando. The dura mater was bulging and tense, some- 
What yellowish and opaque. Incision into it revealed a large clot, which was 
found to extend in every direction under the dura mater. The clot was 
removed. A small clot was also removed from underneath the jia miter by 
incision. The brain was lacerated to a considerable extent. No bleeding 


148 Traumatic Subdural Hemorrhage. 


point was found. The blood and clot were washed out with warm water. 
There were three slight convulsions affecting only the corner of the mouth the 
night after the operation, but no more occurred subsequently. The aphasia 
slowly but completely cleared up. 


No. 64.—Dr. J. W. Elliott. International Medical Magazine (Philadelphia), 
1893, vol. ii., p. 118.—A man, 30 years of age, was admitted to the Massa- 
chusetts General Hospital on November 25th, having been kicked by a horse 
three hours previously. He was unconscious for ten minutes after the injury. 
On admission, he was conscious, but could only speak with difficulty. The 
tongue was protruded to the left when put out. The pupils were equal and 
reacted. Pulse 96. Noother paralyses. On the right side of the skuli there 
was а compound depressed fracture. Ether was given and the depressed 
bone removed. The dura mater, which appeared white and uninjured, bulged 
into the wound and did not pulsate. Distinct fluctuations showed the pres- 
ence of fluid under the dura mater. On incising the membrane a quantity 
of clear fluid escaped, but the pulsating brain was not visible. Another fluc- 
tuating membrane which had the colour of muscular tissue was pushed into 
the opening in the dura mater. On incising this membrane a little clear fluid 
and about an ounce of blood ran out. Pulsating brain convolutions then 
became visible for the first time. Blood continued to pour out of the 
subarachnoid space, and was only controlled by packing gauze deeply in 
between the convolutions. Recovery was complete. 


No. 65.—Mr. Openshaw. Abstracts of the Transactions of the Hunterian 
Society, 1892-3, p. 36.—A man, et. 60, fell from a cart whilst it was in 
motion. He walked into the hospital, where he exhibited considerable 
violence, and was with difficulty persuaded to remain in. There was a scalp 
wound two inches long on the left side of the occipital bone and profuse 
hemorrhage from the left ear. After admission he became more and more 
unconscious and very restless. Two hours later there were no paralyses, 
consciousness was not wholly lost, the pupils were normal. Twenty-four 
hours after admission there was complete paralysis of left arm and leg, 
incessant movements of the right limbs, dilatation of the right pupil with 
failure to react to light, signs of subconjunctival hemorrhage on the right 
side, paralysis of the right internal rectus. Two hours after this, subcon- 
junctival hemorrhage was appearing on the left side and stertorous breathing 
and coma were present. Trephining, without anesthesia, was performed. 
On exposing the dura mater, the middle meningeal artery was intact, but the 
membrane bulged and was non-pulsating. A mass of blood-clot was found 
beneath, and partially removed. There was some improvement after the 
operation, but he sank and died twelve hours later. At the autopsy a large 
clot two and a half inches thick was present beneath the dura mater in the 
middle fossa on the right side. On the left side the petrous portion of the 
temporal bone was fractured, but no vessel of size seemed wounded. 


No. 66.—Mr. Н. W. Page. Lancet, 1898, vol. i., p. 1167.—The guard of a 
train was struck by an open door of & moving train. The blow caught him 
between the eyes, and threw him violently on to the back of his head. He 
was dazed but not unconscious, and in this condition was taken to St. Mary's 


Abstract of Cases. 149 


Hospital, at 1.15 p.m. on December 21st, 1897. On admission, he was 
extremely collapsed but perfectly conscious, answered questions, and gave his 
name and address. From the left ear there flowed blood and cerebro-spinal 
fluid. Respirations 20, pulse 90. No fracture could be discovered, but there 
was some slight swelling in the left temporal region. The pupils were equal 
and reacted sluggishly. There were no unilateral symptoms save the aural 
hemorrhage. Soon after admission he passed into coma. Between the time 
of admission and the time at which he was seen by Mr. Page (2 p.m.) he had 
some clonic movements of the left arm, but these had quickly given way to 
spastic rigidity, which quickly involved all the limbs equally. The coma. 
deepened, the pulse and respiration began to fail, the pupils became unequal, 
the left being much larger than the right, and it was decided to operate. He 
was trephined over the left middle meningeal artery; the dura mater bulged, 
was bluish in colour and non-pulsating. On incision, a considerable amount 
of blood flowed away. As the blood was thought to be chiefly at the base of 
the brain, an irrigator was passed down to this part. There was marked 
improvement in the pulse and respiration, and the left pupil contracted down 
to the same size as the right, but the man never regained consciousness, and 
died six hours later, the temperature having steadily risen to 107° C. before 
death. At the autopsy the subarachnoid space over both hemispheres was 
practically full of blood, both fluid and clotted, but the greatest quantity of 
blood was at the base. There was extensive laceration of the left orbital lobe, 


and anterior extremities of both temporo-sphenoidallobes. There was a most 
extensive basal fracture. 


No. 67.—Dr. J. Ramsay. Inter-Colonial Medical Journal of Australasia 
(abstract in the Journal of the American Medical Association, January 26th, 
1901, p. 261).—A man of 54, addicted to alcoholic excess, was found unconscious 
in the road, having probably fallen from his horse. In the course of an hour 
or two later the man partially recovered consciousness and became greatly 
excited. Forty hours later he had irregular movements and twitchings in the 
right wrist and hand. Later these affected the left wrist and hand, then the 
lower extremities, and finally the left side of the face. General convulsions 
followed, starting on the left side of the face and extending to left arm, left 
leg, and then the right side. The right side of the face was not involved. In 
the intervals the right arm was rigid and the left flaccid. The urine was 
albuminous. The breathing became Cheyne-Stokes in character. He was 
trephined over the right motor area, and a large flat blood clot found on the 
surface of the brain beneath the dura mater. This was removed and the 
cavity left drained with gauze. Two convulsions occurred subsequently, but 


nomore. Some mental and motor impairment remained though lessening 
in degree. 


No. 68.—Sir Benjamin Brodie. Medico-Chirurgical Transactions, vol. xiv. 
р. 327.—А man, 35 years of age, fell out of a cart and struck his head on the 
pavement on November 8th. He was bled by a practitioner in the neighbour- 
hood and afterwards taken to St. George’s Hospital, where he talked and 
reeled like a drunken man. Не was again bled. On November 9th he had 
headache but was otherwise well. He continued so until November 12th at 
9 a.m., when some of the patients in the same ward heard him talking 


VOL. LIX, 12 


150 Traumatic Subdural Hemorrhage. 


incoherently. The house-surgeon was called and found the man insensible, 


motionless, with stertorous breathing and dilated pupils. He was bled from ` 


the arm without effect, and died half an hour after the commence. 
ment of the symptoms. At the post-mortem examination a thin layer of 
blood was found extravasated between the arachnoid and pia mater over the 
posterior part of the two hemispheres. In the lower part of the anterior lobe 
of the cerebrum the substance of the brain had been ruptured, and between 
the dura mater and the arachnoid was about two and a half ounces of blood. 


No. 69.—Dr. Lucius W. Hotchkiss. Annals of Surgery, 36, p. 82.— 
D. McG., æt. 39, fell backwards down some stairs, a distance of about nine 
feet, striking the back of his head. He was picked up unconscious and 
remained so for eight hours. When he recovered consciousness he appeared 
dazed and had difficulty in speaking. Also said to have bled from the right 
ear. He was able to walk up to hospital and was admitted. There were no 
paralyses, but motor aphasia was present. Temperature 101°; respiration 20; 
pulse 90. The urine contained a trace of albumen. There was a small 
abrasion over the right side of the occiput. On the 9th facial paralysis was 
noted. Temperature 102° at noon. On the 10th some bleeding from the 
right ear set in in the early morning. At 8 a.m. the temperature was 101:6, 
the pulse 68, the motor aphasia was practically complete, the grip of the right 
hand was feeble, and there was right facial paralysis. Ether was given and 
trephining over the left middle meningeal artery performed. There was no 
evidence of fracture. Some dark fluid blood was removed from beneath the 
dura mater with an aspirator after which the dura mater was opened and the 
clot exposed. This was firm and moderately adherent to the cortex of the 
brain, It was washed away with a stream of salt solution. Slight cortical 
laceration present. Temporary drainage employed. Two slight convulsions 
occurred after the operation, but his recovery was rapid and complete. 


No. 70.—Dr. Graeme M. Hammond. Journal of Nervous and Mental 
Diseases, December, 1899 (taken from the Lancet, February 24th, 1900, 
where the case is abstracted).—A clerk, 25 years of age, of temperate habits, 
who had suffered for some weeks from albuminuria and granular casts, was 
struck on the left temple with a loaded whip handle in a street fight. He was 
knocked down, but did not lose consciousness, and was abie to get up and 
walk home, though a few days later he was seized with an attack of general 
convulsions of а severe and prolonged character. On recovery of conscious- 
ness it was found that he had completely lost the power to name objects and 
persons. Ophthalmoscopic examination showed slight choking of the right 
disc. A diagnosis of subdural hemorrhage over the posterior part of the 
left superior temporal convolution was made. At the operation (by Dr. 
Seneca Powell) two weeks after the injury, a linear fracture was found in the 
left temporal bone, and a subdural blood clot covered the entire superior 
temporal gyrus. In the posterior part there was a hole into which a probe 
could be passed one and a half inches. The cerebral tissues were here 
lacerated, probably by indirect violence. Patient made a good, but not 
complete recovery. 


Abstract of Cases. 151 


No. 71.—Dr. George Tully Vaughan. American Journal of Medical 
Sciences, vol. 122.—K. M., st. 18, a white man, was admitted to the 
Emergency Hospital, on August 10th, 1899. He had been struck on the 
head with a club and knocked down. On being assisted to his feet he walked 
a short distance, fell again, and lapsed into coma. Examined an hour after 
his injury, he was found profoundly unconscious, breathing deep, sometimes 
sighing, both pupils dilated and immobile. Pulse 60, full, Clonic contrac- 
tions at short intervals of the right arm and leg and sometimes the left arm, 
with persistent tendency of the face to turn to the left side, were found. 
There was а small contused wound of the scalp not extending to the bone 
just above the left ear. Trephining, without an anesthetic, was performed 
over the left fissure of Rolando. The dura mater was found bulging and 
tense, A large black clot was found beneath it about the size of an orange. 
A freely bleeding. artery on the surface of the brain was ligatured. No 
pulsation in the part of the brain exposed was observed. The only change 
after the operation was contraction of the pupils and diminution in the 
frequency of the convulsions, the patient dying two hours later without 
return of consciousness. The necropsy revealed numerous small hemor» 
rhages throughout both hemispheres. 


No. 72.—Mr. Golding-Bird. Guy’s Hospital Reports, vol. xxx.—Thos. D., 
et. 31, admitted into Cornelius ward May 22nd, 1888, suffering from con- 
cussion. He had fallen from a cart one hour before. He vomited on the 
way to the hospital. At 1 p.m., when he was admitted, he could be made to 
answer questions after a fashion, but relapsed at once into irritable 
stupor. Later he became very violent, and passed into coma soon after 
8p.m. Mr. Golding-Bird was called to him at 10 p.m. and found him 
comatose, with stertorous breathing, limbs and face paralysed, pupils inactive 
and dilated, the left more so than the right. The left side of the face 
appeared slightly more paralysed than the right. Pulse 116; Temperature 
102-89. No wound and no signs of fractured base. Over the right parietal 
bone the scalp was bruised and puffy, with extravasated blood. Pressure over 
the bruised area caused extension movements of the left forearm and wrist, 
and greater pressure led to convulsive movements of the left arm and leg. 
No anesthetic was given, but the skull was trephined on the right side just 
anterior to the right parietal eminence. A short fissure of the skull was 
found. An extradural clot was present. As the dura mater was bulging it 
was tentatively incised. A stream of dark blood immediately rose to a height 
of half an inch. A slight improvement in the breathing followed, but he 
died two to three hours later. At the autopsy the only fracture found 
was the one found at the operation. In the arachnoid cavity, chiefly on 
the left side, were three and a half ounces of blood. The left temporo- 
sphenoidal lobe was much bruised on its anterior and under surface. 


Since writing this paper, my attention has been called by 
Mr. Mills, Librarian to Guy's Hospital, to a paper in the 
American Journal of Medical Sciences for April, 1895, on 
Meningeal Hemorrhage, by Drs. Scudder and Lund. In this 


152 


Traumatic Subdural Hemorrhage. 


paper twenty-one cases of subdural hemorrhage were reported. 
Seven of these twenty-one cases are included in the seventy- 
two cases upon which this paper is based. References to the 
remaining fourteen I give below. An examination of these cases 


in no way affects the conclusions arrived at in the above paper. 


References to cases published in Drs. Scudder and Lund’s 
paper aud not reported above :— 


1. 


OD за Qe go to 


10. 


12. 
13. 
14. 


Case 1.—Schneider. Archiv. für Klin. Chir., 1887. 

Case 2. — Ceci. Deutch. Med. Zeitung, 1887. 

Case 5.—Ball. В.М.Ј., 1888. 

Case 6.— Walker. Medical Age, 1888. 

Case 8.—Matas. New Orleans Med. and Surg. Journ., 1889. 

Case 10.—Mills. Journ. Nerv. and Mental Disease, 1890. 

Case 11.—Chiéne. Transactions American Surg. Assoc., 1891. 

Case 12.—Duret. Cong. Trans. de Chir., Paris, 1891. 

Case 14.—Elliot. Massachusetts General Hospital Records, Vol 
281, p. 41. 

Case 15.—Beach. Ibid., Vol. 274, p. 43. 

Case 16. —4A. Т. Cabot. Ibid., Vol. 257, p. 214. 

Case 17.—C. B. Porter. Ibid., Vol. 259, p. 136. 

Case 20.—Mynter. Annals of Surgery, 1894, p. 19, 539. 

Case 21.— Walker. Cincinnati Lancet-Clinic, June 17, 1893. 


CASES OF SUBDURAL HAEMORRHAGE 


Thought to be due to injury, but in which the lesion was found 


1. 


at a post-mortem examination long after :— 

Transactions of the Pathological Society (vol. ii., pt. 2, p. 172) 
* Fracture of the base of the skull, after which the patient lived 
two months.” — Mr. Gray. 

Ibid. (vol. vi., p. 5) :—'* A false membrane lining the smooth surface 
of the dura mater, covering the right cerebral hemisphere, probably 
the result of extravasation of blood from an injury.” —Dr. Ogle. 

Ibid. (vol. vi., p. 8) :—'* Large cyst from the cavity of the aracbnoid." 


—Dr. Quain. 

Ibid. (vol. xxxvi., p. 16) :—'' Hematoma of the dura mater."—Dr. F. 
Charlwood Turner. 

Ibid. (vol. xlviii., p. 10):—'* Hematoma of the dura mater with 


deveiopment of membrane." —Cyril Ogle, М.В. 


Transactions of the Medico-Chirurgical Society (vol. xxviii.) Prescott 
Hewitt’s paper on ‘‘ Extravasations of blood into the cavity of the 
arachnoid.” 


Case mentioned on p. 598 of Bowlby’s Pathology. 








Traumatic Subdural Hemorrhage. 153 


REFERENCES TO PATHOLOGICAL SPECIMENS OF 
SUBDURAL HAEMORRHAGE. 





Through the courtesy of the Curators of the Museums of St. 
Bartholomew’s, London, and St. Thomas’s Hospitals, I was 
enabled to examine the museums of these hospitals with a view 
to finding specimens of subdural hemorrhage the result of injury. 
My search was not very successful, for in five of the largest 
museums, including the three above, our own, and that of the 
Royal College of Surgeons of England, I only found one good 
example of this condition. This was specimen No. 2448 in the 
museum of St. Bartholomew’s Hospital, which is described as 
“ А large clot of blood adhering to the internal surface of the dura 
mater which covered the upper part of one of the hemispheres 
of the cerebrum. The effusion was in consequence of injury.” 
The only other specimen of the condition which I found is No. 
2446a in the same museum, which is described as “ Portions of 
left parietal and temporal bones showing a fracture running 
across the line of the middle meningeal artery. The artery is 
torn across and some blood-clot lies in the groove in the bone. 
From a man, xt. 64, who fell off his cab and was admitted into 
the hospital drowsy and helpless. From this condition he 
rallied and after ten days was able to sit up in a chair; on the 
thirteenth day from the injury he suddenly became comatose 
and died. A post-mortem examination showed a hemorrhage 
into the arachnoid cavity, some of the blood being recent whilst 
the smaller portion evidently dated back to the time of the 
accident. The vessels were atheromatous.” 

In the same museum there is a specimen of subdural hemor- 
rhage in а case of cirrhosis of the liver (No. 2447 b) and one of 
subarachnoid hemorrhage in a case of malignant endocarditis 
(No. 2470 a). 


154 Traumatic Subdural Hemorrhage. 


Specimen No. 1978 in the museum of St. Thomas’s Hospital 
is a “large subdural clot due to rupture of a small aneurysm of 
the middle cerebral artery," from a patient st. 51, who lived for 
a week with hemiplegia, hemianzsthesia, and aphasia, after being 
taken suddenly ill with sickness (Reported by Dr. Sharkey, 
Pathological Society’s Transactions, vol. 27, p. 3). 

In the Guy's museum specimens, Nos. 1591”, 1591®, 1592", 
1605" and 16059, are cases of old hemorrhagic membrane or 
cyst in most cases of unknown origin. 








THE BEHAVIOUR OF 

LEUCOCYTES UNDER THE INFLUENCE 

OF CERTAIN BACTERIAL AND OTHER 
SUBSTANCES. 


By THOMAS EDWARD HOLMES, M.D. 
(Thesis for the M.D. Cambridge.) 


THE following experiments were undertaken at the instigation 
of Dr. Ainley Walker, with the object of determining, if possible, 
the reaction of the leucocytes of rabbits’ blood to various 
bacterial (dead and living cultures) and other toxic products, 
and also to ascertain whether the different forms of leucocyte 
reacted eonstantly with the same kind of injection. 

It is only within recent years that the study of leucocytosis, 
both from a clinical and experimental aspect, has attracted much 
attention. 

As early as 1864, it was shown by Traube and Geschleiden 
that the animal body quickly disposes of bacteria introduced into 
it by artificial means, but it was not until Ehrlich’s valuable 
discovery of the differentiation of leucocytes by the aniline dyes, 
that the histology of the blood was placed on a firm basis. 
Numerous theories have been advanced to explain the germicidal 
power of blood, but, in the light of modern work, no explanation 
which is not open to serious objection was suggested until 
Metchnikoff brought forward his cellular or phagocytic theory. 


156 The Behaviour of Leucocytes under the Influence of 


This eminent observer was, however, compelled to admit in 1889 
that at least part of the bactericidal action in vitro was attribut- 
able to substances present in the serum, which he claimed were 
yielded to it by the leucocytes in the process of coagulation. 
On this question, a large amount of work has been done, com- 
mencing with the observations of Hankin and Kanthack in 1892, 
and subsequently carried on by Loewy and Richter, von Fodor, 
Denys, and Lecelf, Havet, Buchner, Bordet, and many others. 
These observers have shown by their results that :— 

1. The fresh blood of an immune animal possesses a bacterio- 
lytic action which is greatest when the animal concerned presénts 
& condition of marked leucocytosis, and is diminished when the 
leucocyte count falls below the normal. 

2. Sterile pleural exudates rich in white corpuscles possess high 
bacteriolytic power, but if these corpuscles be rapidly separated 
from the fluid by filtration, the bacteriolytic action disappears, 
and is at once restored on their replacement. If, on the other 
hand, the leucocytes are merely broken up and disintegrated by 
alternate freezing and thawing, the germicidal power remains. 

To explain these phenomena, Bouchard advanced the cellulo- 
humoral theory, which involves the simultaneous action of two 
forces—the bactericidal power of the serum, and the phagocytic 
activity of the corpuscular elements. This cellulo-humoral 
theory in its modern form, forms to-day the only really tenable 
position on the general question. I have somewhat digressed 
from the main subject of experimental leucocytosis, but the 
above brief account of the latest opinions on immunity does not 
seem out of place in & paper on at least one important factor, 
the róle of the leucocytes, in the destruction of bacteria and 
other toxic substances. All observers are agreed that bacterial 
and toxic inoculation in animals produces a marked effect on the 
circulating leucocytes. Immediately following such inoculation, 
we have the stage of diminution of total leucocytes to a greater 
or lesser degree, the stage of leucopenia, or hypoleucocytosis; 
this is only temporary, and is followed by a great increase in the 
total number of circulating leucocytes, the stage of hyper 
leucocytosis, or simply leucocytosis. Among the various 








certain Bacterial and other Substances. 157 


substances that have produced these phenomena on injection 
may be mentioned :— | 


Hemoglobin. . Septic fluid. 

Pus. Lymph cells. 
Hemialbumose. Peptone. 

Pepsin. Nucleic acid. 

Nuclein. Leech extract. 
Tuberculin. Pyocyanin. 

Curare. ` Uric acid. 

Urates. Carmine in suspension. 
Dead bacterial products. Living bacterial products. 
Dead bacterial proteins. Filtered yeast cultures. 
Tincture of Myrrh. Extract of Gentian. 
Sodium cinnamate. Animal cells, etc., ete. 


The stage of leucopenia has been practically neglected in the 
present paper, as all blood-counts have been made at least fifteen 
to twenty hours after inoculations; but it will be seen from the 
charts that even as late as this, there was frequently a smaller 
number of circulating leucocytes present than in the blood-count 
previous to injection. 

According to most authorities leucopenia is well established 
within a very short time of inoculation. In some of Lowit’s 
experiments, the number of leucocytes fell in five seconds 
from the time of injection to 1-20 of the number circulating 
before inoculation. In some instances, on the other hand, no 
diminution of leucocytes has been observed, the total number 
gradually increasing from the time of injection. 

Schlesinger, in a lengthy monograph on the subject, observed 
a leucopenia usually two hours, but never later than four or five 
hours after inoculation. He, however, admits that great variations 
occur, and that no definite rule can be made. Most observers 
agree that the polynuclear leucocytes disappear in the stage of 
leucopenia, while the mononuclear forms are scarcely affected, 
but Schlesinger says the lymphocytes are preponderately involved, 
and Muir maintains that all varieties are affected. Sherrington, 
in some experiments on inflammatory leucocytosis, noted that 
the coarsely granular cells disappeared almost entirely in 


158 The Behaviour of Leucocytes under the Influence of 


hypoleucocytosis, and that in the subsequent hyperleucocytosis 
the finely granular leucocytes were strongly in evidence. 
Milroy and Malcolm observed the same phenomena both in the 
blood and marrow after injections of nucleic acid. Durham 
concludes that the coarsely granular eosinophil cell takes a 
minimal share in the process of bacterial destruction. Lowit 
thought the polynuclear leucocytes were destroyed (dissolved up) 
during hypoleucocytosis. Rieder, on the contrary, maintained 
that they were temporarily collected in some region of the 
circulation, which they left after a time to become again dis- 
tributed through the circulation, when a substance inducing 
positive chemiotaxis reappeared in the blood. Werigo sug- 
gested that the leucocytes crowded into the lungs, liver, and 
spleen after the intravenous inoculation of particulate material. 
Goldscheider and Jacob have proved this for the lungs, and 
Everard, Demoor, and Massart pointed out that the medulla of 
bone must also be included. Werigo says the injected material 
is enveloped by the white corpuscles, the latter being arrested 
in the liver, where they transfer the particles to the endothelial 
cells of that organ; the phagocytic cells of the splenic pulp have 
similar functions. Roger and Josué have noted a proliferation 
of “celles medullaires’’ after injections of phosphorus, etc. 
Haushalter and Spillman have also observed important changes 
in the marrow after toxines of bacillus coli communis and 
staphylococcus. Muir, in a recent article, has shown that in 
rabbits, the bone-marrow is the site of multiplication of both 
the finely and coarsely granular polynuclear forms. 

According to Schlesinger, hyperleucocytosis is often the only 
symptom of the infection. In exceptional cases the polynuclear 
leucocytes are increased. In Bullock’s experiments on rabbits 
with sodium cinnamate, an almost pure polynuclear leucocytosis 
was obtained, and Batty Shaw observed the same phenomens 
with similar injections in cats. The increase takes place usually 
on the second or third day after injection (6,000 to 15,000 above 
the normal) and reaches its maximum on the third or fourth 
day. The subsequent fall to normal is gradual; in one of 
Schlesinger’s experiments it was not reached until the fourteenth 
day. 





certain Bacterial and other Substances. 159 


Hyperleucocytosis is not influenced by fever or changes in the 
local infection. This was also pointed out by Sherrington and 
Nicolas and Courmont. 

Besredka, from a large number of experiments with diphtheria 
toxin, concludes that :— 

1. In intoxication by large doses, the polynuclear leucocytes 
describe a curve having a parabolic form, and rise to a 
maximum ten to sixteen hours after inoculation. They decrease 
regularly and rapidly until death. 

2. In intoxications which slowly kill in several days, the 
course of the leucocytes is represented by a curve with oscillations 
“ assez étendues,” having for essential characters— 

a. De se maintenir toujours au dessus du taux normal. 
b. De ne s'interrompre à aucun moment de l'intoxication. 

3. The animal intoxicated with large doses of toxin, and saved 
by serum, remains ill “ polynuclearly’’ during twelve to fifteen 
days, during which the same oscillations as in the slow infection 
occur, but with this difference, that this time, the leucocytes end 
“рат prendre le dessus ce qui si traduit par un retablissement 
progressif et graduel du chiffre normal." 

I have given these conclusions in detail, as they bear very 
closely on a number of similar experiments in this paper. The 
polynuclear hyperleucocytosis has been noted by numerous 
observers in a variety of experimental inoculations, but I have 
been unable to find any precise numerical observations on the 
mononuclear leucocytes, with the exception of those of Bullock 
and Muir. 

Achard and Loeper observed a constant polynuclear leucocy- 
tosis after bacterial injections until the third or fourth day, when 
the polynuclear leucocytes diminished, and ‘the mononuclear 
leucocytes increased in number.” Muir often noticed an 
increase of hyaline leucocytes at a later stage, and suggests that 
the late mononuclear reaction may be due in part to chemiotactic 
substances derived from broken down finely granular leucocytes. 
Besredka says that in the course of immunization against 
diphtheria toxin, each injection of the latter is followed by a 
hyperleucocytosis entirely dependent on polynuclear leucocytes, 


160 The Behaviour of Leucocytes under the Influence of 


but as immunization proceeds the polynuclear forms are less 
prompt to act and are replaced by mononuclear leucocytes. 
Schlesinger states that the lymphocytes may sometimes increase 
very considerably in the later stages of hyperleucocytosis. 

When a fatal issue ensues after inoculation, the leucocytes 
behave somewhat differently. If death occurs after several 
days the hyperleucocytosis is not appreciably different from the 
condition previously sketched, and which occurs in cases ending 
in recovery (Schlesinger). In this observer's experiments, at 
the time of death, the total number of leucocytes had again 
fallen to normal for one or two days, but on a few occasions the 
hyperleucocytosis was still at its maximum. I shall refer to this 
again at a later stage. Schlesinger suggests that the increase of 
leucocytes at death may be either active and chemiotactic, in 
which case the polynuclear leucocytes are increased, or passive 
and purely physical, with an increase of mononuclear leucocytes. 
Gabritchewsky concludes that inoculations of entire cultures 
of bacillus diphtherie producing death, are followed by & 
hyperleucocytosis, which increases progressively till death; on 
the contrary, with an immunized animal, the hyperleucocytosis 
reaches its maximum eight hours after injection and disappears 
completely at the end of twenty-four hours. Sherrington, experi- 
menting with cats, noticed that death was preceded by a stage 
of leucopenia. In some of Schlesinger’s fatal cases, there was 
a gradual diminution of total numbers from the time of inocu- 
lation until only 2,000 per c.cm. or even fewer leucocytes 
were present just before death. In these instances, the same 
observer points out that the polynuclear reaction is small and 
transient. 

Everard, Demoor, and Massart also observed the same 
phenomena in subcutaneous injections of hog cholera, producing 
death in twenty-two and a half hours, and in intravenous injec- 
tions of bacillus anthracis causing death in twenty hours. 

Various theories have been adduced to explain these phenomena. 
Romer suggested that the increase of leucocytes was due to a 
rapid multiplication in the veins, as well as in the blood-forming 
organs, but Kanthack showed that venous blood did not contain 


certain Bacterial and other Substances. 161 


any more leucocytes than arterial blood. Lowit also pointed 
out well-founded objections to Romer’s views, and thought that 
the leucocytosis was due to an increased supply of young 
leucocytes to the blood, which at a later stage developed into 
polynuclear leucocytes. He supposed that this excessive 
production was due to chemical stimulation of leucocyte-forming 
organs by substances shed into the blood-plasma at the time of 
disintegration of the hzemic leucocytes. 

Bruce, Goldscheider and Jacob, Muir, and others, however, 
have clearly shown that the leucopenia occurring after injections 
of such suostances as nucleic acid, peptone, bacterial products, 
extracts of various organs, etc., is due to the accumulation of 
leucocytes in the capillaries of certain organs, especially the 
lungs, liver and spleen. The leucopenia is also due, to some 
extent, to emigration of leucocytes to the site of inoculation, as 
pointed out by Muir. The latter observer, with Ehrlich, 
Goldscheider and Jacob, considers that cheniiotaxis is the all- 
important agent in the production of leucocytosis. The causation 
of the latter within so short a time of inoculation, has been 
much debated in recent years. | 

Erhlich, working with Lazarus, states definitely that leucocy- 
tosis is a function of the bone marrow, and Goldscheider and 
Jacob assert that the rapid occurrence of leucocytosis is due 
to the passage of leucocytes from the bone-marrow to the 
circulating blood. 

Muir is unable to speak definitely as to the mechanism by 
which the increased proliferation is brought about. He says, 
“The passage of leucocytes from the bone-marrow to the blood 
may in itself be sufficient to produce increased multiplication of 
the mother cells. The newly-formed cells will be constantly 
passing into the blood, and on the principle of over-regeneration 
after repeated loss, as expounded by Weigert, a hyperplasia of 
myelocytes may result ; on the other hand, it is possible that the 
substances which act chemiotactically may also directly stimulate 
cellular proliferation.” 

Ehrlich, Engel and Ribbert assert that the granular and large 
mononuclear leucocytes are formed in the bone-marrow, while 


162 The Behaviour of Leucocytes under the Influence of 


the lymphocytes have their origin in the lymphatic glands; 
these observers also say that the large mononuclear forms may 
be formed in the cœlomic cavities. Myers says that the large 
lymphocytes are capable of being transformed into transitional 
cells, and admits that some polynuclear leucocytes are manu- 
factured in the blood-stream from, large mononuclear forms. 
Muir, on the contrary, contends that there is no evidence of the 
transformation from the non-granular to the granular type in the 
circulating blood, and has clearly shown that the bone-marrow 
is the site of multiplication of the granular leucocyte. Gulland, 
Arnold, Uskoff and Frankel maintain that all leucocytes are 
derived from small lymphocytes, and Everard, Demoor, and 
Massart conclude that the different forms of leucocytes are 
evolutionary stages of the saine cell :— 

1. Single nucleated cell with little protoplasm. 

2. Vesicular nucleus with more protoplasm. 

3. Adult polynuclear leucocyte with phagocytic fuuctions 

and protoplasm loaded with granules. 

According to Councilman, Mallory and Pearce, the large 
mononuclear leucocytes are derived from the endothelium of 
lymph and blood vessels and coelomic cavities, and this conclusion 
is the one most generally accepted at the present time. 


METHODS. 





For the purposes of these experiments the diet of the animals 
concerned was very carefully regulated. All edible material was 
removed from the cages at 6 p.m. every evening and the blood 
taken from the ear early each morning before the first meal of 
the day was given. The diet consisted entirely of green food and 
dry biscuits, to which the animals had become accustomed for 
some time before inoculation. Under this treatment they 
remained in good condition and increased in weight when not 
the subjects of bacterial infection. Three months were spent in 
acquiring familiarity with the leucocytes of rabbits’ blood under 
both normal and experimental conditions. During this period, 


certain Bacterial and other Substances. 163 


my results were daily checked by Dr. Ainley Walker until 
sufficient accuracy had been gained. These observations, which 
were regarded as preliminary, have only been recorded in relation 
to the total number of leucocytes. The subsequent observations 
were also checked from time to time by Dr. Ainley Walker, and 
in all cases the two results were found to agree very closely. 
The rabbits selected for inoculation were in every instance well 
grown and healthy, and special precautions were taken to ensure 
a normal condition by counting the blood for several days (in 
some cases a week) before inoculation. If a leucocytosis was 
found to be present the animal was discarded. 

The Thoma-Zeiss apparatus was used for the estimation of the 
leucocytes, and the leucocytes in the whole number of squares 
on the counting chamber were counted. Never less than four 
such counts were made of each diluted drop of blood, and 
frequently where small variations were found to exist, as many 
as eight or ten separate drops of the diluted blood were counted. 
The blood was obtained by pricking the lateral vein of the rabbit’s 
ear with a flat V-shaped needle with both edges sharpened. 
This form of needle makes a very small wound, and one which 
rapidly heals. The larger sized pipette was used for diluting the 
blood, and in the earlier experiments, Toisson’s fluid, prepared 
according to the following formula, was the diluent :— 


Distilled water ios i iu .. 160 с.е. 
Neutral glycerine (30? Вапше)  ... ... 90 c.c. 
Pure Sodium Sulphate... or .. gm. 8. 

j » Chloride ... ы Ge gmd 
Methyl Violet 6 B ... se — .. gm. 025. 


Dissolve the methyl violet in the glycerine with half the 
water added. Dissolve the salts in the other half of the water. 
Mix and filter. Filter before use. 

This stain was employed for estimating the number of the red 
and white corpuscles, but subsequently for the enumeration of 
the leucocytes, a two per cent. solution of acetic acid, with just 
sufficient gentian violet to stain the nuclei, was found to give 
better results. In the case of the red blood corpuscles, the 
number in sixteen squares was counted, and an average taken 


164 The Behaviour <f Leucocytes under the Influence of 


per square. The blood was always counted by the wet method 
as soon as possible after it had been obtained. Throughout the 
experiments, blood-counts were made daily, an interval of 
twenty-four hours separating each count. A dilution of 1 in 100 
was used for all enumerations of the leucocytes. 


The film preparations were stained with Jenner's fluid, but I 
found that three to five minutes was not long enough to stain 
the majority of the films; frequently the latter were left in 
the stain for half an hour or even longer. I tried several 
brands of HEhrlich's triacid stain, but was unable to obtain 
sufficiently good results. 


CLASSIFICATION OF LEUCOCYTES. 


I have made no attempt in these experiments to give a detailed 
account of every form of leucocyte met with, since the wet 
method of enumeration has been used almost exclusively. 

Two main varieties have been distinguished :— 

1. Polynuclear leucocyte with the nucleus in several masses 
united by relatively slender bridges of nuclear material, 
and a granular protoplasm. 

2. Mononuclear leucocyte with a single symmetrical nucleus 
and non-granular protoplasm. 


This variety includes large and small lymphocytes with a 
relatively large and rounded nucleus, and very little protoplasm, 
and large mononuclear leucocytes with a rounded or horse-shoe 
shaped nucleus, and more protoplasn than the former. 


About one hundred films were counted differentially with 1-12 
oil immersion Leitz objective, with the object of determining, if 
possible, some indications of the function of the different varieties 
of the mononuclear leucocyte. The results obtained by counting 
one hundred mononuclear forms in each film are given in the 
tables later, but from the few observations I have made, it does 
not seem advisable to draw any definite conclusions. 

In this differentiation by the film method, I have distinguished 
three forms :— 





certain Bacterial and other Substances. 165 


1. Small lymphocyte.—This is generally about the size of a 
red corpuscle, with a large rounded nucleus occupying 
the greater part of the cell. In some of the experiments 
where a mononuclear leucocytosis was present a great 
number of very small lymphocytes were seen. The 
nucleus stains somewhat indistinctly with Jenner’s 
fluid, while the protoplasm takes the stain deeply. 


2. Large lymphocyte.—This cell has the same essential 
characteristics as 1, with the exception that it is larger, 
always having a bigger diameter that the red corpuscle. 

З. Large mononuclear leucocyte.—This is the mononuclear 
phagocyte of Metchnikoff. It has a fairly abundant 
non-granular protoplasm, and a nucleus which may be 
rounded, horse-shoe shaped, oval, etc. 


DESCRIPTION OF NORMAL Levucocytes oF RABBITS’ Вгоор. 
Brinkerhoff and Tyzzer, in a recent paper on the leucocytes of 

normal rabbits’ blood, give the following classification :— 
Polynuclear leucocytes :— 


1. With affinity for basic stain—mast cells. 
2. Р » acid , —amphophiles. 
3. " » eosin , —eosinophiles. 


Mononuclear leucocytes :— 


1. With strong affinity for basic stain—lymphocytes. 


2. , weak А 5 —large mononuclear 
leucocytes. 

These varieties occur in the following percentages :— 
Amphophiles ... pis 40 to 50 per cent. 
Eosinophiles o , 1 i 
Mast cells г. ba 4 , 8 Й 
Lymphocytes ... з 45 , 90 я 
Large mononuclears ... 2 , 8 


Muir says the lymphocytes number 30 to 40 per cent., but may 
be as numerous as the amphophiles, 


VOL. LIX. 13 


166 The Behaviour of Leucocytes under the Influence of 


Brinkerhoff and Tyzzer maintain that the following factors 
must be considered in drawing inferences from variations in the 
leucocyte count :— 

1. Loss of body heat. 
2. Shock. 

3. Fasting and feeding. 
4. Pregnancy. 


All these factors have been duly considered in the present 
paper. In a large number of normal rabbits in Brinkerhoff's 
and Tyzzer’s paper, the leucocyte counts varied between 4,600 
and 13,400. 


Bullock says the normal number varies between 6,000 and 
9,000, but I agree with the former observers that a wider limit 
than this exists in the healthy rabbit. 


INJECTIONS. 





The following is a list of the various injections used in my 

experiments :— | 

1. Diphtheritic toxin.—This was a specimen of diphtheritic 
toxin which was kindly supplied to Dr. Walker by Dr. 
Vernon Shaw, of the Brockwell Park Laboratories. It . 
was derived from cultures of the bacillus diphtherize 
Americans of Parkes. 


2. Vibrio Metchnikovit.—This was an old laboratory culture 
of this micro-organism. 


З. Bacillus typhoide abdominale. — A stock laboratory 
culture of low virulence, and in constant use in the 
bacteriological department for carrying out the Gruber- 
Durham reaction. In the earlier injections of 2 and 
9 of agar cultures, the growth was washed off the 
surface of the agar with ordinary culture bouillon; in 
the later injections normal salt solution was employed 
for the same purpose. 


certain Bacterial and other Substances. 167 


4. Extract of tubercle bacilli.—This was an ethereal extract 
of dried tubercle bacilli which was brought into 
suspension, after the ether had been driven off, in a 
solution of sodium hydrate having an alkalinity of 
`2 per cent., ?.6., the alkalinity of normal blood. The 
extract was further sterilized by the discontinuous 
method on five successive days before inoculation. 

The tubercle bacilli, which were kindly supplied by 
Professor McFadyean, of the Royal Veterinary College, 
were treated according to the method described by 
, Aronson, who extracted a fatty acid and wax from large 
quantities of bacilli by treatment with alcohol and ether. 

5. Extracted tubercle bacill1—These had been twice 
extracted with boiling ether, and subsequently with a 
mixture of ether and absolute alcohol. They were 
obtained from the same source as 4. 

6. Animal cells.—Red corpuscles were prepared for inocu- 
lation from defibrinated sheep’s blood, which had been 
collected with aseptic precautions, and subsequently 
tested for sterility by centrifugalization and repeated 
washing of the corpuscles with normal (0°85 per cent.) 
salt solution. Renal, ovarian and testicular cells were 
prepared by macerating the organs, which had been 
previously cut into small pieces, in a saturated solution 
of urea according to the method described by Ramsden. 
The material was then rubbed up in a mortar and freed 
aS far as possible from urea by repeated washing and 
centrifugalization. It was then suspended in a few с.с. 
of normal salt solution, strained through a piece of 
sterile muslin to remove connective tissue, etc., and 
injected into the peritoneal cavity of an animal. 

7. Broth.—-Ordinary sterile culture bouillon. 

8. Bacillus .diphtherie Americane.— These were agar 
cultures suspended in normal salt solution. 

9. Staphylococcus pyogenes aureus.—An old laboratory 
culture of staphylococcus aureus. Agar cultures were 
washed off the surface of the agar with normal salt 
solution and so injected. 


168 The Behaviour of Leucocytes under the Influence of 


10. Dead tubercle bacilli from the same cultures as those 
previously mentioned. 

ll. Micrococcus rhewmaticus.—This was an organism which 
was isolated by Dr. Ainley Walker from a case of 
rheumatic fever. It had given rise to acute rheumatism 
in several rabbits. The injections used were from agar 
or blood-agar cultures. 

12. Pneumococcus.—This was a highly virulent organism 
kindly supplied by Dr. Eyre. For the purpose of the 
present investigation it was attenuated by growth in 
ordinary bouillon and frequent re-inoculation in sub- 
culture during several weeks. 

18. Sheep's serum.—Sterile serum obtained from sheep's 
blood which had been collected with as strict aseptic 
precautions as possible, from the slaughterhouse, in 
sterilized flasks, immediately whipped and conveyed to 
the laboratory. 

14. “ Peptone.” — Commercial peptone containing арргохі- 
mately 95 per cent. of albumoses. 


ABSTRACT OF EXPERIMENTS. 


REACTIONS TO VIBRIO METCHNIKOVII. 

Rabbit A. Chart 1.—Two agar cultures seventy-two hours 
old of living vibrio Metchnikovii injected subcutaneously affected 
both varieties of leucocyte, but more especially the polynuclear 
forms. Both kinds reached a maximum (polynuclears, 11,000; 
mononuclears, 7,000) on the third day, and then gradually 
decreased in numbers. There was a slight diminution of both 
varieties in the early stages. 

Three agar cultures twenty-four hours old of living vibrio 
Metchnikovii were again injected fifteen days after the first 
inoculation. There was a marked fall in both forms for two 
days, when they began to increase in number. The number of 
polynuclear leucocytes was highest on the seventh day (10,000 
per c.mm.) and that of the mononuclear leucocytes on the 
eleventh day (10,000 per c.mm.). 








certain Bacterial and other Substances. 169 


Rabbit B. Chart 3.—The injection of one agar culture 
twenty-four hours old of living vibrio Metchnikovii subcutane- 
ously, gave a hyperleucocytosis entirely confined to the poly- 
nuclear leucocytes. An increase of these was noted on the third 
day of 7,000 per c.mm. The mononuclear leucocytes were 
diminished throughout the reaction. 

Rabbit H. Chart 11.—One agar culture twenty-four hours 
old of living vibrio Metchnikovii injected subcutaneously, pro- 
duced a marked increase in the polynuclear leucocytes, the latter 
reaching a maximum of 11,250 per c.mm. on the third day after 
inoculation, and quickly falling again to normal. The mononuclear 
forms did not increase until the fourth day, when they were as 
high as the polynuclear leucocytes. Their fall to the normal 
was more gradual. Cp. Everard, Demoor and Massart. 

A guinea-pig of 850 grammes was injected subcutaneously with 
3:5 с.с. of four days old vibrio Metchnikovii which had been 
heated to 100°. There was a polynuclear leucopenia within an 
hour, and a hyperleucocytosis two hours after inoculation. 
Nineteen hours afterwards the polynuclear leucocytes were 
predominant, and a very large increase of the same kind was 
noted at the twenty-fifth hour, the mononuclear leucocytes 
being at this time very rare. Forty-nine hours after inoculation, 
the polynuclear leucocytes were largely predominant, but the 
mononuclear forms had increased. 5 c.c. of the same culture 
were also injected subcutaneously into & guinea-pig of 1,020 
grammes. No diminution of leucocytes was observed, and the 
hyperleucocytosis was almost entirely polynuclear. 

It will thus be seen that these injections of living cultures of 
vibrio Metchnikovii produce an increase in both forms of 
leucocyte, but more especially the polynuclear forms. 


REACTIONS To ANIMAL CELLS. 


Sheep's red corpuscles.—Rabbit D. Chart 5.—10 c.c. injected 
intraperitoneally produced & diminution of both varieties for the 
first few days. The mononuclear leucocytes rose again on the 
fifth day after inoculation to 7,000 per c.mm., having been about 


170 The Behaviour of Leucocytes under the Influence of 


4,000 for the four previous days. The polynuclear leucocytes 
were only slightly increased; the greatest number recorded 
during the experiment was 4,900 per c.mm. . 

A similar but larger injection (25 c.c.) was given subcutaneously 
in rabbit D, Chart 6, after an interval of nineteen days. In this 
experiment there was an almost pure mononuclear leucocytosis, 
as the polynuclear leucocytes were only increased by about 2,000 
per c.mm. The mononuclear reaction did not occur until the fifth 
and following days; they reached & maximum of 11,000 per 
c.mm. on the sixth day and gradually fell on succeeding days. 

Ovarian cells.—Rabbit F. Chart 9.—The cells of two ovaries 
of a rabbit were injected intraperitoneally, but unfortunately in 
the middle of the reaction the animal aborted and no further 
counts were made. There was, however, a marked increase in 
the mononuclear leucocytes on the third day, the number having 
risen from 4,000 to 8,250 per c.mm. The polynuclear leucocytes 
up to this time were gradually diminishing in numbers. 

Renal cells.—Rabbit G. Chart 10.—Two reactions closely 
following one another will be seen on this chart. In the first 
experiment the dissociated cells of two kidneys of a rabbit were 
injected intraperitoneally, and in the second experiment the cells 
of two kidneys of a guinea-pig were similarly injected. In both 
instances the reaction was again entirely mononuclear, and did 
not take place until the fourth day after inoculation. The poly- 
nuclear leucocytes were not appreciably affected throughout the 
whole period. 

Testicular cells. — Rabbit H. Chart 11.—Intraperitoneal 
injection of the cells of two testicles of a rabbit again gave a 
large mononuclear leucocytosis, and the maximum increase was 
reached on the sixth day. The number of polynuclear leucocytes 
was diminished during the first few days, but on the fourth day 
after injection the total number was slightly above that recorded 
previous to injection. 

It wil be seen, therefore, that in all these experiments with 
cellular inoculations there was a notable increase of mononuclear 
leucocytes four, five or even six days after injection, and no 
appreciable change in the polynuelear leucocytes throughout the 





certain Bacterial and other Substances. 171 


reactions. An exception may perhaps be taken to the first 
experiment with Rabbit D., but although in the increase of mono- 
nuclear forms on the fifth day there was no rise above the 
number recorded before inoculation, the number of mononuclear 
leucocytes had been low for four previous days. | 

These results agree closely with the observations made by 
Bullock on the effect of injections of ox blood corpuscles. In 
his first experiment he injected 13 с.с. intraperitoneally and 
observed a mononuclear leucocytosis from 3,250 to 9,500 per c.mm. 
on the fifth and sixth days, and a similar increase of mononuclear 
leucocytes on the sixth day, with an intraperitoneal injection of 
18 c.c. of the same material. There was also an increase of 
polynuclear leucocytes on the seventh day, but the number of 
these was high before inoculation. 

Bullock found that there was an enormous rise in the immune 
body at the height of the increase of mononuclear leucocytes, 
and that the latter followed the fluctuations of the former with 
regularity. 

The results recorded above appear to justify the conclusion 
that the removal of foreign animal cells is exclusively carried out 
by mononuclear leucocytes. 

Dead tubercle bacillus.—Rabbit E. Chart 8.—The intraperi- 
toneal injection of 10 c.c. emulsion in distilled water of dead 
tubercle bacillus gave a large oscillating polynuclear reaction. 
The great increase of polynuclear leucocytes was noted on the 
fifth day after injection, viz.—14,400 per c.mm., but on the next 
day the number had fallen to 6,500. The number of mono- 
nuclear leucocytes was highest on the third day (10,000 per c.mm.) 
but it remained somewhat high until the eighth day, the number 
of polynuclear leucocytes having already fallen to normal for 
two days. 

Extracted tubercle bacillus.—Rabbit G. Chart 10.—Intraperi- 
toneal injection of 10 c.c. of extracted tubercle bacilli produced a 
slight increase in both kinds of leucocytes, which was greatest 
on the fifth day. The whole reaction was, however, small, and 
was probably influenced to a considerable extent by abortion on 
the second day after inoculation. 


172 The Behaviour of Leucocytes under the Influence of 


Rabbit G. Chart 2.—5 c.c. of extracted tubercle bacilli were 
injected subcutaneously. There was a late leucocytosis affecting 
both varieties. The increase commenced on the third day after 
inoculation, and reached its maximum on the fifth day. A slight 
diminution of total numbers was observed in the early stages. 
An interval of a week separated the two reactions. 

Tubercle bacillus extract.—Rabbit A. Chart 2.—10 с.с. of 
tubercle bacillus extract injected intraperitoneally produced an 
increase in both varieties. The mononuclear leucocytosis was 
slightly larger, and was maintained for three days, while the . 
polynuclear reaction was noted for two days. The increase, 
however, of each kind was only slight. On the sixth day after 
inoculation, this rabbit was again injected intraperitoneally with 
15 с.с. of tubercle bacillus extract. Neither kind was much 
affected for two days, but on the third day, there was an increase 
per c.mm. of 3,500 mononuclear leucocytes, and 2,500 polynuclear 
leucocytes. The number had fallen to.normal on the next day. 

Rabbit G. Chart 10.—Injected with 10 c.c. tubercle bacillus 
extract intraperitoneally. This injection gave a pure mononuclear 
reaction, the mononuclear leucocytes gradually increasing until 
the fifth day, when the number per c.mm. was 8,000. 

Rabbit F. Chart 16.—10 c.c. of tubercle bacillus extract were 
injected subcutaneously. Here again the main effect was on the 
mononuclear leucocytes, their number increasing from 6,750 to 
11,250 per c.mm. on the first day after inoculation. This increase 
was maintained for three days. The number of polynuclear 
leucocytes rose slightly (2,500) on the first day after injection 
but otherwise were scarcely affected. 

The injected material in rabbit A was a first extract of tubercle 
bacilli and may have contained some adherent chemiotactic 
substances besides the tubercle fatty acid. As a mixed reaction, 
though mainly affecting the mononuclear leucocytes, was obtained 
with this injection, the extract was further purified, and in rabbits 
G and F as above a pure mononuclear leucocytosis was obtained, 
this extract apparently consisting of pure fatty acid. It may be 
inferred from these results that the injection of pure tubercle 
bacilli fatty acid causes a pure mononuclear leucocytosis. The 





certain Bacterial and other Substances. 173 


inoculation of extracted tubercle bacilli gave a reaction of both 
varieties, but the injected material was not free from wax, having 
still some acid-fast reaction remaining. 


The injection of unaltered tubercle bacilli produced a reaction 
of both varieties. 


The bearing of these observations will be considered later. 


Sheep’s serum —Rabbit C. Chart 4.—10 c.c. of sheep’s serum 
injected intraperitoneally caused a great rise in number of the 
mononuclear leucocytes, there being a gradual increase from 
4,000 per c.mm. from the day after injection until the fourth day, 
when there were present 15,000 per c.mm. On the sixth day the 
number was 6,500 рег c.mm. The polynuclear leucocytes were not 
affected until the day when the mononuclear forms reached 
their maximum increase, they then rose to 8,000, this being 
6,000 more per c.mm. than on the previous day. 

The number of both kinds had fallen on the sixth day, and as 
there was no great difference in the leucocyte count on the eighth 
day, 20 c.c. of sheep's serum were injected intraperitoneally. 
Twenty hours afterwards the polynuclear leucocytes were found 
to be present in very small numbers, only 2,250 per c.mm. The 
mononuclear leucocytes had increased from 6,000 to 15,000 per 
cmm. At the time of taking the blood for this enumeration the 
animal was very lethargic and blood was only obtained with 
dificulty, as the peripheral circulation was failing. Death 
supervened five hours later, and a post-mortem examination 
revealed the presence of septic peritonitis. 

The failure of the polynuclear leucocytes to react will, in the 
light of. other experiments with living bacterial cultures, possibly 
explain why death resulted so rapidly. 

Human pleural effusions and human serum.— Rabbit Е. 
Chart 7.—This animal was being immunized by Dr. Walker for 
the purposes of other investigations, and I was fortunately able 
to make blood-counts after several of the injections. The 
immunizing effect of the latter is well seen in the charts, the 
reactions gradually decreasing in relation to the total number of 
leucocytes. 


174 The Behaviour of Leucocytes under the Influence of 


10 c.c. of human pleural fluid injected intraperitoneally produced 
& gradual increase of both kinds of leucocyte (but more especially 
the mononuclear form) up to the third day, the numbers then 
being—polynuclear leucocytes 10,000 per c.mm., mononuclear 
leucocytes 14,500 per сот. There was a gradual fall onwards 
until the seventh day, when another injection of 15 c.c. of 
pleural fluid was given. The polynuclear leucocytes were not 
increased during this reaction, but the mononuclear forms, after 
falling to 2,000 on the day after injection, rose to 8,500 per c.mm. 
on the third day after the second injection. 

On the fourteenth day 20 c.c. were again injected. A slight 
hypoleucocytosis was noticed, both kinds being subsequently 
increased, the mononuclear leucocytes on the third and fourth 
days after injection, and the polynuclear leucocytes on the third 
day. Both varieties had fallen to normal on the fifth day after 
the third injection. 

The same animal was injected intraperitoneally after a two 
months’ interval with 20 c.c. of human serum from a case of 
uremia. There was a small decrease in both forms for two days 
and a subsequent slight hyperleucocytosis, involving both mono- 
nuclear and polynuclear leucocytes. The return to a normal 
condition was gradual. 

The reaction to pleural fluid, therefore, appears to affect both 
polynuclear leucocytes and mononuclear forms, but more especi- 
ally the latter, while serum in uremia, presumably containing 
abnormal substances, affected polynuclear leucocytes quite as 
much as.the mononuclear leucocytes. 


STAPHYLOCOCCUS PYOGENES AUREUS. 


1. Dead cultures.—Rabbit F. Chars 9. — One broth culture 
forty-eight hours old of dead staphylococcus pyogenes aureus 
was injected intraperitoneally. This reaction was remarkable 
for the large mononuclear leucocytosis on the fifth day after 
inoculation—an increase from 7,250 to 18,600 per c.mm. The 
number of mononuclear leucocytes for the first few days was 
slightly diminised. The number of polynuclear leucocytes in- 
creased a little on the first day, but diminished for the next 








certain Bacterial and other Substances. 175 


three days. The largest total recorded was on the fifth day, 
namely, 6,400 per c.mm. | 

Rabbit. K. Chart 14.—10 c.c. of a forty-eight hours old broth 
eulture of dead staphylococcus pyogenes aureus, produced an 
increase mainly in the mononuclear leucocytes, these rising from 
4,000 to 12,000 approximately on the second day. The return to 
normal occupied three days. There was a slight increase of 
polynuclear leucocytes (1,750) om the first day, but a subsequent 
fall during four days to the low total of 1,750. 

Rabbit Q. Chart 14.—There was again a marked increase of 
mononuclear leucocytes following the injection of one dead agar 
culture of staphylococcus pyogenes aureus forty-eight hours old, 
especially on the third day, when the number reached 18,400 
per c.mm. This increase was only noted on one day. The 
polynuclear leucocytosis was larger than in the previous experi- 
ment. The highest number recorded was 12,800 per c.mm. but 
on the next day, they had fallen to 8,500, and were still further 
diminished on subsequent days. [6 will thus be seen that 
injections of dead staphylococci produce by far the greatest 
effect on the mononuclear leucocytes, and generally late in the 
reaction. There was practically no increase of polynuclear 
leucocytes in two of the experiments, and in rabbit Q. the 
polynuclear leucocytosis was not very large. 

2. Living cultures. — Rabbit T. Chart 14.— Half an agar 
culture forty-eight hours old of living staphylococcus pyogenes 
aureus produced an extremely large polynuclear leucocytosis. 
On the third day after inoculation, the polynuclear leucocytes 
numbered 24,500 per c.mm., and on the fifth day, 14,000. The 
mononuclear leucocytes also increased to some extent on both 
these days, but the number never exceeded 11,000 per c.mm. 
(7,000 before inoculation), 

With the same injection, there was a similar reaction in 
Rabbit R., Chart 14, allowing for individual susceptibility. 
The polynuclear leucocytes increased in number from 6,000 to 
10,800 per c.mm. on the second day. On the same day, there was 
an increase of 2,000 mononuclear leucocytes, and this was 
maintained when the number of polynuclear leucocytes had 
fallen to normal again. 


176 The Behaviour of Leucocytes under the Influence of 


These two reactions to living cultures form a marked contrast 
to those in which dead cultures were inoculated. 


Everard, Demoor and Massart, found after injecting 1 c.c. of a 
culture of living staphylococcus pyogenes aureus intramuscularly 
a polynuclear leucocytosis which was present until the seventy- 
second hour. Up to this time the mononuclear leucocytes had 
not increased in number. | 


Muir obtained similar results with injections of 1 to 2 c.c. of 
pure cultures of staphyloccus pyogenes aureus having & low 
virulence. A considerable interval, however, elapsed between 
the leucocyte counts in some of his observations. 


These observations show that, while the reaction to dead 
staphylococci, which had been subjected to a temperature of 
100°, was entirely comparable to the reactions to indifferent 
animal cells, the reactions to cultures containing living staphy- 
lococci and their unaltered products affects the polynuclear 
leucocytes most markedly. The latter, therefore, may probably 
be regarded as engaged in the destruction of the micro-organisms 
and their toxins, while the former act in relation to the dead 
cocci precisely as they do with other cells. 


BACILLUS TvPHOIDXE ABDOMINAL. 


Rabbit D. Chart 5.—Subeutaneous injection of 0:5 c.c. of a 
broth culture twenty-four hours old of living bacillus typhoide 
abdominale produced a large polynuclear leucocytosis on the 
third and fourth days. The number of mononuclear leucocytes 
was high (18,000) before injection, but after falling for the first 
few days after inoculation they increased to 12,000 per c.mm. 


Seventeen days after this injection the animal was inoculated 
intraperitoneally with two agar cultures, forty-eight hours old, 
of living bacillus typhoide abdominale. There was an immediate 
rise of polynuclear leucocytes the following day from 2,000 to 
8,000, and this was maintained on the second day after injection. 
During the next three days the number of leucocytes (polynuclear) 
was normal. 








certain Bacterial and other Substances. 177 


The mononuclear leucocytes were only slightly increased for 
four days after injection, but on the fifth day suddenly rose to 
8,000 per c.mm., twice the number they were before inoculation. 

After nine weeks’ interval one forty-eight hour old agar culture 
of living bacillus typhoide abdominale was again injected, the 
animal’s blood having been counted for a week previously. On 
the day after injection (about 20 hours) there was an enormous 
rise of mononuclear leucocytes, consisting chiefly of lymphocytes, 
from 4,250 to 19,750 per c.mm., and an increase in polynuclear 
leucocytes from 3,000 to 11,750 per c.mm. At the same time 
the animal was extremely ill and collapsed (10 a.m.) but its 
condition gradually improved during the day. The number of 
mononuelear leucocytes had fallen to 7,000 on the second day, 
but that of the polynuclear leucocytes increased still further to 
16,660 per c.mm., the latter gradually diminished on the three 
following days, but the number of mononuclear leucocytes during 
the later stages of the reaction was higher than usual, although 
only slightly so. 

Compare this early and sudden mononuclear leucocytosis 
associated with extreme intoxication, with the similar increase 
after injection of infected serum on Chart 4. 

Rabbit H. Chart 11.—One agar culture three days old of 
living bacillus typhoid abdominale produced the greatest change 
in the mononuclear leucocytes during the first few days of the 
reaction, the number rising on the second day from 3,000 to 11,800 
per c.mm., and being maintained with slight variations for four 
more days. The number of polynuclear leucocytes rose on the 
second day from 4,500 to 7,400 per c.mm., but it was not until 
the fifth and sixth days that they were greatly increased. 

The early mononuclear leucocytosis was very similar in the 
last two experiments, but in rabbit H the polynuclear increase 
was late, not being fully established until the sixth day. The 
latter animal, however, was not nearly so seriously ill as 
rabbit D on the day after injection. 


PNEUMOCOCCUS. 


Rabbit N. Chart 6.—Subcutaneous injection of 84 c.c. of broth 
culture forty-eight hours old of dead pneumococcus, In this 


178 The Behaviour of Leucocytes under the Influence of 


experiment, there was an increase of polynuclear leucocytes 
from 3,660 to 10,000 per c.mm., & mononuclear leucocytosis 
from 8,160 to 15,160 per c.mm. on the day after injection, and a 
subsequent rise on the fourth and eighth days of each kind of 
leucocyte. It will be seen from the chart that the increase 
of each variety was coincident in point of time. 

Rabbit F. Chart 16.—The reaction to 0:5 c.c. broth culture 
two days old of living pneumococcus injected subcutaneously 
was only slight. Both kinds were increased, but especially the 
polynuclear leucocytes, which reached a maximum of 7,000 per 
c.mm. on the second day after injection; the mononuclear 
leucocytes attained their greatest number (10,400) on the fourth 
day. 

Schlesinger’s experiments.—Subcutaneous injection of ‘05 c.c. of 
a pneumococcus culture gave a gradual increase of polynuclear 
leucocytes from 4,000 to 9,500 per c.mm. till the ninth hour, while 
the lymphocytes gradually decreased from 8,000 to 8,000 per c.mm. 
until the seventh hour, and remained the same until death, 
which occurred thirteen hours after inoculation. 

A ·15 c.c. broth culture of pneumococcus (diplococcus of Fraenkel) 
producing death on the following day, gave an increase of 1,000 
polynuclear leucocytes on the day of injection, after which both 
varieties gradually diminished till death. Just before death, 
the numbers of polynuclear and mononuclear leucocytes were 
1,000 and 1,750 per c.mm. respectively. 

Sterile broth.—This was given to show the effect of the fluid 
mediums in which some of the cultures were injected. | 

Rabbit F. Chart 9.—10 с.с. injected intraperitoneally produced 
a moderate polynuclear leucocytosis on the following day, the 
number increasing from 3,200 to 10,500 perc.mm. The mono- 
nuclear leucocytes also increased in number from 3,500 to 5,500 
during the same time, and there was a further increase of 
mononuclear leucocytes on the third day, the number then being 
7,250 per c.mm. 

Rabbit H. Chart 11.—20 c.c. injected intraperitoneally gave a 
small leucocytosis of both kinds. This was only maintained for 
one day. 





certain Bacterial. and other Substances. 179 


* PEPTONE.” 


Rabbit O. Chart 13.—1 grm. of peptone in З c.c. normal salt 
solution was injected intraperitoneally. On the following day 
the number of both kinds of leucocyte was diminished. There 
was a progressive increase of the polynuclear forms until the 
fourth day, when the number was 12,250. The number of 
mononuclear leucocytes remained low until the fourth day, when 
there was an increase from 4,250 to 9,750 per c.mm. Both 
varieties had fallen to normal on the fifth day after inoculation. 


DIPHTHERITIC TOXIN. 


Rabbits M. and L. Chart 12, were each injected subcu- 
taneously with :02 c.c. and rabbit A. with 0:2 c.c. of very powerful 
diphtheritic toxin. In all cases there was an enormous 
polynuclear leucocytosis. 

Rabbit M. died during the evening of the first day after 
inoculation. The number of polynuclear leucocytes rose from 
4,000 to 17,000, and the mononuclear leucocytes diminished from 
6,750 to 3,500 per c.mm. 

Rabbit A. died during the evening of the second day after 
injection. On the first day, the number of polynuclear leucocytes 
increased from 4,500 to 9,500 per c.mm., the mononuclear forms 
were slightly diminished. On the morniug of the second day, 
there was a leucocytosis of polynuclear leucocytes of 17,000, and 
of mononuclear leucocytes of 14,500 c.mm. | 

Rabbit L. also died on the second day after inoculation, at 
2.25 p.m. On the first day, the number of polynuclear leucocytes 
rose from 3,250 to 12,000, the mononuclear leucocytes remained 
unaltered. At 10 a.m. on the second day, the polynuclear forms 
had still further increased to 18,500, and the mononuclear 
leucocytes had risen to 12,000 per c.mm. In the blood-count one 
hour before death, the number of polynuclear forms had fallen 
to 5,000, and that of the mononuclear variety to 5,800 per c.mm. 

In the fourth experiment with rabbit J. a much smaller dose 
(005 с.с.) was injected subcutaneously with the view of deter- 
mining, if possible, the behaviour of the leucocytes over a longer 


180 The Behaviour of Leucocytes under the Influence of 


period. There was again a very large and early polynuclear 
leucocytosis, the numbers increasing on the second day from 
6,000 to 20,500. The mononuclear leucocytes did not increase 
appreciably until the third day, when the number rose from 
7,250 to 18,250 perc.mm. The number of polynuclear forms was 
falling at this time. There was a leucocytosis of both varieties 
for three more days, and on the seventh day after injection, the 
mononuclear leucocytes suddenly increased from 11,500 to over 
22,000 per c.mm. Corresponding with the large mononuclear 
increase, there was a slight rise of polynuclear leucocytes. Both 
kinds had fallen to 8,000 on the ninth day after injection. 

Rabbit O. Chart 13, was injected with an even smaller dose 
of toxin, viz., '001 c.c. The reaction was, however, very similar 
io the previous experiment with rabbit J. 

The polynuclear leucocytes were the first to be affected, the 
number reaching a maximum of 10,750 on the second day, and 
then gradually falling to normal. The mononuclear leucocytes 
were not materially altered during the first three days, but on 
the fourth day, the number rose to 10,330 per c.mm., and on the 
fifth day was 8,750. 


These experiments agree with Besredka’s results, in that the 
injection of the diphtheritic toxin produces a large and rapid 
polynuclear leucocytosis, but they also show that the mononuclear 
leucocytes play an important part, and react at a later period. 
In four out of the five experiments, there was a marked increase 
of this kind on the third or fourth day, and in rabbit J. a very 
large mononuclear leucocytosis on the seventh day after inocula- 
tion. No doubt a large number of polynuclear leucocytes are 
destroyed in the process of neutralizing the toxin, and possibly 
the phagocytic action of the mononuclear leucocytes may be 
called into play in removing these, as the late mononuclear 
reaction is very similar to that following injections of the various 
cells which have been previously described. 


It will also be noticed that there is again a sudden preagonistic 


rise of mononuclear leucocytes, as in the injection of infected 
sheep’s serum and bacillus typhoide abdominale. 





certain Bacterial and other Substances. 181 


Micrococcus ВнЕпмАТ1ООВ (living). 


Rabbit O. Chart 13, was intravenously injected with five 
blood-agar cultures forty-eight hours old of very attenuated living 
micrococcus rheumaticus The number of polynuclear leucocytes | 
increased on the first day after inoculation from 2,500 to 10,500 
but fell the next day to 6,000; on the fourth day again the 
number per c.mm. was 9,000. The mononuclear leucocytes reached 
a maximum on the fourth day of 8,750, this being an increase of 
3,750 per c.mm.; for the first three days they remained 
unaltered. 


Rabbit V. Chart 15.—A similar reaction was produced by the 
subcutaneous injection of three agar cultures forty-eight hours 
old. A polynuclear leucocytosis was established on the first day 
after inoculation and was maintained for four days. The mono- 
nuclear leucocytes were unaltered for the first three days but 
their number increased on the fourth day from 6,500 to 9,500 
рег c.mm. 


Rabbit U. Chart 15.—Three agar cultures forty-eight hours 
old were injected subcutaneously. A polynuclear leucocytosis 
was observed on the next day and was maintained more or less 
for two days. The mononuclear leucocytes reacted much earlier 
than in rabbit V. The number increased on the first day from ` 
4,500 to 8,500 per c.mm. and this increase was very nearly 
maintained for three days. These reactions again show the 
early polynuclear reaction to the living organism, and the late 
mononuclear reaction possibly to remove the dead material. 


Schlesinger’s experiments.—1 c.c. of a broth culture of strepto- 
coccus erysipelatus injected subcutaneously produced a poly- 
nuclear leucocytosis which was highest on the fifth day, the 
number of leucocytes increasing from 4,000 to 17,000 per c.mm. 
The mononuclear forms reached а maximum increase on the 
ninth day of 4,800, the total number then being 11,800 per c.mm. 


The number of both kinds of leucocyte was falling at the 
maximum of infiltration. 


VOL. LIX. 14 


182 The Behaviour of Leucocytes under the Influence of 


BacinLus DiPHTHERLE AMERICAN (living). 


The toxin of this organism is very highly toxic, but the 
organism itself is extremely inactive, large doses failing to kill a 
guinea-pig. 

Rabbit P. Chart 15.—0:25 c.c. of an agar culture forty-eight 
hours old of the living organism injected subcutaneously produced 
a fall in polynuclear leucocytes for two days, and a gradual 
increase from the third until the fifth day, but at this time the 
number was only very slightly above that recorded previous to 
inoculation. The number of mononuclear leucocytes increased 
on the third day from 4,000 to 8,750 and remained so until the 
next day. On the 6th day the number had fallen to 4,250 
per c.mm. 

Rabbit 8. Chart 15.—One agar culture seventy-two hours old 
injected subcutaneously gave a leucocytosis on the third day 
almost entirely confined to the polynuclear leucocytes; the 
mononuclear leucocytes were not appreciably altered. 

The two reactions are not comparable to any extent. The 
dose injected was, however, very much larger in rabbit 8, and it 
is possible, with an interval of twenty-four hours between each 
leucocyte count, that the polynuclear forms were at one time 
higher than appears in the instances recorded. 

Schlesinger's experiments.—Injection of broth culture (8 c.c.) of 
bacillus diphtheriae Americans. The number of polynuclear 
leucocytes increased at the fourth hour from 3,800 to 6,500 per 
c.mm., but fell at the sixth hour to about 2,000 and remained 
at 3,000 till death on the following morning. The mononuclear 
leucocytes numbered 10,500 per c.mm. before injection. They 
diminished in the early stages of the reaction, but one hour 
before death the number was 9,000 per c.mm. 

15 c.c. of a broth culture of bacillus diphtheria Americane 
killed with ‘5 per cent. phenol gave a rise and fall on succeeding 
days affecting both varieties, but mainly the polynuclear leuco- 
cytes. The polynuclear leucocytes numbered 25,000 and the 
mononuclear leucocytes 11,000 per c.mm. 

4 cc. of virulent diphtheritic culture injected subcutaneously 
caused a leucopenia during the first few hours, and a subsequent 


certuin Bacterial and other Substances. 183 


increase in both kinds of leucocyte. Previous to death the poly- 
nuclear leucocytes numbered 14,000 (an increase of 9,000) and 
the mononuclear kind 22,000 (an increase of 17,000). 


CONCLUSIONS. 


1. The injection in rabbits of dead non-toxic animal matter, 
such as animal cells and red blood corpuscles, produces a reaction 
exclusively affecting the mononuclear leucocytes. Inoculation 
with pure fatty acid from the tubercle bacillus gives a similar — 
reaction. (Cf. the alleged mononuclear leucocytosis—lympho- 
cytosis—of unmixed tuberculosis). 

2. The injection of toxins produces a pure polynuclear leuco- 
cytosis, unless death ensues rapidly. In the later stages, as 
the number of polynuclear leucocytes diminish, the mononuclear 
leucocytes increase in number, presumably to remove the excess 
of dead material. 

3. The reaction to serum which contains chiefly indifferent 
animal matters, is mainly mononuclear. 

4. Micro-organisms subjected to heat, whereby bacterium and 
toxin are destroyed, produce on injection the greatest effect on 
the mononuclear leucocytes. 

5. The injection of living micro-organisms produces mainly a 
polynuclear leucocytosis, or a mixed leucocytosis in which the 
mononuclear reaction is secondary. 

Much more work must necessarily be done in this direction 
before any definite conclusions can be drawn, but these experi- 
ments, I think, bear out the suggestion that in rabbits, the 
polynuclear leucocytes are chiefly responsible for the destruction 
of toxic products and living bacteria, while the mononuclear 
leucocytes deal chiefly with non-toxic matter and nutritive 
substances. 

Finally, I have to thank Dr. Ainley Walker very sincerely, not 
only for the preparation and inoculation of all cultures, etc., 
but for his kindly encouragement and guidance throughout the 
research. 


184 The Behaviour of Leucocytes under the Influence of — 


Muir. 
Bullock. 


Everard. 


Demoor, 
Massart. 


Haushalter. 
Spillman. 


Roger. 
Josué. 


Ehrlich. ... 
Schlesinger. 


Milroy. 
Malcolm. 


Brinkerhof, 
Tyzzer. 


Bruce. 
Werigo. 


Durham 
Sherrington. 
Romer. 
Batty-Shaw. 
Besredka. ... 


Achard 
Loeper. 


Ramsden. ... 


Hankin 
Kanthack. 


Nicolas, 
Courmont. 


Goldscheider, 
Jacob. 


Lowit. 


Ibid. 


Havet. T 


REFERENCES. 


* The bone-marrow and leucocyte production." Journ. of 
Path., 1901. 

“Оп the nature of hemolysis and its relation to bacterio- 
lysis." Trans. Path. Soc. Lond., 1901, p. 208. 

* Sur les modifications des leucocytes.” Annales de 


l'Institute Pasteur, 1893. 


Compt. Rend. Soc. de Biol. Paris, 1899, p. 678. 
Compt. Rend. Soc. de Biol. Paris, 1899, p. 436. 


“ Die Anamie.'" Histology of Blood. Trans. by Myers, 1900. 
Zeitschrift. f. Hyg. u. Infect, Krank. Leipzig, 1900, p. 349. 
Jour. of Physiol., 1899. Vol. 25, p. 105. 


Jour. of Med. Research. Boston, March, 1902, p. 173. 


Proc. Roy. Soc. Vol. 55, p. 295. 

“Les globules blancs comme protecteurs du sang." Annales 
de l'Institute Pasteur, 1892. Vol. 6, p. 478. 

Journ. of Pathol. Vol. 6, 1897, p. 338. 

Proc. Roy. Soc., 1894. Vol. 55, page 161. 

Berlin Klin. Woch., 1891. No. 36. 

Journ. of Pathol., March, 1902. Vol. 8, p. 70. 

«De 1а leucocytose dans 1а diphtheria.” Annales de 
lInstitute Pasteur, 1898. Т. 12. 

Compt. Rend. Soc. de Biol, Paris, 1901, 52, pp. 486, 487. 


Journ. of Physiol. Vol. 28, July, 1902. Proc., p. 23. 
Proc. Camb. Philosoph. Soc., Feb., 1892. 


«Etude sur la leucocytose dans l'intoxication par la toxine 
diphtherique." Archiv. de Med. Experiment, 1897. 


“u Variationen der Lukocytose." Zeitsch. fur Klin. Med. 
1894. Ва. 25, p. 373. 


'* Studien zur Physiol und Pathol. des Blutes und der 
Lymph." Yena, 1892. 

«Uber die Beziehungen der Leucocyten zur  bactericiden 
Wirkung des Blutes.”  Ziegler's Beitrage zur Pathol. 
Anat., 1897. Bd. 24. 

« Du rapport entre le pouvoir bactericide du sang du chien et 
sa richesse en leucocytes.” La Cellule, 1894, T. 10. 





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certain Bacterial and other Substances. 185 


TABLES. 


The weight is given in grammes. 
The temperature was taken on all occasions in the rectum. 
The figures of all corpuscles (red and white) represent tho number per o.mm. 


RABBIT (1). 


























Day. | Weight. | Temp. | Total Leu. | 
1 2130 100 7950 | 
2 2130 102-9 7500 
3 2170 1006 | 8500 
4 9190 101-4 1500 
5 2175 100°2 — 
6 2120 103 з 
Т^ 2205 102 7000 
8 2180 100°2 6000 
9 2120 102۰2 7000 
10 2120 102-6 6000 Injection of pneumococcus. 
| ? Dose. 
11 2050 104°4 3000 
12 1990 103°8 ` 8000 
13 2010 104-9 8500 
14 1985 104-6 9500 
15 1895 102-4 6000 
16 1840 102-8 12000 
17 1810 100-4 10000 
18 1910 101 ‚ 12000 
19 1880 1024 10500 | 
20 1945 1012 | 9500 | 
21 1910 101 9000 
22 1960 101۰2 9500 
RABBIT (2). 
Day. | Weight Temp. Total Leu. 
1 2165 101 9500 | 
2 2170 100:8 8000 | 8 c.c. T. B. extract, sub- 
cutaneously. 
3 2950 101 11000 | 
4 2265 99:8 6500 | 10 c.c. T. B. extract, intra- 
| peritoneally- 
5 2320 102 18500 | 
6 2290 103 15000 
7 2360 102:2 10000 | 
8 | 9350 102 9000 — 
9 | 2365 102:4 8500 | 
12 |days interval | 
29 2485 102 8000 | 
23 2425 102:2 8000 | 15c.c. T. B. extract, intra- 
| peritoneally. 
24 2400 108 20500 | 
25 2885 100-4 21000 
26 2370 101:2 14000 | 
27 2345 101 29000 | 
28 2820 101°5 24500 
29 2410 101-8 12500 
80 2485 101-6 10000 











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186 The Behaviour of Leucocytes under the Influence of 
RABBIT (8). 


















































+ سے ے 


Day, Weight, Temp. Total Leu. | 
1 9240 99-9 10500 | 
9 e ^ em 
3 س‎ — = 
` 4 2310 101 10000 10 c.c. red corpuscles (sheep), 
intraperitoneally. - 
| 5 2390 102-2 11500 
f 6 |, 2280 101 10500 
| 7 2940 | 1002 13500 
| 8 2310 101 8000 
9 2280 100°6 8500 15 с.е. red corpuscles (sheep), 
| intraperitoneally. 
Wat 10 2300 101 8000 
Whaat 7 days interval 
|| 18 2360 102-4 14500 
Wr 19 2410 100-2 10500 
MEN 20 2440 100-4 12000 
Wha) 21 2475 99-8 10000 
NE 22 2460 99:6 11500 10 с.е. red corpuscles, intra- 
үй peritoneally. 
AW 23 2495 103۰2 45000 
PIN 24 2335 102-5 10500 
| 25 2370 102 18000 
Wi 26 2350 ‚ 102 24000 
a 27 2325 102-8 11500 
im 28 9295 101-9 31500 
b 29 2255 100-9 21500 
M 30 2210 100-8 17000 
ү! 31 — — — 
| | 32 2330 100-6 14500 
t 33 2980 100:9 12500 
Ж 34 2245 101 13500 
| il E | February 24th, 1902, 5 c.c. human serum intraperitoneally. 
i iy March 2nd, 1902 :— 
4 : y | > P ed uam 
1 | Day. Weight. | Temp. Total Leu. | 
i E | = 
A ia 1 1885 101-2 9000 | 
UM 2 | 1900 101 8500 10 c.c. human serum, intra 
WE MI peritoneally. 
РЕВ 3 1900 101-7 11000 
TE | | 4 1825 100-2 14000 
NAT 5 1800 99 13500 
AM 6 1765 100-9 11500 
n ү | 7 1700 102-2 8500 
I ү 8 days interval 
WA I 16 2105 101 16500 | 
ҮЛ | 17 2050 100-2 17000 10 с.с. human pleural fluid, 
ҮЕ intraperitoneally. 
E d 18 1995 102-6 18000 
ҮҮ | 19 | 1895 103 30500 
ҮШҮ 20 1765 100-8 20500 
үү | 21 | 1745 100-6 19500 
| RA 99 252 мефт АД 
i i 23 1790 100-2 17000 
г | 24 1740 100-2 13000 


— 
SS 
ЕЕЕ 
— 
= 
1 


=ч е NON Ду чылт. n шшщ А. 

















certain Bacterial and other Substances. 187 
RABBIT “А”, 
Day. Weight. Temp. Total Leu, - 
1 1585 102-4 9500 
= 1560 101:2 9000 
4 = == ios 
5 1660 101-4 10500 
6 1695 100 9000 
7 1630 103°6 9000 
8 1690 101°7 9000 0:5 с.с. broth culture, 24 hours 
old V.M. heated to 80? O., 
subcutaneously. 
9 1605 103:2 10000 

10 1595 102۰2 8500 

11 — — — 

12 1750 101:2 8000 1 c.c. broth culture, living 
V.M. 24 hours old, subcu- 
taneously. 

13 1825 102-9 8500 

14 1860 102-4 12000 

15 1840 1024 8500 5 c.c. broth culture, living 
V.M. 24 hours old, suFcu- 
taneously. 

16 | 1715 105 2000 

17 1700 108:4 25500 

18 1825 102۰8 11500 

19 1780 103 10000 

20 1850 102۰2 9000 

21 | 1885 102-4 8500 3 agar cultures, 24 hours old 

living V.M., subcutaneously 

22 1735 104 5000 

23 1765 103 20500 

24 1778 108 13500 

25 1780 102۰6 7500 

7 days interval 

88 1720 101:6 8000 3 c.c. broth culture, 24 hours 
old living B.T.A., subcu- 
taneously. 

34 1705 108-4 12500 

35 1685 102:6 10000 

96 |. 2670 - 102-2 7500 

97 |: 1620 102-4 9500 

38 1630 102 8500 

7 days interval 

46 1970 $ 10000 

47 1965 101°6 9000 5 c.c. broth culture, 24 hours 
old living B.T.A., subcu- 
taneously. 

48 1895 103 17000 

49 1885 102°6 22250 

50 1835 102۰2 11500 

51 1810 102۰4 15500 

52 — — — 

53 1910 101:6 14000 

54 1845 102 9000 

55 1790 101:2 10500 

56 — س‎ — 3 agar cultures, 48 hours old 


living V.M. : subcutaneously 





188 The Behaviour of Leucocytes under the Influence of 


RABBIT ‘A’’—continued. 


8 days interval from last count. 


| 
Day. Weight. | Temp, |Total Leu. Poly. Leu. Mon.Leu. 


—À NT ————————— € 


4 


11000 5000 6000 
9000 5000 4000 
8000 5000 8000 

14000 8000 6000 

11000 7000 4000 





= = — 2 agar cultures, 72 hours 
old living V.M. in 
broth, subcutaneously 


-20: Ot боюн 
IIIIII | 


8, 2030 102 14000 8000 6000 
9 | 1985 104:8 | 8000 5000 3000 


22 | 1930 102 8000 4000 4000 | 3 agar cultures, 24 hours 
old living V.M. m 


broth, subcutaneously 
23 | 2025 103 9000 4000 5000 


25 | 1965 103:4 | 3000 2000 1000 
26 | 1930 104 5000 2000 3000 
27 | 1885 103۰4 | 6000 4000 2000 


29 | 2030 104۰2 7000 5000 2000 
30 | 1960 103°8 | 16000 | 10000 6000 
| 31 2000 105:2 | 10000 8000 2000 | 5 c.c. Т.В. extract, sub- 


cutaneously. 
32 | 1985 105 8000 6000 2000 
33 | 1985 104۰8 — 


34 | 1965 103:8 | 16000 6000 | 10000 


36 | 1920 103:6 | 10000 4000 6000 
37 | 1840 103 — 
38 | 1930 1083-8 | 9000 6000 3000 
39 | 1875 108 9000 5000 4000 
40 | 1830 102-2 | 12000 7000 5000 
41 | 1800 103 9000 5009 4000 

















certain Bacterial and other Substances. 189 


RABBIT '*A"—continued. 


15 days interval from last count. 


| 





Day. Weight. | Temp. Total Leu. Poly. Leu | Mon. Leu. 

ЕЕ ТЕЕ ee me HEU! 
1. 2100 | 108-6 | 5500 2500 8000 LT. 
2 | 2090 | 108-4 | 6000 | 2000 | 4000 I TE 
3 2050 | 102:2| 6000 | 1000 | 5000 
4 — — 5000 1000 4000 | 
5 | 2120 102-9 | 6000 2000 4000 | 
6 | 2160 103:6 | 6000 2000 4000 | 
7 = = == == 2 | 
8 | 2195 108:2 | 7000 8000 4000 | 
9 32090 102-8 | 7000 2000 5000 | 10c.c. T.B. extract, intra- 


peritoneally. 
10 | 2020 102-6 | 7000 4000 3000 
11 | 1960 108 10500 4000 6500 
12 | 1985 102:4 ; 8500 2000 6500 
13 | 2020 | 1028 | 8000 2000 6000 


| 
15 | 9980 | 103-8 | 9000 | 4000 | 5000 | 15c.c. T.B.extract, intra- | 


— - == l.. = 
E А SEE 5 ae rece See ences A remm 
МЧ TO Ma PUR uror ur S ty dct we г атте ета: 


cwm UM. 


TEN 


peritoneally. 
16 | 2130 103°6 | 8000 2500 5500 
17 | 2090 108-4 | 8500 4000 4500 
18 | 2040 103 15000 6500 8500 
19 | 2122 103°4 | 8000 8500 4500 


34 | months linterval 


1! 2920 108 10800 5200 5600 
2| 9870 102-7 | 9250 4500 4750 | 0:2 c.c. diphtheria toxin, 
° subcutaneously. 








om 


RABBIT ‘A’’—continued. 


| Small 12 


Large | Large 
Lymph. 


Mon. Leu. Mono. , Lymph. 


Day. Weight. | Temp. Total Leu.' Poly. Leu. 
| | 








9500 
17000 


| 9750 | 105 |14000, 
4| 9700 | 98 | 81500 











| 

MESSER Жыны £s M Башы ыран 

my 185 | 585 | 3780 D 
14500 | 290 | 5220 | 8990 F 


This rabbit died during the evening of the next day, 8 to 12 hours after 
last count, 


190 The Behaviour of Leucocytes under the Influence of 


RABBIT 'B.", 

















Day. Weight. Temp. Total Leu.| Poly. Leu.|Mon. Leu. 
1| 2240 100 7500 

| h 2 | 2215 102 7000 

| 3| 2350 100 11000 

| 4| 2145 100:6 | 15000 
| 5 | 2210 100°6 | 9500 

6 | 2150 102-2 | 9000 

| 7| 2190 102 8000 

| 8 | 2250 101°6 7000 

| 9| 2200 101°6 7000 — — 1 c.c. broth culture, 24 
WE, hours old living V.M., 
Th intraperitoneally. 

I4 711 10 | 2190 102°3 | 3000 

UL 11 | 2150 102:6 | 7500 

WE: 12 | 2140 | 103-2 | 7000 

Ae 13 | 2205 1026 | 8000 

| | 14 — — — 

| 15 | 2205 1026 | 9000 — -— 5 c.c. broth cultures, 24 
dr hours old living V.M., 
LII intraperitoneally. 
A 16 | 2050 102:2 | 14000 | 

qu 17| 2030 | 102-2 | 13000 

hah 18 | 1990 100:8 | 9000 

Ti I 19 | 2040 | 100 9500 

FE 20 | 2020 102-2 | 8000 

| | i] 8 days in |terval 

| ! 29 2210 | 101-5 | 7000 

Ub 30 | 2190 | 101 9000 

(1! 31 | 2200 103 6000 = pet 1 agar culture, 24 hours 
TEM old living V.M., intra- 
| | 32 | 2190 102-6 | 20000 peritoneally. 

| | 33 | 2120 102:4 6000 

a 34 | 2170 102:6 | 17000 

р 35 | 2215 102:4 | 15000 
| m4 46 -- —- — — = 2 agar cultures, 48 pet 
ү] old living V.M., su 
| 3| months |interval cutaneously. 

i 2300 108-2 | 5500 2000 3500 

th 2310 1028 | 6000 2000 4000 

| 2230 102 6000 4000 2000 

| 2235 102°6 6000 2000 4000 

C 2260 108.1 5500 2000 3500 

VP 108-2 | 4000 1000 3000 

i о d s ш 
hA 103 7000 2000 5000 
үң 1 2165 1026 | 8500 2000 6500 | 1 agar culture, 24 day 
qd old living V.M., su 
Б cutaneously. 
LAT 11| 2125 103 5500 2000 3500 
TT 12 | 2005 | 102-6 | 14000 | 9000 | 5000 
t 13 1965 101:6 8000 4000 4000 
|| il 14 | 1995 102:6 | 7000 2000 5000 
ИН! КӨ „= 2 = X Em 

f {| 16 | 2240 | 1028 | 9000 | 4000 | 5000 
FAO 17 | 2160 104:4 | 7000 3500 3500 
18 | 2195 103۰6 7000 3000 4000 





| 

1 

2 

3 

4 

5 

6 | 2125 
7 ed 
8 = 
9 | 2225 
0 











Day. Weight. | 
1| 8990 
9 8190 
9 8095 
4| 2985 
5 2965 
6 2970 
7 S 
8 | 0 
9| 3010 

10 | 3010 

11 2905 

1% 2860 

13 2810 

14 2935 

15 2850 

24 | 2700 

95 | 2685 
26 2595 

27 | 2495 
28 | 9440 
29 — 
30 | 9635 

31 2510 
32 | 2600 
33 | 2640 


certain Bacterial and other Substances. 191 


102 

102 

102-2 
102۰2 
102۰2 
102۰2 
103 

102۰6 
102-9. 
102-4 
102۰4 
103۰6 
101-6 
101 


9500 
14500 
9500 
18000 
6500 
12000 
7500 
7500 
7000 
12500 
15000 
15000 
18000 
10500 


RABBIT 


‚ 


8| days injterval 


100-2 


7500 
18500 
15000 
33000 
29000 
82000 
17000 
11000 

8500 


e C” 


Temp. Total Pau! Poly. Leu. Mon. Leu. 


10 c.c. sheep’s serum, in- 
traperitoneally. 





The observation on the 33rd day was on March 12, 1902. 
March 27th, 1902, 10 c.c. sheep’s serum, intraperitoneally. 





n 


p 


7000 
7000 
6500 
5330 
12000 


9250 


7250 
11660 
12000 
23500 
11000 


8960 


April 9th, 
May 12th, 
October 7th, 1902 :— 

102 | 3270 '1 
1026 | 3270 ;2 
1024 | 8400 !3 
109-8 | 3990 1 
1026 | 3370 |5 
= — ا6 
108 | 3970 | 7 
104 | 9960 !8 
108 | 3380 !9 
102:8 | 3390 :10 
1026 | 3450 |11 
103-8 | 3460 ;12 
= .— : 13 
109-4 | 8450 ;14 
101:6 3270 15 


17250 


| 


^» 


vw 


2250 

500 
3500 
3330 
6000 


3500 
3500 
4000 
2500 
8500 
4500 
2960 
2250 


” 


„ 


4150 


15000 


I 
D 


i 
l 


^ 


10 c.c. sheep's serum, in- 
traperitoneally. 


20 c.c. sheep’s serum, in- 
traperitoneally. 


This rabbit died 4 hours after the last count. A post-mortem examination 
showed the presence of septic peritonitis, 





+ | 192 The Behaviour of Leucocytes under the Influence of 4 


\ 


RABBIT “D.” 





Day.) Weight. | Temp. (Total Leu.| Poly, Leu.|Mon. Leu. 
2260 102:4 | 15000 5000 10000 





2195 102-2 | 11000 3000 8000 

2180 102:2 | 16000 3000 | 13000 | 0-5с.с.24 hours old broth 
culture, living B.T.A., 
subcutaneously. 


м х bM 


5| 9147 | 103-4 | 10000 | 3500 | 6500 
б | 2055 | 108 | 16500 | 9000 | 7500 
{ү 7 | 2020 | 102-8 | 23000 | 11000 | 12000 
| | 8| 9070 | 102 | 12000 | 6000 | 6000 
9 <s msi سک‎ 
10| 2298 | 102 | 17000 | 7000 | 10000 
N 11 | 9990 | 103-4 | 9000 | 4000 | 5000 
| 19 | 9190 | 103 | 11000 | 4500 | 6500 
T 13| 2170 | 102-4 | 13000 | 5000 | 8000 . 
ү! 14 | 9995 | 102-4 | 8000 | 2000 | 6000 
| 


| 15 | 2200 = x = cms . 
n 16 — — — -—- — 2 agar cultures, 48 hours 
had old living B.T.A., in- 
Od traperitoneally. 


17 | 2320 102-4 6000 2000 4000 
18 | 2305 104 12500 8000 45 

19 | 2300 103:2 | 11500 8000 3500 
20 | 2210 102:5 7500 2500 5000 
2220 102 7500 2500 5000 
22 | 2135 102:2 | 11000 3000 8000 


10| weeks linterval 


2500 103۰2 7750 4250 3500 

2520 102°4 7000 2000 5000 

2550 102 12500 5500 | 7000 

2540 102:2 2500 1250 1250 

2570 102.2 8000 3500 4500 v 
— — -— — — 1 broth culture, living 

B.T.A. 48 hours old, 

intraperitoneaiy. 

Chiefly lymphocytes. 

Very collapsed. 


————MÁ— Mv —— 


CM. 
-————————————— > 
bo 
reet 


XT BEC IEEE e 
t= 


Ook tc bor 





| т | 2540 | 102-2 | 7250 | 3000 | 4950 
| 8| 2540 | 98-8 | 31500 | 11750 | 19750 
| 9 | 2450 | 102-4 | 23660 | 16660 | 7000 
| 


А 
L] 
D 


10 | 2390 103 19500 | 12000 7500 
11 | 2380 103:8 | 13000 5500 7500 
12 | 2300 108-6 9000 2500 6500 
13 — — — -— —- 10 c.c. sheep's red corpus 
cles, intraperitoneal): 


= = = 
= Sa AP 
„= _ - 


Е. 14 | 2150 103-6 | 11000 | 3750 | 7250 
|1 1 15 | 2120 103-4 | 5750 1750 4000 
| | 16 | 2080 103-6 | 7160 2660 | 4500 
14. | 17 | 2130 | 103-8 | 7400 | 3200 | 4200 
MM | 18 | 2080 103-2 | 7000 | 3500 3500 
ш | 19 | 2030 108 9000 | 2000 | 7000 
i | 20 | 2010 108-4 | 9500 4500 5000 
| 21 | 2060 102-8 | 5500 2000 3500 
i 99 | 2060 103 3800 | 2160 1640 
| 93 | 9000 | 102:6 | 4250 | 1950 | 3000 





"Рау. Weight. 


RABBIT 


Temp. (Total Leu. Poly. Leu: Mon. Leu. 


certain Bacterial and other Substances. 193 


‘“ D ’’—continued. 


16 days interval. 


ELS REM ыыы cn атчы "сыды үз „ ل‎ o de 


40 | 2220 
41 — 

42 | 2220 
43 | 2170 
44 | 2120 
45 | 2150 
46 | 2140 
47 | 2220 
48 — 

49 | 2080 
50 | 2070 
51 | 2070 


— 8160 8160 5000 
103-2 7000 9950 4750 
105°2 5750 3750 2000 
104°8 7250 4750 2500 
104-2 | 8000 8750 4950 
103:6 8000 2750 5250 
103:6 | 12500 5160 7340 

— 14000 3000 11000 

— 13500 4000 9500 

— 12000 5000 7000 

— 9500 3500 6000 

— 9000 4000 5000 

| 
RABBIT “B.” 


| 

| 25 c.c. sheep's red corpus- 
| cles, subcutaneously. 
| 


June 16th, 1902, 10 c.c. human pleural fluid, intraperitoneally. 
June 20th, , К 
.July 2nd, „p  , 


July 8th, 1902:— 


1) 2245 
2 | 2150 
3 | 2020 
4 | 1985 
5 | 2070 
6 == 

T| 2235 
8 | 2120 
9, 2090 
10 | 2125 
11 | 2215 
12 | 2220 
13 — 

14 | 2335 
15 | 2225 
16 | 2300 
17 | 2280 
18 2270 


19 | 9250 





| 








108 | 4500 
108-4 , 7500 
102-2 | 8000 
` 1015 | 24500 
101:6 | 18000 
102-6 | 14330 
104-2 | 6000 
109-6 - 8500 
109-9 | 13800 
108 ; 7500 
e d еа 

103-4 | 10000 
104-8 | 7000 
108 7000 
103 12000 
— 19500 


| = | 6500 


= 


4000 


2500 | 


00 


7000 


4000 
5500 
5800 . 
2000 


"e | 
4500 
4500 
5500 


5950 
3500 | 


Day. Weight. | Temp. ‘Total Leu. Poly. Leu, Mon. Leu., 


1000 ' 


9500 


3500 
5500 
14500 
11000 


7330 


2000 
3000 
8500 
5500 


5500 


2500 
4000 
6590 
7250 
3000 


„ 


"p 


| 


10c.c.human pleural fluid, 
intraperitoneally. 





15c.c.human pleuralfluid, 
intraperitoneally. 


20c.c.human pleural fluid, 
intraperitoneally. 


194 





Day.| Weight. | Temp. |Total Leu.|Poly. Leu. Mon. Mon. Leu. 
1 | 2570 108 8000 3000 ` 5000 
2| 0 103 9500 5500 4000 
3 | 2480 103.4 | 6660 3660 8000 
4| 2480 1026 | 7000 3500 8500 
5 | 2540 102°6 | 8750 5250 3500 
6 m ss SN n 52 
7 | 2490 103 9500 5500 4000 
8 | 2510 105:6 | 8250 5750 2500 
9 | 2450 105 6250 4000 2250 

10 | 2490 108:2 | 12500 7500 5000 

11 | 2500 108:2 | 12160 6160 6000 

i 2490 108 9000 4680 4320 

14 , 2550 102-2 8000 4000 4000 

15 | 2470 103 933C 4160 5170 

9| days in'terval 

25 | 2450 103:2 | 9750 5000 4750 

2 2450 108-4 | 12000 7250 4750 
7 e = = и oa 

28 | 2550 108-6 | 7250 2750 4500 

29 | 2510 104-2 | 11000 6750' | 4250 

30. 2460 108-4 | 10140 5340 4800 

81 | 2450 108-4 | 22750 | 12750 | 10000 

32 | 2450 108-4 | 14600 8400 6200 

33 | 2450 104 22375 | 14375 8000 

84 | 2450 108-4 | 14000 6500 7500 

85 | 2430 103°4 | 14330 6330 8000 

36 | 2470 108:4 | 16330 7830 8500 

37 | 2420 103:2 | 11875 7000 4875 

38 | 2410 103-2 | 12000 6330 5670 

19 days) interval (from last count 

o8 | 2570 — 12750 5750 7000 

59 | 2580 — 22000 | 15750 6250 

60 | 2580 — 18960 9160 9800 

61 | 2620 — 13200 6800 6400 

62 | 2600 — ^ | 12330 5670 7660 

63 | 2590 — | 16500 8500 8000 

64 | 2629 -— 20000 940) | 10600 

65 | 2570 — 25750 | 14000 | 11750 

66 | 2580 — 5250 5250 


The Behaviour of Leucocytes under the Influence of 


10 weeks interval. 





RABBIT ''E"—continued. 


10500 


20 c.c.human serum (from 
| uremia),intraperiton- 
eally. 


| 





5000000 in distilled 
4700000 water of dead 
5630000 T.B., intra- 
5100000 peritoneally. 
5500000 


5800000 
6050000 
6200000 
5800000 | 


, 1 agar culture, 48 hours 
old staphylococcus 
aureus heated to 80°C., 


| 

Red Corp 

——| 10c.c.emulsion 
| subcutaneously. 











195 


certain Bacterial and other Substances. 


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certain Bacterial and other Substances. 201 


RABBIT “J.” 





Day.! Weight. Total Leu. Poly. Leu. Mon. Leu. 





1| 2670 | 11330 5500 5830 
2; 2660 | 14500 6000 8500 | 0:005 c.c. diphtheria toxin, 
subcutaneously. 
3 | 2610 | 27750 | 20500 7250 
4 | 2610 | 29750 | 16500 | 18250 
5 | 2570 | 26000 | 12400 | 18600 
6 | 2500 | 25200 | 18400 | 11800 
7 | 2470 | 24250 | 12750 | 11500 
8 | 2450 | 38660 | 16330 | 22380 
9 2400 | 15600 8000 7600 
10 2420 | 29160 | 18160 | 16000 


RABBIT “K.” 





Day. | Weight. Total Leu. Poly. Leu. Mon. Leu. Red Corp. | 


— | eS ES OS A E aT 


| | 
1| 2160 | 13750 6500 7250 . 5900000 10 c.c. broth culture, 





| staphylococcus 

aureus heated to100°, 
subcutaneously. 

2 | 2020 | 12250 8250 4000 5700000 

3 | 2060 | 17660 | 6000 11660 | 5700000 

4 2100 10500 2500 8000 ; 5600000 + 

5 2180 !' 8500 2250 6250 | 5600000 . 

6! 2180 4320 1660 2660 5600000 


RABBIT “L.” 





Day. Weight. [Total Leu. Poly. Leu. Mon. Leu. Red Corp. 











1 і 


2120 7000 2000 5000 | == 
2250 | 18500 8750 9750 -— 


2300 | 11250 8250 8000 , 5900000 0:02 c.c. diphtheritic 
` toxin, subcutane- 
ously. 


Wa Со BD سم‎ 


5 2180 20000 | 12000 8000 . 6200000 
6| 2160 30500 | 18500 | 12000 | — 
108.|m. | 


$ 


6 — 10750 5000 | 5750 — — 
1.15 p.m. | 


@ 


The last count was taken one hour before death at 2.15 p.m. on the sixth 
day after injection. 


202 The Behaviour of Leucocytes under the Influence of 


RABBIT "M." 























Day.| Weight. |Total Leu. Poly. Leu.| Mon. Leu. Red Corp. 
1 | 1790 | 9160 3160 6000 — 
2 | 1800 , 12400 5200 |.7200 — 
3 | | | 
4 | 1780 | 10750 4000 6750 | 6000000 0:02 c.c. diphtheria 


| toxin, subcutane- 
| ously. 
5| 1820 | 21160 17660 


| 
| 


8500 . 5600000 
| 


This animal died during the next evening, 4.е., about eight to twelve 
hours after the last count. 


RABBIT “N.” 


| : 
Пау. Weight. |Total Leu. Poly. Leu. Mon.Leu. Red Corp. | 





1| 1860 | 9500 | 2750 | 6750 -— 

2. 1880 | 10500 4160 6340 — | 

3 

4, 1930 | 11800 | 3660 | 8140 | 5600000 | 8jc.c. broth culture, 
| | 48 hours old pneu- 

| mococcus heated 
to 80? C., subcuta- 

| neously. 

5; 1820 | 25160 | 10000 | 15160 5900000 

6 | 1840 | 17160 7000 | 10160 5500000 

7; 1890 | 15750 4000 | 11750 5400000 

8| 1920 | 23140 | 9000 | 14140 | 5800000 

9 1910 | 15750 5750 | 10000 6000000 

10 | 1980 | 14250 5000 9250 — 

11, 1970 | 14800 4140 | 10660 5800000 

12 | 1900 | 23000 8000 | 15000 5700000 

13 | 1950 | 14000 4000 | 10000 5900000 

14 1950 8250 3250 6000 6000000 

15 | 2020 8250 3250 5000 5600000 








certain Bacterial and other Substances. 203 


RABBIT “О.” 


Day. Weight. Total Leu.|Poly. Leu.| Mon. Leu. 





1930 6000 2000 4000 

1970 | 18250 4000 9250 

2000 7000 27750 4250 

2000 | 12000 5250 6750 | ‘001 c.c. diphtheria toxin, subcu- 

taneously. 

1950 | 14625 7750 6875 

2020 | 16500 | 10750 5750 

2050 | 16000 8750 7250 

2040 | 17160 6800 | 10360 

1 2010 | 10250 6500 8750 

1 n == р E 
12 | 2160 8500 2500 6000 | 5 blood agar cultures, living mioro- 
coccus rheumaticus, intra- 

venously in salt solution (3 c.c. 
fluid approximately). 


оомо KP doe 


13 | 2060 | 15000 | 10500 4500 
14 | 2020 | 11500 6000 5500 
15 | 2100 | 12400 | 7400 5000 
16 | 2030 | 17750 9000 8750 
17 | 2090 | 13500 5500 8000 


19 | 2200 | 15000 7250 7750 | 1 gm. ''Peptone" in 8 с.с. normal 
salt solution, intraperitoneally. 
20 | 2100 8250 3500 4750 


21 | 2050 | 14000 9000 5000 ‹ 
22 | 2080 | 11750 7500 4250 
23 | 2050 | 22000 | 12250 9750 
24 | 1990 9400 4000 5400 


26 | 2190 | 12250 4000 7250 


RABBIT “Р.” 





Кеш Кашы. Leu.| Poly. Leu. | Mon. Leu. 





2080 9500 3000 6500 
2080 8250 3500 4750 


Cum И 


4000 | 0°25 c.c. living agar culture, 48 
hours old bacillus diphtheria in 
salt solution, subcutaneously. 


2080 9250 2750 6500 
2050 10750 6750 


| 
6 
7. 9050 | 6750 | 2750 | 4000 | 
8 | 2050 | 13460 | 4800 | 8660 
9 9070 | 15750 | 7250 | 8500 
10, 2090 | 9750 | 5500 | 4250 


. 9000 | 11160 | 5500 | 5660 





204 The Behaviour of Lewcocytes under the Influence of 
RABBIT “Q.” 


Day. | Weight. Total Leu. Poly. Leu. Mon. Leu. 





NS ی‎ i eee 








1 | 3230. | 10750 5000 | 5750 | 

2| 8110 | 15250 9000 6250 | 

: 3070 ges 5400 | 5600 | 

4 = LN 

5 | 2980 | 4000 . 5000 | lagarculture, 48 hours old staphy- 
| | lucoccus aureus heated to 80°C. 
| | | for 10 minutes, subcutaneously. 

6| 2990 | 12750 6000 | 6750 

7 | 8040 | 25000 | 12800 · 12200 ' 

8 | 3130 | 26875 8500 ' 18375 | 

9 | 3150 | 17250 8000 9250 ` 

10 | 3150 : 18360 6000 7660 


RABBIT “R.” 


Day. Weight. Total Leu. Poly. Leu.|Mon. Leu. 











1, 2190 . 8500 3000 5500 

2 | 2170 | 9750 , 5000 4750 

3 | 2180 | 12000 6000 6000 

4 = E س‎ E 

5 | 2180 | 11600 6000 5600 , 05:5 c.c. agar culture, 48 hours old 
| | living staphylococcus aureus in 
: salt solution, subcutaneously. 

6 | 2070 , 10570 6570 4000 

7 | 2090 | 18400 10800 7600 

8 | 2140 10000 4000 6000 

9 | 2120 | 11500 4000 1500 

10 | 2150 ' 13800 7600 6200 


! 


RABBIT “S.” 


- D —— а 
i ی س‎ —————————— ——— ee ж. 22 — M —€— 


Day.. Weight. Total Leu. Poly. Leu, Mon. Leu. 





1 2280 ¦ 10000 3160 6840 
2 | 2850 | 12660 4330 8880 
З 2340 | 15500 . 5750 9750 
4 EN ES x B 
5 | 9460 | 10000 . 3000 : 7000 | 1 agar culture, living bacillus 
| | diphtheria 72 hours old in salt 
| solution, subcutaneously. 
6 | 2410 | 11250 4250 7000 
7 | 2390 | 17500 9500 8000 
8 | 2220 7750 2500 5250 
9| 2410 | 11000 3750 | 7250 
10 5600 


2440 9400 3800 





О 
m 
ve 





Day. . Total Leu. Poly. Leu. Mon. Leu. 


qm wre 





[к 


QU RO 


10 . 





с ооч Ке» 





‚| Weight. 


2250 
2240 
2230 


2250 


2250 
2170 
2050 
2050 
1970 
2050 
1940 


Weight 


2040 
2020 
2020 


2010 


2100 
2070 
2130 
2170 
. 2210 


2110 
2120 
2130 


2150 


2200 
2270 
2290 
2190 
2140 


certain Bacterial and other Substances. 205 


RABBIT 


(¢ Tt 


Total Leu./Poly. Leu.|Mon. TR 


8000 
12500 
10500 


11750 


12500 
15400 
33750 
12330 
25250 
17500 

9750 


11250 


9500 
8250 


7500 





¦ 15000 
· 14000 
13660 


10000 
. 6000 
| 8500 


9000 


13660 
14600 
12250 
15500 
10000 





3250 
4250 
8250 


4750 


8250 
11000 
24500 

6830 
14000 
10160 

5500 


4500 
3500 
4250 


3000 


5950 
2000 
3750 


3000 


6830 
7200 
5750 
6000 
4750 


*-* 


4750 
8250 
7250 


7000 


4250 
4400 
9250 
5500 
11250 
1340 
4250 


RABBIT 





6750 
4000 


RABBIT 


GIGS oe 
| 


Day. Weight. (Total Leu. did ides Leu. Mon. Leu. 


4750 
4000 
4750 


6000 
6830 
7400 


9500 
5250 








= == 


$ agar culture, 48 hours old living 
staphylococcus aureus in salt 
solution, subcutaneously. 


| 
| 
| 
| 


«Uu 99 
. 


ES EE ES ES ES c n ae 


3 agar cultures, 48 hours old living 
micrococcus rheumaticus in salt 
solution, subcutaneously. 


tt Vy.” 


8 agar cultures, 48 hours old living 
, micrococcus rheumaticus in salt 
solution, subcutaneously. 


A CASE OF SUBDIAPHRAGMATIC 
AND HEPATIC ABSCESS CONSECUTIVE 
TO MEDITERRANEAN FEVER. 


By J. W. H. EYRE, M.D., anp J. FAWCETT, M.D. 


In writing of suppuration, the statement has been made by one 
of us! that almost all the micro-organisms pathogenic for 
man possess the power, under certain conditions, of initiating 
purely pyogenic processes in place of, or in addition to, their so- 
called ‘‘ specific actions "—the pneumococcus, and the tubercle 
bacillus, being quoted as familiar instances in support of the 
contention. Additional support is afforded from time to time 
by evidence obtained from the clinical laboratories of our hospitals 
during the routine examination of pus from various lesions. 
Thus at the present time JB. influenze is one of the few 
pathogenic microbes that has not been conclusively shown 
to be capable of taking on a pyogenic róle. Until recently 
Micrococcus melitensis was regarded as another exception, for 
although in many cases of Malta Fever serous effusions have 
been noted (and recorded as probably directly due to the 
activity of this coccus), suppurative lesions, possibly on account 
of their extreme rarity in this association, had not so far been 
attributed to the coccus. During the summer of 1903, some 
observations on the results of the intracranial and subdural 
injection of M. melitensis into rabbits and guinea-pigs indicated 


1 Art. Pyogenic Bacteria (Eyre). Quain’s Dictionary of Medicine. 
Third Edition. 1902. 


308 A Case of Subdiaphragmatic and Hepatic Abscess 


the probability, however, that localised collections of pus might 
well result, in man, from the active multiplication of this 
organism. Тһе lesions produced at, or near, the seat of inocula- 
tion in the lower animals varied in subacute and chrdnic infec- 
tions from localised membranous exudation to suppurative 
meningitis and small pockets of pus. 

Later on, in a case which recently came under our notice, the 
evidence of the causal relationship ot M. melitensis to the sup- 
purative process was so clearly established as to encourage us 
to record it in the hope of eliciting further observations on the 
subject from those who have better opportunities than ourselves 
of investigating the disease as it occurs in man. 

To Mr. Jacobson, under whose care the patient was admitted, 
we tender our thanks for his kind permission to publish the 
details of the case. 

CLINICAL OBSERVATIONS. 

G.T., æt. 38, a coal porter, was admitted into Naaman ward, 
Guy’s Hospital, on July 25th, 1908, suffering from abdominal 
pain. 2 

The patient had been in India for six years and in Malta for 
two years, and in the latter place he contracted Malta Fever.’ 
Since this time he had no illness until the one for which 
he was admitted. 

History of present illness.—Eleven days before admission, that 
is on July 14th, he suddenly felt pains in the stomach while at 
work. He continued at work the following day, but was unable 
to do so afterwards. The pain was continuous and worse on 
standing, or moving about. 

Condition on admission.—A smooth round tender mass, thought 
to be connected with the left lobe of the liver, was felt in the 
epigastrium. The liver dulness extended upwards, higher than 
normal, but the lower edge of the right lobe was not palpable. 
On inspection, the right hypochondrium appeared to be some- 
what more full than the left. A leucocyte count gave 11,400 per 
c.mm. 

The temperature varied from subnormal to 100:6? F. 


? Unfortunately precise data on these points are lacking. 


consecutive to Mediterranean Fever. 209 : 























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July 27th. Mr. Jacobson explored the swelling in the epigas- 
triumYand opened an abscess which was not in the liver, but 
which formed a localised intraperitoneal collection. From this 
date the patient’s progress was on the whole satisfactory, and 
he was discharged on August 25th, 1903, with the wound almost 
healed. 

October ‘2nd. The patient was re-admitted owing to the 
abdominal pains having returned within the last fourteen 


210 А Case of Subdiaphragmatic and Hepatic Abscess 


days. He had also had a “shivering fit," followed by profuse 
perspiration, every day during this period. He looked sallow 
and ill, much more so than on his former admission, and his 
temperature chart (quod vide) showed larger morning and evening 
variations than previously. There was marked fulness in the 
right hypochondriac and epigastric regions, and the upper edge 
of the liver dulness presented a curved line running convexly 
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rib in the middle line in front. By the request of Mr. Jacobson 
one of us again saw the patient and gave the opinion that the 
patient was suffering from a subdiaphragmatic abscess. 

October 8th. A specimen of blood was collected from the 
lobe of one ear and the serum obtained therefrom yielded a 
positive reaction when tested against the M. melitensis. 

October 18th. Mr. Jacobson again operated, on this occasion, 
through the right pleura, and after resecting a portion of a rib 


212 A Case of Subdiaphragmatic and Hepatic Abscess 


and taking careful precautions to shut off the pleural cavity, he 
incised the diaphragm and opened a large abscess cavity beneath it. 
The pus contained therein was thick and of a greenish colour. No 
indication was obtained at the operation as to the cause of the 
abscess. Although the temperature was somewhat lower after 
the operation, it still showed variations from subnormal to 101? F. 
The patient’s condition did not materially alter, and he died 
sixteen days later, on the 29th October, 1903. 


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consecutive to Mediterranean Fever. 218 


Dr. A. Е. Boycott (Gordon Lecturer on Experimental Path- 
ology) performed the autopsy, thirteen hours after death, and 
the following abstract is from the notes made by him :— 

Inspection, 1903, No. 409.—Lungs and pleura.—Right side.— 
Recent pleurisy with thick lymph over the lower lobe and 
between the lobes. In the lower lobe was a large irregular 
cavity with ragged walls, full of thick pus and broken-down lung 
tissue; the contents were odourless. A similar cavity was 
present in the lower part of the upper lobe. Left side.—In the 
lower part of the upper lobe was a small abscess cavity the size 
of à pea, containing thick, yellow pus, and higher up another 
small abscess. 

Abdominal viscera.—The diaphragm on the right side was 
firmly fixed by recent adhesions to the corresponding lung, and 
to the liver, and in the middle of the adherent area was a hard 
white scar. There was no evidence of any recent extension of 
inflammation from the liver to the right lung. | 

The anterior surface of the right lobe of the liver was iieri 
adherent to the scar of the first operation wound, and below 
this a large cavity extended into the substance of this viscus. 

The cavity had cartilaginous walls and thick, yellow, slimy 
contents. In the right lobe there was also a number of abscesses, 
irregular in outline and without any definite walls, and filled 
with thick yellow pus. Microscopically, sections of the liver 
showed large areas of necrotic liver substance, the cavities 
having no definite limiting membrane. 


BACTERIOLOGICAL OBSERVATIONS. 

A specimen of the pus was removed at the first operation 
(July 27th) for bacteriological examination. No suspicion was 
apparently entertained at this time of a connection between the 
previous attack of Malta Fever and the existing abscess, and the 
pus sent to the laboratory was merely stated to have been removed 
from an ‘‘ abdominal abscess." The specimen was consequently 
examined in the routine manner, that is to say, a coverslip film 
preparation stained with carbolie methylene blue, and another 
stained by Gram’s method, were examined microscopically. As 


VOL. LIX. 16 


214 A Case of Subdiaphragmatic and Hepatic Abscess 


no micro-organisms could be dgtected a third film was stained 
by the Ziehl Neelsen method and examined for the presence of 
tubercle bacilli, but again the result was negative. A tube of 
nutrient broth was inoculated with a small loopful of the pus and 
another tube containing an ordinary nutrient agar slant was 
inoculated with a similar amount of pus. The tubes were 
incubated at 37° C. and examined at intervals of twenty-four 
hours until the end of the fourth day, when, being still sterile, they 
were destroyed, and the negative result recorded. If ordinary 
pyogenic cocci or B. colt had been present this procedure would 
almost certainly have revealed their presence. 

About two months later, on October 8th, the clinical 
symptoms prompted the collection of a specimen of the patient's 
blood in order that the serum might bs tested for the presence 
of agglutinins. The serum diluted with sterile saline (0:5 per 
cent.) solution was tested against an eighteen hour broth cultiva- 
tion of B. typhosus and a forty-eight hour broth cultivation of 
M. melitensis, the latter being previously filtered through 
sterile filter paper to remove any small preformed masses 
of cocci. The serum dilutions employed in each case were 1: 20 
and 1:200 and the time of observation limited to half an hour. 
The test as carried out against the typhoid bacillus was com- 
pletely negative, even the 1: 20 dilution showing no evidence of 
clumping of the bacilli at the end of thirty minutes. 

When, however, the М. melitensis preparations were 
examined the cocci were found to be completely agglutinated 
into large masses—no cocci could be seen free in the field--in 
both the 1:20 and 1:200 dilutions within twenty minutes, while 
the control preparations of cocci and sterile broth examined at 
the same time showed active Brownian movement without any 
trace of “clump ” formation. 

The specimen of pus removed for examination at the second 
operation (October 13th) was received in the bacteriological 
laboratory as “ specimen of pus from liver abscess." Consequently 
fresh films were examined microscopically for the presence of 
amoeba dysenterie, but with negative results. Microscopical 
examination of stained film preparations showed the presence 


consecutive to Mediterranean Fever. 215 


of a very few minute spherical bodies which did not retain the 
stain when treated by Gram’s method, but no other micro- 
organisms could be detected. 

A glycerine agar slant cultivation was then made, and in view 
of the small number of organisms present a large platinum loop 
was employed and about two milligramines of the pus planted on 
to the surface of the medium ; а broth culture was also made and 
both these cultivations were incubated wrobically at 37° C. 
(Two control cultivations were prepared and incubated an:robi- 
cally at 37° C., but as no obligate anzrobic organisms made their 
appearance, the culture tubes were discarded after eight days’ 
observation.) 

At the end of some forty-eight hours’ jncubation two small 
colonies had developed upon the agar slant culture, which on 
subsequent microscopical examination proved to be composed of 
minute micrococci similar in size to those noted in the film 
preparations made direct from the pus. When sub-cultivated 
upon various media and tested against the highly diluted serum 
of a rabbit immunised to an authenticated Malta Fever coccus 
the organism proved to be indentical with M. melitensis, and is 
still kept under cultivation in our laboratory collection as strain 
No. о. | 

No other micro-organisins were detected, although the original 
cultivations were kept under observation for a considerable 
period. | 

At the autopsy, on October 30th, the specimens secured for 
bacteriological examination included (1) blood from the right 
ventricle of the heart, (2) swabbings of sero-pus collected from 
the sinus leading from the operation wound to the upper surface 
of the liver, (3) pus from the liver abscess, and (4) the entire 
spleen. | 

The results obtained may be briefly summarised as follows :— 

1. The heart blood on cultivation gave evidence of the 
presence of bacillus coli; but M. melitensis could not 
be detected. 

2. Cultivations were established upon glycerine agar and 
in broth. After incubation at 37? C. for forty-eight 


216 А Case of Subdtaphragmatic and Hepatic Abscess 
consecutive to Mediterranean Fever. 


hours а mixed growth resulted in each of the tubes, 
consisting of B. coli, Staphylococcus aureus, and S. 
albus, and M. melitensis. 

8. Cultivations prepared from the liver pus yielded a mixed 
growth of B. coli, Staphylococcus albus and aureus, 
and M. melitensis. 

4. The spleen surface was thoroughly seared with a red 
hot iron and incieed with a sterile knife. Several 
glycerine agar slants were then inoculated each with 
a loopful of the spleen pulp taken from the centre of 
the organ. Each tube after incubation yielded a 
pure growth consisting of a few colonies, usually 
two or three (none more than three), of M. melitensis. 

In considering these results, it may be concluded that the 
presence of B. coló was in all probability the result of the 
usual post-mortem infection from the alimentary canal, for 
thirteen hours had elapsed between death and the post-mortem 
inspection, and during that interval the body was not kept in 
an ice chamber. 

Further, in view of the result of the bacteriological examination 
of the pus obtained at the second operation (October 13th), the 
demonstration of Staphylococcus aureus and S. albus in pus 
obtained at the autopsy, sixteen days later, may fairly be assumed 
to indicate nothing more than secondary infection of the sinus 
and liver cavity from the skin surface around the wound. 

Therefore, by a process of exclusion, supported by analogy 
derived from animal experiment, M. melitensis remains as the 
organism standing in causal relationship to the pyogenetic 
process observed in this case. | 


[The expense of the inoculation experiments necessitated by this investi- 
gation was defrayed out of a grant from the Royal Society.) 


E asp iis 





M oup try... os 


Pus ЧЁ 


Growths of the Kidney and Adrenals. 





Four-fifths natural size. 


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Growths of the Kidney and Adrenals. 


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Fic. 6. 


DESCRIPTION OF Fics. 5 AND 6. 


These figures represent the kidney removed by Mr. Golding-Bird from case 70. 
The upper end and inner border of the kidney are intact and healthy; the 
growth is situated in the lower end. It possesses a definite capsule which is 
continuous with the kidney capsule, with a fibrous boundary which marks it 
off sharply from the renal tissue, and with the septa which divide the growth 
itself into nodules. Thus the growth consists of a collection of rounded masses 
lying beneath the kidney capsule, and separated from one another and from 
the renal tissue by fibrous partitions. Externally (Fig. 5) some of these 
nodules show a tendency to herniate through the capsule, but none have as yet 
penetrated it. 


The pelvis is not invaded, but is compressed, and those calyces which pass to 
the lower end of the kidney can be seen in Fig. 6 as flattened tubes running 
outside the capsule of the growth. The centre of the growth is occupied 
(Fig. 6) by a very irregular cavity with fibrous walls, which contained old blood- 
clot. It was not possible to demonstrate any connection between this cavity 
and the pelvis. A probe can be passed in several places nearly to the surface of 
the growth in the neighbourhood of the bosses shown in Fig. 5. It is possible 
that this is a hematoma of some standing. In other parts the growth, which 
was naturally whitish, was stained presumably by old blood pigment. 


At the upper left hand edge of Fig. 6 the growth rises abruptly from the 
kidney, but over the junction represented by a dotted line in Fig. 5, the transi- 
tion is gradual, and on making а small incision it can be demonstrated that here 
the kidney forms a kind of cap to the tumour, and that the renal tissue gradually 
thins out over it, till finally only capsule is left. 


The large veins which are seen in an empty condition in the capsule have been 
found in other cases a source of great difficulty to the operator. 


The growth, as a whole, is a typical instance of the nodular form as contrasted 
with the infiltrating (p. 237), and shows the macroscopic characters which are 
connected with adrenal rest growths (p. 241). 


Sections were examined from two different parts of the growth, but although 
the appearances suggested an adrenal origin, they were not definite enough to 
justify a decided opinion, and the examination must be considered inconclusive. 
The consideration of the macroscopic, microscopic, and clinical evidence 
together is in favour of this origin, but does not prove it. 


GROWTHS OF THE KIDNEY AND 
ADRENALS. 


By OWEN RICHARDS, M.B., В.Он. 


In the last twenty years a large number of cases of these growths 
have been recorded, and the technique of nephrectomy has been 
much improved. Nevertheless, the results of treatment compare 
unfavourably with those obtained in other forms of malignant dis- 
ease. This is due partly to the difficulty of making a sufficiently 
‚ early diagnosis, partly to the absence of any certain indications as 
to which cases ате fit for operation. for it is clear that while some 
forms of growth persist for years without metastases, and can be 
totally and permanently removed others disseminate widely in. the 
course of as many months, and are inoperable before they become 
evident. What is needed at the present time is not so much the 
description of rare and anomalous forms of growth (interesting as 
these are from the point of view of pure pathology), as the deter- 
mination of the life-history of those types on which pathologists are 
more or less agreed. If these could be brought into relation with 
clinical signs, and the means of diagnosis so extended and applied as 
to ensure their recognition in an early stage, vastly better results 
could be obtained. As Dr. Kelynack remarks, “ The indiscriminate 
removal of renal growths is neither reasonable nor reassuring "—but 
at present the means of discrimination are inadequate. 

In the present paper those cases of primary renal and adrenal 
growths have been collected which occur in the records of Guy’s 
Hospital between the years 1826—1904. Регігепа], secondary, and . 
small innocent growths have been excluded. The clinical and post- 
mortem records are usually full; histological examination is lacking in 
the earlier cases, and not always decisive, for reasons given below, 
in the later ones. The value of the series is therefore chiefly clinical, 
and as the majority of cases were not operated on, it gives a fair 


218 Growths of the Kidney and Adrenals. 


picture of the natural course of the disease. The cases have the 
great advantage of being entirely unselected, but their number 
(seventy), is a small one to draw numerical conclusions from. 

As regards the arrangement an attempt has been made, 

A. Toclassify the ordinary forms of growth, and give a short 
account of what is known of their life-history and peculiarities. 

B. To consider the clinical course of the cases which have 
occurred in Guy’s Hospital, with special reference to the duration of 
symptoms, and the time and manner in which metastases occurred. 

C. Toreview the available means of diagnosis, and the results 
which have been obtained in the past; and to formulate some 
practical conclusions. 

References to the authorities quoted, and to others, will be found 
in an appendix, arranged alphabetically. A short note of the 
contents of each paper is given (instead of its actual title), and the 
year in which the communication was published ; the references to 
pages which follow authors’ names refer to their original papers, and 
where several papers are by the same author a number is prefixed to 
shew which is referred to. A good bibliography up to 1898 is to be 
found in Dr. Kelynack’s book. This list of references makes no 
claim to completeness, but contains some of the more recent 
work accessible in London, | 

The most important contributions that have appeared lately on 
this subject are those of Walker, Heresco,? Kelynack,? and 
Morris The two last named authors treat the subject as a whole ; 
Heresco deals with the question of operation and its results, as 
shewn by a series of 165 nephrectomies between 1890 and 1899; 
and Walker reviews the pathology, diagnosis and treatment of the 
growths occurring in children, as illustrated by 142 cases and 74 
nephrectomies. A vast deal of pathological work has also been done 
in Germany, especially on those tumours which are referred to the 
growth of adrenal rests. 


1. ‘ Sarcoma of the Kidney in Children.” Annals of Surgery, xxvi. 529, 1897 


2. “ De l'intervention chirurgicale dans les tumeurs malignes du rein." 
Thése de Paris, 1899. 


3. “ RenalGrowths." 1898. Young J. Pentland, Edinburgh and London. 


4. ‘Surgical Diseases of the Kidney and Ureter." 1901. Cassell & Co., 
London. 


Growths of the Kidney and Adrenals, 219 


A.— PATHOLOGY. 
CLASSIFICATION, 

The classifications suggested by Mr. Paul and Mr. Reginald 
Harrison are founded on a division into congenital tumours, and 
those of adult origin. Since many tumours which originate in 
embryonic misplacements make their first appearance in adult. life, 
this criterion is a difficult one to apply with certainty. Dr. Kelynack 
adopts Dr. Newman's grouping, which is as follows: 

(A) Benign. 1. Fibromata: 
a Minute growths, ‘‘ Nephritis interstitialis 
tuberosa.” 
b Simple fibroma. 
c Fibro-cystoma. 
d Fibro-myoma. 
e Fibro-lipoma. 
. Osteoma. 
. Lipoma. 
. Hamatangioma. 
. Adenoma: papillary and alveolar. 
. Papilloma. 


yy © © & WH t 


(B) Malignant. 7. Carcinoma: 
a Encephaloid. 
b Schirrus. 
c Colloid. 
d Epithelioma. 
e Cylindroma. 
8. Lymphadenoma. 
9. Sarcoma: 
a Round-celled. 
6 Spindle-celled. 
c Alveolar sarcoma. 
d Angiosarcoma. 
e Adenosurcoma. 
f Myosarcoma. 
g Myxosarcoma. 
He suggests for use in the future some classification on the 
principle of that recommended by the Royal College of Physicians 


220 Growths of the Kidney and Adrenals. 


(1896), in which tumours (other than cysts) are divided into 
sarcoma, carcinoma, those composed of some form of fully developed 
connective tissue, and those resembling a complex tissue. 

In the present paper a classification on the principle of Hanse- 
mann’s has been employed, based on the origin of the growths, and 
the extent to which they differ from the fully developed tissue. 
ADRENAL GROWTHS. 

Adenoma and “adrenal rest tumours” of the adrenal. 

Sarcoma (? carcinoma). 

RENAL GROWTHS. 
I. From the connective tissue framework, 

a Growths of fully formed connective tissue. 
b Sarcoma. 

II. From the vessels. 
a Angeioma. 
b Endothelioma. 

III. From the epithelium. 
a Adenoma—papilloma. 
b Carcinoma—epithelioma. 

IV. From included tissues. 
* Embryonic” mixed tumours of children. 
Adrenal rest tumours. 

This method of division is simple and has the advantage of clearly 
defining the growths in Class IV., which are responsible for a good 
deal of confusion in the past, as it is difficult to classify them on any 
purely histological basis. It could, perhaps, be further simplified by 
disregarding the angeiomata, and grouping the endotheliomata under 
the heading of sarcoma. 


DIFFICULTIES PECULIAR TO RENAL GROWTHS. 


One of the causes of the confusion which rezgns over the pathology 
of these growths is the situation of the kidney at a kind of develop- 
mental cross roads, so that different tissues becou.e mixed up and 
included in one another. 

The origin of the adrenals is not absolutely certain, but according 
to Keith, the medulla is developed from the cell basis of the semi- 
lunar ganglion, and the cortex from the endothelium covering the 


Growths of the Kidney and Adrenals. 221 


Wolffian ridge, which subsequently invades and replaces the medulla. 
The pelvis and collecting tubules of the kidney arise from a diverti- 
culum of the Wolffian duct near its entrance into the cloaca; this 
grows upwards to join the rest of the organ, which is formed from 
the intermediate cell mass. 

In the foetus of two or three months, according to Grawitz, the 
adrenal is bigger than the kidney, and lies round it, separated only 
by the cells which give rise to the capsule, and covering the whole 
of the organ except the hilum and part of the surface below this. 
Later, the two organs are about the same size, and ultimately the 
adrenal becomes a much smaller mass applied to the head of the 
kidney. The kidney is originally lobulated, and the clefts between 
the lobules gradually close. As the adrenal shrinks upwards por- 
tions of its substance become fixed in these clefts, or to the surface 
between them, and form “rests” of adrenal tissue in the kidney 
capsule; while if the fixation is at the bottom of a cleft, they may be 
actually embedded in the renal substance. Grawitz gives instances 
(1. р. 826-7) where these rests were found in clefts that were still 
recognisable. Sometimes small masses of perirenal fat are included 
in the same way, either alone or in company with adrenal rests 
(Horn, p. 209). 

In the same way renal or Wolffian tissue is (less commonly) 
carried up into the substance of the adrenal, as described by Ricker, 
and well illustrated by case 53 of the Guy’s Hospital series; while 
in the reverse direction Wolffian rests are usually, adrenal rests 
fairly commonly, and renal rests ‘quite conceivably carried down by 
the descent of the genital gland to any point between the kidney and 
the testis or ovary. 

A second source of misplaced tissue in the kidney is found in the 
tubules of the suppressed Wolffian body, which are considered by 
many authorities to be the origin of “ embryonic” tumours arising 
in childhood. In this way there are at least two possible extra-renal 
origins for a tumour which is clinically renal, viz., one adrenal and 
the other Wolffian. 

The other main difficulty is the fact that microscopical examina- 
tion often affords no clue, or a misleading one, to the nature and 
clinical history of a renal growth. Allen and Cherry, after a detailed 


222 Growths of the Kidney and Adrenals. 


examination of 29 specimens, conclude that ** a histological structure 
closely resembling carcinoma, with alveolar arrangement, large 
epithelial cells, and bold nuclei, is compatible with clinical inno- 
cence. The macroscopic and clinical characters of a growth are of 
especial importance in estimating the malignity of any renal 
tumour.” 

Mr. Morris is equally decided on this point (iii., p. 1336). °“ Patho- 
logists and practical microscopists have in many instances given 
totally ditferent interpretations of the same tumour. What one 
regards as a typical renal tumour of accessory adrenal origin, another 
speaks of as aspheroidal-celled carcinoma, another as an endothelioma, 
another as an epithelioma with clear cells, another as a renal 
adenoma ; and again other observers have described them as primary 
angiosarcoma, or alveolar sarcoma, or lymphadenoma.” There is 
plenty cf testimony to this confusion, which chiefly concerns two 
classes of tumours, the embryonic and the adrenal rest growths. 
The synonyms of the latter are given above, the former are variously 
described as rhabdomyosarcoma, sarcoma, carcinoma, myxoma, 
adenoma, and various combinations of these. It follows that any 
generalizations based on the clinical course of, e.g., all the cases 
described in the literature as carcinoma would be quite valueless, 
since they would include instances of embryonic sarcoma, adrenal 
rest tumours, and true carcinuma under a common heading. The 
only cases available for drawing conclusions from are those in which 
a pathologist familiar with these peculiar difficulties has examined 
the case as a whole, clinically, in the post-mortem room, and 
microscopically, and has satisfied himself that it belongs to a certain 
class, Even then the personal equation plays a large part. 


ADRENAL GROWTHS. 
1.—ADENOMATA AND ADRENAL REST TUMOURS OF THE ADRENAL. 


Adenoma occurs (Rolleston i.) most commonly as multiple small 
yellow nodules in the cortex, occasionally as a larger single mass. 
Its structure is usually the same as that of the cortex, but it is 
commonly in a more advanced condition of fatty infiltration. 
Occasionally it breaks down centrally to form a cyst (Craufurd, 
Rolleston iii., Bosanquet) or a hematomaoccurs in it. Dr.Rolleston (ii.) 


Growths of the Kidney and Adrenals. 223 


records a fibro-adenomatous form with large vessels, fibrous stroma, 
and no fatty infiltration. In the Guy’s records they are noted 27 
times in the years 1891-8 (Ze, 1 in 146 cases), but their 
frequency varies with the care with which they are looked for. It 
has been suggested that they cause an adrenal intoxication, rise 
of blood pressure, and cerebral hemorrhage; but in these 27 cases 
cerebral hemorrhage only occurs twice, and the absence of symptoms 
is to be expected from their position in the cortex (of which the 
extract is inactive), and their advanced fatty infiltration. True cysts 
and tubes with epithelial lining may occur in them, and in the 
growths which arise from them, and have been variously explained 
as reversions to a tubular type, the results of degeneration or 
hemorrhage, or renal inclusions. The last have already been referred 
to (р. 221). The growths which arise from adenomata are of the 
kind described below as ** adrenal rest tumours,” and since they occur 
more frequently in connection with adrenal rests in the kidney, and 
there present precisely the same characters, they will be described 
in detail under that heading. Unless they invade the kidney, how- 
ever, they do not give rise to hematuria, but present the symptoms 
described under sarcoma of the adrenal (p. 224). 

Grawitz (1., p. 830), gives a good instance of a large lobulated 
growth of the adrenal, without involvement of the corresponding 
kidney, but with metastases in the lungs and liver. This presented a 
typical adrenal structure. Kelly describes one (p. 290) which had 
involved the surrounding tissues and infected the blood stream. 
Mr. Mayo Robson successfully removed one the size of an orange. 
In this case pain had been present for a year, and tumour for a month, 
but the symptoms were not definite enough to allow of the diagnosis 
being made. The patient was well nearly two years later. A wedge 
from the kidney was removed las well as the tumour. Blackburn 
reports a tumour weighing 6 lbs, with no metastases, which was - 
probably of this character. 

The ditference between adenomata, and ** adrenal rest tumours ” of 
the adrenal which have not yet become malignant, is purely one of 
size. Instances are given by Beadles (iv.), Berdez, Blackburn, 
Kelynack (1., ii.), Moxon, Bland Sutton (ii.) and Wiglesworth, of 
masses of this kind in the adrenal As regards their course the 


224 Growths of the Kidney and Adrenals. 


cases show that they may reach a considerable size without giving 
rise to metastases, but that they may ultimately become malignant, 
and kill the patient by dissemination. 


II. SARCOMA AND CARCINOMA. 


The usual kind of growth in the adrenal is a round or mixed celled 
sarcoma, but there is almost as much uncertainty about these 
growths as about those of the kidney. Otto Ramsay, who has 
collected 67 cases, finds the published diagnoses unreliable. He notes 
that the proportion of ‘ carcinoma” is much greater in the earlier 
records, and probably many of the cases so described would now be 
called adrenal rest tumours. The difficulty is illustrated by Green- 
how’s case, where the Committee of the Pathological Society reported 
that it resembled a medullary carcinoma, but was actually a sarcoma. 
However, Manasse 1s clear that his case (28), is a carcinoma, and 
Ritchie and Bruce describe one with an invasion of the lymph glands 
and pleural lymph channels. The question is an open one, but at 
any rate there are not data enough to discuss the forms separately. 
Considered together, it appears that they occur at any age, and that 
the cardinal symptoms are :— 

1. Languor, weakness, wasting. 

2. Gastro-intestinal disorders, nausea, vomiting, diarrhoea, or 

constipation. 

3. Pain referred in various directions. This does not radiate to 
the groin and testis, but rather straight round the abdomen, 
and by involvement of the phrenic to the shoulder tip. 
(Mayo Robson). 

4. Tumour, usually not retrocolic. 

5. Skin changes. In 3 of the 37 that Ramsay found a clinical 
account of, there was bronzing, and in 9 some change of 
tint, e.g., to a dirty yellow. 

Ramsay found that there was no subnormal temperature, as 
Berdach suggests. . Hematuria was accidentally present, and com- 
plicated the diagnosis in two cases. In 5 the symptoms were wholly 
respiratory, in 8 there were none referable to theadrenals. He puts 
the duration at 6-10 months, Affleck and Leith in a smaller series, at 
2-5 months. Clearly then these growths usually run a rapid course 


Growths of the Kidney and Adrenals. 225 


and are hard to diagnose, in none of the operated cases (Morris) was a 
diagnosis made beforehand. Their tendency to extend upwards 
rather than downwards causes respiratory symptoms to occur 
frequently (Sloukoventoff, Turner, West). Involvement of the kidney 
by a growth primary in the adrenal seems to be relatively rare, the 
kidney capsule offers a remarkable resistance to the passage of growth 
either inwards or outwards. As regards metastases the histories are 
rather incomplete, but they seem to occur frequently and widely. 

Apart from discoloration several curious skin changes accompany 
certain adrenal growths. 

In the Museum of the Royal College of Surgeons is a specimen 
(3518 E), found in a woman of 32, who suffered from mania and 
epileptic fits ; and it is noted that her face and extremities were so 
thickly covered with hair that a razor had been used. 

In Knowsley Thornton’s well-known case (iii.) the patient, a woman 
aged 36, was covered all over with black silky hair and had to shave 
her face. An ovariotomy had been performed six years before. 
Knowsley Thornton removed the tumour, which weighed some 20 
lbs., and after various complications, caused by an abscess which 
burst into the lung, the patient made a complete recovery, and wrote 
nine months later to say that she was now normal in appearance, 
had gained two stone in weight, and could walk or drive any distance. 
Unfortunately she died of intraperitoneal recurrence two years 
after the operation." The structure of the tumour “ reminded the 
observer of the structure of an adrenal," and in the preceding case the 
description of large granular epithelial cells in alveoli separated by 
capillaries suggests that both tumours probably belong to the class 
of adrenal rest growths; though these effects are more likely to be 
due to their chronicity than their nature. An instance of the 
successful removal of such a growth is given above (p. 223), and the 
fact that in Knowsley Thornton's case the symptoms had existed so 
long, and the growth reached so great a size, and yet operation did 
so much good, points to such cases as being among those suitable for 
interference. 

Another small group of cases is recorded by Pitman, Colcott Fox, 
and Dickinson. The patients, in each case girls of 2 or 3, had 

*MS. note in R.C.S. Museum Catalogue, 3507 B. 


226 Growths of the Kidney and Adrenals. 


become in the last year or so dull in intellect, fat, and covered with 
hair. They died with signs of exhaustion and vomiting. 

Dr. Walker, of Budleigh Salterton, has kindly sent me notes of 
the following clinically similar case, in which unfortunately the 
precise origin of the growth was not determined :— 


The patient, a girl, was healthy up to the age of 5, when she became very 
stout and a growth of hair appeared on face, chin, and pubes. At 7 years 
this had grown to the average length of that of a man of 20, and the pubic 
hair was that of an adult. She then lost flesh on the face and limbs, her 
abdomen swelled, and a tumour was observed in the left hypochondrium. 
Slight albuminuria, no hematuria. Eighteen months later she was admitted 
to hospital. She then had the facial aspect of a young man of 20, with black 
silky beard and whiskers. Abdomen distended, urine as before. Ascites was 
present, and she was tapped, whereupon the tumour and an enlarged liver 
became palpable. She died a few days later. Post-mortem: Thorax not 
examined. Liver enlarged and full of growth. Left kidney, the size of a 
cocoanut, consisting entirely of new growth. Right kidney about half this size 
and nearly destroyed by growth. Several mesenteric glands enlarged. Pelvic 
organs healthy, and normally developed for the age. 

No proper examination of the growth was made, put the symptoms 
referred to above suggest strongly that the growth was primary in 
the adrenal, since obesity and growth of hair are not found with the 
common renal growths of children, and the age, sex, and course 
correspond closely with the recorded cases referred to above. 

Amongst the Guy’s cases Case 44 is of great interest (p. 317). 

The nature of this is obscure ; the fact that the masses in the 
skin decreased in size, and that one, 5 inches across, nearly 
disappeared, is against their being secondary deposits of an ordinary 
kind. The pathology of mycosis fungoides is hardly worked out. 
Bowen gives the report of a post mortem examination of one typical 
case of this disease in which the only internal lesions discovered were 
a growth extending along the spermatic cord from both testes to the 
pelvic brim, and nodules in one kidney and the ascending mesocolon. 
In this case the enlargement of the testis was the first symptom, and 
in another, not examined post-mortem, it was an early one. All the 
growths in the first case had the same character as those in the skin 
—and their occurrence along what may be called the “adrenal rest 
tract" is suggestive—but nothing more. In this case also some of 
the cutaneous growths had sloughed off leaving pigmented scars. 

A rather similar case 15 one which Chauffard records :— 


Growths of the Kidney and Adrenals. 227 


The patient, a man of 37, was admitted for chronic diarrhoea of a year’s 
duration. He had loss of appetite, vomiting, and lumbar pain. His urine was 
normal, and no tumour could be felt. In his skin were J10-120 nodular 
tumours, in size from a lentil to a nut, sessile, broadly pedunculated, mobile, 
and asymmetrical. The first appeared 5 years ago. In the skin, which had an 
earthy colour, were some 20 irregular brownish pigment patches the size of a 
sixpence, which had increased in number during the last 3 years. No 
bronzing. The patient wasted and died in 5 months. Post-mortem: The 
nodules, microscopically fibromata, were not connected with the nerves, i.e., 
were not neurofibromata. Both adrenals were enlarged to about 10 X 6cm. 
and were of normal shape. ‘The pancreas and adjacent glands were adherent, 
large, and hard. There were no metastases. Histologically the growth was 
more like an adenoma than a carcinoma, and was primary in the capsules. It 
was thus of quite a different character from the growths in the skin. 

In Mr. Morris’ case (2) the skin over the whole body contained 
scattered nodules the size of peas, but they could not be micro- 
scopically examined; һе considered them metastases. It would 
seem that disease of the adrenals, which in some forms produces 
bronzing or discolouration, may in other cases be associated with 
hypertrophy of either the hair or the subcutaneous tissues, apart 
from metastases. The cause or significance of these rare complica- 
tions is unknown, but Thornton’s case would seem to show that they 
do not necessarily involve a bad prognosis. 

As regards the mental defects in some of these cases, and the very 
marked apathy and weakness in nearly all, Alexander’s researches on 
the adrenal as a source of lecithin, and the association of congenital 
cerebral and adrenal defects, are at any rate suggestive. Mr. 
Beadles (v.) gives it as his impression from experience at Colney 
Hatch that these bodies are particularly lable to hemorrhage 
and degeneration among the insane. 

The clinical course of the remaining Guy’s cases will be referred to 


in Section B. 


RENAL GROWTHS. 
CONNECTIVE TISSUE GROWTHS. 


The small fibromata dignified with the name of “ nephritis inter- 
stitialis tuberosa", are considered inflammatory, and are in any case 
insignificant. Small white fatty masses are fairly often found im- 
bedded in the hidney cortex; these may or may not be encapsuled, 
but in the fresh state are clearly defined by their colour. They 


228 Growths of the Kidney and Adrenals. 


were formerly all classed as lipoma, and are indistinguishable by 
the naked eye, but under the microscope they divide themselves 
into lipomata, adrenal rests, and adenomata with fatty cells. 

The lipomata arise in two ways: 

І. Ву conversion of connective tissue into fat (Alsberg, Warthin, 
Beneke). 

П. By inclusion of small particles of fat in the renal inter- 
lobular clefts, comparable to, and sometimes accompanied by, 
adrenal rests (Grawitz, Horn). 

Calculous kidneys may undergo fatty change (Weir 11.), but these 
are not lipomata. Cases of true lipoma are described by Lazarus- 
Barlow, Parkes Weber (iii.), and others. Pure lipomata are rarely of 
clinical importance, though Alsberg removed a kidney enlarged to 
the size of a child’s head by multiple lipomata, and Warthin 
removed one weighing 2 lbs. 

The usual form of connective tissue tumour is-a mixed one, 
composed of fibrous tissue, smooth muscle, fat, cartilage, ete., in 
varying proportions; these occur in the capsule and grow slowly. 
Busse describes one weighing nearly 20 lbs. which was of 25 years? 
duration. 

Heyder has collected 18 cases operated on for this condition. 
None of them were diagnosed before operation. Ovarian cysts and 
hydatid were the commonest suggestions. Of these 9 were 
* successful,” 8 died at once, and 1 in 5 months. He concludes 
that the symptoms are those of tumour without hematuria, or 
those signs of metastases which would be expected with a malignant 
growth of such size and duration. From the results of operation it 
seems clear that any attempt to remove them without a complete 
nephrectomy will fail. If they are left they may end by becoming 
sarcomatous. The fibrous tumour reported by Sir Samuel Wilks, 
and quoted by Busse and others, has been re-examined in the Guy’s 
Museum and pronounced sarcomatous. In this case the patient 
had had hematuria and pain for ten years, and a tumour for six. 
He died of uremia with no secondary deposits. This suggests 
that the growth was for a long time innocent. 

Busse quotes a case of Tillman's, removal of a fibro-myxoma 
weighing 10 kgs., apparently innocent, but fatal from recurrence 


Growths of the Kidney and Adrenals. 229 


within a year. In any case if such a growth were found it should 
clearly be removed with the kidney. 

These are growths in which several kinds of connective tissue 
take part. They possibly originate in a confusion of embryonic 
elements, whence the variety of their structure; and in any case 
there seems to be no advantage in separating them into groups in 
which any one tissue predominates. 


SARCOMA. 


This group has been made to contain a good many diverse 
growths. The embryonic growths are commonly described as 
sarcoma, and the adrenal rest tumours as alveolar sarcoma, There 
are also cases of angeio-sarcoma, whose nature is still under dispute, 
and of lympho-sarcoma, which is said not to be a primary renal 
growth. 

Freitag has attempted to study the residue of “ ordinary " sarcoma 
which is left when these doubtful classes are removed, and finds 
them relatively rare ; he does not attempt to arrive at a clinical type. 
He divides them into two forms—nodular and infiltrating. Of his 
three instances of the nodular form two are, unfortunately, in- 
accessible to me; the third, in a boy of eight (Van der Byl), is not a 
very good instance, as it appears to be embryonic, and no section 
was cut of it. 

His own case, of the infiltrating form, presents very definite 
features. The patient was a man of 65. The disease ran an eight 
months’ course without hematuria, with pain and weakness as 
the chief symptoms, and no tumour till shortly before death. 
Post mortem, there was no glandular invasion, and no metastases 
anywhere, except a nodule in the other kidney. On the other hand 
the growth had directly invaded two vertebra, two ribs, the psoas 
and the posterior abdominal wall generally. It was a typical example 
of direct invasion as contrasted with blood or lymph diffusion. 
The growth microscopically consisted of every grade of cell, from 
a narrow spindle to a round cell— with a few muscle cells—but was 
mainly spindle cells. It could not be determined whether it started 
in the capsule or the kidney framework. 

Freitag's division into nodular and infiltrating forms is probably 


VOL. LIX. 17 


230 Growths of the Kidney and Adrenals. 


due to the description of these two forms of carcinoma, and is 
based on very few cases. Case 28 of the Guy’s series is very 
definitely nodulated, but unless this feature is found to correspond 
to some structural or clinical peculiarity, as is the case with 
carcinoma, it seemis unnecessary to insist on it. The significance of 
nodular torms of growth is discussed after carcinoma. 

Of the Guy’s cases, No. 28 has microscopically the purest sarco- 
matous structure. Except for an attack of pain 4 years ago the 
course of his illness extends over some three months ; there were no 
urinary symptoms, and invasion was chiefly by the lymphatic system. 
No. 60 has marked local invasion. Other cases are Nos. 50, 45, 31, 
etc. No. 60 is a rapid invasion, 2 months; No. 50, 5 months; 
No. 45, about a year; and No. 31, 6 months. 

If one could draw any conclusions from so few cases, it would be 
that the course of sarcoma is a rapid one, and since invasion takes 
place locally as well as by the usual channels, that it is not suited 
for operation. On the other hand one of Rovsing’s cases was well 
15 months after removal of a spindle-celled sarcoma, and the number 
of definite cases is not sufficient to generalize from. Those that 
begin as innocent mixed tumours, and reach a noticeable size before 
becoming malignant, can be removed in this stage. In these, as in 
other growths, everything depends on early exploration. Diagnosis 
without exposure is shown by Heyder’s cases to be practically 
impossible, even when the growth is large; so that waiting 
is no great help in this respect, and increases the chances of 


malignancy. 


ANGEIOMA AND ENDOTHELIOMA. 


Small angeiomata such as occur in the liver are said to be found 
in the kidney—they are rare and insignificant. The only ex- 
ception to their insignificance is when they are situated on a 
papilla, and give rise to continued hematuria. This condition 
is rare, and probably still more rarely recognized, it is possible that 
some cases of the so-called “essential” hematuria are of this kind. 
Mr. Hurry Fenwick (ii., 64) describes some cases of this condition. 
In one the hematuria had lasted for five years, and had been con- 
sidered hysterical, the side affected was identified by the cystoscope, 


Growths of the Kidney and Adrenals. 231 


the kidney appeared normal, but on incising the pelvis а single 
papilla was found covered with varicose vessels, Excision of this 
cured the bleeding. Mr. Fenwick records a precisely similar condi- 
tion in another kidney, cured by excision of the papilla. In another 
case swabbing the papilla with perchloride of iron proved useless, and 
the kidney was removed at a second operation. In two other cases, 
assumed to be of this kind, incision and manipulation cured the 
hemorrhage, without the pelvis being opened, and the explanation 
suggested is that the blood supply to the affected papilla was 
interfered with. This might explain some of the cases of ‘ essential 
hematuria” which are reported cured by exploration. In a sixth 
case, in which hemorrhage had been present for two years, an incision 
made with this intention gave no relief. The kidney was removed; 
and one papilla was found to have a capillary nevus, or angeioma 
(pp. 74, 75). It is by no means clear whether this condition can 
fairly be called a ** growth," but in view of these cases, it is of some 
clinical importance. Other vascular tumours have been described, 
but a vascular tumour is not necessarily an angeioma. Rolleston and 
Kanthack describe a curious tumour with blood circulating in renal 
tubules, but they do not consider it anew growth. A curious vascular 
growth is described by Holmes, in which the patient had suffered 
from hematuria for two years, and, post mortem, the kidney 
(specimen 3591 in the R.C.S. museum) weighed 30 ozs., and had a 
spongy appearance with the spaces filled with soft vascular growth 
and clots. Pulsation and a bruit: were noticed during life. 
Numerous forms of growth have been described as originating in 
vessel walls—angiosarcoma (de Paoli Manasse Driessen), endothe- 
lioma (Manasse Hildebrand), perivascular sarcoma, venous and 
lymphatic endothelioma (Manasse). A certain number of these are 
probably identical with the adrenal rest tumours, and are considered 
so by those who describe them, or by others (Lubarsch). Others 
are apparently different, but no successful attempt has been made 
to lay down rules for distinguishing them (Lubarsch, Нарѕе:лапп). 
Those that are identical with adrenal rest tumours may be classed 
under that head for purposes of study until the real nature <f the 
growth is determined. The rest, which are not clinically very 
numerous or important, may be considered sarcoma. None of the 


232 | Growths of the Kidney and Adrenals. 


Guy’s Hospital cases come under this heading, though in case 45 a 
concentric arrangement of spindle cells round the blood vessels is 
noted. 


ADENOMA. 


Adenomata occur as small round masses immediately under the 
capsule. They are sometimes encapsuled, often not ; and are 
usually, but not always, white and fatty. One form of pseudo- 
adenoma occurs in connection with granular kidneys, and is 
compared by Albarran to the proliferation of ducts which occurs in 
cirrhosis of the liver. Examples are described by Dr. Parkes Weber. 
Of Sudeck’s 4 cases 3 occur in granular kidneys, but he states that 
they are not of this kind. Others occur (Ricker) in connection 
with scar tissue, apparently by the isolation of renal tubules. 
The genuine adenoma is probably a displacement of Wolffian 
or renal tubules during the formation of the gland. Two 
forms are described, tubular and cystic. The third form, the 
* alveolar adenoma” of Wechselbaum and Greenish, has been identified 
with adrenal rests. Instances of the tubular form are described by 
Ricker and Norman, of the cystic by Edmunds and Dalton. The 
latter usually has intracystic papillary growths, or trabecule. It is 
doubtful if they are really different, or merely stages of the same 
growth. At any rate the clinical importance of the latter form lies 
in its occasional malignancy, of which cases are described by Stanley 
Boyd and Kelynack. No case of this kind was recognized in the 
Guy’s Hospital series, though innocent growths of both kinds are 
occasionally noted. A very striking case of this “ malignant cyst 
adenoma” has been recently (1902) recorded by Voigt. 

The patient, a woman of 38, underwent an abdominal hysterectomy 
for an enlargement of the uterus present 3 years. At the first 
dressing a tumour, hitherto masked, was noticed in the left loin. 
The patient made a good recovery, but died in the course of a few 
hours on the second day after she was allowed to leave her bed. The 
cause of death was pulmonary embolism. The left kidney, with the 
exception of the upper pole, was converted into a mass the size of a 
man’s head, septate, adherent to the aorta, with опе or two enlarged 
glands at the hilum. The adrenal was enlarged by growth. The 


Growths of the Kidney and Adrenals. 233 


lumen of the vena cava was invaded by growth, and there were 
metastases in the liver. The tracheal, cervical and retroperitoneal 
glands, the lungs and pleura were also invaded. The uterus contained 
growth in the centre of four of the fibroids of the ordinary kind 
with which it was studded, and a mass was present in the right 
ovary. The tumours were all essentially papillary cysts, in places 
becoming carcinomatous. They were not the least like adrenal rest 
tumours, and were like papillary adenoma of the kidney. Voigt 
discusses whether thev were primary in the kidney or uterus, or 
whether they were the simultaneous development of misplaced 
embryonic tubules. He decides that the growths in lungs and glands 
were metastases from the kidney growth by the blood and lymph 
stream respectively. The growths in the ovary and in the centre 
of the fibroids he thinks are from .their character not the primary 
source, and from their position not metastases. He decides for the 
view that there has been a simultaneous development of rests 
of the primitive kidney in these three situations. This gains 
probability from the demonstration of what may be called the 
adrenal rest tract, i.e., a tract which extends from the under 
surface of the liver via adrenal, kidney, spermatic or ovarian vein, 
to ovaries, uterus, or testes. "That this is a region along which 
embryonic misplacements are likely to occur is shown by the 
discovery at all points of it of adrenal rests, and at several points of 
the tumours which arise from them. If we imagine rests of the 
primitive kidney substituted for adrenal rests in this displace- 
ment (and “ renal” rests in the adrenal have already been mentioned) 
there is nothing a priori impossible in the primary development 
of “renal” adenomata in any of these situations. The growth in 
the uterus is comparable to Mr. Eastwood's uterine adrenal rest 
tumour, that in the ovary to the rests recorded in this situation 
and in the testes by Ulrich and others. Their simultaneous 
development is again comparable to the condition described by 
Beneke as adrenal system disease. In the instance which he gives 
of this, there was present a simultaneous adenomatous growth of 
adrenal type in both adrenals and both kidneys—and a fair proportion 
of cases are found in which adenomata of the adrenal are bilateral. 
The fact that adrenal rest growths in the kidney are usually con- 


234 Growths of the Kidney and Adrenals. 


geries of separate nodules suggests that where multiple rests exist 
several of them are likely to become active at the same time. 

A case of Thoma’s (vol i, р. 576) is of interest in comparison 
with Voigt’s. In this there was an adenocystoma of the kidney in a 
woman aged 38, accompanied by a similar growth in the vaginal 
wall, and he considers them due to a simultaneous development of 
Wolffian rests. Thoma raises the question whether papilliferous 
cysts of the ovary and papillary cystadenoma of the kidney are not 
essentially the same, both originating in the remains of Wolffian 
tubules. This seems on the whole more reasonable than the other 
view, that they take origin from formed renal tubules. 

As regards their occasional malignancy, in Mr. Stanley Boyd’s 
case there seems to have been local recurrence. In Dr. Kelynack’s 
(p. 119, sey.), there was a liver weighing 111 ozs., full of growth, 
a kidney the size of a child's head, with growth extending from it 
into the vena cava, a few nodules in the lungs, and a few small 
glands. The cysts were mostly filled with blood. Some excellent 
figures are given showing the intracystic papillomata, and the 
character of the deposits in the liver and the thrombus in the renal 
vein. In Voigt's case, where the metastases were even more 
extensive, it is noted that parts of the growth were becoming 
carcinomatous. . 

A corresponding ‘ malignant tubular adenoma” has not been 
described ; but in a ease of Mr. Hurry Fenwick’s (ii., 89), where the 
patient had had hematuria for 53 years from a small renal growth, 
Mr. Targett suggests, from the microscopical appearances, that it 
was originally an adenoma of the tubular type, which had lately 
assumed maliguant characters, The nodular form of carcinoma has 
been attributed to malignant change in adenomata. If it is accepted 
that adenomata may develop simultaneously at several points of the 
adrenal rest tract, and also that they may become carcinomatous, it 
is not neceesary to attribute to cystic or other adenoma any power 
of dissemination without change of type, and the term “ malignant 
adenoma” may be rejected in favour of carcinoma, with considerable 
gain both in clearness and consistency. 

That these growths are not malignant from the start is shewn by 
the frequent discovery of minute specimens post mortem, and by 


Growths of the Kidney and Adrenals. 235 


the cases in which they have been successfully removed, even after 
they have attained some size. An encapsuled cystic adenoma, 24 
inches across, was successfully removed by Dr. Edmunds from a girl 
aged 18, and a cystic tumour with. papillary intracystic growth, 
weighing 2 lbs., was remoyed by Mr. Thomas Smith (sub. Willett) 
from a man of 19. The patient made a good recovery, hunted 
through the next season, and was reported well eighteen months 
later. Mr. Hurry Fenwick's case, mentioned above, was well 6 years 
later. 

It would appear then that adenoma may arise either in the kidney 
or in any part of the “adrenal rest tract," and it may arise simul- 
taneously in several situations. It is probably derived from remains 
of the Wolffian body. It may either remain minute, reach some size 
as an innocent tumour, or become malignant and destroy Ше. While 
it is still innocent it can be successfully removed. 

The relation of this condition to cystic kidney, and simultaneous 
cystic disease of the liver and kidney, lies outside the scope of this 


paper. 
CARCINOMA. 


Just as the study of ordinary sarcoma has been neglected in favour 
of embryonic and other growths, or confused by their inclusion ; so 
the ordinary renal carcinoma has been quite thrown into the shade 
by the enthusiastic interest taken in adrenal rest tumours. 

Sudeck and Graupner, however, endeavour to treat of it by itself, 
and agree in distinguishing two forms, the nodular and the 
infiltrating. The naked eye distinction is that the nodular form 
consists of rounded masses of growth situated in a kidney otherwise 
practically normal, from which they are sharply detined ; while in 
the infiltrating form the kidney as a whole is converted into growth 
by a diffuse malignant invasion. 

In the first case we have a lobulated mass with, perhaps, half a 
normal kidney attached; in the second, a smooth homogeneous 
uniform mass of growth with no trace of kidney tissue. Sudeck 
distinguishes microscopically the little polymorphic cells of the 
infiltrating form from the cylindrical vesicular ones of the nodular 
form, which are often loaded with fat, surrounded by a delicate 


236 Growths of the Kidney and Adrenals. 


stroma rich in vessels, and arranged in nodules separated by fibrous 
septa formed from compressed kidney tissue. He considers that 
those instances which are anything more than adenomata, are 
growths arising in adenomata. From his description it would seem 
that he includes in this class those growths which he calls renal 
adenomata, and other pathologists adrenal rests or adrenal rest 
tumours. 

Graupner concludes that in the infiltrating form the character 
of the cells is that of pelvic rather than tubular epithelium, and that 
growth extends from the pelvis outwards along the urinary canals, 
while at the same time it projects inwards into the pelvis and 
causes hematuria. As for the nodular form, it is developed in the 
cortex, either from the convoluted tubules directly, or indirectly by 
malignant degeneration of renal adenomata. 

A case of the infiltrating form is described by Dr. Beadles, and 
several have been reported in which the kidney is little, if ‘at all, 
enlarged, but is wholly converted into growth. 

"Three successive cases of the nodular form are described by 
Terrillon. 

As regards the clinical course, Israel, who gives examples of both, 
draws the following distinction. The nodular form, he says, remains 
long confined to the kidney (п. 313), generally attains a considerable 
size, is easily palpable from its irregular shape, and can accordingly 
be recognized and treated relatively early in its course. The 
infiltrating form on the other hand does not alter the kidney for а 
long time, either in shape, colour, or consistence, and before any 
such change takes place it gives rise to metastases, so that 
diagnosis and treatment come too late. Clinically, then, the nodular 
form will fall among the cases of long duration which are operable, 
the infiltrating among those which are rapid and inoperable. 

While these classes can be more or less distinguished amongst 
the cases from Gruy's Hospital, the fact that the disease has run its 
entire course makes this much more difficult, for even the nodular 
form will ultimately destroy the whole kidney. 

The most difficult distinction is between the nodular form of 
carcinoma arising in adenomata, and the nodular, cortical, slow- 
growing tumours which originate in adrenal rests.  Sudeck over- 





Growths of the Kidney and Adrenals, 237 


comes this by denying the existence of the latter. Another possible 
solution is to deny the existence of the former, but in all likelihood 
both occur. For clinical purposes there is no particular use in the 
distinction, since their course, according to Israel, is not very 
different. 


NODULAR AND INFILTRATING GROWTHS GENERALLY. 


The distinction between nodular and infiltrating growths, whether 
sarcoma, carcinoma, or any other variety, is probably to be found in 
their course rather than their kind. Some malignant growths are 
undoubtedly based on innocent growths which have been present 
for some time. Such a growth, whether connective tissue, gland 
tissue, or adrenal rest, will, in the course of its innocent development, 
form a defined encapsuled mass situated in an otherwise normal 
kidney. If such a mass then undergoes malignant change it will 
alter its structure and disseminate before its gross physical relations 
to the kidney have time to be materially changed. Its fibrous 
capsule is a very effective barrier for a time against infiltration of the 
rest of the gland. On the other hand, a growth which becomes 
malignant before it has developed such a barrier, or a growth of 
pelvic or renal epithelium which is malignant from the start, will be 
limited by kidney-capsule instead of growth capsule, and will invade 
the tissue within this area, ?.e., it will replace the renal tissue before 
deforming or enlarging the kidney as a mass On this view the 
difference is not in the nature of the growth, the resultant sarcoma, 
or carcinoma, may be of precisely the same kind pathologically ; but 
it is developed in a different relation to the fibrous barriers which 
condition its extensioh. If this is so, it is wrong to erect infiltrating 
and nodular forms of growth into real pathological kinds, although 
certain kinds of growth are from their life-history inclined to one 
or the other course. The real distinction is between growths 
primarily malignant, and innocent growths which subsequently 
become so. This corresponds with the clinical differences, and is 
practically most important. It is an essential distinction which is 
found in all the varieties of renal growth, and the division in the 
clinical section into cases of long and short duration is probably due 
to this, and not to the nature of the growths concerned. 


238 Growths of the Kidney and Adrenals. 


PAPILLOMA. 

Josselin de Jong has published (1904) a review of the 52 cases 
recorded up to date. 

He found that these growths were liable to develop simultaneously 
in several places, e.g. pelvis, ureter, and bladder. Those that were 
anatomically benign passed on into carcinoma, and no single instance 
had occurred which was clinically benign, though on the strength of 
а microscopical examination many had been considered so till they 
recurred. The symptoms were those of kidney growth plus hydro- 
or hemato-nephrosis. Diagnosis may be aided by finding fragments 
in the urine, or by seeing a growth at the opening of the ureter with 
the cystoscope. Treatment is in all cases nephrectomy and the 
excision of the ureter low down. 

Drew’s case illustrates these conclusions very well. He found a 
carcinoma of the kidney, a simple papilloma of the pelvis, and similar 
growths in the ureter and bladder which did not invade the wall. 
Metastases were present in the glands and tissues round. The villi were 
delicate and branching, with round or clubbed ends. He quotes 
eight cases, of which 4 were associated with calculi. One of these is 
Knowsley Thornton’s, another is a specimen in the Guy’s Hospital 
Museum. 

Mr. "Hurry Fenwick (i) has published a case which shows the 


importance of an extensive removal of the ureter. 

The patient, a man of 70, had had hsematuria for two years, With the 
cystoscope blood was found to issue from the right ureter. The kidney on 
this side was accordingly explored (by another surgeon), and nothing abnormal 
found. Two years after this, the patient came again, with a history that, 
hematuria had been present since, and that a piece of villous growth had 
been found in the urine. Blood was again seen to issue from the right ureter. 
Accordingly the right kidney was removed and was found to have its pelvis 
full of villous growth, and its cortex honeycombed with cavities lined with 
the same growth. The patient recovered, but returned in a year's time with 
hematuria. Mr. Fenwick exposed the ureter, which contained a papillomatous 
tuft in its upper part, and excised it as far down as the point where it crossed 
the iliac vessels (both specimens are in the Royal College of Surgeons' 
Museum). There was a subsequent recurrence in the scar which was removed, 
and a deposit in the prostate. The patient died uremic 5 years later. 


Mr. Fenwick also mentions a case the converse of this, in which 
à papilloma was seen at the orifice of the right ureter, and removed, 
but a year later Knowsley Thornton was called on to excise the 
corresponding kidney for carcinoma. 





Growths of the Kidney and Adrenals. 289 


These cases show that in this form of growth the pelvis and 
ureter must be considered together, and that a simple nephrectomy 
without excision of the ureter corresponds to partial excision of a 
carcinomatous organ. This is in accordance with their development 
(p. 221). At the same time, while growths of the pelvis almost 
always invade the kidney substance, growths of the renal substance 
practically never affect the ureter and bladder. 

The first of these two cases shows that a papilloma may remain 
practically innocent for some time, though there is no doubt that it 
always becomes malignant eventually. 

Another point illustrated by the first case is the difficulty of 
recognising this form of growth, even when the kidney is exposed. 
In specimen 3591A, of the Royal College of Surgeons’ Museum, 
presented by the same surgeon, the kidney was found on explora- 
tion to be normal; but its pelvis “was distended with some soft 
material.” On removal there was “a carcinoma of the pelvis, in 
places papilliferous.” 

Three cases of this kind have occurred at Guy’s Hospital. 

In case 27 most of the kidney was converted into growth, but 
there was.a projecting mass springing from a point half way down 
the ureter, which suggests that it originated as a papilloma. 

Case 62 had had hematuria for three years, and the pain, which 
came on in the last three months before admission, may have been 
due to the beginning of a glandular invasion. It is quite in accord- 
ance with De Jong’s observations that, although the disease was far 
advanced, and glandular infection had occurred, the growth was 
microscopically innocent. 

Case 64 illustrates the difficulty of recognising this condition at 
the time of operation. Fortunately this form of growth is one in 
which hematuria is constant, and the passage of fragments of 
growth most probable. Cystoscopy may also be of use, for it defines 
the side affected, and may show a secondary growth at the ureteral 
opening. Such a growth is in itself innocent and no contra- 
indication to operation. 


ADRENAL RESTS. 
At the time when Grawitz wrote his original paper (1883), 


240 Growths of the Kidney and Adrenals. 


adrenal rests in the kidney, if observed at all, were described as 
lipomata. Since that time these structures have been discovered in 
a large proportion of bodies in various situations, and Grawitz’ views 
on the origin of tumours from them (1884) have secured general 
acceptance. 

Adrenal rests have been discovered in the liver, the neighbourhood 
of the adrenal, the celiac plexus, the kidney and its immediate 
surroundings, the broad ligament, the spermatic cord and epididymis 
(Schmorl, Ulrich, Targett, Marchand and others). In fact it seems 
that they may occur at any point in a tract which begins in the 
liver, passes through the adrenals and kidneys, and then follows the 
spermatic or ovarian vein to its termination. Of this the upper 
part represents the region in which the adrenal is formed, the lower 
part the descent of the genital gland. 

In the kidney these rests occur as little whitish subcapsular masses, 
which are by the naked eyeindistinguishable from lipoma or adenoma, 
but under the microscope shew the characters of adrenal cortex and 
medulla (Targett Pitt), though they may contain cortex only (Ulrich), 
or a mass may be found consisting entirely of medulla (Eurich). The 
misplacement occurs in the form of inclusion of the whole or a main 
part (Ulrich) of the suprarenal within the renal, capsule, or thin 
plates or multiple tiny nodules are found in the kidney at some 
distance from the normal adrenal These rests are usually situated 
in the capsule, which encloses them and sends offa layer which 
separates them from the kidney. Sometimes separation is 
incomplete, and the two tissues interdigitate with nothing between 
them. (Ricker.) 

The frequency with which adrenal rests are found is uncertain ; it 
varies of course with the care with which they are looked for. In 
the Guy's Hospital post-mortem records for 1892— 1902, twelve 
are recorded, of which, however, only three were confirmed 
microscopically. : 

As they are minute and liable to occur at any point of a fairly 
long tract, a thorough search for them is never made in any ordinary 
necropsy. One successful method is to cut serial sections of the 
foetal broad ligament. Beneke quotes his colleague Schmorl аз 
finding them in 92% of all bodies; probably they occur much more 


= 


Growths of the Kidney and Adrenals. 241 


often than its usually believed. Clinically they are insignificant 
except as the starting point of adrenal rest tumours, and since they 
are common, and the tumours rare, their presence is not in itself 
important. 


ADRENAL REST TUMOURS. 


This name is perhaps the simplest of the many which have been 
applied to a class of tumours which begin with simple hypertrophy 
of an adrenal rest, go on to form a tumour which is in parts quite 
different from adrenal structure, and after a longer or shorter period 
of clinical innocence, disseminate and cause death. They have been, 
and are still, the subject of much controversy, ever since Grawitz 
published his paper in 1884, “On the origin of renal tumours from 
adrenal tissue.” 

The first dispute was between Sudeck, who denied their adrenal 
origin, and Grawitz, Horn, Lubarsch, and many others who affirmed 
it. 

The second chief issue was raised by De Paoli, Driessen, Hanse- 
mann, and Hildebrand, who asserted that these growths were 
endotheliomata. It is possible to take the view that the cases 
reported are of several different kinds, that they are all adrenal, or 
all endotheliomata. Lubarsch and Hildebrand suggest that as the 
adrenal is the type of a perithelioma, any growth arising from it would 
be likely to have this character. Various side issues were raised 
about the presence of cysts and tubes in these growths, their 
glycogen contents, and other points. Reviews will be found in the 
papers of Gatti (1896), Kelly (1898) and in Borst’s “ Geschwülstlehre," 
(1909). 

At the present time there is an almost universal agreement that 
such growths do occur and have an adrenal origin, but their frequency 
and essential character are both much disputed. They have been 
described alternately as carcinoma and sarcoma, either on the strength 
of divergent views of the origin of the adrenal body, which is not 
yet definitely settled, or on pure histological grounds, which are not 
much more reliable. It is probably not far from the truth to say 
that they look like carcinoma and behave like sarcoma. 

The names, * strum suprarenales aberrate renis (event, maligne),” 


242 Growthe of the Kidney and Adrenals. 


(Grawitz); * hypernephroma” (Burkhardt); “tumours of adrenal 
type" (Lubarsch) ; “adenocarcinoma,” and others, all have dis- 
advantages. Borst decides to call them provisionally “ adrenal- 
tumours,” and allots them an appendix to themselves. 

The name used here is in the same way provisional, and begs the 
question of their origin, but it is impossible to denote this class of 
growths by any name whose connotation nobody will be found to 
dispute. The following description is taken largely from Borst for 
convenience. References to the original papers on which it is based 
will be found in the index. 

The first stage of these growths is a simple hypertrophy of the 
adrenal rest. It conforms entirely to the type of normal adrenal 
cortex, 7.¢., it consists of a fine capillary network in the meshes of 
which lie columns or masses of cells, with their bases applied directly 
to the capillary wall. The cells themselves are large, polygonal, 
epithelioid, with a large definite rounded nucleus and granular vacuo- 
lated protoplasm. They are always more or less infiltrated with fat, 
but are not degenerated, as is shown by the good staining of the 
nucleus. They contain glycogen and lecithin. When the fat is 
extracted the cells are left as large transparent vesicles, with scarcely 
any stainable protoplasm, but with a very definite limiting membrane, 
like that of a plant cell, (Fig. 1.) 

The second stage is one of departure from the type in 
all directions, and a considerable increase of size of the mass as a 
whole. Instead of showing columns one or two cells broad, the cells 
form irregular masses or much thicker columns. The cells themselves 
become either smaller or larger, and some appear with many nuclei, 


or irregular or giant cells are found. The blood vessels become 
broad venous clefts. This may be called the stage of growth. 
(Fig. 2.) 


The third stage—the stage of malignancy—is marked by a further 
departure from the type in some parts of the tumour. The cells 
become polymorphous, long or branched, lose their fatty contents, 
and vary in every possible way from the normal, with the result that 
some fields resemble carcinoma, others sarcoma, while in others the 
original structure is more or less preserved. In some cases there is 
hyaline degeneration of the vessels (Graupner) In some places 


Growths of the Kidney and Adrenals. 





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This is a portion of the growth represented in Fig. 3 x 420. The field con- 
tains alveoli, bounded by capillaries, and here and there are seen the elongated 
nuclei of the single layer of endothelium which forms their walls. In places they 
are irregularly widened, and here blood corpuscles can be seen in the lumen ; in 
the rest of their course they are visible as a thin dark line, marked by occasional 
nuclei. The cells which fill the alveoli are based directly on the capillary endo- 
thelium ; they are large, polygonal, with large definite nuclei and nucleoli, and a 
fairly clear cell-body with a definite boundary. They are arranged in columns 
several cells broad, cut in different planes. In the recent state they were 
probably infiltrated with finely divided fat, but this has been extracted in the 
course of preparation. In one or two places blood can be seen extravasated 
between the cells. 


Growths of the Kidney and Adrenals. 





Another part of the same growth x 280. In this the arrangement is rather 
less definite, and the cells less regular. Тһе type of structure remains the same, 
but the alveoli are less obvious, the cells vary in size, and a number of anoma- 
lous cells are seen, containing dark granules, or two or more nuclei. One or two 
could fairly be described as giant cells, and one has five nuclei in its periphery. 


Mr. Targett has been kind enough to examine this section, and thinks it may 
be best described as hypertrophy of an adrenal rest. It corresponds to the 
* stage of growth” described on p. 242. The character of the cells and their 
relation to the capillaries are the foundation for the terms ‘‘ epithéliome aux 
cellules claires," and “© endo- " or “© perithelioma," which have been applied to 
adrenal rest growths. 


Growths of the Kidney and Adrenals, 243 


papilliform masses of cells project into the lumen of the venous 
spaces. 

The growth as a whole degenerates rapidly and hemorrhage is apt 
to occur into it. The stages described above are not uniform all 
over the growth, and dissemination may occur at any time, so that a 
microscopical examination cannot decide whether the tumour is 
actually malignant or not. It is in any case potentially malignant. 

Growth occurs from several centres simultaneously, as if the same 
stimulus had acted on several rests. The result is a collection of 
nodules lying immediately beneath the kidney capsule, and separated 
from one another, and from the renal substance, by fibrous septa 
formed from compressed kidney tissue. The origin of these septa is 
shewn by the occasional inclusion in them of degenerated renal | 
tubules. Beyond them is a zone of nephritis shading off into 
healthy tissue. Macroscopically the nodulesjare originally white and 
fatty, but they soon break down centrally and their colours vary with 
the extent and date of hemorrhage. The rest of the kidney remains 
for a long time normal. 

These growths might a priori be expected at any point along the 
adrenal rest tract. Mr. Eastwood has supplied a link by finding one 
in the uterus, and he quotes one of Chiari’s in the pelvis, but the 
commonest ‘site 1s the kidney. 

All sorts of criteria have been proposed for diagnosing these 
growths, but none of them are singly decisive. Great stress has been 
laid on the presence of glycogen; which is absent from the kidney, 
most kidney tumours, and the normal adrenal, but occurs in adrenal 
adenomata, adrenal rest tumours, and tumours of various kinds 
elsewhere (Lubarsch). 

Mr. Targett suggests аз the cardinal features the distinct 
capsulation of the growth and its nodules; the characteristic arrange- 
ment of large cells in double columns without lumina, with their bases 
directly applied to the walls of the capillary network which takes the 
place of stroma; and the tendency to fatty infiltration and 
hemorrhage. 

Mr. Eastwood lays down that any tumour of which part exhibits 
a definite adrenal structure is of adrenal origin, and that others are 


not. 


2 44 Growths of the Kidney and Adrenals. 


The presence of definite adrenal structure is accepted by all 
authorities as being necessary to prove an adrenal origin. Practically 
the difficulties seem to be considerable. While the presence of definite 
adrenal structure is good positive proof, the absence of it in the 
sections examined cannot always be held to prove a negative. In the 
more advanced stages whole regions of the growth may have a purely 
sarcomatous, or more commonly carcinomatous aspect, and while 
many ordinary carcinomata have very likely, as Mr. Targett suggests, 
been referred to this extraordinary class, it is probable that 
as many or more of these cases have been classed as ordinary 
carcinoma as a result of the examination of опе section. 
Mr. McWeeney gives a figure of the “ carcinomatous” part of his 
growth, which elsewhere showed undoubted adrenal tissue, and 
Beneke, Lubarsch, Burkhardt, Busse, Ulrich, and others have 
described similar fields. As Manasse puts it (p. 116) “ То establish 
the identity of tumours arising from adrenal rests, we require the 
proof of adrenal tissue, or of the very characteristic adrenal-adenoma 
tissue. This will naturally not always be possible in tumours that 
have progressed far (weit vorgeschrittenen) and in such cases one is 
compelled to leave the precise histological diagnosis open . v 
Burkhardt (p. 109) points out that the most typical parts are often 
destroyed by hemorrhage, to which their structure renders them 
so liable, while adjacent atypical and less vascular parts survive. 

In deciding the natureof a doubtful growth it is necessary to examine 
several different parts of it, and to consider the clinical and naked eye 
characters, as well as the metastases, for while these may vary 
widely from the original type (Askanazy), yet in some cases (Kelly), 
they may be more definitely adrenal than the primary growth. 
It is not suggested that the principle above stated should be 
relaxed, but only that in cases where the macroscopic characters, such 
as those mentioned by Mr. Targett, and the course of the case, are 
in favour of this origin, while the microscopic evidence is opposed or 
inconclusive (as in Maidlow's case), an open verdict should be 
returned. 

As to the frequency with which they occur, there is no good 
evidence. Bayard Holmesasserts that they form one-third of all kidney 
tumours in adults. Kelly in 3098 necropsies found seven primary 


Growths of the Kidney and Adrenals. 245 


renal growths, of which four were of this kind. Other authorities 
regard them as very rare. It is on the face of it unlikely that they 
occur so much more frequently in Germany as the comparison of the 
literature would suggest. 

Several collections of these cases have been made. Lubarsch (1894) 
gives references to 29, including 3 described by de Paoli as 
angiosarcoma. ^ Burkhardt (1900) collects 19 which have been 
operated on. 

Keferences to 41 cases will be found immediately after the 
bibliography. These exclude de Paoli’s cases, but include two of 
Driessen’s and one of MHildebrand’s, which are published as 
endothelioma. The remainder are all published as adrenal rest 
tumours and possess some sort of clinical histories. Many others 
have been published in the form of museum specimens with no 
history, and cases found accidentally post mortem. 

Rupprecht’s case, which occurred in a child of 23, is also excluded. 

Of these 41, 25 occurred in males, 16 in females. 

The ages vary from 30 to 73, with an average of 50. Twenty- 
eight occur between 40 and 60, and five below 40. 

A few cases have been recorded in which they were found in 
early life. Rupprecht’s case was 23, and Bergstrand's 8. The 
kidney shown in Fig. 4, was considered from its size to be 
probably that of a child, but the specimen had no history attached 
toit. ‘Chere is no reason why they should not occur in children, in 
fact from their origin they might be expected to, but apparently it 
is exceptional to find them below the age of 40. 

Hematuria was present at some time in the course of the case in 
26, and was the first sign in 20 out of 39. Burkhardt found it in 
24 out of 30 cases. Three cases of exceptional length occur, one 
with a history of pain for 20 years, and two with tumour for 35 and 
17 years respectively. In all of these hematuria was the second 
symptom, and marked the beginning of activity of the growth. 

Excluding these, the average duration of symptoms is about 
24 years. | 

In three cases the first symptoms were due to metastases in the 
lungs or bones. In 18 cases, pain, tumour, or both, was the first 
symptom. 


VOL. LIX. 18 


246 Growths of the Kidney and Adrenals. 


The appearances of the growths accord with those described above. 

A complete post-mortem examjnation was made in only 19 cases. 
In four of these there were no metastases, and in the successful 
operation cases we may assume there were none. Of the remaining 
15, 11 shewed metastases exclusively by the blood stream. In 
one there was a general peritoneal infection, and in three there 
was, in addition to infection by the blood stream, some glandular 
invasion—but nothing in the least comparable to the cases of general 
glandular infection described below. 

Clearly the typical invasion of these growths is entirely by the 
blood stream, :.e., to lungs, bones and skin. 
| Twenty-eight of these cases were submitted to operation. Of these 
10 died, eight from the operation, two from subsequent accidents ; 
six died of recurrence or metastases in an average of 11 months ; 
eleven went out well and were not further traced ; and, four were 
well, one, one«and-a-half, six and seven years later respectively. 

Some of the cases ran an apparently short course, but it must be 
considered that in the majority of them the course is only reckoned 
to the date of operation; in others the disease may have existed 
much longer than the symptoms. Some undoubtedly disseminated 
early and widely, but the striking feature of them as a group is the 
long duration of certain cases. 

In Askanazy's case the patient had a tumour as a boy, and when 
he did his military training the belt used to give him pain by 
pressing on it. It then disappeared, and re-appeared at the age of 
53, when it took on rapid growth, accompanied by hematuria, and 
ultimately killed him with extensive metastases. 

Grawitzs case had hematuria for 54 years, and passed definite 
fragments of growth soon after the onset. In the two last years he 
was well enough to take his usual active summer holiday. 

Busse reports a case of 6 years’ hematuria, Manasse one of 5 years. 
Lubarsch gives one with slight pain for 6 years and hematuria for 
3 years before operation. Hildebrand has one with 8 years inter- 
mittent hematuria, Perthes one with 5 years. Ulrich gives one 
with pain for 20 years. Driessen has one with 5 years, and Hanse- 
mann one with 17 years history of tumour. 

Even if all these are not accepted at their face value, it is at least 


Growths of the Kidney and Adrenals. 












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FIG 4. 


Growths of the Aidney and Adrenals. 247 


remarkable that in this small collection of cases, ten, or about 25 % 
should have such long histories, and, taken in conjunction with the 
cases found post mortem (p. 261), it is clear that this form of growth 
may not only exist for some time as a clinically innocent tumour, but 
may allow of good general health and active life (as in Grawitz’ case) 
for years after it has progressed far enough to give rise to 
hematuria. 

There seems to be a general agreement as to the clinical characters 
of this group. Burkhardt lays stress on their long latency, which he 
puts at 4-5 years, their proneness to hematuria, and the size to 
which thev attain without giving rise to metastases. 

Lubarsch describes them as existing for years without symptoms, 
and being stirred into malignancy by illness or accident. 

Perthes remarks on their duration, the slight effect they have on 
the general health, and the way in which their structure disposes 
them to hemorrhage. 

Mr. Bland Sutton (p. 129), states that “though these tumours 
are very vascular, and their central parts are often destroyed by 
extravasations of blood, they do not give rise to hematuria, because 
the tumour does not invade the renal pelvis. This is the most 
striking fact in their clinical history.” 

While this is perfectly true of adrenal rest tumours arising in the 
adrenal, it is impossible to agree with it as regards similar growths 
arising in the kidney. Originally cortical, they might be expected 
not to invade the pelvis, but apparently they often do, and other 
authorities seem to have found the frequency of hematuria, rather 
than its absence, the most striking fact in the clinical history. 

Their method of development and extension is well illustrated Бу 
the two specimens shown in Figs. 3 and 4, of which one is in the 
` museum of Guy's Hospital, and the other was obtained from the post- 
mortem room. 

No representation is given of the ordinary adrenal rest, which is 
simply a minute subcortical nodule or plate. Fig. 3 shows a more 
advanced stage. The capsule has been stripped off, and the growth 
is left partly imbedded in the renal cortex, partly projecting from its 
surface as a mass like a cauliflower. The growth as a whole is 
separated from the renal tissue by a distinct fibrous capsule, formed 


248 Growths of the Kidney and Adrenals. 


partly by a layer continuous with the kidney capsule and extending 
inwards from it, partly by a layer of compressed and atrophied kidney 
substance, which is wholly converted into fibrous tissue. Similar 
septa, continuous with this, extend into the growth itself, and divide 
it more or less perfectly into lobules. At the free edge some of these 
have been torn away with the kidney capsule from which they spring, 
leaving the surface irregularly nodular. The histology of this growth 
is illustrated by figures 1 and 2. 

In the second specimen, (fig. 4), which is the one described by Mr, 
Targett (11), a similar growth is shewn in a rather more advanced stage. 
The growth has not gone on to form a circular mass in the cortex as 
might have been expected, but has involved a segment of the kidney 
from cortex to pelvis, so that it forms a wedge, with its base pro- 
jecting from the centre, its apex reaching the mucous membrane of 
the pelvis. As soon as this apex broke down the growth, which is 
by its structure prone to hemorrhage, would have been in commun- 
ication with the pelvis, and free hematuria would have followed from 
a relatively smalland early growth. Several specimens have been 
deseribed with this wedge-shaped extension, which illustrates one way 
in which early hematuria may be produced. 

The cases which have been referred to this class amongst the Guy's 
records are only three— Cases 58, 69 апа 70, From the fact that they 
all occur in the last four years, it is probable that a good many others 
occurred before, but were not recognized as belonging to this class. 
In none of these three cases is the evidence complete (p. 244). 

Case 58 had hematuria as his chief symptom, without palpable 
tumour. His general health does not seem to have been very much 
affected, as he survived three operations, and ultimately died of 
gastric ulcer after the removal of the growth. When he died, nearly 
a year after the first hematuria, no metastases were found in the 
abdomen, and there is no obvious reason why the operation should 
not have been successful. In Case 69 a profuse hematuria was the 
chief symptom, together with pain caused by the clots in the bladder, 
There was some localized pain on the left side. Cystoscopy, with a 
view of localizing the source of the bleeding, would have been 
impossible; not because of the stricture, which offered less obstruction 
than the prostate, but on account of the quantity of blood and clot 


Growtha of the Kidney and Adrenals. 249 


in the bladder. (The case occurred during my house surgeoncy). 
Post-mortem a small growth was found having the capsular relations 
described above, which had given rise to no metastases. Case 70 
is опе in which a growth had existed as a palpable tumour for a 
year, and was then apparently stimulated to growth by an attack 
of influenza, just as others appear to have been by accident or 
childbirth. A year later, with a large tumour, the patient's general 
health was still unaffected. The urine was normal and there was no 
hematuria. Operation was successful, and the patient, who is still 
in hospital, is doing well. 

These cases illustrate very well the long duration without 
metastases, the early hematuria (in two cases out of three), the 
age incidence (all over 50), and the generally benign and operable 
characters of this form of growth. The first case died accidentally, 
the second was easily operable if there had been any indications for 
exploring the kidney, and the third, after certainly two years' duration, 
and probably much longer, seems in a fair way to recovery. 
The tumour in the last case is figured at the beginning of the 
paper, and a description accompanies the figures. (See Figs. 5 and 6.) 

Summary.—A. form of growth may arise from adrenal rests in the 
kidney which is distinguished microscopically by its subcapsular 
position, its encapsulation, its division into round nodules by fibrous 
septa, its white colour, and tendency to hemorrhage and 
degeneration. Microscopically it presents in some parts typical 
adrenal tissue; in others a structure widely different. Its cells are 
often infiltrated with fat, without being degenerated. 

Clinically it occurs between the ages of 40 and 60, and may exist 
for years with the symptoms of tumour or hematuria before it gives 
rise to metastases or affects the general health. In other cases it 
may disseminate early and widely, usually exclusively by the blood- 
stream. 


EMBRYONIC TUMOURS. 


This name (embryonale geschwülste) is a convenient one for the 
sarcomata occurring in children, which are essentially different from 
the adult growths. They are mixed growths (mischgeschwülste) 
arising from misplaced embryonic tissues, connective or glandular, 


250 Growths of the Kidney and Adrenals. 


occurring sometimes before birth, usually in the first five years of 
life. Roughly most growths occurring under the age of twelve fall 
into this class, | 

It is not settled what is their exact origin. They have been 
referred to the Wolffian body (Birch - Hirschfeld, Targett), but 
Pick, in a review of the question, 1901, puts them back to an earlier 
stage, a displacement of undifferentiated mesoderm, while Mr. 
Shattock is inclined to think that they arise from the kidney. | 

They are composed of round cells, spindle cells, and gland tubules, 
in varying proportions. The glandular tissue is in parts regular, in 
parts converted into solid heaps of epithelial cells (adeno-carcinoma). 
In addition to these partially striated muscle tissue, cartilage, and 
fibrous tissue occur. Since different tumours, or different parts of. 
the same tumour, may either contain any one of these constituents 
to the exclusion of the others, or any combination of them, they 
have been described by a corresponding variety of names. They are 
diagnosed mainly by the age at which they occur and their clinical 
characters. Much confusion has been caused by bracketing them 
with the various adult growths which they resemble microscopically. 

They run a rapid course, generally growing from the hilum and 
expanding the kidney over them. The main symptom is tumour. 
Pain is variable, hematuria relatively rare, and the general health 
for some time unaffected. Metastasis occurs usually by the blood- 
stream but sometimes by the lymphaties. The secondary deposits 
are sarcomatous. 

The most satisfactory account of their structure is that of Birch- 
Hirschfeld, and Walker gives a review. 

In 1894 Mr. Targett took these growths as the subject of the 
Erasmus Wilson Lecture. He described and shewed specimens and 
lantern slides of the growths in the College of Surgeons, and other 
London museums. Several of these are reproduced in Dr. 
Kelynack’s book. The classification was based on the primary 
anatomical relation of the growth to the kidney. An example was 
shewn of the round-celled perirenal growth which arises in the 
retroperitoneal tissues in children, and corresponds to the spindle 
celled and lipo-sarcomata of adults which are found in the same 
situation. ‘lhe growth had originated at the hilum and had distorted 


Growths of the Kidney and Adrenals. 251 


the kidney, it had only invaded the renal tissue at one small spot, but 
had compressed and invaded the ureter. These growths may reach a 
very considerable size without producing any other effect on the 
kidney than a deformity due to pressure. 

The true renal growths were divided into subcapsular, hilar, and 
cortical True subcapsular growth lying tbetween the capsule and 
the kidney, as a subperiosteal sarcoma lies between the periosteum 
and bone, is rare, but may occur and reach a considerable size. The 
specimen shewn (3590 R.C.S.) was 8 inches in length, and was obtained 
from a girl aged 3; it was a round celled sarcoma with no glandular 
elements. Some growths were shewn occurring in the cortex and 
containing various cystic and glandular structures. 'lhe common 
form of growth is that starting in the hilum, which by its growth 
“unwraps ” the kidney and expands its capsule. These tumours are 
in more than a third of the cases bilateral, as in the specimens shewn, 
and in the cases recorded by Abercrombie. Some of these contain 
fibrous tissue and striated muscle as well as adenoma. 

The growths which are primary in the adrenal in childhood, were 
also considered. Anatomically they were found to present the 
following features :— 

1. They produce marked flattening of the adjacent surface of 
the kidney, from which they are separated by a distinct layer of the 
renal capsule. | 

2. They push the kidney directly downwards, thereby rendering 
it unusually prominent, or sometimes the kidney becomes stretched 
like a cap over a part of the tumour. 

3. By breaking through their capsule early in the course of 
the disease, the adjacent kidney is invaded and the size of the 
tumour is thereby materially enlarged, The liver and diaphragm 
likewise become speedily involved. 

4. They are not bilateral like the renal tumours of childhood. 


B.—CLINICAL COURSE. 


INCIDENCE. 
The total number of cases of primary growths of the kidney and 


adrenals which I have succeeded in finding in the Guy's Hospital 
records between 1826 and 1903 is 69, and of these 65 died in the 


252 Growths of the Kidney and Adrenals. 


hospital. A total of 22-805 necropsies were performed during this 
period. This gives a proportion of one case in 350, or about ‘28%. 
The renal growths number 52, with a proportion of ‘22% 
Mr. Morris finds 5 in 2:610, or about ‘29, 
Dr. Kelynack gives in two series, 9 in 4505, or °2%, and 
16 in 1400, or ‘4%. 
Clearly the frequency is about :396 of both kinds together, 
and 296 of renal growths. 


AGE. 


It is generally stated that a large proportion of cases occur in the 
first five years of life, that the period from five to 30 is particularly 
free (Bland Sutton), and that after that date liability increases. 

The Guy's cases are more or less in accordance with this, except 
in the absence of infantile cases, probably due to some point in 
hospital management. 

They occur as follows :— 


Five years and under .. - .. 6 cases. 
Between five and 25  .. ka ix. 9. ug 

5 25 „ 30 .. m .. 4 وو‎ 

" 30 , 40 .. л 4 E E 

5 40 , 50 .. b .. 10 , 

- 50 , 00 .. b 2 2L ee 

E. 60 , 70 .. T wa 14 وو‎ 


The last class represents really a higher proportion than appears, 
as other causes of mortality have. accounted for a good many people 
before the age of 60. So that from these cases it would seem that 
the main incidence began at 25 and increased rapidly after 50. 

As regards sex, there were 57 males and 13 females: and, if the 
embryonic and adrenal cases are excluded, 49 males to 8 females. 
Walker and others find the sexes about equally affected in embryonic 
cases, so that the great difference here is probably partly accidental, 
partly due to the fact of the cases being adults. Dr. Kelynack quotes 
several authorities who find the male cases in excess. He himself 
analyses 135 cases and finds the females more numerous up to 40, ' 
the males at ages above 40 in the proportion of 27—19. 

So that it is fair to say that the proportion of the sexes does not 


Growthe of the Kidney and Adrenals. | 258 


differ much in the younger cases, but, with advancing age the male 
cases become much the more numerous. Growth occurred 34 times 


on the right side, 33 on the left. 


CAUSATION. 


The personal and family history of these cases is generally recorded 
in the original reports, though it has been omitted in the abstracts 
appended to this paper. Asa гше it is good ; certainly there is no 
illness or hereditary taint which occurs with constancy enough to 
have any claim to be discussed as a cause. 

The two conditions which are usually considered as possible 
causes are calculus and injury. 

As regards calculus, it may be primary, or secondary to the growth, 

and if it is primary it must occur with some frequency if it is to be 
considered a real cause. 
. Several cases have been reported in which there was reason to 
think the calculus was primary, as by Walsham and Newman 
(c.f. McCormac), and a large number in which the two conditions 
were associated. Jt would be difficult to estimate the proportion of 
eases showing this combination to those of growth without calculus, 
or calculus without growth, but probably it would be a small one. 

The composition of the calculus is of importance, since a phosphatic 
one is more likely to be secondary to changes in the kidney. 
Rovsing quotes an interesting case where a small concretion passed 
was found to consist of calcium carbonate. The case was operated 
on for calculus, and a growth was discovered containing little centres 
of caleareous degeneration like the one passed. No calculus was 
present. 

In the Guy's series, five cases are associated with stone, viz., 6, 27, 
33, 56, and 57, and there are two preparations in the museum (1703, 
1652), which illustrate the combination. Case 6 has no history. 

Case 27 passed a calculus the size of a pea one year after the 
beginning of hematuria and three years before death. This is the 
case which had a papillomatous growth in the ureter, and we may infer 
(De Jong) that it was associated with a papilloma in the pelvis, and 
that the original growth was probably pelvie, and therefore quite 
possibly caused by the stone. 


254 Growths of the Kidney and Adrenals. 


Case 33 has a small uric acid calculus at the top of the ureter. 
The growth arose “in the head of the kidney,” sparing the lower 
end. It does not sound like a pelvic growth, and calculus can hardly 
be held responsible for growths elsewhere. 

Case 56 is one with a history of 15 years hematuria, many calculi, 
a growth in the pelvis, and no metastases. In this case the 
calculi may quite well have been the cause, though they took some 
time to bring about the result. 

Case 57, like the last, is accompanied with suppuration, and has 
a large branched calculus. Examination of the growth showed an 
epithelioma with squamous cells, and a ** marked bird's nest arrange- 
ment." This points to the growth being pelvic. 

So in three of these cases there is some evidence that the growth 
is pelvic in origin (whereas most growths are cortical), and associated 
with stone. In the other two there is merely the association. On 
the whole, it is probable that in some cases calculus is the 
cause of a malignant growth in the pelvis, though only a very small 
proportion of cases with calculus develop growth, and only a small 
proportion of renal growths are associated with calculus. 

The question of injury is full of fallacies, since it is impossible to 
tell whether the growth was present parr the injury, and how the 
injury affected the kidney. 

Walker discusses the relation of injury to embryonic growths, and 
comes to the conclusion that it cannot be cansidered a real cause. 

In the present series one of the embryonic cases (4) gives a 
history of a blow, and Case 68 (infantile adrenal growth) of a fall. 
Of the adults, 2, 16, 26, 32, 39, 41, 42, 55, 61, 67, have histories of 
some sort of injury. Cases 2, 16, 41, 55, have injuries preceding 
symptoms by periods from seven months downwards. In 26, 
symptoms came on a month after a severe labour, and in 70 after 
influenza. 

Of the others, symptoms came on in 67 in a fortnight, in 61 at 
once, and in 32 in two days; while in 39 and 42, although active 
symptoms seemed to be induced by a fall in one case and a mis- 
carriage in the other, yet tumour and pain had been noticed before 
this date. 

It is possible for the healthy kidney to be injured by an accident, 


Growths of the Kidney and Adrenals. 255 


but the accident has to be a severe one to reach it in its sheltered 
position, What probably happens in most of the cases is that 
growth is already present when the accident occurs. The period of 
latency, of some renal tumours at any rate, is a long one, and the 
cases which are found accidentally post mortem show that they may 
reach some size unnoticed. A growth is affected by injuries which 
would not hurt a normal kidney, and the injury either brings about 
hematuria, or determines the passage of the hitherto benign tumour 
into a malignant state. In 39 and 42, this was apparently the case, 
and in 67, 61, and 32, the interval is short for an entirely new 
growth to originate and give rise to symptoms. 

Busse reports a case where a man fell carrying a sack, and 
immediately developed hematuria, which lasted till within six months 
of his death 6 years later. The injury was considered for purposes 
of compensation to be the cause of his illness. Post mortem, he 
was found to have an adrenal rest tumour, with deposits in the 
lungs. ‘The fall cannot have originated an adrenal rest tumour, but 
it possibly determined its growth, or, at any rate, its bleeding. 

So that it seems probable that while calculus in rare cases is a real 
cause of renal growth, injury is more likely to be the determining 
cause of the progress of a growth already present. 


COURSE OF THE CASES. 


In considering a case of growth of the kidney clinically there is 
no need to discuss whether it is innocent or malignant, for nearly 
all growths which can be recognized during life are ee and 
the few exceptions are very likely to become so. 

The only practical question when once the diagnosis has been 
made, is whether local invasion and metastases have rendered 
operation useless or impossible. No treatment other than complete 
excision need be seriously considered. Coley’s fluid has proved 
useless, and medical treatment is merely palliative. 

As will be seen from the preceding section it is usually difficult to 
diagnose the nature of a growth post mortem; during life it is 
impossible. The most that can be done at present is to study the 
natural history of the cases, and endeavour to distinguish real 


256 Growths of the Kidney and Adrenals. 


clinical kinds which may or may not be found later to coincide with 
the real kinds of histology. 

The most important distinction for the surgeon is between those 
cases which remain long localized and operable, and those which 
become generalized at once. The distinction of next importance is 
bet ween those which infect lymphatics and invade locally, and those 
which disseminate only by the blood stream. For in the second class 
there is the possibility of complete local removal and prolongation of 
life, even if unrecognized metastases are already present. In the 
first, anything like even a local removal is, for anatomical reasons, 
wholly out of the question. 

The adrenal and embryonic cases will be first mentioned, and then 
the remaining cases considered en bloc from the clinical side. 


ADRENAL GROWTHS, 


The cases of adrenal growth in the Guy’s series are 12 in number, of 
which two have already been referred to in the pathological section, 
53 and 44. The others are 3, 15, 22, 30, 36, 40, 49, 59, 65, 68. 

They fall into very distinct clinical types, both as regards their age, 
incidence and duration. 

Three of them occur in children less than a year old, 65, 49, 30, 
and one in a child of 24 (68). 

Six occur between the ages of 25 and 46, i.e., in young adult life 
(cases 59, 40, 36, 22, 15, 3.) 

Thus there is the same interval of immunity that occurs in 
growths of the kidney. 

Again, as regards their duration, case 59 had pain for 44 years 
and tumour for a year. The duration of case 15 is uncertain. The 
remainder, including all the infantile cases, had a maximum duration 
of 8 months, and an average of 4 months. 

Of the cases occurring in infancy, one (65) presented a tumour at 
birth and died in two weeks ; another had rapid generalization in the 
skin and bones from the age of 2 months. The third is a case ofa 
growth which gave rise to no symptoms, and the fourth had had 
tumour for a month, but shewed no other symptoms till a day or two 
before death. | 

Clearly nothing could have been done for these cases. 


Growths of the Kidney and Adrenals. 257 


Of the rapidly fatal growths in adults, the symptoms of pain (in 
one case (40) going to the shoulder), weakness, vomiting, wasting, and 
tumour, with normal urine, occurred in different degrees. In one 
case (40) there were secondary deposits in the skin. In cases 22, 36 
the growth spread through the diaphragm into the lungs. 

None of them give the impression that anything could have been 
done for them. 

Case 59 ran a wholly different course. Assuming the pain to have 
been due to the same cause throughout, the tumour had been in 
existence for 44 years, and it had been palpable for a year. Yet at 
the time of death the only metastases were “ one or two nodules the 
size of a pea” in the lungs. 

None of the viscera were affected, directly or indirectly. It is 
possible that operation at the time when the tumour was first 
discovered would have saved this patient. At the time when it was 
undertaken it was too late. But the operation would have been an 
exploratory one, for there were no localizing symptoms, and no 
mention is made of the weakness, vomiting, etc., which marked the 
other form of growth. As to its structure, the long duration and 
late diffusion by the blood stream are in accordance with what is 
known of adrenal rest tumours ; the microscopic examination neither 
excludes or confirms this. 

Of the rest, four were not examined, and five were small 
round-celled sarcoma. Case 40 is described as carcinoma. It 
has this in common with the case just described, that the glands 
are not infected. 

Cases 40 and 15 are the only two adult cases in which both 
adrenals are the seat of growth, and these and 68 are the only cases 
in which the kidney is invaded. In case 15 the ovaries both contain 
growth in addition, this is either a case of ** adrenal Stem disease," 
or retrograde infection by the ovarian veins. 

Summary.—The Guy's Hospital cases of primary adrenal growth fall 
into two different classes. 

1. A rapid growth occurring in 4 infants and 6 adults, spreading 
locally by extension, and diffusing by both lymph and blood channels, 
giving rise to weakness, vomiting, etc., and destroying life in an 
average time of 4 months—inoperable. 


258 Growths of the Kidney and Adrenals. 


2. А slow growth occurring in one adult case, encapsuled, with 
no local extension, and late diffusion by the blood stream only; 
giving rise to no symptoms except tumour and pain, and not 
destroying life for 44 years from the first symptom, during part of 
which period it could have been successfully removed. 


EMBRYONIC GROWTHS. 


In the Guy's Hospital series only three cases of kidney growth 
occur which could be referred to this class, at 2, 11, and 5 years 
respectively. ‘This is much below the usual proportion ; Pick (quoted 
by Kelynack) states that 60% of all cases occur below five years of 
age, and Dr. Kelynack in his own series of 162 cases finds 84 or 529/, 
below 10 years of age, of which 74 were under 5. Probably the 
explanation is that relatively few children were taken into this 
particular hospital. 

Of these cases very little need be said. In case 12 the only 
symptom was a large tumour, which gave rise to no metastases. 
In cases 4 and 47, there is in each case a history of injury. In 
both, the growth extends into the vena cava and thence to the heart ; 
in 47, the pulmonary artery is blocked by it, and the liver is enlarged 
to three times its normal size by- deposits. In none was there 
hematuria, and only transient pain is noted. 

These fully bear out the conclusions quoted above, that the chief 
symptom is tumour, usually without hematuria, and that metastasis 
occurs chiefly by the blood stream. 

In case 12, as the tumour had already been noticed some months, 
it is possible that interference in an earlier stage with modern 
methods might have been successful. Case 4 came in moribund, and 
47 was already rather advanced, for although signs of metastases 
were not present on his admission, his general health had failed for 
some time. 


RENAL GROWTHS IN ADULTS. 


CLASSIFICATION BY METASTASES. 


There are several ways in which a renal growth may disseminate. 
The chief ones are the blood stream, the lymph channels, the ureter, 
and direct extension. 


Growthe of the Kidney and Adrenals. 259 


T. — Dissemination by the blood stream. 


This probably occurs sooner or later in all these growths, it has 
been said to be a character of renal growths rather than of any 
particular kind of growth, so that for purposes of classification 
it is only important when it occurs independently of the other 
methods. 

The usual way in which it occurs is that the growth comes to lie 
free in branches of the renal vein. It then extends to the adjacent 
vena cava, and either cavses thrombosis of this vessel and extends 
upwards as a malignant thrombus towards the right auricle, as in 
cases 4, 55, 60, etc., or fragments are detached and form deposits 
in the lungs, more rarely in the bones of the cranium, ribs, muscles, 
and skin. Another way is for the growth to involve and penetrate 
some branch of the portal vein, giving rise to deposits in the liver. 

In some cases the veins are thrombosed, the clot invaded, and a 
retrograde extension takes place. In case 19 thrombosis reached in 
this fashion down the iliac and femoral veins, and growth extended 
up the portal vein to the liver and down the mesenteric veins to 
their termination in the mucous membrane of the bowel, where it 
produced *'heap-like elevations." А. similar retrograde infection 
along the spermatic vein is reported and discussed by Sutter, in a 
case where the growth extends all down the cord to the testis. 

Two classes of tumours which disseminate in this way almost 
exclusively are the embryonic and adrenal rest growths. In some 
cases the metastases are out of proportion to the primary growth, as 
in a case of Lówenhardt/s, where a deposit in the clavicle had 
existed for four years and reached the size of a man’s head without 
the primary renal growth making its presence known. In case 50 
the only symptom was a deposit in the sternum. 


П. Dissemination by the Lymphatics. 


Here again almost any growth will invade the adjacent glands at 
the hilum of the kidney after a certain time, probably by direct 
extension. Case 7 is an example of a blood extension with one or 
two glands at the hilum, and it is noted that the kidney “could be 
easily turned out " with them, so that they would not have been a 
bar to operation. Oontrast with this case 43, a pure lymphatic 


260 Growths of the Kidney and Adrenals. 


invasion, where the vena cava and lungs are normal, + but the 
mesenteric portal, axillary, and inguinal glands are all infected, 
and case 54, in which the cervical glands are involved. Invasion of the 
liver may occur via the portal glands, and invasion of the pleura is 
noted in case 48 as occurring along the lymphatic channels. 

It is clear that in a certain number of cases invasion takes place 
primarily by the lymph channels. It is necessary to include in this 
class cases where a blood infection has supervened late on an 
original lymph infection—as in case 10, in which lymph infection 
extends down to the inguinal glands and up to the mediastinal, 
but death was brought about by a shower of emboli in the lung, 
noticed at the post-mortem examination to be recent. 

On the other hand, cases where there are only one or two glands 
in the neighbourhood of the kidney—as in Nos. 7, 12, 24, 29, 46— 
may be excluded from this class. 

А good number of cases have invasion by both routes, and these 
fall into neither class, or rather into both. From the surgical 
point of view, both the lymphatic and the mixed invasion render 
local removal impossible; whereas a blood invasion, even with a 
gland or two at the hilum, does not. Of course, no operation would 
be undertaken if metastases were known to be present, but it is 
impossible in any case to be sure that there are none. 


IIL—By the Ureter. 


This mode of extension is probably peculiar to the papillomata, 
and case 27 is the only instance among the Guy's cases. It is 
possibly a question of multiple primary growth rather than 
implantation. In the other forms of growth fragments are often 
passed down the ureter, but they never infect it: 


IV.—Direct Extension. 

This is not common in renal growths, and its rarity is due to the 
presence of a capsule. As suggested above, sarcoma developing in 
rather than within, the capsule, and growths of the adrenal which 
lie outside it, seem to have more marked powers of local extension. 
It is a bar to operation. It occurs in cases 6, 15, 22, 26, 27, 31, 34, 
48, 52, 54, etc. In case 1 there is a direct invasion of the peritoneal 
cavity with peritonitis and multiple growths, 


Growths of the Kidney and Adrenals, — 261 


CASES OF INDEFINITE DURATION. 


Growths found post mortem in patients who showed no symptoms 
during life. 


Two of these cases are adrenal—49 and 53. 

Of these, the latter is a mixed tumour already described, contain- 
ing renal and adrenal tissue, and is essentially an adenoma. Its 
claim to inclusion depends on its size. The former is the size of a 
pea, and is described as a round-celled sarcoma; it occurred in a child 
of eight months, and is possibly the early stage of a malignant growth. 

The remaining cases, 18, 21 and 38, occurred in adults, and are of 
considerable interest. 

Case 18 is described in the * Transactions of the Pathological 
Society for 1875," vol. XXVIL, p. 204. The other kidney was 
granular, and contained—apparently—adenomata. The growth in 
the affected kidney consisted of large round masses, and the cells, 
from their character and infiltration with fat, suggest an adrenal 
origin ; though, as the case occurred 10 years before the publication 
of Grawitz's paper, this was not discussed while the specimen was 
fresh. There were no metastases, but the growth had in many 
places come to lie free in the veins, and there is no doubt that dis- 
semination would ultimately have occurred by the blood stream 
(p. 259). 

In cases 38 and 21. there were no secondary deposits. These 
growths were nodular, alveolated, marked off from the remaining 
kidney substance, and showed hemorrhage into their substance. 
These characters and the transparency of the cells in 21 (ethéliome 
aux cellules claires), and the fact that the growths had reached some 
size without metastases, are all in accordance with what is known of 
adrenal rest tumours, but are not sufficient grounds for referring 
them to that class. At the same time it is noticeable that several of 
the tumours reported as having been found in this way have been 
adrenal rest tumours. Buday describes one in a man of 63, 
encapsuled, nodular, with big glassy cells and fatty infiltration. 
This resembled, in its position in the kidney, the one represented 
in Fig. 1. Driessen describes one the size of a child's head, 
found in a case of pneumonia (case IIL). Ulrich quotes another 


VOL. LIX. 19 


262 Growths of the Kidney and Adrenals. 


(case II.), and Grawitz describes one found in a woman who 
died of an operation for hernia, where the kidney was enlarged to 
three times its natural size by a growth which had given rise to no 
metastases. These four were all definitely adrenal rest growths. 
Dr. Hebb describes a growth in a man brought in moribund; but 
here the growth seems to have caused death by pulmonary embolism, 
though there were no metastases. The patient was walking in 
St. James’ Park when he became faint, and was taken into hospital 
unconscious. The growth was a collection of nodules, and the 
description is not unlike an adrenal rest tumour. Mr. Beadles 
(i., ii, iii) describes seven renal tumours found in lunatics; but 
it is not stated in all of them what symptoms, if any, occurred 
during life. In two there seem to have been none; in one 
hematuria referred to an accident; three of them showed no 
metastases. In the same way growths of the adrenal have been 
found accidentally ; Mr. Wiglesworth describes one the size of an 
orange. 

So that, excluding шейи adenomata and minute growths of 
unknown character, of which many occur scattered through the Guy’s 
records, it seems that ina fair number of instances a renal tumour has 
reached a considerable size without giving rise either to symptoms 
or metastases, and has been found accidentally on the death of 
a patient from some other cause. This is quite consistent with the 
cases mentioned elsewhere in which a tumour has been noticed for 
years before the appearance of any other sign, and with the long 
course of other cases. That the growths are not actively malignant 
for some time is shown by the rarity of metastases; that they 
ultimately become so is illustrated by the relation of the growth to 
the veins in case 18, and by the embolism in Dr. Hebb’s case. 1n 
both of these it was a blood stream infection which finally occurred. 
Some of these cases have been seen to be adrenal rest tumours; 
others resemble them in various characters. It is probable that a 
large proportion of them are of this kind, but there are no grounds 
for asserting that they all are. Any growth which passed through 
a stage of innocence might be found in this way. Their significance 
as illustrating the long latency of some renal окап is independent 
of any guesses at their origin. 


Growths of the Kidney and Adrenals. 263 


CASES CLASSIFIED BY DURATION OF SYMPTOMS. 


The fallacy of this division is that the duration of symptoms is no 
index of the length of the disease. The cases which are found post 
mortem show this clearly. ‘The occurrence of hematuria is an 
accident in the course of the growth; a tumour may be detected 
(Israel) when it is the size of a cherry, or it may remain impalpable 
even when its presence is presumed and its size considerable (case 58), 
while pain is a capricious symptom with many causes. Especially in 
cases in which a large mass is noticed for the first time on admission 
to hospital, we may presume that it has existed for along time 
without symptoms. 

Still this method of division has its РИЯ since the duration 
of symptoms represents the longest interval before the natural end 
of the disease at which surgery can intervene, and the importance of 
early operation cannot be overrated: moreover since the error is 
usually in the same direction the results suffice for comparison. 

We may exclude from consideration the cases of adrenal and 
embryonic growth, one or two cases discharged well, and five which 
were found accidentally post mortem, Of the 46 which remain 
the average duration of life was some two years. They are divided as 
follows :— 

Under six months  .. % .. 18 | 99 


Between 6 months and 1 year .. 4 

Between l year and 2 years .. v3 м 78 
Between 2 and 3 years v3 T ss (0 
Over 3 years .. "^ ёе T .. 10 


Twenty-two, or nearly half, had a course of less than a year, while 
one was alive 12 years from the first symptoms, and one at the end 
of seven years had no metastases. They may be considered in two 
classes—30 of less than two years’ duration, 16 of over two years. 


SHORT CASES. 
1, 2, 5, 8, 9, 10, 13, 16, 17, 20, 26, 28, 31, 32, 33, 40, 41, 42, 45, 
48, 50, 52, 54, 55, 57, 58, 60, 66, 67, 69. 
LONG CASES. 
7, 19, 23, 24, 25, 27, 34, 35, 37, 39 13, 46, 51, 62, 68, 70. 


264 Growths of the Kidney and Adrenals, 


SYMPTOMS. 

Not much is to be gained by comparing the pain in these cases, 
as it is due to numerous causes (p. 267), and is very variable. Tumour 
was noticed in 15 of the short cases, and is not mentioned in 15. 
In the long cases it was present in 12, absent in 3. Hematuria was 
present in 13 of the short cases, absent in 17. In the long cases it was 
present in 12 cases, absent in 4. The metastases in the short cases 
were absent in 3, universal in 9; 7 were by thé blood stream, 9 by 
the lymphatics. In those running a course under six months, they 
were universal in 8; by the blood stream in 4, and by the lymphaties 
in 5. Inthe long cases three are not available (62, 63, 70) ; of the 
rest, 2 were by both, 4 by neither, 1 by the lymphatics, and 6 by the 
blood stream. The only long case (43) in which dissemination was 
chiefly by the lymphatics, is also one of the minority as regards 
tumour and hematuria. Its claim to inclusion depends on a history 
of epigastric pain, worse after meals, extending over 23 years. 

Converting these figures into percentages and comparing them, it 
is seen that in this small series of cases dissemination by both ways 
is commoner in the short cases, in the proportion of 2} to 1, and 
dissemination by the lymphatics, in the proportion of nearly 5 to 1. 
Dissemination by the blood stream, on the other hand, is commoner 
in the long cases in the proportion of 8 to 5. Зо that in these cases 
those of long duration extend by the blood stream rather than the 
lymphatics, those of short duration are relatively much more apt to 
extend by the lymphatics, or by both together. 

As regards symptoms, a definite tumour is noted more commonly 
in the long cases in the proportion of 3t02. This is not important, 
it depends on the metastases in the short cases occurring early, 
before the tumour has time to become palpable, and occurring locally, 
so as to mask it. 

Hematuria is relatively more common in the long cases, in the 
proportion of nine to five, and that this is not the result of their 
length is shown by the fact that it is the initial symptom in more 
than half of them. 

The most remarkable, and clinically the most important, difference 
between these groups of cases is in their onset. 

The long cases‘begin 8 with hematuria, 4 with tumour, 4 with pain. 


Growths of the Kidney and Adrenals. 265 


Apart from these definite symptoms there is, as a rule, not much the 
matter with their general health for some time. Thus case 19 had 
had hematuria for 2 years at the time of his last admission, but he 
had been walking 10 miles daily for the last 9 months about his 
business, 24 boasted himself to have kept nearly continuously drunk 
for З years; 25,35 and 70 were not troubled by their tumours, 37 went 
about with intermittent hematuria for 7 years, 46 bore children, 51 
and 62 seem to have gone about in the intervals of hematuria, 
63 went round various hospitals, and so on. So that roughly, at 
their onset, these cases presented the three classical signs, or some 
combination of them, and nothing else. Their general health was 
fairly good. 

The beginning of the short cases is rather different. Eight (i.e. 
about 1) have a definite hematuria, and three began with tumour. 
Eleven were markedly ill, and this was their first and main symptom, 
and of these, one had paralysis (9), and one (80) presented 
metastases in the deltoid and ribs ОЁ the others, three came in 
for edema or ascites (55, 66, 48) and one for blockage of the 
ureter (52). Case 16 suffered solely from symptoms due to 
metastases in the brain, 40 had subcutaneous deposits before 
admission, and 50 came in for a secondary deposit in the sternum. 

So that these cases, most of them, showed clinically a very 
different picture. In about a third of them hematuria and tumour 
were the first signs, in most of the others illness was the most 
marked feature, and in many of them other symptoms, due to 
metastases or interference with the big vessels, showed that the case 
was hopeless from the beginning. | 

The importance of this difference in the symptoms during the 
early stages is very great. The cases of embryonic tumour show 
(Bland Sutton p. 124) how little the presence of a renal tumour in 
itself affects the general health, and this is borne out in adults by 
the cases of long duration in this series. The * malignant cachexia” 
however, is produced as soon as direct extension or metastases 
affect any vital function, and in the kidney this is likely, for 
anatomical reasons, to occur soon. So that, apart from demonstrable 
metastases, any early failure of the general health, in excess of that 
due to pain or loss of blood, should raise the suspicion that the case 


4 


266 Growths of the Kidney and Adrenals. 


is one of the rapidly malignant group, and the same applies to any 
symptoms whatever, apart from pain, tumour, and hematuria. 

Cases of long duration are by no means rare. A good many are re- 
corded in the older literature. Of the more modern ones some have 
already been mentioned under the heading of adrenal rest tumours, and 
in a specimen of this kind, presented by Mr. Hurry Fenwick to the 
Royal College of Surgeons’ Museum, (A3584B,) there was a history of 
hematuria extending over 34 years. 

Of those that do not belong or have not been referred to this 
class, there is one on which Alm performed a successful nephrectomy 
whieh had had hzmaturia for 6 years and tumour for 3; and 
Kammerer reports a case of a woman: who had had tumour for 
6 years, with a recent rapid increase in size. With the cystoscope it 
was seen that no urine came from the affected side, and the colon 
was inflated and found to pass in front of the lower end of the 
mass, Nephrectomy was performed, and when the patient died a 
month later from an embolism, it was found that there were no 
metastases. Mr. Lunn reports a case with a history of 6 years' 
hematuria, a growth weighing 44 lbs. and projecting into the vena 
cava, and no metastases other than a small mass in the other kidney. 
Mr. Rushton Parker removed a renal tumour which had been 
noticed for more than seven years. The patient died of recurrence a 
month later. No doubt riany other cases could be collected. When 
it is considered that the duration of symptoms is necessarily shorter, 
possibly many years shorter, than the duration of the disease, it is 
abundantly clear that some of these growths run a very slow 
course indeed. 

Other cases may be fatal in a few weeks, as in Brault’s case (11 
weeks) and cases 22 (18 weeks), 26 (2-3 months), 52 (5 weeks), 6U 
(2 months) The difficulty is to distinguish cases of a growth which 
lias been latent for some time and then takes on a rapidly malignant 
course, from those in which the growth is rapid from the start; but 
there can hardly beany doubt that the latter class exists. 


SUMMARY. 


From the clinical aspect both renal and adrenal growths in adults 
separate themselves into two classes. 


Growths of the Kidney and Adrenals, 267 


1, Those which run a rapid course, invade locally, by the lymph 
channels, and the blood stream, present a variety of symptoms, and 
affect the general health almost from the first. 

2. Those which exist and give rise to the classical symptoms of 
pain, tumour, and hematuria, or some of these, for a long time, often 
many years, before they cause any other symptoms or affect the 
general health. These growths are, as a rule, encapsuled and 
disseminate by the blood stream. When situated in the kidney they 
often cause an early hematuria; when in the adrenal, this symptom 
is absent, but they give the signs of other adrenal growths, and 
sometimes cause changes in the skin. 

Histologically a considerable number of the latter class have been 
found, both in the kidney and adrenal, to have the structure of 
adrenal rest tumours. They also include the “nodular form” of 
carcinoma, and it is probable that this class includes any other cases 
in which, as in these, a benign growth precedes the malignant one. 

The first class includes mixed celled sarcoma of the adrenals, and 
the infiltrating form of carcinoma, The first class will probably 
always be inoperable ; the second are, owing to.their symptoms, their 
method of extension, and their duration, capable of complete removal 
in their early stages. 

DIAGNOSIS. 
PAIN, 

This is a very uncertain symptom, but occurs in all cases sooner 
or later, and may, as in Brault’s case, be the chief or only sign. As 
a rule it is local, and radiates down to the groins, thighs or testes. 
In adrenal growths it is sometimes referred to the tip of the shoulder 
via the phrenic (Robson), and in renal growths tenderness is some- 
times noted in the corresponding Head's area (cases 43, 51, 64). 

Its causation is various ; it may be due to direct pressure on a 
single nerve (case 8), or to involvement of the lumbar or even sacral 
nerves by extension or metastases. Gastric pain is caused by 
adhesions or involvement of the solar plexus; colicky pain is 
produced by the passage of blood clots, and vesical pain by their 
pressure on the bladder. Local pain depends usually on stretching 
or a local inflammation of the peritoneum; spinal pain on erosion of 
the vertebral bodies. 


268 Growths of the Kidney and Adrenals. 


It is no safe index of the character or extent of the growth, for 
quite large tumours may run an almost painless course. At the 
same time it seems to be most severe in the more malignant forms. 

The chief value of the symptom is that it may occur early and 
lead to a thorough examination. In itself it is merely an indication 
that something is wrong. | 


TUMOUR. 


Tumours which have reached a size at which they give rise to 
седеа, venous obstruction, lung compression and the like, are easy 
enough to recognise. What is needed for successful treatment is 
their recognition while they are still very small. 

Amongst the factors which render this difficult are obesity, ascites 
and tenderness. Further, only the lower end of the kidney is accessible, 
and most growths occur in the upper end. Enormous masses may be 
hidden away under the vault of the diaphragm, especially on the left 
side, and yet be impalpable (Rovsing, p. 414). Again, the infiltrating 
form of growth and the kind which invades locally are very difficult 
to feel compared to those which grow as nodular masses projecting 
from a normal kidney. The patients themselves very rarely take effec- 
. tive notice of a tumour till it has attained a fair size, unless it i5 
accompanied by pain. By the time other symptoms drive them to 
seek advice the tumour is easy to recognize, and its recognition 
correspondingly useless. | 

At the same time palpation is very important, for precisely those 

growths (viz, the nodular), which are easiest to appreciate, are also 
the mest suitable for treatment. Israel lays great stress on palpation, 
chiefly on account of the success which has attended it in his hands. 
Others, less experienced or less fortunate, consider it relatively 
unimportant. In one case (p. 306), a patient, a man of 21, came to 
Israel with hematuria, and he was able to feel a lump the size of a 
5pfennig piece in the anterior surface of the lower end of the 
kidney. This increased to the size of a cherry in the course 
ofa month. The kidney was removed and a growth found 
extending from cortex to pelvis. The patient was well eleven 
years later (Heresco). Microscopically the growth was a medullary 
carcinoma. 


Growths of the Kidney and Adrenals. 269 


In another case (p. 307), a girl of 6 had hematuria, and it was 
found that the blood came from the left ureter. The kidney was 
normal to palpation. Two months later it was found that the 
kidney was a little longer than the other, and had a diffuse smooth 
swelling on the middle third of its anterior and outer surfaces. 
Later a prominence like a distended pelvis was felt at the hilus. 
The kidney was accordingly exposed, and to careful palpation 
gave a sensation as if it had imbedded in it a harder mass the 
size of a hazel nut. On splitting it a medullary tumour was found 
at the depth of 4 m.m., extending along a pyramid and projecting 
as a rounded polypoid mass into the pelvis. Microscopically it was a 
sarcoma. The child was well 5 years and 10 months later (Heresco). 

In yet another case, a man of 48, with hematuria, it was possible 
with great difficulty at the third attempt to feel on the lower end 
of the left kidney a prominence the size of a cherry. The kidney 
was excised; the growth proved to be a sarcoma, and the ponent 

was well three years later (Heresco). 
` These are very brilliant results, but it must be remembered that 
itis only under certain conditions that a growth at this stage is 
palpable at all. For the growth must be of a certain kind, in a 
certain sort of patient, in a certain part of the organ, and according 
to Professor Israel must be sought for in a certain way, i.e., with 
the patient lying on the sound side. One might fairly add that it 
must be sought for by some surgeon of Professor Israel's experience 
and capacity. Now these conditions are rarely combined ; 
practically the case at this stage is usually in the hands of a man 
in general practice, who is not likely to make a large number of 
examinations, or to feel at the first attempt what Israel feels, 
* with great difficulty " at the third. 

Moreover, tumour by itself is often misleading, Rovsing (case 7 of 
lus series), tells how he explored the wrong side because the 
diseased kidney was impalpable, the sound one hypertrophied. 

At the same time, Professor Israel’s results are very good compared 
to those obtained by other surgeons, and his experience a large one. 
In the third paper referred to he summarizes his results at the time 
(1896). .Of 17 cases of nephrectomy for growth, 2 had died at once, 
one a year later from acute peritonitis (no metastases), and three 


270 Grow'hs of the Kidney and Adrenals, 


were still under treatment. Of the remaining 11, 6 were well and 
free from recurrence at periods of 9, 715, 5, 4, 3, and ls years 
respectively. These results he attributes to early diagnosis, rendered 
possible by palpation, and to convince the sceptical he made a 
drawing of the last-mentioned case (where the growth was the size 
of a cherry, situated two fingers' breadth from the lower end of the 
kidney), and demonstrated its accuracy at the operation. 

It is noticeable, however, that in all these cases there was 
hematuria. This was the cause of the cases being examined in the 
first instance, and if it had been absent no amount of small 
prominences would Lave led to their exploration. Israel's advice that 
all surgeons should acquire the same skill in palpation is a counsel of 
perfection, but the lesson which these cases seem to convey is, that 
when there is an unexplained unilateral renal hematuria, the kidney 
should be carefully palpated, and then, whether a tumour is 
demonstrated or not, it should be explored. It is only in this way 
that the disease can be attacked sufficiently early —and early inter- 
ference is essential to success. 


HAMATURIA AND URINARY CHANGES. 


The value of hematuria can hardly be overestimated. Not only is 
it a frequent symptom, but it often occurs quite early. Morris 
quotes Denaclara as finding it as the first symptom in 68:8 per cent. 
of a series of 168 adult cases. 

In the Guy's cases, at any rate, it occurred relatively most often 
and most early in the cases which were best suited for operation. 
Moreover, it is a symptom that the patient is prompt to notice and 
seek relief from. A man who would diagnose and treat his own 
pains, and not notice a fair-sized tumour, sends for his doctor in 
alarm at the first occurrence of a free hematuria. So that this 
symptom is one that can hardly be missed, and it occurs early in 
precisely those cases in which prompt treatment is most likely to be 
successful. At the same time it has many other causes, of which the 
one most often confused with growth is calculus. Bleeding from a 
growth is sudden, profuse, and independent of any apparent cause. 
16 is not usually provoked by movement, or diminished by rest and 
dieting (42) ; someti nes, however, it follows an injury. At first blood 


Growths of the Kidney and Adrenals. 271 


is nearly pure, and causes great pain by clotting; later, as it diminishes 
clots of the pelvis or ureter are often passed (51, 61, 64, 58). It 
continues for a few days, and then passes off altogether, usually to 
recur in a few weeks or months. In the interval the urine is 
normal, and commonly free from albumen, but blood corpuscles can 
often be demonstrated microscopically. After recurring several’ 
times, the bleeding may cease altogether, either from the blockage 
of the ureter or because the whole kidney is converted into growth 
and secretes no urine to wash the blood down. It is in the nodular 
vascular growths, such as adrenal rest tumours, where most of the 
kidney is functionally intact, that bleeding is most constant and 
persistent. | 

The first point to establish in a case of hematuria is whether the 
blood comes from the kidneys or bladder. The intimate mixture of 
blood and urine, the passage of ureteral clots, the possibility of 
getting fluid in the bladder clear enough to use the cystoscope, and 
the normal appearance of the bladder when this is done, are all 
important points. In case 58 this difficulty was only decided by 
cystotomy. If the bleeding is renal, the next question is which side 
it comes from. Generally, other symptoms are present to settle 
this, but if not, Heresco warmly recommends catheterization of the 
ureters. Latterly, a safer and simpler method has been introduced, 
in which various kinds of vertical partitions are introduced into the 
bladder, and urine from each side collected and examined separately. 
Mr. Lynn Thomas gives instances of its successful application. This 
has the additional advantage of allowing an estimation to be made of 
the urea excretion of the unaffected kidney without a separate 
catheterization, and is far easier to carry out. If an unilateral renal 
hwmaturia is found, and the diagnosis lies, as it often does, between 
stone and growth, the next step is be explore without waiting for 
further evidence. If the case is one of calculus there is no 
advantage in waiting; if it is one of growth, delay will probably 
be fatal. Mr. Hurry Fenwick says (ii. p. 99) ** 1t should, I am sure, 
be a golden rule to explore every case of profuse renal hemorrhage, 
and to be prepared for nephrectomy.” 

Apart from hematuria, a systematic examination of the 
urine is of great help in differential diagnosis, The presence of 


2712 Growths of the Kidney and Adrenals. 


gravel, tubercle bacilli or casts may clear up the case. The specific 
gravity is unaffected by growth, and, as a rule, the urea excretion is 
normal. An extreme instance is a case of Israel's, in which a woman 
dying with a carcinoma the size of a man’s head excreted 33°7 gr. 
urea daily. Rovsing reports a case in which he abstained from 
operation on account of a deficient excretion of urea; the patient 
died of uremia, and both kidneys were found to be involved in the 
growth. The specific gravity may be of value in excluding cystic kidney, 
a condition which is accompanied by tumour and intermittent 
hematuria. 

A case of this condition associated towards the end with an 
adrenal growth is recorded by Dr. Lee Dickinson. The patient 
had suffered from tumour and hematuria for eight years. During 
the last six or seven months he showed progressive weakness and 
languor, and a dirty brown pigmentation appeared on the face, neck, 
and axille, with a few patches elsewhere. At the necropsy the 
kidney was found nearly entirely cystic, and the other kidney had 
hypertrophied and weighed 10 ozs. This accounted for the earlier 
symptoms; the later ones were due to a sarcoma of the adrenal with 
local invasion and secondary deposits. 

An important positive sign which is rarely found is the passage of 
pieces of growth. Dr. Penrose records a case where tumour cells 
were passed, and post mortem a piece of growth the size of a nut lay 
loose in the bladder, while a similar mass grew from its neck. 
Rovsing found growth in the urine of cases 3, 6, and 7 of his series. 
It is noticed in some of the Guy’s cases (23, 52, 58, etc.). In case 23 
a distinct piece of villous growth was passed two years before death, 
imbedded in blood clot. 

Hematuria is presumably caused by the breaking down of growth 
in the pelvis, so that it is during and after attacks of bleeding that 
fragments are most likely to occur. If the clots were examined and 
the urine centrifugalized on several occasions as a routine measure 
this sign would be more often obtained. Probably it occurs most 
often with the papillomata, but in case 23 the growth seems to have 
begun in the cortex. It is not possible to determine the earliest 
appearance of this sign, for as a rule it was not looked for, or the 
search not mentioned, before the cases came into hospital. It is only 


(тои оў the Kidney and Adrenals. | 273 


owing to the circumstance of case 23 having been admitted twice 
that it is possible to assert that it occurred relatively early. 

In a case of Grawitz's, an adrenal rest growth in the kidney, 
branching tufts ending in fine round knobs, and covered with a thick 
layer of large nucleated oval or irregular epithelial cells, were found 
in the urine 54 years before death, and practically at the beginning 
of the hematuria. Lubarsch mentions finding tumour cells іп the 
urine (Case 7); and cells of various kinds are very often found, but 
they can never have the positive value of the tufts and fragments 
described above. 


EXPLORATORY PUNCTURE. 


This is warmly recommended by Israel, whose opinion is entitled 
to respect. In three cases he has extracted cells of growth, and 
even where this was wanting he has been able to satisfy himself that 
the tumour was solid, and to demonstrate, by the hematuria which 
followed the puncture, that it was renal. 

On the other hand the nature of a growth cannot be diagnosed 
from a few cells, and the test is not infallible as regards the nature 
of the mass. For a needle may easily pass between the loculi of a 
pyonephrosis, or draw off fluid from a hydronephrosis dependent on 
growth. | | | 

The method was adopted in eight of the Guy's cases. In four 
cases blood or fluid was obtained, in two “rounded cells”; in one 
“gelatinous matter"; and in one nothing.. The diagnosis was not 
materially forwarded, and of these eight cases two immediately 
developed acute suppurative peritonitis, and a third died five days 
later. Exploration through a lumbar incision would give vastly 
more information, and would hardly have a higher mortality. How- 
ever cleanly the puncture may be done it is liable, in the absence of 
adhesions, to put a septic cavity in communication with the peri- 
toneum (Case 29). 


X RAYS. 


These might be of great service in demonstrating the presence of 
a calculus where hematuria and pain are the chief symptoms, and 
the diagnosis lies between calculus and growth, Negative results 


274 Growths of the Kidney and Adrenals. 


are not trustworthy, as Mr. Lucas has recently pointed out. Except 
for this purpose the rays have not been much used. One case (61) 
was skiagraphed with a negative result. Heresco gives an instance 
(157) where the tumour was shown in a radiograph lying under the 
diaphragm in a case where it was not palpable. This might be of 
value in some circumstances, and is always worth trying as a routine 
measure. 


VARICOCELE. 


Some stress has been laid on this symptom as indicating a glan- 
dular infection, and as contra-indicating operation. The frequency 
with which it occurs is unknown, as it is not marked when the 
patient is lying down, and the clinical reports are usually concerned 
with patients in bed. It has some significance as showing that 
there is interference with the return of, blood along the spermatic 
vein, in cases where it has come on recently in a patient of middle 
age-——beyond this it proves nothing. Mr. Morris found it with 
a tumour of the adrenal, and it may be dependent on pressure of 
the tumour on the veins, without metastases, or on thrombosis of 
the main trunk. As Heresco and others point out, varicocele may 
oceur without glands, and glands without varicocele, and varicocele 
may disappear after a successful operation (Wallace), so that this 
symptom in itself cannot be held to contra-indicate operation. _ 


LATE SYMPTOMS. 


From a practical standpoint the numerous late symptoms which 
are described in detail in cases dying in the medical wards are of no 
importance, and the various ways in which the disease terminates 
may also be neglected. It is essential to make an early diagnosis, 
and it is almost equally essential to recognise when a case has 
become inoperable, but nothing is to be gained by studying the 
infinite variety of symptoms which are secondary to an enormous 
mass in the abdomen, or to metastases in the brain. 


SIGNS THAT A CASE HAS BECOME INOPERABLE. 


Instances have already been given in which the first symptoms 
are those due to metastases; such cases are inoperab from the 


Growths of the Kidney and Adrenals, 276 


start. But in other cases it is often very difficult to decide whether 
any extension or metastases has occurred. The duration and size 
of the growth and the amount of pain and hematuria give little or 
no information on this point. Signs of mischief in the lungs and 
pleure, enlarged liver, paralyses, and edema are among the commoner 
symptoms, but since there is no situation in which deposits may not 
occur, nothing short of a thorough general examination of the 
patient is of any use. 

Perhaps the most important sign is failure of the general health. 
Tt has been pointed out in the © cases of long duration," (p. 265). 
and repeatedly observed in children, that a renal tumour in itself is 
quite compatible with the enjoyment af active life. It is usually 
only when the growth escapes from the capsule and invades sur- 
rounding structures, or gives rise to metastases in vital parts, that 
the condition called cachexia sets in. So that when a patient has 
had symptoms for some time, and then his health begins rapidly to 
fail, or where his illness is out of proportion to his pain or loss of 
blood, it is probably wise to abstain even from exploration. As Mr. 
Jacobson says, * When the history makes it probable that the 
growth has got beyond the earlier stage, when there isany extension 
to the lymphatic glands or other viscera, when there is nausea, 
emaciation, or a temperature inclined to fall, th« time for operation 
has gone by." But supposing that none of these signs are present, 
and that an operation is taken in hand, it is still necessary to regard 
it as in the first instance an exploration, and to be prepared to desist 
if it becomes clear that no good can be done. Direct invasion of 
muscles, and a lymphatic invasion extending beyond the few glands 
situated actually on the hilum, are good reasons for stopping, while 
large tumours and extensive adhesions without invasion are 
merely mechanical difficulties which may or may not be 
superable. 

An instance is case 41. Here there was a large tumour, pain, 
and a history of hematuria, with signs of mischief in the lungs, but 
these might well have been due to pressure of the mass. Otherwise 
the very extensive growth found post mortem seems to have given 
rise to few, if any, positive signs. At the same time the patient 
was noted to be pale and sallow, and he had becn invalided for 19 


276 Growths of the Kidney and Adrenals. 


weeks. Mr. Lucas explored, found evidence of glandular infection, 
and desisted ; a course amply justified at the autopsy. 

In a case of Abbé’s, where he left behind two enlarged mesenteric 
glands, the child was well for four and a-half years, and then died 
of growth in the other kidney, which was probably entirely 
independent. But in an infant the mesenteric glands are not 
the usual route of invasion, nor is growth the only cause of their 
enlargement. 

A case of Israel’s has been quoted as shewing that a growth is in 
itself toxic by resorption. The case was an advanced one in a woman 
of 43, with hectic fever, vomiting, and signs of nephritis, On 
removal of the tumour all these signs disappeared, to reappear soon 
afterwards with the recurrence of the growth. But this was an 
inoperable case, in which the only object was to afford relief, 
metastases were presumably already present, and it is hardly fair to 
conclude from it that a growth in itself causes illness, when there 
are so many instances in which it does not. 

So neither of these two cases can be said to controvert the principle 
that glandular infection and disproportionate illness contra-indicate 
operation. 


EXPLORATION. 


This is by far the most satisfactory means of diagnosis, and under 
modern conditions there is no reason why it should not be freely 
used, if the whole question is fairly and fully explained to the 
patient, and his consent obtained to any further’ operation which 
may be found necessary. 

Rovsing in one case explored the suspected side, found it normal, 
and under the same anesthetic explored the other, found a growth, 
and successfully removed it. This shows, if proof were necessary, 
that even a very thorough examination of a kidney does not do it 
any harm, for in this case the explored kidney had to do the whole 
work of the body at once. This patient had a recurrence in the scar 
four years later; this was excised, and he was well 53 years from 
the first operation. | 2 

Iu exploration from behind the pelvis can be felt, calculi 
detected, the substance of the kidney palpated with a nicety im- 


Growths of the Kidney and Adrenals. 277 


possible through the parietes, and what is more important 
still, the kidney can be seen. For most growths are cortical, and 
most growths are white, and their colour marks them out even 
before they become palpable. Of the Guy's cases all those that 
were operated on may be said to have been explored, in the sense 
that every operation is an exploration. But in case 58 the kidney 
was exposed in the absence of a palpable tumour, and in 
uncertainty as to the side affected, and the result fully justified 
this course. In case 51 two explorations were carried out, in the 
first the kidney was found rather large and hard, in the second, 
two months later, its anterior surface was found covered with 
white warty growth. On the first occasion the kidney was 
punctured and palpated. There is nothing in the report to show 
whether the anterior surface was examined or not. If it had been, 
it is possible that the colour of the growth would have led to its 
detection. The small amount of metastasis present post mortem 
suggests that its removal on the first occasion might have been 
successful. Another class of cases in which even exposure of the 
kidney leaves the diagnosis doubtful is that of the papillomata, where 
a fulness of the pelvis is in the early stages often the only sign. 
However, in the two cases of this kind a right conclusion was 
arrived at. It would seem to be essential to examine both surfaces 
of the kidney in a good light, to palpate the substance, and examine 
the pelvis before pronouncing it normal. 

A large proportion of the recorded cases seem to have been 
submitted to the surgeon far too late, Descriptions of universal 
adhesions, networks of enlarged vessels, and tumours so large that 
they: have to be delivered piecemeal, contrast in a very striking 
way with Israels cases quoted above, where the growth formed a 
slight projection on an otherwise healthy kidney, and nephrectomy 
was correspondingly easy and successful. All surgeons are agreed 
that early diagnosis is the one thing essential to success, 
most allow that without exploration it is difficult, with it 
usually easy. 

It is true that some large tumours have been successfully 
removed, but this is no justitication for allowing any given tumour 
to become large. The course too often followed has been to watch 


VOL. LIX. 20 


278 Growths of the Kidney and Adrenals. 


the case till unmistakable symptoms have settled at once the 
diagnosis and the prognosis, and then to send it to a hospital ora 
surgeon for operation. Compared with this method of dealing 
with malignant disease the purchase of the Sibylline books (which 
it closely resembles) was a prompt and business-like transaction. 

If surgeons are to explore early they must be content to do so 
on the grounds of hematuria alone, or tumour alone—that is to 
say, hematuria or tumour of a certain kind, the hematuria 
apparently causeless, profuse, unilateral, renal, the tumour rounded, 
solid, slightly mobile, retrocolic. Israel's successful cases in most 
other surgeons’ hands would probably have been cases of hematuria 
without tumour.  Rovsing's successful case (well 5 years 4 months) 
had a kidney that could not be felt on the affected side. McWeeney's 
case (well 4 years) had no hematuria. Perthes’ case (well 5 years) 
had no hematuria. Jordan’s (Heresco, well 53 years) had hema- 
turia without tumour. Clearly these successes have been gained 
in many cases by exploring on the strength of one of these 
symptoms alone, and of the two, hematuria of the kind described 
above is the more significant. Of course, if exploration is freely 
` "used a certain number of kidneys will be exposed on wrong 
diagnoses. Of these none need be damaged, and many of those in 
which the bleeding is due to other causes can be cured. `A few un- 
necessary incisions are а cheap price deliberately paid for early 
diagnosis in malignant cases. 

Exploration in an early stage has been urged particularly oy 
Kuster and Rovsing. The latter sums the whole matter up thus: 
(p. 450) “And so my belief is that if we would only keep the 
possibility of malignant growth before our eyes in every case of 
renal hematuria whose cause is not quite obvious, and promptly 
apply all our resources to determine ‘the cause of the bleeding, 
that in future successful results of nephrectomy for growth would 
become considerably more numerous—and if only surgeons would 
undertake exploration more frequently and more boldly, but at 
the same time resign themselves to leave colossal adherent tumours 
wholly alone . . . . I am sure that the mortality of this operation 
could be brought from its present considerable height almost to 


zero." 


Growths of the Kidney and Adrenals. 979 


METHODS OF OPERATION. 


As regards the two main methods, the anterior transperitoneal and 
the lumbar, there seems to be a general preference for the latter. 
The actual incision must be made to suit the individual case. The 
mortality of the anterior incision used to be about twice as great as 
that of the lumbar, partly from sepsis, partly because this method 
was used for very large growths, too big to be got out through the 
loin. This difference has now disappeared, and the mortality in 
adult cases is about the same. In children the anterior method is 
still the more fatal (Негеѕсо). ‘The peritoneum is likely to be 
opened in any case, but the posterior incision gives better access. 
The whole question is discussed in Mr. Jacobson's “ Operations." 
Israel and others urge that the fat and glands should be cleared out 
in every case, just as the axilla is stripped in cancer of the breast. The 
cavity should then be pulled open with broad retractors, dried, and 
inspected with a good light; after which tears in the peritoneum are 
sewn up and the wound drained. If necessary clamp forceps may be 
left on the pedicle. | Abbé's successful case (8 years) and Bloch’s 
case, were instances of partial resection of the kidney, a proceeding 
which might be adopted in exceptionally suitable cases. 

Apparently early interference in carefully selected cases is much 
more important than any points in the technique. In case 39 death 
occurred on the table from detachment of a malignant thrombus by 
manipulation; and a similar case is recorded by Kuster (1.). It is 
important to avoid rupture of the capsule if possible. In a case of 
Perthes' (F1.) this led to recurrence in the scar by contamination of 
the wound. Early interference would diminish both these special 
risks as well as those common to all operations. 


RESULTS OF OPERATION. 
A.—ADRENAL GROWTHS. 


Not very many operations have been done for this condition, and 
in no case has it been diagnosed beforehand. 

Mr. Morris has published three cases, and Mr. Mayo Robson 
three, with reference to nine others—most of them proved fatal soon 
after operation 


280 Growths of the Kidney and Adrenals. 


In the case of Knowsley Thornton’s already mentioned (p. 225), 
operation brought about a great improvement in the patient’s health 
and allowed her to resume active life. Unfortunately she died of 
recurrence two years later, but this result may be considered 
satisfactory, and as the tumour weighed 20 lbs. at the time of 
operation the case may be considered one in which operation came 
too late, rather than one which was inoperable. 

Mr. Mayo Robson removed an adrenal tumour the size of an 
orange together with a wedge from the kidney, and the patient was 
known to be well nearly two years later. 

Curtis (1900) showed a woman, aged 49, from whom he had 
removed an adrenal growth a year and a half before. In this case 
the urine was practically normal; the symptoms were dyspepsia and 
discomfort, and the chief positive sign was tumour. The growth 
partly involved the kidney, and the two together weighed 2 lbs. 2 ozs., 
and measured 16 x 17 inches. 

In Mr. Mayo Robson's successful case the growth was an adrenal 
rest tumour, in Knowsley Thornton’s case the description of the 
specimen in the catalogue of the Royal College of Surgeons’ Museum 
suggests that it was of the same kind, and in Curtis's no details 
are given. It is known that these growths occur and reach some size 
in the adrenal (p. 222), and it is probable that the operable cases of 
growth will be found to be mostly of this kind. 

In case 59 there was a history of four years' pain and a year's 
tumour with scarcely any metastases, so that probably early explora- 
tion with no diagnosis, or a wrong one, would have saved the patient ; 
at the time when she reached the hospital it was too late. So that 
although the infantile adrenal growths, and the majority of those in 
adults, are likely to remain inoperable, the cases quoted above show 
that in a certain number early operation has a good chance of 
success. In these, even more than in renal growths, it is necessary 
to explore early, for hematuria practically never occurs, the tumour 
is often not retrocolic, and the characteristic symptoms are vague 
and late. In the case of growths that reach a considerable size 
under the vault of the diaphragm on the left side, it is possible that 
skiagraphy may be of some use, but as a general rule it is unlikely 
that a correct diagnosis will ever be made without an incision. 


Growth of the Kidney and Adrenals, 281 


RENAL GROWTHS. 
I.—IMMEDIATE RESULTS. 


Heresco finds that the immediate mortality, i.e., the proportion of 
cases dying within a month of the operation, was about 60 per cent. 
before 1890, and has since been reduced to less than 20 per cent. 
In his 53 cases in infants he found a mortality of 17 per cent. as 
against one of 60 per cent. in cases occurring before 1890. Probably 
this figure is too low, as Döderlein in a series of 47 cases (1894) 
finds it 40 per cent., and Walker in 74 cases finds it 36 per cent. 

Of the nine completed nephrectomies in the Guy's series one died 
of gastric ulcer, two died at once, and one in two days. The five 
others, which are the five most recent, all survived the operation 
over a month, three were sent out well, one transferred to an 
infirmary, and one is still in the hospital. This fully agrees with 
the improvement in immediate results found by Heresco. 

Apart from sepsis and a wrong selection of cases there is a 
high immediate mortality connected with nephrectomy. This 
is due to various causes, but one on which Israel is inclined 
to lay stress is a nephritis of the other kidney from chloroform. 
Rindskopf has made observations on this point, and finds that 
it occurs in a slight form in about one-third of all cases 
operated on under this anmsthetic, and in 82 per cent. of operations 
on the kidneys. It is shown by the passage of casts, albumen, etc., 
coming on a day or two after operation and lasting two or three 
days. In most cases it passes unnoticed, and in fatal cases it can 
only be detected by the microscope and is consequently usually 
missed. In case 6 of his series Israel satisfied himself that this was 
the cause of death. In case 42 of the Guy's series death followed two 
days after the operation with vomiting. It is noted that chloroform 
was administered for nearly two hours. Post mortem the remaining 
kidney was noticed to be “anemic.” Possibly death was due to 
this cause. The question of chloroform intoxication as a whole is 
discussed by Kocher (Operations-lehre, p. 15 seg.). The reason of its 
special importance in these cases is that it-affects a kidney on which 
an exceptional strain is suddenly put. 

Whatever may have been the causes of death in the older cases 


282 ` Growths of the Kidney and Adrenalé, 


it is clear that the immediate mortality has been much reduced by 
modern methods, and is now about 20 per cent. 


IL—REMOTE RESULTS. 
ADULTS. 


It is difficult to draw any safe conclusions as to the proportion of 
cures from any series of cases collected from the literature. The 
fact of publication generally involves selection, apart from any that 
may occur in the compilation of a series, and the after-history is 
incomplete in most. Негезсо has written for th» after- histories of а 
large number of published cases, and his results are consequently 
much fuller than any to be extracted from the rest of the literature, 
but his conclusions are subject to the limitations suggested above. 
Of his 112 adult cases 89 survived the operation, and he obtained an 
after-history in 62 of them. Of the cases seen after three years 10 
were well at periods up to 7 years. One died without recurrence at 
+ years 9 months, and one died of recurrence in 3} years. So that 
11, or 10 per cent. were ‘‘ cured ” in the sense that they were known to 
be well at the end of three years and are not known to have had 
recurrence since. Fifteen others were well at the end of a year. 
One of these then died from another cause. Three had recurrence 
between one and three years. In all 22 are known to have had 
recurrence, and in 27 there is no history. So it is established 
beyond doubt that of this series of cases some proportion over 10 
per cent. were * cured" by operation in the sense defined abore, 
and a number of others were well at the end of a year. 

Heresco classifies the results according to the form of growth, but 
this is very unsafe ground, for reasons already stated. Theloperative 
results of the adrenal rest tumours have already been mentioned 
separately. 


CHILDREN. 


Heresco has 56 infantile?;cases, and an after-history in 24. Of 
these 16 died of recurrence, 8 were alive at periods varying from 9 
months to 6 years, 4 being over 3 years. 

Walker collected 74 cases, and found that 27 died of the operation, 
28 had recurrence, 15 were lost sight of, and 4 survived over 3 years. 


Growths of the Kidney and Adrenals, 283 


Since the publication of his paper one of these cases (Abbé) has 
died of recurrence after 4$ years, and one of his incomplete cases 
(Malcolm) has since been reported well at the end of J0 years, and 
another (Döderlein) at the end of 6. He found 5:4 per cent. of 
cures, and an average duration of 16 months of life in the operated 
cases, as opposed to 3 months in those unoperated. These alterations 
would bring the proportion of cures to 6'7 per cent. 
The following are the successful cases up to date :— 


SUCCESSFUL CASES OF NEPHRECTOMY FOR GROWTH IN CHILDREN, 


SURVIVAL OVER З YEARS. 


No SUBSEQUENT RECURRENCE REPORTED. 



















Age and Sex Reference to 



















Malcolm | Girl, 144 yrs.| Trans. Clin. Soc. | Letter to Mr. Bland | 10 yrs. 
XXVII. 94 Sutton. Tumours, 
innocent and mal- 
ignant. 1903. p. 126 
Abbé Girl, 144 yrs. | Annals of Surgery Annals of Surgery 8 yrs. 


XIX. 58 XXXI. 760 


Döderlein | Girl, 7 yrs. | Cbl. f. d. Path. der | Letter from Perthes to 


6 yrs. 
Harn-Organe V. 5 Heresco. p.89 





Israel Girl, 6 yrs. | Lang. Archiv. Letter to Heresco. 519 yrs. 
XLVII. 307 p. 124 
Israel Boy, 14 yrs. si Ibidem 5 yrs. 
p. 322.438 
Schmid Boy. +; yr. | Münch Med. Woch.| Cbl. f. Chirurgie 8 yrs. 
XXXIX. 256 XX. 612 


Abbott Girl, 1 yr. | Letter from Mr. | Child seen well Dec., 


4} yrs. 
Abbott. 1904. O.R. ty 


These figures are an understatement of the amount of success 
obtained, for so many cases are lost sight of, and it has been seen 
that at least two of Walker’s “cases with incomplete history " have 
since turned out to be cures. 


As regards Abbé’s case of recurrence after 43 years, the second 
growth oceurred rapidly, at the end of a considerable interval, in the 


284 Growths of the Kidney and Adrenals. 


other kidney—it is not likely to be an actual recurrence, but rather 
a fresh development—and if this view is taken, the case is really one 
of * death from intercurrent affection." | 

Mr. Abbott proposes to publish his case in full at a later date, 
but in the meanwhile has been so kind as to furnish me with the 
following particulars, and to give me permission to include them. 

Nellie A., aged 1, was admitted to the Evelina Hospital with growth of the 
right kidney. The operation was performed on March 29th, 1900. A long 
oblique incision was used, opening the peritoneum in its anterior part. 
Great difficulty was experienced during part of the operation. The child did 
well afterwards. The tumour was thought by Mr. Targett to be a columnar- 
celled carcinoma; it was mixed in structure. and Mr. Shattock was inclined 
to think ita sarcoma. On May 6th, 1902, the child was re-admitted to 
St. Thomas' for what was considered to be recurrence in the abdominal wall 
and għands. A large piece of abdominal wall and muscles was removed right 
down to the iliac crest, also some lumbar glands. These and the wall were 
dense, hard and fibrous, and contained a fluid that looked like pus in numerous 
loculated spaces. There had never been any temperature. No cultivation 
grew from this fluid, and no trace of growth was found in the parts removed, 
The child made a good recovery, though it had a large hole in its abdominal 
wall, which was much weakened. 


The child was last seen on December 7th, 1904. There is no 
sign of recurrence; the scar is flush with the skin unless the 
child coughs or cries, when a small hernia appears, chiefly at the 
upper end, this is easily controlled by a belt and pad; the opposite 
kidney is very readily palpable, and is enlarged, presumably by a 
compensatory hypertrophy. 

A good many other successful adult cases might no doubt be 
collected from the literature, or by writing to the surgeons. For 
example, two are mentioned in Heresco's preface, one of Krénlein 
(well 13 years) and one of Israel's (well 11 years). Fenger reports 
one well 74 years, and Knowsley Thornton one well 7 years. In 
the last-mentioned the tumour weighed 11 lbs., had been present for 
six years, and was said to resemble adrenal tissue. Probably it was 
an adrenal rest growth. Maidlow’s case was well 3 years later 
(Bland Sutton, p. 131) ; in this case the growth weighed 7 los. But 
a few cases more or less make no difference to the conclusion which 
the recorded cases fully establish, that in some cases of renal growth 
a permanent cure can be obtained by operation. Although the 
successes are not very numerous, it must be remembered that they 


Growtha of the Kidney and Adrenals. 285 


are all relatively recent. Heresco had difficulty, he says (p. 30) in 
finding two or three cases before 1890 which had survived opera- 
tion for more than a year. There is no difficulty now in finding 
a number that have survived more than three. 

The difference that has been brought about in the outlook is 
well seen by comparing the two last editions of Mr. Butlin's 
Operative Treatment of Malignant Disease. In 1887 all operation 
is practically condemned. In 1900, Mr. Bruce Clarke is able to 
write about this operation: “There are reasons for hoping that 
better results may be obtained from it in the immediate future. 
The mortality due to the operation is already very much lower 
than it was, and is likely to be still further diminished by careful 
attention to the diagnosis of the disease in the earlier stages.” 

The infantile cases are less promising than the adults. Not only 
does the disease sometimes begin before birth, but hematuria is 
relatively rare, and the diagnosis is generally made when a large 
tumour is already present; while infants are not in any case good 
subjects for extensive abdominal operations. The selection of 
suitable cases is also extremely difficult. Abbé was unable to state 
any points that distinguished his successful cases from the 
unsuccessful at the time of operation. Since, however, the disease 
is inevitably fatal, and there is a slight chance of success, there can 
be no doubt that operation in suitable cases is justified. 

In adult cases there is no encouragement in the results quoted 
above for interference in all cases or at all stages. Probably, as in 
children, the majority of cases will remain inoperable. What can 
reasonably be expected is that early diagnosis will raise the total of 
successes, and careful selection increase their proportion to the 
number of nephrectomies performed. 


SUMMARY. 


Our knowledge of the different forms of growth is increasing, 
but at present it is impossible to diagnose them during life, and 
their separation after death presents peculiar difficulties. Clinically 
both renal and adrenal growths fall into two classes, one, rapid, 
diffuse, disseminating early and affecting the general health; the 
other, slow, encapsuled, disseminating late and usually by the 


286 Growths of the Kidney and Adrenals. 


blood stream, and giving rise to pain, tumour, or hematuria for 
some time'without other symptoms. The essential difference between 
these classes is probably that the latter consists of those growths 
(whatever their structure) which exist as innocent tumours for some 
time before they become malignant, whereas the former are malignant 
from the start. Since in certain kinds of tumours, such as the 
adrenal rest growths, a benign stage is the rule, whereas in others, 
such as pelvic carcinoma, it is the exception, it is natural that the 
majority should impress their secondary characters on the class ава 
whole. Consequently we find the latter class showing the same 
preference for dissemination by the blood stream that is shewn by 
the adrenal rest growths, but less absolutely. ` 

Since carcinoma, epithelioma, sarcoma, and malignant adrenal rest 
growths may any of them be preceded for variable periods by 
adenoma, papilloma, connective tissue growths, and innocent adrenal 
rest growths respectively it will probably never be possible to 
connect the structure of a growth absolutely with its clinical course. 
At the same time there are grounds for thinking that growths of an 
adrenal type are relatively more likely to run a slow and favourable 
course. 

The diagnosis of the presence of a growth may be much helped by the 
employment, in addition to the usual methods of examination, of 
the cystoscope and urine separator, by a repeated examination of 
the urine and the deposits obtained by centrifugalizing it, and by the 
X-rays. Diagnosis is often impossible without exploration, and if 
suspicion of a growth is aroused by any single symptom, of which 
hematuria of a certain kind is the most important, this should be 
employed without delay. No hematuria should ever be left unac- 
counted for, and as few tumours as possible. Disproportionate failure 
of the general health and evidence of metastases forbid operation ; 
varicocele, skin changes, and tumours of a moderate size do not. 
The immediate mortality of the operation has been much reduced 
since 1890, and is now about 20 per cent. Before that date 
scarcely any successes were recorded; since then it has been found 
possible, in cases taken early, to bring about a fair number of 
complete cures extending over three years or more. The whole 
question turns on early diagnosis, and much better results 


Growths of the Kidney and Adrenals. — 287 


may confidently be expected if adults in whom there is any 
suspicion of this disease are at once submitted to a thorough 
examination, including, if necessary, exploration through a lumbar 
incision, It is unlikely that a corresponding improvement will 
be obtained in the growths that occur in children, but the results 
justify operation in carefully selected cases. 

In conclusion, I should like to express my thanks to those 
members of the Staff who have kindly allowed me to use their 
cases, and particularly to Mr. Jacobson, to whose кар енин апа 
encouragement this paper owes its existence. 


ADRENAL REST TUMOURS. 


References will be found in the index under the following 
names :—Grawitz, Johnson, Israel (2), Busse (4), Askanazy, Beneke, 
Gatti, Manasse, Burkhardt (4), Lubarsch (5), Kelly (2), Hildebrand 
(3, ‘‘endotheliomata”’), Holmes, Perthes (3), Boyd, Ulrich (3), 
Graupner, Fairbairn, McWeeney (2), Driessen (2.“ endothelio- 
mata”), Hansemann, Lówenhardt. These all occur in the kidney, 
and have some kind of clinical history. 

For other instances of this form of growth, see under Rupprecht, 
De Paoli, Bergstrand, Bland Sutton (p. 130), Eastwood, Kuster, 
Targett, Thelwall Thomas, Knowsley Thornton, and the authors 
mentioned above, also the cases figured, and those included in the 
Guy's series, 58, 69, 70. 


288 Growthe of the Kidney and Adrenals. 


BIBLIOGRAPHY. 


ABBE. I. 1894. Annals of Surgery, XIX., 58. Three nephrectomies in 
children, one partial. 


и. 5 i » " 92. Discussion. 
II. 1895, 3 be XXII., 269. Discussion, cases shown. 
Iv. 1897. т $i XXV.,360. Recurrence in one case. 
v. 1898. з % XXX. 317. А nephrectomy. 

vi. 1900. ss XXXI., 760. Case reported well 8 years. 


ABRAM. 1900. Journal of Pathology and Bacteriology, VJ., 384. Carcinoma 
arising in glomeruli. 

ABERCROMBIE. 1880. ‘Trans. Path. Soc., XXXI., 168. Three cases em- 
bryonic growth at hilum of both kidneys. 

ADDISON. 1855. ‘ Disease of the Suprarenal Capsules.” A collection of the 
published works of the late Thos. Addison, M.D. Wilksand Daldy. 1868. 
Vol. XXXVI. of the New Sydenham Society. 

AFFLECK AND LEITH. 1896. Edinburgh Hospital Reports, IV., 287. Sarcoma 
of adrenals, references to 20 cases. 

ALBARRAN. 1897. Ann. des Mal. des Org. Génito-urinaires, pp. 243, 387. 
Adenoma and epithelioma. 

ALEXANDER. 1892. Ziegler’s Beiträge, XT., 145. Structure and function of 
adrenals, and their relation to the nervous system. 

ALLEN AND CHERRY. Report of Australian Inter. Med. Congress, 1890, 
Histology of 29 cases of primary renal growth. 

ALM. 1894. B.M. J., ii., epitome 296. Cancer of kidney, hematuria 6 years, 
tumour 3 years, nephrectomy, recovery. 

ALSBERG, 1881. Langenbeck’s Archiv., XLIV., 458. Removal of a large 
lipoma. 

ASKANAZY. 1893. Ziegler’s Beitrage, XIV., 33. One case of adrenal rest 
tumour, and remarks. 

BACALOGLY. 1898. Bull. de la Soc. Anat. de Paris, XII., 21. Carcinoma, 
39 (m.), extensive glandular infection. 

BEADLES. I. 1893. Trans. Path. Soc., XLIV., 98. A large renal tumour 
found post mortem, 
hematuria. 

II. 1897. à „ XLVIII., 241. Adeno-carcinoma found 
post mortem, with 
epithelioma of larynx. 

III. 1898. Е „ XLIX., 179. Infiltrating carcinoma, 
and four other cases. 

у. y » „ » 260. Fibroadenoma of ad- 
renal. | 

у. 1899. РА ,; L., 214. Lesions of adrenals in 
the insane. 


Bibliography. 289 


BENEKE. 1891. Ziegler’s Beiträge, IX., 440. One case, Malignant change in 
adrenal rests. 

BEBDACH. 1889. Wien Med. Woch., XXXIX., 357. Diagnosis of adrenal 
sarcoma, case. 

BERDEZ. 1892. Arch. de Méd. Exper. Paris, IV., 412. Adrenal tumour found 
post mortem. 

BERGSTRAND. 1897. Ann. des Mal. des Org. Gé6nito-uraines, XV., 202. 
Adrenal rest tumour in boy of 8, tumour for a year. 

BIERHOFF. 1900. New York Med. Journal, LXXI., 805. Cystoscopy in a 
case of carcinoma. 

BIRCH-HIRSCHFELD. 1. 1894. Centralblatt f. d. Path. der Harn.-Organe. V., 

5, 88. Embryonic growths. 
п. 1898. Ziegler's Beiträge, XXIV.. 343. Histology of 
embryonic tumours. 

BLACKBURN, 1888. Journal of American Med. Ass, X.,389. Tumour of 
adrenal found post mortem. 

Borst. 1902. Geschwülstlehre, Wiesbaden. Review and bibliography. 

BOSANQUET. 1901. Trans. Path. Soc. LII., 64. Adrenal cysts found post 
mortem, references. 

Воүр, STANLEY. 1898. Trans. Path. Soc., XLIX. Malignant papillary adenoma. 

Boyp. Am. Journ. Med. Soc., CXXIII., 1069. Adrenal rest tumour. 

BowEN. 1897. Journal of Cutaneous and Genito-urinary Diseases, p. 65. 
Mycosis fungoides. | 

BRAULT. 1891. Semaine Médicale, IL, 249. Rapid infiltrating growth, great 

| pain, explored. 

BREWER. 1901. Annals of Surgery, XXXIV., 827, Exploration without 
tumour, well 1 year. 

BRITISH MEDICAL ASSOCIATION. Discussion. , B. M. J., 1899, II., 1273. 

BRUCE-CLARKE. Butlin’s ' Operative ‘Treatment of Malignant Diseases.” 
1900 edition. 

Bruns. 1898. Ziegler's Beiträge, XXIV., 375. Spindle-celled sarcoma. 

BUDAY. 1898.  Zieglers Beiträge, XXIV., 501. Occurrence of cysts in 
adrenal tumours. 

BURKHARDT. 1900. Deutche Zeitschrift für Chirurgie, LV., 91. Adrenal 
rest tumours, four cases, review. 

Busse. 1899. Virchow’s Archiv, CLVII., 346. Fibromyoma, Embryonic 
tumours. 

BuTLIN. 1887. “Operative Treatment of Malignant Disease." First edition. 

CAILLE. 1895. Archives of Pediatrics, XII., 594. Adrenal sarcoma of 
infant, metastasis in neck. 

CARPENTER. 1902. Rep. Soc. Diseases of Children, IL, 69. Adrenal sarcoma 
in child, zt. 2. 

CHAPMAN. 1897. West London Medical Journal, p. 201. Two cases of renal 
growth. | | 

CHAUFFARD, 1896. Bull. et Mém. de la Soc. Méd. des Нор. de Paris, XIII., 
777. Growth of adrenal, multiple fibromata in the skin ; pigmentation. 

CoHN. 1894. Berlin Klin. Woch., XXXI., 266. Sarcoma of adrenal, girl 
set. 9. 

CoLEy. 1897. Med. News of Philadelphia, p. 467, Embryonic growth 
nephrectomy, recurrence in 5 months, Coley's fluid, death in 1 year. 


290 Growths of the Kidney and Adrenals. 


ORAUFURD, RAYMOND. 1899. Trans. Path. Soc., L., 212. Cyst of adrenal 
adenoma. | 
- Ourtis. 1900. Annals of Surgery, XXXL., 759. Adrenal growth removed, 
well 1 year. * 
DALTON. I. 1884. Trans. Path, Soc, XXXVI., 247. Infant, growth of 
adrenal or liver. 
п. 1899. King's Hospital Reports, V., 217. Papillary adenoma, 
found post mortem. 

Day. 1880. Trans. Path. Soc., XXXII., 142. Capsular growth 9} lbs. 

. DEAVER. 1902. Annals of Surgery, XXXVI., 87. Two nephrectomies for 
growth. 

DE Jona, JOSSELIN. 1904. Ziegler' Beiträge, XXXV., 205. Papilloma. 

DELAFIELD AND PRUDDEN. 1902. Pathological Anatomy. 

DELÉTRE AND RAIMONDI. 1897. Bull. Soc. Anat. Paris, II., 112. Infiltrating 
growth, fatal in 2 months. 

рк PaoLr. 1891. Ziegler’s Beiträge, VIII., 140. Three cases angiosarcoma 
(1 adrenal rest growth). 

DICKINSON v, sub. Fox, CoLCOTT. Sarcoma of adrenal in a child, overgrowth 
of hair, etc. 

DICKINSON, LEH. 1894. Trans. Path. Soc. XLV., 129. Cystic kidney and 
sarcoma of adrenal in а man æt. 57. Hæmaturia and tumour, 8 years, 
pigmentation, languor. 

DóDERLEIN. 1894. СЫ. f. d. Path. der Harn-Organe, V., 3. Embryonic 
growths, statistics. 

DREW. 1897. Trans. Path. Soc., XLVIII., 130. Villous carcinoma of pelvis, 
papilloma. 

DRIESSEN. 1893. Ziegler's Beitrage, XIL, 65. Endotheliomata, occurrence 
of glycogen. 

x» DUNNING. 1895. Annals of Surgery, ХХІ, 223. Embryonic growth, nephrec- 
tomy, recurrence in 9 months. 

‘EARLE AND WEAVER. 1894. Journal of Am. Med. Ass., page 980. Adrenal 
sarcoma, set. 2. | 

Eastwoop. 3902. ‘Trans. Path. Soc., LIII., 153. Adrenal rest tumour in 
the uterus ; review. 

EDMUNDS, 1892. Trans. Path. Soc., XLIIL, 89. Cystic adenoma. 

EuRICH. 1896. Journal of Path. and Bact., р. 504. Growth composed of 
adrenal medulla. 

FAcGE, HILTON. 1875. ‘rans. Path. Soc., XXVII., 204. Report оп Case 18 
of the Guy's series. 

FAIRBAIRN. 1902. Trans. Path. Soc., LIII., 184. Adrenal rest growth, 
excision (Bland Sutton, p. 129). | 

` FENGER. 1898. Annals of Surgery, XXX., 386. Nephrectomy: for growth. 
well 73 years. 

ENVIR, HURRY. 1. 1897. Trans. Med. Soc., XX., 237. Papilloma, cystos сору. 

II. 1903. Obscure diseases of kidney.. J. and A. Churchill. 

FLETCHER. 1901. ‘Trans. Path. Soc., LII., 199. Embryonic growth. 

Fox, Соһсотт. 1884. Trans. Path. Soc., XXXVL, 460. Sarcoma of adrenals, 
overgrowth of hair. 

FRANKEL. 1886. | Virchow's Archiv., CIII, 244. Growth of adrenals, 
nephritis, uremia. 


Bibliography. 291 


FREITAG. 1898. Ziegler's Beitráge, XXIV., 363. Sarcoma of adult kidney ; 


review. N 
FRUITNIGHT. 1895. Archives of Pediatrics, XH., 881. ‘Trial of Coley's 


fluid. к 
GATTI. 1896.  Virchow's Archiv., CXLIW, 467. Summary of question of 
adrenal rest tumours. 
«GIORDANO. 1892. Ann. des Mal. des Organes Génito-urinaires, X., 584. 
Growth of pelvis, nephrectomy. 
GRAUPNER. 1898. Ziegler's Beiträge, XXIV.,385. Adrenal rest growth. 
399. Kinds of carcinoma. 
GRAWITZ. I. 1883. Virchow's Archiv. XCIII., 39. “ On the nature of so- 
called lipoma,” 
п. 1884. Langenbeck’s Archiv., XXX., 824 Origin of tumours 
from adrenal rests. 
. GREENHOW. 1866. Trans. Path. Soc., XVIII, 260. Growth of adrenal, no 
metastases. l 
GUILLEMAIN. 1891. Gaz. hebd. de Méd., LII., 619. Methods of diagnosis. 
Guyon. 1900. Ann. des Mal. des Org. Gen AS ANSE: XVIII., 1. Diagnosis 


of renal growth. 
HABERSHON. 1866. Guy's Hospital Reports, XII., 423. Report of Case 15 


of Guy's series. 

HANSEMANN. I. 1896. Deutsch. Med. Woch., p. 52. On Endothelioma. 

| п. 1902. Zeitschr. t. Klin. Med., XLIV., 1. Tumours, adenoma, 

endothelioma, etc. 

HAWTHORNE. :1894. Glasgow Med. Journal, XLI., 148. Growth with 
glandular invasion. 

HEBB. 1895. Westminster Hosp. Reports, IX., 121. Latent growth, sudden 
embolism. 

HEKTOEN AND RIESMAN’s Text book of Pathology, 1901. 

HERESCO. Thèse de Paris, 1899. Results of 165 nephrectomies for growth, 


bibliography. 

HEYDER. 1890. Archiv. f. Сурак, XXXVIIL, 301. Growths of the kidney 
capsule. 

- HILDEBRAND. I. 1894. Langenbeck's Archiv., XLVII., 225. Three cases 


` endothelioma, glycogen. . 
II. 1894. Langenbeck's Archiv., XLVIII., 343. Various cases. 
HoLMES, BAYARD. 1898. Journal Am. Med. Ass, XXXI., 403. Adrenal. 
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HOoLMES. 1872. Trans. Path. Soc., XXIV., 149. Vascular pulsating growth. 
Horn. 1891. Virchow’s Archiv, CXXVI., 191. Adrenal rest growths, 
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recurrence in nine months. 
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III. 1896. Deutsch Med. Woch, XXII., 345. Further cases and 
' remarks. 
JACOBSON AND STEWARD. Operations of Surgery. 1902. 
„ JOHNSON. 1899. Annals of Surgery, XXIX., 329. Three cases of growth. 


292 Growths of the Kidney and Adrenals. 


JONES. 1891. Med. Chron., Manchester, XXVL Recurrent papilloma. v. 
Kelynack, p. 223. 

JORES. 1894. Deutsch. Med. Woch, 209. Two cases of adrenal growth, 
structure of adrenals. 

KAMMERER. 1891. New York Med. Journal, LIII., 79. Опе case. 

1896. Annals of Surgery, XXIII., 747. “Cancer” in a woman, 
æt.60. tumour 6 years, 
nephrectomy, acci- 
dental death, 1 month, 
no metastases. 

1899. » 5 XXIX., 753. Nephrectomy, well 5 
months. 

1901. " -— XXXIV.,828. Death from recurrence 
in 2$ years. 

KEITH. 1902. “Human Embryology and Morphology.” 
KELLY. 1898. Ziegler's Beiträge, XXIII., 280. Review, three adrenal rest 
tumours, adenomata, and other cases. ' 
KEYES. 1903. “ Diseases of the genito-urinary organs." 
KELYNACK. “Renal Growths," 1898. 
I. 1896. Journ. Anat. and Phys, X., 539. Adrenal adenoma. 
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ш. 1897. Med. Chron., Manch., 401. Growths of adrenals. 
Iv. 1897. Journal Path. and Bact., IV., 236. Malignant cyst 
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KUSTER. I. 1890. Berl. Kl. Woch., XXVII., 641. Death on table from 
detachment of growth, successful removal of adrenal 
rest growth. 
п. 1897. СЫ. ғ.а. Path. дег. Harn-Organe., VIII., 583. Diagnosis 
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LANCEREAUX. 1890. Union Méd. de Paris, XLIX., 289. A case. 
LANGHANS. 1890. Virchow's Archiv, CXX., 28. Glycogen contents of 
tumours. 
LAZARUS. 1894. Berl. Kl. Woch., XXXI., 498. Adrenal sarcoma in a child of 4. 
LAZARUS, BARLOW. 190). B.M.J.,IL, 24. Two cases of true unencapsuled 
lipoma. 
Lzvt, EMILY. 1896. Archives of Pediatrics, XIII., 97. Table of nephrec- 
tomies for embryonic tumour. 
LOWENHARDT. 1888. Deutsch. Zeitschr. f. Chir., XXVIII., 583, Adrenal 
rest tumours. 
LUBARSCH. I. 1894. Virchow's Archiv., CXXXV., 149. Adrenal rest tumours, 
* cases, glycogen. 
II. 1594. is is CXXXVIL, 191. Reply to Sudeck. 
IH. 1902. Ztschr. f. Kl. Med., XLIV., 491. Reply to Hansemann, 
characters of adrenal rest tumours. 
LUNN. 1891. Trans. Path. Soc., XLII., 186. Hæmaturia 6 years, no pain, 
tumour weighed 43 lbs., no metastases. 
МсВовмеү, 1894, v. sub. Johnson. Annals of Surgery, XX, 373. 


Nephrectomy, boy æt. 10, discussion. 


Bibliography. 293 


McCormac. 1888. B.M.J., I., 533. Epithelioma and calculus. 

MCWEENEY. 1896. В. М. J., I., 323. Two adrenal rest tumours, figures, and 

review. 

MACKINTOSH. 1895. Lancet, I., 1371. An embryonic case. 

MAIDLow. 1898. В. M.J., I., 426. Growth removed weighing 7 lbs., nature 

uncertain, well 3 years. (Bland Sutton, p. 131.) 

MALCOLM. I. 1894. Trans. Clinical Soc.,XXVII.,94. Nephrectomy for em- 
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II. 1895. » 8 XXVIII., 287. Child shown well. 

III. 1896. Trans. Path. Soc., XLVII., 119. Sarcoma, girl æt. 19 
symptoms 2 years, removal, recurrence. 

IV. 1902. Lancet, II.,1197. Shows embryonic case, well 10 years. 

MANASSE. І. 1895. Virchow’s Archiv., CXLII. 164. Adenoma, kinds of 


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ligaments. 

MARTIN. 1896. Lyon Méd. One embryonic case. 

MORRIS. I. “Surgical Diseases of the Kidney." 1901 

п. 1893. B.M.J.,1.,1. Five nephrectomies. 
ш. 1899. » 11,1336. Four cases of adrenal growths. 

Moxon. 1868. Trans. Path. Soc., XX., 385. Adrenal adenoma, size of a 
chestnut. . 

MULLER, HELLMUTH. 1896. Virchow’s Archiv., CXLV., 339. Origin of 
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MURCHISON. 1870. Trans. Path. Soc., XXI., 240. Bilateral papilloma. 

NEWMAN. 1896. Glasgow Med. Jour, XLV., 179. Carcinoma following 
stone, ` 

NORMAN. 1893. Trans. Roy. Acad. Med. Ireland, XI., 377. Tubular adenoma 

OGLE. 1864. Trans. Path. Soc, ХУІ, 250. Adrenal sarcoma, child st. 3 
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PARKER, RUSHTON. 1897. Medical Press and Circular, II., 456. Tumour 
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PAUL. Liverpool Med. Chir. Journal, WV., 102. Embryonic growths, 

PENROSE. 1893. Trans. Path. Soc., XLIV., 96. Passage of fragments of 
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PERRY. 1888. В. M.J., I., 1382. Growth of adrenals. 

PERTHES. 1896. Deutsch. Zeit. f. Chir., XLII., 201. Adrenal rest growths, 
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Pick. 1901. Berl. Kl. Woch., XXXVIII., 299. On the origin of embryonic 
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POLLARD. 1884. Trans. Path. Soc., XXXVI., 272. Carcinoma and calculi. 

РОМСЕТ. 1897. Lyon Médicale, LXXXV., 122. Transperitoneal nephrectomy. 


VOL. LIX. 21 


294 Growths of the Kidney and Adrenals. 


RAMSAY, OTTO. 1899. Bull. Johns Hopkins, 20. Review of adrenal growths, 
RICKER. I. 1896. СЫ. f. Allg. Path., VII., 363. Renal elements in adrenal 


rests, etc. 
п. 1897. У „ VIII., 417. Adenomata and adrenal rests. 
RINDSKOPF. 1893. Deutsch. Med. Woch., 854. Effect of chloroform on the 


kidneys. з 
Ris, Ев. 1891. Beitrüge zur. Klin. Chir., VIL, 146. Three nephrectomies іп 
adults. 
RITCHIE AND BRUCE. 1890. Trans. Edin. Med. Chir. Soc., IX., 67. Carci- 
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ROBSON, MAYO. I. 1895. Clinical Journal, VIL, 98. Two nephrectomies, 
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п. 1899. B. M. J., IL, 1100. Three operations for adrenal 
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RoBERTSON. 1885. Trans. Glasgow Path. and Clin. Soc., II., 352. Encapsuled 
nodular growth, general diffusion, illness, death with obscure symptoms. 
RoLLESTON. I. 1895. Goulstonian Lectures on the Adrenals, B. M. J., I. 


629. 
» Trans. Path. Soc. XLVI., 150. Fibro-adenoma of 
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TI. 1899. T © „ 4L., 214. Cyst of adrenal adenoma. 


ROLLESTON AND KANTHACK. 1894. Journal of Pathology, 11., 80. Anomalous 
mass in kidney. 
RovsisG. 1895. Langenbeck's Archiv., XLIX., 407. Diagnosis and treat- 
ment of renal tumours in adults. 
ROYAL COLLEGE OF PHYSICIANS. 1896. Nomenclature of Diseases, p. 335. 
Classification of tumours. 
RUPPRECHT. 1890. СЫ. fur Gyn&k., XIV., 592. Adrenal rest tumour in а 
child æt. 24; quoted also in Trans. Path. Soc., XLVII., 128. 
ScHMID. I. 1892. Münch Med. Woch., XXXIX., 256. Embryonic growth, 
nephrectomy. 
u. 1893. Centralblatt f. Chirurgie, XX., 672. Embryonic nephrec- 
tomy, well 3 years. 
SCHMORL. 1891. Ziegler’s Beiträge, IX., 523. Adrenal rests in liver and 


sòlar plexus. 
SHARKEY. 1881. Trans. Path, Soc., XXXIII., 195. Growth beginning in 


glomeruli. 

SHATTOCK. 1894. В.М.Ј., II., 1176. Renal origin of embryonic growths. 

SHORT. 1896. Birmingham Med. Кес. XXXIX., 159. Case, great pain, late 
tumour, general invasion. 

SLOUKOVENTOFF. 1895. Gazette Méd. de Paris, 581. Growth of adrenal, 
symptoms pulmonary. 

STEELE. 1896. Med. and Surg. Reporter., LXXIV., 136. Embryonic, well 


2 years. 
STEINER. 1896. Berlin Klin. Woch., XXXIIL, 565. A nephrectomy by 
Israel. 
SuDECK. I. 1893. Virchow’s Archiv., CXXXIII., 405, Adenoma and car- 
cinoma. 
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reply to Lubarsch. 


Bibliography. 295 


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п. 1884. Journ. Anat, and Phys, XIX., 458. Adrenal 
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Threenodularlocalized 
growths, weighing 


TERRILLON. 1890. Bull. et. Mem. Soc. de Chir., XVI., 431 | #85» 750, and 1,500 
1890, ,, T " „ ХУІ, 474] 818: respectively, 


р" „ „ә ХҮП, 116 | !emoved by opera- 
im tion. The first case 


was well 28 months 
later. 

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THOMAS, LYNN, 1904., B. M. J., IL, 11. Use of urine separator in a case of 

growth. 

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п. 1884, S dh » XXXVI., 269. Papilloma 
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II. 1890. Trans. Clin. Soc, XXIII., 153. Adrenal 

Ko tumour, woman, æt. 36. Overgrowth 
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THURSTON. 1898. St. Thomas' Hosp. Rep., XXVII., 124. Growth and calculi. 

TREYER. 1899. Corr. Bl. Schweiz. Aerzte.. XXIX., 614. Growth with 

glandular infection. 

TURNER, CHARLEWOOD. 1885. Trans. Path. Soc., XXXVI., 464. Growth of 

adrenals, symptoms pulmonary. 

ULRICH. 1895. Ziegler’s Beiträge, XVIII., 589. Adrenal rests and their 

growths, lipomata. 

VAN DER BYL. 1855. Trans. Path. Soc, VIL, 268. Embryonic growth. 

VILLENEUVE AND NEPVEN. 1890. Bull. Soc. Chir. de Paris, XVI, 221. 

Colloid epithelioma, operation, recovery. 

VoiGT. 1902. Arch. für Gynik., LXVI., 658. Malignant papillary adenoma. 

WALKER. 1897. Annals of Surgery, XXVI., 529. Sarcomata in children. 

WALLACE. 1902. Trans. Med. Chir. Soc., Edin., XXL, 170. Two cases, an 

* adenocarcinoma " in a woman, æt. 30, nephrectomy, well in three weeks; 
and one year later: a sarcoma, man, eet. 53, one year ago hematuria, double 
varicocele, partial excision, varicocele cured. 


e 


296 Growths of the Kidney and Adrenals. 


WALSHAM, 1885. St. Barth. Hosp. Reps., XXI., 125. Calculus and growth. 
WARTHIN. 1897. Journal of Pathology, IV., 404. Fibrolipoma, 2 lbs., two 
years' duration, removed. 
+ WEBER, PARKES. I. 1896. Trans. Path. Soc., XLVII., 117. Lymphosarcoma. 
п. 1898. Ў » XLIX.,176. Papillary adenoma. 
ш. 1899. a. 5 L., 179. Multiple adenomata in 
contracted kidney, 
» 181. True lipoma. 
WEIR. т. 1887. Annals of Surgery, VI., 38. Papillary cystadenoma, 
operation, recovery. 
II. 1897. " B XXVI., 128. Calculus, kidney con- 
verted into fat. 
WENTWORTH, 1896. Archives of Pediatrics, XIII., 321, 341. Embryonic 
growths, review. 
, WEST. 1879. Trans. Path. Soc., XXX., 419. Growth of adrenal, pulmonary 
symptoms. 
WHITE, HALE. 1897. Guy's Hospital, Gazette 11. Diagnosis of renal growth. 
1884. Trans. Path. Soc., XXXVI., 464. Sarcoma of adrenal, 
considered secondary. 
WIGLESWORTH. 1892. Liverpool Med. Chir. Journal, XII., 254. табар ОЁ 
adrenal, size of an orange, found post mortem. 
~ WILKS. 1868. Trans. Path. Soc., XX., 224. Fibrous growth of kidney. 
+ WILLETT. 1895. Trans. Path. Soc., XLVI., 86. (a) Embryonic tumour, 
recurrence in 11 months. (b) Papillary adenoma successfully removed. 


Appendix of Cases. 297 


APPENDIX OF CASES. 


CASE 1. Infection of peritoneum, glands, and lungs. T.G., et. 18 (m.), was 
admitt»d under Dr. Cholmeley, September 8th, 1830, and died September 21st. 
He had been an invalid several months, with pain, wasting, and a large tumour 
which reached from hypochondrium to groin on the left side. Post Mortem: 
there were a few small tubercles (nature undecided) beneath the right pleura, 
tubercles in both lungs, and in the diaphragmatic pleura. (An examination 
made in 1890 shows that the main disease here is tuberculous.) Theabdomen 
contained dirty brown fluid and shreds of recent false membrane. The peri- 
toneum was thickly sprinkled with fungoid tubercles of various sizes, like 
boiled sago. (These were examined in 1893 and found to be spheroidal celled 
carcinoma.) ‘The descending colon passed over a tumour the size of a half- 
quartern loaf situated in the kidney. ‘Towards the top a part of this organ 
was found much distended and stretched, but in other parts it retained its 
natural structure. Elsewhere nothing could be discovered but the mere tunic 
distended over the substance of the tumour, which consisted of fungoid . 
material having the consistency of mortar, yellow, and in some few points 
semi-transparent. Traces of cysts and debris of vessels were to be dis- 
tinguished in it. Pelvis healthy. Other kidney healthy. ‘The absorbent 
glands near it, and those about the aorta, were loaded with opaque fungoid 
material and fungoid tubercles. Liver and spleen normal, their peritoneal 
covering tuberculated, as the peritoneum elsewhere. Green book X. 4T. 





Case 2. Short history, glands invaded.—A. K. M., xt. 67, was admitted 
under Mr. Cooper, July 30th, 1831, and died August 14th. He had a fall four 
months ago, injured his Joins, and coughed up some blood. A few days ago 
he had retention; the catheter brought away chocolate-coloured bloody 
urine. Hzematuria continued, and was accompanied by pain in the back and 
left side. He died with a bloody diarrhoea. Post Mortem: Lungs emphyse- 
matous and congested. On one of the bronchi of the left lung a mass, the 
size of a walnut, whitish, breaking down in places. Liver—one small solid 
deposit on the surface. Right kidney large, ureter dilated and thin, “а little 
gut." Left kidney enlarged, adjoining it a mass like a kidney in size and 
shape surrounding the aorta. The upper half of the kidney contained a 
scirrhous mass which rendered it twice its normal size. This seemed to have 
developed in the kidney, and to have encroached on its natural structure, 
(destroying a full half), from which it was ill-defined. It was rounded and 
nodular in form, a soft scirrhous growth with cyst formation and parts of 
almost medullary softening. There was some appearance of a ragged vege- 
tation sprouting into the superior infundibula. The mass round the aor 
consisted originally of glands, one was breaking down into a large eyst. Green 
book XVII. 140. 


298 Growths of the Kidney and Adrenals. 


CASE 3. Growth of adrenal, two months’ pain, invasion of liver, lungs, and 
glands.—S. B., æt. 29 (m.), was admitted under Dr. Addison on November 
2nd, 1842, and died on December 20th. Two months ago he had pain in the 
left loin and could not move his leg freely—no other symptoms. A tumour 
was felt on admission at the lower margin of the liver, which increased in size 
daily. He referred to the loin as the seat of pain. November 15th, explored 
by trocar — a few drops of blood issued—died five days later. Post Mortem: 
a few breaking-down masses in the lungs the size of marbles. Liver a mass of 
growth. Mes:nteric glands enlarged. A firm oval mass consisting of fungoid 
disease of the suprarenal body, cerebriform, but having oval portions the size 
of nuts, of cheesy consistency. Kidneys healthy, the whole reached to and 
thru-t up the spleen. Miscellaneous Inspections XXXII. 83. 





CASE 4. Embryonic growth, invading vena cava and auricle. —M. W., xt. 
2 years 9 months (f.) Admitted under Dr. Addison, January 25th, 1845, and 
died January 26th. Scarlatina 9 months ago, blow on side 6 months ago, 
history of vomiting. Post Mortem: Lungs free. Right kidney bigger than 
two adult kidneys. A good part of its tissue detached by 2:3 ozs. of very 
bloody fluid. The kidney retained a good deal of its form and tissue, being 
expanded by the growth within, which had escaped widely downwards as a 
heematoid mass, the rest medullary. “Vena cava and both renal veins dilated 
with very soft and bloody fungus, adherent, distinctly a growth, i.e., organized 
into the right hepatic veins ard auricle, a round nob the size of a walnut 
almost a clot of black blood, but containing serous cells or cysts, the whole 
variously cerebriform, fluid, and bloody.” Left kidney, soft, pale, and dull. 
Liver, a probable deposit posteriorly. Spleen, “ill defined peas—perhaps 
cerebriform.” Miscellaneous Inspections XXIII. 91. 





CASE 5. Growth spreading by vena cava to pulmonary artery.—W. M., xt. 
40 (m.). Admitted uuder От. Addison, March 3rd, and died October 10th. He 
had been “ill” for 12 months; urine free from hzematozine. Post Mortem: 
Right lung singularly full of water, and all the first branches of the pulmonary 
artery filled with pale brain-like fungus, The pericardium contained red fluid 
and scabrous fibrin. Left kidney nearly half the size of a liver, very full of 
fungus, cerebriform, or like soft cartilage. Pelvis filled with fungus. Calyces 
2inches long. Left renal vein and an inch of vena cava full of fungus, and 
above two or three fingers of organized growth—pale, fragile, and unequal. 
Right kidney enlarged, free. Liver contained one dark red tuber the size of a 
bean. Miscellanevus Inspections X XXIII. 205. 





CASE 6. Growth, calculi, direct invasion extending through diaphragm, 
abnormal adrenal.-—J. S., et. 35 (m.). Admitted under Dr. Gull, December 18, 
1852, and died January 13th, 1853. No history is available. Post Mortem: 
On opening the peritoneum a large fungoid mass was seen passing up from 
beneath the liver, but unconnected with it, passing up under the stomach and 
invading its outer coats but not its mucous membrane. It arose from the left 
kidney, the whole of which was infiltrated with growth. It invaded the inter- 
costal muscles and ribs 11 and 12, and extended backwards through the 
muscles, forming an external tumour. The kidney presented a mass of growth, 
dead in the centre, sprouting at its circumference. The pelvis contained an 


Appendix of Cases. | 299 


irregular nodulated calculus of pelvic shape; four others occupied cysts or 
dilated calyces beneath the capsule. The capsule was not invaded except at 
the hilum. The malignant mass passed through the diaphragm, invaded the 
left pleura (causing pleurisy), and in one or two places reached the lung. Right 
lung, one or two small deposits on the surface. Liver, 12 separate deposits. 
Right kidney healthy, 14 times the normal size. The suprarenal capsule was 
adherent to the body of the kidney and apparently beneath the tissue, but at 
the position where it was adherent the cortex appeared contracted; whether 
this was the result of inflammation or an abnormal position it is difficult 
to say. Miscellaneous Inspections XX VII. 35. 





CASE T. Two years’ history of tumour, metastases in lungs amd bones, 
glands free.—T. H., et. 69 (m.). Admitted under Dr. Addison, February 18th, 
1857, and died April 23rd. Well until two years ago, when he felt tightness in 
his abdomen, a tumour discovered after some months’ ill-health. On admission 
very feeble. Large mass, evidently renal, in right side of abdomen, which can be 
raoved bimanually, Hematuria. Post Mortem : Lungs and pleura full of growth, 
bronchial glands free. The tumour is almost all kidney, very few of the 
adjacent glands are involved. The ascending colon passes in front of it, the 
vena cava and aorta are displaced to the left. Mesenteric glands free. One 
mass the size of an egg in the right lobe of the liver adjoining the kidney. 
Left adrenal large, one deposit the size of a pea. Right adrenal involved in 
the growth, and forming a lump the size of an egg on top of it (the growth 
had evidently begun in both adrenals from a localised deposit). At one end 
remains of the capsule are seen, about one-half was destroyed. Right kidney 
quite circumscribed, and can be turned out easily with the adrenal and a few 
infected lymphatic glands, the whole the size of a fcetal head. On section a 
firm and fairly uniform mass of growth, some soft and growing, some breaking 
down and caseating. On closer examination a bit of healthy kidney was still 
seen intact, and in parts the mucous membrane of the pelvis remained, so that 
when the growth was removed the original form of the organ could be seen, 
and the method ofinvasion. Ureter normal and free, its channel joined the 
cancer in the pelvis. Renal vein full of a mass of soft growth, protruding 
into the vena cava. Nodule in right epididymis. Deposit in inner condyle of 
right humerus, destroying the joint. Growth from medulla of right tibia. 
Insp. 1857, 80. ' 





CASE 8. Five months’ pressure on nerves, no metastases,—M. R., æt 57 (m.). 
Admitted under Dr. Habershon, July 16th, 1856, and died October 29th. 
gouty—a drinker. In May last had sudden pain in course of left dorsal 
nerve, apparently causeless, which grew worse. He was admitted to hospital, 
no disease could be found, urine normal—discharged unrelieved. Re- 
admitted under Drs. Habershon and Hughes, September 13th.  Relieved by 
blisters. October 22nd. became soporous, urine drawn off was scanty and 
highly albuminous, died a week later. Post Mortem: Lungs normal; heart, 
some vegetations on mitral and aortic valves. Mesentery and glands normal, 
liver cirrhosed. Peritoneal surface of spleen covered by whitish tubercular layer 
fin. thick, cancerous (1 capsulitis). In the vena cava a loose ante-mortem clot 
an inch long, opposite renal veins, softened centrally. Right kidney engorged, 
patch on surface such asis seen with a diseased mitral—nothing cancerous. Left 


300 Growths of the Kidney and Adrenals. 


kidney, substance engorged, tubules filled with granules and cells, surface 
granular. Pelvis nearly obliterated by cancerous growths. Thickening round 
pelvis leading to pressure on left dorsal nerve. At the pelvis were several 
masses the size of walnuts, two had dense fibrous envelopes and cheesy 
degenerative contents of fat granules and nuclei. Adjoining and encroaching 
on the kidney was a rather larger mass, softened from effused blood, and 
presenting under the microscope abundant large nuclei and blood. In the 
kidney structure near this part was a small mass of effused yellowish-white 
product, consisting of large cells, some containing two large nuclei, others 
large nuclei nearly filling the cells, others free. Znsp. 1856, 210. 





Cast 9. Haematuria 3m., paralysis 2m., infection of glands, spine, and 
lungs. —S8. W., et. 58 (f.). Admitted under Dr. Hughes, December 5th, 1857, 
and died January 21st, 1858. She was admitted for hematuria of three 
months' duration. She had been ailing for about a year, and for two months 
had been unable to walk. On admission paraplegia increased and bed-sores 
appeared. Post Mortem: Body much wasted. The cancerous growth in the 
abdomen had destroyed a large part of the spine. It seemed as if the bodies 
had been attacked separately, as two of them had quite disappeared and 
the intervertebral discs were in contact. Above this the bones were black 
and necrosed, and connected with some suppuration in the back. The lower 
dorsal and upper lumbar vertebrae were thus diseased, and the disease had 
extended into the spinal canal. The membranes of the cord were black and 
sloughy, and the medulla within was quitesoft. Both lungs contained numerous 
nodules of cancer, mostly on the surface, one or two pedunculated ; bron- 
chial glands infected. Liver, peritoneum, pancreas, normal. The lumbar 
glands formed a large malignant mass. Museum specimen 1649. 

The left kidney is somewhat enlarged and laid open to show its substance 
thickly beset with soft nodules of growth ğ-1 in. across. On the reverse, 
similar nodules are seen to project from the surface of the organ, and there 
is one prominent bossy growth measuring 2% in. across, to which the capsule 
is adherent. Histologically the deposit consists of a fibrous stroma, the 
alveoli of which arelined with cubical epithelium, some of tbem being also 
filled with spheroidal cells. “ Cylindrical and spheroidal carcinoma." Jnsp 
1857, 11. 





CASE 10. А year's vague illness—extensive glandular | infection —later- 
invasion of luwngs.—W. G., et. 30 (m.). Admitted under Dr. Willis, January 11th, 
and died February 1st. He had been ailing for about a year, and gradually 
becoming anzmic and weak, but with no positive symptoms. He had been 
considered phthisical, but the physical signs of this were wanting. On 
admission he was bedridden and anemic, but had no pain or symptoms to 
localise his illness; there was some inconsiderable crepitus at the apices of 
his lungs. Idiopathic anemia, Addison’s disease, and deep-rooted disease 
about the stomach were discussed. Post Mortem : Wasted ; right leg swollen, 
Small masses of recent growth scattered throughout the lungs. At the apices 
old healed phthisical cavities, and a few minute tubercles. Bronchial glands 
full of caseous deposits. Liver normal. Right kidney much enlarged and 
nearly destroyed by growth, which was probably primary here. The growth 
passed to the hilus but did not break through it, and it was still outside the 


Appendiv of Cases. 301 


vein, though the latter was compressed. Ureter and pelvis unaffected. The 
neighbouring glands and the whole lumbar chain were infected, and through 
these the deep inguinal below, and the mediastinal above. Vena cava com- 
pressed and nearly blocked by adherent thrombus ; there was no growth within 
the vein. Glands round pancreas very firm; no doubt their pressure on 
the thoracic duct had been a cause of emaciation. Small deposits in left 
adrenal; left kidney normal. Insp. 24. 





CASE ll. Vague history—metastases in lungs—no others. —E. P., æt. 62 (f.). 
Admitted under Dr. Barlow, March 5th, 1861, and died May 17th. She came 
in with a history of pain in the chest and diarrhoea, and said that some time 
ago she used to throw up everytning she took. She was wasted. Albuminuria 
was present and cedema of legs. She continued to have diarrhea and occa- 
sional vomiting. (Report ends.) Post Mortem: Body wasted. Numerous 
small secondary deposits in both lungs. Liver, glands, adrenals, normal. Other 
kidney not described. Right kidney much enlarged by growth, the upper 
half replaced by a round tumour, which had not come through the capsule, 
but within projected into the pelvis. On section soft and medullary, the 
interior containing yellow degenerating masses. Insp. 1861, 92. 





CASE 12. Embryonic tumour, no metastases.—'Y. H., et. 11 (m.). Admitted 
under Dr. Gull, February 11th, 1863; died February 27th. He was sent up 
from Swindon with a large abdominal tumour, which had been growing for 
some months. It sprang from the left side, and presented obscure fluctuation. 
The boy was ill and thin. Mr. Birkett explored and extracted a little 
gelatinous matier. Post Mortem: Body very thin. Lungs normal Large 
tumour present in left loin, reaching from diaphragm to pelvis, and nearly 
reaching the right side. It touched the parietes in front, so that the intestines 
lay coiled up in a small space on the right side and the transverse colon above. 
The descending colon ran down the front aspect of the tumour. On examining 
the posterior surface, the left kidney was seen stretched over the tumour, and 
about twice its usual size and length; its upper part was free, its lower part 
involved in the disease. The anterior part of the organ was almost destroyed, 
especially below; above the upper part was untouched, even its anterior 
margin. Contents semi-fluid. The growth at the lower part seemed at first 
sight to be soft cancer, but emitted no juice on pressure, and corresponded 
rather to recurrent fibroid. Some parts had a gelatinous fluid in the 
meshes. Insp. 1863, 51. 





Case 13. Tumour 23m. hydronephrosis, glandular and slight lung invasion. 
—W. S. xt. 60 (m.) Admitted urder Dr. Barlow May 26th 1864, died 
August 21st. Six weeks ago he noticed a swelling the size of the palm of the 
hand below his left ribs, fixed, not moving with respiration. Urine acid, no 
albumen. Tumour increased and became painful, and evidently contained 
fluid. On July 24th there was pus in the urine. Mr. Foster put in a trocar, 
and drew off 2-3 pints of bloody fluid. (е cyst soon filled again, and the 
patient sank and died. Post Mortem: A few deposits in lungs. The tumour 
was clearly an enlarged carcinomatous kidney. The great bulk of it was a 
Cyst chiefly filled with blood. When this was emptied, white masses of fibrin 
were seen adherent to its walls, and nodules of growth in them. Тһе lower 


302 Growths of the Kidney and Adrenals. 


part of the kidney was composed of fungous masses, and at the upper end, 
where remains of kidney substance were seen, some distinct masses of 
cancer existed. ‘These were connected with similar masses in the lumbar 
glands. Med. Reports p. 34. Insp. 1864, 207. 





Cask 14. Paralysis, deposits in skull, glands, liver.—J. R., xt. 34 (m.). 
Admitted under Mr. Cock, October 21st, 1863, and died November 11th. He 
was admitted with partial paralysis, attributed to an injury to his back, and 
lived three weeks. His mind was enfeebled. Post Mortem: Numerous 
cancerous deposits between skull and dura mater. Spine not examined. 
Numerous patches of tubercle all over the surface of both lungs. Cancerous 
deposits in glands near stomach. Liver full of deposit, cirrhosed, and hard. 
The deposits in lumbar glands, kidney, etc., involved the adrenals, These 
were 2-3 times their usual size, and at first sight seemed quite destroyed. A 
section showed a mass of effused blood, with white growth round the edges, 
and covered in one case partially, the other completely, by flattened cortex. 
On the top of one kidney and in contact with the suprarenal body was a large 
tumour, bigger than the kidney itself, containing a quantity of debris, and in 
a few places well-marked growth. A careful section showed that the cancer 
had grown in the kidney, destroyed its upper part, and expanded the true 
capsule of the kidney over it. Insp. 1863, 271. 





CASE 15. Gronth of adrenals. Weakness, vomiting, pain, local invasion, 
deposits in both kidneys and ovaries.—K. B., set. 38 (Ё). Admitted under Dr. 
Habershon, June 16th, 1866. Her health had been failing for 8 years, and 
the duration of the growth was uncertain. The most marked symptoms were 
abdominal pain, emaciation, loss of appetite, weakness, vomiting, sallow- 
ness, and the presence of a tumour. Post Mortem: Lungs normal. 
No evidence of pressure on thoracic duct. Two large tumours connected 
across spine by enlarged glands and pushing cola forwards, extending 
above kidneys, and pushing up liver and spleen. Liver flattened and 
capsule invaded over an area 5 inches in diameter, where it touched the mass. 
Spleen notadherent. Both adrenals enlarged to 3-4 times the bulk of a kidney. 
Both kidneys separable, the right touching at one point only, the left applying 
itself to a convexity of the lower end of its adrenal. Kidneys irregular, 
almost destroyed by masses of growth developing in the cortex. Only the 
lower part of the right kidney normal. Growth encephaloid. Liver free. 
Glands near the growth enlarged. Both ovaries, the size of a walnut and 
kidney potato respectively, were infected with growth. Insp. 1866, 177. 
Guy's Hosp. Rep. XII., 423. 





CasE 16. Death from metastases in brain and thorax, abdominal glands 
free. —G. C., æt. 51 (m). Admitted under Dr. Habershon, February 22nd 1870, 
and died March 10th, 1870. Seven months ago he fell and hurt his back, 
lately he has had loss of memory and fits in which he does not lose conscious- 
ness, Paralysis of right side followed; he became nearly comatose, but 
could protrude his tongue when asked. He lost his speech, either from 
aphasia or dementia. Urine never procured. Post Mortem: Left side of 
brain much flattened. A spherical tumour occupied the left vertex, the size of à 
billiard ball, containing cysts, vascular, with much cheesy degeneration. Round 


Appendix of Cases. ` 303 


it the hemisphere for two-thirds of its extent was in a state of yellow 
softening. In the pleura some 20 growths, the size of 4 pea to a bean. Lungs 
themselves free. Bronchial glands infected. Venacava stuffed like a small 
sausage with ante mortem clot of various ages. Evidently there had till 
recently been a way for blood to creep through the interstices of the clot, 
which extended down to the iliac veins. Liver, mesenteric, and lumbar 
glands quite free. Adrenals free. Right kidney, 30 oz. swollen into a 
cancerous mass, which was still within the capsule at nearly all points, but at 
some few was growing through as fungoid nodules. On section a good deal of 
necrosis, cysts few and small. Veins of kidney full of ante mortem clots, and 
the pelvis filled by a dark brown decolorizing clot which extended down to the 
upper end of the ureter. Here the cancer sprouted through into the tube and 
obstructed it, causing distension of the pelvis. ‘The cancer in the ureter had a 
soft papillary growth, its growing margin in the kidney was in the form of 
soft red vascular masses, it came. chiefly around the roots of the pyramids as 
marble-sized spherical growths. Testes normal. Insp. 1870, 54. 





CASE 17. Hematuria 21 months, tumour 1 month —invasion of liver and 
some glands.--J. C., æt. 34 (m.). Admitted under Dr. Habershon May 6th 1879, 
and died May 2ith. Twenty monthsago he had hematuria, and since then he has 
lost much flesh. A month ago he first noticed a tightness of the abdomen 
after meals, this got worse and the hepatic region became tender. On 
May 1st he again had hematuria. On admission there was a tumour occupying 
the right hypochondriac, lumbar, and iliac regions. ‘The epigastrium was dull. 
Urine dark, 1028, small red clots. While in the hospital he had an interval 
free from hematuria, and then a recurrence. Tenderness and swelling 
increased. On the 26th while walking across the ward he fainted and died in 
а few minutes. Post Mortem: Pleurz healthy, and lungs, except for some 
compression of the right base. Heart normal. Liver, 148 oz., full of large 
masses of growth, some circumscribed, some infiltrating, all of them diffluent 
and creamy. Lumbur glands a little large and very cream-like on section. 
Adrenals normal. Left kidney, 11 oz., dark and hard enough for the kidney 
of cardiac obstruction. The vessels are healthy and not blocked by the 
tumour. Right kidney, 69 oz. filling right loin and crossing the mid-line, 
ascending colon pushed forward and adherent to the front ofit. Right lobe 
of liver adherent and displaced upwards. Surface lobulated, growth 
encapsuled except where it adheres to the liver. Vessels not plugged or 
abnormal. On section a large fibrocystic mass retaining the shape of the 
kidney, but with no trace of renal tissue. Cysts full of soft red ard brown 
creamy fluid. Right hydrocele. Testes normal. Microscopically : cells of all 
shapes, many angular or epithelioid. “ Therefore the growth may be called 
medullary carcinoma.” Insp. 1879, 202. 





CasE 18. Bronchitis—growth found post mortem-—no metastases—M. H., set. 
67 (f.). Admitted under Dr. Pavy, July 9tb, 1873, and died July 14th, 1873. 
She had had a cough 18 years, and for the last month, cedema of the legs. 
On admission she was thin, with the signs of bronchitis. (Edema of legs and 
of the body wall, chiefly on left side; ascites. Liver palpable below ribs, 
Urine, 1022, albumen, granular casts. Post Mortem: pleurisy, emphysema, 
cedema of lungs, bronchiectasis, a dissecting varix of left fe oral vein. Liver, 


304 Growths of the Kidney and Adrenals. 


vena cava, etc., normal. Left kidney, 44 ozs. granular, some small cysts, surface 
speckled with minute yellow grains, which microscopically were of some solid 
opaque fatty material. Right kidney, 7 ozs., smcoth, with similar yellow points, 
Described in the catalogue as ‘‘a kidney of normal size, of which the structure 
is for the most part replaced by a mass of growth, which in the recent state 
was soft and yellowish. On section the growth consists of an aggregation of 
nodules partially separated from each other by fibrous tissue. The pelvis is 
dilated, and at either end of the kidney is a shell of persistent cortical sub- 
stance. On the reverse a mass of growth is seen occupying the hilum and 
projecting into the renal vein.” It was noted at the post mortem that in 
addition to this another mass tbe size of a walnut lay in the channel of 
another dilated bunch of veins, probably going to join the trunk outside the 
organ. Even within the hilus it was evident that a good deal of the mass lay 
within dilated venous channels. Histologically the growth is a medullary 
spheroidal-celled carcinoma with areas of colloid degeneration. In the post 
mortem report the growth is described as full of fat globules, looking like a 
very fatty liver. After a time however, it became evident that these globules 
were inside cells of a very irregular form, with large oval nuclei. Some were 
of the shape of cylindrical epithelium, some pear-shaped, some granulated. The 
growth was not suppurating but infiltrated with fat. Even the most recently 
growing parts presented the same peculiarity. In the report to the Patho- 
logical Society it is noted that the cells were not degenerated but infiltrated 
with fat. On hardening, a portion shewed the characteristic alveolar structure 
of a carcinoma. Many cells contained two nuclei. Znsp. 1873, 219. Museum 
Specimen 1647. Med. Rep. 194. Trans. Path. Soc. XXVII., 204. 





CASE 19. Two years hematuria—invasion of portal venous system.—W. H., 
æt. 47 (m.). Admitted under Dr. Willis, January 4th, and died February 20th. 
He has had hematuria two years, and has been admitted three times previously. 
For the last 9 months he has been able to walk ten miles daily. He now 
comes in for hematuria, ascites, and pain at the umbilicus and bladder. The 
abdomen is distended and dull, except over the stomach and descending colon. 
A mass. fills the left lumbar and part of the left iliac and hypochondriac 
regions. Abdominal veins distended. Edge of spleen palpable over the 
tumour. Urine 1026—turbid—no albumen. Only about half-a-pint is passed 
daily. Ascites and pain increased, nausea came on, and cedema of the lower 
half of the body. He gradually sank and died. Post Mortem: There was one 
infected gland behind the manubrium, and a deposit the size of a marble in 
the left lung. Otherwise the thorax was healthy. ‘The vena cava inferior 
contained clot of 3-4 weeks’ duration, reaching down the iliac and femoral veins. 
Peritoneum free, it * was projected highly in spots, but did not take on the 
cancer action.” The mesenteric veins were distended with cancer down to 
the branches which ran over the intestinal walls; they were thickened and 
contained a pink creamy diffluent material. The veins were involved where their 
branches crossed the cancerous kidney: here the cancer thrust itself up in 
large masses, which were softened within to a cyst-like appearance. The liver 
was full of cancer. . . . . It appeared certain that the cancer came 
generally into the liver along the portal channel. In the same way it reached 
the colon also, and from the ends of the cancerous veins it grew into the 
mucous membrane of the bowel in heap-like elevations showing a remarkable 





Appendix of Cases. 305 


preference for the mucous rather than the peritoneal surface. Left adrenal 
involved in the growth. The left kidney formed a mass thewize of a cocoanut, 
the colon passed down in front of it and was adherent at one point. The 
organ preserved its general outline and had a thick capsule. There were 
effusions of blood into the remains of the pelvis and on the surface of the 
séction. The left testis contained a nodule of growth. Jnsp. 1874, 51. Med. 
Rep. 342. 





CASE 20. Hamaturia 9 months, hydronephrosis —local invasion without 
metastases.—J. С., æt. 66 (m.). Admitted May 12th, 1873; re-admitted under 
Dr. Moxon December 17th 1873, and died February 27th, 1874. He has had 
bronchitis five years. Twenty years ago he had a sudden attack of hematuria. 
In May, 1873, he passed blood. He was twice admitted to hospital for this. 
In June he noticed pain, and there was a dull elastic fulness in the left hypo- 
chondrium. Bleeding then ceased, but recurred in August, and again later. 
On re-admission it had been copious for the last seven weeks. There was then 
pain in the left side, and à dull rounded mass in the left loin. Liver dulness 
normal. Systolic aortic murmur. Urine was 30-40 oz. daily, alkaline, 1020, 
It contained blood, but no clots or casts. Bleeding and pain continued. During 
January the daily urine sank to 14 ozs. and became purulent. The tumour 
became rather bigger and more distinct. Post Mortem: Pleura and lungs 
free. Aortic stenosis. Mitral failure. Fibroid degeneration of left ventricle». 
Liver free, perihepatitis. No glands or thrombosis mentioned. Capsulitis of 
spleen. The left kidney formed a flattened tumour over which ran the de- 
scending colon. It contained two collections of reddish purulent urine. On 
emptying these the lower part collapsed ; the upper remained as a solid mass 
of firm whitish growth infiltrating the structures to the inner side of the kidney 
and the side of the spine and round the aorta, which was at one place com- 
pletely surrounded. The lower part was an ordinary sacculated kidney, with- 
outsecreting structures. The new growth was in places growing into the septa, 
and even fungating into the cavity. The growth was doubtless in the kidney ; 
its exact site could not be made out. It infiltrated the surrounding structures, 
and the glands round the aorta were full of it. Elsewhere no secondary 
growths. Right kidney granular, arteriosclerosis. Znsp. 1874, 76, Med. Rep. 300. 





CASE 21. Growth found post mortem, death from fractured base.—J. C., 
æt. 55 (m.). Admitted and died December 13th, 1870, under Mr. Bryant. 
He fell, fractured the base of his skull, and died. The post mortem showed 
the condition diagnosed. Apart from this, the left kidney was occupied at 
its upper and hinder part by a lobulated cystic tumour as big as an orange. 
It proved to be solid and composed of a gelatinous alveolated tissue with 
blood extravasated into its cortex. It was distinctly in the substance of the 
organ. It was very soft, and seemed hardly organised at all. In the pyramids 
` of the kidney were many cysts filled with the same mucous material. Fat at 
the hilus free. The rest of the kidney and the adrenals were healthy. Micros- 
scopically the growth is cellular and alveolar, the cells are very difficult 
to recognise owing to the peculiar glassy change they have undergone. It is 
described as colloid. and cylindrical celled carcinoma. Insp. 1875, 494. 
Museum Specimen, 1650, 


306 = Growths of the Kidney and Adrenals. 


CASE 22. Growth of adrenal, local and glandular infection, extension through 
diaphragm.—J.8., œt. 25 (m.). Admitted under Dr. Pavy, April 19th, 1876, 
and died June 7th. Perfectly well up to six weeks ago. He then, while 
digging, was seized with a sudden pain in the left side, which forced him to 
lie down, and since then he has been in bed with continuous pain, aggravated 
by solid food, and some vomiting. On admission he was sallow and wasted, 
his abdomen was not distended, but there was a painful hard solid mass, 
resonant on percussion, in the left hypochondrium. Urine normal. Heart and 
lungs normal. Pain went on, one day he had retention, which passed off. The 
wasting increased, and the tumour became rather less definite in outline. On 
April 24th he developed a left-sided pleurisy. On June 5th his liver was 
noticed to be hard and enlarged. Just before death he passed a quantity of 
blood from the bowel. Post Mortem: Diaphragmatic pleurisy right side 
(slight). Left pleura contained two or three pints of fluid. On the surface 
of the diaphragm was a layer of fleshy growth, which had extended through it. 
Lungs free, the left compressed. Mediastinal glands all enlarged and fleshy. 
The left side of the diaphragm infiltrated by growth. Kidneys normal. A 
large mass was present in the left hypochondrium, pushing forward the stomach 
and transverse colon. On separating the coils of intestine below this a cavity 
was opened full of dirty fecal fluid. An acute peritonitis was present, 
possibly due to escape from this, the surfaces were covered with lymph, and 
there was half-a-pint of fluid in the pelvis. Mesenteric and lumbar glands 
enlarged, white, and succulent. The spleen had to be shelled out of the mass, 
and the upper end of the kidney was embedded in it. It extended beyond 
the stomach, which adhered to it, involved parts of the pancreas, and merged 
into a mass of enlarged glands which lay along the front of the spiue. It 
surrounded, but did not invade, the portal vessels. The adrenal was much 
enlarged and converted into a fleshy mass of growth. It seemed provable 
the disease had begun in this organ. Right adrenal normal. No communica- 
tion could be found between growth and intestine, and the terminal 
hemorrhage is unaccounted for. Insp. 1876, 223. Med. Rep. 210. 





CASE 23. Hematuria over 2 years. No secondary invasion.—H. D., zt. 69 
(m.) Admitted under Dr. Habershon, March 18th, 1876; re-admitted May 
16th, 1878, and died May 18th. Since 1873 occasional nausea and malaise. 
Early in March 1876 he suddenly felt sick and passed half-a-pint of bright 
blood, and later blood mixed with urine. He developed a cough and a shooting 
pain in the left loin. Bleeding was increased by exertion. At his first 
admission there was tenderness in the left loin and hematuria. He remained 
in nearly three months, and on one occasion it was noted that he passed some 
villous growth enclosed in a clot. After his discharge he had hematuria with 
intermissions of as long as six weeks. On May 16th, 1878, he had suppression 
of urine for 36 hours. He was admitted, and three pints of blood were drawn 
off with a catheter at different times during the next two days. Post Mortem: 
Lungs, liver, lumbar glands, adrenals, normal. Right kidney fully twice the 
normal size, nodulated on the surface, and two-thirds of it occupied by a soft 
yellow alveolated growth. It seems to have started in the cortex, for the 
pyramids are still discernible in the growths almost untouched. There is part 
of the lower end of the kidney which is uninvaded by growth—this is granular 


Appendix of Cases. 307 


on the surface. The other kidney is granular and both contain cysts. The 
arteries are thick. Prostate the size of a Tangerine orange. Insp. 1878, 187. 
Med. Rep. 338. 

CASE 24. Haematuria З years, metastases іп bones.—W. A., set. 34 (m.). 
Admitted under Dr. Moxon, June 15th, 1874; died August 4th. He has 
hardly been sober for five years, except when he was illin bed. Quite well till 
three years ago, when he had hematuria. He has had two attacks since, one 
21 years and one 2 months ago. A month ago he woke up with “pins and 
needles " and total paralysis of left arm and shoulder, present since. On 
admission cannot move left arm. Pain in left fore-quarter. Weakness left 
knee. Pain in head. Chest normal. Urine 1012 no albumen. The left 
arm improved a little in hospital, then got worse, and the right arm became 
weak also. A “ postpharyngeal abscess'' of 4 oz. was evacuated. His legs 
became weak and entirely paralysed by the end of July. Two “cold 
abscesses ” appeared on the left side of his chest. Post Mortem: Many 
deposits of growth in both vault and base of cranium, and one in the 4-5 
cervical vertebrz, infiltrating the tissues in front. Two ribs оп the right side 
had masses replacing their centre. Pleura and lungs normal. On the anterior 
surface of the right auricle a growth the size of a pea, 3-4 nodules in the liver. 
A few lumbar glands adjoining the left kidney were slightly enlarged with 
white growth. A secondary nodule in each adrenal. Right kidney normal. 
Left kidney a large mass of soft cancer, triangular in shape, the lower end 
globular. The mass was composed of red, white, and yellow substance in 
various stages of degeneration. At the upper end some kidney substance was 
spread out over the growth, as if it had began near the pelvis and made its 
way outward. The pelvis was much dilated, and large polypoid masses of 
growth projected into it. The renal vein was invaded and blocked by a mass 
of growth. Microscopically the growth was composed of all kinds of cells, 
mostly angular and epithelioid, of all sizes. The stroma was fibrous, and did 
not tend to a definite areolation. Jnsp. 1874, 317. Med. Rep. 92. 





CASE 25. Tumour 12 years, hematuria 14 years— General visceral infec- 
tion.—H. S. æt., 49 (m.). Admitted under Dr. Moxon, August 2nd, 1876, and 
died September 4th, 1876. Twelve years ago he noticed asmall movable lump the 
size of a pigeon’s egg in the left lumbar region, which was painless. Fifteen 
months ago he had intermittent hematuria over some 3 weeks, this has not 
recurred since. Seven months ago he began to lose flesh, and 6 weeks ago he 
noticed a rapid increase in the size of the lump, and an aching in the legs. 
He thinrs this is the same lump that he noticed originally, not a fresh one. 
For the last week it has been painful. On admission he was wasted, the left 
side of the abdomen from ribs to ilium was filled with a solid dull mass, 
crossed vertically by the descending colon, nodular, and movable on bimanual 
palpation. Urine, 1015, albumen, no blood. He became weaker, suffered from 
a varying amount of pain, and on August 14th, became delirious and remained 
so till his death. The tumour increased in size, Post Mortem: lungs full of 
secondary nodules, soft, most of them under ğ-inch across. Liver, 620z.a few 
scattered nodules. Mesenteric glands much enlarged with deposit, some of 
which is caseating. Left kidney 47 oz., a mass of cancer arranged to some 
extent in nodular masses. A large part of this had undergone caseation, and 
there were also fibrous patches. The recent growt): was soft and pulpy. 


308 Growths of the Kidney and Adrenals. 


Some cysts contained a dark brown fluid. No renal substance left. Right 
kidney, several little nodules of secondary deposit. Insp. 1876, 363. Med. 
Rep. 323. 





CASE 26. Rapid glandular invasion—death in three months.—M. L. (E), 
et. 41. Admitted under Dr. Willis,September 11th, and died September 27th. 
Family and personal history good. Thirtsen children besides miscarriages, 
Only three alive, of whom two are hydrocephalic idiots and one deranged. The 
others died of hydrocephalus at about two or three years of age. On June 30th. 
she had a severe labour. She got up three weeks later, and was attacked with 
shivering, vomiting, and pain in right loin and epigastrium. She went to bed 
for a week and then noticed a swelling in the right side. On admission she 
was wasted, the skin dry and pig mented, ankles swollen, nausea constant. 
Urine 1030, acid, albuminous. Right side of abdomen hyperesthetic. Hard 
tender mass continuous with liver. This is dull and the rest of the abdomen 
tympanitic. She lay in a listless state with occasional vomiting (no jaundice), 
and died with signs of heart failure. Post Mortem: the whole dorsal and 
lumbar spine was infiltrated with growth, which also involved the right lower 
ribs and subpleural tissue. Both lungs were studded with nodules of hard 
growth, in size from a pea to a walnut, which were more numerous on the 
surface. Blood-stained fluid in right pleura. Bronchial glands unaffected. 
Liver enlarged and studded with soft growth, especially on the right side. 
The liver, right kidney, glands, aorta, and vena cava were fused into one 
shapeless mass of growth. The vessels were compressed but not involved, and 
a clot which filled the left common iliac vein was apparently innocent. There 
was a nodule in the ilium near the ilioccecal valve. Right kidney showed 
a fairly healthy structure below and inside, where it was wasted and anaemic. 
The growth was soft and medullary, and looked oldest above. There was one 
small nodule in the left kidney, and of the adrenals the right was cancerous, 
the left healthy. Dr. Willis thought the right kidney the primary source, no 
other possible origin was found. Insp. 1877, 361. Med. Rep. 309. 





CASE 27. Calculus 4 years, hematuria, direct extension to liver, growth in 
ureter, no other metastases.—W. P., et. 58 (m.). Admitted under Dr. Moxon, 
May 1st, 1878, and died J uly 11th, 1878. Four years ago he had hematuria and 
pain. Three years ago he passed a calculus the size of a pea ; he continued to pass 
blood up to the present. In February he was seized suddenly with severe pain in 
the right side while in bed. In April he had dysuria, the passage of clots, and 
pain, which has continued. There is no vomiting, appetite is good, the liver 
normal; urine 1022, contains blood. A mass is felt bimanually deep in right 
loin, He went on with occasional hematuria and pain in the right, and later 
in the left loin, and lost flesh. A nodule appeared in the lower edge of the 
liver, which by the end of June extended two inches below the ribs, He 
became drowsy and unconscious, and sank. Post Mortem: All the viscera 
were healthy except the liver and kidneys. The right kidney formed a large 
irregular mass adherent to the liver. A large, firm, infiltrating growth 
occupied its upper half, growing round the adrenal, and changing its substance 
into caseous growth only recognizable as adrenal by its position and a little 
brownish pigment. Thence the mass grew upwards into the right lobe of the 
liver, and had spread from here through the liver substance as firm white 


Appendix of Cases. 309 


circular nodules. The lower part of the kidney was involved in growth but 
less regularly. This part was caseous, more like a scrofalous kidney. 
Pelvis dilated and sacculated. The ureter was dilated and thickened, and 
for its upper half its mucous membrane is covered by a vascular growth from 
its surface. This seemed to have begun half way down the canal, and growing 
thence had pushed upwards as a clot might do, forming a mould of the ureter 
at the upper part,and merely attached below. Bladder and other kidney 
normal. Microscopically : large round cells, some of them rather like epithelium 
— “ а medullary cancer rather than sarcoma.” Insp. 1878, 263. Med. Rep. 251. 





CASE 28. Three months history—universal extension.—R. C., æt. 54 (m.), 
Admitted under Dr. Pye-Smith, April 7th, 1879, died April 22nd. Has bad 
malaria and syphilis. Five years ago, on his way to work, he felt a sudden pain 
in the right hypochondrium, which sent him to bed and kept him there seven 
weeks. He was weak, but had ao other symptoms. He has had a slight 
cough for five years, and has been sick now and then, generally in the early 
morning. Two months ago he began to have pain in the back and weakness, 
and for three months has had loss of appetite and flesh. Six weeks ago he 
gaveup work. The pain is in the lumbar spine, epigastrium, and left hip. 
On admissiou—Fulness of right side of abdomen, swelling the size of the 
palm of the hand between ninth rib and navel. A nodule in the skin 2 inches 
above pubes. There isa solid mass in this position; pressure on it causes 
pain in the back. Liver normal. Lungs, signs of slight bronchitis. Urine 
1025, acid, albumen, 30 ozs. daily. The veins on the left side of the chest and 
abdomen are the larger. The growth does not cross the mid-line, and has a 
definite lower edge at the navel. Pain and a good deal of vomiting continued. 
With a trocar some blood and large granular round cells were drawn off. This 
was followed by acute pain, especially in the right shoulder. The patient 
grew feebler, and his bronchitis worse. Died April 22nd. Post Mortem: 
Right pleura, some pleurisy. Right lung covered with nodules, mostly very 
small but some as big as peas or beans, most numerous in the superficial 
Jayers of the lung tissue. None in parietal or visceral pleura. Mediastinal 
glands much enlarged, especially in front of the left bronchus, where they 
formed a mass the size of a small apple. Abdomen, lymph and pus all over 
between the viscera. Liver, 90 ozs. ; three or four large, several small, nodules ; 
the biggest the size of an orange, this formed the tumour felt during life. 
All the larger growths are caseating and softening centrally. The lumbar and 
mesenteric glands, full of caseating growth, formed a large mass about the 
aorta. Each adrenal contained a minute nodule of growth. Right kidney, 
5 ozs., normal, with a minute fibroma in one pyramid. Left kidney, 213 ozs., 
nearly destroyed by what was clearly the primary growth. This occurred in 
lobulated masses, some of which were white and medullary, and growing 
into the little that remained of the renal tissue as a lobulated mass. It 
also projected into the interior of the pelvis as a firm lobulated growth, 
discoloured on the surface as if it must have bled during life. (No hematuria 
is known to have occurred.) One part of the growth formed a circumscribed 
encapsuled round mass, the size of a small apple. This was universally 
caseating, and was thought to be the starting point of the disease. Micro- 
scopically : the growth consisted of a closely interlaced mass of spindle cells and 
cells with long pointed processes. There was no trace of any alveolar arrange. 


VOL. LIX. 22 


310 Growths of the Kidney and Adrenals. 


ment. The nuclei are not large, the cells not epithelioid. Acetic acid caused 
no increased opacity, but there was a good deal of granular matter present 
before it was added. Insp, 1879, 162. Med. Rep. Clinical, 240. 





CASE 29. Growth, aspiration, peritonitis, No metastases..—F. S., et 50 [m.). 
Admitted under Dr. Pavy, February 2nd, 1880; died February 6th. The 
history cannot be found, but on admission he had anesthesia of one side of 
the face, paralysis and wasting of the left side of the tongue, and a large soft 
tumour in the right side of the abdomen. This was punctured on the 5th, and 
a dirty brown fluid drawn off. Pain in the abdomen immediately set in; he 
sank and died. Post Mortem: Brain normal. No disease affecting IX. or 
V. anywhere. Trunk of IX. in anterior triangle full-sized white and glisten- 
ing. No note of XII. Left side of tongue contrasted markedly with right, 
it was flabby, pale. and thin. Microscopically : an excess of fat and connective 
tissue ; the muscular fibres retained their striation, but one or two were 
granular. Lungs and heart normal. Liver normal. Left kidney 6 oz., pale 
and fatty. Au acute suppurative peritonitis with creamy yellow pus. Colon 
adherent to mass and pushed down by it. The right kidney formed a large 
cystic tumour the size of an adult’s head, projecting forwards. Part of its 
anterior wall was free, and no doubt after puncture some of its contents 
had escaped into theabdomen, But to theright side it adhered to the aorta, 
and behind it was an abscess in the iliacus extending towards the groin. The 
cyst held two pints of red-brown fluid, foetid, with the look and smell of an 
unencysted hepatic abscess. Wall rough and thick. Growing from its upper 
part was a soft flocculent mass of new growth, on section almost encephaloid, 
emitting a creamy juice, discoloured and sloughing Оп the surface.  Ureters 
and bladder normal. Microscopically : this was a true carcinoma, cells large and 
of varying shape, with immense nuclei, often two or three, and large nucleoli. 
There was a distinct alveolar structure. Insp. 1880, 67. 





CASE 30. Congenital sarcoma of adrenal, deposits in skull and skin. —F. B., 
æt. 6 months (m.). Admitted under Dr. Pye-Smith, August 25th, 1881, and 
died September 25th, 1881. The infant was admitted with swellings in the 
head, left arm, and leg. The parents were healthy and the child born at full 
term. When he was 2 months old a lump appeared on the posterior fontanelle 
which has grown quickly since, and is now the size of an orange. soft and 
fluctuant. Other lumps have appeared and grown rapidly since. The swellings 
increased in size and the child lost strength. One mass destroyed the right 
eye, others appeared on the legs and elsewhere. Post Mortem ; the tumours 
on the calvarium were situated in the bone and projected both outwards and 
inwards, there were three, one described above, and one in each frontal bone. 
They were soft and full of blood, the inner and outer halves of each were 
separated by a thin worm-eaten layer of theoriginal bone. Dura free. Brain, 
spine, and lungs normal. A growth in the posterior bronchial glands. Liver, 
94 oZ., contained six patches of growth 1j-in. by 1ğ-in. across. Some mesen- 
егіс glands a little enlarged. Adrenals both replaced by a soft vascular growth. 
With the exception of a projecting hematoma on the left side they retained their 
normal shape, but measured about 4-in. by 3-in. each. Kidneys normal. Left 
arm, a nodule l-in. across in the subcutaneous tissue. Right leg, a similar 
larger one. Right thigh, one 23-in. long, lying in a cavity in the muscle, of 


Appendix of Cases. 311 


which the bottom was formed by thickened periosteum. Ribs бапа 6 were 
infiltrated about the centre foc some 2-in. by a soft growth containing bony 
spicules. The growth was a small round celled vascular sarcoma. 

Insp. 1881, 289. Med. Rep. 71. 





CASE 31. Signs of bronchitis six months, growth found post mortem, locally 
infiltrating, 8 inches long. -P. S., еб. 55 (m.). Admitted under Dr. Fagge, 
June Ist, 1881, and died July Ist. А porter, used to lifting heavy weights. 
He complains of cough and wasting for the last five months, with night sweats. 
No hemoptysis. There are the physical signs of bronchitis, with wasting and 
pyrexia. Diagnosis, phthisis. Urine normal. Temperature, from 102° or 103° 
to 99:69. He gradually sank and died. Post Mortem: Lungs emphysematous, 
cedema. No phthisis, scarcely any bronchitis. Heart, brown atrophy. 
Peritoneum contained fluid. Stomach and intestines normal. Liver atrophic. 
Spleen shrunken. Right kidney and adrenal normal. Left kidney, an oval 
mass, 8 inches long, retained the shape of the organ. A good deal of the upper 
end was healthy, the lower part was occupied by some bosses of malignant 
growth which formed rounded tumours the size of three or four small apples, 
partly caseating, partly fibrous, clearly the primary growths. They grew into 
the kidney pelvis projecting from the mucosa as flat nodules with depressed 
centres the size of a shilling. Ureter free. Calyces scarcely dilated. In front 
was & large mass of glands infiltrated with growth, which was softer than 
that in the kidney, white and homogeneous, not encephaloid. Growth 
extended into the left psoas. The large veins were compressed, but contained 
no clot or extension of growth. Microscopically a sarcoma, large round or 
oval cells with vesicular nuclei, a few with two nuclei These in parts formed 
the great bulk of the tumour, embedded in a granular and fibrillated' matrix. 
In other places there is much fibrous tissue. Some spindle cells here and 
there. ‘The growth has considerable tenacity. Insp. 1881, 198. 





CASE 32. Tumour three months, metastasis in lungs.— J. G., æt. 64 (m.). 
Admitted under Dr. Fagge, July 28th, 1881, and died September 20th. Nine 
months ago pleurisy left side. Three months before admission a bale of wool 
fell on his left side, and on the second day after he noticed a tumour there, 
He had a good deal of pain, increased on movement. The mass increased 
and filled the left side of the abdomen, the patient got thinner and gradually 
sank, Urine contained a few pus cells, otherwise normal. Post Mortem: Three 
patches of growth the size of a shilling in right pleura. Three nodules right 
upper lobe. Left lung studded with hard grey nodules. Left side of abdomen 
full of growth, over which passed the descending colon. The rest of the 
intestines lay to the right. The mass was lightly adherent over 3 inches 
to the anterior abdominal wall. Liver, 54 ozs., fatty. No glands noted. 
Right kidney normal. Left kidney, 7j lbs. All the kidney left was a piece 
half the size of a small orange. Growing from this was the large tumour, the 
upper part solid, irregular, bossy, white; the lower lacerable and red. 
Insp. 1881, 284. 





OasE 33. Large growth, tumour one year, hardly any metastases or in- 
vasion.—R. B., Bt. 49 (m.), Admitted under Dr. Moxon, March 10th, 1881, and 
died March 25th. Family and personal history good. A year ago he had pain 


312 Growths of the Kidney and Adrenals. 


in the left loin and noticed a mass the size of the palm of his hand. The pain 
was intermittent, at times severe. Two months ‘ago hzematuria—he passed 
about half-a-pint of blood in two days. On admission, blanched, wasted, 
cedema of both legs (especially the left), which has been present some five 
months. Superficial abdominal veins dilated. A tumour fills the left and 
central part of the abdomen, it is round, hard, solid, and dull. Lungs normal. 
Urine normal. He was relieved from pain by morphia and died in a fortnight. 
Post Mortem: one enlarged gland in lower end of mediastinum. A few 
mesenteric glands slightly enlarged but no definite growth in them. All the 
large veins free, lungs and liver free, lumbar glands not mentioned. In the 
other kidney several white nodules from half-a-pea downwards. They were 
softer than the growth on the other side, and yielded a small amount of 
milky juice, the remaining structure was pale but healthy. Bladder and 
testes normal. An enormous mass in left side of abdomen, the colon ran 
as a small compressed tube vertically down the median line. The tumour was 
very elastic and had a dense tunica-albuginea-like capsule. Pancreas spread 
out and flattened in front of it, adrenal behind it. Neither was invaded. 
Vessels enlarged but normal. Ureter normal but blocked by a small uric acid 
calculus. The lower part of the kidney was healthy, and rose so abruptly 
from the mass that the tumour seemed extrarenal, but careful examination 
showed kidney substance spread out over the lower end of the tumour, which 
had grown in its head. On section blood clot and a tough yellow fleshy 
material, which microscopically consisted of a tough fibrous material with a 
number of leucocytes in the spare juice. Insp. 1881, 91. Med. Rep. 286. 





CASE 34. Growth of kidney and adrenal —23 years’ history—local invasion— 
metastases in intercostal space. —T. R., et. 37 (m.). Admitted under Dr. Willis, 
December 13th, 1882, and died July 29th, 1883. Two years before admission, 
and ten weeks after recovery from rheumatism, he began to have attacks of 
pain in left hypochondrium which used to cause him to take to his bed at 
intervals of three or four weeks. In October, 1881, %.¢. fourteen months ago, 
he suddenly passed -pint of blood, and went to hospital for four months, 
during the first fortnight of which he used to pass blood and clots. This has 
not recurred since. He got better and went to Dover for three months. He 
then began to vomit half-an-hour after his meals, tohave the pain constantly, 
and to lose flesh. Six weeks ago he developed worse pain in the abdomen, 
groin, and root of the penis. On admission a tumour, noticed last month, 
filled his abdomen from ribs to ilium, it was tender, dull, solid, smooth, and 
presented a notch anteriorly. The urine was normal, now and always. During 
his stay the mass did not markedly increase, the pain and sickness varied. 
Post Mortem: In the right intercostal space close to sternum was a mass of 
fleshy, partly caseous growth, l-in. by à-in. Lungs normal. The stomach 
hardly more than a tube, passing vertically down over the mass, and then 
bending sharply to the pylorus. Liver normal. Pancreas flattened. Mesenteric 
glands normal. Several lumbar glands infiltrated. Right kidney normal. 
The left kidney formed a large lobular mass, and filled the left side of the 
abdomen from diaphragm to pelvis. The stomach and colon ran down 
vertically in front of it, the pancreas imbedded in its anterior surface. Every- 
thing in front of the twelfth dorsal and first lumbar vertebree was infiltrated, 
but the bones were unaffected. The vena cava was displaced and adherent. 


Appendix of Cases. 313 


its wall puckered by infiltration. Left renal vein blocked by a tongue of 
growth which grew into it and projected from it into the cava. ‘The muscles 
behind were infiltrated, and near the spine the tissues were yellow and 
gummatous. The mass itself was in two parts, one yellow, firm, elastic, into 
which the ureter ran --clearly the kidney, but without any renal tissue. The 
other softer, containing much blood and pigment, apparently a larger adrenal. 
No other adrenal was found this side. Microscopically the structure was the 
same, much of it fatty, the rest like а myxoma, but on careful examination 
round and oval nuclei were seen contained in large irregular cells of extreme 
delicacy, whose outlines were hardly visible. Nothing definitely cancerous 
about it, it looked like a sarcoma with mucoid degeneration. The right 
adrenal containel a large mass of fleshy growth very similar microscopically 
Insp. 1883, 262. 





CASE 35. Five years’ history—nephrectomy—shock—a few nodules in lungs 
and liver.—M. W., el. 54 (£). Admitted under Dr. Moxon, on October 1st, 
1883; and died November 12th. The patient had had hematuria for five years, 
and a tumour had been felt in her abdomen since 1880. She was admitted 
with a large movable mass in the right Join, from which a little blood was 
obtained by puncture. The urine contained blood and pus. November 11. — 
Nephrectomy by Mr. Jacobson under chloroform and ether, lasting 13 hours, 
She became cold, pulseless, semi-conscious, and died. Post Mortem: The 
lungs contained two or three nodules of a firm, soft, white growth. One was 
l inch across. They contained epithelioid cells of various shapes. In the 
vena cava lay a little growth-like clot, which was considered innocent. The 
ligatures were satisfactory, and the peritoneum was shut off from the wound. 
There was one small nodule in the liver. Adrenals normal. Left kidney, 
uterus, etc., normal. Right kidney: A large nodular mass oocupied two- 
thirds of it, in greater part caseating, the edge formed by fungating growth. 
The rest of the organ was swollen and cedematous-looking, as it is when 
the vein is obstructed. Pelvis dilated. On subsequent examination, „Mr. 
Jacobson found the renal vein completely blocked and invaded by growth. 
which, however, had not gone far enough to in any way hamper the operation. 
Insp. 1883, 394. 





CASE 36. Growth of adrenal, direct extension to mediastinum, З months’ 
history:—J. W., et. 32 (m.). Admitted under Dr. Goodhart, January 5th, 1885, 
and died January 31st. Three months ago he began to feel ill, lost, his appetite, 
and had swelling of the feet. Seven weeks ago he fell so ill that he took to 
bed and has stayed there since. The last week or so he has passed little urine 
and that thick and high coloured. On admission, weak and wasted. Urine 
normal. Some cedema of ankles and wrists. No pain. Tenderness on 
pressure over left kidney. Тһе себет gradually subsided. In a fortnight's 
time he developed pleurisy at the right base. A week later 52 ozs. of purulent 
fluid were withdrawn, and he died a few cays later. Post Mortem: Left 
pleura thickly coated and lung compressed. Right side healthy. Glands in 
posterior mediastinum malignant, hard,and white. Growth had spread along 
bronchi into lungs. Nowhere had it ulcerated into the bronchi. There was 
an irregular mass at the bifurcation of the trachea. Largest gland the size of 
a pigeon’segg. Right adrenal normal, Left adrenal, 20 ozs., wholly converted 


314 Growths of the Kidney and Adrenals. 


into a malignant mass retaining its original shape. It had not infiltrated 
the tissues round or compressed veins. It was retroperitoneal and pushed the 
pancreas forward. Most of it was soft and breaking down. There were 
occasionally hard whitish nodules, with here and there a peculiar yellow tint 
like that of the vanished adrenal. The growth could easily be shelled out 
from the surrounding tissues—it adhered to the top of the kidney. It had 
grown in the direction of least resistance—up and out. The cesophagus was 
implicated from the bifurcation of the trachea down. The interior was 
ulcerated, and this entered the lung, forming a sac the size of a Tangerine with 
malignant walls leading from the cesophagus. Nothing else abnormal. 
Glands, liver, and lungs free. Insp. 1885, 43. 





CASE 37. Seven years’ hematuria, no metastases.—S. H., æt. 60 (m.). 
Admitted under Mr. Durham, August 18th, 1885, and died August 99th. 
In 1878 he first noticed bleeding from the penis. He had retention, the 
passage of a catheter was inetfectual, but a warm injection brought away a 
quantity of clotted blood and urine. In 1880 he had a similar attack and was 
treated two or three weeks. Some time afterwards Dr. Foster noticed enlarge- 
ment of the right side of his abdomen. In July, 1885, pain came on and 
lasted three weeks, acd since then there has been no blood noticed. On 
admission, a mass in right loin moving on respiration; dull. Its limits are 
1 inch below ribs, 1 inch to right of umbilicus, ğ-inch below umbilicus. No 
fluctuation. Veins are more distinct on this side of the chest and abdomen. 
Urine 1020, acid, a trace of blood. August 2156, operation; oblique incision. 
Large perirenal veins. Kidney punctured with a trocar. No fluid escaped, 
wound closed. The urine became ammoniacal, and the patient died ina week. 
Post Mortem: No peritonitis. Right kidney, 53 ozs., firm and hard. Renal 
vein tortuous and dilated. Posterior part of kidney adherent round wound. 
On section no kidney tissue remained, the upper part was yellow and 
caseating, with oily masses, the lower was tougher, and showed cysts filled 
with recent hemorrhage. Into this mass the ureter opened freely. Mesenteric 
and lumbar glands, lungs, liver, other kidney, and all other organs healthy and 
free from metastases. Insp. 1885, 270. Surg. Rep. 111, 36. 





CASE 38. Cerebral hemorrhage, growth of kidney found post mortem. H.H., 
æt. 55(m.). Admitted under Dr. Taylor, November}1 9th, 1885 ; died December 3rd. 
He was admitted recovering from a sudden loss of consciousness. He remained 
drowsy and had headache. Then he had one or two fits, became comatose, 
and died. Urine, 1018, normal. Post Mortem: Extensive cerebral hzemor- 
rhage. Left kidney: upper half converted into a white malignant growth 
sharply defined from the healthy part. There were опе ог two minute nodules 
in the perirenal tissue. No healthy kidney tissue at the upper end. There 
were two nodules of growth in the lower end of the organ the size of marbles. 
Pelvis normal. Glands, lungs, liver, &c., normal. «sp. 1885, 389. 





CASE 39. Passage of growth by vena cava to heart. Tumour 4 years, growth 
and death in three months after miscarriage. E.T., et. 25 (f.). Admitted under 
Mr.Howse January 26th, 1886 ; died March 2nd.—Never very healthy; apparently 
ansemic and tuberculous. Three children alive; eldest 4. On December 18th a 
miscarriage, preceded by a month's bleeding from vagina. Ever since then she 





Appendiv of Cases. 315 


has been in bed. Every attempt to get up brings on bleeding, Loss of flesh, 
weakness, bad appetite, Two or three times difficulty in micturition. For 
four years she has noticed a swelling in the right side of her abdomen. 
Originally the size of an egg, it grew gradually at first, more rapidly since her 
miscarriage, and is accompanied by а little pain; more latterly. On admis- 
sion ill and weak. А so.id, smooth, hard mass in right side of abdomen, 
reaching 15 inches to left of umbilicus. Resonance between this and the 
liver. The mass itself dull. Urine 1027; albumen, blood. Temperature 
100—103°. Dr. Hale White diagnosed sarcoma of the kidney. Dr. Hor- 
rocks found the tumour was not uterine. Intermittent hzmaturia was present 
fora month. Operation, March 2nd; anterior incision. The patient died 
during the separation of the growth. Post Mortem: Lungs studded with 
minute growths, of which even the smallest are soft and creamy. Mediastinal 
glands full of growth. Right ventricle contained grumous delicate clots, . 
suggesting growth, and similar masses were present in the vena cava and 
renal vein. Mr. Howse suggests that in the course of his manipulations he 
must have caused some of this very soft growth to pass into the cava, and so 
produce this embolism. The mass in the heart is microscopically identical 
with that in the kidney. Тһе liver contained several small secondary nodules, 
the largest 4 in. across. One or two lumbar glands much enlarged by soft 
creamy growth. Left kidney large, healthy. Right kidney still retained its 
normal shape, and at the upper end its normal appearance, the whole forming 
a mass 9 by 6, with a fibrous loculated basis. 'l'he greater part was composed 
of a soft, cream-like substance, which flowed out and left a flaccid stroma. 
The renal vein was full of stuff of this sort, and when washed away the wall 
was covered with fibrous shreds which seemed to be the stroma of the growth. 
There were two or three isolated nodules in the lining membrane of the vena 
cava. Microscopically, the grcwth consisted of a large granular epithelial 
type of cell with many nuclei. The kidney had been separated from its bed 
as far as the hilum, and presented a pedicle capable of being dealt with by 
ligature. Insp. 1886, 82. Surg. Rep. 121, 26. Specimen in museum. 





CASE 40. Growth of kidney and adrenals, invasion of skin and lungs.— 
В. E., et. 46 (m.). Admitted under Dr. Pitt, November 18th, 1888, and died 
December 13th. Six months ago he had pains in right hypochondrium, 
Shooting to the left shoulder and down both legs to the feet, often followed 
by a short attack of jaundice and dark urine. Four days ago the dark urine 
was clotted in the morning. He has lost flesh six months, and in the last 
three weeks little hard tender nodules have appeared beneath his skin. The 
pain has been less lately. On admission, he cannot lie on the right side. 
Several subcutaneous nodules, movable, are present on scalp, neck, arm, back, 
and leg. The abdomen is tender, and there is a round hard mass in the right 
loin, which ends 2 inches to right of navel and reaches 3 inch below it. It 
moves independently of the liver. There is a sulcus, which is resonant, between 
it and the ribs above and in front. Urine normal during his stay. November 
26th, Mr. Jacobson removed a nodule from the scalp, which proved to be a 
scirrhous carcinoma with a moderate amount of stroma, not very hard. 
November 29th, he passed into a condition of mental weakness, which lasted 
till death. Post Mortem: No pigmentation. Cranial bones not invaded. 
Brain normal, Lungs, tubercle both apices (microscopically). Secondary 


316 Growths of the Kidney and Adrenals. 


deposits from the size of a pea to that of a pigeon's egg. Secondary nodules 
one in the pericardium, one in the liver. The peritoneum, abdominal and 
thoracic glands, and all other organs free. Both adrenals entirely occupied 
by growth, the left larger, though the grcwth was in right kidney. No normal 
tissue left, possibly the growth was primary here. Left kidney normal. Right 
kidney anterior half normal. Posterior half replaced by a mass of growth as 
big as the kidney, which projects beyond its upper end. It is contained within 
the capsule, and breaks through it at two places only. It is composed of soft 
rounded areas, separated by fibrous bands of compressed kidney tissue. There 
is an intermuscular growth in the loin, the size of a pigeon's egg. Ureter 
normal. The growth isin all situations a carcinoma varying from schirrus 
to encephaloid. Jnsp. 1888, 446. Med. Rep. 250. 





CASE 41. Pain five months—exploration—death—eaxtensive glandular infec- 
tion.—P. D., et. 48 (m.). Admitted under Mr. Lucas, February 28th, 1989 and 
died March 10th. Eighteen months ago he had a fall on his back, and has 
since had several attacks of lumbago. Four and a-half months ago he had 
severe pain in the right loin, and has been invalided since. Hzematuria several 
times. Occasional passage of long clots. On admission: No hematuria; 
patient pale and sallow. In right hypochondrium and loin a smooth, hard, 
solid tumour, surrounded by resonance, except where it joins the liver. Flank 
dull. Mass movable and separate from the liver, which is enlarged, smooth, 
and tender. Abdomen rigid; veins distended, Bad entry right lung; ráles; 
bronchial breathing. Left lung not so bad. Tenderness along spine, not 
localized. Operation, March 4th: Kidney explored, two or three glands excised 
and others felt on the posterior wall of the abdomen; wound closed. He 
sank and died in six days. Post Mortem: Spine eroded in upper dorsal region 
by extension of growth from lung. All along the thoracic spine were deposits 
in the glands over the heads of the ribs. Some pleuritic effusion right side, 
Lungs both studded with nodules of growth, chiefly in the pleura, but also in 
the lung substance along the vessels. Mediastinal and bronchial glands 
infected. Vena cava thrombosed from opposite the renal vein down to the 
junction of the common iliacs, and thence into the left common and internal 
iliacs. The thrombus did not fill the vessel, and was covered with p.m. clot. 
Large mass of glands behind duodenum. Liver stuffed with secondary nodules, 
firm. No deposits in portal fissure. Lumbar glands converted into large 
masses of growth. Left kidney: one small deposit. Right kidney nearly 
all converted into a mass of growth which fungated into the pelvis, but did 
not block the ureter. All round it deposits in glands and adjacent tissue. 
Renal vein full of growth which spreads along it to vena cava. Small secon- 
dary deposits in right ureter 3 inches from pelvis. Microscopically both 
growths consisted of small alveoli, filled with large spheroidal epithelial cells. 
Insp. 1889, 103. Surg. Rep. 56. 





CASE 42. Five weeks’ hematuria, nephrectomy, death, invasion of vena cava 
and lungs.—J. W., et. 17 (m.). Admitted under Mr. Lucas, November 20th, 
1890, and died November 30th. Seven weeks ago he fell 8 feet and hurt his left 
side. Previously to this he had for some time had a dull aching pain in the 
left hypochondrium. Five weeks ago he began to pass blood ; this lasted nine 
days, intermitted for a week, recurred, and has been present since, unaffected 


Appendix of Cases. 317 


by rest and milk diet. Rigors and loss of flesh. On admission: Firm smooth 
tumour in left loin and hypochondrium, resonant in front, not fixed, not 
fluctuating, reaching to umbilicus, and 1 inch from mid-line. Urine 1030, 
acid, blood, urea about 300 grains. Operation, November 28th: Anterior 
incision. Kidney adherent, covered with large veins. Nephrectomy. 
Counteropening and drainage. Chloroform was given for 1 hour 50 minutes. 
The patient was restless and sick, and died two days later. The kidney 
removed weighed 2 Ibs. 4 ozs. and measured 7 x 43 inches. It was nodular on 
the surface. On section soft, hzemorrhagic, degenerate in patches. Post 
Mortem: A few small nodules in both lungs and pleure. Adrenals and liver 
normal, Left renal vein was filled, from the ligature to the vena cava, with a 
thrombus composed of growth covered with clot. There was a large irregular 
polypoid mass protruding into the vena cava, which at first looked like clot, 
but microscopically was composed of very large cells filled with fatty granules, 
resembling epithelial cells in size and shape. No blood or peritonitis in the 
abdomen. In the pedicle and round it were some glands containing secondary 
deposits, and masses of growth which might have been extensions from the 
renal tumour. Right kidney, 5 ozs., normal. Bladder normal. Insp. 1890, 
462. Surg. Rep. 166A. 





CASE 43. General glandular invasion, lungs free.—M. Y., st. 62 (m.). 
Admitted under Dr. Taylor, July 15th, 1890, and died January 18th, 1891. 
Admitted for epigastric pain and wasting. Two years ago he had epigastric 
pain, worse after meals, usually aching, rarely shooting in character. A year 
ago he got worse, has been invalided since, and in bed since February, with 
loss of flesh; no sickness or flatulence. For the last 18 months he has had 
shooting pains from his buttocks to his feet. On admission: He has moder- 
ately enlarged glands in the left axilla and the groins. He is suffering from 
“Таг Molluscum.” His abdomen is retracted and resonant. Liver dulness extends 
to 4 inch from the navel. Lungs normal. Urine, 1010, normal. Feces some- 
times colourless. During his stay he had variable pain, and tenderness is 
once recorded at a spot at the outer border of the erector, 1 inches above 
the iliac crest. He was sometimes sick, and sometimes had white stools. On 
the whole he gained weight (rising from 95 lbs.in September to 99 lbs. in 
December), but lost strength, Repeated attempts: failed to detect any 
abnormal mass in the abdomen. Three weeks before death he passed blood 
and casts for the first time. Post Mortem: Axillary glands enlarged. Pleurisy 
left side. Lungs and thoracic glands free from growth. Liver contains two 
deposits the size of peas, and the glands in the portal fissure are infected. 
Adrenals, spleen, left kidney, normal. The mesenteric glands round the head 
of the pancreas are infected, and are the size of pigeon’s eggs. The pancreas 
itself is half its natural size, but otherwise both gland and duct look healthy 
and contain no growth. The right kidney contains a growth the size ofa 
cricket ball in its centre, which is degenerating. Microscopically ; The growth 
is scirrhous carcinoma with spheroidal cells. The deposits in the axillary 
and mesenteric glands show more epithelial cells and less stroma. Jnsp. 1891 
26. Med. Rep. 280. 





CASE 44. Sarcoma of adrenal—mycosis fungoides—no metastases.—J. B., 
æt. 16 (m.). Admitted under Dr. Pye-Smith, January 17th, 1891, and died 


318 Growths of the Kidney and Adrenals. 


March 30th. Personal and family history good, no syphilis. A year ago he 
was treated for itching all over. In July the sore on the right shoulder 
appeared and was followed by those on the left scapula and right loin. On 
admission, lungs, heart, and urine normal. On the right eyelid is a 
mass the size of a filbert, of which the surface is granulating. All over the 
chest the skin is covered with dry epidermis. On the spine of the left scapula 
is an inflamed patch 5 ins. across, raised, with a central depression, which has 
vertical edges and is filled with slough. There is a granulating patch on the 
right shoulder, and a few raw patches on the outer side of the right leg. On 
both surfaces of both arms the skin is dry and pigmented in patches, in some 
places there is scabbing. Over the right loin isa large swelling, the skin round 
itis inflamed, and there is a patch of slough on its lower and outer part. 
Diagnosis: Mycosis fungoides. February lith.—All the raw patches de- 
creasing in size. They give rise to a copious serous exudation. March 6th.— 
The place on the left shoulder has nearly disappeared, that on the right has 
increased a little, and is now 4 ins. by 5 ins, and raised 1ğ in. from the 
surface. March 10th.—Chromic acid injected into mass on loin. March 
19th.—The patch over the eye is worse, the left forearm is nearly well, the 
right arm is raw from the shoulder to the elbow, a new patch has appeared 
below left scapula and two on the left arm. March 26th.—Sinking. Right 
arm better, left worse, back the same. March 30th.—Died. Post Mortem: 
Tumours as noted above. Brain and spine normal. Pleurz adherent, hypo- 
static pneumonia, and at the base of the right lung a gangrenous patch; 
adherent pericardium. Liver, 89 ozs., fatty and cirrhotic. Capsulitis of 
spleen. Left adrenal normal. Right adrenal, 44-ozs, enlarged by a fleshy 
growth which quite obscured the normal structure. It was vascular, witha 
few caseating patches and measured 21 ins. by 1i ins. Kidneys, bladder, 
testes, and all else normal. The tumour of the back and adrenal were histo- 
logically the same. They consisted of an aggregation of small round cells 
quite uniform in size and shape, with little stroma. "They did not seem to 
differ at all from small round-celled sarcoma. Insp. 1891, 107. Med. Rep. 311. 





CASE 45. About a year's duration; hematuria 6 months; some minute 
metastases in lungs.—J. J. æt. 43 (m.). Admitted under Dr. Goodhart, 
March 28th, 1891, and died April 26th. Admitted for hematuria and wasting. 
Good history, personal and family. In February, 1890, he had violent pains 
іп the epigastrium which laid him up for a month. They came on suddenly 
and made him sick. In October he noticed his urine dark, with clots, and he 
had pain. He recovered, went to work, and in a few weeks had recurrence. 
Hematuria has been presént off and on since. A month ago he had congestion 
of the lungs. He thinks he has been losing flesh a year; more rapidly the 
last six months. On admission: Right lung normal, left lung dull from 
fourth rib down, with a rub. Systolic bruit. Urine, acid, 1025, blood and 
pus. During hisstay hehad several rigors and rises of temperature. Some 
bloody serum was drawn off from his chest, and he showed signs of a mass in 
the abdomen, though the palpation of it is not noted. Post Mortem: Lungs, 
three nodules of growth, average size of.a pea. On the right side recent 
pleurisy and broncho-pneumonia. On the left side the lower lobe is airless from 
compression. Thoracic glands normal. There was a large mass in the upper 
left abdomen ; spleen pushed up, colon pushed forward and collapsed but not 


Appendix of Cases. 319 


compressed. ‘The lower internal edge reached the middle line as low as the 
bifurcation of the aorta. Liver, spleen, and lymphatic glands normal 
Stomach, pancreas and spleen lightly adherent. Adrenals—Right, normal ; 
left, absorbed in mass. Right kidney normal. Left kidney: In upper part 
was a cavity holding grumous mess and clot ; in the middle is a white growth. 
partially encapsuled ; lower end normal. Microscopically: sarcoma with some 
long spindle cells, the fibrous arrangement often being concentric round the 
blood vessels. Insp. 1891, 146. Med. Rep. 341. 





CASE 46. Tumour 18 months, nephrectomy, shock, one gland ‘infected.— 
А, W., æt. 29 (f.). Admitted under Dr. Shaw, May 30th, 1891, and died 
June 15th. Five years ago shegused to have a variable aching pain in the 
right side, under the lower ribs, while doing her work as housemaid. Three 
years ago she married, and has two children. She had a miscarriage (at three 
months) six weeks ago. She has noticed the present tumour for 18 months. 
The pain, which has always been localized, is worse lately. No hematuria, 
There is an irregular, smooth, fairly movable mass in the right half of the 
Abdomen. Its long diameter is oblique, running from just below and to the 
left of the ensiform cartilage to just above and behind the right anterior 
superior iliac spine—above it is prominent and cystic. Nothing else, 
abnormal. Urine normal. June 8th: Aspirated; blood drawn off—no cells 
seen. June 18th: Operation; nephrectomy; followed by death in two hours. 
Post Mortem : Lungs and heart normal. The cavity left by the nephrectomy 
was found in a satisfactory state, but at the upper end was a nodule the size 
of a hen's egg adherent to the adrenal. This was the pedicle of the tumour, 
and not a secondary deposit. One gland beside the aorta was infected. 
Adrenals, left kidney, liver, and other structures normal. Microscopically the 
growth is a round-celled sarcoma. The Museum catalogue thus describes the 
affected kidney :—A right kidney, at the inner margin of which is situated an 
oval tumour 33 inches in its longest diameter. It is closely applied to the 
hilum of the kidney, and the renal vein crosses its anterior surface. The 
kidney has been laterally compressed and moulded to the convexity of the 
tumour. Anteriorly the growth is nodular, some of the nodules projecting 
into the dilated renal vein. On the back the surface is rough and was firmly 
adherent. On section the growth is composed of homogeneous material 
traversed by strands of translucent fibrous tissue. Histologically it has the 
structure of a spheroidal-celled carcinoma with abundant stroma (c.f. diagnosis 
above). Insp. 1891, 220. Med. Rep. Clinical, 338. 





CASE 47. Sarcoma ina child, invading liver and pulmonary artery.—T. M., 
æt. 5 (m.). Admitted under Mr.Durham, November, 1892, and died January 4th, 
1893. Three months ago he fell over a stool, and for a few days had pain in the 
left side. A fortnight later he began to lose flesh, and has continued to do so 
since. Ten days ago a tumour was observed in his abdomen. On admission : 
hard tense tumour in left side of abdomen. Liver normal Urine normal. 
December 13th: Exploration with a needle; blood and a few masses of round 
cells, some containing pigment. "The tumour continued to grow rapidly; the 
liver extended to 21 inches below the costal margin, superficial veins became 
distended, and the average excretion of urine sank from 11 ozs. to 4 ozs. Post 
Mortem; Lung—Small patches of collapse, probably pneumonia. Left pul- 


320 Growths of the Kidney and Adrenals. 


monary artery filled by a mass of soft adherent growth, which cortains no 
blood pigment. Left renal artery dilated. The vein admits a small finger, and 
contains adherent clots, softened centrally. Liver, 59 ozs. (normal is 19), 
reaches to umbilicus; contains many soft diffuent nodules. Right kidney 
normal. Left kidney: 54 ozs.; no renal tissue. Growth included in capsule, 
but breaking through it at a few points; soft, and caseating centrally. 
Ureter normal. Microscopically: In the liver, numerous nodules of round- 
celled sarcoma, composed of rapidly-growing cells, 8 д in diameter. A few 
were ovoid, 24 u by 8 u. ‘They stained deeply, and were granular. The 
nucleus took up nearly the whole cell. Lungs showed only broncho-pneu- 
monia. Insp. 1893, 11. Surg. Rep. 163, 48. 





° 

CASE 48. Hematuria one year, edema and ascites а few weeks, infection of 
lymph and blood channels.—C. K., æt. 58 (m.). Admitted under Dr. Goodhart, 
April 28th, 1893, and died May 22nd. Admitted for wasting, weakness, and 
ascites. A year ago he noticed blood in his urine, and three weeks later had 
pain in his loins and passed more blood with clots. A few weeks before 
admission he noticed his legs swelliny, and soon afterwards his abdomen. 
Urine has been scanty lately. On admission: Abdomen tense, abdominal 
veins dilated, liver slightly enlarged, urine 1014, а trace of albumen, (7) cirrhosis 
of liver. Ascites increased, and he died. Post Mortem: Pleura over the lower 
right lobe infiltrated, white lines showing course of infection along the 
lymphatics. Bronchial glands infected. Heart, ante mortem thrombus in 
right auricle continuous with that in vena cava. Upper half of vena cava 
swollen to twice its natural size, and full of clot, which looked malignant, and 
was softening centrally. The lower half is filled with hard adherent clot, 
which extends into the iliacs. Right renal vein thrombosed. 110 ozs. clear 
fluid in the peritoneum. Liver slightly enlarged, contains one secondary 
growth. Abdominal lymphatic glands affected. Left kidney normal, cortex 
cystic. Right kidney, twice normal size, irregular, soft, studded with masses 
of growth, no renal tissue apparent. Microscopically: Alveolar carcinoma, 
masses of cubical cells divided off by fibrous partitions. Јлзр. 1893, 187. 





CasE 49. Death from pneumonia at 8 months. Sarcoma found in adrenal.— 
A. M., et. 8 months (f.). Admitted under Dr. Perry (Clinical), August 13th, 
1894, and died August 23rd. Admitted for cough and wasting of one month’s 
duration. Temperature, 102°. Post Mortem: Pleurisy and broncho-pneu- 
monia right side. Left adrenal normal. Right adrenal contained a white 
growth with hemorrhages into it, the size of a large pea, which microscopically 
was found to be а round-celled sarcoma. Kidneys normal. Insp 1894, 334. 





CASE 50. Six months’ course, deposits in sternum, lungs, glands, liver.— 
T. T., et. 64 (m.). Admitted under Dr. Hale White, January 28th, 1895, and died 
March 23rd. He has been healthy, but many years ago he lost his memory 
for a year, and after this had a goitre which was seen and eventually removed 
by Sir James Paget. He has been quite well till September, 1894, when he 
had a pain in the left chest with cough and wasting, which have continued 
since. There is now a small lump on the third costal cartilage beside the 
sternum, fluctuating, anà surrounded by a tender area. Puncture of this 
yielded blood and large multinuclear cells, bigger than lymph cells. 


Appendix of Cases. 321 


Pulsation was transmitted through the swelling. Lungs normal. 
Urine normal. Mr. Dunn considered there was an inoperable growth, 
probably primary in the sternum. The further course of the case 
was increased pain, bronchitis, pneumonia, the appearance of a mass 
below the left clavicle, swelling of left arm, and extension of the sternal swell- 
ing. Post Mortem: Sternum and third and fourth left costal cartilages 
eroded by soft red growth. Both lungs contain vascular nodules of growth, 
many cystic or broken down centrally. Liver, a few nodules. Some 
abdominal lymph glands infected. Adrenals partly destroyed by growth. 
Left kidney: Lower third occupied by mass of tough white growth, 
nearly as big as a normal kidney, soft in places. Above, an encapsuled 
nodule not broken down at all, ? adenoma of accessory adrenal. Right 
kidney : several deposits of tough white growth, also a small nodule rather 
like the adenoma in the other kidney. Microscopically an oval-celled sarcoma 
with caseous change. Insp. 1895, 95. Med. Rep. Clinical, 58. 





Case 51. Hematuria 5 years, two explorations, ligature of ureter, death. 
Recent secondary deposits in pleura, no other metastases.—A. E., æt. 54(m.). Ad- 
mitted under Mr. Lucas, October 8th, 1896, and died January 27th, 1897. Five or 
six years ago he had dull aching pain in loins, upper thighs, and testes. He then 
passed some blood in the urine and the attack ceased in 24 hours. Since then 
he has had similar attacks once or twice a year, lasting about a day. Two 
years ago the attacks became longer, and the blood more plentiful. In the 
last year he has had three or four more severe attacks. Twelve days ago he 
passed pure blood and was dependent on a catheter for five days, since then 
the urine has been normal. Urine acid, 1022, no blood or pus, a little albumen. 
He had pain over the 11th & 12th dorsal and lst lumbar vertebre (renal 
Head’s area). He continued to have intermittent passage of blood, some thin 
clots up to 74-ins. in length. Operation, November 10th.—Kidney large, hard, 
firm, and smooth. No enlarged glands felt, no calculus detected, no 
fluctuation, wound closed. ‘The patient’s condition remained the same. 
Urine averaged 50 to 60-ozs daily. It gradually became purulent and 
ammoniacal. Operation, January 27th.—lIncision through the old scar. 
Kidney much enlarged, a nard nodular, whitish growth projected from it 
anteriorly. It was firmly adherent and the patient’s condition was bad. The 
ureter was ligatured and the wound closed. Death followed in seven hours. 
Post Mortem; Left pleura, 10 small nodules j-in. across. Lungs, liver, 
supraienals, lymphatic glands, all other viscera examined and found free from 
growth. A few cysts in the left kidney. Right kidney, 31l-ozs., a large 
irregular mass of hard growth, only slight traces of renal tissue. Micro- 
scopically, a sketch showing an alveolar arrangement. Jnsp. 1897, 34. Surg. 


Rep. 168. 


CASE 52. Rapid course, glandular and direct extension, blockage of ureter 
a month before death the first symptom, abnormal adrenal.—k. O., et. 54 (m.). 
Admitted under Dr. Pitt, January 11th, 1897, and died January 24th. He 
was healthy till December 20th, 1896, when he began to have difficulty in 
passing water, which lasted a fortnight. He could only pass small amounts 
and desired to do so very frequently. On December 29th he passed 5 oz. of 
bloody urine on two occasions, this was his first and last hematuria, Sub- 





322 Growths of the Kidney and Adrenals. 


sequently he suffered from pain and sleeplessness. On admission he was thin 
and anxious. There was a hard nodular tumour in the right side of the 
abdomen, separated from the liver by a band of resonance. It extended into 
the right loin and filled a space bounded by umbilicus, iliac crest, and liver. 
A transverse ridge crossed its lower part, and there was a tender area near the 
umbilicus. ‘The hand could be carried beneath its left edge. Bad entry 
right base. Urine 1020, acid, albumen, pus. Microscopically: bloodstained 
fragments in the urine, (? growth.) After admission he went rapidly downhill, 
vomiting without relation to food, and sleeping badly. Post Mortem: One 
deposit in a mediastinal gland. Head of pancreas and submucosa of duodenum 
infiltrated. The colon, which passed over the front of the tumour, was small 
and adherent, but not infiltrated. In the right iliac fossa a growth, 3 inches 
across, due to the kidney tumour, and extending down as a large cord in the 
course of the right ureter. Secondary deposits in the mesenteric glands. Left 
kidney, 74 ozs., normal. Attached to its upper end was a piece of adrenal, and 
on examination it was clear that the adrenal tissue extended into the renal 
tissue, as sometimes happens with adrenal rests. The patch of adherent 
adrenal was not homogeneous, but consisted of separate flattened nodules, and 
appeared to be above the capsule, though, as section showed, some of it went 
beneath it. Right kidney occupied and almost wholly destroyed by a large 
white softish growth, which extended down the ureter and partly blocked it, 
producing hydronephrosis. At the lower and inner part of the organ the 
growth had penetrated the capsule and formed a large nodular mass, which 
infiltrated the head of the pancreas and appeared as a white substance 
beneath the mucosa of the second and third parts of the duodenum. 
Mucosa of bladder normal, but at the orifice of the right ureter was а 
sloughing growth the size of a Brussels sprout, and this was connected 
with the growth mentioned above. Histologically the growth was a round- 
celled sarcoma. Insp. 1897, 28. Med. Rep. Clinical, 44. | 





CASE 53. Death from suppuration in the liver, “renal rest" forming part of 
adrenal tumour found post mortem.—W. 8., æt. 55 (m.). Admitted under 
Dr. Shaw. ‘The patient died with suppurative cholecystitis and cholangitis, 
fistula into the duodenum, and liver abscess. The liver section gave rise to 
a Suspicion of actinomycosis. Kidneys normal. In the right adrenal was a 
round soft yellow tumour the size of a fives ball, containing one or two 
hemorrhages. Microscopically it showed some normal adrenal tissue con- 
taining numerous spaces filled with blood. Around this adrenal tissue, but 
separated from it by a thick and irregular capsule of fibrous tissue, was 
kidney tissue containing a large number of glomeruli. In places there 
were large numbers of glomeruli, and hardly any tubules, but a number 
of small round cells, and also large cells resembling in character the supra- 
renal cells. Dr. Bryant noticed several glomeruli, the inner surfaces of the 
capsules of which were lined by these cells. Insp. 1897, 95. 





CASE 54. Short course, local and glandular extension.—' T. G., vet. 62 (m.). 
Admitted under Dr. Goodhart, April 1st, 1897, and died April 29th. Admitted 
for cough and shortness of breath. He has lost flesh for the last 12 months. 
For three months has had cough with dyspnoa and occasional difficulty in 
swallowing. On admission: Resp. 28. Dulness and diminished breath sounds 


Appendix of Cases. 323 


from sixth rib down on right side. Edge of liver at navel, surface firm and 
rough. Some ascites. Enlarged abdominal veins. Large hard gland left side 
of neck. He grew worse and on April 12th had cedema of the right leg which 
subsequently spread to the other leg, scrotum, and body wall. Glands appeared 
in groins and over clavicle. Urine contained indican. Post Mortem: 
Growth in the cervical glands. 68 ozs. fluid in right pleura. Growths under 
‘pleura and in lungs. Medastinal glands infected. White patches in muscle 
of left ventricle. 48 ozs. fluid in the abdomen. Right kidney much enlarged 
and nodular from protrusion of white masses of growth which extended in all 
directions to involve liver, vena cava, and retroperitoneal glands. On section 
the kidney was full of a soft white or grey vascular growth. Hardly any trace 
of renal tissue. The vena cava was invaded by growths which formed a layer 
on its inner wall for 43 inches below the hepatic fissure. Below this it was filled 
with a thrombus extending to the division of the iliacs. Retroperitoneal 
glands full of growth and lumbar vertebre eroded. Pancreas normal. 
Secondary deposits liver and left kidney. Znsp. 1897, 167. 





CASE 55. Rapid course, invasion by blood stream, по hematuria.—J. McN., 
æt. 50 (m.). Admitted under Dr. Pitt, May 11th, 1898, and died May 13th, 
He has had malaria, syphilis, and pneumonia. In October last he fell and 
strained his right side and subsequently had pain for some days. In January, 
while convalescent from pneumonia, he had severe pain in theright side for a 
week,-followed by pain down the inner side of the right thigh, and the whole of 
the opposite leg became swollen. A few days later the right leg did the same. 
He has been losing flesh since. In February he noticed a swelling of the 
abdomen. On admission: Thin, legs and right side of chest and abdomen 
cedematous. Не always lies on his right side. A large smooth uniform dull 
mass fills the right loin, its edge runs from 1} inch below the navel to the 
ninth costal cartilage. It does not move with respiration. An exploring 
needle withdrew only blood. Urine 1022, a trace of albumen, no blood. 
Lungs: Bad entry right base, ráles behind ; rub in second space in front. He 
developed signs of pleurisy on the left side, and died May 13th. Post Mortem: 
Secondary growths throughout both lungs. Small masses of detached growth 
in right side of heart. No ascites. Abdominal lymphatic glands normal. 
Adrenals normal. Mass in liver 4 x 25 inches, signs of recent hemorrhage. 
Large tumour in situation of right kidney, consisting of growth in the capsule 
of the kidney. There is old hemorrhage in the centre. Only a small piece of 
renal tissue remains at the lower end. The growth has invaded the vena cava, 
wbich is filled with ante mortem thrombus. Left kidney rather granular. No 
microscopical report. Insp. 1898, 191. Med. Rep. Clinical, 212. 





CASE 56. Calculus—nephrectomy—growth.—J. C., æt. 30 (m.). Admitted 
under Mr. Lane, June 7th, 1898, and died June 24th. Previous history good. 
Fifteen years ago pain in right side and red urine. ‘hese attacks occurred 
about once a year for some time ; they then became more frequent, and for the 
last five years have occurred once a month. In October 1897 he was operated 
on for calculus, at Newport, Four operations were performed and five stones 
removed. He was admitted to Guy's with a foul discharge from a large renal 
fistula, His general condition was good. Urine 1020, acid, albumen, pus, no 
blood; urea, 1:3 per cent. Operation, June 15th: Kidney enlarged, adherent, 


324 Growths of the Kidney and Adrenals. 


full of pus; containing three stones the size of filberts. A large abscess 
extended up beneath ribs and diaphragm. The kidney was removed piecemeal, 
part of the pelvis was left. Afterwards he was depressed, vomited from time 
to time, and died nine days later. Urine averaged 16 ozs., urea 1'4 per cent. 
Post Mortem: The remains of the right kidney consisted of the pelvis, in which 
there was a mass of fungating growth, which Dr. Perry thought was certainly 
growth and not granulation tissue. Suppuration had extended upwards 
behind the peritoneum, and the fibrous tissue in the portal fissure was itself 
infiltrated with pus. Downwards it had extended to the pelvis, causing retro- 
peritoneal cellulitis, and there was pus in the rectovesical pouch, and a local 
peritonitis. The stomach and duodenum had adhesions to the liver and 
gall-bladder respectively. All other organs normal. The other kidney 
weighed 8 ozs. and was healthy. Insp. 1898, 243. Surg. Rep. 69. 





CASE 57. Calculus, pyonephrosis—epithelioma—lymphatic — infection— 
4 months’ cowrse.—E. L., st. 48 (m.). Admitted under Dr Shaw, March 
21st, 1899, and died May 21st. Cystitis 23 years ago: recovery. Other- 
wise well till January last when he felt vaguely ill and began to 
lose flesh. No hematuria. On admission: A large hard tumour in 
the right side, moving on respiration. Lower and inner edges distinct 
and hard, upper edge 1 inch below ribs. It extends into the loin, 
down to the iliac crest, inwards nearly to the mid-line. It is dull, but 
traversed by a vertical band of slight resonance. Complete dulness behind. 
Base of right lung compressed. Urine 1016, acid, nothing abnormal. Urea 
1:7 per cent. On March 30th, there was a peritoneal rub and some fever 
There was albumen inthe urine; no blood. Tumour tender. On April 4th 
a discharge of pus in the urine began and lasted three days-—it contained no 
tubercle bacilli. On the 10th the rub and pain had disappeared. He lost flesh 
(7 lbs. in a month) and had a recurrence of tenderness, but not any increase in 
the tumour. Pain and cedema of the feet and ankles developed, and he died 
May 21st. Post Mortem: No deposit in lungs or heart. Vena cava pressed on 
but not infiltrated. The liver contains soft yellow nodules up to 2 inches 
across fluid centrally. Abdominal lymphatic glands are enlarged. Right 
kidney bigger than two fists, upper end loosely adherent to the liver, and 
behind it an abscess containing 15 025. pus. The capsule is perforated 
here. Round it the kidney tissue is very thin. Inside a large branched 
calculus was found surrounded by pus, and filling the dilated pelvis and 
calyces. The lower half or more of the kidney is replaced by a soft, yellow 
growth which had bulged towards the spine and infiltrated the neighbouring 
lymphatics, and had pressed on and almost entirely occluded the vena cava, 
which below it was blocked by ante mortem thrombus. Microscopically: An 
epithelioma with a marked bird’s nest arrangement of cells; it looked very 
much like epithelioma of the cesophagus, the cells being squamous in 
appearance. Jnsp. 1899, 161. Med. Rep. 109. ` 





Cass 58. Adrenal rest tumour, hematuria, cystotomy nephrectomy —death from 
gastric ulcer.—J. M., æt. 68 (m.). Admitted under Mr. Golding Bird, September 
18th, 1899 ; re-admitted November 28th; died March 2nd, 1900. When 13 
years old had a kick in the left loin, followed by 7-8 years incontinence. Mic- 
turition always frequent. Pajn over sacrum last two years. In April, 1899, he 











Appendix of Cases. 325 


had hematuria—no injury—no pain. ‘This persisted, with occasional 
difficult micturition from passage of clots. The attacks lasted 5-6 days, with 
intervals of freedom of about the same length. Some clots were the size and 
shape of a finger. On admission the left kidney seemed rather the larger, but 
a week later no difference could be felt. Urine 1020, acid; blood and pus 
present. On one occasion a mass of epithelial cells was found undergoing 
fatty degeneration: Operation, October 19th:  Cystotomy. The only 
abnormality found was a small ulcer on the left of the trigone, which was 
scraped. The patient went out, but continued to have the same symptoms. 
He was re-admitted, and although the swelling of the left kidney, noted above, 
had not recurred, it was decided to explore this side. Operation, November 
30th: Kidney found enormously enlarged and covered with dilated veins. 
The upper and anterior borders could not be reached, and at the lower end a 
large knob projected down into the pelvis. The patient's general condition was 
so bad that the wound was closed. Operation, February 20th: A vertical in- 
cision was made, 7inches long, which was afterwards extended. The peri- 
toneum was opened, and both kidneys explored. ‘The left kidney, which was 
adherent behind and above, was with difficulty removed. Eleven days later 
the patient passed a quantity of blood and slough from the rectum, and died, 
Pathologist's report: ‘This section shows a diffuse deposit of carcinoma. The 
cells are very clear, and in alveoli, the walls of which are composed of very fine 
fibrous tissue, the appearance suggests a suprarenal origin for the tumour. 
Mieroscopically the pedicle removed was free from growth. Post Mortem: 
Only a partial examination allowed. Abdominal wound healthy ; some 
brick-red fluid, probably broken-down blood, along course of psoas. Pedicle 
firmly ligatured, and no growth could be seen extending into it. Right kidney 
and liver normal. Some blood in the intestines. Stomach contained two 
pints of clot. On the lesser curvature, within 4 cm. of, the cesophagus, was an 
ulcer 7 x 5 cm., the edges rounded and thickened, the floor formed by the 
muscular coat. It looked like a chronic ulcer, and there was no infiltration of 
growth intoit. In the centre of its floor was a minute opening leading 
directly into one of the vessels along the lesser curve of the stomach. 

Surg. Rep. 509 


CasE 59. Growth of adrenal, no invasion or metastases, 4 years’ history. — 
E. S., et. 30 (f.). Admitted under Dr. Perry, November 9th, 1900, and died 
November 27th. In 1896 she first felt pain in the side, where she feels it now. 
This has since been intermittent. Frequent menstruation began then and 
lasted till May, 1900, when the function ceased. In November, 1899, she had 
a sharp attack of pain in the right side, and saw a doctor who diagnosed a 
small ovarian tumour. In August she was told she had enlarged liver and 
pleuritic effusion. In September her chest was tapped and 2 ozs. blood-stained 
fluid withdrawn. She has since had more pain. She cannot lie on the right 
side. There is now dulness and absence of sounds from the fourth rib down- 
wards, and a small dull area on the left side. Voice-sounds audible 
everywhere. No ráles. The liver, hard, with a rounded edge, is felt to 
reach to 13 inches from the right iliac crest. In the region of the gall bladder 
is a small round tumour, separable from the liver, not moving on respiration, 
not painful, not connected with the pelvis. Per rectum a hard mass the size 
of a small apple on the anterior wall Urine alkaline. November 19th : Liver 





VOL. LIX. 93 


326 Growths of the Kidney and Adrenals. 


bigger. Temperature always normal. Swelling in right iliac fossa less 
definite. Red corpuscles 5,240,000. Hydatid discussed. November 26th: 
Mr. Fripp made a vertical incision at the outer border of the rectus. Liver 
normal. Midway between its anterior and posterior surfaces was a swelling 
whose surface was covered with large veins. It displaced the kidney down- 
wards and the peritoneum went on to it straight off the liver. It had no 
pelvic attachments, The wound was packed to form adhesions. November 
27th: Packing removed—mass incised—blood and pulpy material issued. 
The cavity was packed and death followed in a few hours. Post Mortem: 
Lungs, lower third compressed from below, emphysematous, по 
evidence of old pleurisy. The lungs contained one or two nodules of 
growth the size of a pea. The liver was pushed up and the kidney downwards 
by a large encapsuled growth between them, 26 x 21 cm. Above it was 
firmly adherent to the under surface of the right lobe of the liver, and the edge 
of this was thinned out over it in front so much as hardly to be felt even post 
mortem when the hand was passed from liver to growth. Although adherent 
there was no invasion of the liver, nor did it invade any neighbouring viscera. 
On section the capsule enclosed a soft red growth with an irregular firmer 
yellow mass in its centre. No trace of the right adrenal found, Dr. Fawcett 
thought that this was the origin of the tumour. Left adrenal normal. Both 
kidneys normal, the right displaced downwards. Microscopically: An 
extremely vascalar growth—great part of it having been destroyed by blood 
extravasation. Where not destroyed it consists of a mass of cells with very 
little fibrous tissue between them. Insp. 1900, 420. Med. Rep. 389. 





CASE 60. Two months’ course, deposits in skin, pleura, liver, glands. —H. 8., 
st. 34 (m.) Admitted under Dr. Bryant, November 30th, 1900, and died 
December 23rd. A tinplate worker, always healthy. At’ the end of October, 
1900, he began to have pain in the loins shooting down the thighs, which got 
worse. Three weeks later he took to his bed. He has lost weight and strength. 
The pains come on with no apparent. cause. The right leg has become weaker than 
the left, and there is pain in the left foot. In the right deltoid is a swelling 
the size of & marble, soft and movable, which has been there three weeks. 
Another is present, loosely attached to eighth rib in the right axillary line 
(where the shears touched him), this is larger and of rather older date. First 
dorsal spine prominent and tender, fourth dorsal tender. Chief reference of 
pain is to first and second sacral, and the posterior third of the iliac crest. 
Nothing abnormal to be felt here. Knee-jerk increased. Ankle clonus present. 
Liver and spleen impalpable. Chest normal. Urine 1005, alkaline, nothing 
abnormal, urea 1:3 per cent. Diagnosis, sarcoma or subacute myelitis. At 
first the patient improved, and his legs gained power. On December 17th 
his liver was found enlarged, and this increased till death. An intention 
tremor of the hands. was noticed, and he finally died with hiccough and 
delirium. Post Mortem: The lumps noticed in life proved to be secondary 
nodules between muscle and deep fascia, softening centrally. Spinal cord 
normal. Thyroid acrophied, a yellow fibrous patch (not growth) in each lobe, 
Lungs normal. Right pleura, nodules of growth from a pin's head to a pea ; 
recent pleuritic adhesions. Recently extravasted blood in the pericardium. 
The pulmonary artery contained an ante mortem thrombus, derived 
probably from the auricle. Liver, 3091 gr, yellow, mottled. Right lobe 


Appendix of Cases. 327 


infiltrated and replaced, some small nodules the size of a pea. Left lobe 
infiltrated and softening. Pancreas and giands invaded. Right kidney, 
584 gr., upper half occupied by a white mass 6 cm. across. This had invaded 
the perinephric tissue on the inner side ; on the outer it was coated with renal 
tissue. Left kidney, several deposits the size of a pea. Adrenals normal. 
Dr. Fawcett considered the kidney growth undoubtedly primary. Micro- 
scopically: The kidney showed a mixed spindle and round-celled sarcoma. 
The liver was invaded by growth, which in parts where the tissue is not 
wholly replaced seems to run along the course of the hepatic veins and 
interlobular capillaries, the intralobular veins are in many cases filled with 
growth. ‘he liver cells are cloudy and atrophic. Insp. 1900, 451. Med. Rep. 397. 





CASE 61. Carcinoma, nephrectomy, discharge. H. B., et. 55 (m.). Admitted 
under Mr. Jacobson, November 8th, 1901, and discharged January 15th, 1902. 
Six months ago he caught his foot in a hole while running, had a pain in his left 
side, and an hour later passed urine containing much blood. For some time 
he passed highly coloured urine, and had recurrences of pain. Three months 
ago a tumour appeared in his left side, and he occasionally passed clots, one 
8 inches long and as thick as whipcord. He could not sleep on his right side, 
as a mass seemed to fall across. On admission: A movable tumour in left 
renal region. Skiagram showed nothing abnormal. The diagnosis lay between 
a latent calculus dislodged at the time of the accident, and blood calculus. 
Operation, November 22nd: Kidney found enlarged and low down. It was 
bossy with what was clearly malignant growth. The structures at the hilum 
were matted together and difficult to recognize. Clamps were applied to them, 
Near the origin of the renal vessels was a grey mass, probably growth. The 
whole was removed as completely as possible, and the patient made a good 
recovery. Mr. Targett has examined a section of the growth and thinks it is 
a degenerating carcinoma. Surg. Rep. 17. 





Case 62. Papilloma of pelvis, nephrectamy, death from recurrence.—H. K., 
æt. 53 (m.). Admitted under Mr. Symonds, July 25th, 1902, and discharged 
October 19th. Previous history good. Three years ago he noticed that his 
urine was very dark, and again a year later. In the last three months pain 
has begun to occur in the right loin, groin, and testes, and a fortnight ago he 
had difficulty in passing his water, caused by clots. On admission: Right side 
of abdomen rigid, in right loin a large tender trilobed mass. Hydrocele right 
side and pain in right testes and thigh. Operation, July 30th: Kidney 
on exposure dilated and contained much dark fluid, with which escaped pieces 
of papillomatous growth. Pelvis and ureter thickened and dilated, one gland 
enlarged. The whole kidney and upper end of ureter removed. The 
pelvis was found choked with papilloma, and hardly any kidney substance 
was left. The patient recovered and went on fairly well fora month. At the 
end of six weeks he complained of pain in the left loin, and a mass could be 
felt there, which was considered likely to be secondary deposit. He went 
gradually downhill, and was ultimately discharged to an infirmary where he 
died. Microscopically the growth was of a delicate papillary nature. There was 
only a small amount of cellular tissue at its base. and nothing to suggest 
malignancy. Surg, Rep. 828. 


328 Growths of the Kidney and Adrenals. 


CASE 63. Six years pain, по hematuria, nephrectomy.—S. W., æt. 36 (f.). 
Admitted under Mr. Jacobson, April 4th, 1902, and discharged May 16th. Twelve 
years ago a difficult labour, no other illness. Six years ago she began to have 
severe pain in the left loin and was for several weeks an in-patient at two 
London hospitals, where floating kidney and neuralgia were diugnosed. She 
was then treated for seven months for laceration of the cervix. Since then 
she has remained well till a fortnight ago, when she began to have severe 
intermittent pains in the back, increased by movement. On admission: 
Dyspepsia, general condition good. Pain limited to left inguinal and lumbar 
regions, coughing painless. A mass can be felt in the left loin at the level of 
the iliac crest, dull, tender, moving with respiration, and about 2-ins. by 2-in. in 
size. Urine normal, urea 1:5 per cent., leucocytes 9000. Diagnoses suggested 
were growth, and pyo-nephrosis with calculi. Operation, April 15th: Oblique 
incision, kidney enlarged with grey patches on the surface, no calculi found, 
ureter healthy, no thrombosis or glands. It weighed 15 ozs., and only a small 
part near the hilum remained normal. The microscopical section was un- 
recognizable. The patient made a good recovery. Surg. Rep. 186. 





CASE 64. Papilloma—15 months’ hematuria, nephrectomy.—G. Q., st. 60 
(m.). Admitted under Mr. Jacobson, November 23r4, 1902, and discharged 
January 1st, 1903. History good. Fifteen months ago he first noticed that his 
urine was sometimes tinged with blood, especially after exercise. A year ago 
he felt a weakness in his back, aud nine months ago he began to have attacks of 
sharp, shooting pains below the right ribs. Eight months ago he had a fall, 
and after this the pain got worse and extended across the right iliac region 
and down to the testes. Two months ago he passed a clot 2 inches long, the 
thickness of a toothpick. On admission: He seems healthy, except when his 
pain is present. There is some tenderness of the right loin and rigidity of 
abdominal muscles. The right kidney is more easily felt than the left. He 
cannot sleep on the left side as a mass seems to fall across. Urine, 1024, 
acid; blood and pus present. December 3rd, operation: The kidney was 
punctured, incised, and explored with the finger. It bled freely. The kidney 
was clearly a damaged one, though neither calculi or growth could be demon- 
strated. The ureter was cut low down and the kidney removed. On exami- 
nation it was found to have a villous mass at the beginning of the ureter lined 
by cubical epithelium. The epithelium also invaded the substance of the 
kidney. Mr. Targett considered the growth malignant. The patient made a 
good recovery and was discharged January Ist. Snrg, Rep. 21. 





CASE 65. Congenital sarcoma of adrenal, infiltration of liver.—W. M., æt. 
2 weeks (m.). Admitted under Dr. Perry, January 17th, 1902, and died 
January 18th. The child’s abdomen was noticed to be swollen two days after 
birth. It has since become bigger. There was anuria for the first two days, 
and a bullous rash over back and thighs since the first day. Legs, lower back, 
and abdomen cedematous, Abdomen distended: superficial veins running up 
from umbilicus. Upper and right half of abdomen dull. Lungs normal, 
Respiration 64. January 18th: Temperature 102° morning. 104° evening. 
The only urine obtained (5 02.) contained no albumen. Post Mortem: Slight 
broncho-pneumonia both lungs. A little ascites. Liver much enlarged, yellow, 
mottled, infiltrated throughout with what looks like new growth. It weighs 





Apnendix of Cases. 329 


1850 grms., and the capsule is normal. Glands in portal fissure are also 
infiltrated. Right adrenal normal. Left adrenal, a large tumour 2X 15 incbes, 
is quite independent of the kidney. Alternate layers of creamy white and 
deep red. In the centre many little yellow gritty points. Right kidney normal. 
Left kidney attached to tumour. Microscopically the adrenal shows a superficial 
layer of normal adrenal cortex, enclosing a small round-celled very vascular 
sarcoma. In part the cells of the tumour are arranged round the edges of 
small masses of homogeneous substance of uncertain nature. The liver 
presents a structure similar to that of the adrenal tumour. Only slight 
remains of normal liver tissue can be found. Insp. 1902, 36. Med. Rep, 
Clinical, 68. 





CASE 66. Five months’ course, extensive lymphatic and local invasion—blood 
invasion.—A. M., æt. 33 (m.). Admitted under Dr. Hale-White, May 8th, 1902, 
and died, August 27th. Came in for swelling of the leg. History good. 
He was well till March last, when he began to feel ill and run down, and had 
pain in hips, groins, and thighs, these got worse and his feet were always 
cold. He has been laid up two weeks. On admission, temperature 101° 
right leg cedematous from foot to groin, veins on leg and abdomen distended, 
femoral vein a hard cord. Liver normal, chest normal, urine normal. (Edema 
and pain decreased. In the middle of June he lost power in his right leg, but 
retained sensation. Atthe end of Junea little fluid was drawn off from his left 
pleura. Meanwhile pain and paralysis varied. About a month later there was 
cedema in the other thigh, the enlargement of veins and upward flow in them was 
marked, there was some fixed dulness in the left flank, and an enlarged and 
nodular liver reaching to within two inches of the navel. Carcinoma of the 
pylorus was discussed. In the course of August he developed paresis of both 
legs and loss of sphincter control, the liver increased in size, sensation became 
abnormal, and finally two days before death there was some blood in the urine. 
Post Mortem : A solid mass of growth surrounded the cavity of the pelvis and 
adhered to its inner wall. It compressed all the vessels and the sacral plexus, 
but had not invaded the bladder and prostate. ‘The right common iliac was 
thrombosed at its upper part. Over the prominence of the sacrum and on 
either side was a solid mass of growth continuous with that in the pelvis, and 
extending up on either side of the vertebral column as far as the crura of the 
diaphragm. The vena cava was invaded and completely blocked by the 
growth, the aorta surrounded but nov invaded. The mass was continuous with 
deposits in the lymphatic glands, and on tho left side with the kidney, which 
was much enlarged. It extended into the spinal canal by the intervertebral 
foramina over the lower 9 cm. of its length, and for this distance there was a 
layer of growth on the anterior surface of the dura mater. The nerves of the 
lumbar plexus were completely surrounded. Sections of the spinal cord 
were normal to the naked eye. On cutting through the muscles of the back 
in the lumbar region, a secondary mass was discovered which had spread 
through from the mass in front of the vertebra between the laminz. The 
lungs showed old adhesions and were studded with nodules of new growth 
almos t all the size of peas. In the thorax was a tubular mass of growth 

) cm. broad along the side of the aorta continuous with that in the abdomen. 
Azygos vein thrombosed. Heart, 210 gr. A worm-shaped cylinder of white 
growth hung from the vena cava into the right auricle for 3 cm., and 


330 Growthe of the Kidney and Adrenals. 


another polypoid mass the shape of a gourd adhered to and projected out of the 
auricular appendix, this was 5 cm. long. Liver, 4320 gr., enormously 
enlarged by deposits. Spleen normal. Lumbar glands and those in the 
portal fissure infected. Adrenals normal. Right kidney normal. Left kidney, 
710 gr., enlarged by a mass of white growth which nearly replaced the renal 
substance. It was firmer than that in the liver and was considered the primary 
source. The glands at the hilum were enlarged. There was acute cystitis. 
Microscopically : A carcinoma with alveoli of varying sizes and shapes, lined 
mostly by a short cubical epithelium, with comparatively little stroma. The 
growths in lungs, liver, and pelvis were similar, that in the lungs being rather 
more fibrous than the rest. Insp. 1902, 375. Med. Rep. 173. 





CASE 67. Six months hematuria, growth, calculs, blood and lymph invasion.— 
M.S., et. 53(m.). Admitted under Mr. Jacobson, September 3rd, 1903, and 
died September 10th. He has been a heavy drinker, and has had a hernia for 
the last seven years. Six months ago he dislocated his right shoulder and 
bruised his right thorax and loin, and a fortnight later he had hematuria for 
three days. Three months ago he began to have attacks of acute pain in both 
loins, lasting some five hours at atime, and generally occurring at night. Two 
months ago the pain became localized in the right loin; for the last three 
weeks this has been worse, a tumour has appeared, and micturition has been 
frequent and occasionally painful On admission: He looks as if he had 
peritonitis. His abdomen is tense and tender, especially in the right loin, 
where an ill-defined fluctuating dull tumour is present. Liver enlarged. 
Pulse 130. Temperature 100°4°. Respiration 48. Urine 1015, acid ; a trace of 
albumen. Leucocytes 32,500. September 4th: A transverse incision was 
made in the right loin behind and pus let out. He developed bronchitis and 
died. Post Mortem: 14 pints of fluid in each side of the chest. Lungs: 
bronchiectasis, cedema, nodules of growth. Liver contained growth. Right 
kidney adherent al) round and converted into a shell of renal tissue enclosing 
large masses of growth, pus, and four or five big branched calculi. Growth 
was present in the appendix, the pancreas was enlarged and congested, the 
lumbar and mesenteric glands enlarged and hard. Other viscera healthy. 

Surg. Кер. 812. 





CASE 68. Sarcoma of adrenal and kidney in a child, no metastases.—E. J.. 
zt. 2 years and 7 months (f.. Admitted under Sir Cooper Perry, May 26th, 
1903. Admitted for swelling of the abdomen. Five weeks ago she fell down- 
stairs, and a week later a swelling was noticed in the right side of the abdo- 
men, which has been steadily increasing in size. On May 26th she was sick, 
and in a good deal of pain. She was brought up to the hospital, and at once 
admitted. The legs were found to be slightly cedematous and drawn up 
towards the abdomen, which was much distended, especially on the right 
side. The superficial veins were dilated, and a hard tumour could be felt 
extending from 1} inch above Poupart’s ligament upwards to the right of the 
umbilicus and outwards into the flank, becoming continuous with the liver. 
There was dulness all over the tumour. No specimen of urine was obtained. 
The child became collapsed, and died within twenty hours of admission. Post 
Mortem : No pleurisy ; lungs healthy, base of the right one compressed and 
airless from the abdominal tumour pushing up the diaphragm. Stomach dis- 


Appendix of Cases. 331 


placed to left, cecum, appendix, and lower part of ascending colon pushed for- 
ward bya large tumour. No ascites. Abdomen distended by a large mass 
in the right half. No growth in the liver, but the tumour had gradually pushed 
it over to the left side and at the same time become firmly attached to it, so 
that it appeared as if the tumour was actually hepatic. On making a vertical 
section of the mass it was found to be composed of two parts, a lower spherical 
mass in the right kidney, capped by another much larger mass, which seemed 
to have originated in the right adrenal, of which no trace could be found. 
Both tumours were soft and very friable, and in appearance and consistence 
resembled hemorrhagic brain substance. Renal vessels not thrombosed. Some 
normal kidney tissue could be seen forming a kind of capsule to the lowest 
parts of the tumour. The growth was a small round-celled sarcoma. Insp. 
1903, 192. 

CASE 69. Adrenal rest tumour, hematuria, no metastases.—J. К, æt. 68 
(m.). Admitted under Mr. Golding Bird, June 5th, 1903, and died June 11th. 
Admitted for retention and hematuria. Family history good, personal 
history : repeated gonorrhea, syphilis, cystitis, stricture. He has been passing 
a catheter at intervals. On June 4th he had retention, and a quantity of 
bloody urine was then drawn off with a catheter, which was tied in, but had 
to be removed as it soon became clogged with blood. On admission, bladder 
distended, and renal pain, worse left side. Catheter used and bloody urine 
drawn off. For the next four days he continued to have hematuria, and to be 
dependent on a catheter. On the 9th the bladder was washed out with 
hazeline; much blood. Temperature 104°. On the 10th, A.C.E was given, 
and a suprapubic cystotomy performed. Blood clot was extracted, and a 
small prostatic adenoma (thought at the time to be growth). The bladder 
was washed out with hot water and hazeline, and a tube fixed in. The next 
day he died. Post Mortem : Old tubercle both apices, pleural adhesions over 
the posterior and diaphragmatic surfaces of the right lung. Lungs cedematous 
behind, emphysematous in front, in the left lower lobe were several patches 
of early septic bronchopneumonia. Pigmentary degeneration of myocardium, 
Adrenals normal. Kidneys 213 gr, left 130. There was a spherical nodule 
of growth 4 cm. in diameter, which projected from the upper inner posterior 
surface of the left kidney. ‘The capsule could be stripped from it, but it was 
continuous with the kidney capsule below, and could not be separated from 
it, and it opened into the pelvis, which was considerably dilated and deeply 
congested. From the appearance it seemed to have bled freely into the pelvis. 
The growth was soft, hemorrhagic, and streaked with yellowish areas. From 
its position and appearance it looked like a neoplasm originating in an adrenal 
rest. Bladder full of blood clots, some ulceration, a few small polypoid 
masses at the beginning of the urethra, otherwise nothing abnormal. Mucous 
membrane deeply stained. Prostate enlarged, no carcinoma. Several 
phleboliths in the prostatic plexus. Microscopically, the primary growth was 
a carcinoma of the suprarenal, (probably carcinoma originating in a supra- 
renal rest was meant, for the adrenals are noted as being normal.) Jzsp. 1903, 


213. Surg. Rep. 292. 





CASE 70. Adrenal rest growth. Tumour 2 years. Nephrectomy. Recovery. 
—G, H., æt, 59 (m.) Admitted under Mr. Golding Bird, November 4th 


332 Growths of the Kidney and Adrenals. 


1904. Family and personal history good. А swelling had been 
noticed in the left side for two years. A year ago, after an attack 
of influenza, it began to cause discomfort. There was no pain—only 
a heavy feeling. There was never any hematuria. On admission, the patient's 
general appearance was healthy. His abdomen bulged on both sides, more 
markedly on the left. On palpation the right side of the abdomen} was 
normal, and the liver not enlarged. On the left side a large mass could be 
felt, situated chiefly in the left lumbar region, but extending up into the left 
hypochondrium and forwards iuto the umbilical region. This was hard, did 
not fluctuate, had an ill-defined shape, and moved on respiration. By placing 
the hand behind the left loin it could be moved downwards and forwards. 
It was slightly tender. The mass felt uniform all over, except at 
a point immediately above the anterior superior iliac spine, where 
a movable tube could be felt, apparently continuous with the sigmoid. 
In. the course of examination, gas could be felt to pass through 
this. A knob could be felt at the anterior inferior angle of the mass, 
but no notch could be found. The costal angle was much increased. 
The bladder was not enlarged, and nothing abnormal was felt per rectum. 
Urine 1022, acid. No abnormal constituents. A blood count showed nothing 
abnormal. Fluid was drawn olf by an exploring syringe, and on examination 
showed ordinary blood with a few short chains of cocci. Nothing grew from 
these in six days at the temperature of the body. Operation: A.C.E. was 
administered, and the breathing failed. The patient was restored by artificial 
respiration, and an exploratory incision was made, 4 inches long, vertical, just 
above the left anterior superior iliac spine. The descending colon was found 
pushed forwards by an extra-peritoneal tumour which bulged up between the 
two layers of the descending meso-colon, and reached forwards nearly to the 
aorta. The pancreas and spleen felt normal. As the tumour was clearly renal, 
this incision was closed, and an oblique one made for 7 inches from the tip of 
the last rib to the thickest part of the iliac crest. The quadratus was not 
divided. The tumour was found covered with a tough capsule. This was 
divided, and the mass separated out with great difficulty by the hand. During 
this proceeding the thin inner capsule was torn. The separation of the mass 
from its outer capsule was quickly performed, and the tumour drawn down and 
pushed out of the lumbar opening. A large pedicle could be seen, consisting 
of the renal vessels and ureter; this was secured by a Staffordshire knot of 
thick silk, divided, and the whole mass freed. Owing to the patient's condi- 
tion, it was found necessary at this stage to infuse 35 oz. into the axilla. The 
wound was then washed out with mercury perchloride lotion, and two large 
drains fixed in. The patient's condition was very bad immediately after the 
operation, but improved rapidly in the course of the next few days, and is 
now satisfactory. The tumour will be found figured and described at the 
beginning of the paper. | 


A CASE OF SEVERE HAMOCYTOLYSIS. 


By G. T. WRENCH, M.B., anp J. H. BRYANT, М.р. 


Ss о е d 


In the following case of a girl, æt. 10, hemocytolysis was 
present in such a marked degree, and the blood exhibited such 
extraordinary changes, that we have deemed it worthy of record. 
For a few days a fatal result appeared to be inevitable, but 
recovery took place eventually at the end of three weeks, with 
complete restoration of the blood to normal. 

Florence C., æt. 10, was admitted into Miriam ward on April 
19th, 1902, under the care of Dr. Bryant, for profound anemia. 
Three years ago she had an attack of measles, otherwise she had 
always been strong and healthy. Her parents considered her to 
be a strong child, and stated she rarely suffered from any 
ailments. 

On April 11th, 1902, t.e., eight days before admission, she was 
playing in the yard when she slipped and fell, striking her left 
side in the region of the spleen, against the shaft of a cart. She 
went indoors and complained to her mother of the injury, but 
soon went out again and resumed her game. She appeared to be 
quite well for the next two days. 

On Sunday, April 14th, she complained of feeling ill; loss of 
appetite and headache. Her parents thought she had a bilious 
attack and took little notice until April 16th, when they observed 
that she had changed colour, her face being pale and of a some- 
what yellowish tint. The pallor increased up to the time of her 
admission on April 19th. During this time she was able to take 
nothing but milk, or milk and egg. She was sick after food, 


334 A Case of Severe Hemocytolysts. 


usually about three times a day, was very thirsty and complained 
of her tongue being rough and dry. There was no evidence of 
hemorrhage and she had no rash. She was constipated for three 
days. She had neither headache nor mental symptoms. 

Her parents are strong and healthy. She has six brothers 
and sisters, all of whom are living and well. On Friday, April 
19th, she was admitted into Miriam ward. 

Condition оп admission.—Temperature 98°, pulse 96, respira- 
tions 24. She was а well-nourished child but markedly anemic. 
The skin, however, had a curious yellowish-brown tint more like 
that of Addison's disease than of simple ansmia. She was very 
restless and was continually yawning. She had a wild look about 
the eyes although she was not delirious. 

Circulatory system. — The impulse was seen and felt in the 
fifth left intercostal space, just beyond the nipple line. There was 
no thrill. The superficial cardiac dulness commenced above in 
the third left space and externally extended just beyond the - 
nipple line. At the apex there was a systolic murmur which 
could be heard all over the front of the chest, but which was best 
marked in the pulmonary area. It was also traceable into the 
carotids and along the.abdominal aorta and external iliac arteries. 
During a full inspiration the heart-beat was much slowed. There 
was & doubtful bruit de diable just above the clavicle but it was 
difficult to dissociate it from the systolic bruit. 

Abdomen.—The abdomen was not distended. It was supple 
and there was no tenderness. The edge of the liver could be felt 
just below the costal margin in the right nipple line. 

The spleen was enlarged. It could be felt half an inch anterior 
to the left nipple line, and below, it extended to within a finger's 
breadth of the level of the umbilicus. It was not tender. The 
edge was regular, sharp, and well defined. 

Skin.—No rash present. | 

Respiratory and nervous systems.—There were no abnormal 
signs. 

The urine was acid and contained neither blood, sugar, pus nor 
albumen. 

The vomit contained no blood and no free hydrochloric acid. 


A Case of Severe Hemocytolysis. 335 


The feces were carefully examined for parasites and ova but 
none were detected. | 

Blood.—(In describing the different kinds of blood-cells, the 
nomenclature of Ehrlich, as given by Cabot (8rd edition) was 
used and all differential counts were made from specimens stained 
by Ehrlich’s triacid stain. The blood-counts -were made with 
the Thoma-Zeiss hemocytometer and the hemoglobin was 
estimated by Marie's hemoglobinometer, and once by the specific 
gravity method). 


April 19th.— 

Red blood corpuscles ... 989°300 per cubic millimetre. 

Hemoglobin see ... 2T per cent. 

Nucleated red corpuscles ... — 27:600 per cubic millimetre. 

White id T .. 69:000 i Р 
Polymorphonuclear ... 66:4 per cent. 
Small lymphocytes .. 28:9 j 
Large lymphocytes e. 24 Р 
Myelocytes i sae 58 : 
Eosinophiles ... .. 20 я 
Eosinophile myelocytes... 0:2 Ў 
Transitional 5 .. 60 " 


A microscopical examination of the films showed the majority of 
the red corpuscles to be undersized. A large number of red cells 
were nucleated. The nuclei were bipartite, tripartite or irregular. 
Some of the bipartite cells were dividing in equal proportion and 
with division of the protoplasm, suggested cell division. Some of 
the nuclei were deeply stained, probably old corpuscles, others, 
especially those of the large erythroblasts, were pale blue. Many 
of the red corpuscles showed well-marked polychromatophilia. 
There was no poikilocytosis, the corpuscles retaining their normal 
contour, nor were there fragments of broken corpuscles. The 
white corpuscles, although greatly increased in number, did not 
display any disproportion in their relative percentage, except for 
the presence of a few myelocytes. 

She was given an ounce of peptonized milk every hour and 
large nutrient enemas every six hours.* 0:6 c.c. of cacodylate of 
soda solution was injected into the axilla at 10 p.m. 


* À sterile solution was used which contained 0.05 gm. i.e. $grain of 
Cacodylic Acid in 1 c.c. (17 minims). 


336 A Case of Severe Hemocytolysis. 


She was very restless during the night and made several 
attempts to get out of bed, and was once found sitting on a chair 
by her bed. 

April 20th. She was in much the same condition as on admis- 
sion. She was rational with her own relations, but with nobody 
else. The bowels were opened, but both urine and fæces were 
passed unconsciously. The motion was very dark, but contained 
no blood. There was no epistaxis, hsematemesis, melena, 
hematuria nor purpura. She did not complain of pain. The 
spleen was the same size as on the 19th. Her grandmother, 
who had watched her from the beginning of her illness, considered 
her colour better to-day. The highest recorded temperature was 
99:8? at 10 am. At 6 p.m. the pulse was 160, and the lowest 
rate was 136 at 10 a.m. Urine: 1022, pinkish deposit of urates, 
urea 2:05 per cent., no albumen, sugar, bile, pigment or indican; 
a little urobilin was detected. At 9 p.m, 0:9 c.c. of cacodylate of 
soda solution was injected into the axilla. 


The eyes were examined and a few retinal hemorrhages were 
seen. 

The blood-count showed the following :—- 

Red blood corpuscles i5 = .. 1,164,500 
White blood corpuscles ... з Ps 105,500 

The differential count was not markedly different to that made 
on the 19th, except for the smaller percentage of polymorpho- 
nuclear cells (53:8 per cent.), the larger percentage of small 
lymphocytes (28:8 per cent.), and the appearance of new cell-like 
bodies which were not present in the films made and examined 
on the 19th. 

They did not conform to any type of leucocyte described 
by Cabot, Ewing, or Von Limbeck. They have been placed in 
the list of the differential counts amongst the leucocytes and named 
“ vacuolated bodies." In appearance these “ vacuolated bodies" 
presented fairly definite masses of protoplasm which took on 
basic stains either lightly or darkly, but asa rule to a tint that 
was less deep than the nuclei of the concomitant leucocytes. 
This stained protoplasm was much vacuolated, and was bound 


A Case of Severe Hemocytolysis. 837 


together by a kind of fibrillar network. The margins of the 
vacuoles were either closely defined or merged into the blue- 
stained protoplasm. These bodies varied greatly in size but the 
average was considerably above the measurement of the leucocytes. 
Some only measured 9u by 10и, but many as much as l6y by 
14u or even 12y by 28и. 


At first it was thought they might be basophiles, but their 
staining reactions with Jenner's stain and methylene blue did 
not correspond with this kind of cell. True basophiles were seen 
only on one day (April 24th). The shape of the vacuolated bodies 
was often irregular with protrusions comparable to the pseudo- 
podia of amceba. A few specimens of fresh blood were examined, 
but nothing of a parasitic nature was noticed. No special search 
with a warm stage was made for parasites, as this interpretation of 
the bodies was not thought of at the time. "They had no definite 
nucleus, and no granules. 

With Jenner's stain they presented a similar uniformly stained 
vacuolated mass. With eosin and methylene blue they presented 
the same appearance as with Ehrlich's triacid or Jenner's stain. 
Sometimes similarly stained uniform, but unvacuolated, protoplasm 
was seen with fine oxyphile granules near them and occasionally 
these fine granules were observed apart from any protoplasm, as 
if lying loose in the blood-stream or separated from their cell in 
the process of making the film. 


April 21st. She was in much the same condition, but the 
spleen was a little smaller. The tendency to delirium was still 
present. The eyes were examined and hemorrhages into both 
retine were found. She appeared to have a slightly better 
colour. She was still troubled with vomiting. The highest 
recorded temperature was 99:4? at 2 p.m., and the lowest 97:8? 
at 6 p.m. A few uric acid crystals were found in the urine. 

She was given some bread and milk, but vomited it soon after- 
wards. Plasmon 3j. and Extract of Malt 511. was ordered for her, 
to be taken three times a day. 

22nd. She was improving in every respect, being more 
sensible and of a better colour, and the spleen was appreciably 


338 A Case of Severe Hemocytolysis. 


smaller; 13 minims of cacodylate of soda solution were injected 
into the axilla. | 

23rd. She was less anemic in appearance and much more 
sensible. The spleen was smaller. The temperature was 99°; 
20 minims of cacodylate of soda solution (}2grs.) were injected 
subcutaneously at 11.45 a.m. 

24th. А further improvement in her colour and also in her 
manner was noticeable. The spleen was a little smaller. Urine 
acid, no albumen, urea 2:4 per cent.; no uric acid crystals; 
Indigo red present but no indican blue: no urobilin. 14 minims 
of cacodylate of soda solution (#gr.), were injected into the 
axilla at 11.45 a.m. 

25th. She appeared to be steadily improving in every respect ; 
10 minims of cacodylate of soda solution were injected. 

26th. The spleen was smaller. Urine: 1025; acid, urobilin 
present. 15 minims of cacodylate of soda injected. 

27th. She felt and looked comparatively well. She was now 
able to take (minced) fish for dinner and bread and milk for 
breakfast; 15 minims of cacodylate of soda solution injected. 
Urine 1025 ; a good deal of urobilin was present. 

28th. The administration of one-fifth grain of cacodylate of 
soda in the form of a pill three times a day was now commenced. 

29th. She looked quite well She had no pain and was able 
to take full diet without any discomfort. 

May 1st. The mucous membranes were still a little pale. 
Systolic murmurs were audible in the pulmonary and mitral 
areas. The cardiac impulse was in the fifth left space about 
three-quarters of an inch outside the nipple line. The spleen 
was just palpable below the left costal margin. 

3rd. The spleen was not palpable. 

9th. She was discharged, having been up and about the ward 
for several days. Her colour had greatly improved. She had a 
distinct red tint about the cheeks, but elsewhere the skin was 
sallow. She was no longer sick and the bowels acted regularly 
every morning. No hemic murmurs could be detected. Neither 
the spleen пог the liver could be felt beneath. the costal margin. 
The retine presented a normal appearance. 


339 


A Case of Severe Hemocytolysis. 
















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340 A Case of Severe Hemocytolysis. 


One of the most interesting points to be determined in this 
case was the cause of the yemarkable changes in the blood. The 
parents attributed her condition to the injury she had received 
in the region of the spleen and the enlargement of that organ, 
which was discovered on her admission with its subsequent 
diminution in size as she recovered, seemed to corroborate this 
view and to point to some injury or to some derangement in 
the function of the spleen as the most likely cause of the anaemia. 

What pathological changes would account for such an enormous 
decrease in the number of red blood corpuscles (939,333 per c.mm. 
t.e. to about 18 per cent. of normal) the relative large amount of 
hemoglobin (27 per cent.) giving a colour index of 1:5, the 
leucocytosis (69,000 per с.п.) and the extraordinary number 
of nucleated red copuscles (27,600 per c.mm.) ? 

In all respects, with the exception of leucocytosis, the changes 
resembled those which are usually found in advanced cases of 
pernicious anemia. In all marked examples of this disease the 
leucocytes are diminished in number, frequently below 4,000 per 
c.mm. and even to 2,000 or 1,500. Leucocytosis, when it does 
occur in the course of pernicious anemia in adults is invariably 
due to some such complication as hemorrhage or suppuration, 
but in children it takes much less to induce leucocytosis. 
In this case no complication was discovered to account for it. 
Pernicious anemia is rare at such an age as ten, and further, the 
onset is much less acute and recovery is much more protracted ; 
additional reasons which help to exclude a diagnosis of this 
disease. 

The extreme pallor, the restlessness, and the constant yawning 
suggested the possibility of a severe hemorrhage. There was no 
history of epistaxis, hematemesis, hemoptysis, nor of any other 
form of hemorrhage, nor did a careful physical examination of 
the chest and abdomen yield any signs of an internal hemorrhage. 

The injury to the left side and the enlargement of the spleen 
made us consider whether that organ had been ruptured and 
bleeding had occurred into the peritoneal cavity. 

A simple hemorrhage, however, would hardly account for such 
marked changes in the blood. As a result of the loss of a 


A Case of Severe Hamocytolysis. 341 


considerable quantity of blood there is a diminution in the 
number of red blood corpuscles, and the hemoglobin is much 
reduced, so that the colour index is usually below ‘one. ‘The 
presence of such a large number of nucleated red corpuscles was 
compatible with a severe hemorrhage, for alter the loss of a 
considerable quantity of blood it is usual to find a large number 
of normoblasts and microblasts in the blood. Ewing writes, 
* Small and repeated hemorrhages, on the other hand, have led 
to some of the most severe forms of anemia ever recorded in 
which the morphological changes of pernicious anemia are 
pronounced, but the prevailing feature of the blood is the loss of 
hemoglobin.” It is usual to get a leucocytosis after hemorrhage, 
but the number of leucocytes per cubic millimetre do not as а 
rule exceed 40,000. А differential count shows a relative 
lymphocytosis. There are no grounds for supposing that in this 
case there had been repeated small hemorrhages. If the anemia 
was due to hemorrhage it must have been connected with the 
injury to the side and to bleeding into or from the spleen. 

The enlargement of the spleen suggests the possibility of some 
disorder or derangement of the function of that organ as a result 
of the injury. 

In two cases of splenectomy (of the healthy spleen) mentioned 
by Dr. Rolleston (Clifford Allbutt's System of Medicine, vol. lv.). 
the following group of symptoms occurred :— 

1. Progressive loss of strength and weight and of emaciation. 

. Extreme anemia. 

A daily rise of temperature 1? to 3? Fahrenheit. 

. Increased frequency of the pulse. 

. Fainting attacks, with increased pallor of the surfacc. 

. Headache, drowsiness and great thirst. 

. Severe griping pains in the abdomen and pain in tho legs 
and arms. In one case tenderness along the tibia, which was 
thought to indicate compensatory changes in the red marrow of 
the bones. 


8. Enlargement of the external lymphatie glands, which 
remained permanently increased in size. 


VOL. LIX. 24 


342 A Case of Severe Hemocytolysis. 


9. Blood changes, which consisted of a diminution in the 
number of: the red blood corpuscles and an increase in the 
number оЁ leucocytes. 

In this case, with the exception of 7 and 8, all these symptoms 
were prominent and striking, especially the diminution in the 
number of red blood corpuscles and the increase in the number 
of leucocytes. 

Could the injury, which she had received in the region of the 
spleen, in some obscure manner, have put that organ temporarily 
out of action, as when splenectomy removes the splenic function 
from the living subiects ? 

This explanation, however, was by no means satisfactory. In 
the first place, we were not able to find any previous record of 
such severe hemocytolysis and illness following an injury in the 
splenic area, and in the second place, the injury was slight, for 
there was no external evidence of it in the form of bruising, and 
the child, as has already been stated, was quickly enabled to 
return to her play. 

Casting around for some other cause we naturally thought, in 
the absence of any evidence of hemorrhage, of the possibility of 
her condition being due to the influence of some poison. Cabot 
(Clinical Examination of the Blood, 3rd edition) quotes a case 
reported by Brandenburg of acute anemia with marked leuco- 
cytosis as the result of poisoning by chlorate of potash and 
another case, reported by Ehrlich and Lindenthal of a similar 
condition due to poisoning by nitrobenzol. 

This last mentioned case is also quoted by Ewing (Clinical 
Pathology of the Blood, 1st edition, 315). The blood became 
chocolate-coloured ten hours after the initial symptoms and 
methemoglobin was visible by spectral analysis until the eighth 
day. On the fifth day the red cells were reduced to 2,975,000 
and before death fell to 200,000 per cubic millimetre. Poikilocy- 
tosis was noted on the third day. Nucleated red corpuscles 
were first seen on the third day, and on the ninth day 24,700 
to the cubic millimetre were counted. On the ninth day the 
leucocytes rose to 61,000. The hæmoglobin fell to 40 per cent., 
so that with 900,000 red blood corpuscles to the cubic millimetre 





A Case of Severe Hemocytolysis. 848 


and this percentage of hemoglobin the colour index was 
remarkably high. “ Тһе morphological characters of the blood 
described by Ehrlich and Lindenthal probably represent an 
extreme degree of the effects upon the blood of the entire group 
of anilin poisons.” 

Some such poison, we thought, might have been the cause of 
the hæmocytolysis in our case but all enquiries and efforts at 
discovering such a cause proved to be unavailing until six weeks 
after the patient’s discharge, when our suspicions received con- 
firmation in an unexpected manner. The quarterly gas bill was 
sent to the father of our patient and found to be considerably 
more than usual, in fact was nearly double the amount of the 
corresponding quarter for the previous year. Recalling our 
persistent questioning as to the possibility of his daughter having 
taken some poisonous substance, he looked for a leak in the gas- 
pipe of her bedroom and discovered an escape of gas which was 
situated under the floor immediately over which her bed was 
placed. We feel justified therefore in attributing the illness of 
our patient to the subacute toxic effects of coal gas. ` 

We did not notice any marked difference in the general naked- 
eye appearance of the blood; it certainly was not a bright cherry 
red nor was it chocolate coloured. We did not obtain a history 
suggesting hemoglobinuria, nor after admissicn did we find any 
evidence of such a condition. Although we have not been able 
to find a similar case of anemia which has been attributed to 
chronic coal gas poisoning, we are of opinion that this form of 
toxzemia is the most satisfactory explanation of this interesting 
and remarkable case. 

The rapid recovery was also of very great interest, but whether 
it was due to the treatment with cacodylate of sodium or to the 
change of environment, and so the removal of the apparent cause, 
we prefer to leave an open question. 

She was examined two months after discharge. She was quite 
healthy and the blood-count was normal. 





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A COLLECTION OF CASES IN WHICH 
THE OPERATION OF EXCISION 
OF THE HIP-JOINT HAS BEEN 
PERFORMED FOR DISEASE OF THE 
JOINT. 


By A. R. THOMPSON, M.B, Сн.В., F.R.C.S. 


SURGICAL REGISTRAR. 


THE object of the appended collection of cases is, primarily, to 
elicit the history of those patients in whom excision of the hip- 
joint has been performed for disease of that joint, and in whom 
the operation has succeeded, either partially or completely; in 
arresting the disease. EE 

But, in order that the collection of cases may be made’ more 
just, fuller, and more interesting, there have been added those 
cases in which disease of the hip-joint continued, and eventually 
resulted in amputation, through the upper part of the thigh, 
or in death, a previous excision of the hip-joint having been 
performed. 

It is advisable to point out in this place that the term **disease 
of the hip-joint” indicates tuberculous disease, but two cases 
have been included in the collection which were probably not 
tuberculous (cases 10 and 30). 

Forty cases in all have been traced since the operation of 
excision of the hip-joint was performed. Letters were addressed 
to many more, but in answer to some, no replies were recelyed ; 


948 A Collection of Cases in which the Operation of Excision of 


and, it may fairly be assumed that some of the cases were 
prevented from answering letters, or attending personally at the 
hospital, by the intervention of death. Of these forty cases 
which have been traced, definite information of their history after 
excision has been secured in all but three cases, concerning 
which, however, some information has been obtained. 


These forty cases, with four exceptions, have been under the 
care of surgeons at Guy’s Hospital during the years 1896 to 
1903. Two patients were operated upon by Sir Henry Howse, 
and Mr. Symonds respectively, before 1896. Two patients were 
operated upon at other hospitals. 


The interval which has elapsed between the excision of the hip 
and the examination of the patient by the writer, or the records 
of actual events in the surgical reports of Guy’s Hospital, varies 
from nineteen years to six months. In two cases, more than 
ten years have elapsed between the operation of excision, and the 
writer’s examination, or the actual records of failure or success; 
in fourteen cases more than five years; in four cases more than 
three years; in twelve cases more than one year; whilst in 
five cases less than a year has intervened between the operation 
of excision of the hip and examination. 


Three cases have not been included amongst these figures, 
owing to death immediately following excision of the hip in two 
cases, and incompleted history in the third case. 


The results may be considered under three heads; first, the 
cure of the tuberculous process; secondly, the deformity pro- 
duced by the operation; thirdly, the utility of the limb after 
the operation, and the ability of the patient to enter upon the 
various duties of life after excision of the hip has been performed. 
The cure of the tuberculous disease may first be considered. 


Three results may occur after excision of the hip. First, in 
some cases excision has had eventually to be followed by 
amputation, through the hip-joint, or a fatal termination has 
occurred at some time after the operation. These cases have 
been reckoned by the writer as failures. Secondly, those cases 
in which there is no sign of continuation of disease, as evidenced 


the Hip-joint has been performed for Disease of the Joint. 349 


by abscess or sinus-formation, have been reckoned as successes. 
Thirdly, those cases which still show sinus-formation, or 
evidence of abscess-formation, have been reckoned as partial 
failures. There is certainly a difficulty in accurately classifying 
these partial failures, for whilst some are undoubtedly progressing 
towards recovery, others are as surely progressing towards ampu- 
tation, or perhaps even early death. 

In six cases, out of the total number collected (15 per cent.) 
death has occurred since the operation. Two deaths resulted 
from shock immediately following surgical interference (cases 
24 and 33). Two deaths have occurred from progressive tuber- 
culous or lardaceous disease (cases 21 and 85); whilst two patients 
have died outside the hospital (cases 2 and 25). As the last 
two cases were discharged in a considerably worse condition than 
when they were admitted, it may be justly considered that death 
occurred from complications or sequele associated with the hip 
trouble. In two of these cases death took place in spite of 
amputation through the hip-joint 

Eight other cases are known to have had amputation performed 
at the hip-joint after excision of the joint. Thus excision of the 
hip-joint resulted in failure in fourteen cases (35 per cent.). 

The failures, represented either by death or amputation through 
the hip-joint, excluding the deaths actually due to operation and 
excluding an unusual case of nineteen years' interval, occurred 
on an average three years after excision of the hip-joint 

There are in the present series of cases eleven partial failures, 
that is to say, that in 27:5 per cent. of the cases there are still 
sinuses present. In fifteen cases, or in 37:5 per cent. the results 
of excision of the hip-joint have been successful. 

A more detailed analysis of the cases may now be made. 
There are, in this collection of cases, fourteen females and twenty- 
six males. Whilst in each sex there are eight successes, there 
are five failures amongst the females against nine failures amongst 
the males, and one partial failure amongst the females against 
nine partial failures amongst the males. These figures seem to 
show that the males have the same power to resist the progress 
of disease after excision as the females, but, owing no doubt to 


350 A Collection of Cases in which the Operation of Excision of 


greater activity in life, have less power to resist the continuation 
of disease. 

For the purposes of comparison with other forms of treatment 
of hip disease the following facts may be stated. The cases of 
excision of the hip may be divided into three groups. The first 
group comprises those cases in which excision of the hip-joint 
has been performed before the formation of an abscess or sinus. 
In this group there are seven cases with three successes, three 
failures and one partial failure. The second group comprises those 
cases in which an excision was performed, when abscess-formation 
was present, but no sinuses. In this group there are twenty cases, 
made up by seven successes, seven failures, and six partial failures. 

The third group comprises those cases in which sinus-formation 
had occurred when excision was performed. In this group there 
were nine cases with three successes, two failures and four 
partial failures. Four cases in which the history was imperfect 
have not been included under these headings. The mortality in 
the first group was 14 per cent., in the second 18 per cent., in 
the third 22 per cent. 

The failures, that is those cases in which death occurred after, 
or amputation followed, excision, amounted in the first group to 
43 per cent., in the second to 35 per cent., and in the third to 
22 per cent. Thus, as regards the failure or otherwise of excision 
of the hip, it may be concluded that excision is more favourable 
when an abscess has formed than when it has not, since failures 
are more common with excision performed before, rather than 
after, an abscess has formed. | 

As regards the age of the patient, there were sixteen cases 
over the age of ten whose hips were excised; of these there were 
eight successes, or 50 per cent. of the total number. In twenty- 
four cases operated upon under the ‘age of ten, there were eight 
successes, representing 33 per cent. of the total number. In 
none of the cases actually examined by the writer, twenty-three 
in number, was there any evidence of advancing lardaceous or 
tubercular disease, but in eleven cases there were sinuses 
present near the site of operation, indicating continuation of the 
disease. Many of these sinuses appeared superficial, and a 


Hip-joint has been performed for Disease of the Joint. 351 


single scraping might have been expected to effect a cure, but 
if the vagaries of the tuberculous process be considered, even these 
cases cannot fairly be considered as cures. Sinuses, however, 
do not appear to prevent patients from enjoying life or earning 
money. Thus, one case (29) whose hip was excised by Mr. Lucas 
was delighted to come up from Worthing and to spend a few 
days in town. Не was thoroughly happy, although about every 
three months a sinus appeared, which quickly healed up. Another 
patient (38) performed his duties as night watchman although 
sinuses are still present (May, 1904). 


Defornuty.—The next point to be considered is that of the 
deformity produced by the operation of excision of the hip. 
The deformity is usually well marked, and is chiefly due to the 
shortening of the limb on the side of the excised joint. 


In every case examined with a view to discovering the amount 
of shortening, the writer found that the great trochanter is 
displaced directly upwards on to the dorsum ilii, the tip of the 
great trochanter being generally nearly as high as the level of the 
anterior superior spine on the same side. In the great majority 
of cases this displacement of the great trochanter upwards is 
responsible for all the shortening; but in six cases there was 
marked shortening below the knee, amounting in each case to 
at least an inch (cases 12, 14, 23, 26, 28 and 30). 


It is not easy to obtain an exact history of the forms of splints 
used, or length of time for which they were applied after 
excision, but the displacement upwards of the trochanter 
occurred irrespective of the application of splints; thus, in one 
case splints were still being used seven years after the operation 
of excision, and in this case the displacement upwards was just 
as marked as in those cases in which splints had been discarded 
shortly after operation. 


Moreover, in those cases where special efforts were made 
by the surgeon, either by the introduction of wire joining the 
upper part of the femur to the acetabulum, or by special care 
exercised over the application of splints and position of the 
limb, the displacement upwards of the trochanter was just as 


352 А Collection of Cases in which the Operation of Excision of 


marked eventually as in those cases where no such special 
precautions were taken (vide cases 1 and 15). 

In some of the cases of excision of the hip seen at the Out- 
patient department, lordosis of the spine indicating flexion of the 
artificial joint is marked, but in the writer’s series of cases, out 
of twenty-two observed, only seven showed lordosis. 

The obvious disadvantage of flexion of the artificial joint is the 
great increase in apparent deformity which it causes, and the 
enormous boot which must be worn by the patient; in one case 
a boot with a sole nine inches thick was being worn by the 
patient, and in this case there was only three and a half inches 
actual shortening. In no case was there scoliosis of a permanent 
nature. 

In conjunction with the deformity, the question of wasting of 
the whole limb may be considered. 

In all the cases seen, the wasting was very apparent on the 
same side as the excision; and in these cases where the results 
have otherwise been successful, massage might be tried with 
advantage, as not only might it strengthen the lower limb, but 
it might also prevent the shortness of the tibia which occurs in 
some cases, and further might improve movements in the knee 
and ankle; and thus further compensation than that afforded by 
the pelvis and spine might be afforded for the loss of the natural 
hip-joint. 

Utility of the joint.—The utility of the new joint after excision 
now demands attention. In all the cases seen by the writer, the 
utility of the new joint was good, except in one case (28), in 
which an excision of the hip has been performed, and in which, 
for all the use the patient was making of the limb, amputation of 
the lower limb at the hip-joint might just as well have been 
performed as excision. 

In all the cases, except three, the whole weight of the body 
could be borne upon the artificial joint between the dorsum ilii 
and the femur. In no case did the great trochanter rise in the 
slightest degree when this test was carried out. 

Two of the most intelligent patients told the writer that they 
could do everything in the way of movements, except bend down 


the Hip-jount has been performed for Disease of the Joint. 353 


in such a way as would enable them to fasten their shoe on the 
side of the excised joint. 

An interesting question which may now be raised is that of 
mobility in the new joint. The writer was led to believe, before 
he made enquiries for himself, that flail joints were fairly 
common after excision of the hip. They are, according to the 
present collection of cases, rare. In this series only one case is 
found. In seven cases there was free mobility of the new joint, 
and in three cases there was partial mobility. In thirteen cases 
the joint was fixed. The mobility of the joint seems, however, 
to influence the formation of sinuses, for in eleven cases of 
movable joint, sinuses were present in six, and in thirteen cases 
of fixed joint three only had sinus-formation. 

These figures are not perhaps of much value if considered by 
themselves, but when taken in conjunction with the experience 
of the relative value of excision or erasion of the knee-joint, they 
seem to indicate that disease is more likely to recrudesce with a 
movable than with a fixed joint. 

In the hip-joint, mobility after excision may be exceedingly 
useful to the patient; thus, a child, Alice E. B. (not included in 
collection of cases), was admitted into the Waterloo Hospital for 
Children in 1899. Her right hip was excised by Mr. Marmaduke 
Sheild in the same year. 'The wound healed up and she was 
discharged. In 1902, she was re-admitted for left hip disease. 
Since then she has been using crutches, and wearing a patten 
on the right boot, so that the right hip has been in constant 
use for two years. The artificial joint is movable in every 
direction, and the great trochanter does not rise higher than 
its fixed position on the dorsum ilii, when the weight of the whole 
body is thrown upon the artificial joint. 

Finally, the ability of patients to attend to the ordinary duties 
of life after excision of the hip has been performed may be 
considered. 

Seven patients, who had reached the money-earning period of 
life, were obtaining fair wages and working hard. One was 
working nine hours a day as a clerk and earning thirty shillings 


354 <A Collection of Cases in which the Operation of Excision of 


a week; another was earning one pound a week; another was 
earning eight shillings a week, and was working eleven hours a 
day; others, younger, were earning five shillings a week or 
thereabouts; whilst another, preferring to live the life of a 
pitiable invalid, though quite capable of working, received eight 
shillings a week from clubs. A female patient, whose hip was 
excised by Mr. Golding-Bird for acute arthritis, following upon 
a miscarriage, told the writer that she had had after the 
operation the best labour and confinement she had ever 
experienced. One of the female patients living in Bermondsey, 
aged twenty-two, and exceedingly pretty, was still unmarried, 
and for this condition of single life, apart from private reasons 
which the writer did not enquire into, the deformity must be 
held responsible. 


The preceding remarks and the conclusions which may fairly 
be considered to arise therefrom may be now summarised in 
round numbers. Out of two hundred cases in which the hip- 
joint has been excised, seventy may be expected to be the subjects 
of progressive disease, and of these thirty may be expected to 
die from continuation and spread of the disease. Fifty-five will 
rank as partial failures, in that in these sinuses will persist. In 
many of these cases, however, sinuses wil] not interfere with the 
wage-earning capacity or happiness of the individual. Seventy- 
five cases may look forward to a complete recovery. Two cases, 
however, amongst these will have a flail joint. The majority of 
cases, whether sinus-formation is present or not, will have useful 
joints. The best result, however, namely, a useful joint, with 
free mobility and without any sinus, only falls to the lot of 
twenty-five people out of two hundred, there being in this series 
of forty cases only five such excellent results. 


the Hip-joint has been performed for Disease of the Joint. 855 


SYNOPSIS OF CASES. 


These are arranged in three classes :— 


1. Those cases in which excision was performed for hip- 
disease, and in which neither abscess nor sinus-formation 
had occurred before excision. 

2. Those cases in which excision was performed for hip disease 
and in which an abscess had formed, but no sinus-forma- 
tion had taken place before excision. 

3. Those cases in which excision was performed for hip disease 
and in which an abscess had formed and sinus-formation 
had taken place before excision. 


Class 1 comprises cases numbered from 1 to 7 inclusive. 
7 cases—3 successes T ... Cases 1, 8, 5. 
3 failures ies ... Cases 2, 6, 7. 


1 partial failure (that is sinuses still existed after 
excision) Case 4. 


The successful cases showed two movable and one fixed 
joint. 

The cases which terminated in failure showed one death and 
two amputations through the hip-joint. In the cases of failure 
the joint was movable. 


CASE 1.—Alice B., æt. 16. Mr. Golding-Bird, 4, 1898. Twelve months’ 
history of hip disease previous to admission on 27th October, 1897. Excision 
of hip on 9th December, 1897. No sinuses nor abscesses found. Healing 
took place by primary union. Efforts made to keep femur in acetabulum, 
and one month after operation there is a record of one inch shortening. 
Splihts and crutches discarded two months after discharge from hospital. 
On May 21st, 1904, six and a half years after operation, general and local 
condition was good. No signs of sinus-formation were present. The excised 
joint was movable and useful. The great trochanter did not rise at all 
when the weight of the body was borne upon the excised joint. There was 
two inches shortening due to slipping up of great trochanter. There was 
wasting of the thigh on affected side, amounting to two inches, and of leg 
three-quarters of an inch. This patient works eleven and a half hours a day 
as button-hole maker, earning eight shillings a weok, and although decidedly 
pretty, is unmarried. 


356 А Collection of Cases in which the Operation of Excision of 


Case 2.—Fred D., æt. 8. Sir Henry Howse, 130, 1896. Admitted March 
26th, 1896. Hip disease in second stage Excision of hip, May 1st, 1896. 
No sinuses nor abscesses found. Patient made no progress for some time, and 
on August llth, 1896, amputation, through the hip-joint, was performed. 
Sinuses persisted after amputation, and the patient died on August 10th, 
1898, at home. When he was discharged from Guy’s Hospital, he shewed 
signs of phthisis at the apex of the right lung. 


Case 3.—Elizabeth H., æt. 6. Sir Henry Howse, 126, 1901. Six months’ 
history of hip disease. Head of femur excised, 15th March, 1901. Complete 
healing by June 30th, 1901. Sinus appeared and was scraped in August, 
1901. Patient discharged with sinus practically healed, on September 20th, 
1901. Examined in May, 1904, three years after operation. Three inches 
shortening on affected side, made up by slipping up of great trochanter. 
Great trochanter does not rise when weight of body is borne upon excised 
joint. Joint fixed, and useful. Wasting of thigh amounts to one and three- 
quarter inches; wasting of leg to half an inch. Lordosis present, amounting 
to twenty degrees of flexion of artificial joint. Patient is in good local and 
general condition. | 


CASE 4.—Rose S., æt. 6. Mr. Davies Colley, 417, 1897. Nine months’ 
history of hip disease. Excision of head of femur, 15th June, 1897. No 
ubscess nor sinus present. Healing occurred by July 12th, 1897, by primary 
union. Examined May, 1904, seven years after operation. Three-quarters 
of an inch shortening, due to slipping up of great trochanter. Great trochan- 
ter does not rise when weight of body borne upon excised joint. The joint is 
movable and useful, and whilst the patient’s general condition is very good, 
there is sinus-formation present. 


CASE 5.—Ernest T. H., æt. 22.—Mr. Golding-Bird, 254, 1897. Two years’ 
history of hip disease. Head of femur excised, 10th November, 1896. 
Healing practically complete when patient was discharged on February 3rd, 
1897. Examined in May, 1904, seven years after operation. One and a 
quarter inches shortening in the affected limb, due to slipping up of the great 
trochanter. The great trochanter does not rise when the weight of the body 
is borne upon the excised joint. Joint movable and useful. Wasting of 
thigh amounts to one inch, and of leg to one and a half inches. There is no 
spinal curvature; good local condition. Although this patient has a cured 
tuberculous condition of his left knee and has lupus on his left heel, his 
general condition is good and he is considered as & success. 


Case 6.—George L., «t. 7. Mr. Jacobson, 213, 1903. One year's history 
of hip disease. Excision of hip when patient was aged seven in 1896, by Mr. 
Davies Colley. No mention of abscess or sinus. Sinuses formed after opera- 
tion. Patient was able to flex his hip through sixty degrees, but other 
movements were absent. Mr. Jacobson performed amputation through the 
thigh on 28th July, 1903. 


the Hip-joint has been performed for disease of the Joint. 857 


CASE 7.—Arthur H., et. 20. Sir Henry Howse, 390, 1899. Three years 
history of hip disease. Excision of hip on the 28th of July, 1898. No 
abscess nor sinus-formation. Sinuses formed after excision, and amputation 
through hip-joint, performed on the 18th of July, 1899. Dr. Emil Harden- 
berg tells me that the condition of the patient is quite good now. 


The second group (Nos. 8 to 27), comprises those cases in 
which excision was performed when an abscess had formed, but 
when there was no sinus-formation, and comprises twenty cases 
in which there were seven failures, namely, two deaths and five 
amputations (cases 11, 19, 20, 21, 24, 25 and 26). There were 
seven successes, in three of which the joints were movable 
(cases 8, 18 and 23), and in four of which the joints were fixed 
(cases 9, 10, 12 and 26). In four cases of partial failure 
(13, 14, 15 and 17), the joint was in each case fixed :— 


CASE 8.—DanielS., et. 5. Sir Henry Howse, 1901. One year's history 
of hip trouble. Abscess had formed and was discovered over great trochanter 
on October 11th, 1900. Excision of hip on October 18th, 1900. The wound 
had almost healed on November 23rd. Examined July, 1904, four years 
after operation. One and а quarter inches shortening, due to displacement 
upwards of great trochanter. Great trochanter does not rise when the weight 
of the body is borne upon the excised joint. The hip-joint on the other side 
is in the second stage of hip disease. The local condition on the side of the 
excised hip is bad, sinuses being present. The excised joint is movable in 
all directions, except that abduction and internal rotation are not possible. 


CasE 9.—Jessie N., æt. 10. Mr. Lucas, 377, 1897. Two years’ history of 
hip disease. Abscess formed anteriorly; nosinus. Excision of hip performed 
on the 17th of November, 1896. Healing by primary union was complete by 
the 3rd December, 1896. A special note is made in the report, that shortly 
before patient's discharge from hospital there was one inch shortening on the 
affected side. Examined in May, 1904; seven years after operation. Two 
and a quarter inches shortening on affected side, due to slipping up of great 
trochanter. Great trochanter does not rise when the weight of the body is 
borne upon the excised joint. The joint is fixed and useful. Some lordosis, 
although not marked, is present. Wasting of thigh amounts to three inches, 
and of leg to one and a quarter inches. Good local and general condition. 
Patient works in a tin factory eleven hours a day, and earns five shillings 
and sixpence & week. 


Case 10.—Mrs. P., et. 34. Mr. Golding-Bird, 266, 1896. Acute arthritis 
of hip, followed upon a miscarriage in 1896. Abscess-formation occurred. 
Head of femur excised on May 28th, 1896. Complete healing by June 30th, 


VOL. LIX. 25 


358 A Collection of Cases in which the Operation of Excision of 


1896. Examined May, 1904, eight years after operation. There is two inches 
shortening, due to slipping up of great trochanter. Great trochanter does 
not rise when the weight of the body is borne upon the excised joint. The 
joint is fixed and useful. Wasting of the thigh amounts to one inch, and of 
leg to one and a half inches. There is no spinal curvature. Good local and 
general condition. Patient performs housework; she has had one child 
since the operation. 

Case 11.—Charles M., et. 11. Sir Henry Howse, 83, 1897. Three years’ 
history of hip disease. Abscess-formation anteriorly in upper part of thigh. 
Excision of hip on 26th July, 1896. Sinus-formation is present. Amputa- 
tion through hip-joint on 18th February, 1899. Patient made a good 
recovery. 





Case 12. —Frederick M., et. 6. Mr. Lucas, 121, 1897. Sixteen months’ 
history of hip disease. Abscess had formed on anterior aspect of upper part 
of thigh. On 19th November, 1896, incision of the abs-ess and excision of 
the affected hip. Healing, by primary union, complete on 27th December, 
1896. Examined in May, 1904, seven years after operation. Two inches 
shortening, one inch being made up by slipping upwards of great trochanter, 
and one inch being due to shortening of leg below knee, measurements being 
taken from a triangle [bounded above by curved lower and internal border of 
internal condyle of femur; below by upper and inner edge of the internal 
tuberosity of tibia, and externally by inner border of patella and ligamentum 
patelle], to the tip of the internal malleolus. The great trochanter does not 
rise when the weight of the body is borne upon the excised joint. The joint 
is fixed and useful. Wasting of thigh amounts to three and a half? inches, 
and of leg to one and a half inches. There is no spinal curvature, and no 
sinus, but the general condition of the patient is scrofulous. 


CASE 13.—George T., æt. 5. Mr. Golding-Bird, 585, 1897. Two years’ 
history of hip disease. Excision of hip on the anterior aspect of thigh at the 
upper and outer part on the 31st July, 1897. Complete healing by December 
6th, 1897. Examined May 23rd, 1904, seven years after the operation. Two 
inches shortening on affected side, due to slipping up of great trochanter. 
Great trochanter does not rise when the weight of the body is borne upon 
the excised joint. The excised joint is fixed, and useful. There is no spinal 
curvature. The wasting of the thigh amounts to three inches, and of the 
leg to one and a quarter inches. The local and general conditions are good. 


` Case 14.—George N., et. 5. Mr. Golding-Bird, 381, 1897. Sixteen 
months’ history of hip trouble. Abscess formed over great trochanter. 
Excision performed on January 12th, 1897. Formation of many sinuses, 
which had, however, nearly healed on discharge of patient from hospital on 
October 25th, 1897. Examined May, 1904, seven years after the operation. 
Two inches shortening, made up by slipping upwards of great trochanter for 
one inch, and one inch shortening below knee (points for measurement as in 
case 12). Great trochanter does not rise when the weight of the body is 
borne upon the excised joint. The joint is fixed and useful. Sinuses are 
present over joint. Wasting of thigh amounts to two and a half inches, and 


the Hip-joint has been performed for Disease of the Joint. 859 


of leg to one-quarter inch. General condition is scrofulous, but not tuber- 
culous. Bryant’s double splint was used in this case, it was discarded shortly 
after discharge from hospital. Crutches were used for twelve months after 
discharge. There is very littel lordosis of spine. 





CASE 15.—James G., et. 5. Mr. Golding-Bird, 213, 1897. Seven months’ 
history of hip trouble. Abscess formed in anterior and upper part of thigh. 
Excision of head of femur, February 22nd, 1897. The wound healed by 
primary union, but patient contracted diphtheria whilst in Guy’s Hospital, and 
was sent to a fever hospital. Mr. Golding-Bird saw the patient on June 10th, 
1897, when splints were discarded. The condition noted then was, that the 
hip was firmly anchylosed and that there was only а quarter of an inch 
shortening. Examined May, 1904, seven years after operation. Patient 
has not used any support for two years. Two inches shortening, due to 
slipping up of great trochanter. Great trochanter does not rise when the 
weight of the body is borne upon the excised joint. The joint is fixed, and 
useful. The thigh is wasted, being two and a half inches less in circumfer- 
ence than the other one. Wasting of the leg amounts to three-quarters of 
an inch. No spinal curvature. General condition is poor, the child looking 
very delicate. . There is an abscess pointing under the scar, which is 
stretched, but not yet broken. This abscess, according to the parents, is the 
first sign of recurrence of disease since the operation. 


° Case 16.—Gladys C., æt. 11. Mr. Symonds, 1902. Five months’ history 
of hip trouble. Excision of head of femur on the 20th of June, 1902. 
Caries of acetabulum with an intrapelvic abscess was discovered. Sinuses 
formed after operation, but healing had taken place by August 1st, 1902. 
The parents informed the writer in December, 1903, that sinuses were present 
and that there was about two inches shortening: 





Case 17.—John D., æt. 5. Mr. Symonds, 1902. First symptoms of hip 
disease are said to have appeared in March, 1902. On May 5th, 1902, an 
abscess formed over great trochanter, and so, shortly after this date, the 
head of the femur was excised: sinuses formed, and were continually being 
scraped. In October, 1902, it is recorded that there was one inch shortening. 
Examined July, 1904, one year after operation. One inch shortening due to 
displacement upwards of great trochanter. Joint is fixed and useful. 
Wasting of thigh amounts to one and a half inches; there is no wasting of 
the leg. There is no spinal curvature, good general condition, but sinuses 
are still present over excised hip. Patient still uses crutches, and a Thomas’ 
single hip splint. 


Case 18.—Frederick O., et. 8. Mr. Symonds, 19, 1908. Excision of head 
of femur on November 20th, 1902. Hoffa’s plaster splint, Liston’s long 
splint and Thomas’ double splint were applied in succession. Patient dis- 
charged on. February 12th, 1908, with no splint and with half an inch 
shortening.. . Examined July, 1904, twenty-one months after operation. 
One inch shortening, due to displacement upwards of great trochanter. 
Great trochanter does not rise when the weight of the body is borne upon the 


360 А Collection of Cases in which the Operation of Excision of 


excised joint. The joint is movable and useful. Wasting of thigh amounts 
to one inch. There is no wasting of the leg, and there is no spinal curvature. 
Good local and general condition ; there are no sinuses. 


Case 19.—Fred C., et. 5. Mr. Jacobson, 20, 1902. Four months’ history 
of hip trouble. Abscess formed over great trochanter. Hip excised on the 
29th September, 1899. Thomas’ splint was used till July, 1903. Sinuses 
formed and persisted: there was a fixed joint. Amputation, through hip 
joint, July 20th, 1901. Patient was discharged on January 29th, 1902, 
having made a fair recovery. 


Case 20.—Eliza H., et. 5. Sir Henry Howse, 42, 1899. In 1880 excision 
of hip performed for hip disease ; abscesses and sinuses continually forming 
and being treated in a conservative manner. Amputation through hip was 
performed in January, 1899 (nineteen years after previous excision). Patient 
was discharged, practically well, in October, 1899. 


Case 21.—Joseph C., æt. 7, Mr. Davies-Colley, 259, 1896. Excision of 
hip for tuberculous hip disease with abscess but no sinus-formation in 1891. 
Abscesses and sinuses persisted. Lardaceous disease set in. Amputation 
through hip-joint performed in 1896. Patient died October 18th, 1897. 


Case 22.—Walter W., æt. 35 Sir Henry Howse, 442, 1897. Excision of 
head of femur in April, 1897. Abscess-formation had taken place. June 7th, 
1897, patient was discharged, having made a good recovery. On November 
24th, 1903, six years after operation, sinuses were forming. Patient wears 
an ordinary boot, with the heel raised an inch. 


Case 23.—John R., æt. 14. Mr. Lucas, 115, 1896. Two years’ history of 
hip trouble. On October 6th, 1896, excision of head of femur was done; 
abscess found in thigh ; wound healed by primary union and patient was 
discharged on November 13th, 1896; the excised joint being stiff. Examined 
May 21st, 1904, eight years after operation. Three inches shortening, two 
inches of this being due to slipping up of great trochanter, and one inch to 
shortening of leg below knee (the same points being used for measurement as 
in Case 12). Great trochanter does not rise when the weight of the body is 
borne upon the excised joint. The joint is partially movable and useful. 
Wasting of thigh amounts to five inches, and of leg two. Good local and 
general condition; no sinuses present. Patient works nine hours a day, and 
is earning thirty shillings per week. 


Case 24.—Dolly T., et. 4. Mr. Lucas, 1897. No details as to history. 
Admitted on 20th May, 1897. Head was excised on the same day; death 
occurred same evening, immediately after the operation. 


Case 25.— Harriet B., et. 49. Mr. Lucas, 2, 1898. Hip disease had 
existed for 28 years. Abscesses and sinuses had continually been forming, 
but for three years previous to admission there had been no abscess nor 
sinus-formation. On October 15th, 1897, the head of the femur was excised, 
and ‘еп route ’’ an abscess was opened. Patient's wound was not closed on 
January 815%, 1898; death, frem husband's information, occurred in 1900. 


the Hip-joint has been performed for Disease of the Joint. 861 


CASE 26.—Augusta C., et. 4. Mr. Symonds, 1890. One year’s history of 
hip trouble. Excision on March 25th, 1890, when an abscess was found, but 
no sinuses; healing took place by primary union, and patient was discharged 
on April 26th, 1890. A Bryant’s double splint was used for fourteen months 
after discharge, then Thomas’ single splint was used for six months. 
Examined in June, 1904, fourteen years after excision. three inches short- 
ening, two inches of this being due to rising of great trochanter, and one inch 
due to shortening of leg below knee (measurements as in Case 12). Great 
trochanter does not rise when weight of body borne upon excised joint. Joint 
fixed and useful. Wasting of thigh amounts to three inches, and of leg to 
two inches. There is so much tilting upwards of pelvis on the affected side, 
that patient wears a boot with a nine inch heel, and there is lordosis 
amounting to thirty degrees of flexion in hip-joint. Good local and general 
condition. No trace of sinus-formation. 


Case 27.—Ellen R., et. 16. Mr. Symonds, 1908. One year’s history of 
hip disease. Spinal caries also present. Excision of hip in 1902; intra- 
pelvic abscess found ; sinus-formation occurred. In middle of 1903 lardaceous 
disease set in and amputation through hip-joint was performed; sinuses 
persisted. Patient discharged, and was last heard of in October, 1904, when 
her condition was improved. 


The third group, Nos. 28 to 36, comprises those cases in which 
excision was performed after abscess and sinus-formation had 
taken place. There were three suceesses, in two cases (30 and 31) 
with fixed joints, and in one, case (32) with a movable joint ; 
two failures, both having fatal termination, and four partial 
failures, three with movable joints (cases 28, 29 and 34); case 
28 showed a flail joint. The other partial failure, case 33, shows 
no record as to mobility or fixity :— 


CasE 28.—James William B., et. 5. Sir Henry Howse, 58, 1897. Two 
years’ history of hip disease. Abscess and sinus-formation. Excision of hip 
on 12th March, 1897. Complete healing on 31st December, 1897. Examined 
in December, 1903, six years after excision. Four inches shortening of 
affected limb, three inches being due to displacement upwards of great tro- 
chanter, and one inch to shortening of leg below knee (measurements as in 
case 12). Great trochanter does not rise when the weight of the body is 
borne upon the excised joint; the joint is flail and is of no apparent use to 
the patient. There is slight lordosis. Talipes equinus present, and sinus- 
formation continua!ly recurring. Patient still uses crutches. 

CasE 29. Fred J., et. 51. Mr. Lucas, 315, 1902. Three years’ history 
of hip trouble. Sinus-formation had occurred. Excision of head of femur 
in May, 1902. Wound completely healed by granulatiors in July, 1902. 
Examined May, 1904, two years after operation. Two and a half inches 
shortening of affected limb, due to slipping upwards of great trochanter, 


362 А Collection of Cases in which the Operation of Excision of 


Great trochanter does not r'se when weight put upon it, but weight of body 
cannot be borne upon excised joint. The joint is movable in all directions. 
The generel condition of the patient is good. Sinus continually forming, 
` healing and re-forming. Wasting of thigh amounts to two inches, and of leg 
to three-quarters of an inch; there is no spinal curvature. Patient does no 
work, but obtains e ght shilling a week from clubs. 





Сазе 30.- John B. A., et. 13. Sir Alfred Fri p, 99, 1900. Four months’ 
history of hip trouble, possibly pysemic in origin. Sinus-formaticn took 
place. Excision of head of femur in August. 1901. Discharged practically 
well on October 12th, 1900. Examine May, 1904, four years after excision. 
There was four and & half inches shortening, three and & half inches being 
due to slipping up of great trochanter, and one inch due to shortening of leg 
below knee (measurements as in case 12). Great trochanter dces not rise 
when weight of body is borne upon the excised joint. The joint is fixed and 
useful; no s'nuses present. The wasting of thigh amounts to one and a half 
inches, and of leg to only a quarter of an inch. "There is no spinal curvature 
of a permanent nature. Patient used crutches for one and a half years after 
his discharge from the hospital. This boy is healthy, well developed, but 
short. Two of his brothers were also well developed, but well over six feet in 
height. 


Case 31.—Harry Y., æt. 12. Mr. Symonds, 289, 1903. Uncertain history, 
but in 1902 sinuses formed in connection with hip disease. The head of the 
femur was excised in May, 1903; sinuses had completely healed by August, 
1903. Patient discharged in 1908. Examined by Mr. T. C. Lucas, R.A.M.C., 
May, 1904. Three-quarters of an inch shortening in affected limb. The ex- 
cised joint is flexed very much. There is some lordosis of the spine. The 
joint is fixed and useful. Wasting of thigh amounts to two and three-quarter 
inches. There is no wasting in the leg; general condition is good. 


Case 32.—Elizabeth B., et. 7. Mr. Symonds, 1902. Nearly two years’ 
history of hip disease. Abscess and sinus-formation occurred. Head of femur 
excised in October, 1902. Examined in July, 1904, twenty months after 
excision Two and а half inches shortening, due to displacement upwards of 
great trochanter. Great trochanter does not rise when the weight of the body 
is borne upon the excised joint. The joint is movable and useful. There is 
no special curvature. Wasting of thigh amounts to half an inch, and of leg 
to a quarter of an inch. No sinuses present ; good general condition. 


Case 33.—Wm. T., æt. 12. Mr. Golding-Bird, 287, 1897. Ten months’ 
history of abscess and sinus-formation in connection with hip trouble. 
Excision of head of femur on October 4th. Death from shock on same night. 


CasE 34.—Keith H., æt. 5. Sir Henry Howse, 27, 1902. One year's history 
of hip disease, with three months' history of abscess and sinus-formation. 
Excision of head of femur April 1st, 1902. Patient discharged on May 3rd, 
1902, with wound partially healed. Examined July, 1904, two years after 
excision. There is one and three-quarters of an inch shortening, due to 
slipping upwards of great trochanter. Great trochanter does not rise when 
weight of body is borne upon the excised joint. The joint is movable and 


the Hzp-joint has been performed for Disease of the Joint. 368 


useful. Wasting of thigh amounts to three and three-quarter inches ; wasting 
of leg, two and a half inches. No obvious spinal curvature. The boy is 
delicate. Sinuses continually forming, healing and re-forming. 


Case 35.— Wm. C., æt. 8. Mr. Davies Colley, 1, 1899. Admitted in 
September, 1898, with double hip disease and extensive abscess and sinus- 
formation on the left side. Excision of head of right femur on the 18th 
October, 1898 Sinuses persisted. Lardaceous disease set in, and patient died 
on April 30th, 1899. 


CASE 36.—Wm. T., æt. 19. Mr. Lucas, 1902. Two years’ history of hip 
disease. Abscess formed and sinus appeared three weeks previous to excision 
of hip on May 12th, 1902. May, 1904, patient wrota a letter to say he was 
doing work as night watchman; his general health was good, but sinuses 
were continually forming, healing and re-forming. 


In the following group the history of the cases is imperfect :— 


CASE 37.—Minnie G., under care of a Russian Surgeon ten years ago. 
Excision of hip-joint ten years ago, ?.e., 1894. Examined July, 1904, when 
under care of Mr. Steward. Two inches shortening on affected side, due to 
slipping up of great trochanter. The whole weight of the body can be borne 
upon the excised joint without the trochanter being displaced upwards. 
There is marked flexion of the excised joint. Local and general conditions 
are good. Flexion has been overcome by an operation performed by Mr. 
Steward. 


CASE 88.—Harry A., 14, out-patient, under care of Mr. Steward. Operation 
of exoision of hip in 1901. Examined July, 1904, three years after operation. 
Three inches shortening on affected side, due to slipping upwards of great 
trochanter. Excised joint cannot support weight of body. Good local and 
general condition. Wasting of thigh amounts to three and a half inches; 
wasting of leg amounts to two inches; по lordosis. 


Case 39.—Margaret А. A., et. 13. Sir Henry Howse, 164, 1898. Excision 
had apparently been performed at Leicester some time previous to amputa- 
tion through hip-joint by Sir Henry Howse in 1898. 


Салве 40.—Samuel C. T., æt., 18. Sir Henry Howse, 40, 1901. No history 
given by clerk in notes previous to excision on the 16th September, 1897. 
Abscess and sinus-formation had occurred some time before excision. 
Multiple sinuses formed about the hip, which was freely movable. An 
amputation was performed through the hip-joint in 1901, four years after 
excision, and in December, 1903, the boy was remarkably well. 


364 А Collection of Cases in which the Operation of Excision of 
the Hip-jount has been performed for Disease of the Joint. 


TABLE showing period of time between Excision of the Hip-joint 
and Amputation through the Hip-joint, or Death :— 


CasE 2. 
6. 

9. 

11. 

19. 

20. 

21. 


24. 
дб. 
27. 
33. 
85. 
89. 


40. 


Interval. Result. 
Two years Death. 
Seven years ... Amputation. 
One year aes " 
T wo and a half years i 
Two years " 
Nineteen years Pus m Р 
Five years... Amputation ; death in following 

year. 

Immediately after operation Death. 
Three years ... : 
Six months ... see Amputation. ` 
Immediately after operation Death. 
Six months .. 5 
Uncertain Amputation. 
Four years " 


N 
The writer owes a debt of gratitude to the surgeons at Guy's 
Hospital for their kindness in allowing him to utilise their cases, 
‘and especially to Mr. Steward for his suggestions, also to Mr. F. 


H. Fuller for his kindness in tracing certain cases. 


NOTES FROM THE 
ACTINOTHERAPEUTIC DEPARTMENT 
AT GUYS. 


A YEAR'S EXPERIENCE. 


By G. SICHEL. 





Turis Department is at present in its infancy. The first case, 
a recurrent carcinoma mamma, began treatment with X-rays on 
18th August, 1903. Up to August 5th, 1904, sixty-one patients 
have attended the department. These sixty-one cases were as 


follows :— 
Malignant disease i m ie es A 
Rodent ulcers  .. ix ие sio ie 8 
Lupus  ... s - ids т .. 12 
Mycosis fungoides um a VT sv x 
Glossitis ... eh EM bis T ew. 32 
Chronic rhinitis ... = wit КП ia г: 
Lupus erythematosus... d — ws d 


58 


This leaves eight cases unclassified which will be shortly 
referred to at the end of this paper. 


366 Notes from the Actinotherapeutic Department. 


MALIGNANT DISEASE. 


CASE 1.—N. S., female, æt. 48. Recurrent carcinoma of left breast. She 
was operated on two years ago by Sir A. D. Fripp. A small lump appeared 
again seventeen months after; four months ago began X-ray treatment else- 
where, which had to be stopped for six weeks on account of X-ray burn. 
Treatment here extended from 18th August, 1908, to 30th October, 1903. 
Twenty-five sittings of X-rays for at first ten, later fifteen minutes. Cossor’s 
tube was used. Twenty-six sittings of the static breeze, fifteen minutes 
each, from a large Wimshurst machine. 


Remarks.--The X-rays and static breeze were applied alternately in the 
hope of preventing the recurrence of an X-ray burn. Result.—No increase 
of tumour in two months; no pain. No cure, but alleviation. Patient left 
to return to her home in Norfolk and promised to attend Norwich Hospital 
for further treatment. I wrote to the house-surgeon of Norwich Hospital in 
July last, but he told me she had not been attending there. 


CASE 2.—C. P., male, et. 69. Extensive recurrent epithelioma of mucous 
membrane of mouth and right cheek, no enlarged glands. Treatment lasted 
from 20th August, 1903, to 23rd December, 1908, when he had to give up 
coming from weakness. X-rays, forty-two sittings; static breeze thirty- 
three times. The static breeze was applied when redness of the skin (? from 
the X-rays) threatened dermatitis. A large Cossor’s tube was used, and on 
sixteen occasions, with the X-rays externally, 5 mgms. of radium bromide in 
a glass tube were applied inside the mouth. As far as I could judge, he 
did not benefit in the slightest and the treatment was & complete failure. 


Case 3.—G. D., male, æt. 54. Carcinoma of the lower jaw. Не had been 
operated upon six months previously. Came up in an almost hopeless condi- 
tion. Only attended four sittings of X-rays with Cossor's tube and then ceased 
to appear. Three of the sittings lasted twenty minutes, and one fifteen 
minutes. There was reddening of the skin and apparently some softening 
of the anterior part of the growth. ‘There was no benefit to the patient, but 
the tumour was far too advanced and the treatment far too brief to expect 
any. 


CasE 4.—E. M., an old Welsh woman who could not speak English. 
Epithelioma of right side of scalp which began five years ago. 
Very foul; a few cervical glands enlarged. Treatment began on 31st August, 
1908, and continued until 16th November, 1903. Thirty-seven sittings of 
X-rays with large Cossor's tube, generally for fifteen minutes. Treated seven- 
` teen times with the negative static breeze. 


Remarks.—W. B. Hardy and Miss E. G. Willcock found that in certain 
experiments the activity of radium emanations was increased in the pres- 
ence of NaCl, so I used to sponge over the growth with a strong solution of 
common salt before treatment. The disease was naturally slow in growing, 
and I do not believe she received the slightest benefit from the treatment. 
She left at her own wish to gohome. The epithelioma had spread and the 
glands in the neck had broken down. . 


367 


Notes from the Actinotherapeutic Department. . 


@ ‘DI 





*Fo61 “Алеплдә,] pSr пәхңе[, 


т ‘DI 


'£o61 ‘19q0190 u18 use, 





368 Notes from the Actinotherapeutic Department. 


Case 5.—J. K., male, et. 46. Lymphosarcoma of the glands of the neck, 
which had been operated upon twice. The growth presented a large oozing 
fungating mass protruding behind the angle of the jaw. Treatment:—Eleven 
X-ray sittings with Cossor's tube, fifteen minutes each, five sittings with static 
breeze. As there was no benefit, and the sarcoma increased, he gave it up to 
submit to a third operation. 


CASE 6.—A. W., female, et. 70. Recurrent carcinoma of the breast. Mr. 
Lucas had removed the left breast four years ago. The recurrent growth 
was extremely painful and tender, and the left arm was swollen. Treatment 
lasted from the 16th September to the 31st December, 1903. X-rays (Cossor's 
tube), sixteen times, of ten to fifteen minutes each sitting. Static electricity, 
negative breeze, for fifteen minutes, forty-three times. Positive charges, ten 
times. 

Remarks.—Pain was much alleviated in this case, and she was certain she 
got more relief from the static electricity than from the X-rays. Neverthe- 
less she steadily became worse and had to desist from attending owing to left 
pleuritic effusion, due to extension of the growth. 


CASE 7.—S. M., female, st. 50. Inoperable carcinoma of cervix uteri 
sent by Dr. Horrocks. Treatment.—Six sittings of X-rays by small Cossor's 
tube. 

Remarks.—No benefit, and patient too ill to continue treatment. 


CASE 8.—L. H., female, et. 63. Sent by Mr. Dunn. Began twenty-six or 
twenty-seven years ago as a small wart. Has been operated upon. Came here 
with what looked like a rodent ulcer of the right cheek, lip and ala of nose. 
Treatment lasted from 8th October, 19083, to 12th February, 1904. Fourteen 
sittings of X-rays with Cossor's tubes. Eleven sittings of static negative 
breeze. Forty-six sittings of 5 mgms. of radium bromide. Remarks.—Entire 
failure to do good; ulcer increased in size (see photographs) and continued 
extremely tender and painful throughout. At times it appeared to be com- 
mencing to heal and then all would break down again. ~ The radium bromide 
was supplemented by the NaCl treatment mentioned in case 4, also by 
applying oxygen from a cylinder over the ulcer, on the supposition that the 
action of radium depended upon the presence of this gas, and would therefore 
be more efficient in the presence of an excess. I also painted over the 
surface of the ulcer with a solution of methyl blue in collodion, on the 
supposition that the rays at the red end of the spectrum might be harmful. 
However, I afterwards found with the spectroscope that my solution painted 
on glass did not prevent the red rays coming through. Towards the end the 
case had more the appearance of an epithelioma than а rodent ulcer, and as 
such it is classified here. (Figs. 1 and 2.) 


CASE 9.—J. K., æt. 65, sent here for treatment for carcinoma of the cervix 
uteri after operation by Mr. G. B. Smith. Treatment lasted from 25th 
September, 1903, to 6th October, 1903. ‘Seven sittings with X-rays (Cossor's 
tube), in all one anda half hours Оп 6th October examined by Dr. Horrocks 
and Mr. G. B. Smith and no growth could be found. There was no further 
treatment, as patient was very sore after examination, and on 12th October 
she was discharged to a convalescent home. 


Notes from the Actinotherapeutic Department. 369 


Remarks.- -I am indebted to Mr. Hicks, the Obstetrical Registrar, for 
further information respecting this case. She was re-admitted into Patience 
ward under Mr. G. B. Smith from November 28th to December 13th, 1903. 
There was undoubted growth of the cervix, and a piece removed showed that 
16 was an epithelioma. She never came to my department again. 


CASE 10.—L. M., female, æt. 29. Carcinoma of the cervix, sent for treatment 
after operation on 14th October, 1908. "Treatment commenced 26th October, 
1908, and went on till 8th February, 1904. Thirty sittings, fifteen minutes, 
X-rays, with small Cossor tube. 

Remarks.—Absolute failure to do any good with either pain or growth. 


CASE 11.—E. M., female, et. 25. Inoperable case of carcinoma of the cervix 
uteri. Treatment lasted from 29th October, 1903, to 11th January, 1904. 
Thirty sittings of X-rays (small Cossor’s tube), fifteen minutes each. 

Remarks.—Absolute failure to do any good. 





CASE 12.—H. W., female, æt. 45. Inoperable carcinoma of the cervix uteri, 
sent by Dr. Horrocks. Treatment from 23rd November to 23rd December, 
1903. Ten sittings of X-rays (Cossor’s tube). 

Remarks.—Absolute failure to do any good ; бөй had to give up 
attending owing to excessive weakness. 





CASE 18.—M. B., female, et. 69. Epithelioma of the cervix uteri operated 
upon by Dr. Horrocks thirteen days before she was sent here. Treatment 
from 21st December, 1903, to 5th January, 1904. Nine sittings of X-rays, 
(Cossor’s tube), of fifteen minutes each. No benefit from treatment. 





Case 14.—M. C., female, æt. 44. Sent by Dr. Horrocks. Carcinoma of the 
cervix uteri. Operation in August and again in December, 1903. Recur- 
rence. Treatment commenced on 23rd December, 1903, and lasted till 
26th April, 1904. X-rays, forty-three sittings of fifteen minutes. Acting on 
Dr. Horrocks’ suggestion this treatment was supplemented on eighteen 
occasions by the action of radium. 

Remarks.—Probably some alleviation. When the radium was applied as 
well, the X-rays were applied externally, with 5 mgms. of radium bromide 
‘in a glass tube in the vagina, and on sixteen occasions there was а radio- 
active screen on the back, in the lumbo-sacral region as well. I am afraid 
that this case also must be looked upon as a failure. 


Case 15.—G. H., male, æt. 53 Recurrent epithelioma of the right cheek, 
very extensive and inoperable. Treated from 12th February to 25th April, 
1904. X-rays from a large Cossor’s tube, thirty-five sittings of fifteen minutes. 
No benefit whatever. 


CASE 16.—E. H., female, æt. 62. Inoperable carcinoma of the cervix uteri. 
Treated with. X-rays, small Cossor tube, in vagina from 15th February, to 
19th May, 1904. Forty-two sittings of fifteen minutes. 

Remarks. — Absolutely no beneficial effect on growth.. She told me she 
was never free from pain except during the actual application of the rays. I 
last saw her on 13th June; she was very ill, much emaciated, and in great 
pain. 


370 Notes from the Actinotherapeutic Department. 


CASE 17.—E. K., female, æt. 45. Recurrent epithelioma of the vulva. Nine 
sittings of radium bromide for fifteen minutes, except the first, which was 
only five minutes. Patient did not persevere with the treatment and left in 
statu quo. She attended from 29th February to 7th March, when she ceased 
attending owing to menstruation, and again from 21st to 815% March. 


Case 18.—M. W., female, et. 61. Inoperable carcinoma of the cervix 
uteri. Attended from 10th March to 7th April. Fifteen sittings of X-rays for 
fifteen minutes each. Small Cossor tube used per vaginam. No apparent 
benefit. 


CAsE 19.—M. S., female, æt. 60. Recurrent carcinoma of the breast sent 
to me by Mr. Rowlands. Treatment lasted from 14th March io 7th April, 
during which time she had thirteen sittings of X-rays lasting fifteen minutes 
each. 

Remarks.—At the end of the treatment Mr. Rowlands took her into 
Bright ward to remove a mass of glands in the neck. Both he and the 
patient were of opinion that the recurrence which had been treated with 
X-rays had got smaller. The tube used was a hard one, averaging a six- 
inch alternative spark. Deane-Harnack’s apparatus was used. 


Case 20.—A. H., female, æt. 37. Scirrhus of the left breast in such an 
advanced stage that she could hardly stand alone. Given X-rays for fifteen 
minutes on one occasion ; she never attended again. 

Remarks.—This is an example of the hopeless condition in which many 
cases are when they are sent for X-ray treatment as a dernier resort. They 
are not fair tests from which any reliable deductions can be drawn. 


Case 21.—F. B., female, æt. 38. Inoperable carcinoma of the. cervix uteri. 
Seven sittings with X-rays for ten minutes each, except the last, which was 
fifteen minutes. She said she felt better, but ceased to attend, so do not 
suppose she felt any real benefit. 


Case 22.—L. T., male, æt. 54. Recurrent epithelioma of the sole of the 
left foot. 18th February 1904, admitted under Mr. Lane with a fungating 
ulcer, two and a half inches by one and a half inches, which began in an old 
Scar two years before. 'The skin behind the ulcer was covered with scabs. 
Numérous hard but painless glands in left groin. On' 17th February the 
mass was removed and skin grafting was performed. 8th March, slight 
recurrence of growth in two places. 22nd March to 5th May, X-ray 
treatment, twenty sittings of fifteen minutes. Ulcer healed up, but the 
raised indurated border remained. On 9th April two bits were removed and 
found by the pathologist to be still epitheliomatous, He went home, to 
Wales, and so treatment was discontinued. 

Remarks.—I think that in this case the rays had decidedly a beneficial 
influence, but in view of the microscopical. examination it is more than 
probable that the improvement observed will be only temporary. 





CASE 28.—C. S., female, et. 54. Recurrent carcinoma mammæ. Had 
been operated upon twice for carcinoma of the right breast. Only attended 
four times for X-rays. It is useless to try and draw any deductions from this 
case. 


Notes from the Actinotherapeutic Department. 





371 


Fia. 4. 


Taken 4th January, 1904. 


Fio. 3. 


Taken 14th October, 1903. 


372 Notes from the Actinotherapeutic Department. 


Case 24. —M. E , female, et. 49. Sent by Mr. Jacobson. Right breast was 
removed for carcinoma about eighteen months before ; now has a recurrence 
about the size of small orange in the scar and attached to the ribs. Treatment 
commenced on 28th April, and is still continuing at the time of writing, 7th 
August, 1904. Forty-three sittings with X-rays usually of ten minutes 
duration. On 24th June, Mr. Jacobson was kind enough to take her into 
Dorcas ward to keep her under observation; when the effect of embedding 
5 mgms. of radium bromide in a glass tube, into the centre of the growth 
was tried, it was put in in three different places by Mr. Adams (Mr. Jacob- 
son's dresser) and finally removed on 15th July, when the X-ray treatment 
was continued. With the exception of easing the pain, of which the patient 
is certain, there is apparently no benefit. The growth is much larger than 
it was and patient, who is most cheerful and hopeful, is becoming cachetic. 





Case 25.—S. W., female, æt. 47. Extensive carcinoma of the cervix 
uteri which had been operated upon and partially removed. Attended four 
times for X-ray treatment and then did not appear. 


Case 26.—D. W., female, et. 67.  Atrophic scirrhus, left breast, sent to 
me by Mr. Steward. She has only noticed it a year, but thinks she has had 
it longer. The nipple is much retracted, and there is a puckered-in, red, 
linear, ulcerating scar, deeply attached, in the lower part of the left breast. 
Treatment commenced cn 20th June, 1904, and she is still attending (Tth 
August). She has had twenty-two sittings of the X-rays lasting ten minutes 
each. On the whole, there is some improvement locally; there is less 
discharge, and the growth is at all events no larger than it was; on the 
other hand, I am afraid the patient is slowly losing flesh. 


CasE 27.—E. S., female, et. 50. Recurrent carcinoma mamma. Has 
been operated upon three times in three years. Multiple carcinomatous 
nodules of the skin, sent by Mr. Lucas on 14th July, 1904 ; still under treat- 
ment, 7th August, 1901. Has had eleven sittings of X-rays usually ten 
minutes each. The largest nodule, which is ulcerating, has been picked 
out for treatment. No change so far. 


Conclusions as regards malignant disease.—Of the above 
twenty-seven cases, eight (viz., 3, 5, 7, 9, 12, 20, 23, and 25) шау 
be disregarded as being of any value, since either from being in 
too advanced a condition, or from want of immediate alleviation, 
their attendances were too meagre to prove the value or otherwise 
of the treatment. And here we must remember that it is 
practically only inoperable cases which have been sent to this 
department. Of the other nineteen cases, there was some allevi- 
ation (2.е., relief of pain) and perhaps some retardation of growth 
in five (viz., 1, 6, 14, 19 and 22). About two (26 and 27) I 
would give no opinion at present, and they are stil under 


+ —— ee — Um = 


VOL. 


Notes from the Actinotherapeutic Department. 


Mie | Mx tono лау 
f aj M 


iz =) 
olia pe 
А pe) т, 

yt 





LIX. 


378 


Fic. 6. 


Taken 29th January, 1904, 


Fic. 5. 


Taken 1oth December, 1903. 


^D 
с 


374 Notes from the Actinotherapeutic Department. 


treatment; the other 12 must, I regret to say, be recorded as 
absolute failures. 

As regards the details of treatment, I have always used 
high tubes, which accounts for the fact that no case of dermatitis 
has occurred. Several cases of decided reaction (t.e., redness 
and loss of hair) have occurred, but the appearance has soon 
subsided on the cessation of treatment. The current used has 
varied from four to six ampéres at about ninety volts. The 
alternative spark gap of the tubes which have been used is about 
six inches. 

The results cannot be looked upon as very hopeful, perhaps 
lower tubes, which I now intend to try, will give better resulta, 
at the same time, as the cases sent were practically hopeless, 
it is well to remember that in about one case out of every three 
one may hope to lessen pain or retard growth for a time. It is 
interesting to note that in case 6 pain was more relieved by 
static electricity than by the X-rays. 


RODENT ULCERS. 


CASE 1.—J. L., male, æt. 72. Rodent ulcer of the left temple, had been 
operated upon six times. Treatment: five sittings of X-rays, one of the 
static breeze, after which treatment was discontinued and he was operated 
upon by Mr. Jacobson. 


CASE 2.—G. T., male, æt. 65. Rodent ulcer over the right lower jaw; 
another situated higher on cheek had been operated upon (see Figs. 4 and 5). 
Forty-two sittings of 5 mgms. radium bromide in a glass tube. Treatment 
lasted from 14th October to 31st December, 1903. A depressed scar was left. 
He was last seen on 28th July, 1904. There was no recurrence. The treat- 
ment was generally supplemented by a preliminary bathing with NaCl solution 
and the ulcer painted over with a solution of methyl blue in collodion, but 
I do not think these preliminaries can have been of much help (see Figs. 
3 and 4). 


CASE 3.—L. E., female, et. 38. Small rodent ulcer near the inner canthus 
of the right eye (see Figs. 5 and 6). Had twenty applications of radium 
bromide 15 mgms. in glass tube, fifteen minutes at a time. "Treatment lasted 
from 9th December, 1903, to 25th January, 1904. Ulcer healed leaving a 
soft, slightly pink scar. I again saw her on lith March, when there was 
some very slight thickening to be seen at the upper part of the scar. A slight 
warty lump subsequently formed here, which was again treated on 22nd and 
29th April, and 6th and 13th May, 1904, when it had become much smoother 
and she discontinued her attendance. Thirty-minute sittings were given on 
the last three occasions, 


375 


Notes trom the Actinotherapeutic Department. 


`#обт цолер U36 uox I, 


„соу 


*£061 ‘2940320 114 UJEL 





376 Notes from the Actinotherapeutic Department. 


CASE 4.—G. C., mile, et. 71. Rodent ulcer the size of a shilling just in 
front of the right ear. Attended for seven applications and then discontinued 
coming. The ulcer was beginning to improve. He was given X-rays for 
fifteen minutes a time. 

CASE 5.—M. G., female, æt. 58. Small rodent ulcer of the left upper lip. 
Treatment from 3rd May to 15th July with a compound salt of 
radium and barium of seven thousand radio-active units, one dec’grm, 
behind a mica shield in a vulcanite holder, thirty-five sittings of thirty 
minutes each. After niue sittings the ulcer appeared almost healed and 
then in spite of treatment relapsed and even got a little bigger. From 18th 
July to the present time radium bromide 5 mgms. in a glass tube has been 
used and the ulcer appears to be slowly healing; some redness of the 
surrounding skin has been caused. Patient is not anxious to have an 
operation. She has had in all thirty-five applications of radium and 
barium and eleven of radium bromide. So far the case must be looked upon 
as а failure, and if the patient consents I shall discontinue treatment and 
recommend her for operation. 


CASE 6.—A. G., female, et. 69. Multiple rodent ulcers of the right cheek. 
Operated upon four years ago. Has had four applications of radium bromide 
and is still under treatment. 


Case 7.—T. M., male, æt. 60. Rodent ulcer of the right cheek. Was operated 
upon five years ago. Has had eight applications of X-rays of ten minutes 
each; is still under treatment. Patient says there is less discharge. 


Case 8.—W. J., a middle aged Welshman, who can only speak a little 
English. Rodent ulcer attacking nose. Began treatment on 16th June, 
and is still under treatment. Twenty-two sittings with X-rays. The ulcer 
appears to be spreading in one direction and healing in another. Treatment 
changed to radium bromide, of which he has only had one sitting at the time 
of writing (7th August). If in another week the spreading on the one side 
still continues I shall discontinue the treatment and send him to one of the 
surgical staff with a view to operation. 


Conclusions as regards rodent ulcer.—Out of the eight cases 
three are still under treatment (6, 7 and 8) and two (cases 1 and 
4) failed to persevere with it. This leaves three cases for con- 
sideration; of these I think two (cases 2 and 3) may be considered 
successful, and one (case 5) a failure. These were all treated 
with radium salts, and I think the failure may be perhaps due to 
inefficient therapeutic value in the salt used, or to the fact that 
besides the mica shield I also used a thin sheet of gutta-percha 
tissue to prevent the radium getting spoilt by moisture from the 
skin. Rodent ulcer has been shown to be amenable to X-rays 





Notes from the Actinotherapeutic Department. 377 


in other people’s hands, but I have not been able to give them a 
fair trial yet, except in case 8, where they failed. Radium is 
useful, because it could be applied at a patient’s own home. 


LUPUS. 


CASE 1.—L. S., female, et. 21. A small, recurrent, but very thick and 
obstinate patch on the upper lip (see Figs: 7 and 8). Treatment lasted from 
18th September, 1903, to 7th March, 4904. She had in all one hundred and 
five sittings, of which forty-four were X-rays, using Cossor’s lead-glass tubes ; 
six radium bromide, and fifty-five ultraviolet light from an iron spark lamp ; 
in the last fourteen ultraviolet sittings L. Miller’s lamp was used, but the 
previous application had been by a very inefficient instrument by another 
maker. The sittings were usually fifteen minutes each and only once was 
any reaction obtained. At the end the hard lumps were touched with pure 
carbolic; this was done twice. A pale soft scar was left. At various times 
she was prescribed Iron, Arsenic, Potassium Iodide, Perchloride of Mercury, 
and Extract of Malt. Locally Ung. Picis Carbonis. I had a letter nearly 
two months after she left to say that the cure persisted. 

Remarks. —The treatment was unduly long, a great deal I think on account 
of the inefficient instrument used before the Leslie Miller lamp. 


CasE 2.—M. M., female, et. 31. Extensive lupus on the chin, right cheek 
and right ear with superficial ulceration and much scabbing. Had been 
treated with X-rays from July to November, 1902, and discharged as almost 
cured; it recurred and was again treated with X-rays from March, 1903, to 
February, 1904, with absolutely no benefit. She was then sent here for the 
light treatment. Treatment began on 8th February, 1904, and has continued 
to the present time. She has had in all fifty-four sittings, all with the Leslie 
Miller iron spark lamp, except one with radium and one with the Lortet- 
Genoud modification of Finsen’s lamp. She is nearly cured at the time of 
writing, 7th August, 1904, and what was an unsightly ulcerating area, is now 
smooth scar tissue with a few scattered apple-jelly nodules here and there. 


Case 3.—J. F., male, æt. 22. Lupus all over the front of his chest, the right 
side of the face and left cheek. Sent up by Dr. J. Richards. I failed to do the 
slightest good in this case, either with light or X-rays. He attended from 
5th January to 10th May, 1901, and had in all eighty-four sittings. Опсе 
radium was applied. I tried Leslie Miller’s lamp, another iron spark lamp, 
a carbon arc lamp, kindly lent me for trial by the Dowsing Company, and 
Cossor’s tubes for the X-rays. We had not the proper Finsen lamps installed 
at this time. As before stated, the treatment proved an utter failure, although 
some reaction was obtained on several occasions. 





Case 4.—H. P., female, æt. 17. Lupus non-exedens of right thigh, lupus 
exedens of right foot, of which there was much deformity with loss of the big 
toe. "Treatment commenced on 28th March, 1904, and has continued to the 
present time. Sixty-two applications to thigh, all, except three, ultraviolet 
lamp, Miller. Sixty-one applications of X-rays to foot. Besides this, on 


378 Notes from the Actinotherapeutic Department. 


two occasions very hard nodules in the thigh were touched with pure phenol. 
There is great improvement in the foot and a good deal in the thigh. The 
sittings for both foot and thigh were usually fifteen minutes. The case is still 
under treatment. Much benefit has accrued, and I hope to effect an entire 
cure. 


Case 5.—M. F., female, æt. 21. Lupus non-exedens of right cheek 
Had been operated upon. Treatment commenced on 25th April, 
1904, and is still being continued. She has had thirty-five sittings with 
Miller's iron spark lamp, varying from three to ten minutes, and twelve with 
the Lortet-Genoud lamp of thirty minutes each. There is great improve- 
ment, and a soft pliable pale scar is replacing the lupoid tissue. 

CASE 6.—C. R., male, æt. 20. Lupus of the skin in front of the neck, 
patch rather larger than a five-shilling piece. Treatment began on 18th 
May, 1904, and still continues (7th August, 1904). Thirty-five sittings with 
Miller's lamp. Improvement is taking place, but slowly, probably because 
the soft tissues of the neck prevent sufficient pressure being used to produce 
proper anæmia of the part. 


CASE 7.—A. C., female, æt. 50. Extensive lupus of the face; a good deal of 
destruction ofthe nose; ulceration. Treatment began on 8th June, and is being 
continued. Seventeen sittings of ten or twelve minutes with X-rays, four 
with the iron spark lamp, six to ten minutes, twelve with the Lortet-Genoud 
lamp of thirty minutes each. There is marked improvement. The X-rays 
were used in the ulcerated parts which were too tender to stand pressure. 








CASE 8.—R. M., female, æt. 24. Lupus of the gums. Sent up by Dr. Mason, 
of Sudbury. Has been operated on for lupus of face, nose, and lip, seven 
times. This was finaily cured at the London Hospital after fifteen treat- 
ments of one hour each. The present trouble of the gums has come on later. 
A good deal of ulceration and loss of central incisors in upper jaw. Treat- 
ment began on 28th June, and still continued. Fourteen treatments of ten 
minutes each with X-rays which seemed to do no good, then nine sittings 
with radium bromide of thirty minutes each. "There is now, I think, some 
improvement, 7th August, 1904. 

Case 9.—F. H., female, æt. 26. Small patch of lupus on the right cheek, 
also a spot in the right nostril. Treatment began on 12th July and is being 
continued. X-rays thirteen times, ten minutes each. Miller's lamp and 
Lortet-Genoud lamp once each, but discontinued as efficient pressure 
was impossible. Great improvement. 


Case 10.—E. C., female, æt. 8. Several patches of lupus on the face and 
limbs. Those on the limbs are being scraped, those on the face treated with 
the Lortet-Genoud lamp. She has had ten sittings of thirty minutes each, and 
one of ten minutes with the iron spark lamp and is improving, she is still 
under treatment. 





CASES 11 and 12.—Are of such recent date that no purpose can be served 
by reporting their treaument. 


Notes from the Actinotherapeutic Department. 379 


Conclusions as regards lupus.—Omitting the last two cases 
(11 and 12) I have to record entire failure to do any good in one case 
(No. 3), a (at all events temporary) cure in one case, marked 
benefit in four cases, and slight improvement in the others, some 
of which have not had time to show any decided change. Up 
to the present we have had to work with very scanty apparatus, 
but when the new department is fully opened our results should 
be much better. 


MYCOSIS FUNGOIDES. 


On 1st March, 1904, F. E., a strongly-built man, æt. 36, was 
brought to Sir Cooper Perry’s out-patients, suffering from 
patchy, pigmented, rough blotches all over the trunk, arms and 
legs, with somewhat extensive ulceration about the left nipple, 
which was itself enlarged as a red, moist granulomatous mass, to 
the size and appearance of a raspberry. 

Patient says the disease began in childhood. When about 
eight years old his mother took him to a doctor because his 
legs used to come out in bright red spots, especially after 
washing. These spots used to come and go, but gradually the 
skin grew rough, first on the legs and then on the arms. His 
father died from “influenza” at seventy-four, and his mother 
from “paralysis,” also aged seventy-four. He has four brothers 
and two sisters alive and well, another brother died from “ kidney 


, 


disease," and another died after ‘“operation”’ for (?) intestinal 
obstruction. He is a married man, and has two children 
(girls), quite healthy, and his wife is also healthy. He had 
* pleurisy,” he thinks, on the right side, when fourteen; was 
troubled with varicose veins, stil present, when 18, relieved by 
applying a Martin's bandage; ‘‘ slight inflammation of thelungs " 
when 20. About six months ago he found a slight abrasion of 
the skin below and a little to the inner side of his left nipple; he 
treated it himself with boracic ointment for six weeks, and during 
this time it scabbed over, but then the scab came off, leaving an 
ulcer ; this has gradually spread since, until it is now about the 
size of the palm of the hand. The skin, generally, is dry and 
rough, and in many places a brawny red, these brawny patches 





L 4 


380 Notes from the Actinotherapeutic Department. 


being sometimes a slightly deeper colour at the edges, which are 
slightly raised. In other patches there is slight branny des- 
quamation, and on the back of both upper arms the condition 
resembles ichthyosis. The face and head are free. He suffers 
from itching, which is evidently only slight, as there are no 
scratch marks; this itching has been more marked during the 
past few months, and is worse when he is hot or is in bed. He 
says his hands always swell in winter. 


Sir Cooper Perry diagnosed mycosis fungoides, and it was 
resolved to treat him with X-rays. Treatment commenced on 
March 2nd. The X-rays were applied direct to the ulcer and 
fungating nipple, by means of a Deane-Harnack apparatus from 
a very high tube, which probably averaged about a 6-inch 
alternative spark gap. 

The sittings on each occasion lasted fifteen minutes, 
except twice, when they were only ten minutes each. On the 
12th April, after twenty applications, the chest was healed; 
patient was then found to have a small scabbed place on his back 
about the size of a threepenny-bit. Between 12th and 29th 
April this was given seven applications, and appeared healed. 
On 10th May, however, he came back again, the scab on the back 
having re-formed. He attended very irregularly until the 21st 
June (10 attendances), and the place on his back grew decidedly 
bigger. І impressed on him the necessity for regular treatment, 
and it has now practically healed again after twenty-three further 
sittings (7th August, 1904). Besides the local effects, a general 
improvement was clearly observed in the condition of the skin. 
The nipple now is normal in size and appearance, and where the 
ulcer was situated is now & deep pink patch of soft pliable skin, 
to which the term scar is hardly, perhaps, applicable. He was 
not given any internal medicine, and the only local application 
was & simple ointment and lint to protect the ulcer from pressure 
of his clothes. In the Epitome of Current Medical Literature 
* British Medical Journal," 9th April, 1904, is mentioned a case 
treated by A. E. Carrier (Journ. Cutan. Diseases, February, 1904), 
where, as here, although no cure is claimed, a distinct and 
remarkable effect has been obtained by X-rays in a disease which 


— 7''"Uu 





Notes from the Actinotherapeutic Department. 381 





Taken 1oth March, 1904. 





Taken 12th April, 1924. 


Fig. 10. 


882 Notes from the Actinotherapeutic Department. 


is almost uniformly fatal, and for which no other treatment is 
known. 

Scholtz, Norman Walker and H. G. Brooke have also reported 
good results in this affection (Freund).  Radcliffe-Crocker des- 
cribes three types of mycosis fungoides: I. The most common 
where there is some form of dermatitis antecedent to the tumour- 
formation. II. The rarest where recurrent attacks of lymphan- 
gitis lead up to an elephantiasic thickening of the skin, and finally 
tumour-development. III. Where tumours develop without 
antecedent dermatitis. 

It is interesting to note that the present case is an example of 
type I., whereas Carrier's case seems to belong to type III. 

I would add that the patient's private doctor, who had taken 
great interest in the case, had applied all the usual remedies with- 
out any good result. 

I have to thank Sir Cooper Perry for his kindness in allowing 
me to publish these notes on his case (see Figs. 9 and 10). 


GLOSSITIS. 


Case 1.—J. R., male, æt. 54. Suffering from ‘‘Sore tongue" for over a 
year. He has been attending a doctor for eighteen weeks. He now has a 
greatly thickened tongue covered with fissures and bald patches. He was 
sent to me by Mr. Lane, who considered the condition of the tongue was 
likely to end in epithelioma. The tongue was extremely painful and tender. 
Treatment began on 3rd March and ended on 16th May, 1904. Three sittings 
of X-rays of fifteen minutes each and eighteen of radium bromide. There 
was so much improvement that Mr. Lane advised him to discontinue the 
treatment. I saw him again on 13th June and llth July, when he was 
still keeping well. He used a chinosol mouth wash during the treatment. 

Remarks.—-In view of the chronicity and possible termination of the 
disease in malignancy, I think this case is well worth noting. 

(NoTEÉ.—The day after writing this the patient returned complaining of his 
tongue being sore again. It was, however, still looking well. Treatment was 
recommenced.) 


Case 2.—F. N., male, et. 31. Sent fcr treatment by Mr. Steward. 
Tongue swollen and fissured, smooth in places, superficial ulceration in 
others. Curious white elevated papules in parts of the ulcers, which, as Mr. 
Steward suggested, looked like a fungous growth, but which was examined 
by Dr. Eyre with negative result. The same condition existed on the palate. 
There is one slightly enlarged, soft, gland in the left submaxillary region. He 
says he has had the disease all his life. No history of syphilis; has been 
married eight years. Suffered from dyspepsia and measles during his child- 
hood. Finger nails ara very thin, and those of right thumb and left index 





Notes from the Actinotherapeutic Department. 383 


thickened as in onychomycosis. Treatment lasted from 21st June to 22nd 
July, 1904. Fourteen sittings of ten minutes each with X-rays. On two 
occasions the treatment was discontinued as the tongue got rather more 
sore than usual. He had to discontinue treatment in order to revurn to his 
work. The tongue was slightly improved, being not so swollen and ulcerated. 
This may or may not have been due to the treatment, and, as he said, his 
tongue varied from time to time. 


CHRONIC RHINITIS. 


Case 1.—H. A., male, middle aged. Chronic, purulent, scabby, thickened 
condition of the upper lip, apparently dependent upon a chronic profuse, 
watery discharge from the nose from which he has suffered for twenty-four 
years. He is inclined to indulge somewhat freely in alcohol. He has been 
under treatment since April, 1904, and has been treated with X-rays, positive 
static charges, and high frequency currents; is decidedly better but is liable 
to relapses. 


Case 2.—L. B., female, æt. 29. Sent for treatment by Mr. Steward, on 
account of a chronic watery nasal discharge from both nostrils accompanied 
by sneezing. Has suffered from it for a year. Has been treated with high 
frequency currents since 81st May, 1904, and expresses herself as being very 
much better. She is still attending. 


е 


LUPUS ERYTHEMATOSUS. 


Case 1.—E. B., female, ext. 49. Lupus erythematosus discoides over 
right eye, patch about the size of a half-crown. Treated from 4th December, 
1908, to 7th April, 1904, with X-rays, negative stwtic breeze, high fre- 
quency currents and radium. It seemed at one tim: to improve with the 
static breeze—the scaliness disappeared and there was less thickening of 
the edges of the patch—eventually, however, after trying all the above 
remedies, the case had to be given up as I entirely failed to do any good, in 
fact she got worse instead of better. 


UNCLASSIFIED CASES. 


These were eight in number and will be just shortly referred 


to— 

Case 1.—R. D., male, æt. 25. Sent by Sir Alfred Fripp for a hard bony 
swelling in left occipital region, the result of an accident some time previously ; 
inveterate headache and insomnia. Given ten sittings of the negative static 
breeze for fifteen minutes each. . Cured of headache and sleeplessness. 


` Oase 2.—M. H., female, et. 17. Small brown mole on loft cheek. Given 


two sittings of radium and barium and two of X-rays, no change, so шей 
advised to have it excised, which was done. 


U 


384 Notes from the Actinotherapeutic Department. 


Case 3.—Е. W., male, æt. 32. For an ulcer on back of his left hand of 
fourteen months’ duration, which followed an injury with a pair of scissors. 
It would not heal. Has been excised twice but recurred. Is now surrounded 
by а suspicious induration. Has had a course of potassium iodide. Sent 
to me by Mr. Dunn. Was extremely suggestive of commencing malignant 
disease. No microscopical examination had been made. Treatment from 
16th May to 20th July, 1904, forty-two sittings with X-rays, fifteen minutes 
each; discharged cured. Quite healed and no induration. 


CASE 4.—A. G., female, æt. 18. Old infantile paralysis of left lower 
extremity, trophic congestion and ulceration in small patches on toes and 
ankle. Treated with X-rays, galvanism and faradism. Some improvement. 


CASE 5.—A. O., female, æt. 24 years. Suffering from chronic membranous 
ophthalmia of the left upper lid. Had five sittings of radium bromide for five 
minutes each, but then developed measles and treatment had to be 
discontinued. 


CASE 6.—  — female, æt. —. Warts оп hand. Attended twice for radium 
treatment and then discontinued coming. 


Case 7.—H. P., female, et. 19. Sent to me as а case of lupus, as which 
at first I regarded it. I started treatment with a Leslie Miller lamp, and 
later with radium. Latterly І came to the conclusion that my diagnosis was 
wrong, and that it was a case of erythema dependent upon indigestion. 
Treated with Salol and Sodium Sulphate, and subsequently Mist. Acidi Co., 
with only applications of lanoline locally. She appeared to get quite well. 


CASE 8.—L. L., female, æt. 30. Sent up as а case of lupus. Extensive 
ulceration on the back of her right leg which she has had for twenty-seven 
years. Has had X-rays tried for five months without any benefit. Was treated 
from 9th June to 18th July with first Pot. Iod. and Hyd. Perchlor., and later 
nerve and general tonics. Locally mercurial applications. The ulceration all 
healed. From 18th to 26th July, at patient’s earnest request, she was given 
the ultra-violet light treatment from a Leslie Miller lamp. When last seen 
all the ulcers were healed, but a red-coppery area was left covered with 
scaly epithelial debris resembling ichthyosis. 


NorTE.—I would like here to acknowledge my indebtedness to 
all the members of the Staff whose names are mentioned in the 
foregoing, and to Mr, Pullen, the electrician of the department, 
for his help, especially with the photographs, for which he is 
chiefly responsible. 


SPECIMENS RECENTLY ADDED 
TO THE, PATHOLOGICAL MUSEUM. 


By LAURISTON E. SHAW, M.D., 


Sm COOPER PERRY, M.D, 
AND 
JOHN FAWCETT, M.D. 


HEART. 


2309 Imperfect Septum Yentriculorum. 

The base of a heart mounted to show at the upper part 
of the septum a small fistulous communication between the 
two ventricles. The opening in the left ventricle is situated 
just below the attached border of the right anterior aortic 
cusp. 

William P., st. 19, was admitted under Dr. Pye-Smith with a 
cerebellar tumour, from which he died ten weeks after admission. 
While in the hospital a loud systolic bruit was heard over the heart, 
its point of greatest intensity being in the pulmonary area. At the 
autopsy the heart was found to weigh twelve and a half ounces, the 
other viscera with the exception of the brain being healthy. See Insp., 
1897, No. 49. 

2316 Pulmonary Stenosis. 

A heart divided by a vertical incision to show the aorta 
and pulmonary artery, both arising from the right ventricle, 
the wall of which is somewhat thicker than that of the 
left ventricle. The pulmonary valves are fused together, 
forming a thick membranous cone, with a central aperture 
not more than a line in diameter. The trunk of the pul- 
monary artery is small and its walls are thin. The two 





Up 


286 Specimens recently added to the Pathological Museum. 


ventricles communicate with each other by an opening, 
admitting the index-finger, at the highest part of the 


septum. 


John V., et. 17, was admitted under Dr. Pye-Smith for dyspnea 
and attacks of syncope. On admission his lips were cyanosed, his 
fingers clubbed, and a systolic bruit was heard in the third left inter- 
costal space close to the sternum. While in the hospital the patient 
had two epileptiform seizures, and blood and albumen were found in 
the urine. He died two months after admission, and at the autopsy 
the heart was found to weigh fifteen ounces and the kidneys were 
congested. See Insp., 1898, No. 404. 


2322 Congenital Malformation of Heart and Great Vessels. 
The thoracic viscera of a foetus mounted to show the 

aorta arising from the right ventricle, and giving off from 

its arch two vessels taking the place of tbe right and left 
branches of the pulmonary artery, the main trunk of which 

is absent. The descending aorta passes over the right 


bronchus. 
From a foetus prematurely born in Mary ward in 1888. 


2328 Congenital Malformation of the Heart and Vessels. 

An infant’s heart mounted to show a large cavity rep- 
resenting the right ventricle, from which the aorta and 
pulmonary artery arise side by side. A red rod is passed 
through the upper part of the interventricular septum into 
the cavity of the undeveloped left ventricle, which does not 
communicate with the left auricle. This auricle is very 
small and possesses a well-developed appendix; it has a 
free communication through the foramen ovale, with the 
dilated and hypertrophied right auricle. 


Margaret B., æt. 3 months, was admitted under Dr. Hale White 
in a moribund condition, and died two hours later. A loud systolic 
bruit, associated with a thrill, was heard all over the cardiac area. 
At the autopsy patches of collapse were found in the lungs. There 
were no malformations other than those of the heart and large vessels. 
See Insp., 1897, No. 108. 


2330 Dilated Coronary Sinus. 
A heart seen from behind and presenting at the situation 
of the coronary sinus a thin-walled sacculus measuring 
an inch and three quarters in its longest diameter. It 


Specimens recently added to the Pathological Museum. 387 


2424 


2426 


. 2429 


communicates by an aperture, admitting the tip of the 
little finger, with the right auricle. The foramen ovale 


is patent. 


From a female infant, æt. 11 months, who died from epiphysitis 
and osteomyelitis. The viscera, with the exception of the heart, were 


normal. 
Presented by Mn. TaAncETT, 1900. 


Chronic Endocarditis of Aortic Valve. 

An infant's heart laid open to show the aortic cusps 
thickened, two of them being coherent. At the point 
of union of these cusps, there is & small mass of 


fibrinous deposit. 


Ellen L., et. 11 months, was admitted under Dr. Pitt in a moribund 
condition and died on the following day. The child had been in the 
hospital a short time previously and was then noticed to have a systolic 
basic bruit, which was believed to be due to congenital heart disease. 
Before death a to-and-fro bruit was heard at the base of the heart. 
At the autopsy the lungs presented patches of collapse, the other 
viscera being normal. See Insp., 1892, No. 465; and Trans. Path. Soc., 
vol. xliv., p. 28. 


Ulcerative Endocarditis of Aortic Valves. 

A portion of a heart mounted to show the aortic valves 
extensively destroyed by ulceration and partially encrusted 
by fibrinous deposit. On the reverse of the specimen a 
similar deposit is seen attached to the wall of the pulmonary 
artery a little above the valve, which itself appears to be 


norinal. 


Francis S., et. 25, was admitted under Dr. Perry with signs of 
valvular disease of the heart, supposed to be due to an attack of 
rheumatic fever, from which the patient had suffered six months 
previously. He died ten days after admission, and at the autopsy the 
heart was found to weigh nineteen ounces. There were patches of 
broncho-pneumonia in the lungs and the kidneys were infarcted. See 
Insp., 1891, No. 340. 


Ulcerative Endocarditis. Perforation of Aortic Valve. 

A portion of a heart mounted to show ulcerative 
endocarditis affecting the aortic and mitral valves, the 
aortic being also affected by chronic disease. The two 
anterior semilunar cusps are much thickened, and are 
fused so as to form a single large flap. The posterior 


888 Specimens recently added to the Pathological Museum. 


cusp presents a rounded perforation fringed with vegeta- 
tions. In the neighbourhood of the valves are seen the 
orifices of three small aneurysms. Тһе aortic cusp of the 
mitral valve together with its chorde tendiniz presents 
numerous small septic vegetations. 


Joseph H., st. 46, was admitted under Dr. Taylor for dyspnoea and 
dropsy, having previously suffered from rheumatism. On admission 
bruits were heard in both mitral and aortic areas and there wasa 
petechial rash upon the legs. The patient died the day after admission, 
and at the autopsy the liver and spleen were found to be enlarged and 
the kidneys were scarred. See Insp., 1894, No. 195. 





2487 Aortic Stenosis. 


The base of a heart mounted to show the aortic cusps 
forming a rough dome-like septum, with its convexity 
towards the arch of the aorta. The valve is extremely 
rigid and calcareous, and the aperture resembles a button- 
hole rather less than half an inch in length. There is 
a considerable calcareous deposit in the mitral valve 
continuous with that in the semilunar cusps. 


From a hawker, xt. 37, who was found dead in the snow. His 
friends believed him to have been in good health. The heart weighed 
fifteen ounces. 


Presented by Mr. A. С. ELLIMAN, 1891. 


2488 Aortic Stenosis. 


The base of a heart mounted to show the aortic orifice 
obstructed by the cohesion of the semilunar cusps. Two 
of the cusps are united to form a thick fibrous septum, 
whilst the left anterior cusp presents a large nodular 
excrescence, bare of endothelium and infiltrated with 
calcareous deposit. The mitral valve is also thickened: 
The epicardium is roughened by old adhesions. 








Louisa H., æt. 58, was admitted under Mr. Higgens with opacity of 
the cornea and closure of the left pupil, for which irridectomy was 
performed. There were physical signs of aortic and mitral disease, 
with symptoms of chronic cardiac failure, from which she died nine 
days after her admission. At the autopsy the heart was found to 
weigh thirteen ounces, and the lungs were in a condition of brown 
induration. See Insp., 1891, No. 193. 





Specimens recently added to the Pathological Museum. 889 


2462 Stenosis of Cardiac Valves. 


The base of a heart mounted to show a considerable 
degree of stenosis of the aortic, mitral, and tricuspid 
valves. The pulmonary valve is normal. There are recent 
vegetations on the mitral curtains. 


Emma M., et. 30, was admitted under Dr. Taylor for general cedema 
and hemoptysis, associated with a systolic bruit at the apex of the 
heart. She had had four attacks of acute rheumatism. The patient 
died four days after admission, and at the autopsy the heart was 

found to weigh fifteen ounces and the viscera were congested. See 
Insp., 1895, No. 61. 


2463 Aortic Stenosis. Fibroid Heart. 


A portion of a heart, which in the recent state weighed 
twenty-two ounces, mounted to show the aortic orifice 
reduced to a narrow chink, half an inch in length, between 
the edges of two of the cusps. The valves are thickened 
and loaded with calcareous deposit. A section through the 
hypertrophied wall of the left ventricle shows several white 
patches of fibroid change in the myocardium. The other 


valves are healthy. 


George R., st. 61, was admitted under Dr. Taylor for dyspnoea 
and anasarca of nine months’ duration. He had had a winter cough 
for twenty years. On admission there were physical signs of pleuritic 
effusion, and of aortic stenosis and mitral regurgitation. Paracentesis 
thoracis was performed, and the patient died two days after his 
admission. At the autopsy the heart was found to weigh twenty-two 
ounces, the kidneys were granular, and there was a deposit of urate 
of soda in the great-toe joint. See Insp., 1898, No. 406. 


2505 Four Pulmonary Semilunar Valves. 


A portion of a pulmonary artery considerably hyper- 
trophied and measuring four inches in circumference. Its 
orifice is guarded by four nearly equal semilunar cusps, all 
of which are thickened and opaque but of normal shape. 


From a congenital idiot who died at the age of 50 in the Norfolk 
County Asylum. He had suffered from subacute rheumatism and died 
from chronic cardiac failure. At the autopsy the heart was found to 
weigh thirty-two ounces, the mitral orifice being considerably dilated. 
The viscera were congested. 

Presented by Dr. J. RoBERTSON, 1898. 


VOL. LIX. . 27 





390 Specimens recently added to the Pathological Museum. 


2621 Pulmonary Stenosis. 

The base of a heart mounted to show the cusps of the 
pulmonary valve united to each other to form a thin 
conical septum, in the summit of which is seen a narrow 
opening measuring half an inch in length and a line in 
width. On the edge of the orifice there are a few minute 
vegetations. 

Phoebe B., æt. 50, was admitted under Dr. Pye-Smith for an 
abdominal tumour associated with vomiting and emaciation. There 
was & loud rasping systolic bruit audible all over the chest, loudest in 
the second left intercostal space. The patient died about four months 
after admission, and at the autopsy a malignant growth was found in 
the colon invading the duodenum. The heart weighed nine and a 
half ounces. See Insp., 1899, No. 10. 


AORTA. 
2588 Coarctation of the Aorta. Hypertrophied and Dilated 
Heart. 

An aorta with the base of the heart. At the junction of 
the descending aorta with the arch there is a constriction 
whereby the lumen of the vessel is narrowed so as to 
barely admit a fine probe. Below the constriction the 
vessel is normal, while above it is considerably thickened 
by atheromatous deposit, and somewhat diminished in 
calibre for a distance of about an inch. The aortic valves, 
two in number, are thickened, and the adjacent portion of 
the aorta atheromatous. 

Thomas M., æt. 45, was admitted under Dr. Pye-Smith for dyspnea 
and cedema of the legs. Не had had ‘‘ rheumatic gout” seven years 
previously, and was in bed two months. Since this time he had 
suffered with cough and palpitation of the heart. In October, 1898, 
he was admitted under Dr Pitt with pleurisy, associated with hyper- 
trophy of the left ventricle and albuminuria, At the autopsy the 
heart was found to be generally hypertrophied and dilated, weighing 
twenty-three ounces, The lungs were in a condition of ‘‘ carnification,”’ 
and there were some recent infarcts in the kidneys. See Insp., 1899, 
No. 142. 


2539 Occlusion of Aorta. 

The base of the heart with the great vessels and the lower 
end of the trachea. At a point immediately below that at 
which the still patent ductus arteriosus joins the aorta the 
vessel is completely occluded. Below the site of the 


Specimens recently added to the Pathological Museum. 891 


2540 


2542 


occlusion, the aorta, which appears thin and healthy, is 
diminished in size by about one-half, and above as far as 
the origin of the left subclavian artery it is still further 


diminished. 


Eliza S., st. circa 45, was admitted under Dr. Horrocks for 
pregnancy and heart disease. She had born eight children alive, the 
last pregnancy being one year ago. On admission she was dyspnoeic 
and had some bronchitis and albuminuria, in addition to signs of 
valvular disease of the mitral and aortic orifices. Labour was induced, 
but patient’s condition did not improve, and she died seventeen days 
after admission. At the autopsy aortic stenosis was found. See Insp., 
1899, No. 441. 


Malposition of the Aorta. 


A heart with its great vessels, the trachea, and the main 
divisions of the bronchi dissected to show the aorta crossing 
the right bronchus and passing behind the lower end of the 
trachea. There is no innominate artery, the right common 
carotid and subclavian arteries arising directly from the 
arch of the aorta. The ductus arteriosus, which springs 
from the pulmonary artery in the normal position, crosses 
the left bronchus to be attached to the left subclavian 


artery. 


Eliza D., æt. 74, was admitted under Mr. Lucas after having been 
run over. She died as the result of the injuries received. See Insp., 
1888, No. 379. 


Aorta perforated by a Bone impaoted in the 
(Esophagus. 

A portion of a thoracic aorta and of an wsophagus, 
mounted to show a fistulous communication between the 
two tubes indicated by a red rod. The opening in the aorta 
is situated just below the origin of the subclavian artery: 
On the wall of the cesophagus opposite to the perforation 
is an ulcer leading into the connective tissue between the 
cesophagus and the trachea. In the recent state a piece 
of chicken-bone occupied the position of the rod. 


Francis N., st. —, was admitted under Dr. Goodhart, having 
swallowed a chicken-bone a week previously. On the evening before 
she died she was found in a fainting condition on her bed, and on 
being raised she immediately vomited about half a pint of blood. 





392 


2547 


2550 


Specimens recently added to the Pathological Museum. 


Hemorrhage recurred on two occasions during the next few hours, 
and eventually proved fatal. At the autopsy seven ounces of blood-clot 
were found in the stomach, and the intestines also contained a con- 
siderable quantity. See Insp., 1898, No. 112. 

Rupture of the Aorta into the Pericardium. 

A left ventricle with the first part of the aorta laid open 
to show, an inch above the semilunar valves, a ragged 
laceration through the inner coat of the vessel, large enough 
to admit the tip of the little finger. On the reverse of the 
specimen the outer coats of the aorta are seen to have 
been separated over a considerable area, and to present a 
longitudinal tear, which, in the recent state, communicated 
with the pericardial sac. The interior of the aorta appears 
healthy. At the apex of the left ventricle there are some 
patches of fibroid’ myocarditis, over which the pericardium 
has been adherent. 


From a woman, et. 26, who was found dead in front of a grate that 
she was about to clean, having been seen in her usual health a few 
minutes before. She had been confined of a seven-months’ child at 
twenty-one years of age, and had suffered from symptoms of syphilis. 
At the autopsy the pericardium was found distended with about a pint 
and a half of fluid blood, in addition to a large amount of coagulum. 


Presented by Dr. J. COLLISON MORLEY, 1889. 


Aortitis. 


The first part of an aorta laid open to shew the vessel, 
for a distance of two inches from the semilunar valves, to 
be thickened and its interior irregularly corrugated. This 
condition is clearly defined from the healthy aorta beyond 
by a raised sinuous margin. The semilunar valves are 
thickened and much deformed, and appear to have been 
partially destroyed by ulceration. 


Mary S., æt. 14, was admitted under Dr. Taylor for anemia and 
dyspnoea, with an enlarged heart and aortic incompetence. She died 
shortly after an attack of vomiting. At the autopsy the heart was 
found to be generally dilated and hypertrophied. The mitral, tricus- 
pid, and pulmonary valves were all normal. There were infarcts in 
the lungs and kidneys. See Insp., 1901, No. 332. 














a er u a J goa 4AVWA US VAY 


The base of a heart with the first part of the aorta. The 


semilunar valves are greatly thickened and deformed. Two 
are united together, their point of union being marked by а 
mass of calcareous deposit. Just above the valves there is 
a localised thickening of the aorta, forming a raised plaque 
with a well-defined sinuous margin which almost encircles 
the vessel and extends upwards for a distance of one inch. 


John S., a blacksmith, æt. 31, was admitted under Dr. Pye-Smith 
for pain in the chest, dyspnoea, and cedema of the legs, associated with 
an enlarged heart and а ‘‘to-and-fro,’’ bruit, which was audible all 
over the front of the chest. Death occurred suddenly, fourteen days 
later. At the autopsy the heart was found to be dilated and hyper- 
trophied (weight twenty-iwo ozs.), and on the surface of the liver were 
several scar-like patches, which, however, did not penetrate the sub- 
stance of the organ. The testes were healthy. See Insp., 1896, No. 7. 


2564 Aneurysm of the Aorta and Innominate Artery 
surrounding the Clavicle. | 
A portion of the arch of an aorta, which is extremely 
atheromatous, and has been laid open to shew at its upper 
part the orifice of an aneurysmal sac plugged by firm blood- 
clot. Above the aorta is seen the sac of the aneurysm 
which measures about four inches in diameter. Its wall 
has been partially removed, and reveals the greater part of 
the right clavicle, which, bared of its periosteum and 
eroded, has been separated from its sternal end and projects 
into the sac. A red rod marks the course of the arch of 
the aorta. 


Alfred H., æt. 62, was admitted under Dr. Fawcett for a large 
aneurysm of gradual development projecting from the upper part of 
the right side of the chest. There was a history of venereal disease. 
At the autopsy the right pleura was found to be thickened and adherent 
and the right lung compressed, as was also the trachea to a slight 
degree. Parts of the manubrium, the clavicle, and the first two ribs 
were eroded, The outer wall of the aneurysm was formed by some of 
the muscles attached to the clavicle and the overlying skin. The 
aorta was dilated, and very atheromatous throughout. See Insp., 
1902, No. 80. 


VOL. LIX. 28 





394 


Specimens recently added to the Pathological Museum. 


2575 Aneurysm of the descending Aorta communicating 


2577 


with the (Esophagus and the Left Bronchus. 


Portions of the thoracic aorta and of the cesophagus and 
trachea. The aorta is extremely atheromatous and dilated, 
and in the recent state presented a saccular aneurysm 
arising from the descending portion, and eroding the bodies 
of some of the dorsal vertebrae. The red rod marks an 
opening from the wall of the aneurysm into the adjacent 
cellular tissue. There are openings in the cesophagus and 
the left bronchus, whereby an indirect communication was 
established between these tubes and the perforation in the 
wall of the aneurysm. 


John G., et. 53, was admitted under Sir Cooper Perry for severe pain 
in the chest, of some months' duration, increased by taking food. 
Death took place suddenly from hemorrhage. At the autopsy the 
trachea and main bronchi were filled with recent clot. See Insp., 
1904, No. 30. 


Aneurysm of the Aorta opening into the Pericar- 

dium. 

The base of a heart with the first part of the aorta laid 
open to shew, two inches above the semilunar valves, the 
circular orifice of an aneurysmal sac, which admits the 
thumb. The sac is ovoid in shape, measuring four inches 
in its longest diameter, and presents on its lower and 
anterior aspect a small laceration into the pericardial 
cavity. 

Frank F., æt. 24, was admitted under Dr. Shaw, in a collapsed 
condition, having fainted while at work an hour previously. He was 
almost pulseless, and his lips and face were blanched; he died five 
minutes after reaching the ward. At the autopsy & gumma was found 


occupying the apex of the left ventricle, and another in the pancreas, 
See Insp., 1899, No. 151. 


2578 Aneurysm of the Aorta opening into the Pericar- 
dium. 

The base of a heart with the first part of the aorta laid 
open to shew, just above the junction of the anterior and 
right posterior cusps, the circular orifice of an aneurysmal 
sac, through which the tips of three fingers can be passed. 








2590 


2592 


LUG YUU ID UVUIU 111 DLLME, зало w viis vr wag wiu aaa em اا‎ 
three and a half inches in its longest diameter. In the 
recent state, a small communication was discovered between 
the sac and the pericardial cavity. The surface of the peri- 
cardium is roughened by a soft fibrinous deposit. 


Arthur P., æt. 30, was admitted under Dr. Washbourn, having been 
found in his cart ір a moribund condition. He was cyanosed and in 
intense pain. There was a great increase in the area of precordial 
duiness. Subsequently pulsation was detected to the right of the 
sternum and a pericardial rub was heard. On the morning of his 
death he had an attack of syncope, and succumbed in a few minutes. 
At the autopsy the pericardium was found to contain sixteen ounces of 
blood-clot, some of which was decolorised. See Insp., 1896, No. 179. 


Aneurysm of the Arch of the Aorta invading the 
Trachea. 

The arch of an aorta laid open to shew on its posterior 
wall, immediately beneath the origin of the common carotid 
and subclavian arteries, a smooth circular opening large 
enough to admit the tip of the little finger, and leading into 
an aneurysmal cavity about the size of a walnut. On the 
reverse of the specimen the sac is seen to have bulged into 
the trachea, considerably narrowing its lumen. On the 
prominence thus produced there are two teat-like projections, 
over which the mucous membrane is partially destroyed, 
exposing the blood-clot in the sac. 


Albert D., et. 42, was admitted under Dr. Taylor for a cough of 
about six weeks’ duration, during which period he had on one occasion 
brought up about an egg-cupful of bright red blood. He was very 
dyspnosic, and a loud respiratory stridor was present. Signs of 
bronchitis were audible all over the lungs, and he shortly developed 
pneumonia, to which he succumbed. At the autopsy diffuse broncho- 
pneumonia with pleurisy was found, and the aorta was atheromatous. 
See Insp., 1904, No. 142. 


Aneurysm of the Aorta compressing the Superior 
Vena Cava. | 
Half of the ovoid sac of an aortic aneurysm, measuring 
five inches from above downwards and three inches from 
side to side. It arises from the first part of the aorta, and 
the aortic orifice, guarded by its semilunar valves, can be 


996 Specimens recently added to the Pathological Museum. 


seen on the middle of the lateral wall of the sac. The 
superior vena cava, which courses over the posterior wall of 
the sac, has been laid open to shew its lumen considerably 
encroached upon by the pressure of the aneurysm. 


Henry J. T., et. 50, was admitted under Dr. Shaw for orthopnea 
cyanosis and dulness over the right side of the chest. There was some 
bulging of the „chest wall, but no pulsation. General anasarca was 
present. At the autopsy, parts of the sternum and of the third, fourth 
and fifth ribs were eroded. The right pleura was thick and adherent, 
and there was double hydrothorax. See Insp., 1890, No. 28. 


2600 Aorta opened by Epitheliomatous Ulcer of the 
(Esophagus. 

A thoracic aorta, with the cesophagus laid open from 
behind, to shew a small oval communication between the 
two tubes situated about two inches below the level of the 
bifurcation of the trachea. In the aorta the edges of the 
perforation are smooth and free from evidence of disease, 
while in the cesophagus there is a crateriform malignant 
uleer, the base of which is partly formed by the outer wall 
of the aorta. Histologically the wall of the ulcer is infil- 
trated with squamous-celled epithelioma. 


William S., et. 52, was admitted under Dr. Taylor for difficulty in 
swallowing, and died suddenly, six weeks later, from profuse hemorr- 
hage. At the autopsy the stomach was found to be distended by a 
large mass of blood-clot. See Insp., 1895, No. 106. 


2601 Aorta opened by Epithelioma of the (Esophagus. 

A thoracic aorta mounted to shew, at the junction of the 
arch with the descending portion, a small opening com- 
munieating with the cesophagus. This opening is seen to 
be situated in the midst of a large cancerous ulcer, which 
involves the upper two-thirds of the gullet, and histologically 
has the structure of a squamous epithelioma. 


From a man who died suddenly after bringing up a large quantity of 
blood. 


Presented by Dr. Bryan, of Leicester Infirmary, 1898. 


2602 Aorta deformed by Spinal Caries. 

A portion of the thoracic aorta, presenting in its course a 
sharp bend with its concavity to the right, which resulted 
from a curvature of the spine, due to caries. The aorta is 
very small, and its inner coat is somewhat atheromatous. 


Alice M., et. 38, was admitted under Dr. Pye-Smith for symptoms 
of lardaceous disease following upon psoas abscess and spinal caries. 
She died six days after admission, and at the autopsy the spine was 
found to be affected by caries in the dorsal and lumbar regions. There 
was interstitial and tubal nephritis. See Insp., 1897, No 278. 


2608 Calcification of the Abdominal Aorta. 

An abdominal aorta with its terminal branches laid open 
from behind to shew its lining to be thickened and irregular, 
and in some places removed by ulceration. The deeper 
coats are infiltrated by calcareous deposit, which for the 
last two inches of the aorta has converted the vessel into a 


rigid bony tube. 


Joseph H., et. 72, was admitted under Mr. Golding Bird for gan- 
grene of the right foot. The leg was amputated, but two days later 
the stump became gangrenous, and he died four days afterwards from 
asthenia. At the autopsy the heart was found to weigh ten ounces, 
and the valves were competent. There was very little atheroma in the 
ascending portion and arch of the aorta, but the iliac arteries and those 
of the lower extremities shewed considerable calcareous degeneration 


of their coats. See Insp., 1895, No. 465. 


2617 Healed Aneurysm of the Abdominal Aorta. 

A portion of the abdominal aorta with its terminal 
branches laid open from behind to shew, just above its 
bifurcation, an aneurysmal sac, produced by the protrusion 
of the anterior wall of the vessel over a distance of three 
inches. The wall is rigid from calcareous deposit, and the 
interior is partially filled with firm blood-clot. 


This specimen was taken from a woman who died in the Stepney 
and Poplar Sick Asylum in 1897. 


Presented by Mr. A. B. CARTER. 


398 Specimens recently added to the Pathological Museum. 


2624 Embolism of the Abdominal Aorta. 


The lower end of an aorta with its terminal branches, as 
far as the femoral arteries. There is a large mass of firm | 
partially decolorised blood-clot occupying the last inch of 
the aorta, and occluding both common iliac arteries. From | 
this mass of thrombus there extends softer and dark red 
blood-clot into the greater number of the vessels forming 
the preparation. 


Emma H., æt. 40, was admitted under Dr. Perry in a collapsed con- 
dition, with an irregular and very rapid pulse, and died twenty-one 
hours later. She had been seized with acute pain in the abdomen, 
followed by sickness, eight hours before admission. Albumen was 
present inthe urine. At the autopsy an extreme condition of mitral 
stenosis was found, and the left auricular appendix was full of ante- 
mortem clot, which projected out into the cavity of the auricle. The 
left renal artery was plugged by clot; the aorta was free from disease. 
See Insp., 1903, No. 15. 


PULMONARY ARTERY. 
2628 Atheroma of the Pulmonary Artery 


A heart with the pulmonary artery laid open to shew 
numerous patches of atheroma situated chiefly in the 
main divisions of the vessel, the trunk itself appearing 
normal. The patches are raised, and of a yellowish colour, 
contrasting with the healthy surrounding parts. The right 
ventricle is dilated and hypertrophied, its wall measuring 
half an inch in thickness; the tricuspid valve is thickened 
and the mitral orifice considerably narrowed. 


Henry W., æt. 22, was admitted under Dr. Taylor, for heart disease, 
for which he had been an in-patient three times previously during 
1891-1892. The physical signs pointed to the presence of mitral 
stenosis and regurgitation, with tricuspid incompetence. At the 
autopsy the heart was found to weigh eighteen ounces. The branches 
of the pulmonary artery in the lungs were dilated and atheromatous. 
See Insp., 1894, No. 81. 





2637 Thrombosis of the Pulmonary Artery. 


A pulmonary artery with its main divisions laid open to 
shew, in its right branch, a mass of adherent thrombus, 





Specimens recently added to the Pathological Museum. 399 
7 


having а granular surface and a pointed extremity towards 
the heart. 


John N., æt. 20, was admitted under Dr. Taylor for morbus cordis, 
from symptoms of which he had suffered for six years. He presented 
the pbysical signs of mitral stenosis and tricuspid incompetence with 
general anasarca. While in the hospital he had numerous attacks of 
urgent dyspnoea, in one of which he died. At the autopsy the right 
side of the heart was found to be enlarged, both mitral and tricuspid 
valves being fibrous and shrunken. There was thrombosis in the right 
veutricle and the left subclavian vein, and in the lower part of the in- 
ferior cava extending into each iliac vein. There was old and recent 
infarction of lungs and kidneys. See Insp., 1892, No. 237. 


2642 Sarcomatous Thrombus in Pulmonary Artery. 

The pulmonary artery of a child, mounted, to shew in its 
left division a mass of malignant deposit adherent to its 
wall and partially occluding its lumen. The deposit is of 
soft consistency, has a rough surface, and histologically 
has the structure of a sarcoma. 


Thomas M., et. 5, was admitted under Mr. Durham for a large 
tumour on the left side of the abdomen, which proved to be a sarcoma 
of the kidney. The child became emaciated and dyspneic, and during 
the latter part of his life cyanosed. At the autopsy the liver was found 
to be much enlarged by secondary deposits. The kidney-tumour 
weighed thirty-four ounces. See Insp., 1893, No. 11; and Trans. 
Path. Soc., vol. xliv., 1898, p. 48. 











LIST 


OF 


GENTLEMEN EDUCATED AT GUY’S HOSPITAL 


WHO HAVE PASSED THE 


EXAMINATIONS OF THE SEVERAL UNIVERSITIES, COLLEGES, 
&c., &c., 


IN THE YEAR 1903. 


ülnibersity of Oxford. 


Degree of Doctor of Medicine. 
G. G. Davidson. 


Degree of Master in Surgery (M.Ch.) 
F. E. Fremantle. ; 


Second М.В. Examination. 
Medicine, Surgery, Midwifery, Forensic Medicine and Public Health. 


J. M. Bickerton. | P. N. Blake Odgers. | W. E. Robinson. 
A. R. Wilson. 





Anibersity of Cambridge. 


Degree оў Doctor of Medicine. 
J. G. Taylor. 


Final Examination for the Medical and Surgical Degrees. 


Part II. 
H. A. Ackroyd. J. S. Cooper. C. M. Murray. 
E. Bigg. — H. A. Cutler. F. Richmond. 
A. R. Brailey. J. H. Donnell. c R. D. Smedley. 
W. H. Brailey. F. B. Manser. A. Wylie. 

Part I. 
A. R. Brailey. R. E. French. C. W. Ponder. 
S. Child. A. H. Miller. C. M. Stevenson. 
J. S. Cooper. Е. W. М. Palmer. B. H. Stewart. 

A. Wylie. 





402 Gentlemen admitted to Degrees, £c., in the year 1903. . 


Second Examination for the Medical and Surgical Degrees. 


F. A. Barker. C. F. Fothergill. | C. W. Greene. 
R. Davies-Colley. G. W. Goodhart. | С. W. de Р. Nicholson. 


Examination in Sanitary Science. 
A. Armer. | G. E. Richmond. | G. Warwick Smith. 


Gnibersity of London. 
Examination for the Degree of Doctor of Medicine. 


T. P. Berry. Е. С. Gibson. W. М. Robson. 
G. Clarke. S. Hodgson. L. E. Stamm. 
D. Forsyth. G. E. Richmond. C. Tessier. 


H. Nolan (State Medicine). 
Obtained the Gold Medal. 


Examination for the Degree of Master in Surgery. 
G. E. Manning. | R. P. Rowlands. 


Examination for the Degree of Bachelor of Surgery. 
First Division. 


H. Watts. 
Obtained the Gold Medal. 


C. H. Robertson. 
Obtained Honours. 


H. McD. Parrott. | A. M. Webber. | G. T. Wrench. 
Second Division. 

J. Evans. G. Lewin. | N. Ivens Spriggs. 

T. Holmes. E. H. B. Milsom. W. C. Swayne. 


Examination for the Degree of Bachelor of Medicine. 


May. 
Second Division. 

W. F. Box. | E. G. Goldie. H. McD. Parrott. 
J. Braithwaite. A. C. H. Gray. G. W. Smith. 
Н. S. Brown. G. Lewin. E. W. Strange. 
F. W. Fawssett. L. H. Moiser. | H. Tipping. 
L. S. H. Glanville. D.L. Morgan. D. H. Trail. 

| A. H. E. Wall. 





Gentlemen admitted to Degrees, Ёс., in the year 1903. 408 


October. 
First Division. 
G. T. Wrench. 
Obtained Honours in Medicine and Forensic Medicine. 


C. D. Pye-Smith. | Н. Watts. 


Second Division. 
N. Ivens Spriggs. 


Obtained Honours in Medicine and Forensic Medicine. 


A. M. Webber. 
Obtained Honours in Forensic Medicine. 


P. R. Bolus. R. A. Greeves. E. H. B. Milsom. 
H. M. Goldstein. R. Larkin. H. F. B. Walker. 
B. H. Wedd. 


Intermediate Examination in Medicine. 


January. 


Entire Examination. 
Second Division. 
E. H. Adams. E. M. Harrison. 


W. P. Purdom 
T. H. Barton. H. 8. Knight. F. A. Sharpe 
R. J. Bentley. E. F. Milton. H. A. Watney 
G. Hamilton. T. C. Pocock. F. T. H. Wood 

Physiology only. 

Second Division. 

I. R. Cook. 
А July. 


Honours Examination. 


G. Cockcroft. 
Obtained the Exhibition and Medal in Anatomy and Honours in Physiology 
and Histology. 


T. B. Layton. 
Obtained First Class Honours in Anatomy. 


J. 8. Bookless. 
Obtained Honours in Anatomy. 


Entire Examination. 
First Division. 
W. H. Trethowan. 


Second Division. 


Е. Alban. Е. С. Lowe. P. S. Mills. 
A. W. Berry. P. F. McEvedy. Н. F. Vandermin, 
С. С. A. De Villiers. W. Н. Miller. Т. Е. Wilson. 


Physiology only. 
Second Division. 
P. C. P. Ingram. 


MEL TR 





404 Gentlemen admitted to Degrees, £c., in the year 1903. 


Preliminary Scientific (M.B.) Examination. 


January. 
Entire Examination. 
First Division. 


S. C. H. Air. | E. L. W. Mandel. | M. D. Price. 
Second Division. 

H. R. Bastard. A. L. Gardner. H. E. Perkins. 

R. C. V. Edsall. J. B. Martin. S. G. Tracy. 


Chemistry and Experimental Physics. 








M. E. Ball. T. Evans. B. McDermott. 
A. F. W. Denning. H. J. Henderson. T. E. Price. 
J. B. Dunning. K. H. Hole. G. F. Syms. 
Biology. 
S. S. Brook. | G. B. Harland. | D. Reynolds. 
| H. J. Smith. 
July. 


Entire Examination. 
First Division 
M. M. Adams. | H. B. Carter. | E. L. M. Lobb. 
T. Stansfield. 


Second Division. 


S. Chelliah. | W. Johnson. | A. E. Lees. 
P. S. Price. 


Chemistry and Experimental Physics. 


5. S. Brook. | G. B. Harland. 
Biology. 
M. E. Ball. K. H. Hole. B. McDermott. 
J. B. Dunning. H. C. Lucey. N. A. D. Sharp. 


Intermediate Examination in Science. 


Honours Candidate recommended for a Pass. 
8. G. Tracy. 


Intermediate Examination in Science and Preliminary Scientific 
Examination conjointly. 
H. A. Sanford. 





Gentlemen admitted to Degrees, £c., in the year 1903. 405 


` Anibersity of Burham. 


Examination for the Degree of Doctor in Medicine. 
H. C. Sturdy. 


Examination for the Degree of Doctor of Medicine for Practitioners 
of Fifteen Years’ Standing. 
G. F. Hugill. | E. Sharpley. 


Final Examination for the Degrees of Bachelor of Medicine 
and Surgery. 


B. Glendining. | J. G. O. H. Lane. | A. A. Miller. 
A. Reid. 


Third Examination. 
C. M. Anthony. | B. W. Lacy. 
Chemistry and Physics. 


First Examination. 


L. K. Fdmeades. |, T. H. V. King. 
J. F. Young. 


Anatomy and Biology. 


Н. С. W. Allott. | E. R. H. Joynt. 
H. F. Joynt. 


Royal College of Physicians of Fondon. 


Elected to the Fellowship. 
A. P. Beddard. | E. Goodall. 


Eramination for the Diploma of Membership. 
J. G. Taylor. 


Final Examination for the License. 


January. 
W. F. Box. i W. H. Cole. 1 A. W. Iredell. 
A. R. Brailey, | F. W. Fawssett. | C. B. Penny. 
S. Child. =” P. W. Hamond. |. V. M. Wallis. 





406 Gentlemen admitted to Degrees, «c., in the year 1908. 


odds 


K. Black. 

P. R. Bolus. 

J. S. Cooper. 

C. F. Fraser. 

J. Goss. 

G. W. C. Hollist. 


July. 


. E. Iredell. 
. Larkin. 


Piggott. 


Op NEKO 


. H. 

. A. Peall. 
. P. 

. D. 


October. 
‚ S. Jones. 


‚ С. Lucas. 
. H. Wallace. 


inizi 


B. Milsom. 


Pye-Smith. 


. Collins Lewis. 


. Robinson. 
. Shattock. 

. Wedd. 

. Winckworth. 


A. M. Webber. 
R. Willan. 


Royal College of Surgeons of England. 


F. E. Fremantle 


J. G. O. H. Lane. 


W.G. Mumford. 


Final Examination for the Fellowship. 


E. A. Peters. 
C. H. Robertson. 


First Examination for the Fellowship. 


T. H. Barton. 
L. H. Burner. 
G. Cockcroft. 


R. Davies-Colley. 


A. G. Jones. 


T. B. Layton. 
G. C. F. Robinson. 
W. Welchman. 


Examination for the Diploma in Public Health. 


R. F. Clark. 


H. Hewetson. 


Final Examination for the Membership. 


R. G. Anderson. 
P. C. V. Bent. 
S. C. Bowle. 

W. Johnson. 

J. H. Atkins. 
W. H. Bowen. 
P. W. L. Camps. 
J. A. Andrews. 
J. B. Ball. 

A. S. Bankart. 
G. N. Bartlett. 
W. F. Box. 

A. R. Brailey. 

S. Child. 

J. D. Bridger. 
G. L. Buckeridge. 
C. H. Dawe. 

J. F. Douse. 

E. G. Goldie. 

H. M. Goldstein. 





January. 
. Cole. 


W. H 
F. W. Fawssett. 
P. W 


. Hamond 


April. 
C. Mann. 


Pearson. 
Rahim. 

‚ W. Read. 

. Roberts. 


. C. 
. Moir 
. D. 

. I. 


ij ira 


W. Iredell. 
B. Penny. 
M. Wallis. 


SaS 


F. C. Robinson. 
C. R. Shattock. 
H. Watts. 

B. H. Wedd. 
H. С. Winckworth. 


Gentlemen admitted to Degrees, «tc., т the year 1908. 


K. Black. 

P. R. Bolus. 
J. S. Cooper. 
С.Е. oo 


9. W. С. Hollist 


| V. Bent. 


H 

A. 

>Р. Piggott. 
. D. Pye-Smith. 


October. 


H. 8. Jones. 

W. Collins Lucas 
T. C. Lucas. 

F. H. Wallace. 


A. M. Webber. 
R. Willan. 


Society of Apothecaries of Rondon. 


. Bradbury. 
‚ Collier. е 


G. І. Buckeridge. 


Н. V. Bagshawe. 
R. T. Collins. 
A. С. Н. Gray. 


H. C. Keats. 





E. Н. Griffin. 
D. В. T. Griffith. 
G. В. S. Soper. 


| A. W. Iredell. 


F. M. M. Ommanney. 


S. L. Pallant. 
C. H. Robertson. 


W. A. G. Stevens. 


F. J. Turner. 
A. J. Urquhart. 


Habal Medical Serbice. 


| F. M. V. Smith. 


Royal Army Medical Corps. 


G. Warwick Smith. 


F. J. Turner. 


M. C. Wetherell. 


Indian Medical Berbice. 


W. E. J. Tuohy. 


407 


408 Medallists and Prizemen. 


MEDALLISTS AND PRIZEMEN, 
JULY, 1904. 


Open Scholarships in Arts. 


Sydney John Darke, Owen’s School, Islington, £100. 
Jean René Perdrau, Royal College, Mauritius, £50. 
Guy Barton Cockrem, King’s School, Canterbury, Certificate. 


Open Scholarships in Science. 


Harry Archibald Sanford, Guy's Hospital, £150. 

Leonard Tilsley Baker, Dulwich College, £60. 

William Johnson, Guy’s Hospital Equal 
Vincent Townrow, University College, sheffield} Certificates. 


Scholarship for University Students. 
Charles William Greene, Emmanuel College, Cambridge, £50. 


Open Scholarships in Dental. Mechanics. 


October, 1903, Robert Charles Basker Shaw, £20. 
May, 1904, George Packham, £20. 


Junior Proficiency Prizes. 


Kenelm Hutchinson Digby, £20. 
Ernest William Giesen, £15. 

Thomas Edmund Ashdown Carr, £10. 
George French Stebbing, Certificate. 


The Michael Harris Prize for Anatomy. 
Kenelm Hutchinson Digby, £10. 


The Sands Cox Scholarship in Physiology. 


Ernest William Giesen, £15. 
` Kenelm Hutchinson Digby, Certificate. 


The Hilton Prize уот Dissections (1908). 


Patrick Francis McEvedy, £3. 
William Henry Miller, £1. 
William Henry Trethowan, £1. 

(1904 Kenelm Hutchinson Digby, £1 18s. 4d. 
Ernest William Giesen, £1 13s. 4d 
Christian Hugo Rippman, £1 18s. 4d. 


Medallists and Prizemen. 409 


The Arthur Durham Prizes Jor Dissection. 


Furst Year's Students. 


Edward Leslie Martyn Lobb, £5. 
Thomas Stansfield, Certificate. 
William Johnson, Certificate. 
Howard Bernard Carter, Certificate. 


Senior Students. 
Ernest William Giesen, £15. 


Dental Prizes. 


Furst Year's Students. 


Robert Charles Basker Shaw, £10. 
Arthur William Parrott, Certificate, 


Practical Dentistry Prize. 


James William Mawer, £10. 
Julian Bollard, Certificate. 


Travelling Dental Scholarship. 
John Edmund Spiller, £100 


The Beaney Prize for Pathology (1903). 
Neville Ivens Spriggs, £34. 


The Treasurer's Gold Medal for Clinical Medicine. 
Arthur Frederick Hertz. 


The Treasurer's Gold Medal for Clinical Surgery. 
Arthur Frederick Hertz. 


The Golding-Bird Gold Medal and Scholarship in Bacteriology. 


Charles Morley Wenyon, £20. 
Maurice George Louisson, Certificate. 


VOL. LIX. 29 


410 Hospital Appointments held in the year 1903. 


THE PHYSICAL SOCIETY. 


Honorary President, —Sir Samuel Wilks, Bart., M.D., LL.D., F.R.S. 
Secretaries.—E. I. Spriggs, M.D., R. P. Rowlands, M.S. 


Presidents. 


Kenneth Black, G. Evans, M.B., E. H. B. Milsom, M,B., B.S., H. F. B. 
Walker, M.B., F. W. M. Palmer, B-A., G. A. Ticehurst, B.A., W. M. Mollison, 
B.A., A. R. Brailey, B.A., M.B., B.C., H. C. Cameron, M.A., J. 8. Cooper, 
M.A., M.B., B.C., A. F. Hertz, B.A., M.B., B.Ch., P. A. Peall, M.B., G. 
Russell, M.B., N. I. Spriggs, M. B., B.S. 


Photographic Committee. 
E. W. Shenton, D. H. Trail, M.B., H. Mann, M.B. 


The Society’s Prize of £10 was awarded to Mr. N. Ivens Spriggs, M.B., 
B.S., for his paper on “ The Diagnosis and Treatment of Coma,” and Mr. J. 
Sephton Cooper, M.A., M.B., B.C., gained the Treasurer's Prize of £5 for his 
paper, ** The Uses of Light and Electricity in Surgery.” 


CLINICAL APPOINTMENTS HELD DURING THE 
YEAR 1908. 


HOUSE PHYSICIANS. 


H. Barber. d C. Tessier. S. Hodgson. 
G. T. Wrench. M. J. Rees. H. A. Cutler. 
D. H. Trail. G. Evans. 


HOUSE SURGEONS. 


C. H. Robertson. F. C. Wetherell. A. R. Thompson. 
O. W. Richards. E. Faulks. | H. Parker. 
C. R. Howard. T. Morland Smith. 
ASSISTANT HOUSE SURGEONS. 
M. J. Rees. D. H. Trail. N. N. A. Houghton. 
F. L. Thomas, E. Faulks. O. W. Richards. 
A. R. Thompson. P. W. Hamond G. Evans. 
F. D. S. Jagkson . F. H. Parker C. R. Howard 
B. Glendining. T. Morland Smith. B. H. Wedd 
D. L. Morgan. G. E. Malcomson. H. Tipping 
F. W. Fawssett. K. Black. H. C. C. Mann. 
A. R. Brailey. H. S. Brown. L. S. H. Glanville. 
ASSISTANT HOUSE PHYSICIANS. 
S. Hodgson. G. T. Wrench. M. J. Rces. 
H. A. Cutler. G. Evans. D. H. Trail. 
B. Glendining. G. E. Malcomson, 


Hospital Appointments held in the year 1903. 


UO bo to 


RESIDENT OBSTETRIC ASSISTANTS. 


А. С. Н. Gray. 
F. L. Thomas. 


H. Tipping. 
R. G. Anderson. 
A. R. 

H. C. C. Mann. 
W. F. 

F. H. Wallace. 

B. 


Glendining. 


F. H. Wallace. 

S. C. Bowle. 

E. H. B. Milsom. 
A. M. Webber. 

Н. М. Woodward. 


Н. Вагрег. 
R. Moyle. 
S. C. Bowle. 


C. J. Pinching. A. C. Ransford. 
L. H. Moiser. G. S. Robertson. 
N. Blake Odgers. F. D. S. Jackson 
| CLINICAL ASSISTANTS. 
K. Faulks. T. Morland Smith. 
Evans. H. S. Brown. 
H. Wedd. N. I. Spriggs. 
E. Malcomson. K. Black. 
W. Fawssett. L. S. H. Glanville. 
W. Strange. C. H. Reinhold. 
Goldie. P. A. Peall. 
W. Hamond. C. R. Howard. 
CLINICAL ASSISTANTS IN THE MEDICAL WARDS. 
H, Ackroyd. H. D. Smart. 
Н. F. B. Walker. F. P. Hughes. 
J. S. Cooper. P. A. Peall. 
G. A. Ticehurst. C. D. Pye-Smith 
H. H. Jenkins. M. G. Louisson. 
Е. С. Myott. 
CLINICAL ASSISTANTS IN THE SURGICAL WARDS. 
Е. С. В. Knight G. L. Buckeridge. 
J. W. Раад. P. L. Bolus. 
J. M. Barrionuevo. F. G. Goble. 
P. F. Minett. M. B. Taylor. 
J. Cook 


. Cole. 
. Lowe. 


. F. 

. Richards. 
. Webber. 

. Bridger. 

. Carter. 
'anklin. 
ussell. 

. Cheyney. 
acs. 

. Pollard. 

. Myott. 


SOR PUER 


> Ei Ede 
као 
®© et 
"X 


. Cook. 

. S. Littlejohns. 
. C. Hughes. 

. O. Musson. 
. D. Wyatt. 


cp c 
gm 


. P. Costobadie. 
. B. Cocker. 

. M. Wenyon. 
. о. Williams. 


mo» 


Kynaston. 


Hb pg EE Om} 


SURGEONS’ DRESSERS. 


M. G. Louisson 
W.S. Orton. 
M. J. Mottram 
R. M. Rendall. 
E. Lloyd. 

G. H. Rees. 

B. Moiser. 

C. P. Harvey. 
F. Rogerson. 

J. W. Barrionuevo. 
A. F. Hertz. 

A. M. Benett. 


H. M. Clarke. 

‚ Е. Minett. 
Felton. 

M. Stevenson. 
R. Beaumont. 
J. Orpen. 

M. Longson. 
Doudney. 

P. Lewis. 

. A. Chisholm. 
. Turner 


G. W. C. Hollist. 


. Jenkins. 
. Maybury. 
. Ticehurst. 

. S. Dismorr. 

. Payne. 

. M. Palmer. 
.F. Robinson. 
. Thomas. 

. Rowlands. 
arnes. 

. Clatworthy. 
. Mollison. 
. May. 

‚ Wells. 

. Roome. 


Ma Pa 


EE ug Bg 


tik 

کج 
Ф‏ 
n‏ 


eming. 
. Sheaf. 
eeve. 
. Clarke. 

. Davies. 

. S. Dyson. 
. Mitchell. 
. Wyatt. 

aher. 


EEHUPHzEPLPUIZLHHELHOHNOOQ»IE 
E 


BOS" OR 


411 


412 Hospital Appointments held in the year 1903. 


. Prentis. 
useell. 


ei 


. F. Minett. 

. S. Littlejohns. 
. M. Stevenson. 
. M. Roome. 

. M. Wells 

. Cook. 


o 


. B. Cocker. 

. O. Williams. 

. Maher. 
. M. Wenyon 

. P. Costobadie. 
A. C. Greene 

. de L. Robinson 
. C. Cameron. 
. H. Macalister 
. F. Greening. 
. H. Oliver. 
. H. Miller. 


со Asa dd Hua aoo 


G. Goldie. 
W. Dadd. 
H. Clatworthy. 
J. 


E. 
J. 
J. 
M. J. Mottram. 


. Barrionuevo. 


C. P. Harvey. 
J. E. Spiller. 
D. Isaacs. 

A. M. Benett. 
B. B. Westlake. 
W. Reeve. 


. P. 

. V. Mitchell 

. H. Clough. 

. À. Chisholm. 

. Turner. 
R. Preston. 
Jacobson. 
Crew. 


Barron. 
Langdale. 
Pollard. 


> | 


DENTAL SURGEONS’ DRESSERS. 


C. F. Fraser. 

H. D. Smart. 

F. H. Wallace. 

L. S. Н. Glanville. 


. W. 

. D. 

. D. 

. A. P. Costobadie. 
. D. 
. M. 

ОМ. 


ASSISTANT SURGEONS’ DRESSERS. 


. Н. Clatworthy. 
. N. Ma 


ay. 
. W. Routley. 

. Rogerson. 

. R. Beaumont. 
P Orpen. 


. Welchman. 


b" 
un 
© 
P, 
Ф 
m 


. Doudney. 
. G. Davies. 
. W. Allen. 
‚ В. O’Brien. 
. E. French. 
. D. Crofts. 
. McPherson. 
. C. N. Dickey. 


xa A A gie dal HD 


C. H. Dawe. 

C. H. Reinhold 
E. H. B. Milson 
G. H. Rees. 


CLINICAL ASSISTANTS IN MEDICAL OUT-PATIENTS. 


S. C. Bowle. 
F. Richmond. 
R. D. German. 
J. B. Copland. 
H. H. Jenkins. 
W. N. May. 


. Tipping. 

. W. Fawssett. 
. H. Donnell. 
. Black. 

. Watts. 

. À. Greeves. 
. H. Reinhold. 
J. S. Cooper. 
B. Moiser. 

B. Muir. 

C. E. Iredell. 


H. M. Goldstein. 
F. C. Robinson. 
J. Goss. 

T. C. Lucas. 

P. P. Cole. 


OPHTHALMIC DRESSERS. 


R. G. Anderson. 
A. R. Brailey. 


J 

R 

M. G. Louisson. 
H. Meade King. 

E. L. Ward. 

G. A. Ticehurst. 

L. H. Frankenberg. 


H. Moyle. 

B. B. Westlake. 
E. J. Crew. 

M. J. Mottram. 
C. M. Murray. 


. Woodward. 
. Strange. 
. Osburn. 
. Winckworth. 
. Pye-Smith. 
. Smart. 
. Carter. 
rlisle. 
. Hollist. 
. Wilson. 


> OO bh O m 
Ro pmUUS OE 


Hospital Appointments held in the year 1908. 


413 


DRESSERS IN THE THROAT DEPARTMENT. 


B. H. Wedd. 

N. I. Spriggs. 
C, H. Reinhold. 
E. L. Ward. 

G. Louisson. 
у, Payne. 

Е. В. Walker. 
А, 


М. 
О. 
Н. 
G. Ticehurst. 


B. B. Westlake. 
B. H. Stewart. 


. Myer 

Littlej ohns. 
Hughes. 
Oliver. 
Costobadie. 
Lennox Jones. 
Greening. 

Scales. 


. R. 
. S. 
. C. 
. H. 
. P. 
. H. 
. F. 
Е. 
М 
. М. Langdale. 
‚ A. Р. Costobadie. 
B. O’Brien. 
. C. Cameron. 
. H. K. Macalister. 
. McPherson. 
. P. Purdom. 
. S. Knight. 
. A. Sharpe. 
. B. Smith. 
. T. Wight. 
. W. Nicholson. 
M 
G 
R 
. C. 
. F. 


vus о eae as 


. M. Roome 
2. C. Hughes. 
. A. Chisholm. 
. Alcock. 
. de L. Robinson. 
. M. Langdale. 
. H. Macalister. 
. A. 
. E. 


=, 


Sharpe. 
Rendle. 


PAOmS soap ' 


E. G. Goldie. E. W. Strange. 
L. 8. H. Glanville. E. H. B. Milsom. 
S. L. Pallant. G. S. Robertson. 
K. Black. H. Watts. 
A. M. Webber R. G. Anderson. 
F. H. Wallace. H. M. Woodward. 
P. P. Cole. H. H. Carter. 
T. C. Lucas. | D. R. Pike. 
CLERKS IN THE THROAT DEPARTMENT. 
C. S. Morris F. Barnes. 
3. F. Hardy M. B. Taylor. 
R. M. Rendall A. H. Miller. 
MEDICAL WARD CLERKS. 
J. O. Musson. A. Leeming. 
P. A. 8. Dyson. A. M. Roome. 
J. Cook. P. F. Minett. 
R. Edridge. S. M. Wells. 
C. M. Stevenson. L. J. Orpen. 
H. M. Clarke. E. W. Sheaf. 
L. Doudney. R. O. Williams. 
F. M. Longson. T. Turner. 
A. H. Clough. A. B. Cocker. 
R. P. Lewis. H. V. Mitchell. 
L. G. Davies. Е. Alcock. 
R. A. Chisholm. J. A. C. Greene 
С. W. R. Preston. R. W. Allen 
A. D. Crofts. М. С. Dickey 
М. де L. Robinson. R. D. Barron 
F. D. Crew. R. E. French 
A. H. Miller. M. Maher 
E. Patterson-Clavier. G. Hamilton 
E. H. Adams. R. T. Bentley 
M. Leckie. E. F. Milton. 
A. H. Watney. F. T. Н. Wood 
В. В. Metcalfe. T. Norman. 
К. S. Harper. E. E. Rendle. 
A. Morris. T. C. Pocock. 
G. N. Bartlett. T. H. Barton. 
L. H. Burner. W. S. H. Burney 
T. R. Harvey. E. White. 
J. H. Mayston. G. H. Morris 
H. G. Gibson. A. 8. M. Palmer 
ASSISTANT PHYSICIANS’ CLERKS. 
E. W. Sheaf. A. Leeming. 
A. R. Beaumont. R. Felton. 
F. Lennox-Jones. H. V. Mitchell. 
R. P. Lewis. T. Turner. 
F. M. Longson. W. C. Dickey. 
F. D. Crew. A. H. Miller, 
E. Patterson-Clavier. H. C. Cameron, 
T. C. Pocock. F. T. H. Wood. 
H. F.. Wight. R. S. Harper. 
E. B. Smith. G. Hamilton. 


414 Hospital Appointments held in the year 1908. 


. A. C. Greene 
. Allen. 

. 0 Brien. 

. Crew. 


. Dickey. 
. Wingent. 
. Adams. 
. Milton. 


е. 


C. H. Dawe. 
A. C. Osburn. 
G. F. Hardy. 


H. S. Jones. 

J. Bromley. 

M. J. Mottram. 
B. Moiser. 


D 


. Robinson. 
. M. Palmer. 
. R. Preston. 
W 


"mn mnorz 


. C. Bowle. 
eeve, 


M. Palmer. 
Mollison. 


puuman 


.R 
.H. 
. L. Ward. 
. W. 
. M. 


. H. Macalister. 


Frankenberg. 


SURGICAL WARD CLERKS. 


Н. М. Langdale 


V. А. Р. Costobadie. 
М. де L. Robinson. 


R. E. French. 
A. H. Miller. 
. M. Barron. 
. Hamilton. 


Litchfield. 
Lowe. 
Eyles. 

R. Norton. 


ое 


J 
A 
F 
P 
G 
H 
H 
‚Н 
. М. Bartlett. 
‚ С. 
‚ ©. 
. W. 
. L. 
S 
. G. 
W 
. W. 


C. H. Reinhold. 
E. Lloyd. 
Е. Р. Hughes. 


AURAL SURGEON’S DRESSERS. 


C. H. Denyer. 
F. H. Wallace. 


W.'T. Meade King. 


F. G. Goble. 


A. Pallant. 


H. 
W. H. Robinson. 
H. 
T. B. Layton. 


POST-MORTEM CLERKS. 


Е. С. Robinson. 
E. H. B. Milsom. 
F. G. Goble. 

E. C. Myott. 

R. M. Rendall. 





. D. Crofts. 

. С. Cameron. 
. McPherson. 

. W. Nicholson. 
. Maher. 

. Leckie. 

. S. Knight. 
. T. H. Wood. 
. S. Harper. 
. C. Pocock. 
. B. Ball. 

. R. Harvey. 
. F. Fothergill. 
. S. M. Palmer. 
. R. Cook. 

. Morgan. 


ті 


. Alban. 

. F. McEvedy. 

. C. De Villiers. 

. M. Ockwell. 
7. Н. Trethowan. 
. Vandermin. 


о 


CLERKS ІМ THB SKIN DEPARTMENT. 


T. Morland Smith. 
E. Morgan. 


. Е. N. Jupp. 


H. Watts. 
C. M. Murray. 


ASSISTANT SURGEONS’ CLERKS. 


R. Moyle. 

B. H. Stewart. 
E. Lloyd. 

Е. Р. Hughes. 
W.N. May. 


‚ Black. 
T 

. R. Wilson. 
‚Р. 

‚ Н. Jenkins. 
. H. 

.E 


F. Kynaston. 


POP D> ga 


. McF. Pollard. 
. V. Maybury. 


. O. Mann. 
. Wilson. 
. Lacy. 
. Woodward. 


i daos 
©. 
OE 


. G. Seagrove. 
‚ Peall. 
. Morris. 
. Spiller. 
. Mottram. 
loyd. 
‘Rendall. 


ok. 
. Minett. 
. Rees. 
. Mvott. 
. M. Palmer. 
аасв. 
. Maybury. 
rrionuevo. 
. Lictlejohns. 
. Beaumont. 
. Prentis. 
. Clatworthy. 


dard aed 


a ta pe p SH P» OH Ed (o I EH ed d i S OP IU t pL E > Ш 


SCR 


. B. Travers. 
. Watts. 
. O. Bradbury. 
oyle. 
. Hamond. 
. Fraser. 
. M. Beadnell. 
. Westlake. 
. Rey. 
. Lucas. 
\ckroyd. 
. Payne. 
. Pike. 
. Taylor. 
. Bickerton. 
'omley. 
. Maybury. - 
A. Ticehurst. 
. M. Mollison. 


o 
SE 


e 


Meade King. 


Frankenberg. 


Hospital Appointments held in the year 1903. 415 

OBSTETRIC DRESSERS. 
H. Watts. F. G. Goble. 
B. W. Lacy. Н. С. С. Mann 
G. 8. Robertson. J. Goss 

. R. Larkin. M. J. Zottram. 

| W. Е. Box. | P. A. Реал. 

' J. Е. Prentis. ‚ P. P. Cole. 
C. J. З. Dismorr. O. V. Payne. 
Е. В. Lowe. А. М. Benett. 
E. J. Crew. 

EXTERN OBSTETRIC ATTENDANTS. 

D. H. Smart. F. H. Wallace. 
E. L. Ward. G. Carlisle. 
G. F. Hardy. M. B. Taylor. 
H. O. M. Beadnell. L. H. Fraakenberg. 
Е. Р. Hughes. В. А. Greeves. 
В. Н. Stewart. J. F. Rey. 
F. Barnes. F. Rogerson. 
C. D. Pye-Smith. A. F. Hertz. 
A. M. Webber. M. G. Louisson. 
O. V. Payne. G. A. Ticehurst. 
H. H. Carter. W. S. Orton. 
H. H. Jenkins. P. P. Cole. 
J. D. Thomas. H. F. B. Walker. 
A. E. F. Kynaston. B. Moiser. 
J. M. Pollard. W. N. May. 
R. P. Rowlands. C. G. Dismorr. 
R. D. Bridger. G. H. Cheyney, 
E. W. Routley. M. Maher, 
R. Frankiin. C P. Harvey. 
A. M.. Benett. A. H. Clough. 
J. E. Scales. W. M. Mollison. 
G. S. F. Robinson. L. Myer. 
A. M. Roome. | J. O. Musson. 

CLERKS TO ANZESTHETISTS. 
P. R. Bolus G. F. Hardy. 
J. S. Cooper K. Black. 
B. H. Wedd P. A. Peall. 
C. D. Pye-Smith W. F. Box. 
E. L. Ward. R. Moyle. 
B. H. Stewart : Е. G. Goble. 
R. A. Greeves D. Isaacs. 
E. H. B. Milsom H. S. Jones. 
C. R. Shattock. H. F. B. Walker. 
W. T. Meade King. C. E. Iredell. 
F. H. Wallace. A. M. Webber. 
M. G. Louisson. H. H. Jenkins. 
E. H. Griffin. J. W. Dadd. 
C. M. L. Cowper. J. S. Cooper 
R. M. Rendall. R. Willan. 
W. H. Bush. | E. W. Routley 
E. C. Myott. H. H. Carter 
E. C. Hughes. | R. D. Bridger 
A. M. Benett. | W, N. May. 
B. W. P. P. Cole. 


. H. Rees. 
. Barnes. 


ee 


Lacy. | 


416 Hospital Appointments held in the year 1908. 


DENTAL SCHOOL | 
APPOINTMENTS HELD DURING THE YEAR 1903. 


DENTAL HOUSE SURGEONS. 


H. Croot. 
F. W. Parfitt. 


| E. Farrant. 


| H. P. Aubrey. 


ASSISTANT DENTAL HOUSE SURGEONS. 


G. L. Dymott. H. P. Hooper. F. W. Parfitt. 
W. H. Elwood. A. E. D. Prideaux. С. W. Randall. 
B. H. Martin. N. McL. Nibbs. | 








DEMONSTRATORS IN THE CONSERVATION ROOM. 


E. N. Plummer. C. W. Randall. W. H. Elwood. 

B. Glendining. B. H. Martin. J. H. Williams. 

N. McL. Nibbs. E. L. Pilbeam, i Н. Poyton. 

P. H. Hickman. J. W. Mawer. | A. Hammond Smith. 


N. McL. Nibbs. W. W. Vaughan. H. C. Collett. 

W. H. Elwood. F. N. Palmer. P. H. Hickman. 

T. R. B. Ellis. S. H. Peatfield. J. Stevenson Brown. 

S. H. Barlow. V. S. Houchin. J. F. Ryder. 

R. A. Scott. J. H. Williams. E. White. 

E. L. Pilbeam. A. E. D. Prideaux B. H. Martin 

R. Roberts. H. C. Malleson. W. H. Yeo. 

F. J. Goodman. H. Poyton. A. Hammond Smith. 

C. W. Randall. C. L. D. Taylor. G. E. Wood. 

R. J. Messent. H. E. H. Tracy. H. E. Warren Williams. 

J. W. Mawer. G. G. Timpson. R. E. Mungal 

J. B. Ball. F. H. Fuller. C. D. Wallis 

F. S. Vin». H. A. Pallant. J. Н. Williams. 

P. E Luce. F. A. Beckley A. H. Harris. 

F. L. Aubrey. F. A. Husbands H. J. Snowden. 

S. D. Marshallsay. W. Elwood J. Bollard. 

A.A. Forty. W. J. Wormald. H. M. Peacock. 
DRESSERS IN THE EXTRACTION ROOM. 

H. Poyton. T. L. Smith G. E. Rice. 

J. H. Williams. P. H. Hickman. S. D. Marshallsay 

R. M. Pearson. J. S. Vogvell. F. J. Goodman 

A. A. Forty. F. H. Fuller. F. A. Beckley 

H. J. Snowden A. Hammond Smith. E. J. Sheppard 

P. E. Luce. J. W. Mawer. F. S. Vine. 

W. Elwood. W. J. Wormald. F. A. Husbands 

W.J. C. Timberlake. J. Bollard. G. E. Wood. 

F. L. Aubrey. H. J. Russell. H. G. Pearce 

W. E. Cook H. A. Pallant. L. B. Moore 

A. Angell. H. M. Peacock. C. D. Wallis 

C. L. Pemberton. A. В. Durant. * R. G. Yates 

D. G. Wearing. H. Snell. А. S. Thomas 

H. E, Alexander. A. W, Parrott, 


R, G. H. Warner, 


DRESSERS IN THE GAS ROOM. 


Hospital Appointments held in the year 1903. 


417 


JUNIOR AND CASUALTY DRESSEBS. 


. L. Pilbeam. 

. Poyton. 

. J. Goodman. 
. Warren Williams. 
. Mawer. 


. Pallant. 
wood. 
. Wormald. 
. Peacock. 


ig se 
gupg оны: 

3 

© 


J. F. Ryder. 

. L. D. Taylor. 
. H. Yeo. 

. Fuller. 
3. Timpson. 
. Luce. 

. Aubrey. 

. Beckley. 
. Marshallsay. 
llard. 

‚ Houchin. 


ee 
SS 


. Peatfield. 
. Williams. 
. Messent. 
‚ Н. Tracy. 
. Mungal. 
. Snowden. 
arris. 
. Forty. 
. Husbands. 
. Pearce. 


Heer ШЕШЕН · 
moet 


Qe > 


DRESSERS IN THE CONSERVATION ROOM. 


. H. Martin. 
. Oates. 


v. 


Randall. 


Houchin. 
oyton. 

. D. Wallis. 

. H. Hickman. 
. L. Mason. 

. W. Bartle. 

. Glendining. 

. E. Holman. 

. E. Wood. 

. £i. Collett. 

. N. Palmer. 

. A. Scott. 

. W. Parfitt. 

. MeL. Nibbs. 
. W. Wallis. 

. A. Helyar. 

‚ J. Wormald. 
. A. Pallant. 

‚ б. Vine. : 
. A. Husbands. 
. О. Mungal. 

. Elwood. 

. E. Н. Tracy. 
. J. Sheppard. 
‚ В. Durant. 

‚ В. Moore. 

. A. Beckley. 


Eda sa a sane me duc alee 


. L; Aubrey. 

. A. Husbands, 
‚ М. Pearson. 
. S. Vine. 

. Angell. 

‚ A. Forty. 

. J. Sheppard. 
L. Pemberton. 
. S. Thomas. 

. E. Rice. 

‚ G. Wearing. 


UG» Ob > > ba чн 


. W. 

. E. Warren Williams. 
. S. 

.P 


. J. Messent. 
. L. Palmer. 
. Stevenson Brown. 


. V. 
.J. 
. E. Derriman. 
.H. Lennox-Jones. 
. H. Peatfield. 
. В. Beaumont. 
. J. Green. 
. H. Williams. 
. F. Minett. 

. Н. Elwood. 

. R. Penford. 

0. Trotter. 

. E. Luce. 

. N. Plummer. 

. White. 

. B. Cocker. 

. A. Beckley. . 
‘Hammond Smith. 
. Williams. 

: Mawer. 

. Pearson. 
‚ Luce. 
|. E. Cook. 
A. Angell. 


S о E 


P gn» B 
eR Se 


‚ А. А. Forty. 


R. А. Scott. 


A. Hammond Smith. 


PROBATIONARY DRESSERS. 


F. H. Fuller. 
J. W. Mawer. 
W. J. Wormald. 


W. J.C. Timberlake. 


W. E. Cook. 

J. S. Vogwell. 
L. B. Moore. 

N. P. Rodgers. 
H. E. Alexander. 
H. Snell. 
R. G. Yates. 


C. J. B. Kliszezwski. 
A. E. D. Prideaux. 
W. W. Vaughan. 

A. Harris. 


J 

. E. Preston. 

. E. Williams. 

. D. Marshallsay. 
. F. Ryder. 

. C. Malleson. 
. J. Goodman. 
. Bollard. 

. G. Timpson. 
. H. Williams. 
. G. Pearce. 

. M. Peacock. 
. Randall. 

. Malleson. 

. Aubrey. 

. Fuller. 

. Russell. 
. Vogwell. 


ENEE 


. Hammond Smith. 
. M. Peacock. 
. A. Beckley. 
. A. Pallant. 
. Elwood. . 
. J. Bollard. 
SL Gillett. 
. Scott-Foster. 
. W. Parrott. 
. G. H. Warner. 


GUY’S HOSPITAL. 





MEDICAL AND SURGICAL STAFF. 
1904. 
Consulting Physicians: Sir SAMUEL WILKS, Bart., M.D., LL.D., F.R.S. 
F. W. 


Pavy, M.D., LL.D., F.R.S.; 


P. 'H. Pyz-SMITH, M.D., 


F.R.S.; J. F. Goopnanr, M.D., LL.D. 
Consulting Surgeons: THomas Bryant, M.Ch. ; Sir Henry G. Howse, M.S. 
Consulting Obstetric Physician: A. L. GALABIN, M.D. 
Consulting Physician for Mental Diseases: G. Н. SíAvaaEg, M.D. 
Consulting Aural Surgeon.—W. LAIDLAW Punvres, M.D. 
Consulting Anesthetist.—Tom BIRD, Esq. 


Physicians & Assistant Physicians. 


FREDERICK TAYLOR, M.D. 
W. Hare WHITE, M.D. 
G. Newron Pirr, M.D. 
SIR Cooper PERRY, M.D. 
L. Е. SHaw, M.D. 

J. H. Bryant, M.D. 

J. Fawcett, M.D. 

A. P. BEDDABD, M.D. 


Obstetric Physicians. 
P. HORROCKS, M.D. 
J. H. Taraetr, M.S. 


Assistant Obstetric Physician. 
G. BELLINGHAM Өмттн,М.В.,В.8. 


Physician for Mental Diseases. 
MAURICE CRAIG, M.D. 


Physician in charge of Skin 
Department. 
SIR COOPER PERRY, M.D. 


Anesthetists. 
G. RowELL, Esq. 
Н. F. LANCASTER, M.D. 
C. J. OGLE, Esq. 
P. TURNER, M.S. 
А. W. ORMOND, Еве. 
H. T. Hicks, Esq. 
D. Коввүтн, M.D. 
A. G. Levy, M.D. 


Bacteriologist. 
J. W. Н. ЕүвЕ, M.D. 


Medical Registrars and Tutors. 
Н. В. FRENCH, M.D., B.Ch. 
Н. BABBEB, М.В. 


Obstetric Registrar and Tutor. 
Н. T. Hicks, Esq. 


Curator of the Museum. 
J. FAWCETT, M.D. 


Surgeons & Assistant Surgeons. 
В. CLEMENT Lucas, B.S. 
C. Н. GOLDING-BIRD, M.B. 
W. Н. A. Jacosgon, M.Ch. 
CHARTERS J. SYMONDS, M.S. 
W. ARBUTHNOT Lang, M.S. 
L. A. Dunn, M.S. 
SIR ALFRED Fripp, M.S., О.В. 
C.V.O. 
F. J. STEWARD, M.S. 
Ophthalmic Surgeons. 
C. HiGGENS, Esq. 
W. А. BBAILEY, Esq. 
Surgeon in charge of Throat 
Department. 
F. J. STEWARD, M.S. 
Surgeon in charge of Aural 
Department. 
C. H. Facas, M.S. 
Surgeon in charge of Actino- 
therapeutic Department. 
G. SICHEL, Esq. 
Dental Surgeons. 
F. NEWLAND-PEDLEy, Esq. 
W. A. Maaas, Esq. 
R. WYNNE Rouw, Ево. 
Assistant Dental Surgeons. 
Н. L. PiLLIN, Esa. 
M. F. Hopson, Esq. 
J. B. PanFITT, Esq. 
J. L. Payne, Esq. 
Radiographer, 
E. W. H. SHENTON, Esq. 
Surgical Registrar and Tutor. 
A. R. THOMPSON, M.B., Ch.B. 
Ophthalmic Registrar and Tutor. 
A. W. ORMOND, Esq. 


Lying-in Charity. 


Mr. TARGETT AND Mr. BELLINGHAM SMITH. 


Dean of the Medical School and Warden of the College. 
H. L. Eason, M.D., М. 8, 


LECTURERS AND DEMONSTRATORS. 


Clinical Medicine ... ... ... 
Clinical Surgery 


Medicine ; 
Practical Medicine 
Surgery 


Operative Bug 
Practical Surgery 


Practical Obstetrics ... 
Mental Diseases ... 
Ophthalmic Surgery ... 
Dental Surgery ... 
Aural Surgery ... ... 
Diseases of the Skin ... 
Diseases of the Throat 
Electro- Therapeutics... 
Actinotherapeutics 
Anasthetics... ... 
Hygiene and Public Health 
Pathology 


Pathology 
Morbid Anatomy 


Morbid Histology and Bacteriology 
Medical and зма 101100004 


Classes .. 
Bacteriology 


Forensic Medicine 
Anatomy 
Practical Anatomy 


Phystology ... - 
Practical Physiology ... 


Materia, Medica and Therapeutics ... 


Practical Pharmacy ... 
Chemistry ТР 
Practical Chemistry ... 
Experimental Physics — ... 


.. THE PHYSICIANS AND ASSISTANT PHY- 


SICIANS. 


. THE SURGEONS AND ASSISTANT SUR- 


GEONS. 


. DR. TAYLOR AND Dr. HALE WHITE. 
. DB. FRENCH AND Mr. BARBER. 
‚ Мв. Lucas AND MR. GOLDING-BIRD. 
. SIR ALFRED FRIPP AND MR. STEWARD. 
es ooo oo Mr. A. R. THOMPSON. 
Midwifery and Diseases of Women... 
.. MR. Hicks. 
. Ов. M. CRAIG. 
.. Мв. BRAILEY. 
. Mr. Wynne Rouw. 
. Мв. Faaae. 
. SIR COOPER PERRY. 
‚ MR. STEWARD. 
.. DB. BRYANT. 
. Mr. G. SICHEL. 


Рв. HORROCKS AND MR. TARGETT. 


Мв. ROWELL. 


. Ов. SYKES. 
e ‚. DR. Рітт. 
Gordon Lecturer on Experimental 


. рв. Boxcorr. 


. Dr. FAWCETT AND Dr. BEDDARD. 


Mr. BELLINGHAM SMITH AND Dr. EYRE. 


. Dr. FAWCETT AND Mr. STEWARD. 


. Dr. EYRE. 

. SIR THOMAS STEVENSON. 

. Mr. Dunn AND SIR ALFRED FRIPP. 
. MR. FAGGE, Mr. ROWLANDS AND 


Mr. TURNER. 


... DR. PEMBREY. 
. Dr. PEMBREY, Dr. SPRIGGS AND 


Dr. FORSYTH. 
Dr. Bryant. 


. THE HOSPITAL PHARMACIST. 

. Ов. WADE. 
. DR. WADE, MR. RYFFEL AND Мв. BALL. 
. PROFESSOR  REINOLD, 


F.R.S., AND 


Мв. BALL. 


. MR. ASSHETON, DR. STEVENS AND 


Мв. TURNER. 


420 Scholarships and Prizes. 


The Hospital contains 652 Beds, of which 588 are in constant occupation. 





Special Classes are held for Students preparing for the University and 
other Higher Examinations. 


APPOINTMENTS. 


All Hospital Appointments are made strictly in accordance with the 
merits of the Candidates, and without extra payment. There are 24 
Resident Appointments open to Students of the Hospital annually without 
payment of additional fees, and numerous Non-resident Appointments in the 
general and special departments. The Queen Victoria Ward provides 
accommodation for gynecological and maternity cases. 


ENTRANCE SCHOLARSHIPS. 
YEARLY IN SEPTEMBER. 


Two Open Scholarships in Arts, one of thé value of £100 open to Candi- 
dates under 20 years of age, and one of £50 open to Candidates under 25 
years of age. Two Open Scholarships in Science, one of the value of £150, 
and another of £60, open to Candidates under 25 years of age. One Open 
Scholarship for University Students who have completed their study of 
Anatomy and Physiology, of the value of £50. 


PRIZES AND SCHOLARSHIPS 


Are awarded to Students in their various years, amounting in the 
aggregate to more than £650. 


DENTAL SCHOOL. 


A recognised Dental School is attached to the Hospital, which affords to 
Students all the instruction required for a Licence in Dental Surgery. 


NEW SCHOOL BUILDINGS. 


The new Theatre and Laboratories, opened in June, 1897, by H.R.H. The 
Prince of Wales, afford every facility for practical instruction in Physiology. 


COLLEGE. 


The Residential College accommodates about 59 Students in addition to 
the Resident Staff of the Hospital. It contains a large Dining Hall, Reading 
Room, Library, and Gymnasium for the use of the Students’ Club. 


For Prospectus and further information, apply to the Dean, Dr. Eason 
Guy's Hospital, London Bridge, S.E. 


THE STAFF OF THE DENTAL SCHOOL. 
1904. 


Dental Surgeons. 
F. NEWLAND-PEDLEY, F.R.C.S., L.D.S.E. , 
W. A. Maces, L.R.C.P., M.R.C.S., L.D.S.E. 
R. WYNNE Rouw, L.R.C.P., М.Б.С.8., L.D.S.E. 


Assistant Dental Surgeons. 


H. L. PILLIN, L.D.S.E. J. В. Parritt, L.R.C. P., M.R.C.S., 
M. F. Hopson, L.D.S.E. L.D.S.E. 
J. L. PAYNE, І. R.C.P., M.R.C.S., 
L.D.S.E. 


Demonstrators of Practical Dentistry. 


E. B. DowsETT, L.R.C.P.,M.R.C.S., С. S. MORRIS, L.R..O.P. M.R.C.S., 
L.D.S.E. L.D.S.E. 
P. S. Campxin, L.D.S.E. F. J. PEARCE, L.D.S.E. 
J. E. SPILLER, L.D.S.E. 


Anesthetists. 
H. F. Lancaster, M.D. А. W. ORMOND, F.R.C.S. 
С. J. OGLE, M.R.C.S. P. Turner, M.S. 


R. P. RowLANDS, M.S., F.R.C.6. Н. T. Hicks, F.R.C.8. 


Lecturers. 

‘Dental Anatomy and Physiology.—Mr. Maaas. 
Dental Surgery and Pathology.—Mr. WYNNE Rouw, 
Operative Dental Surgery.—Mr. PARFITT. 

Dental Mechanics.—Mr. PAYNE. 

Practical Dental Mechanics.—Mr. PILLIN. 

Dental Materia Medica.—J. H. Bryant, M.D. 
Dental Bacteriology.—J. W. Н. Eyre, M.D. 

Dental Microscopy.--E. І. SPRIGGs, M.D. anD D. Forsyru, M.D. 
Dental Metallurgy.—J. WADE, D.Sc. 

Practical Dental Metallurgy.—Mr. Hopson. 
Curators of Dental Museum.—Mr. PAYNE AND Mr. DowseEtr. 
Dean.—Dr. Eason. 


GUY’S HOSPITAL REPORTS. 


The Fifty-eight Volume. Edited by J. H. Bryant, M.D. 
and F. J. STEWARD, M.S. Price to Subscribers, 6s.; to Non- 
Subscribers, 10s. 6d. Postage free. 


CONTENTS. 


1. On Disease of the Heart due to Over-Indulgence in Alcoholic Drinks. By 
W. Hale White, M.D. 


2. A Contribution to the History of the Intravenous Injection of Drugs; 
together with an Account of some Experiments on Animals with Anti- 
septics ; and a Bibliography. (Thesis for the M.D. Oxon.). By J. M. 
Fortescue-Brickdale, M.A., M.D. 


3. Eosinophilia in Skin Diseases. By Herbert French, M.B., B.Ch., Oxon., 
M.R.C.P. Lond. 


4. Some Cases Illustrating the Influence of Heredity in Angeio-Neurotic 
CEdema. By C. A. Ensor. 


. Malignant Disease of the Stomach; with Appendix of Cases, 1826—1900. 
By Sir Cooper Perry, M.D., and Lauriston E. Shaw, M.D. - 


Qt 


List of Gentlemen Educated at Guy's Hospital who have passed the 
Examinations of the several Universities, Colleges, etc., in the year 
1902. 


Medallists and Prizemen for 1908. 

Clinical Appointments held during the year 1902. 
Dental Appointments held during the year 1902. 
Medical and Surgical Staff, 1903. 

Lecturers and Demonstrators, | 


The Staff of the Dental School, 1908. 


J. & A. CHURCHILL, Great Marlborough Street. 




















| 








UNIVERSITY OF MINNESOTA 
biom,per ser.3:v 44 

Stack no.61 

Guy's M 

Guy's Hospi 


LOOT