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(^ EDITED BY t | N
Ug H. BRYANT, M.D,
AND
F, J. STEWARD, M.S.
iə 7 25. . ә.
VOL. LVI.,
BEING
JE THIRD SERIES.
> MDCCCCII.
boe os
PRINTED BY ASH AND CO., LIMITED,
SOUTHWABK STREET,
SE,
LONDON,
BOROUGH,
42,
II.
III.
IV.
VI.
VII.
VIII.
IX.
CONTENTS.
PAGE.
. On a Method of Stretching, Dividing, or Excising a
Portion of the Lingual Nerve, with Cases. By R.
CLEMENT Lucas, B.S. " də 2 1
Case of Congenital Cavernous Angeioma of Right
Hand. Ligature of Brachial, and Five Months
Later, of Radial and Ulnar Arteries. Cure
Permanent Ten Years Later. By W. H. A.
JACOBSON, М.Сн. ... дә T .. 18
A Case of Splenic Anemia. By Lauriston E.
SHAW, M.D. xi дә e 6 20
Some Conditions in which Opium is Dangerous. By
A. P. BEDDARD, M.D. er Em .. 35
. A Research upon the Nitrogenous Metabolism in a
Case of Bright's Disease. (With Tables. By J.
A. Вотгев, M.B., B.S. Lond., and H. S. FRENCH,
B.A., B.M., B.C. Oxon. d bas ҝә 49
Roentgen-Hay : 75007 of, Renal "Calculus, LY E
W. H. Викебби * 2577575 . 91
Bacteria in mia "yu. H “Вида M.D. ... 99
A Case of Seppe Mod. By FREDERICK
TayLoR, M.D. i is D .. 109
Blue Urine. By A. P. Bepparp, M.D. ... i 127
4176105
IV. Contents.
X. Reduction en Masse. (With Tables.) By R. P.
Rowranps, F.R.C.S...
XI. On Enteric Fever. Being an Investigation into the
Bacteriological Condition of the Urine, and in
some Cases of the Kidney in this Disease. (With
Table). (Thesis for the M.D. Cambridge.) By
STANLEY E. Denver, C.M.G., M.A., M.B., B.C.,
D.P.H.
XII. A Cardiographic Tracing, Showing Asynchronous
Action of the Ventricles. By THEODORE FISHER,
M.D.
XIII, On Acute Septic Inflammation of Young Bone
Growing from Cartilage. By R. LawrorD KNAGGS,
M.C. Cantab.
XIV. Some Notes on the Ætiology of Strabismus. By
ARTHUR W. ORMOND, F.R.C.S.
XV. Specimens Recently added to the Pathological
Museum. By Lauriston E. SHaw, M.D., and E.
CooPER Perry, M.D...
XVI. List of Specimens added to the Dental Museum.
By J. PENIS PAYNE
* vs v
e a .... ve
IU ә ie 27
° .. ... e
List of 2 : Educated at" ‘Guy’ 5 “Hospital who
have passeşi ; tbe: ха анырды: of the several
Univertitted, Göleges, tv it (he Year 1899
Clinical Appointi is bil: dia the Year 1899
Dental Appointments held during the year 1899
PAGE
131
153
211
221
243
265
283
. LIST OF ILLUSTRATIONS.
PLATES.
TO FACE
PAGE.
Mr. E. W. H. SHENTON.
Illustrating his Paper on Roentgen-Ray Diagnosis
of Renal Calculus. Figs. I. to XXIII. se "98
Dr. FREDERICK TAYLOR.
Illustrating his Paper on A Case of Suppurative
Pylephlebitis T i» ie ms 112
Dr. R. LAwFORD KNAGGS.
Ilustrating his Paper on Acute Septic Inflammation
of Young Bone Growing from Cartilage. Figs. I.
to XXVI. 222, 224, 226, 228, 230, 232, 236, 238, 240
CHARTS.
Messrs. J. A. BUTLER AND Н. S. FRENCH.
Ilustrating their Paper on A Research upon the
Nitrogenous Metabolism in a Case of Bright’s
Disease ... a nd 355 .. 60
Dr. FREDERICK TAYLOR.
Illustrating his Paper on A Case of Suppurative
Pylephlebitis . дә . aie .. 118
vi. List of Illustrations.
WOODCUTS.
PAGE
Mr. R. P. RoVLANDS.
Illustrating his Paper on Reduction en Masse. Figs.
I. to VII. ... 133, 134, 135, 136, 137, 138, 139, 151
Dr. THEODORE FISHER.
Illustrating his Paper on A Cardiographic Tracing,
shewing a Synchronous Action of the Ventricles.
Figs. I. to XI. -— “с bi 217-219
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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
Ackroyd, H., B.A., Guy’s Hospital
Adams, A. R., Guy’ s Hospital
Adams, C. E., Guy's Hospital
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. E., Llandrillo, Corwin, North Wales
Aikins, M. H., M.D., Burnhamthorpe, Ontario, Canada
Airy, H., M.A., M.D., Stoke House, Woodbridge, Suffolk
Alban, E., Guy's Hospital
Alcock, F., Guy's Hospital
Aldis, A. W., 20, Lansdown Crescent, Cheltenham
Alexander, H., Sundon House, Church Hill, Walthamstow
Alexander, K. B., M.B., Guy's Hospital
Alexander, S. R., M.D., Gatefield House, Faversham
Allan, A. P., M.D., B.S., Abbotsford, 74, Croham Road, South
Croydon
Allen, R. Westmore, Guy's Hospital
Allen, R. William, M.A., Guy's Hospital
Allison, G. F. E., Guy’ 8 Hospital
Allport, A., 28a, Moorgate Street, E.C.
Allport, E. 'G., B. A., Guy's Hospital
Alston, W. E., B.A., M.D., B.C., Wheathampstead, St. Albans
Anderson, C. T., Cape Town, South Africa
Anderson, G. E. C., M.D. , Cape Town, South Africa
Anderson, K., Guy's Hospital
Anderson, R. G., Guy's Hospital
Anderton, J. E., Thornfield, New Mills, Derbyshire
Andrews, J. A., B.A., Guy's Hospital
Andrews, Richard J., Homefield House, -— Exeter
Anthony, C. M., Guy’ s Hospital
Archer, A., Bourne Hill, Pembroke Road, Clifton, Bristol
VOL. LVIl. 9
x. List of Subscribers.
Ashby, E., 58, Bootham, York
Ashwell, H. G., 74, Mansfield Road, Nottingham
Ashwin, R. H., M. D., High Street, Market- VVeighton, East Yorks
Assheton, R., M.A., Grantchester, ‘Cambridge
Atkins, F. D., Chalk Pit House, Sutton, Surrey
Atkinson, T. Reuell, M.D., Cardigan House, Chadwell Heath,
Essex
Aubrey, H. P., Guy’s Hospital
Audland, W. E., 5, Oxford Street, Wellingborough
Bacon, H., Guy's Hospital
Badcock, G. Wallace, Lulworth, Rushey Green, Catford, S.E.
Badeock, J. H., 140, Harley Street, W.
Bagshawe, H. V., Uppingham, Rutland
Baines, J. C., Etonhurst, Malvern
Balderston, R., M.B., 30, Park Road, Forest Hill, S.E.
Baldwin, F. 15. Judge, Cawdor House, Rotherham
Baldwin, H. R., M.D., New Brunswick, New Jersey, United
States of America
Ball, J. A., M.D., The Gables, Bromsgrove
Ball, M. E., Guy’ s Hospital
Ball, W. C., B.A., 19, Lewisham Hill, S.B.
Barber, H., ‘Guy’ 8 Hospital
Barkshire, F., Guy's Hospital
Barlow, S. H., Guy's Hospital
Barnard, J. H., M.D.,8, Place Carnot, Aix-les-Bains, Savoie, France
Barnes, F., Guy's Hospital
Barnett, G. S. H., Guy's Hospital
Barrett, A. E.; 123, Holland Park Avenue, W.
Barrionuevo, J. M., Guy's Hospital
Barron, J. B., 35, The Grove, Ilkley, Yorkshire
Barron, R. M., Royal Victoria Hospital, Netley
Barrs, A. G., M. D., 22, Park Place, Leeds
Bartholomew, A. A., 31, West Hill, Wandsworth, S.W.
Bartle, F. W., Guy's Hospital
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, 2, Courtfield Road, Gloucester Road, S.W.
Barton, T. H., Guy's Hospital
Bascombe, E. D., Melford Lodge, Bournemouth
Basker, C. = Guy’s Hospital
Bastard, H. R., Guy’s Hospital
Batchelor, F. C., M.D., A. M. P. Buildings, Prince’s Street,
Dunedin, New Zealand
Batchelor, F. S., Moray Place, Dunedin, New Zealand
Bates, J. E. L, Guy's Hospital
Beadel, A. J., Guy's Hospital
Inst of Subscribers. xi.
Beadnell, H O. M., Guy's Hospital
Beale, E. Clifford, M.A , M.B., 23, Upper Berkley 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. Archer, Australia
Station
Beard, F., M.B., The Crossways, South End, Croydon
Beaumont, A. R., Guy's Hospital
Beddard, A. P., M.A., M.D., B.C., 44, Seymour Street, Portland
Square, W.
Bedford, G. H., Harbottle, Rothbury, Cumberland
Beeby, Walter T., M.D., Sheringham, Norfolk (summer), and
Rapalls, Liguria, Italy (winter)
Beley, G., c/o Mrs. Beley, 35, Wemyss Road, Blackheath, S.E.
Bell, A. H., Guy's Hospital
Bell, A. O., 46, Worple Road, Wimbledon, S.W.
Bell, H. T. S., Milton, near Brisbane, Queensland
Bellingham-Smith, E., Guy's Hospital
Benett, A. M., Guy's Hospital
Bennett, H., Builth, Breconshire
Bennett, J., 9, Mason Avenue, Croydon
Bent, P. C. V., Guy's Hospital
Bent, S. C. H., Guy's Hospital
Bent, V. T. C., Guy's Hospital
Bentley, H., B.A., Guy's Hospital
Bentley, R. J., Guy's Hospital
Berry, A. W., Guy's Hospital
Berry, H. P., M.B., The Priory, Grantham
Berry, H. T., 66, Pembridge Villas, Bayswater
Berry, T. P., M.B., St. Saviour's Infirmary, East Dulwich Grove,
S.E
Bethell, H. W., Guy's Hospital
Bett, Staff-Surgeon W., R.N., H.M.S. Minerva, Cruiser Squadron.
Beven, Octavius, M.D., B.S., 3, Balham Grove, S.W.
Bevers, E. C., B.A., Guy's Hospital
Bickerton, J. M., B.A., Guy's Hospital
Bigg, E., Guy's Hospital
Biggs, T. Strange, West Coombe, Hassocks, Sussex
Binns, H. T., Guy's Hospital
Birch, George, 105, Downs Road, Lower Clapton, N.E.
Bird, Tom, M.A., 594, Brook Street, W.
Birdwood, R. A., M.A., M.D., Park Hospital, Hither Green,
Lewisham, S.E.
Bisshopp, Francis R. B., M.A., M.D., B.C., Belvedere, Mount
Pleasant, Tunbridge VVells
Blachford, J. V., M.D., 87, Belvedere Road, Upper Norwood, S.E.
Black, G., M.B., Hurstpierpoint, Hassocks, Sussex
xli. Inst of Subscribers.
Black, J., Guy's Hospital
Black, K., Guy's Hospital
Black, O., Guy's Hospital
Blackler, H. J., M.B., Braconfell, Redhill
Blasson, Thomas, Billingborough, near Folkingham, Lincolnshire
Blatherwick, H., The Laurels, Dulwich, S.E.
Bligh, W., M.D., B.S., Minley, Caterham Valley
Bolus, H. P. B. A., M. B., B.C., Haddon, Beckenham, Kent
Bolus, P. R., Guy’s Hospital
Booker, C. W., 12, Church Terrace, Lee, S.E.
Bookless, J. S., Guy’s Hospital
Booth, E. H., M.D., 1, Cambridge Road, Hove, Brighton
Booth, Lionel, M. D., Sherburn House, Durham
Boswell, J: Lo; JJ M.D. , Crawley Grange, Newport Pagnel
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., 7, Marine Terrace, Herne Bay
Bowle, 8. C., Guy’s Hospital
Box, W. F., Guy's Hospital
Bradbury, J. C. O., Guy’s Hospital
Brailey, A. R., B.A., Guy’s Hospital
Brailey, W. H., B.A., Guy’s Hospital
Brailey, W. A., M.A., M.D., 11, Old Burlington Street, W.
Braithwaite, C. B., M.B., The Sycamores, Golcar, near Hudders-
field
Braithwaite, J., Guy's Hospital
Brayne, R. E., Guy's Hospital
Bredin, R., M.B., Valparaiso, Chili
Bremner, R. À., 47, Queen Street, Exeter
Brenton, W. H., 44, Cobourg Street, Plymouth
Brereton, Captain F. S., M.D., R.A.M.C., Eskdale, Birkdale,
Southport
. Bridger, J. Dell, Guy's Hospital
Bridger, R. D., Guy's Hospital
Bright, T. D., Guy's Hospital
British Medical Journal, The, 429, Strand, W.C.
Brock, E. H., M.D., 21, Streatham Hill, S.W.
British Medical Association Library, 429, Strand, W.C.
Brogden, R. W., M.B., B.S., 12, Lower Brook Street, Ipswich
Bromley, F. W., Guy's Hospital
Bromley, J., Guy' s Hospital
Bromley, J. B. Castle Hedingham, Essex
Brook, S. S., Guy's Hospital
Brookhouse, C. T., M.D., 19, Wickham Road, Brockley, S.E.
Brookhouse, H. O., Guy's Hospital
Brooks, B., Sonning near Reading
List of Subscribers. xiii.
Brown, G. Minter, Princess Christian Hospital, Pinetown, near
Durban, Natal |
Brown, H. S., Guy's Hospital
Brown, H. W., M.B., Guy’s Hospital
Brown, J. Stevenson, Guy's Hospital
Brown, 8. C., Guy's Hospital
Brown, T. E. Burton, C.I.E., M.D., 185, Willesden Lane, N.W.
Browne, R. H. J., Staff-Surgeon, R.N., Royal Yacht Osborne,
Portsmouth
Bruce, H. W., M.D., B.S., Guy’s Hospital
Brundrett, G. T., Guy's Hospital
Brussels, Académie Royale de Médecine de Belgique, Palais des
Académies (per the Secretary)
Bryan, C. H. R., Guy’s Hospital
Bryant, J. H., M.D., 4, St. Thomas’s Street, S.B.
Bryant, Thomas, M.Ch., 27, Grosvenor Street, W.
Bryden, F. W. A., The Priory, Godalming
Bryden, R. J., 21, Harmer Street, Gravesend
Brydone, J. M., M.B., B.C., Guy’s Hospital
Bubb, C. H., 15, Queen’s Avenue, Muswell Hill, N.
Buckell, C. A. W., Guy’s Hospital
Buckeridge, G. L., Guy’s Hospital
Bullbrook, J. A., Guy’s Hospital
Bunting, James, Earlham, Torquay
Burghard, F. F., M.S., 86, Harley Street, W.
Burnett, Captain S. H., M.B., C.M., Indian Medical Service,
Surgeon-General’s Office, Bombay
Burner, L. H., Guy’s Hospital
Burney, W. H. S., Guy's Hospital
Burt, A., 143, Uxbridge Road, W.
Burton, Herbert C., Lee Park Lodge, Blackheath, S.E.
Burton, T., Guy’s Hospital
Burton-Brown, F. H., M.A., M.B., B.Ch., 3, Via Venti
Settembre, Rome
Bush, W. H., Guy’s Hospital
Busteed, J. H., Ellesmere, Shropshire
Butcher, H. O. F., Ware, Hertfordshire
Butler, H. A. G., c/o J. B. Forster, Esq., South Parade, Ban-
galore, India
Butler, H. R. C., Oaklands, Abbey Road, Torquay
Butler, J. A., M.B., B.S., Guy’s Hospital
Butt, F. K., Constitutional Club, Northumberland Avenue, S.W.
Cadel, N. P., Agincourt House, Camberley, Surrey
Caldecott, C., M.B., B.S., Earlswood Asylum, Redhill, Surrey
Cameron, J., Guy’s Hospital
Campbell, H. J., M.D., 36, Manningham Lane, Bradford, Yorks
Campkin, P. S., 80, Wilton Place, Belgrave Square, S.W.
xiv. List of Subscribers.
Camps, P. W. L., Guy's Hospital
Cann, F. J. H., M.B., Sefton House, Dawlish, Devon
Canning, H. A. E., 11, King’s Terrace, Southsea
Capes, R., 181, Grove Lane, Denmark Hill, S.E.
Card, L. O., Guy’s Hospital
Carden, W. A., St. Luke’s Mission, Chemulpo, Corea
Cardiff Medical Society (per A. P. Fiddian, M.B., Cardiff)
Carey, Francis, M.D., Villa Carey, Grange Road, Guernsey
Carlisle, G., Guy’s Hospital
Carling, W., B.A., M.B., B.C., 11, Roseberry Terrace, Highland
Road, Southsea
Carpmael, C. E., M.B., B.S., Marle Green, Heathfield, Sussex
Carr, T., M.D., 15, Albert Terrace, Blackpool
Carr, T. E. Ashdown. Guy’s Hospital
Carrell, G. N. P., 51, Woodland Road, Ilford
Carrington, W. H., 8, Battersea Rise, S.W.
Carter, A. H., M.D., B.S., Guy’s Hospital
Carter, H. H., Guy’s Hospital
Cawston, A. E., Guy's Hospital
Cazenove, W. R., St. Andrew’s, Billing Road, Northampton
Chandler, H. S., Guy’s Hospital
Chaning-Pearce, A., M.D., Shalmsford Street, Chartham,
Canterbury ; à
Charles, H. E., 82, St. Helen's Road, Swansea
Chatterton, G., P. O. Box 11, East London, South Africa
Cheesman, J., M.D., Buckingham
Cheyney, G. H., Guy's Hospital
Chicken, Rupert C., Forest Road, West Nottingham.
Chignell, L. A., Guy's Hospital
Child, S., B.A., Guy's Hospital
Childe, Major L. F., M.B., Sir Jamsetjee Jeejeebhoy Hospital,
Bombay
Chilton, F., Guy's Hospital
Chinneck, H. E., Guy's Hospital
Chubb, W. L., M.D., Darenth House, Sandgate
Churchill, G. B. F., Guy's Hospital
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., 6, The Crescent, Wisbech, Cambridgeshire
Clarke, G., M.B., Guy's Hospital
Clarke, Henry, H. M. Prison, Wakefield, Yorkshire
Clarke, W. F., M.D., B.S., 2, Baron’s Court Road, West Kensing-
ton, W.
Clatworthy, J. H., Guy's Hospital
Claxton, E. I., B.A., Guy's Hospital
Clayton, E., 47, Devonshire Street, Portland Place, W.
Cleveland, A. J., M.D., 45, Shooters Hill Road, Blackheath, S.E.
List of Subscribers. "
Clifford, S., Guy's Hospital
Clogg, A. H., Guy's Hospital
Clough, A. H., Guy's Hospital
Clowes, E. F., ** Grantley," Wotton-under-Edge, Gloucestershire
- Clowes, N. B., 45, London Road, Reading
Cobb, W. E. S., 12, Drakefield Road, Upper Tooting, S.W.
Cock, E., Guy's Hospital
Cock, F. W., M.D., M.S., 1, Porchester Houses, W.
Cock, J., 17, Morton Crescent, Exmouth, Devon
Cock, W., 147, Queen's Road, Peckham, S.E.
Cockcroft, G., Guy's Hospital
Cocker, A. B., Guy's Hospital
Cogan, Lee F, 51, Sheep Street, Northampton
Cohen, E., Purley, Surrey
Cohen, M. W., Guy’s Hospital
Coish, H. J., Guy’s Hospital
Colelough, W. F., B.A., M.B., B.C., Guy’s Hospital
Cole, P. P., Guy’s Hospital
Cole, W. H., Guy’s Hospital
an F. 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
Collett, H. Edgar, Guy’s Hospital
Collier, H. W., M.B., B.S., Murillo House, High Road Lee, S.F.
Collier, T., 5, Westgate, Ripon
Collington, F. A., 28, Much Park Street, Coventry
Collins, E. A., Guy’ s Hospital
Collins, G. T., M.B., Guy’s Hospital
Collins, H. W., Wrington, near Bristol
Collins, M. A., Guy’s Hospital
Collins, R. T., Guy's Hospital
Constant, F. C., 15, Queen’s Street, Cheapside, E.C.
Cook, James Wood, Barnstaple, Devon
Cook, J., Guy’s Hospital
Cook, I. R., Guy’s Hospital
Cooke, L., Guy’s Hospital
Cooke, T. A. B., New Milford, Pembrokeshire
Cooper, F. W., Guy’ S Hospital
Cooper, H., M. A., M.D., B.Ch., Fownhope, Ewell Road, Surbiton
Cooper, J. S., B.A., Guy’s Hospital
Copland, J. B., Guy’s Hospital
Coplans, M., M.B. , Guy’s Hospital
Copley, S., İnnes Road, Stamford Hill, Durban, Natal
Corfe, E. W., St. Catherine’ s, Queen’s Road, Maidstone
Corin, H. J., 9, Suffolk Place, Pall Mall, S.W.
Costobadie, H. P., Guy's Hospital
Costobadie, V. A. P., Guy's Hospital
xvi. List of Subscribers.
Couchman, E., 64, Croham Road, Croydon
Counsell, H. E., 27, Banbury Road, Oxford
Cowper, C. M. L., Guy's Hospital
Cox, J. H., 232, Alfreton Road, Nottingham
Craig, M., M.A., M.D., B.C., Bethlem Hospital, S.E.
Cranston, H. S., Guy's Hospital
Creasy, R., Windlesham, Bagshot, Surrey
Cregeen, J. Nelson, 21, Prince's Avenue, Liverpool
Cressy, A. Z. C., Wallington, Surrey
Crew, John, J.P., Higham Ferrars, Northamptonshire
Crofts, A. D., Guy’s Hospital
Croot, H., Guy’s Hospital
Cross, F. G., Guy's Hospital
Crosse, W. H., M.D., 45, Dover Street, Piccadilly, W.
Croydon Medical Book Club (per Dr. T. A. Richardson, 87, London
Road, West Croydon)
Cruickshank, J. D., The Lodge, Chingford, Essex
Cuff, H. E., M.D., North-Eastern Fever Hospital, St. Ann's
Road, South Tottenham
Cuff, R., M.B., 1, The Crescent, Scarborough
Cunningham, John, M.B., Campbeltown, Argyleshire
Currie, Andrew S., M.D., 81, Queen's Road, Finsbury Park, N.
Currie, O. J., M.B., 18, Longmarket Street, Maritzburg, Natal,
South Africa
Curtis, F., Guy's Hospital
Cutler, F. J., Guy's Hospital
Cutler, H. A., Guy's Hospital
Dadd, J. W., B.A., Guy's Hospital
Daglish, R. R., J.P., New Romney, Kent
Dakin, W. R., M.D., 18, Grosvenor Street, W.
Daldy, A. M., M.D., B.S., 25, Claremont Road, Surbiton
Dallas, A., McCabe, Guy's Hospital
Dalton, B. N., M.D., Selhurst Road, South Norwood, S.E.
Daniell, George Williamson, Blandford, Dorsetshire
Davidson, G. G., B.A., Guy's Hospital
Davies, A. H., B.A., M.B., B.C., Guy's Hospital
Davies, Ebenezer, Brunswick House, Swansea
Davies, F. VV. S., 21, Newport Road, Cardiff
Davies, J., M.D., 87, Cambridge Gardens, Ladbroke Grove, W.
Davies, W. T. F., D.S.O., M.D., B.S., Post Office Box 1750,
Johannesburg, Transvaal
Davies-Colley, H., B.A., Guy’s Hospital
Davy, Henry, M.D., Southernhay House, Exeter
Daw, S. W., Guy’s Hospital
Dawe, C. H., Guy’s Hospital
Dawson, R. B., Guy’s Hospital
Dawson, W. J. O., Portarlington, College Place, Southampton
List of Subscribers. xvii.
Day, F. G., Guy's Hospital
Day, T. M., Harlow, Essex
Day, W. L. M., Guy's Hospital
Deane, E., Greenham Villa, Caversham, Reading
Deck, E. F., Guy's Hospital
Delbruck, R. E., B.A., M.B., B.C., Embankment Chambers,
Villiers Street, Strand, W.C.
De Mierre, A., 6, Seaside Road, Eastbourne
Dencer, W. H., Guy’s Hospital |
Denham, N., 1, Albemarle Road, Beckenham, Kent
Denman, R., Port Victoria, Mahé, Seychelles
Denning, A. W. F., Guy’s Hospital
Dennant, W. A., Guy’s Hospital
Denny, Surgeon H. R. H., R.N., H.M.S. Magnificent, Channel
Squadron
Dent, H. L, Guy’s Hospital
Denyer, C. H., Guy’s Hospital
Derriman, W. E., Guy's Hospital
Desprez, H. S., Shoreham, Sevenoaks
De Villiers, C. C. A., Guy’s Hospital
Dickey, W. C. McN., Guy's Hospital
Dickson, A. C., Guy's Hospital
Digby, K. H., Guy's Hospital
Dimock, E. C., 85, Victoria Road, Aldershot
Dismorr, C. J. S., Guy's Hospital
Dobson, T. H. B., M.B., Guy's Hospital
Docra, C. G., Guy's Hospital
Dodd, A. H., 49, Church Road, Hove, Brighton
Dolman, A. J., General Dispensary, Lincoln
Donald, J. A., Guy’s Hospital
Donnell, J. H., Guy’s Hospital
Doudney, L., Guy’s Hospital
Douglas, W. T. Parker, M.B., Ivy House, Newbury, Berks
Douse, J. F., Guy’s Hospital
Dovvsett, E. B., 1, Gloucester Street, Portman Square, W.
Drake, G. H., 35, Old Elvet, Durham
Drew, H. W., Eastgate, East Croydon
Drewitt, A., 15, Prospect Place, Harrogate.
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. W. E. Froggie, 30, Springfield,
Dundee
Dunn, L. A., M.S:, The College, Guy's Hospital, S.E.
Duran, Carlos, and Nunez, Daniel, San José, Costa Rica
Durant, A. R., Guy's Hospital
Durham, F., M.B., 52, Brook Street, W.
Durham, H. E., M.A., M.B., B.C., Physiological Laboratory,
Cambridge
xviii. List of Subscribers.
Dymott, G. L., Guy s Hospital
Dyson, P. A. S., Guy s Hospital
Eager, Reginald, M.D., Northwoods Asylum, Frampton Cotterell,
near Bristol
Eason, H. L., M.B., B.S., Guy's Hospital
Eastes, George, M.B., 35, Gloucester Place, Hyde Park, W.
Eastes, G. Leslie, M.B., B.Sc., 62, Queen Anne Street, S.W.
Eastes, T., M.D., 18, Manor Road, Folkestone _
Eccles, H. D., Monganui, New Zealand
Edey, T. H., Guy's Hospital
Edmonds, W. H., Guy's Hospital
Edridge, Ray, Guy's Hospital
Edwards, C., City of London Asylum, near Dartford, Kent
Edwards, C. D., B.A., M.B., B.C., Alton Lodge, Woodford
Green, Essex
Edwards, F. H., M.D., Camberwell House, Peckham Road, S.W.
Edwards, O., 34, Etnam Street, Leominster
Edwards, W. H., Trevone, Knollys Road, Streatham, S.W.
Elcum, D., M.D., 41, Montpellier Terrace, Cheltenham
Elliott, C. C., M.D., B.S., Sea Point, Cape Town, South Africa
Elliott-Blake, H., 3, Ellasdale Road, Bognor
Ellis, G. G., 49, Sandgate Road, Folkestone
Elphinstone, R., Forest House, Silverstene, Towcaster, North-
amptonshire
Elwood, W. H., Guy’s Hospital
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., Guy’s Hospital
Evans, 4. H., Broomfield, Crosby Road North, Waterloo, Liver-
pool
Evans, J. R., Ammanford, Carmarthenshire
Evans, J., Guy's Hospital
Evershed, A. R. F., 49, Knollys Road, Streatham, S.W..
Every-Clayton, L. E. V., M.D., B.S., Emsworth, Hants
Evison, F. A., March, Cambridgshire
Ewart, J. H., Eastney, Devonshire Place, Eastbourne
Ewen, H. W. , Kynance, York Avenue, East Cowes, Isle of Wight
Eyles, A. W. , Guy’ s Hospital
Fagge, C. H., M.S., 22, St. Thomas’s Street, S.E.
Fagge, R. H., High Street. Melton Mowbray
Farr, H. A., J.P., Heath House, Andover, Hants
Farrant, E., Guy’s Hospital
Faulks, E., Guy’s Hospital
List of Subscribers. xix.
Faweett, J., M.D., B.S., 26, St. Thomas's Street, S.E.
Fawley, T. B., Guy's Hospital
Fawsett, F. W., Guy's Hospital
Fawsitt, Thomas, 46, Union Street West, Oldham
Fearn, I. R., Guy's Hospital
Featherstone, J. W., Guy's Hospital
Felton, R., Guy' 8 Hospital
Fenn, C. D., Park House, Diss, Norfolk
Field, Ernest, M.D., C. M., 8, Belmont, Bath
Field, G. H., B.A., M.B., B.C., Cedarlea, Poole Road, Bourne-
mouth, West
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., Sind Club, Karachi, Bombay,
India
Floyd, S. G., M.D., B.S., Llandrindod Wells, Radnor
Forbes, A. H., Guy’s Hospital
Forman, H. Baxter, M.D., 11, Bramham Gardens, South Ken-
sington, S.W.
Forsyth, D., Guy”s Hospital
Fort, H. R. T., B.A., Chorleywood, Rickmansworth
Fortescue-Brickdale, J. M., M.A., M.B., B.Ch., Uppingham,
Rutland
Forty, D. H., Edbrook, Wotton-under-Edge, Gloucestershire
Foster, A. L., Guy’s Hospital
Foster, C. M., M.D., 1101, Yonge Street, Toronto, Canada
Foster, O. H., M.A,, | M. B., Hitchin, Hertfordshire
Fountaine, D. O., c/o T George, Esq., Pollicott, Thane, Oxon.
Fowke, F. W., Byfield, R.S.O., Northants
Fox, A. D., Guy’s Hospital
Fox, F. N., Guy’s Hospital
Fox, H. E. C., M.B., Surgeon R.N., H.M.S. Duke of Wellington,
Portsmouth
Fox, H. J., Guy's Hospital
Fox, J. A., Tregea House, Penzance
Francis, 4. S., Guy's Hospital
Frankenburg, L. H., B.A., Guy's Hospital
Franklin, R., Guy's Hospital
Fraser, A., M.B., 22, Shooters Hill Road, Blackheath, S.E.
Fraser, C. F., Guy's Hospital
Fraser, J. A., Western Lodge, Romford, Essex
Frazer, E. H., M.D., B.S., Helena House, Great Union Road,
St. Heliers, Jersey
Fremantle, F. E., B.A., M.B., B.Ch., 39, Moore Street, Lennox
Gardens, S.W.
French, H. S., B.A., M.B., B.Ch., Guy’s Hospital
Fripp, A. D., C.B., C.V.O., M.S., 19, Portland Place, W.
xx. Inst of Subscribers.
Frost, E. B. M., 216, Queen's Road, New Cross, S.E.
Fry, A. Cradock, B.A., M.B., Priory House, Wellesley Road,
Colchester
Fry, J. F., Shepton Mallet, Somersetshire
Fuller, Courtenay J., 38, Nightingale Place, Woolwich
Fuller, W. A., Guy’s Hospital
Gabriel, A. M., Hazlewood Lodge, Enfield
Gaffney, E. J., Guy's Hospital
Galabin, A. L., M.A., M.D., 49, Wimpole Street, W.
Galton, J. H., M.D., Chunam, 14, Sylvan Road, Norwood, S.E.
Ganney, W. E., 4, Fairfield Road, Old Charlton, Kent
Gardner, A. L., Guy's Hospital
Gardiner, J. J., Guy's Hospital
Gardiner, J. N., B.A., M.B., B.C, Glenwood, Auckland Road,
Upper Norwood, S.E.
"Gardner, P. H., Five Ways, Torquay
Garner, W. L, B.A., M.B., B.C., The Limes, Ampthill, Beds.
Garrard, C. R. O., 30, Broad Street, Pendleton, Salford
Garrard, W. A., Chatham House, Rotherham, Yorkshire
Gater, A. W., Guy’s Hospital
Gathergood, B. W., M.D., Terrington St. John’s, Lynn, Norfolk
George, A. L., Guy’s Hospital
German, H. B., Guy’s Hospital
Gibson, F. G., M.A., Guy's Hospital
Gibson, J. H., 1, Lansdown Road, Aldershot
Giles, W., Guy's Hospital
Gilford, H., Norwood House, Reading
Gill, J. MeD., 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., Guy's Hospital
Glendining, B., Guy's Hospital
Glendining, R., Guy's Hospital
Glenn, C. H., B.A., M.B., B.C., Guy's Hospital
Giesen, E. W., Guy's Hespital
Glover, 4. A., M.B., West Malling, Kent
Glover, J. Alison, B.A., M.B, B.C., Guy’s Hospital
Goadby, K. W., The Mall, Wanstead, N.E.
Goble, E. W., Guy's Hospital
Goble, F. G., Guy's Hospital
Godson, A. H., B.A., M.B., B.C., 68, 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
Goldie, E. G., Guy's Hospital
Golding-Bird, C. H., M.B., 12, Queen Anne Street, Cavendish
Square, W |
List of Subscribers. xxi.
Goldstein, H. M., Guy's Hospital
Goodall, E. W., M.D., Homerton Fever Hospital, N.
Goodey, A., Guy's Hospital
Goodhart, J. F., M.D., 25, Portland Place, W.
Goodman, W. J., Guy's Hospital
Goss, J., B.A., Guy's Hospital
Gosse, H. W., Eccleshall, Staffordshire
Gowing, Benjamin C., Weirfield, Penistone, Yorkshire
Goyder, David, M.D., 88, Great Horton Road, Bradford, Yorks
Graham, G. H., M.D., Buckingham Gate Gardens, James Street,
S.W.
Graham-Smith, G. S., B.A., M.B., B.C., Guy's Hospital
Granger, E. B., Little Milton, Tetsworth, Oxon
Gray, A. C. H., Guy's Hospital
Greaves, E. H., Amersham, Bucks
Green, A., M.B., Burlington Street, Chesterfield, Derbyshire
Green, A. W., 4, Wardrobe Place, St. Paul’s Churchyard, E.C.
Green, N. W., Guy' s Hospital
Green, R. J., Guy’ s Hospital
Green, T. J., Guy’s Hospital
Greene, J. A. C., Guy’s Hospital
Greenfield, D. G., M.B., Guy’s Hospital
Greening, G. F., Guy’s Hospital
Greenwood, E. Climson, 19, St. John’s Wood Park, N.W.
Greenwood, J. H., 8, Park Road, Kingston-on-Thames
Greenwood, P., 155, High Street, West Norwood, S.E.
Greeves, R. A., Guy s Hospital |
Grellet, H. R., Guy’s Hospital
Griffin, E. H., B.A., Guy's Hospital
Griffin, T. H., Guy’s Hospital
Griffin, W. E., Guy's Hospital
Griffith, H. D., Guy's Hospital
Griffith, O. Wynne, 3, Church Place, Pwllheli, N. Wales
Gromitt, J. W., Guy's Hospital
Grose, H. N., Guy's Hospital
Grove, W. Reginald, B.A., M.B., B.C., St. Ives, Hunts
Groves, C. E., F.R.S., Kennington Green, S.E.
Growse, J. L., Bildeston, Suffolk
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)
Gwatkin, A. J., 49, Grand Parade, Brighton
Gwynn, 8. T., M. D., St. Mary's House, Whitchurch, Salop
Gwyther, H. W., Guy' s Hospital
binis до S. H., M.D., 88, Harley Street, Cavendish Square,
xxli. List of Subscribers.
Hall, F. W., M.D.. M.S., 18, College Street, Hyde Park, Sydney,
New South Wales
Hall, Surgeon R. W. B., H.M.S. 1, Pelham Road, Southsea
Hamilton, E. T. E., M.D., M.S., B.Sc., Post Office Box 1750,
Johannesburg, Transvaal, South Africa
Hamilton, G., Guy’s Hospital
Hammond, J. A. B., M.B., Guy’s Hospital
Hamond, P. W., Guy’s Hospital
Hancock, W. I., 7, Royal York Villas, Clifton, Bristol.
Handley, W. S., M.D., M.S., 41, Devonshire Street, W.
Hardenberg, H. F. H., M.B., Duffield House, Upton Road,
Watford
Hardy, G. F., Guy's Hospital
Hare, Major E. C., Indian Medical Service, Gauhati, Assam,
India
Harland, G. B., Guy's Hospital
Harnett, C. J., M.D., Atlas House, Parade, Margate
Harper, R. S., Guy's Hospital
Harries, T. D., Grosvenor House, Aberystwith
Harrington, R. G., Guy's Hospital
Harris, E. B., 1, Holy Innocents’ Road, Tottenham Lane,
Hornsey, N.
Harris, J., M.D., B.S., 127, Elizabeth Street, Hyde Park, Sydney,
New South Wales
Harris, R., M.B., 18, Duke Street, Southport
Harris, W. J., B.A., M.D., B.C., 37, Bell Street, Shaftesbury
Harrison, A. J., M.B., Failand Lodge, Guthrie Road, Clifton,
Bristol
Harrison, E. M., Guy's Hospital
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, C. P., Guy's Hospital
Harvey, 4. S. S., M.D., 1, Astwood Road, Cromwell Road, South
Kensington, S.W.
Harvey, T. R., Guy's Hospital
Hawkins, H., Broxbourne, Herts
Hayes, R. H., 4, Courtfield Road, Gloucester Road, S.W.
Hayes, T. E. D., M.D., High Street, Reigate
Hayward, John W., Whitstable, Kent
Hazell, F., M.B., B.S., 1, Bouquet Street, Cape Town, South
Africa
Heap, E. F. G. T., Guy's Hospital
Heatherley, F., M.B., B.S., Endellion, New Ferry, Cheshire
Heddy, William Jackson, 46, Redcliffe Gardens, S. W.
Helm, J. K. A., Guy's Hospital
Henderson, E. E., B.A., M.B., B.C., 12, Kensington Square, W.
Henderson, H. J., Guy's Hospital
List of Subscribers. xxiii.
Henderson, W., Guy's Hospital
Henson, W. J., Elmsett Hall, Wedmore, Weston-super-Mare
Hertz, A. F., B.A., Guy's Hospital
Hetley, Henry, M.D., Beaufort House, Church Road, Norwood,
S.E
Hewetson, Captain H., R.A.M.C., Station Hospital, Rangoon,
Burma
Hickes, C., Guy's Hospital
Hickes, P. L., Guy's Hospital
Hickman, H. V., M.B., Overton House, Wanstead, N.E.
Hicks, J. T., Guy's Hospital
Hicks, R. G., 4, Paragon, 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.
Hills, H. J., Guy's Hospital
Hills, William Charles, M.D., The Chantry, Norwich
Hilton, C. T., M.B., B.S., Guy's Hospital
Hinchliff, C. J., 211, Selhurst Road, South Norwood
Hind, Wheelton, M.D., Roxeth House, Stoke-on-Trent
Hindle, F. T., Hill Croft, Askerne, Doncaster
Hinton, J. H., Guy's Hospital
Hirsch, L., Guy's Hospital
Hitchins, F. C., St. Austell, Cornwall
Hobson, J. M., M.D., Glendalough, Morland Road, Croydon
Hodgson, C. R., M.D., B.S., Marlborough House, Balham Hill,
S.W
Hodgson, 8., 201, Brixton Hill, 8.W.
Hodson, Frederick, Hornsea, Hull
Hodson, J. E., Guy's Hospital
Hogarth, B. W., M.D., B.S., 11, Erving Terrace, Morecambe
Hogarth, F. W., Guy's Hospital
Hogg, R. Bowen, Timaru, Canterbury, New Zealand
Holden, H. C., Workington Hall, Cumberland
Holford, T. C., Guy's Hospital
Hollist, G. W. C., Guy's Hospital
Holloway, S. F., Holmwood, Bedford Park, W.
Holman, A. E., Guy's Hospital
Holman, C., M.D., J.P., 26, Gloucester Place, Portman Square, W.
Holman, F. K., Galeston, Eton Avenue, South Hampstead, N.W.
Holman, H. J., 1, Hardwick Road, Eastbourne
Holmes, T., M.B., Holm Lea, Forton, near Garstang
Holmes, T. E., B.A., M.B., B.C., Guy's Hospital
Hood, Donald W. C., M.D., 43, Green Street, Park Lane, W.
Hooper, H. P., Guy's Hospital
Ы. Му. В., Caversham Lodge, Gosbrook Road, Caversham,
xon
XXIV. List of Subscribers.
Hopkins, C. L., B.A., M.B., B.C., Kent County Asylum, Barming
Heath, Maidstone
- Hopkins, F. G., M.A., M.B., B.Sc., Lynfield, Tenison Avenue,
Cambridge
Hopson, M. F., Grove House, Rosslyn Hill, Hampstead
Horrocks, P., M.D., 45, Brook Street, W.
Horsley, C. D., B.A., Guy’s Hospital
Horsley, H., 60, London Road, Croydon
Horton, J. H., c/o W. Watson & Co., Bombay
Houghton, N. N. A., Guy’s Hospital
Houchin, V. S., Guy’s Hospital
Howard, U. R., B.A., Guy’s Hospital
Howard, J. A., M.D., 8, Herne Hill, S.E.
Howard, R., M.A., M.B., B.Ch., Devon House, Buckhurst Hill,
Essex
Howard, Wilfred, New Buckenham, Norfolk
Howe, J. D., Deepdale House, Burrow Road, Preston
Howell, J., M.B., B.S., General Hospital, Cheltenham
Howell, J. B., 86, North Side, Wandsworth Common, S.W.
Howell, T. A. I., Cleeve House, West Hill, Wandsworth, S.W.
Howse, H. G., M.S., 59, Brook Street, W.
Hubbard, Thos. Wells, Barming Place, Maidstone
Hudson, A. B., Vine House, Cobham, Surrey
Hughes, F. P., Guy’s Hospital
Hugill, George F., 32, Bedford Hill, Balham, S.W.
Hull Medical Society, c/o Dr. J. McNidder, Anlaby Road, Hull
Humphreys, F. R., 27, Fellows Road, N.W.
Humphreys, G. F., Guy's Hospital
Huntley, E., M.B., B.S., 8, Trinity Road, Tulse Hill, S.F.
Hutchinson, F. E., Belgrave, Leicester
Hyslop, T. B., M.D., C.M., Bethlem Royal Hospital, S E.
Ince, Lieut.-Colonel John, M.D., Montague House, Swanley, Kent
Ingram, P. C. P., Guy's Hospital
Iredell, A. W., Guy's Hospital
Iredell, C. E., Guy's Hospital
Isaacs, D., B.A., Guy's Hospital
Jackson, F. D. S., Guy's Hospital
Jackson, P. J., 216, Great Dover Street, S.E.
Jackson, T. L., B.A., M.B., B.C., Cheadle, Cheshire
Jackson, T. S., Fleatham, Liss, Hants
Jacobs, J. M. C., 21, Castle Street, Shrewsbury
Jacobson, T. B., Sleaford, Lincolnshire
Jacobson, W. H. A., M.A., M.Ch., 66, Great Cumberland Place,
Hyde Park, W.
Jalland, W. H., D.L., J.P., St. Leonard's House, York
James, Newton, Guy's Hospital
List of Subscribers. XXV.
Jaynes, V. A., 157, Jamaica Road, S.E.
Jenkins, H. H., Guy’s Hospital
Jepheott, C., M.A., M.B., B.C., 8, The Northgate, Chester
Jiménez, R., Guy’s Hospital .
Jiménez, J. J., San José, Costa Rica, Central America
Johnson, H., Guy’s Hospital
Johnson, R. H. C., Guy's Hospital
Jones, A. G., Guy’s Hospital
Jones, B., M.D., Leigh, Lancashire
Jones, F. Felix, Llanfyllin, near Oswestry
Jones, G. H. West, Southgate, Eckington, Derbyshire
Jones, H. J., 167, Lillie Road, 8.W.
Jones, H. S., Guy's Hospital
Jones, H. W., Guy's Hospital
Jones, J. Edwards, D.L., J.P.. M.D., Bryn-y-ffynon, Dolgelly,
North Wales
Jones, Robert, 11, Nelson Street, Liverpool
Jones, R. W., Guy's Hospital
Jones, Surgeon Murray P., R.N., H.M.S. Wildfire, Sheerness
Jones, S. H., 9, Wimpole Street, W.
Jones, W. Makeig, M.D., Beaumont, Torquay
Jones, W. W. C., Guy's Hospital
Joslen, H., ** Ducie," Chapelton, P.O., Jamaica
Joy, G. P., Guy's Hospital
Judson, T. R., 44, Mill Lane, West Derby, Liverpool
Jupp, E. N., Guy's Hospital
Keall, C. A. H., 81, Clarendon Road, Holland Park, W.
Keates, H. C., M.B., Guy's Hospital
Keele, S., 8, Highbury Place, N.
Kellock, W. B., M.D., 94, Stamford Hill, N.
Kelsey, Surgeon A. E., R.N., Redhill, Surrey
Kemp, G. L., M.D., Worksop, Notts
Kempe, A. M., 53, Church Road, Bournemouth
Kendall, G., Battle, Sussex
Kendall, Walter B., Greenheys, King’s Wear, Devon
Ker, Hugh Richard, Tintern, 2, Balham Hill, S.W.
Ker, W. P., Guy’s Hospital
Kerby, R. J., Speenhamland, Newbury
Key, B. W. M. A., 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
Kingcombe, A. P., Towcester, Northamptonshire
Kingsford, E. C., Carntyne, Brondesbury, N.W.
Kinsey-Morgan, A., M.D., 1, Stanhope Gardens, Bournemouth
Kitchin, E. H., Guy’s Hospital
Kitching, C. M., M.D., 10, New Street, Cape Town, South Africa
VOL. LV). 3
Xxvi. List of Subseribers.
Kliszczewski, C. S., Guy's Hospital
Knaggs, R. Lawford, M.A., M.D., M.C., 27, Park Square, Leeds
Knight, F. C. R. M., Guy's Hospital
Knight, H. S., Guy's Hospital
Knowles, C. H., Casamajor Road, Egmore, Madras
Knowles, G. F., Guy's Hospital
Kynaston, A. E. F., Guy's Hospital
Lacey, B. W., Guy's Hospital
Lacey, E. E., Guy's Hospital
Lacey, T. Warner, M.D., 26, Nightingale Place, Woolwich
Lacey, W. J. M., Clyde House, 6, Ware Road, Hertford
Lamb, C. J., Guy's Hospital
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.
Landon, T. W. H., Hackbridge, Carshalton
Lane, W. Arbuthnot, M.S., 21, Cavendish Square, W.
Langdale, H. M., Guy's Hospital
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
Larkin, R., Guy's Hospital
Larking, A. E., M.D., 4, London Street, Folkestone
Latimer, H. A., M.D., 202, St. Helens Road, Swansea
Lavers, N., M.D., Camberwell House, Peckham Road, S.E.
Lawry, R. C., Guy's Hospital
Layton, T. B., Guy's Hospital
Leader, H., M.B., 407, Fulwood Road, Ranmoor, Sheffield
Leathes, J. B., B.A., M.B., B.Ch., St. Thomas's Hospital, S.E.
Leckie, M., Guy's Hospital
Ledger, A. V., Guy's Hospital
Leeds School of Medicine Library (per the Secretary of Yorkshire
College, Leeds)
Leeming, A., Guy's Hospital
Leigh, W. W., J.P., Treharris, R.S.O., South Wales
Lewin, G., Guy's Hospital
Lewis, A. C., Wingham, near Dover
Lewis, R. P., Guy's Hospital
Lewis, W. C., Guy's Hospital
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., 95, Wimpole Street
Litchfield, P. C., Guy's Hospital
Inst of Subscribers. xxvil.
Littlejohns, A. S., Guy's Hospital
Littlewood, J. O., West Hill Drive, Mansfield, Nottinghamshire
Lloyd, E., B. A., Guy’ s Hospital
Lloyd, M., M. D., Vale Villa, Llanarthney, R.S.O., Wales
Lockwood, J. P., Faringdon, Berkshire
Lockyer, G. E., Purley Rectory, Maldon, Essex
Long, D. S., B.A., M.D., B.C., 71, Micklegate, York
Longhurst, E. A., Guy's Hospital
Longson, F. M., Guy's Hospital
Loosely, W. H., 14, Stratford Place, W.
Loud, F., Albion House, Lewes
Louisson, M. G., Guy's Hospital
Love, A. E. B., Richmond Villa, Bournemouth
Loveday, W. D., Becket House, Wantage, Berks
Lowe, E. C., Guy’ s Hospital
Lowe, F. B., Guy s Hospital
Lovve, G. C., Guy’s Hospital
Lowe, W. E., 23, Alderbrook Road, Balham, S.W.
Lucas, H., Huntingdon
Lucas, R., Clement, B.S., 50, Wimpole Street, W.
Lucas, T. C., Guy’s Hospital
Luce, R. H., B.A., M.B., B.C., 42, Friargate, Derby
Lucey, H. C., Guy’s Hospital
Luscombe, T. B., Cromer House, Teddington
Lush, Wm. George Vawdrey, M.D., 12, Frederick Place, Wey-
mouth
Lyne, W. C., Guy’s Hospital
McAlpin, J. G., 73, London Road, Leicester
McCarthy, J., McC., M.D., St. George's, Wellington, Salop
McDermott, B., Guy’s Hospital
McEvedy, P. F., Guy’s Hospital
McGavin, L. H., 21, Montagu Street, Portman Square, W.
McGill University Medical Library, Montreal, Canada
Magowan, P. D. F., Guy’s Hospital
McGregor, G., Verona, New Road, Portsmouth
McLachlan, A. R., Guy’s Hospital
MacLehose, Messrs. James & Sons, 61, St. Vincent Street
Glasgow, (2 copies)
MacIlwaine, S. W., Lyndens, Redhill
Mackern, George, M.D., Calle Florida, 484, Buenos Ayres
Maggs, W. A., 16, Hanover Square, W.
Mahomed, A. G., Astolat, Poole Road, Bournemouth
Maillard, Surgeon W. J., V.C., M.D., R.N., Oakfield House,
Pembroke
Maisey, C. T. B., 137, Cheetham Hill Road, Manchester
Maisey, F. T., Charlbury, Oxon
Makepeace, A. J., Hertford Chambers, Coventry
xxvili. List of Subscribers.
Malcolm, J. D., M.B., C.M., 15, Portman Street, Portman
Square, VV.
Malcomson, G. E., Guy s Hospital
Mallam, G. B., Hall Place, Sparsholt, near VVantage
Mallam, VV. P., 169, Uxbridge Road, Shepherd”s Bush, W.
Malleson, H. C., Guy s Hospital
Manby, Alan R., M.D., Bast Rudham, Norfolk
Manchester Royal Infirmary (per The Secretary)
Mandel, L., Guy’s Hospital
Manfield, G. H. H., North Stafford Infirmary, Stoke-on-Trent
Manley, J. H. H., M.A., M.B., 20, New Street, West Bromwich
Mann, H. C. C., Guy’s Hospital
Manning, T. Davys, M.B., B.S., Hoddesdon, Herts
Mansell, E. R., 44, Wellington Square, Hastings
Manser, F., The Priory, Church Road, Tunbridge Wells
Manser, F. B., B.A., Guy”s Hospital
Manson, P. T., M.B., 21, Queen Anne Street, W.
March, E. G., M.D., 41, Castle. Street, Reading
Marriott, Hyde, B.Sc., M.B., The Limes, Hall Street, Stockport
Marriott, O., Guy's Hospital
Marriott, R. B., Swaffham, Norfolk
Marshall, C. H., Guy's Hospital
Marshall, J., 143, Grange Road, S.E.
Marshall, W. L. W., Oak House, New North Road, Huddersfield
Martin, Albert, M.D., Ingestre Street, Wellington, New Zealand
Martin, B. H., Guy's Hospital
Martin, F. J. H., Perim, Arabia
Martin, James P., Slope of the Bank, Box, Wilts
Mason, A. L., Guy's Hospital
Mason, C. H., Guy's Hospital
Mason, W. Inglis, J.P., Sudbury, Suffolk
Matcham, Alfred, 116, St. George's Road, Southwark, S.E.
Mathews, A. L., Guy's Hospital
Mathews, H. D., 39, Brook Street, W.
Matthews, T. A., Guy's Hospital
Maurice, H., 1, Peahen Chambers, St. Alban
May, W. N., Guy's Hospital
Maybury, A. V., Guy's Hospital ;
Mayer, C. A. E., Guy's Hospital
Mayston, J. H., Guy's Hospital
Mayston, R. W., M.D., Hill View, Erith Road, Erith
Meachen, G. N., M.B., B.S., 27, New Cavendish Street, W.
Mead-King, W. T. P., Guy's Hospital
Meek, J. W., M.D., 329, Norwood Road, Herne Hill
Mellin, E. H., Guy's Hospital
Mesquita, S. B. de, M.D., B.S., 1, Highbury New Park, N.
Messent, R. J., Guy's Hospital
Metcalfe, B. B., Guy's Hospital
Last of Subscribers. xxix.
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.
Mickley, George, M.A., M.B., M.C., Freshwell House, Saffron
Walden, Essex
Millbank-Smith, H. J. M., Broadwater Villa, Broadwater Road,
Worthing
Miles, T. G., Guy’s Hospital
Miller, W. H., Guy’s Hospital
Milligan, R. A., M.D., Ardmae, Northampton
Mills, C., Guy’s Hospital
Milis, P. S., Guy’s Hospital
Milsom, E. H. B., Guy’s Hospital
Milton, E. F., Guy’s Hospital
Milton, W. T., M.B., M.S., 33, Greenvale Road, Eltham
Milward, J., M.D., Cardiff
Minett, P. F., Guy’s Hospital
Mitchell, H. E. H., Guy's Hospital
Mitchell, H. V., Guy's Hospital
Moffat, H. A., B.A., P.O. Box 595, Bulawayo, South Africa
Moir, G., Guy’s Hospital
Moiser, B., Guy’s Hospital
Moiser, L. H., Guy’s Hospital
Molleson, W. M., Guy's Hospital .
Moon, A. L., Guy’s Hospital
Moon, F., 20, Bryanston Street, Portman Square, W.
Moon, R. O., M.A., M.B., B.Ch., 16, Peter Street, Winchester
Moore, A. M., Holland Road, VVestham, Weymouth
Moore, W. H., 18, Chureh Street, Kidderminster
Morgan, A. L., Guy' s Hospital
Morgan, E., Guy's Hospital
Morgan, J., J.P., Mount Hazel, Pontryd-y-Groes, R.S.O.,
Aberystwith
Morgan, T., Guy’s Hospital
Morgan, W., Guy’s Hospital
Morice, C. G. F. ., M.D., Greymouth, New Zealand
Morrell, J. G., Guy's Hospital
Morrell, R. J., Guy’s Hospital
Morres, F., Guy’s Hospital
Morris, Arnold, B.A., Guy’s Hospital
Morris, C. S., Guy’s Hospital
Morris, F., Guy s Hospital
Morris, G. H., Guy’s Hospital
Morris, H. E., Guy's Hospital
Morse, T. H., 41, All Saints' Green, Norwich
XXX. List of Subscribers.
Moss, E., M.D., B.S., 6, King Street, Wrexham
Mothersole, R. D., M.D., M.S., 44, St. George’s Terrace, Bolton
Mottram, M. J., Guy’s Hospital
Moyle, H. H., Guy’s Hospital
Moyle, R., Guy’s Hospital
Mugford, S. A., 135, Kennington Park Road, S.E.
Muir, B., Villa Vecchia, Davosdorp, Switzerland
Mullins, R. C., B.A., M.B., B.Ch., Civil Surgeon, Imperial
Yeomanry Hospital, Elandsfontein, South Africa
Munden, C., Ilminster, Somerset
Munden, W. P. H., Guy’s Hospital
Mungal, R. C., Guy’s Hospital
Munro, D. J., M.B., B.S., c/o Dr. F. H. Morison, Raglan Place,
West Hartlepool
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, Shirley F., 22, Endsleigh Street, Tavistock Square,
W.C
Murray, C. M., B.A., Guy's Hospital
Musgrove, E. H., 55, High Street, Merthyr Tydvil
Muspratt, C. D., M.D., B.S., Tantallon, Madeira Road, Bourne-
mouth
Musson, J. O., Guy's Hospital
Mutch, R. S., M.D., The Manor House, Brixton Hill, S.W.
Myer, L., Guy's Hospital
Myott, E. C., Guy's Hospital
Naish, G., Beechcroft, Anstey Road, Alton, Hants
Nash, A. C., Guy's Hospital
Nash, P. J., Guy's Hospital
Nash, W. G., Welford, Rugby
Nason, J. J., M.B., Church House, Stratford-on- Avon
Nathan, M. P., 179, Barrack Street, Perth, Western Australia
Neale, B. G., Cromhall, near Falfield, R.S.O., Glosters
Ness, K. C., Street House, Essex Road, Watford
Newland-Pedley. F., 82, Devonshire Place, W.
Newnham, W. Н. C, M.B., Chandos Villa, Queen's Road,
Clifton, Bristol
Nicholson, Surgeon C. R., R.N., H.M.S. Cambrian, South East
Coast of America
Nicholson, J. W., Red Hall, Gainsborough
Nicholson, T. M., M.A., 245, Roundhay Road, Leeds
Nisbet, F. J., 11, "Heene Terrace, Worthing
Norburn, A. Е, М. D., Kidbrooke Lodge, Oldfield Park, Bath
Norman, A., 35, Coleherne Road, Earls Court, S.VV.
Norman, T., Guy s Hospital
Northampton General Infirmary Library (per the House Surgeon)
Inst of Subscribers. ХХХ.
Northcott, J. F., В.А., M.B., 179, Adelaide Road, South Hamp-
stead, N.W.
Norton, E. L. R., Guy's Hospital
Norton, O. S., Guy s Hospital
Nunn, G., Guy s Hospital
Nunneley, John A., M.B., 29, Royal Crescent, Bath
Oates, J. A., Guy’s Hospital
O’Brien, A. B., Guy’s Hospital
Ockfield, C. M., Guy’s Hospital
Oddy, A. E., 5, Duchess Street, W.
Odgers, P. N. Blake, B.A., Guy’s Hospital
Ogle, C. J., 1, Cavendish Place, W.
Oldham, C. J., 38, Brunswick Square, Brighton
Oldham, Montagu W., M.D., 56, West Gate, Mansfield
Oldman, C. E., M.D., "The Grange, Bletchingley, Surrey
Olver, S. H., 41, Devonshire Street, Portland Place, W.
Ommanney, F. M. M., 42, Kidbrooke Park Road, Blackheath, S.E.
Oram, R. G., Guy's Hospital
Oram, R. R. W., Cremyll, Bolingbroke Grove, Wandsworth
Common, S.W.
Ormond, A. W., Guy’s Hospital
Orton, W. S., Guy’ s Hospital
Osborn, A. G; M.B., Children’s Hospital, Great Ormond Street,
W.C.
Osburn, A. C., Guy’s Hospital
Owen, S. Walshe, 10, Shepherd’s Bush Road, W.
Pakes, A. E. H., B.Se., Guy s Hospital
Pakes, W. C. C., 12, Benson Road, Forest Hill, S.E.
Paliologus, A. L., 14, Beckenham Road, Beckenham
Pallant, H. A., Guy”s Hospital
Pallant, S. L., Guy’s Hospital
Palmer, A. E., 15, High Street, Loughborough, Leicestershire
Palmer, Clement, Barton-under-Needwood, Burton-on-Trent
Palmer, C. L. , Guy’ s Hospital
Palmer, FT N., -Guy’s Hospital
Palmer, F. R. E. , Collington Villa, Lee, Kent
Palmer, F. W. M., B.A., Guy's Hospital
Palmer, H. T., Guy's Hospital
Palmer, J. Irwin, 47, Queen Anne Street, W.
Palmer, P. H. Hayes, St. Elmo, Belvedere Road, Upper Norwood
Pantin, C. S., M.D., B.S., 1, Albert Terrace, Douglas, Isle of Man
Paramore, Richard, M.D., 2, Gordon Square, W.C.
Parfitt, F. W., Guy's Hospital
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.
` XXXİL List of Subscribers.
Parker, F. H., B.A., Guy’s Hospital
Parker, W. G., Guy’s Hospital
Parrott, H. McD., Guy’s Hospital
Parry, R., M.B., Ty Newydd, Carnarvon
Partridge, A. A. H., M.A., M.B., B.Ch., St. Germains, Grove
Road, Sutton, Surrey
Paterson, E. H., Guy’s Hospital
Paul, Frank T., 38, Rodney Street, Liverpool
Pavy, F. W., M.D., F.R.S., 35, Grosvenor Street, W.
Payne, J. Lewin, 44, Devonshire Street, W.
Payne, O. V., B.A., Guy s Hospital
Peacock, R., Guy’s Hospital
Peake, W. H., M.D., B.S., Marden, Kent
Peall, P. A., Guy’s Hospital
Pearce, F. J., Normanhurst, The Butts, Brentford.
Pearse, A. S. J., M.A., M.B., B.C., 110, Cathedral Road, Cardift
Peatfield, S. H., Guy’s Hospital
Peers, E. C., Guy's Hospital
Pedley, J. Kennerley, 3, Mount Sion, Tunbridge Wells
Pedley, S. E., The Terrace, 18, Peckham Road, Camberwell
Pedrick, P. V. S., Guy's Hospital
Pegge, Charles, Baglan House Asylum, Britton Ferry, Gla-
morganshire
Pellow, C. J., Guy's Hospital
Pellow, L. H, Guy's Hospital
Pembrey, M. S., M.A., M.D., B.Ch., Parkside, Clever Green,
VVindsor
Pendlebury, J. P., Knowles House, Ormskirk
Pendred, V., M.D., Crohill, Pendennis Road, Streatham, S.W.
Penfold, F. W. H., Rainham, Kent
Penford, W. R., Guy’s Hospital
Pennell, G. H., M.D., English Club, 77, Calle S. Martin, Buenos
Ayres
Pennington, 8. A. B. C. C., Holt, Norfolk
Penny, C. B., Guy’s Hospital
Penny, E., M.D., Hermitage, Marlborough
Percival, G. H., M.B., 66, Abingdon Street, Northampton
Perkins, H. B., Highfield, Barking, Essex
Perkins, J. S. Steele, B.A., Guy's Hospital
Pern, L., Guy's Hospital
Perry, C. E., M.D., 1, Castle Hill Avenue, Folkestone
Perry, E. C., M.A., M.D., Superintendent's House, Guy's Hospital
Peters, E. A., B.A., M.D., B.C., 13, Cadogan Place, Belgrave
uare, W.
Philipps, A. E., 50, Epple Road, Fulham, S.W.
Phillips, E., Guy's Hospital
Phillips, G. R., Guy's Hospital
Phillips, F. B. Willmer, M.A., M.D., B.Sc., 7, Harpur Place,
Bedford x
List of Subscribers. xxxiii.
d
Phillips, P. J., Guy’s Hospital
Phillipps, W. A., M.D., 18, John Street, Berkeley Square, W.
Pigeon, H. W., M. À., M. C., 6, Albion Street, Hull
Piggott, A. P. , Guy’ S "Hospital
Pike, D. R., Guy' s Hospital
Pike, N. H., M.B., Heckmondwike, Yorks
Pilkington, F. W., Kencott House, Lechlade, Glos.
Pillin, H. L., 33, George Street, Hanover Square, W.
Pinching, C. J., B.A., Guy's Hospital
Pinching, Charles J. W., 76, New Road, Gravesend
Pinder, G., M.D., B.C., Hazeldean, Farncombe Road, Worthing
Piper, S. A., Guy's Hospital
Pitt, G. Newton, M.A., M.D., 15, Portland Place, W.
Plimmer, H. G., 28, St. John's Wood Road, N.W.
Plummer, E. N., Guy's Hospital
Plummer, W. E., Wenchow, Shanghai, China
Plomley, John Fred., M.D., Knightrider House, Maidstone
Plumley, A. G. G., M.B., 28, Bond Street, Wakefield
Pocock, T. C., Guy's Hospital
Poland, John, 2, Mansfield Street, Cavendish Square, W.
Pollard, C., M.D., 23, Foregate Street, Worcester
Pollard, G. S., Midsomer Norton, Somerset
Pollard, J. M. W., Guy's Hospital
Poole, T. B., M.D., B.S., 53, Trinity Road, Wimbledon, S.W.
Poole, 8. K., Guy's Hospital
Poole, W., C.M.G., B.A., M.B., B.C., H.B.M. Legation, Pekin,
China
Poolman, A. E., B.A., c/o National Provincial Bank of England,
9915, Oxford Street, W.
Portsmouth Medical Library (c/o F. Lord, Esq., 16, Landport
Terrace, Southsea)
Powell, J. W., Guy’s Hospital
Poyser, R. C., Guy's Hospital
Prall, S. L., 19, Elgin Mansions, Maida Vale, W.
Prentis, J. E., Guy's Hospital
Preston, A. E., Guy's Hospital
Preston, C. W. R., Guy's Hospital
Price, A. E., M. D., M.S., Thanet Lodge, Bromley, Kent
Price, John A. PS M. D., 124, Castle Street, Reading
Price-Jones, C., M .B., 7, Claremont Road, Surbiton
Prideaux, A. E. D. , Guy’ s Hospital
Prince, P. C., Egremont, Reigate
R Staff-Burgeon VV. VV., R.N., Royal Hospital, Greenwich,
Purdom, VV. P., Guy”s Hospital
Purves, W. Laidlaw, M.D., 20, Stratford Place, Oxford Street, W.
Puzey, Chauncy, 71, Rodney Street, Liverpool
Pye-Smith, C. D. , Guy’ s Hospital
XXXİV. List of Subscribers.
Pye-Smith, P. H., B.A., M.D., F.R.S., 48, Brook Street W.
Pye-Smith, R. J., 450, Glossop Road, Sheffield
Rake, H. V., “ St. Ives," Fordingbridge, Salisbury
Ramsden, W., M.A., M.B., B.Ch., Pembroke College, Oxford
Ramskill, Josiah, 29, Meadow Lane, Leeds
Randall, C. W., Guy's Hospital
Randall, R. M. H., M.D., Goodwood, Coper's Cope Road,
Beckenham
Ransford, A. C., Guy's Hospital
Ransford, L. U., Guy's Hospital
Ransford, T. D., 6, Queen's Square, Bath
Ransford, W. R., Guy's Hospital
Rattray, M. J., Guy's Hospital
Rawlings, J. Adams, Bryn Awel, Sketty, Glam.
Ray, Edward Reynolds, 15a, Upper Brook Street, W.
Ray, G. W., Guy's Hospital
Rayson, H. K., Frazerburg, Cape Colony, S. Africa
Read, W. W., Guy's Hospital
Reader, S., Guy's Hospital
Recordon, R. B., 27, South Tay Street, Dundee
Rees, G. H., Guy's Hospital
Rees, M. J., Guy's Hospital
Reeve, E. F., Guy's Hospital
Reeve, W., Guy's Hospital
Reeves, A., 6, Streatham Hill, S. W.
Reeves, J. K., 66, Upper Tulse Hill, S.W.
Reid, A., The Cranes, Tooting, S.VV.
Reid, H., 200, St. Helen s Road, Swansea
Reid, P. J., 29, High Street, Aldershot
Reinhold, C. H., Guy’s Hospital
Reinold, A. W., M.A., F.R.S., 9, Vanbrugh Park, Blackheath
Rendall, R. M., Guy’s Hospital
Rendall, W., Maiden Newton, Dorset
Rendle, E. H., Guy s Hospital
Rey, 4. F., Guy s Hospital
Reynolds, B. G., “ Silverhowe," College Park, N.W.
Reynolds, D., Guy”s Hospital |
Reynolds, L. G., Toddington Villa, Plashet Lane, Upton
Park, E.
Reynold”s, L. L. C., Guy’s Hospital
Reynolds, R. J., Guy's Hospital
Reynolds, W., Guy’s Hospital
Reynolds, W. P., 128, Stamford Hill, N.
Richards, D. H., Guy’s Hospital
Richards, Owen W., M.A., Guy’s Hospital
Richardson, E. H., M.D., 31, 1-2 Peachtree Street, Atlanta,
U.S.A.
Inst of Subscribers. XXXV.
Richardson, H., 530, Commercial Road, E.
Richardson, T. A., 87, London Road, West Croydon
Richardson, W. S., M.D., *Melbury," Christchurch Road,
Bournemouth
Richmond, B. A., M.B., B.S., B.Se., Murillo House, High Road,
Lee, S.E.
Richmond, F., Guy's Hospital
Ricketts, T. F., M.D., B.Sc., Hospital Ships, Long Reach,
Dartford, Kent
Rivers, A. T., Guy's Hospital
Rix, B., 2, Mount Ephraim Road, Tunbridge Wells
Roberts, Astley C., Badlesmere, Eastbourne
Roberts, C. Gordon, M.A., M.B., B.C., Halstead, Essex
Roberts, E., Guy's Hospital
Roberts, H. W., Ashdown Villa, Wickham Terrace, Lewishaui
High Road, S.E.
Roberts, J. Lloyd, B.A., M.D., B.S., B.Se., 20, Prince's Avenue,
Liverpool
Roberts, R., Guy s Hospital
Roberts, R. J., M.A., M.B., B.C., 63, Gladsmuir Road, Whitehall
Park. N.
Roberts, T. H. F., Guy s Hospital
Roberts, VV. O., Guy”s Hospital
Robertson, C. H., Guy’s Hospital
Robertson, G. S., Guy”s Hospital
Robertson, W. I., M.D., St. Annes, Thurlow Park Road, West
Dulwich
Robinson, F. C., Guy s Hospital
Robinson, F. VV., M.D., Nev North Road, Huddersfeld
Robinson, G. C. F., Guy's Hospital
Robinson, 4. F., Guy s Hospital
Robinson, J. H., Guy s Hospital
Robinson, M. de L., Guy”s Hospital
Robinson, S. W., Guy's Hospital
Robinson, T., Guy”s Hospital
Robinson, VV. E., B.A., The VVhite House, Sonning, Berks.
Robson, H. Sheddon, J.P., B.A., 8, North Bailey, Durham
Robson, VV. M., M.B., Guy’s Hospital
Rodman, G. Hook, M.D., Heathcote, East Sheen, S.W.
Rogers, W. G., M.S., M.D., P.O. Box 810, Johannesburg,
Transvaal
Rogerson, F., Guy’s Hospital
Roome, A. M., Guy’s Hospital
Roots, W. H., Kingston-on-Thames
Roper, A., M.D., Colby, Lewisham Hill, S.H.
Roper, R. S., Guy's Hospital
Ross, H. B., Guy's Hospital
Routh, C. F., M.D., Purbeck House, Clarence Parade, Southsea
XXXVI. List of Subscribers.
Routley, E. W., Guy's Hospital
Rouw, R. Wynne, 7, Wimpole Street, W.
Rowell, G., 6, Cavendish Place, Cavendish Square
Rowland, E. W. S., 299, Oxford Road, Reading
Rowland, F. W., M.D., B.S., 6, Waterloo Place, Brighton
Rowland, W. J., B.A., M.B., B.S., 7, St. George's Road, Brighton
Rowlands, R. P., The College, Guy's Hospital
Rowlands, Richard P., Guy's Hospital
Rowlett, A. E., 7, London Road, Leicester
Rowley, A. L., 54, Terrace Road, Aberystwith
Royal College of Physicians, London, S.W.
Royal College of Surgeons, London, W.C.
Royal College of Surgeons in Ireland, Dublin
Royal Medical and Chirurgical Society, Hanover Square, W. (2
copies
Russell, G., Guy’s Hospital
Russell, G. H., M.D., Cromwell House, 235, Stockport Road,
Manchester
Russell, H. J., Guy’s Hospital
Russell, J. W., M.A., M.D., 72, Newhall Street, Birmingham
Rust, A. B. W., Guy’s Hospital
Ryffel, J. H., B.A., 10, Onslow Gardens, Highgate, N.
Ryle, R. J., M.D., 15, German Place, Brighton
Rymer, 4. F., 13, Old Steine, Brighton
Sadler, H. G., 3, De Castro Terrace, Wincheap, Canterbury
St. Mary’s Hospital, Manchester (care of the Librarian)
Saffery, F. G., 20, Talfourd Road, Peckham, S.E.
Salter, A., M.D., B.S., 154, Jamaica Road, Bermondsey, S.B.
Salter, C. E., M.D., B.S., St. Nicholas Parade, Scarborough
Sams, V. S., The Elms, West Worthing
Sandoe, J. W., M.D., B.S., Broad Clyst, near Exeter
Sangster, Charles, 148, Lambeth Road, S.E.
Sargood, G. F., Glencoe, Queen's Road, Kingston Hill
Sarjant, F. P., M.B., 1, Grosvenor Terrace, Withington, Man-
chester
Saunders, S. M., Guy's Hospital
Saunders, 8. J., Guy's Hospital
Saundry, J. Baynard, M.D., 81, Greenwich Road, Greenwich
Savage, G. H., M.D., 3, Henrietta Street, Cavendish Square, W.
Saward, A. H. M., 14, Highland Road, Upper Norwood, S.E.
Scales, J. E., Guy's Hospital
Schofield, G., M.D., Bloxham, Banbury
Scott, A., M.D., Bocking, Braintree, Essex
Scott, Alfred, 141, Marine Parade, Brighton
Scott, A. L., Westbourne Villa, Ealing Dean, W.
Scott, B., Hartington, Bournemouth
Scott, P., Guy’s Hospital
List of Subscribers. xxxvi.
Scott, R. A., Guy's Hospital
Scott, R. J. H., 28, Circus, Bath
Seagrove, R. St. G., Guy’s Hospital
Searle, W. R., Trinity Terrace, London Road, Derby
Secretan, W. B., M.B., Guy’s Hospital
Segreda, F. A., San José, Costa Rica, Central America
Sewill, J. Sefton, 94, Cavendish Square, W.
Shadwell, St. C. B., M.D., Lynhurst, Orford Road, Walthamstow
Shannon, S.S. H., Guy’ 8 Hospital
Sharpe, F. A., Guy's Hospital
Shattock, C. R., Guy's Hospital
Shaw, C. Knox, 19, Upper Wimpole Street, W.
Shaw, F. H., 33, Warrior Square, St. Leonards-on-Sea
Shaw, Lauriston E., M.D., 64, Harley Street, W.
Sheen, A. W., M.D., M.S., 2, St. Andrews Crescent, Cardiff
Sheffield Medico- Chirurgical Society (Dr. W. T. Cocking, 277,
Glossop Road, Sheffield)
Sheldon, T. Steele, M.B., Parkside Asylum, Macclesfield
Shells, W. F. M., G. P. O. Sydney, New South Wales
Shelswell, O. B., "Sibford, Mitcham
Shelton, H. L., Guy’s Hospital
Shelton-Jones, E., Guy's Hospital
Shepperd, A., Guy' s Hospital
Shillitoe, A., B. A., M.B., B.C., 2, Frederick’s Place, Old Jewry,
E.C.
Shipman, George Wm., Grantham, Lincolnshire
Shorter, H. G., Paragon House, Hastings
Shoveller, J. S., Guy’s Hospital
Shufflebotham, F., M.A., M.B., B.C., 12, London Road, New-
castle-under-Lyme
Shute, G. S., M.D., 2, Granby Place, Northfleet, Kent
Sichel, G. T. S., R.N., Royal Naval Hospital, Haslar, Gosport
Sigler, Geo. A., M.D., Liberty, Union County, Indiana, United
States of America
Simpson, G. S., Guy’s Hospital
Smalley, J. T. , Guy' s Hospital
Smart, H. D., Guy s Hospital
Smedley, R. D., B.A., Guy’s Hospital
Smith, A.H, Guy’s Hospital
Smith, D. Wilberforce, M.B., Guy’s Hospital
Smith, F. M. V., Guy’s Hospital
Smith, F. W., Guy’s Hospital
Smith, G. Bellingham, M.B., B.S., 24, St. Thomas’s Street, S.E.
Smith, G. Warwick, Guy”s Hospital
Smith, J. Snowden, West Street, Tavistock, Devon
Smith, James William, 18, Hall Gate, Doncaster
Smith, M. R., Guy’s Hospital
Smith, T. Morland, Guy’s Hospital
xxxviii. last of Subscribers.
Smith, W. A. L., M.A., M.B., B.C., 8, Chamberlain Street, Wells
Smyth, F. Sidney, “ Castleacre," Adelaide Road, Brockley, S.E.
Solomon, W. H., Guy’s Hospital
Soper, A. W., Guy’s Hospital
Soper, G. B. 8., Guy's Hospital
Soper, N. B., Guy's Hospital
South London Medical Reading Society (per Dr. John Durno,
168, Cold Harbour Lane, Camberwell, S.E.)
Spiller, J. E., Guy's Hospital
Spon, H. J., 29, Southwark Bridge Road, S.H.
Spriggs, E. Ivens, M.D., 26, St. Thomas's Street, S.E.
Spurgin, Herbert P. 89, Abington Street, Northampton
Spurgin, Thomas, Manor House, Ongar, Essex
Spurgin, W. H., 7, Graingerville, Newcastle-on-Tyne
Spurrell, C., Poplar and Stepney Sick Asylum, Devon's Road,
Bromley-by-Bow, E.
Stamford, R. B., Heathtield, near Alfreton
Stamm, L. E., M.B., B.Sc., Guy's Hospital
Stamp, L. D., Guy's Hospital
Staple, A. H., 53, Marlborough Street, Oldham
Starling, E. A., M.B., Chillingworth House, Tunbridge Wells
Starling, E. H., M.D., 8, Park Square West, Regent’s Park, N.W.
Starling, H. J., M.D., 55, Carlton Hill, N.W.
Statter, H. B., M.D., Snapethorp, Wimborne Road, Bournemouth
Stebbing, G. F., Guy’s Hospital
Steinhaeuser, J. R., M.B., B.S., Lewes
Stephens, L. E. W., Emsworth, Hants
Stephens, R. F., High Cross House, St. Austell
Stevens, A. M. A., 11, Clapham Park Road, S.V.
Stevens, E. O., Guy's Hospital
Stevens, G. J. в, 1, Newington Green, N.
Stevens, John, Guy’ s Hospital
Stevens, R. Ingram, 1, Devonshire Villas, Ditton Road, Surbiton
Stevens, T. G., M.D., B.S., 8, St. Thomas's Street, S.E.
Stevens, W. S., Guy s Hospital
Stevenson, C. M., Guy’s Hospital
Stevenson, T., M.D., 160, Streatham High Road, S. W
Steward, F. J., M.B., M.S., 24, St. Thomas's Street, S.E.
Stewart, B. H., B.A., Guy's Hospital
Stewart, H. M., M.A., M.D., B.C., Walton House, 508, Lordship
Lane, S. E.
Stewart, W. G., M.B., B.S., 48, Longton Grove, Sydenham, S.E.
Steweni, G. H., Biverslee, Hydro Avenue, West Kirby, Cheshire
Stocker, John Sherwood, M.D., 2, Montague Square, W.
Stoehr, F. O., B.A., M.B., B.Ch., Guy's Hospital
Stoke Newington, Clapton, and Hackney Medical Book Society
(per F. Wallace, Esq., Foulden Lodge, Upper Clapton)
Stoker, F. O., 23, Westland Row, Dublin
List of Subscribers. XXXİX.
Stothard, W. J., 163, Palatine Road, Didsbury, Manchester
Stott, E., Guy’s Hospital
Strange, E. W., Guy's Hospital
Strasburg University Library
Stringfellow, E., The Chestnuts, Taunton
Stroud, A. C., Guy's Hospital
Strover, H. C., Ivel Lodge, Sandy, Beds
Stuart, E. O., 30, The Common, Woolwich
Stuart, Major S. O., care of Dr. E. O. Stuart, 30, The Common,
Woolwich
Sturdy, H. C., Hospital for Diseases of the Chest, Victoria
Park, E.
Sturges-Jones, W. E., care of London and Pacific Petroleum
Co., Payta, Talara, Peru, South America
Styer, A. St. J., 25, Old Steine, Brighton
Suffolk Medical Book Society, per W. E. Harrison, The Ancient
House, Ipswich
Sumerling, B. J., 66, St. Edward Street, Leek, Staffs
Sutton, C. R. A., M.A., M.D., B.C., Maison Rouge, Sidcup
Swan, R. H. J., M.B., B.S., 8, St. Thomas's Street, S.E.
Swayne, F. G., M.A., M.B., B.C., 140, Church Road, Upper
Norwood, S.E.
Swayne, J. G., M.D., 74, Pembroke Road, Clifton, Bristol
Swayne, W. C., M.D., 8, Leicester Place, St. Paul's Road, Clifton,
Bristol
Sweet, S. H., Guy’s Hospital
Swinhoe, G. M., Park House, New Swindon
Sykes, J. F. J., M.D., D.Sc., 40, Camden Square, N.W.
Syms, G. F., Guy’s Hospital
Symonds, C.J., M.D., M.S., 58, Portland Place, W.
Ta'Bois, F. W., 2, Mornington Villas, Woodford Green, Essex
Та Bois, L., 53, Harley Street, W.
Tanner, John, M.D., 19, Queen Anne Street, Cavendish Square,
W
Targett, J. H., M.S., 6, St., Thomas's Street, S.E.
Tasker, B. G., 12, Goldstone Villas, Hove, Brighton
Taylor, Arthur S., M.D., Douglas House, Surbiton Hill
Taylor, Frederick, M.D., 20, Wimpole Street, W.
Taylor, H. Owen, M.D., Oxford Street, Nottingham
Taylor, J. G., B.A., M.B., B.C., 5, Upper Northgate Street,
Chester
Taylor, C. L. D., Guy’s Hospital
Taylor, M. Bramley, Guy’s Hospital
Tebbitt, H. R., 42, High Street, Tunbridge Wells
Telling, W. H. M., M.B., B.S., General Infirmary, Leeds
Terry, H. B., Woodchurch, near Ashford
Terry, R. H., Guy's Hospital
x]. List of Subscribers.
Tessier, C., M.B., Guy's Hospital
Thacker, H., Guy's Hospital
Thomas, A., M.B., B.S., North Parade, Aberystwith
Thomas, F. L., Guy's Hospital
Thomas, Jabez, Ty Cerrig, Swansea
Thomas, J. D., B.A., M.B., B.C., Bushey Heath, Herts
Thomas, J. D., Guy's Hospital
Thomas, T. P., B.A., Guy's Hospital
Thompson, A. R., Guy's Hospital
Thompson, D., Kirkston, Spa Road, Radipole, Weymouth
Thomson, C. B., 2, Granville Park, Lewisham, S.E.
Thorne, J. M., The Square, East Retford, Notts
Thorpe, G. E. Knight, 77, Gell Street, Sheffield
Thorpe, W. G., M.D., 34, Bedford Hill, Balham, S.W.
Ticehurst, A. R., J.P., Winstowe, St. Leonards
Ticehurst, C. S., “ Kemps," Hawkhurst, Kent
Ticehurst, G. A., Guy's Hospital
Ticehurst, N. F., B.A., M.B., B.C., Guy's Hospital
Tilbury, R., Farleigh Wallop, Basingstoke
Timpson, G. G., Guy's Hospital
Tinsley, Seth, Guy's Hospital
Tipping, H., Guy's Hospital
Todd, G., Sydenham, Torquay
Tolhurst, St. John A. M., Guy's Hospital :
Tongue, E. J., Huzelwood, Shooters Hill, Kent
Tracy, H. E. H., Guy's Hospital
Tracy, D. P., 88, Grosvenor Road, Highbury, N.
Tracy, S. G., Guy's Hospital
Trail, D. H., Guy's Hospital
Travers, O. B., Guy's Hospital
Travers, Otho R., San Nicolas, St. Leonards-on-Sea
Trethowan, W. H., Guy's Hospital
Trotter, A. O., Guy's Hospital
Tubby, A. H., M.S., 25, Weymouth Street, W.
Tuchmann, M., M.D, 113, Fellows Road, Hampstead, N.W.
Tuohy, W. E. J., Guy's Hospital
Turner, A. H., Guy's Hospital
Turner, F. Douglas, M.B., New North Road, Huddersfield
Turner, F. Meadows, M.A., M.D., M.C., South-Eastern Fever
Hospital, New Cross, S.E.
Turner, F. J., Guy's Hospital
Turner, H. A., Ely Lodge, Lismore Road, Eastbourne
Turner, H. E. B., Guy's Hospital
Turner, H. Gunton, Holmwood, Bournemouth
Turner, H. S., Balgownie, 211, Bridge Road, S.W.
Turner, J. Sydney, 81, Anerley Road, Anerley, S.E.
Turner, J. N., Guy's Hospital
Turner, P., M.B., B.S., B.Se., Guy's Hospital
List of Subscribers. xli.
Turner, T., Guy’s Hospital
Turner, V. E., Guy’s Hospital
Tweney, S. J. St. H., Calvert House, Mansell Terrace, Swansea
Tyson, W., M.A., M.B., B.Ch., The Beeches, Lowestoft
Tyson, W. J., M.D., 10, Langhorne Gardens, Folkestone
Uhthoff, John C., M.D., Wavertree House, Brunswick Place,
Hove, Brighton
University College Library, London, Gower Street, W.C.
Urquhart, A. J., Guy's Hospital
Valeria, I., Guy’s Hospital
Vandermin, H. F., Guy’s Hospital
Van Someren, E. H., Palazzo Soranzo, S. Polo, Venice
Vaughan, W. W., Guy's Hospital
Veasey, Henry, Aspley-Guise, Woburn, Bedfordshire
Vernon, T., Guy's Hospital
Viney, J. E., M.A., M.D., Harcourts, Chertsey
Visick, H. C., 11, Goldsmid Road, Brighton
Vorah, R. P., Rutlam, Central India
Wacher, F., Monastery House, Canterbury
Wacher, G., Guy's Hospital
Wacher, H., Guy's Hospital |
Wacher, S., St. George's Place, Canterbury
Waddy, H. E., Rhossili, Brunswick Road, Gloucester
Wade, J., B.Sc., 7, Trinity Square, S.E.
VVadson, 8. P., Guy's Hospital
Wainewright, R. S., M.D., 49, Wickham Road, Beckenham, Kent
Waite, D. A., M.A., 37, Westbourne Park Road, Bayswater, W.
Wakefield, C. F., Lincoln Lodge, Horley, Surre:
Wales, E. G., Downham Market, Norfolk
Wales, T. Garneys, Downham Market, Norfolk
Walker, A. W., Rue de l’ Académie, 17, Athens
Walker, F. E., Guy's Hospital
Walker, H. F. B., Guy's Hospital
Walker, S., J.P., Ashleigh, Middlesborough
Walker, T. M., Hook Norton, Banbury
Walkington, T., Guy's Hospital
Wall, A. H. E., Guy's Hospital
Wallace, F. H., Guy's Hospital
Wallace, R. U., M.B., Cravenhurst, 148, Stamford Hill, N.
Waller, W. A. E. Rugby
Wallis, C. D., Guy's Hospital
Wallis, D. H., Guy's Hospital
Wallis, H. W., Guy's Hospital
Wallis, M. E. A., 31, Thistlewaite Road, Upper Clapton, N.E.
VOL. LVI. 4
xlii. List of Subscribers.
Wallis, R., Guy's Hospital
Wallis, S. S., 287, Roman Road, Bow, E.
Wallis, V. M., Guy's Hospital
Walters, J. Hopkins, 15, Friar Street, Reading
Walton, J. W., Guy's Hospital
Ward, E. L., Guy's Hospital
Ward, J. L. W., Clasdir, Merthyr Tydvil
Warlow, F., Inglesant, Drummond Road, Bournemouth
Warner, P., Rydul, Woodford Green, Essex
Warren-Williams, H. E., Guy's Hospital
Wartski, J. L., 30, Upper Baker Street, W.
Washbourn, J. W., C.M.G., M.D., 6, Cavendish Place, Cavendish
Square, W.
Wason, R. L., 421, Green Lanes, Harringay, N.
Watney, H. A., Guy's Hospital
Watson, C. F., c/o The High Commissioner, Jebba, Northern
Nigeria, West Africa
Watson, D. P., Guy's Hospital
Watson, W., 1, Clifton Villas, Rochester
Watson-Smyth, C. A., Guy's Hospital
Watts, H., Guy's Hospital
Way, Montague H., Kenilworth Lodge, Clarendon Road, Southsea,
Hants
Weaver, E. A., Guy's Hospital
Webb, G. B., M.D., Colorado Springs, Colorado, U.S. America
Webb, H.. J., 166, Church Street, Stoke Newington, N.
Webber, A. M., Guy's Hospital
Weber, Sir Hermann, M.D., 10, Grosvenor Street, W.
Wedd, B. H., Guy's Hospital
Weir, Patrick A., M.A., M.B., C.M., Lieut.-Col. Indian Medical
Service, c/o H. 8. King & Co., 65, Cornhill, E.C.
Welchman, F. E., Guy's Hospital
Welchman, W., Guy's Hospital
Wellesley-Garrett, À. E., Dalkeith House, Leamington
Wells, S. M., Guy's Hospital
Wenyon, C. M., Guy's Hospital
Wetherell, F. C., M.B., Guy's Hospital
Wetherell, M. C., Guy's Hospital
Whatley, J. L., Guy's Hospital
White, W. Hale, M.D., 65, Harley Street, W.
Whitlow, H. L., Guy's Hospital
Whitinore, F. C., Guy's Hospital
Whitworth, Wm., St. Agnes, Scorrier, Cornwall
Wight, H. F., Guy's Hospital
Wilkes, J. Hamilton, 70, Frithville Gardens, Shepherd's Bush, W.
Wilkin, L., B.A., Guy's Hospital
Wilkins, J. C. V., Lerryn, Lostwithiel, Cornwall
Wilkinson, J. C., 1, Elwick Road, Ashford, Kent
Last of Subscribers. xliii.
Wilks, Sir Samuel, Bart , M.D., LL.D., F.R.S., 8, Prince Arthur
Road, Hampstead, N.W. |
Willan, G. T., Melton Mowbray, Leicestershire
Willan, G. T., junr., Guy’s Hospital
Willan, Reginald, Guy's Hospital
Willan, Richard, Guy's Hospital
Williams, A. E., Guy s Hospital
Williams, Fleet-Surgeon E. H., R.N., c/o C. W. Williams, Esq.,
Brick Court, Temple, E.C.
Williams, R. E., M.B., 21, The Common, Woolwich
Williams, R. O., Guy's Hospital
Williamson, N., M.D., New Brunswick, New Jersey, United
States of America
Wilson, A. R., B.A., Guy's Hospital
Wilson, T. F., Guy's Hospital .
Wilson, W., M.B., C.M., 184, Goldhawk Road, Shepherd's Bush,
W
Wilson-Smith, T., M.D., 17, Brock Street, Bath
Wiltshire, H. P., Guy's Hospital —
Winckworth, H. C., Guy's Hospital
Wingent. R. M., Guy's Hospital
Winslow, W., M.B., B.C., Watlington, Oxon
Witcombe, R. S., Guy's Hospital
Wohlmann, A. S., M.D., B.S., 9, Gay Street, Bath
Wood, C. D., The Old House, Dorrington, Shrewsbury
Wood, F. T. H., Guy's Hospital
Wood, F. S., Westbourne House, Sheffield
Wood, G. E., Guy's Hospital
Wood, J. A., Guy's Hospital |
‘Wood, P. M., Esher, Holden Street, Ashfield, Sydney, N.S.W.
Wood, Walter R., 21, Old Steine, Brighton
Woods, F. Lindsay, B.A., Guy’s Hospital
Woodward, H. M. M., B.A., Guy’s Hospital
Wordley, A. W., 20, Champion Park, S.E.
Wornum, G. Porter, 58, Belsize Park, Hampstead, N.W.
Worthington, H. E., The Sycamores, Birchington-on-Sea
Worts, C. C., Fordham Lodge, Colchester
Wragg, E., Guy's Hospital
Wright, G. A., M.B., 84, St. John Street, Manchester
Wright, H. S., Guy's Hospital
Wright, H., 71, Kennington Park Road, S.E.
Wright, H. H., Ospringe Road, St. John's College Park, N.W.
Wyand, E. H., Guy's Hospital
Wyatt, H. D., Guy's Hospital
Wyatt-Smith, F., M.B., c/o R. J. Neild, Esq., River Plate House,
Finsbury Circus, E.C.
Wylie, Angus, B.A., Guy's Hospital
-
xliv. List of Subscribers.
York Medical Society (care of Richard Turner, M.B., C.M., 48,
Bootham, York)
Young, F. C., B.A., M.B., B.C., Homesdale, Twyford, Berks
Young, John, M.D., 45, Stamford Hill, N.
Zorab, A., Guy's Hospital
IN EXCHANGE.
The St. Bartholomew's Hospital Reports
The St. Thomas's Hospital Reports
The Westminster Hospital Reports |
The Royal London Ophthalmic Hospital, Moorfields, E.C.,
Reports
The Edinburgh Medical Journal (care of Messrs. Oliver and Boyd,
Tweeddale Court, Edinburgh)
The Dublin Journal of Medical Sciences (care of Messrs. Fannen
and Co., Grafton Street, Dublin)
The Birmingham Medical Review (care of Dr. Saundby, 83a,
Edmund Street, Birmingham)
The Bristol Medico-Chirurgical Journal (care of L. M. Griffiths,
Esq., 11, Pembroke Road, Clifton, Bristol)
The Liverpool Medico-Chirurgical Journal (The Medical Insti-
tution, 1, Hope Street, Liverpool)
The Thompson-Yates Laboratories' Report, University College,
Liverpool
The Editors, The Medical Chronicle, The Owens College,
Manchester
Quarterly Medical Journal (care of The Editor, 342, Glossop
Road, Sheffield)
The Pharmaceutical Journal, 5, Serle Street, W.C.
The Transactions of the Hunterian Society
The Transactions of the Obstetrical Society of London
Transactions of the Odontological Society (care of the Hon. Sec.,
Odontological Society, 20, Hanover Square, W.)
Transactions of the Medical Society of London (care of W. R.
Hall, Esq.), 11, Chandos Street, Cavendish Square, W.
The Practitioner (care of Cassell & Co., Ludgate Hill)
The Medical Review, 70, Finsbury Pavement, E.C.
Library of Surgeon-General’s Office, U.S. Army, Washington,
D.C. (per Mr. B. F. Stevens, U.S. Government Despatch
Agency, 4, Trafalgar Square, London, W.C.)
xlvi. In Exchange.
The American Journal of the Medical Sciences (care of Messrs.
Lee Bros. & Co., Philadelphia, U.S.A.)
The Brooklyn Medical Journal, c/o Dr. James McF. Winfield
1313, Bedford Avenue, New York City, U.S. America
The Journal of Nervous and Mental Diseases (care of Dr. C. H.
Brown, 25, West 45th Street, New York)
Transactions of the College of Physicians, Philadelphia, U.S.A.
Transactions of the New York Academy of Medicine, care of
Librarian, 17, 19 and 21, West 43rd Street, New York
The Medical News (care of Lea Brothers & Co., 111, Fifth
Avenue, Con. 18th Street, New Yor«, U.S.A.)
Johns Hopkins Press, Baltimore, Maryland, U.S.A.
Le Progrés Médical (care of Dr. Bourneville, Rue des Écoles 6,
Paris)
Revue de Médecine (Monsieur le Docteur Lepine, 30, Place
Bellecour, Lyons)
Annals of the Pasteur Institute (Le Bibliothécaire Institut Pasteur,
Rue Dulot, Paris)
Mémoires de la Société de Médecine et de Chirurgie de Bordeaux
(care of Dr. Demons, Hópital St. André, Bordeaux)
Archives d'Électricité médicale (care of M. J. Bergonié, 6 bis Rue
du Temple, Bordeaux)
Le Bulletin de la Sociéte d'Anatomie et de Physiologie de
Bordeaux (care of M. le Dr. X. Arnozan, 27 bis, Pavé des
Chartons, Bordeaux)
Verhandlungen der Berliner medicinishen Gesellschaft (care of
Herr B. Fränkel, Bibliothek der Berliner medicinischen
Gesellschaft, Ziegelstrasse, 10, Berlin, N.)
Centralblatt, für Chirurgie (care of Messrs. Breitkopf und Hartel,
Leipzig)
Centralblat für. klinische Medicin (care of Messrs. Breithopf und
Hártel, Leipzig)
Centralblat für Innere Medicin (care of Messrs. Breithopf und
Hartel, Leipzig) i
Upsala Lükareförenings Fórhandlingar (per Prof. Hedenius
Bibliothéque de lu Société des Médecins, Upsal, Suéde)
Clinitchesky-Journal (care of Dr. V. Norobieff, Vosdvijenka,
maison N-4-7, logement N-1, Moscow)
ON A METHOD OF STRETCHING,
DIVIDING, OR EXCISING A PORTION OF
THE LINGUAL NERVE, WITH CASES.
By R. CLEMENT LUCAS, B.S.
SURGEON To Guy’s HOSPITAL.
In the British. Medical Journal of November 15th, 1884, there
appeared an editorial note’ on a method of stretching the lingual
nerve, which I devised for a case of intense neuralgia of the
tongue, after failing to give permanent relief by division of the
nerve, when following the older method suggested by Mr. Hilton
for the relief of pain due to cancer of the tongue.
The progress made in the methods of removing the tongue
for cancer has practically eliminated the cases for which Mr.
Hilton originally suggested division of the lingual nerve.* In
those days of conservative surgery, when the lingual artery—
trivial little vessel that it is—was held up as a terror to
surgeons, and when the operation of placing a ligature upon it
was deemed of tragic importance, when surgeons feared to
approach the tongue with knife or scissors and were satisfied
that ‘caustic or cautery were the only available remedies—when
the presence of a cancerous gland was regarded as a sign that no
operation could be of avail—in those primitive days of elementary
1 Brit. Med. Journ., Vol. ii., 1884, p. 975.
2 Guy’s Hospital Reports, 1850, p. 253.
2 On a Method of Stretching, Dividing, or Excising a
surgery, the idea of Mr. Hilton that temporary relief from the
agonizing pain of tongue-cancer might be brought about by
division of the lingual nerve, came and lived as a valuable sugges-
tion, but does not appear to have been acted upon by others till
ten or twelve years later. 1 take it for granted that now there
lives not a surgeon who with a case of cancer of the tongue
before him would dream of performing a palliative operation.
His thoughts would be concentrated on removing as thoroughly
as possible the growing disease, and even in the most advanced
cases, where vitality was not actually on the ebb, he would
proceed by excision to relieve the patient of the reeking decom-
posing mass which prevents him from taking nourishment, and
by its foator renders him objectionable both to himself and to his
friends.
Although the cases for which Mr. Hilton suggested neurotomy
of the lingual have passed into another category, there still
remain certain other conditions which call urgently for surgical
interference. They are happily rare, but anyone who has
witnessed the intense agony and distress caused by a chronic
neuralgic condition of the tongue will know how anxious such
patients are to be relieved of the maddening pain. The etiology
of such cases is often obscure. Some, no doubt, may be found
associated with a gouty diathesis, others with syphilis, but in
many cases the medical attendant will be entirely at a loss to
explain the cause of the intense recurring agony. Every possible -
remedy will have been tried without avail. Anti-podagric and
anti-syphilitic remedies will have been poured in, every nerve
tonic and every anodyne tried, all the soporifics administered in
succession, but the patient only wakes to renewed distress. Solid
food cannot be taken into the mouth without exciting stabbing
pains and salivation, and the patient gradually wastes from lack
of sleep and nourishment. What other causes than those
mentioned may be at work to produce such painful results must
generally be a matter of conjecture. Neuritis following typhoid
fever or influenza is a condition which apparently picks out
special nerves indiscriminately, and some of these cases may
have such origin. Outgrowths of bone about the foramen ovale
Portion of the Lingual Nerve, with Cases. 3
may be another possible cause, but I am inclined to think that
the throbbing lancinating pain so often experienced in these cases
must be dependent on the throb of the companion artery on the
sensitive nerve. So long ago as in my student days, in a prize
essay before the Guy’s Physical Society, I drew attention to the
interesting fact that almost every nerve of the head and face
subject to neuralgic pain passed through a small bony aperture or
canal in company with a small artery. Differences in the calibre
of this small artery, I argued, might be as much the cause of
neuralgic pain by pressing the nerve against the sides of the bony
foramen or canal, as alterations of function or pathological con-
ditions affecting the nerve itself. In the young, functional
sympathetic disturbances frequently disturb the calibre of the
vessels ; and in the aged, degenerative changes in the wall of the
vessel might lead to similar consequences. How far these
various suggestions may be justified, apart from clinical observa-
tion, it is difficult to forecast, for proper pathological investigation `
of such cases is most difficult ever to obtain. This is certain,
whatever may be the cause, nothing short of surgical operation
will in the majority of cases bring about any permanent relief.
It was for one of these cases of agonising neuralgia that I first
operated by dividing the lingual nerve after the manner described
by Mr. Hilton, a procedure which I found both difficult to perform
and unsatisfactory in its results. But subsequently, when the nerve
had united, I devised and carried out the operation it is the object
of this paper to bring into prominence, which is extremely simple
to perform and highly beneficial in its effect.
HILTON'S OPERATION.
Mr. Hilton thus describes the operation that he performed:
“Му dresser, Mr. Morgan, drew the tongue (which was much
congested with blood) forwards, upwards, and towards the
patient’s right side. I then divided vertically, with a small knife,
the mucous membrane, and submucous tissue to about three
quarters of an inch in length, opposite the molar teeth; over the
hyo-glossus muscle, and across the position of the sublingual
gland; the progress of the operation was much impeded by the
almost constant flow of blood, chiefly venous, into the wound;
—
4 On a Method of Stretching, Dividing, or Excising a
but by continuing deeply by the side of the tongue this first
incision, through the upper edge of the sublingual gland, I
exposed the nerve, and laying hold of it with forceps I divided it
with scissors. . . . The bleeding was stopped by a piece of sponge
dipped in a strong solution of alum, being forced into the wound.
Exactly one month from the date of the division of the nerve she
began to feel again on the left side at the tip of the tongue.”
It will be noticed that this operation, allowing for the increased
difficulty caused by the presence of a cancerous growth, proved
to be one not easy of performance, that a vertical incision three-
quarters of an inch in length was made across the course of the
nerve, and that it had to be carried deeply by the side of the
tongue and through the upper edge of the sub-lingual gland before
the nerve was reached. The operation was complicated by free
hemorrhage, which was only stopped by plugging the wound
with a sponge steeped in a strong solution of alum.
Moore’s OPERATION.
Twelve years after Mr. Hilton’s suggestion was made Mr.
Charles H. Moore, of the Middlesex Hospital, again drew atten-
tion to the temporary relief from pain that might be obtained by
dividing the lingual nerve or nerves in cases of cancer of the
tongue.’
He, however, recommended an improved method of dividing
the nerve at a point further back than that at which Mr. Hilton
operated. He describes his operation as follows: ‘‘ The guide to
the nerve in the latter situation is the last molar tooth. On
passing the finger into the mouth within and beyond that, the
bulging alveolar ridge can be felt narrowing as it ascends into the
thin coronoid process. Behind, below, and parallel with the
ridge, is the nerve. A line drawn inside the lower jaw, from the
crown of the last molar tooth to the angle of the jaw, would cross
it at right angles about half an inch from the tooth. An incision,
therefore, in the direction of such a line, three-fourths of an inch
in length, and carried through the mucous membrane to the inner
surface of the bone, must divide the nerve. It is advisable to
operate with a curved bistoury, since the alveolar ridge would
3 Med. Chir. Trans., vol. xlv., 1862, p. 47.
Portion of the Lingual Nerve, with Cases. 5
shield the nerve from the edge of a straight knife. It is also
advisable to be careful in observing the position of the alveolar
ridge, or, in its absence the edge of the toothless gum curving up
to the ramus. In one of my earlier cases, in which there were
no teeth to serve as a guide, I cut too far back and missed the
nerve, being probably misled by a mass of the tumour which was
adherent to the inner side of the lower jaw.”
This operation would appear to be a decided advance on that
originally carried out by Mr. Hilton, inasmuch as a definite guide
is pointed out for finding the nerve, and the trunk of the nerve is
divided farther back. But it presents several disadvantages
which render its successful performance doubtful. In the first
place, the “bulging alveolar ridge” caused by the last molar
tooth, is only present when the tooth remains in situ, and in Mr.
Moore's own experience, when ““ there were no teeth to serve as
a guide," he himself failed in his endeavour to divide the nerve.
With the extraction or loss of the last molar, and consequent
absorption of the alveolus, Moore's guide is lost and a blind cut
is made over the supposed position of the nerve. Another defect
in Moore's cperation is that he does not expose the nerve to view,
so that whether or not the operation has been satisfactorily com-
pleted cannot be ascertained until after the patient has recovered
from the anesthetic.
THE AUTHOR’S OPERATION.
The operation which I devised seventeen years ago, but the
exact details of which have never been published, depends for its
accurate performance upon the anatomical fact that the lingual
nerve passes from the outside of the internal pterygoid muscle to
the lateral aspect of the tongue. When the jaws are widely
separated the anterior edge of the internal pterygoid muscle is
put on the stretch and holds the nerve outwards in contact with
the jaw. If now the tongue be forcibly drawn out of the mouth
and towards the opposite ear, the edge of the pterygoid muscle
forms a point d'appui from which the nerve can be made tense.
Under these conditions the nerve forms a tense bow-string under
the mucous membrane, which can be both seen and felt. Thrown
thus into prominence its position becomes so evident that it
6 On a Method of Stretching, Dividing, or Excising a
cannot be missed, and it is completely under the control of the
surgeon.
The details of the operation are as follows:—A sand pillow is
placed under the hollow of the patient’s neck, so that the mouth
can be freely opened. A Gowan’s or Mason’s gag is introduced
on the opposite side to that on which the operation is to be
performed, to fix the jaw open, and a blunt hook retractor, whose
prongs are an inch and a half apart, is used to widen the mouth
and retract the cheek on the side of the operation. Next a stout
ligature is run through the tip of the tongue close to the septum,
but on the side of the operation, so that no pain may be felt in
this wound after the nerve has been stretched. This ligature is
tied in a loop and is used to draw the tongue forcibly out of the
mouth towards the ear of the opposite side. A tense fold of
mucous membrane then appears running from the inner aspect
of the jaw along the side of the tongue, with a hollow above and
below. This fold is caused by the stretched nerve which lies in
the free edge of the fold. Should swelling prevent the appear-
ance of the fold when the tongue is forcibly drawn to the other
side, the tense nerve can still be readily felt beneath the mucous
membrane with the forefinger.
The next stage is to pass a fine sharp hook, such as is used in
cleft palate operations, from below upwards through the fold of
mucous membrane and under the nerve. In this way the nerve
is securely held. An incision about a quarter or half an inch in
length through the mucous membrane, in a line with the nerve,
then exposes the trunk ; a blunt aneurysm needle is passed under
the nerve and the sharp hook removed. The nerve is now com-
pletely isolated and may be divided, excised, or stretched
according to the surgeon’s views as to what will best relieve the
patient.
The steps of the operation, as just detailed, were first worked
out on the dead subject and implicitly followed in the first opera-
tion performed in 1884. Subsequently, I have not generally
troubled to use the sharp hook, as if the tongue be sufficiently
tense, the nerve cannot be missed in cutting through the mucous
Portion of the Lingual Nerve, with Cases. 7
membrane over it. A fine suture may be used to close the
small wound in the mucous membrane.
Performed in this way the operation is practically bloodless,
and compares very favourably with the incision across the course
of the nerve into the side of the tongue and upper part of the
sub-lingual gland, as performed by Mr. Hilton.
It is impossible, if the details are followed out, that the
surgeon can fail, for the operation rests on an unalterable anato-
mical fact, the relation of the nerve to the internal pterygoid muscle
and the side of the tongue. In this respect it is very superior to
. Moore's operation, which depends on a guide which is not
constant, the alveolar prominence below the last molar tooth
disappearing with the loss of that tooth. Moreover, as I before
pointed out, Moore's operation is a blind: one, for no attempt is
made to expose the nerve, and it can only be a conjecture, till
after recovery from the anssthetic, that the nerve has actually
been divided. Further, it is inapplicable to stretching of the
nerve, which I maintain is a far more satisfactory operation than
division, being more lasting in its effects, and allowing of repeti-
tion should the pain recur.
An account of this operation was given by the late Mr. W.
Morrant Baker,‘ in Heath's Dictionary of Practical Surgery, but
I believe it did not find its way into the ordinary text-books or
works on operative surgery, either then or since. Much indeed
that is original or of value is apt to be lost in a dictionary, owing
to the disconnected nature of adjacent articles.
The following cases illustrate the advantages of the operation:
CASE 1.—W. A., mt. 48, was admitted into Guy's Hospital,
under Mr. Clement Lucas’s care, on October 30th, 1884. He
had suffered from both syphilis and gonorrhoea in former years, and
his wife had had three miscarriages and no living child. He had
suffered from tumoufs about his body, which came and dis-
appeared. There were two in front of the right leg, one on the
forehead, and one on the outer side of the right eye, which has
been breaking down for some time. He had knocked his left leg,
4 A Dictionary of Practical Surgery. Edited by C. Heath. 1886, vol. i.,
p. 654.
8 On a Method of Stretching, Dividing, or Excising a
which had been ulcerating for some months, in consequence. He
was, however, admitted on account of an exceedingly painful con-
dition of the right side of his tongue. He was in a medical ward
a year ago an account of the painful tongue, and Mr. Lucas then
saw him and divided the nerve. This gave him temporary relief,
but the pain returned a few weeks later. Six or seven years ago
the patient’s tongue first began to trouble him, causing him great
pain when eating or talking. He has suffered more or less ever
since. Patient is rather pale but fairly well nourished. There is
a swelling on the outer side of his right eye, an inch and a half by
one inch, discharging serqus fluid on the inner side. Another
swelling is situated on the front of his right leg, an inch and a —
half in length by three-quarters of an inch, larger at some times
than at others. On the outer side of this is the scar of an old
swelling over the fibula, about an inch in diameter. There is also `
a raised lump at the junction of the middle and lower thirds of
the tibia. On the front of the left tibia is a granulating sore as
big as a walnut. His tongue is very red, and tender underneath
on the right side. Near the base is a small tender lump about
the size of a pea, which is excessively tender, and is probably the
site of the former operation. The pain is much greater at one
time than another. Talking and eating bring it on, and the pain
seems to paralyse the tongue so that he cannot move it. He was
ordered fifteen grains of iodide of potassium, with tartrate of iron
three times a day.
The operation.—On November 11th, 1884, chloroform was
administered, Gowan’s gag was introduced between the molar
teeth on the left side, and the right cheek was drawn back by a
large pair of hook retractors. A stout silk ligature was next
placed through the tip of the tongue, and by means of this the
tongue was drawn forcibly out of the mouth and towards the left
side. As a consequence the lingual nerve was made to stand out
as a band beneath the mucous membrane at the posterior and
lower part of the tongue, where it could be readily felt to roll
under the finger. A sharp hook was next passed through the
mucous membrane from below upwards underneath the nerve so
as to fix it. Being held firmly by this hook, Mr, Lucas cut
Portion of the Lingual Nerve, with Cases. 9
through the mucous membrane over the nerve for about half an
inch, then passed a blunt hook under it. The sharp hook being
withdrawn, Mr. Lucas pulled forcibly on the nerve, first forwards
then backwards, so as to thoroughly stretch it. There was
scarcely any bleeding.
November 12th. The patient suffered scarcely any ill effect
from the anesthetic, and he has felt none of the old pain in his
tongue since the operation. He can now move his tongue about
without exciting any pain.
November 19th. The small operation wound has healed. He
has had no pain in the tongue since the operation, and can now
eat and talk with comfort. The sore on his left leg has healed
and the discharge from the place near his right eye has ceased.
The lump on his right shin has also gone down. He was dis-
charged to day.
RE-ADMISSION THREE YEARS LATER.—W. A., æt. 51, was re-
admitted into Job ward on June 15th, 1887, on account of a
recurrence of the pain in his tongue. He was a pale, thin, worn
looking man. He described the pain as if his tongue was being
sawn across, and sometimes he had difficulty in swallowing.
The same operation was repeated, except that Mr. Lucas did not
trouble to put the sharp hook under the nerve before cutting
down on it. The nerve was thoroughly stretched and he was
immediately relieved of all pain. |
He was discharged on June 24th, quite free from pain. He
attended among my out-patients and took iodide of potassium for
many months after his discharge, but no recurrence of pain was
noted, and I believe the second operation resulted in a complete
cure.
CASE 2.—Miss P., a maiden lady, set. 65, was brought to see
me on December 17th, 1885, by a member of ‘the hospital staff.
She was a tall, thin, delicate looking old lady, living in easy
circumstances with her sister. For more than twelve months
she had suffered from an acute stabbing, neuralgic pain on the
left side of her tongue. It comes on whenever she talks or eats,
and for some time she has been unable to swallow anything but
fluid diet and sops. The pain is so intense that it causes tears
10 On a Method of Stretching, Dividing, or Excising a
to flow from her eyes. When the pain first came on she had a
badly fitting set of false teeth, but the replacing of these by
others fitting correctly did not relieve the pain. At one time
some pain was felt in the lips on the left side, due probably to
the sympathetic irritation of the buccal branch of the third
division of the fifth nerve, but this pain did not continue.
December 19th, 1885, Mr. H. Davis gave an anesthetic and
I operated in a similar way to that already described. When the
nerve was exposed, and I was stretching it with an aneurysm
needle, I noticed something immediately beneath it, which proved
to be the duct of the submaxillary gland. The two cords could
be readily traced by traction, the one to the papilla by the side
of the frenum and the other to the side of the tongue. A fine
catgut suture was used to close the small wound in the mucous
membrane after stretching the nerve. The effect of the operation
was to completely relieve her of the pain. I saw her some four
years later, when she still remained free from pain, except for an
occasional slight reminder. She then began to show symptoms
of cancer of the bowel, of which she died some time after.
Case 3.—F. L., a retired officer of the Indian Civil Service,
consulted me May 6th, 1890, on account of intense neuralgia of
the right side of his tongue. He was fifty-six years of age,
plethoric and bronzed by the Indian climate. He had had
syphilis many years ago, and also suffered from occasional
attacks of gout. He had been a heavy smoker, but had lately
given it up as it seemed to aggravate the pain in his tongue. The
latter was white with chronic superficial glossitis, commonly
known now as leucoplakia. There were several irregular sharp
edged fangs and broken teeth, for which I sent him to a dentist to
have them filed down. This palliative treatment gave him no
relief, though the appearance of his tongue slightly improved.
On June 2nd, 1890, I operated on his tongue, pulling it out by
means of a silk suture put through the tip, cutting on to the
prominent band of the lingual nerve and stretching it with an
aneurysm needle passed beneath it. When he recovered from
the ansesthetic he said the pain was entirely relieved. I saw this
gentleman from time to time for several years and he remained
Portion of the Lingual Nerve, with Cases. 11
İree from the pain in his tongue. He died three years ago in a
fit of apoplexy. "
CASE 4.—The widow of a clergyman, who had suffered a good
deal of privation and much trouble, consulted me on February
16th, 1897. She was fifty-eight years of age, and since her meno-
pause had been generally in weak health. She was a thin, pale,
nervous-looking woman, who had been put to great sorrow by the
extravagance of her son, and had denied herself many of the
ordinary necessaries of life. For the last eighteen months she
had lived entirely on slop food, owing to agonising pain on the
right half of her tongue. When she moved it in eating or speak-
ing, a plunging, stabbing pain shot along the side to the tip and
seemed completely to paralyse it. She had been in the habit of
taking opium and chloral to gain sleep at night, and her nervous
system generally was in an unsatisfactory state.
On February 22nd, I stretched her right lingual nerve by the
method described, and it gave her immediate relief. It was some
time before she could be persuaded to take a rational amount of
food even when not suffering from pain, as she seemed to fear
that mastication would cause it to return. She greatly improved
in general health after the operation, and has not, I understand,
had return of pain in the tongue; but, from what I hear, she has
not been cured of the habit of taking opiates which was fostered
by the pain she used to suffer and by the trouble she had had to
endure.
The foregoing cases sufficiently illustrate the great relief that
can be brought about by the operation, and the ease with which
it can be performed.
VOL. LVI. 5
CASE OF CONGENITAL CAVERNOUS
ANGEIOMA OF RIGHT HAND.
LIGATURE OF BRACHIAL, AND FIVE
MONTHS LATER, OF RADIAL AND
ULNAR ARTERIES. CURE PERMANENT
TEN YEARS LATER.
By W. H. A. JACOBSON, M.CH.
` N. A., æt. 18, was sent to me at the Royal Hospital for Children
and Women, in 1891, with the following congenital condition of
the right hand. The patient could give no account of the
disease in its earlier stage. Her mother is dead. These cases
of angeiomata of the hand, or elsewhere, appear to form two
groups. In one the disease is congenital and begins as a neevus.
In the other the mischief first shows itself much later in life, and
dates, in some cases, to an injury. But they are still cavernous
angeiomata, not arterio-venous aneurysms or aneurysms by anasto-
mosis. All the fingers showed, back and front, and along their
lateral margins, bluish-purple swellings, involving the skin and
subcutaneous tissues. Here and there these swellings contained
knotty nodules, as if phleboliths were present. The thumb was
14 Case of Congenital Cavernous Angetoma of Right Hand.
not involved. The whole of the little and ring fingers, and the
upper half of the second finger were the parts chiefly affected.
The nail-bed of the index finger showed a chronic onychia, and
the nail was unusually dry, discoloured, and inclined to break up
longitudinally. Some of the swellings felt just like sacs full of
blood, others, especially those in the palm, felt spongy, as if com-
posed of cavernous tissue. All could be affected by pressure,
being imperfectly emptied and at once filling up again. Owing to
the presence of these swellings on the fingers it was impossible to
say if the digital arteries were enlarged. In places, e.g., on the
back of the index finger, large varicose veins the size of an adult
internal saphena ran upwards to spongy masses situated on the
dorsum of the metacarpus, e.g., over the second and third spaces.
These swellings appeared to be continuous with other puffy
swellings in the palm, less defined owing to the thicker cover-
ings. When those on the dorsum were compressed, those in the
palm increased in size. Elsewhere, e.g., over the palmar aspect
of the pisiform -bone, swellings distinctly puffy but not discoloured
were present. Apart from these angeiomata the hand was not
increased in size, measurements of the bones showing no increase
over those on the left side; nor was there any change in the size
and appearance of the forearm and arm.
The pulsation of the right radial and ulnar arteries was more
distinct than on the opposite side. Pulsation was also visible over
some of the largest of the above described spongy swellings,
especially in that over the palmar aspect of the first phalanx of
the middle finger. No thrill could be detected anywhere. The
chief complaint of the patient was that the hand felt big and
clumsy, and, when warm, intensely itchy. The puffiness interfered
with her writing or using a needle; points of much importance
as she was being trained as a sehoolmistress. The swellings were
always larger in cold weather, and when the hand was allowed
to hang down. On two occasions when one of the fingers was
accidentally cut, the bleeding is described as having been furious
and difficult to arrest.
March 13th. Ether was given. As puncture with the fine point
of the Pacquelin’s cautery caused no clotting, merely free jets of
Case of Congenital Cavernous Angeioma of Right Hand. 15
venous blood, and as the pulse in the right radial and ulnar
arteries was markedly increased compared with that in the fellow
vessels, the right brachial’ was tied in the middle of the arm
with a carbolised silk ligature.
The only difficulty met with in finding the artery was the large
size of the basilic vein and the vene comites. All pulsation below
at once stopped. The hand became cold and the level of the
masses of vascular tissue at once sank down, and to the feel
became markedly flaccid. Two days later very faint pulsation
could be detected in the radial artery.
March 28rd. Numerous setons of aseptic chromic gut were
passed into the chief vascular masses, now flaccid, and knotted
am situ. An incision was made over the varicose veins on the
back of the hand, and when these were exposed they were found to
be continuous, as was expected, by means of neevoid tissue passing
through the second and third spaces with the spongy tissue in the
palm. The veins were tied and removed. As much of the
cavernous tissue as seemed safe was cut away, while two deep
setons were passed into the spongy tissue which ran through
the spaces, knotted in situ and brought out between the sutures
which united the wound on the back of the hand.
The next few weeks, as the setons were withdrawn, fresh ones
were introduced, the fingers were kept bandaged with narrow
rolls of salalembroth gauze, wrung out of carbolic acid lotion
(1 in 40). The patient was kept under observation for some
months after the wounds had healed, in order that pressure could
be maintained by means of narrow roller bandages.
In August she was readmitted. The puffy swellings and masses
of spongy tissue had everywhere disappeared save on the back
of the index, ring, and little fingers. A little was also present
in the pulp of the ungual phalanges of the three outer fingers,
some swelling, still feeling like cavernous tissue, persisting in
the palm. But at each of these spots the amount of the disease
1 It will be noticed below that in Sir W. Lawrence’s case ligature of the
radial and ulnar arteries failed, though here the angeiomatous condition
affected only one finger. Also in Mr. Poland’s case (vide infra), in which
& vascular condition affected the dorsum and sole of one foot, ligature of the
dorsalis pedis and tibials failed also.
16 Case of Congenital Cavernous Angevoma of Right Hand.
itself and the bluish discoloration were extremely diminished.
Elsewhere its former existence was only shown by brownish
depressed and very distinctly pigmented scars. Extension of the
fingers was complete; flexion was possible to about two-thirds of
the full movement only. The fingers were now nearly free from
the former feeling of fulness, clumsy bigness, and itching.
While the repeated insertion of catgut setons had had much to
do with the great improvement of the disease in the fingers, I
was averse to using them in dealing with the swelling which
persisted in the palm. In the fingers the setons had been intro-
duced on the back and sides, safely away from the thece. But
the disease which persisted in the palm lay deeper, at the base
of the hypothenar and between this and the thenar eminences,
just over the place where the tendons are crowded together. As
the setons would have to be introduced deeply here, I preferred
to run the risk of tying the radial and ulnar arteries.
This was done on August 18th. Feeble pulsation was present in
the radial; none in the ulnar. Each stroke of the knife was
accompanied by universal, free, punctate oozing; on this
account a few threads of horsehair were used for drainage.
Several fresh setons of catgut were introduced into the
patches of disease still present in the pulps of the index,
little, and ring fingers. The hand became cold after the opera-
tion, but there was no waxy pallor. The limb was well wrapped
up in cotton wool. The two incisions for ligature of the arteries
healed without drawback, and no ulceration or threatening of
gangrene followed. Henceforward the only treatment employed
was firm bandaging of the fingers and hand. After an interval
of ten years I am able to give the permanent result of the above
operations. They show how complete has been the cure. I
quote the account as given by the patient herself and a lady who
has been; throughout, much interested in her. Since N. A. left
my care I have had no opportunity of seeing her.
“N. A. is now 27. She is head-mistress of a school in North
Wales, with an average of forty-five children. After being under
your care she was able to pass her three examinations, including
at each of the three times a good deal of fine sewing, knitting and
Case of Congenital Cavernous Angetoma of Right Hand. 17
drawing maps. She now teaches sewing, knitting, writing and
drawing, herself drawing freely on the black-board for the
children. She is in good health and does not suffer from her
hand in any way, except that during the winter, cold weather
makes it ache.”
As angeiomata of the extremities and especially the hand,
though happily not common, are extremely difficult to cure
radically, the following references to a few cases illustrating, as
some of them do, the difficulty sometimes met with in bringing
about a radical cure, and the severity of some of the steps taken,
may be of interest.
The well-known surgeon of New York, Dr. Abbe, brought
before the New York Surgical Society (Annals of Surgery, 1894,
Vol. i., p. 364), a boy, nine years of age, with an “ aneurismal
varix’’ occupying the ring, middle, and index fingers, as well
as the palm and dorsum of the right hand. When the patient
was a baby a small nevus was first noticed on the dorsum of the
middle finger near the middle joint. This remained quiescent
many years, but afterwards grew a little larger. About a year
ago he sustained a deep cut with a knife at the base of the
thumb; soon after, the nsvoid degeneration took on a rapid
enlargement, until it attained very marked dimensions. The
fingers affected have become several times larger than normal.
There is a thrill at the base of the thumb, and apparently a
connection between the artery and veins at that point, from
which point, also, the rapid invasion of the neighbouring parts
started. There is undoubtedly some increase in the size of the
radial artery all the way up the forearm, but it is likely that this
is only coincident with the increased supply of blood demanded
by the finger enlargement. There was no question in the family
about the rapidity of the growth during the year since the
accidental cutting, yet it was not possible to say that there was
no connection between the arterial venous plexuses before that
time. As there was a very local aneurismal thrill at a point quite
near to the scar in this hand, Dr. Abbe believed that there was
a connection between a rather large artery and a venous trunk
close to the chief enlargement, and therefore preferred to call
18 Case of Congenital Cavernous Angeioma of Right Hand.
the condition one of aneurismal varix rather than angeioma
With regard to treatment, he had operated on one case success-
fully which resembled the one now before the society. The
whole arm was involved from the hand to the shoulder, presenting
a sponge-like appearance, but there was not the bruit nor the history
of traumatism with more or less rapid increase afterwards. He
tried several methods, resorting to excision of a part, to the actual
cautery, and cautery with a wire loop, cutting through the masses
in planes with the cautery wire. He also tried Roser’s method,
with the septic setons suggested by Professor Esmarck, who
witnessed the cautery operations. But in a case like the present
one he would be inclined to cut down upon the point of apparent
anastomosis and excise that portion. He intended also to try
the Roser method again. |
Dr. A. P. Gerster looked upon the case not as one of aneurysm,
but of arteriovenous angeioma, a condition very frequently con-
genital and growing with the growth of the individual, involving not
only the vessels, but all the tissues, even the skeleton of the parts
affected. He described a similar case, one entire lower extremity
up to the buttock being involved. Ultimately the veins became
thrombosed, and very severe attacks of phlebitis occurred, accom-
panied by high fever and serious interference with the circulation
of the limb, so that superficial gangrene of the skin developed in
several places. In order to ward off a possibly fatal complica-
tion which was threatened in this manner, he finally amputated
the limb through the diseased tissues. The vascularity of the
cut surface was so great that he had, according to the statement
of Dr. Kinloch, of Charleston, who assisted him, to tie about
seventy-five arteries, yet the surface was still practically a spongy
opening, which would have caused fatal hamorrhage the moment
constriction was removed. In order to secure against the possi-
bility of secondary hemorrhage, he resorted to the plan of closing
the entire surface by buried sutures, commencing at the peri-
osteum and going out to the skin. The wound healed by first
intention, and the patient was well seven years after the opera-
tion. In another case, that of a boy eleven or twelve years of
age, the disease being limited to the toes, foot and heel, the
Case of Congenital Cavernous Angeioma of Right Hand. 19
external iliac was first tied, and, as a consequence, rather exten-
sive gangrene of the skin near the disease and of the bellies of
both peronsi muscles developed, and the boy's foot had to be
amputated. He finally recovered. The bones in both cases
were decidedly enlarged, as ascertained by exact measurement.
Other instances of the grave importance which may sometimes
be attached to these cases of angeioma of the hand are shown by
two of the following cases. |
Professor Spence (Medical Times £ Gazette, vol. ii., 1875, p.
209) related the following cases. “ An infant of six weeks was sent
to my care on account of a deep-seated erectile tumour occupying
the palm of the hand and extending up to the wrist. The tumour
had been growing rapidly, and at one point the skin was thin and
discoloured. I used injection of perchloride of iron, and part
consolidated. Again it was used and the consolidation was
followed by inflammation and separation of a small central slough.
From the ulcerated surface bleeding took place, and though
arrested by local application of the perchloride, it returned from
time to time, and as the child's life was thus endangered, and the
growth seemed rather to increase than to diminish, I was forced
to amputate through the forearm when the infant was eight weeks
old. She made a very rapid recovery, but with the loss of a hand.
I show you here the cast of the hand of an infant affected with
deep-seated pulsating erectile tumour very similar to the former.
In this case I applied electrolysis during three months while the
child was under my care in hospital, and by several applications
of the battery the growth began to consolidate and contract. As
it was inconvenient for the mother to remain in hospital, I asked
Dr. Connel, of Peebles, who had sent the case to me, to conduct
the remainder of the treatment." It is stated that ‘‘the cure was
. eompleted," but we have no information how long afterwards the
case was watched.
The following case is reported by Dr. Russell (Medical Gazette,
vol. xviii., p. 173). It appears to belong to the second or non-
congenital group of these cases. “ The woman, et. 41, had two
swellings, each about the size of a walnut, extending one
from the extremity of the ring, the other from that of the little
20 Case of Congenital Cavernous Angeioma of Right Hand.
finger to the middle of the fingers, of a violet colour and
spongy feel, and of a structure resembling a placenta. They
shrunk under pressure, but recovered their size on its being
removed; throbbed strongly, as did all the vessels of the arm,
and were excessively painful. The radial and ulnar arteries
were enlarged, the latter tortuous, the basilic vein had assumed
the appearance so commonly seen in a varicose vein of the leg.
She stated that the disease had commenced five years before, on
the tip of the ring finger, just under the nail, by a bleeding,
without any previous symptom, while engaged in wringing
clothes. At first she observed a little speck, which ulcerated,
cicatrized, and then gradually formed a little violet-coloured
pulpy tumour, bleeding frequently and sometimes freely. In
three years more a similar tumour appeared on the little finger of
the same hand. The bleeding and inconvenience increased much.
I recommended removal of the fingers at the metacarpal joints,
which she declined. After some weeks she returned, willing to
submit to anything. The disease had now extended so far as to
form one aneurysmal tumour at the junction of the two fingers,
the placenta-like appearance reached now to the wrist, the arm
was of an erythematous hue to the elbow, the tumour had ulce-
rated and sloughed, and the carious phalanges protruded from the
gangrenous fingers, which were enlarged and dreadfully painful.
The pulsation and size of the arteries and veins had considerably
increased up to the axilla. I first tied the ulnar artery at the
wrist and then amputated the metacarpal bones of the ring and
little fingers at the carpus, being obliged to cut within the verge
of the purple mass. The stump healed well. "Three years after
she called to thank me. All the morbid affections had long
subsided, the vessels of the arm had resumed their natural
appearance, and with the assistance of the thumb and two
fingers she was enabled to follow her occupation of a laundress.””
The following case is of interest, (1) from the failure of ligature
of the radial ulnar arteries, and (2) from the treatment adopted
later. It will be seen that the mischief was probably congenital
and affected one finger only. The case is given by Mr. Wardrop
Case of Congenital Cavernous Angeioma of Right Hand. 21
(Med. Chir. Trs., Vol. ix., p. 216). It is related in the words of
Sir William Lawrence.
““ A woman, twenty-one years old, has been for the last three
or four years under the care, first of Mr. Hodgson and sub-
sequently of myself, for a pulsating tumour of the finger, of the
description which has been called aneurism by anastomosis. She
does not remember its commencement, but rather supposes that
it had existed from the time of birth; it increased in size, and
began to be troublesome about four years ago. The complaint
occupied the ring finger of the right hand, there was a general
fulness of the first phalanx, but the chief swelling was on the
palmar surface and ulnar side of the finger, the circumference of
which may probably have exceeded the natural dimensions by one
third. The swelling was soft and compressible ; the vessels com-
posing it obscurely discernible through the skin, and gave it a
slightly reddish or livid tint. There was a sensation of heat in it,
and it was rather warm to the touch. It pulsated strongly, just
like an aneurism. The digital artery of the corresponding side was
very large, and conspicuous by its size and strong pulsation in
the palm of the hand. The veins at the back of the finger, hand,
and forearm were turgid, and the integuments of the hand, on its
dorsal surface marked by a line of discolouration exactly like that
which remains after a bruise. Having ascertained that the beat-
ing could be stopped entirely by pressing on the radial and
ulnar arteries at the same time, and having tried ineffectually for
several months compression and other external means, Mr.
Hodgson tied both the trunks mentioned. The consequences of
the operation were an entire cessation of the beating, collapse of
the swelling and relief of pain, but these symptoms all
recurred in a few days, and were just as bad as before." Com-
pression being again unavailing and amputation of the finger
being refused, Sir W. Lawrence operated as follows :—
“To cut off the supply of blood I made a circular cut close to
the palm, through all the soft parts, excepting the flexor tendons
with their theca, and the extensor tendons. The digital artery,
which had pulsated so evidently in the palm of the hand, was
fully equal in size to tho radial or ulnar of an adult, and was th
22 Case of Congenital Cavernous Angeioma of Right Hand.
principal nutrient vessel of the disease. After tying this and
the opposite one we were much surprised at finding so strong a
jet of arterial blood from the other orifices of these two vessels
as to render ligature necessary. The occurrence, however, dissi-
pated any apprehensions that might have been entertained
respecting the subsequent supply of the finger. The edges of the
incision were brought together by four sutures, but could not be
very satisfactorily united in consequence of the tumor, and indeed,
the whole finger beyond the cut swelling considerably. The
wound of the incision healed slowly: the swelling subsided, but
did not entirely disappear; and the integuments recovered their
natural colour. The pulsation and the pain were put an end to.
At the present time ”—the interval after the operation is not
given, but was, perhaps, two years —“ there is still a fulness of
the part, but without any beating, and some minute red vessels
are visible in the skin.”
In reporting a case of cavernous angeioma of the hand in our
Hospital Reports, one naturally refers to a closely similar case of
* Erectile Tumour of the Foot," fully reported by Mr. Poland in
these Reports for 1868-1869. The wax models, copied from a
dissection of the part by Mr. Howse, show the presence in the
sole of the foot of cavernous tissue very similar to that in the palm
of the hand of my patient.
The patient was a girl of nineteen. The mischief here dated
to an injury to the foot from the fall of a desk ten years before.
Cavernous tissue was present in this case both in the sole, where
it was continuous with the plantar arteries, and in the dorsum
where it was connected with the dorsal artery and internal
saphenous vein. Mr. Howse who wrote as a supplement to
Mr. Poland’s article a full account of the anatomy of the growth
was inclined to think that it originated in the walls of the arteries
and veins, as small growths were found arising in the walls of the
digital vessels and the internal saphenous vein quite unconnected
with the larger masses of erectile tissue. In this case the dorsal
artery was first tied, as pressure on this vessel controlled the
pulsation in the cavernous tissue on the dorsum. Pulsation
reappearing, the posterior tibial artery was tied in its lower third.
Case of Congenital Cavernous Angetoma of Right Hand. 23
Symptoms completely disappeared, and pressure by a pad and
bandage was ordered, the patient leaving the hospital. The
swelling on the dorsum reappeared, and as pressure on the
anterior tibial just above the ankle commanded this, the artery
was tied at the above spot. Once more the swelling, pain, and
throbbing disappeared, only to return in three or four weeks.
Amputation was now performed through the leg, a good recovery
following. |
In a similar case of cavernous angeioma of the foot it would be
interesting to know the result of first tying the femoral artery
and then, if needful, the tibials low down.
CoNCLUSIONS.
(i.). The importance of curing early any nevus on the hand
or foot.
(ii.) Ligature of the main artery first, and, later on, if needful,
of the radial and ulnar or tibial arteries, offers the speediest and
simplest method of treatment in these cases, where the arteries,
veins and capillaries are all affected, and cavernous tissue is
present as well. The above treatment may be supplemented by
the use of sterilised setons and firm bandaging, but it is unlikely
that these will cure any cavernous tissue which persists after
ligature of the main trunk only. Ligature of the radial and ulnar
or tibial arteries alone is not likely to bring about a radical cure
judging from Mr. Hodgson’s case—here only one finger was
affected—and that of Mr. Poland.
(iii.) If the criticism is offered that tying the radial and ulnar
just above the wrist, after ligature of the brachial, is a dangerous
step, I admit its fairness. I would reply that any other treat-
ment of the cavernous tissue which still persisted in the palm, as
by setons, excision, or electrolysis, was not promising, owing to
the close contiguity of the flexor tendons, together with the
nerves and the depth at which the mischief lay. In taking the
further step I was influenced by the following points. Five
months had elapséd since the ligature of the brachial artery.
The patient was young and her vessels free from endarteritis. As
it was clear that the anastomoses round the elbow-joint had
24 Case of Congenital Cavernous Anqetoma of Right Hand.
brought sufficient blood into the ulnar and radial arteries to feed
the disease which persisted in the palm, it might be expected
that, after ligature of the radial and ulnar arteries just above the
wrist, sufficient blood would find its way by means of the inter-
oseous and carpal arteries, and those abnormal channels which
would be likely to exist in such a case of eighteen years’ duration
to carry on the life of the hand.
A CASE OF SPLENIC ANJEMIA.
By LAURISTON E. SHAW, M.D.
PHYSICIAN TO Guy's HOSPITAL.
In the fifty-second volume of these Reports Dr. Frederick Taylor
has recorded a typical case of Splenic Ansemia. Unfortunately
no post-mortem examination could be obtained, but the clinical
aspects of the case leave no room for doubt that the disease
belonged to the group to which the title splenic anemia has been
given. In the last few years the number of cases recorded as
examples of this condition has rapidly increased, and many
varying more or less from the type originally described have been
included. Osler has collected a series of fifteen cases which
occurred in his own practice during twenty years, and
has recorded them in the American Journal of the Medical
Sciences for January, 1900. In his paper he has drawn atten-
tion to the diseases for which this condition is likely to be
mistaken, and has given a brief summary of. the main clinical
features. To this communication, to Dr. Taylor’s paper above
referred to, and to the article on Splenic Anemia by Samuel
West in Clifford Allbutt’s System of Medicine, the reader is
referred for particulars as to the nature and history of the
disease. In recording the present case some points of special
interest will alone be dealt with.
Splenic ansemia, has naturally attracted great attention because
it appears to be the only uniformly fatal disease in which it is
possible that the extirpation of an enlarged spleen may save the
26 A Case of Splenic Anemia.
patient’s life. In Dr. Taylor’s case the possible advantages of an
operation were pointed out to the patient’s friends, but operation
was declined. In the case I am about to record I regret that no
operation was proposed. This was not due to a want of appre-
ciation of its possible advantages, but to the uncertainty of the
diagnosis. Although the possibility of the case being one of
splenic anemia was before us from the time of the patient's
admission to the hospital, and although I had the advantage of
consultations with several of my colleagues, I was unable to
satisfy myself that the association of enlargement of the spleen
with heematemesis might not be due to some condition which was
recoverable without operation, or was beyond the possibility of
relief by surgical means.
I do not wish to be understood as advocating that in all cases
of splenic ansemia the spleen should be removed. İn any case in
which the diagnosis can be confidently made, and in which, not-
withstanding medicinal treatment, the disease makes steady
progress, splenectomy is justified. In endeavouring to estimate
the value of this treatment, two points must be borne in mind.
Already a, case has been recorded in which good results seemed
to follow the operation, but in which a few years later death
ensued, and the post-mortem examination showed the enlarge-
ment of the spleen to have been due to cirrhosis of the liver.
At present, also, our knowledge of the life-history of the disease
is very imperfect. From some of Osler’s recently reported cases
it appears that the disease may exist much longer than the period
of two years, which was until Jately stated to be its maximum
duration. Even should a patient survive splenectomy for twelve
years, we cannot say for certain that this is in consequence of,
and not despite the operation. It must not be forgotten that at
one time splenectomy was regarded as a proper proceeding in
leucocythemia. It is now altogether abandoned, on account of
the serious risk of uncontrollable hemorrhage, due to the altered
state of the blood. Neither in leucocythemia nor in splenic
anemia have we any definite knowledge as to the actual cause of
the disease, nor can we say for certain whether the enlarged
spleen is a primary or secondary factor in the pathology. Until
A Case of Splenic Anemia. 27
our knowledge is greater our treatment must be empirical.
Experience has proved that no immediate ill effects follow the
removal of the spleen in splenic anemia. Extended knowledge
will shew whether the good effects are permanent, and whether
simpler measures can be relied upon to produce equally good
results.
The following notes are from the report written by Mr. H. M.
Hardy :—
Lily D., set. 10 years, was admitted into Guy's Hospital on
January 19th, 1898, for a tumour in the abdomen.
Family history.—The father and mother are quite healthy.
The father is a bricklayer’s labourer. Two brothers died in
infancy, the remainder of the family, three in number, are healthy.
Previous history.—The child has bronchitis every winter. She
has had measles, whooping cough, and chicken-pox. Has always
been considered by her mother to be a weakly child, often com-
plaining of headache. She has always lived at Greenhithe, in
Kent.
History of present iliness.—On December 26th, 1897, viz.,
twenty-four days before admission, while in her usual health the
patient awoke at 4 a.m. and called out that she was going to be
sick. She immediately vomited half-a-pint of blood mixed with
food. The vomiting of blood was repeated four times on the 26th
of December, and twice on the 27th. The medical man who was
called in to see the child noticed a tumour in the abdomen.
Since the attack of hamatemesis the patient has been pale and
has lost flesh. There has been no acute pain, and no further
gastric disturbance.
Condition on admission.—The patient is anemic, the skin having
a yellowish tinge. She is fairly well nourished. The temperature
is 99°, the respirations are 28 per minute; there is no cough or
dyspnoea, and the physical examination of the lungs reveals no
abnormality.
The pulse is 100, small, regular, and compressible. There is
a soft blowing systolic murmur at the apex, but no obvious enlarge-
ment of the heart. The apex beat is in the fourth space.
VOL. LVI. 6
28 A Case of Splenic Anema.
The specific gravity of the urine is 1012, its reaction neutral,
there are no abnormal constituents.
The lips are pale, the tongue moist, the appetite is good; the
bowels are regular.
On examination of the abdomen, the spleen is found to be much
enlarged, forming a tumour reaching from the costal margin to
the left iliac fossa. Its inner edge is sharp and well defined, and
close to the costal margin a notch can be felt. The tumour moves
freely on respiration.
The liver dulness is not increased, but the edge of the organ
can be felt to descend below the costal margin on deep inspira-
tion and is perhaps a little harder than normal.
The abdomen appears to be distended and the veins over it are
unnaturally visible. No ascites can be detected.
Examination of blood.—Heemoglobin, 80 per cent.; red cor-
puscles, 3,300,000 per cubic millimetre; white corpuscles, no
. Increase.
The patient was put on Mist. Ferri Tartarati Sil. ter die, with
farinaceous diet and beef-tea.
January 31st. The edge of the liver is clearly felt just below the
costal margin and is thought to be a little harder than normal.
There is some increase in the amount of abdominal distension.
The hemoglobin has increased to 45 per cent.
February 2nd. The backs of the eyes appear quite normal.
No һәзтоггһаре can be detected.
8rd. The blood is examined to-day and gives the following
results :— Red discs, 3,000,000; hemoglobin, 60 per cent.; white
corpuscles, two or three only seen in the field.
6th. Temperature 102°. Slight epistaxis this morning. Patient
complaining of headache and some pains in the joints. The
medicine has been changed to a mixture containing two drops of
Liq. Arsenicalis, and two grains of Ferri et Am. Cit. each dose.
The patient is on fish diet.
14th. The spleen is harder but not materially altered in size.
Heinoglobin, 50 per cent.; red corpuscles, 4,000,000; white
corpuscles, no excess. Circumference of the abdomen at the level
of umbilicus, twenty-three inches.
A Case of Splenic Anemia. 29
15th. Patient to-day vomited about a pint of blood, at first
bright red and later dark in colour. A few hours after the
hematemesis the spleen was noticed to be very much diminished
in size.
17th. The patient vomited half a pint of blood yesterday and
a smaller quantity to-day. The spleen is still more diminished
in size.
18th. No more hematemesis. The circumference of the
abdomen is twenty-one and three-eighths inches, being one and
five-eighths inches less than it was the day before the recent
attack of hsematemesis. Since the vomiting the patient has
been fed on peptonised milk and nutrient enemata.
23rd. The spleen is larger again. It reaches from the seventh
rib to within an inch of the anterior superior spine and forwards
to within two inches of the umbilicus.
March 1st. The abdomen is more distended. It measures
twenty-three inches.
5th. Blood: red corpuscles, 2,850,000 per cubic millimetre ;
hemoglobin, 30 per cent.; white corpuscles 1 to 912 red.
llth. Another attack of hamatemesis. Vomiting at 4 p.m.,
again at 11 p.m. Altogether two pints of fluid were brought up,
chiefly consisting of blood.
12th. To-day two or three ounces of blood were vomited in
the morning, and more than a pint in the afternoon. The
circumference of the abdomen is twenty and three-quarter inches.
The liver and spleen both seem diminished in size.
14th. No more hematemesis. Patient is looking very anemic.
There is a systolic bruit at the apex and another of different
character over the pulmonary area. Abdomen twenty and a
half inches.
25th. Urine 1020, normal. Abdomen much distended, circum-
ference twenty-four and a half inches. Some dülness in right
flank which disappears on rolling patient on to the left side. No
thrill. Liver is felt well below the costal margin.
28th. Slight epistaxis this morning.
April 5th. Red corpuscles, 4,250,000; hæmoglobin, 45 per
cent.; white corpuscles, no excess.
30 A Case of Splenic Anemia.
13th. Spleen seems larger and is very hard, it reaches within
a. finger’s breadth of the crest of the ilium.
May 5th. Patient vomited several times to-day. The vomited
matter is blood-stained. The spleen feels softer.
6th. Slight recurrence of hamatemesis.
14th. Patient looks very pale and ill. The abdomen is
generally tender, especially so over the spleen.
15th. There is a small quantity of dark brown vomit to-day.
20th. She looks brighter, but is absolutely colourless.
June 6th. There is much pain in the abdomen, aggravated
by coughing.
10th. In great pain, frequently sick, no heematemesis.
13th. Constant sickness. Bovvels open nine times in the
last twenty-four hours. Some of the motions contain blood.
14th. The patient became collapsed and died this morning.
The post-mortem examination was made by Dr. Perry. The
following abstract is from his report of the case :—
The mucous membrane of the stomach was pale. No ulcer or
other source of hemorrhage was detected.
The spleen weighed fourteen ounces, and on its surface were
numerous small tufts resembling the vascular tufts seen on the
surface of the liver in chronic venous engorgement. On section,
the structure of the organ appeared normal.
The liver was little, if at all enlarged; it was pale on section,
and appeared normal but for some tough adhesions around the
gall-bladder.
The heart was normal, weighing four and a-half ounces.
Recent ante-mortem thrombus was found in several vessels.
Just at the commencement of the right branch of the pulmonary
artery there was a small ante-mortem thrombus, about the size
of a pea, reddish grey in colour, and adherent to the wall of the
vessel.
The main trunk of the portal vein was found plugged with
recent thrombus, which did not extend into the branches of the
portal vein in the liver. The veins of the stomach were not
thrombosed. The superior mesenteric vein was plugged, and
there was some thrombosis of the terminal portion of the inferior
A Case of Splenic Anemia. 31
mesenteric. At the lower part of the small intestine there was
an area of intense congestion, the part affected being the last
eight inches or so of the ileum. The upper limit of the conges-
tion was well marked, while the lower was less well defined. On
the surface of the congested bowel was a thin deposit of lymph,
and the peritoneal cavity contained an ounce or two of bloody
fluid. On gently squeezing the intestine some fecal exudation
took place through several small apertures. The mucous mem-
brane at this part was of a dark red colour, granular on the
surface, and evidently undergoing coagulation necrosis. Tracing
up the superior mesenteric vein from this part it was found to be
plugged throughout, and the thrombus was continuous with the
thrombus in the portal vein. The main splenic vein was plugged
by somewhat adherent ante-mortem thrombus. This thrombus
was only about an inch in length, and did not appear to be con-
tinuous with that in the portal vein.
The thrombosis in all the vessels was obviously of very recent
date.
The rest of the viscera examined were normal.
I have recorded this case at some length as one of splenic
ansemia, because it seems desirable that we should carefully com-
pare all cases of enlarged spleen of obscure origin associated
with anemia, in order to determine whether there is a group of
cases sufficiently defined to warrant us in giving them a special
name and searching for a common cause. It is probable that,
owing to the interest lately aroused in this subject, and to the
satisfaction usually experienced in making a definite diagnosis,
most obscure diseases associated with splenic enlargement will
be classified as “splenic anemia.” This will ensure such cases
being carefully contrasted, and will assist the task of subdivision,
which, I believe will soon be found necessary. As long as we
can, we force anomalous cases into existing groups of well-
established diseases, making light of the features in which they
fail to conform to the type. As soon as a new disease is ''dis-
covered,” the anomalous cases, which have with difficulty been
retained in a large number of quite dissimilar groups, are trans-
ferred to this new place. Thus it is the number of recorded cases
82 A Case of Splenic Anemia.
of splenic anemia is rapidly increasing, and the dissimilarity of
many of the cases is very striking.
I am by no means certain tbat my case would be accepted as
an instance of splenic ansemia by all those who have written on
the subject or have recorded cases. If it is not, however, I do
not know under what other well-established disease it should be
classified,
It certainly was not a case of leucocytheemia, nor cirrhosis of
liver, nor malarial cachexia. While the case was under my care
I regarded it as one of portal obstruction, attributing the
enlargement of the spleen and the bamatemesis to the results of
impeded circulation, and the anemia to the repeated loss of
blood. I thought it possible that we should find some organic
cause for such portal obstruction in cirrhosis of the liver, in
thrombosis of veins, or in permanent obstruction by enlarged
glands or by condensed fibrous tissue. As already stated, the
question of splenic ansemia was fully considered at the bedside,
but no definite opinion, either for or against the diagnosis was
expressed. The child did not come under observation till it had
suffered from profuse hematemesis, and there was no evidence
that it had suffered from anemia until after it had lost a
large amount of blood. A feature of the case which, to my
mind, pointed to portal obstruction, was the diminution in the
size of the spleen which followed the various attacks of hema-
temesis and the subsequent progressive swelling of the abdomen,
which was obviously not due to, although it kept pace with, the
enlargement of the spleen.
The post-inortem proved the absence of any cause of portal
obstruction, and practically established the case as one of splenic
anemia.
But there is a strong suspicion in my mind that, as is common
whenever a new disease is “ discovered,” we are forcing into a
single group cases which further knowledge will lead us to
differentiate.
Samuel West, writing in 1898, and analysing the symptoms of
the cases recorded up to that date makes the following state-
ment :—
A Case of Splenic Anemia. 33
“ Heemorrhages.—The tendency to bleeding is pronounced ; the
hemorrhages are usually of slight degree and of the nature of
oozing; but they frequently recur, are very difficult to control,
and add greatly to the anemia. € € * * From the gastro-
antestinal organs hemorrhage 4s rare, and if any large amount
41 48 probably associated with some secondary lesion. A case is,
however, recorded by Dr. Douglas Stanley, in which, although
profuse and fatal hematemesis took place, no lesion in the
stomach was found after death."
In Osler's collected cases, on the other hand, profuse hema-
temesis is a very common symptom. Out of a total of fifteen
cases, eight suffered more or less from hamatemesis, and in several
cases bleeding occurred from no other organ than the stomach,
and in some as in this case I am now recording, the recurrent
heematemesis appears to have been the direct cause of death.
The question that I desire to raise, and which indeed seems
forced upon us by the dissimilarity of Brühl's and Osler's cases,
is whether we are not dealing with two quite separate groups ?
In one group the course of events appears to be (1) large spleen,
(2) anemia, (3) general hemorrhagic tendency ; in the other, (1)
large spleen, (2) local gastric hemorrhage, (3) anemia.
Douglas Stanley’s case, many of Osler’s cases, and the case
now recorded, should be placed in the second group. Most of
Brühl”s cases and Dr. Taylor’s case belong to the first group. In
estimating the value of splenectomy in the treatment of splenic
ansemia, it must be carefully considered to which of these groups
the case belongs. The hope of good being done by the operation
should certainly be greater in cases belonging to the second
group.
SOME CONDITIONS IN WHICH OPIUM
IS DANGEROUS.
By A. P. BEDDARD, MD.
SENIOR DEMONSTRATOR OF PHYSIOLOGY.
İT happens occasionally that a patient dies so soon after an
ordinary dose of opium—and this applies especially to hypo-
dermic injections of morphia—as to leave but little doubt that
the opium has been the immediate cause of death. It seems of
some practical importance, therefore, to enquire what class of
patients are thus liable to be killed by a small dose of opium, and
how the opium brings about rapid death.
On turning to Allbutt’s System of Medicine, as the largest
English text-book, for guidance in giving opium in diseases of the
kidneys, heart and lungs, the following statements bearing on the
subject are found :—“ Opium and its derivatives should be rigidly
avoided in the convulsive and every other stage of organic
albuminuria, save only with the lardaceous kidney, where they
are permissible and sometimes useful, but not when this condition
is productive of convulsion or other uremic symptom.”
In the article on acute pericarditis, only two statements are
made :—“ Should the pain be severe, opium may be given,
Dover”s powder being a useful preparation; or morphia may be
administered subcutaneously and repeated as occasion demands.”
And in speaking of severe cases with dyspnoea, cyanosis and
want of sleep :—“ Subcutaneous injection of morphine may be
imperatively demanded, even if risky. Dr. Cheadle speaks
highly of nepenthe for ehildren.” The article on disease of the
36 Some Conditions in which Opium is Dangerous.
aortic area of the heart mentions generally the value of the
hypodermic injection of morphine in heart disease, quotes
Leonard Hill to the effect that ‘‘morphine is one of the best
vaso-constrictors and cardiac tonics we possess," and gives the
following warnings :—“ Of the drawbacks to the continuous use
of morphine I may refer to the article on the subject. Like any
other potent remedy it must be used seasonably and discreetly.”
The article on diseases of the mitral valve mentions that ‘‘ In a
considerable number of cases manifesting distressful symptoms of
dyspnoea and insomnia no agent succeeds so well as morphia.
By far the best way of administering it in cases of cardiac disease
is by hypodermic injection. The first dose should be small—
one-sixth or one-fourth of a grain—but this may he increased
subsequently to half a grain. Care should be taken that the
administration shall not become habitual." The article on
angina pectoris, after speaking of the use of the nitrites, goes on
to say :—‘‘ When pain is not relieved by this treatment, arterial
spasm having been eliminated as its cause, the use of subcu-
taneous morphia is indicated, due care being exercised with
regard to the dose in view of the possible presence of kidney
disease; if this factor be excluded, the degree of pain would
regulate the dose and the combination of atropine would be
useful as a, heart stimulant. The free use of oxygen inhalation
is of very great value in all cases in which cardiac failure is a
marked feature. . . . . Oxygen inhalation is particularly
indicated in those cases in which morphia is found necessary ;
and when the paroxysm is over and sleep induced, the gas should
be allowed from time to time to fortify the air immediately above
the patient's mouth and nose.”
In the treatment of pneumonia it is stated that for severe
sleeplessness opium ‘‘has been forbidden lest its use should
increase cyanosis, diminish respiratory efforts and lead to fatal
coma. These fears are far from groundless. When there is
extensive consolidation or much bronchitis, when the patient is
livid, and the expectoration scanty, i& would be bad practice to
give this drug." And further on, “ In many cases of pneumonia
the danger is not directly from suffocation, it is rather from the
Some Conditions in which Opium is Dangerous. 97
effects of a continued high temperature upon the heart, the
impending weakness of the respiratory muscles and the exhaustion
of the reflex activity of the nervous centres. In such cases ten
grains of Dover's powder, five grains of compound soap pill,
fifteen to twenty drops of laudanum are often invaluable and
succeed when all other hypnotics are powerless. An additional
warrant for the use of opium is dilatation of the pupils. The
presence of" albumen, if only of pyrexial origin, is no counter-
indication ; but if the patient be a subject of chronic Bright's
disease we must forego the use of this valuable drug, or use it at
his peril, to escape a still more imminent danger.” Again, in the
treatment of attacks of spasmodic dyspnea in emphysema with
bronchitis it is stated that ‘‘The desirability of employing
morphia in such cases will depend chiefly on the relative pre-
ponderance of the spasmodic or catarrhal factor. The nearer the
attack approaches in character to one of true asthma, the greater
is the probability of relief from a subcutaneous injection of
morphia; whilst, on the other hand, if the dyspnea be chiefly
due to the accompanying bronchitis, the use of morphia may be
attended with the greatest danger.”
The advice contained in the above extracts may be briefly and
fairly summarised as follows :—Opium in albuminuria due to neph-
ritis is so dangerous as to be inadmissible, presumably, although
it is not so stated, because the disease of the kidneys will interfere
with the elimination of the morphia in the urine. In cardiac
failure due to various diseases of the heart, opium is in some
cases excellent treatment, in others it is less safe, although in
what the danger really consists and how it may be clinically
recognised is not very precisely stated. In acute inflammation
of the lungs opium may be highly dangerous, but here again the
exact nature and cause of the danger is not made very clear.
When, however, we turn to the known physiological actions of
opium and its method of elimination from the body as the basis
on which to guide us in the use of it in disease, it becomes
doubtful whether much of the above quoted advice can really be
founded on facts. However opium is introduced into the body,
whether by the alimentary canal or subcutaneously, it or its
88 Some Conditions in which Opium is Dangerous.
products of oxidation in the body are ultimately eliminated from
the blood almost entirely by the mucous membrane of the
stomach and intestines. Minute quantities of it do leave by the
kidneys, but the most reliable work on the subject shows them to
be insignificant. This at once raises a doubt as to whether
opium must of necessity be dangerous in all cases of organic
albuminuria ; this doubt is further strengthened by the following
considerations: Cases of acute uremic convulsions; of uremic
dyspnoea and of puerperal eclampsia are not infrequently now
treated by hypodermic injections of morphia, and treated with
success. If opium were really dangerous in renal disease simply
because of its non-excretion in the urine, then it ought to be
equally dangerous in any condition in which the secretion of
urine is very slight, as in shock, acute peritonitis, acute intestinal
obstruction and collapse generally, also in the backward venous
pressure of cardiac and pulmonary disease, in all of which the
secretion of urine may be as nearly suppressed as in nephritis;
yet in many of these conditions opium is not considered an unsafe
remedy. Again, many of the fatal cases are not of patients
suffering with organic renal disease at all, and simply because a
patient passing albuminous urine dies after a dose of opium, it
does not follow that death is caused by the kidneys failing to
excrete the morphia.
Turning now to the physiological actions of opium, we find
that besides its depressing action on the higher parts of the
central nervous system, whereby it relieves pain, its chief well
recognised effects are—(1) its special depressing action on the
cells of the respiratory centre, and (2) its action on the heart as a
powerful cardiac stimulant and on the vasomotor centre, causing
vasoconstriction of the peripheral arterioles. It is by a careful
consideration of these two effects that we find an explanation of
the cases under consideration and also the main indications of
when and when not opium is dangerous.
It is a mistake to think that even in health the contraction of
the heart and the elastic recoil of the larger arteries are the only
forces used to send the blood round the circulation. The so-
called respiratory pump is more or less necessary, we will
Some Conditions in whieh Opium is Dangerous. 89
therefore consider its mode of action. In man, in the erect
posture, the chief problem of the venous circulation is how to
get the blood from the legs and abdomen back to the heart
against the force of gravity; when in the horizontal position,
although the action of gravity is eliminated, a proper return of
blood from the abdomen is still a matter of prime importance to
the circulation and requires a special mechanism to ensure it.
The return of blood from the legs is largely carried out by the
compression of the deep veins by the limb muscles, and though
important, its importance is slight as compared with the question
of the return of blood from the abdomen, the readily distensible
veins of which could hold the total circulating blood. A properly
maintained abdominal circulation is therefore of great importance
to the whole body, and especially to the brain. It is controlled
by two mechanisms, one to prevent an undue quantity of blood
from ever reaching the abdominal veins, namely, the vasomotor
centre and nerves keeping the splanchnic arterioles in various
degrees of constriction, and a second to actively empty the
abdominal veins, namely, the respiratory pump.
This pumping action of the respiratory movements combines
the two actions both of a suction pump and of a force pump.
The suction action takes place only during inspiration and is
produced by the increased negative pressure in the thorax
actively sucking blood from the abdomen into the thorax. In the
absence of exertion during health, that is with a strong heart,
elastic arteries and a properly acting vasomotor centre, this
suction adequately empties the abdominal veins and fills the right
heart. The force-pump action of the respiratory movements is
more complicated, but can be much more powerful. The
abdomen is a muscular box completely filled by viscera and
blood-vessels, and since the venous blood is the only content
which can rapidly vary in quantity, it follows that the firmness
or laxity of the abdominal walls will determine the size of the
abdominal veins, and, therefore, the quantity of blood they
contain at any given time. When the diaphragm descends in
inspiration the abdominal viscera and veins are compressed and
venous blood is forced out of the abdomen into the right
40 Some Conditions in which Opium is Dangerous.
ventricle. This, however, can only take place provided that the
muscles of the abdominal wall, under control of the respiratory
centre, are capable of resisting the increased intra-abdominal
pressure and do not materially stretch. Consequently we find
that in some forms of dyspnoea and in muscular exertion, at the
same time that the diaphragm descends, the abdominal walls are
not only not allowed to give at all, but are actively contracted in
order to ensure this pumping action. The power of this force-
pump is great, and when in vigorous action it would inevitably
overstretch the right ventricle were the latter not supported by
the tough inelastic pericardium. In urgent dyspnoea of circu-
latory origin this pump is capable of driving blood straight
through the distended right ventricle into the lungs; and during
expiration the lungs are compressed and the blood driven onwards
into the left ventricle. Thus by itself the respiratory force pump -
can to a large extent carry on the circulation apart from the
heart, but as has been already explained, in health, this force-
pump is only used during exertion and in disease either to
supplement the pumping action of the right ventricle or under
special circumstances to fill it as well. The respiratory suction-
pump is, of course, always at work to a greater or less extent—to
a less extent in the horizontal position and to a greater extent in
the foot down position. But even in the horizontal position and
with a healthy heart it is probable that the circulation as a whole
could not be maintained for long without the action of the
respiratory pump.
In order to understand the relation that the respiratory pump
has to circulatory failure, it is necessary to consider the effect
that circulatory failure has upon the respiratory centre. This
centre by the respiratory movements maintains a proper inter-
change of gases in the lungs and also helps to keep up a
proper circulation throughout the lungs, we therefore find that
it is wonderfully sensitive, not only to the quality but also to the
quantity—or rather the velocity of flow—of the blood it revives.
The circulation may fail, either on the arterial or venous side, or
both, and it makes a considerable difference to the respiratory
centre how it fails.
Some Conditions in which Opium is Dangerous. 41
On the arterial side the circulation fails either from failure of
the vasomotor centre, as in shock, or from failure of the left
ventricle, as in the early stages of uncompensated aortic disease.
In both cases the blood is properly aerated, but there is an
exaggeration in rate or amplitude of the respiratory movements
due to the low aortic blood-pressure and the consequent less
rapid flow of blood through the medulla. With regard to this
dyspnoea, we have to ask ourselves, Is it of any vital importance
for carrying on the circulation and is it therefore any contra-
indication to the use of opium? In both cases the dyspnea is of
the suction-pump type, and its object seems to be to hurry blood
from the venous system into the right heart and to get it pumped
into the left side in order to raise the arterial blood-pressure and
so improve the cerebral circulation. In shock and other similar
conditions the most effective way of raising the arterial blood-
pressure is to replace the action of the vasomotor centre by a
firm bandage round the abdomen, and if this be done the dyspnea
will either cease or at least be not in any way essential to the
circulation. In such a case morphia is not only not contra-
indicated, but may do good both by depressing the brain and
rendering it less susceptible to afferent inhibitory impulses, but
also, by causing peripheral vaso-constriction, and by stimulating
the healthy and in this case underworked cardiac muscle.
In aortic disease with comparative failure of the left ventricle
alone, the dyspnoea again is simply the expression of the effect
that a low mean general arterial blood-pressure has upon the
respiratory centre. The dyspnoea is undoubtedly an attempt to
improve the circulation through the medulla on its arterial side,
but it is not, as such, essential to the circulation as a whole.
Consequently it is not only safe to reduce dyspnoea and subjective
distress by opium, but the opium, by its action on the heart and
blood-vessels, will improve the circulation on its arterial side and
steady the heart. |
When we come to cases of failure of the right ventricle we find
a totally different circulatory condition. Whenever the muscle of
the right ventricle begins to fail from overwork, however caused,
it dilates, the residual blood in it is increased, and the more it
42 Some Conditions in which Opium is Dangerous.
dilates the more work the muscle has to do to send out an
adequate quantity of blood. Therefore, a vicious circle is easily
set up, the arterial blood-pressure falls, whilst that in the veins
rises and the velocity in the pulmonary, coronary, and especially
the cerebral circulations, is greatly slowed. The whole circulation
would run a great risk of coming to a standstill unless the
respiratory pump came to the assistance of the right ventricle.
The respiratory centre is stimulated partly by the less well
aerated blood supplied to it, and partly by the less rapid flow of
blood through the whole brain. It has already been pointed out
that the respiratory force-pump is of great power, and at first
sight it might seem a doubtful benefit to pump more blood into
the already over-dilated and labouring right ventricle. This
difficulty, however, is only apparent, and is overcome in two
ways. In the first place, by the support of the tough inelastic
pericardium, which is able to withstand a pressure of nearly two
atmospheres and limits the capacity of the heart by about one-
half, so that blood forced into the right ventricle under these
circumstances can not simply distend it further, but must force
blood out of the ventricle into the lungs; and in the second
place, by the position of orthopnea which the patient assumes.
By allowing the force of gravity to act on the column of blood in
his inferior vena cava, he practically bleeds himself into his
abdominal veins, and by the action of his respiratory pump he
drives or sucks appropriate quantities of blood through his right
ventricle into the lungs. It is practically true to say that when-
ever a patient with right-sided failure assumes this position his
right side is engorged and would be benefited by venesection.
And further, the degree in which his respiratory pump is really
carrying on the circulation may be gauged by observing the
degree in which the abdominal muscles are contracted during
inspiration, and the lungs are emptied into the left ventricle by
an expiratory dyspnea.
It is almost unnecessary to point out that whenever the
maintenance of the circulation depends materially, as it does in
this case, upon the action of the respiratory pump, opium, by
its specific action on the respiratory centre may be a dangerous
Some Conditions in which Opium is Dangerous. 43
drug. Of course it is and may be given time after time with
impunity, and even with benefit to the patient; here we are only
concerned in pointing out in what the danger consists and that
the margin of safety is not great and extremely difficult to estimate
clinically.
It is in cases of pericarditis with effusion that the most powerful
and urgent use of the respiratory force-pump is seen. During
inspiration blood has to be driven through the compressed right
auricle on into the ventricle in order to fill it, and during expiration
the lungs have to be compressed in order to drive blood through
the strangled left auricle. In most cases of general circulatory
disturbance due to heart failure the dyspnoea is wholly com-
pensatory and beneficial, but in pericarditis with or without
myocarditis, or in pericarditis with effusion, there is another side
to the question. The heart is now only supported by a softened
. and distensible pericardium, and the force of the respiratory pump,
although necessary to carry on the circulation, at the same time
stretches the pericardium and dilates the heart, it may be acutely
and irreparably. It may be necessary and even advisable to
give opium in these cases but it is certainly a dangerous drug and
must be treated as such.
In almost any case of angina pectoris morphia may be safely
given during the acute attack, not because these attacks may not
be accompanied by considerable cardiac and general circulatory
failure, but because the pain itself to a large extent prevents any
depressant action of opium on the respiratory centre.
In acute inflammations of the lungs diminished aeration of the
blood is a possible cause of severe dyspnea. This may be
present alone or combined with right-sided failure, and the
difference between the two cases is well seen in the way they
respond to treatment by inhalations of oxygen. If the right
ventricle be acting well and the cause of the dyspnoea be want of
proper aeration of the blood, oxygen inhalations may for a time
improve the dyspnoea ; if, however, the right ventricle has failed
as well, the inhalations will appear to produce but little effect on
the dyspnea. But even in this latter case inhalations of oxygen
do real good because, quite apart from the benefit the eardiac
VOL. LVI. 7
44 Some Conditions in which Opium is Dangerous.
muscle will derive from a supply of better blood, the safety of the
whole circulation lies in the very fact that the respiratory centre
normally is and should be kept as susceptible as possible to
changes in the quality and quantity of blood supplied to it. It
is serious enough that the centre may become gradually narcotised
by CO,, but to dull it further by opium may be to remove the
only effectual defensive mechanism the patient has. As Sir
Thomas Watson well says, “ Opium is a ticklish remedy in these
cases. Many a patient—some within my own knowledge—
labouring under general or extensive bronchitis, have been put so
soundly to sleep by a dose of opium on going to bed that they |
have not waked again.” It is a familiar fact that but few patients
showing Cheyne-Stokes’ respiration, associated with right sided
failure, recover. This is only another way of saying that by the
time the respiratory centre is so exhausted or poisoned that it can
only respond with an intermittent activity, the circulation is in
imminent danger of stopping.
It has been frequently pointed out that in acute pulmonary
disease the size of the pupils may be used to indicate whether or
not opium may be safely given. In the quotation given above it
is stated that in certain stages of pneumonia ““an additional
warrant for the use of opium is dilatation of the pupils." It
would perhaps be even better to say that constriction of the
pupils is an additional contra-indication to its use. In the early
stages of disturbance of the cerebral circulation and of CO,
poisoning the pupils gradually constrict, and by the time they
are markedly constricted, the patient is dull and takes but little
notice of what goes on around him; in the final stages of poisoning
the pupils dilate again and the patient becomes more or less
unconscious. In the early stages the respiratory centre is
stimulated and the patient sits up in bed and gives his respiratory
pump full play; in the later stages the centre becomes poisoned,
exhausted and less regularly active, and the patient sinks down in
bed, like his centre, unable to respond further to calls upon him.
The size of the pupils, therefore, is some indication of the amount
of risk the respiratory centre will run during the next few hours
of being poisoned. If the pupils are already small, opium is
Some Conditions in which Opium ts Dangerous. 45
contra-indicated, but if they are not, from that one observation
alone it would be unsafe to infer that opium might be given
without risk. In fact, in pulmonary disease, just as in cardiac
disease, before opium is given, in any case the question that has to
be decided is to what extent the respiratory centre is by its
present activity carrying on the circulation, and therefore to what
extent is it safe to reduce its excitability by opium.
In organic albuminuria, we have seen that it is hard to believe
that opium is necessarily dangerous, and yet such a widespread
belief must have some foundation on fact. On the other hand,
various considerations have led us to believe that opium may
be dangerous in serious right-sided failure with or without
albuminuria. Considered from the paint of view of their
circulation, all cases of nephritis may be divided into two groups
—(1) those with an arterial blood-pressure decidedly above the
normal—apart, of course, from mere thickening or rigidity of the
arterial wall—and (2) those with an arterial pressure that is not
above the normal or even distinctly below it. To deal with group
(1), which includes the minority of the cases which we have to
treat. A high arterial blood-pressure is to be expected in all
cases of nephritis, and yet it is seen rarely in cases of chronic
nephritis when they come under treatment, more frequently in
cases of genuine acute nephritis, sometimes in uremia, and more
often in eclampsia. This rise in arterial blood-pressure is only
possible provided the cardiac muscle is acting forcibly and well ;
and as long as this continues to be the case, opium might be
safely given. But it is necessary to remember that a really high
arterial blood-pressure, when prolonged, greatly increases the
work of the left ventricle, and may so rapidly do so as to cause
even acute dilatation of the heart and general circulatory failure ;
and that simply because a case is one of acute nephritis, for
instance, and has a high arterial blood-pressure, it does not
follow that it will continue to have it for long; that convulsions,
like severe cough, throw an enormous strain on the right
ventricle, and of themselves cause a general circulatory dis-
turbance, lowering arterial and raising the venous blood-pressures.
Consequently a heart may begin to fail at any moment, and fail
46 Some Conditions in which Opium is Dangerous.
rapidly, letting down the arterial blood-pressure as it fails. This
is true not only of uremic, but of any convulsions; thus it is a
well recognised fact that even a small dose of morphia may be
extremely dangerous and even fatal in status epilepticus. Further,
it must be remembered that in, at any rate, uremia and
eclampsia there is circulating in the blood one or more poisons
of whose properties we know little, except that they affect
especially the cells of the central nervous system, and as in the
case of CO, poisoning this might well make us careful of adding
another depressant like opium. As in the case of CO, poisoning,
too, the size of the pupils is of some help to us, for smallness of
the pupils contra-indicates the giving of opium. It is impossible
to say whether this constriction of the pupils in urzmia is due to
a special poison or simply to the less perfect aeration of the blood
and disturbance of the cerebral circulation, or to both, but in any
case its significance is much the same.
There is one condition, namely, uremic dyspnosa, in which
morphia has been found of great value. The type of respiration
is a һурегрпова, t.e. a mere exaggeration in rate and amplitude
of the normal respiratory pump, and as such it does the circulation
nothing but good. This dyspnoea is not due to circulatory failure
nor to imperfect aeration of the blood but is of central origin and
presumably due to the action of some poison on the respiratory
centre. It frequently occurs as an early and it may be the sole
symptoms of uremia, and provided the heart is working well there
could be no objection to treating it by morphia.
Group (2) contains the bulk of the cases of nephritis when they
come before us for treatment. Presumably their arterial blood-
pressure was once above normal, and that it is no- longer so may
be due to their nephritis becoming cured, but most frequently it
is due to some degree of cardiac failure, much more rarely to
collapse. Putting the cases due to collapse aside—and they are
readily recognisable—it may be broadly said that opium may be
highly dangerous in any case or stage of nephritis in which the
arterial blood-pressure is markedly below the normal; just as
it may be in cardiac and pulmonary disease and for the same
reasons.
Some Conditions in which Opium is Dangerous. 47
The conclusion has thus been reached that the danger of opium
in all these cases is due to its depressing action on the respiratory
centre, whereby the centre either gives less assistance to a failing
circulation or is made too dull to respond to a call for further
help. And it must be noted that these remarks apply with even
greater force to doses of opium given at night, a time when right-
sided circulatory failure is nearly always aggravated and the
activity of the central nervous system depressed.
It is impossible here to discuss further the points on which we
have to rely clinically for estimating in any given patient the
degree in which the respiratory centre is carrying on the circula-
tion. But it must be pointed out that lividity means more
than imperfect aeration of the blood, for the total cessation of
respiration may not cause any cyanosis. This condition is
frequently seen in cases of severe intracranial pressure in which
the heart may go on beating for half an hour after respiration
has stopped. This means that the blood, although excessively
venous, has accumulated, not in the superficial veins at all but
almost entirely in the great abdominal veins; and it has done
so, because both the mechanisms for keeping the blood from stag-
nating in the abdominal veins, namely, the vasomotor centre and
the respiratory pump, have ceased to act. When, therefore, we
see lividity we know that the vasomotor centre is still working, for
if its activity decreased the cyanosis would also begin to disappear.
There is still the question of the smallness of the dose which is
sometimes fatal, and here failure of elimination, not by the kidneys,
but by the alimentary canal, probably plays an important part.
In a healthy indvidual morphia begins to be excreted into the
stomach two and a half minutes after a hypodermic injection.
Nothing is known as to the effect that right sided cardiac failure
has upon this excretion, but judging from the fact that right sided
failure means stagnation of blood in the abdominal veins, and that
this backward pressure often has a marked effect upon the
serectory activities of the alimentary canal, it is hard to believe
that the excretion of morphia will in such cases be as rapid as in
health. It is this derangement of the circulation through the
alimentary canal which probably explains the occasional serious
effect of a small dose of opium in cases of cirrhosis of the liver.
48 Some Conditions in which Opium 18 Dangerous.
It is necessary to say a word about the action of opium on the
heart and blood-vessels. The exact action on the heart is that
it causes the cardiac muscle to dilate more during diastole and
contract up more during systole, and hence it increases largely
the amount of blood sent out at each systole. It appears, there-
fore, to be a direct stimulant to the cardiac muscle and renders
a slightly irregular heart regular again. It also contracts the
peripheral arterioles by stimulating the vasomotor centre; this
chiefly affects the splanchnic area, and the effect here may be so
great, that the arterioles of the skin are forced open and dilated.
In a physiological experiment in which powerful respiratory
movements are kept going by mechanical means at a certain rate,
no matter what effect the opium may have on the animal’s
respiratory centre, the total effect of opium on the circulation is
very like that of digitalis. But in man the conditions are
different. Here the total effect of opium on the circulation is the
difference of two opposite actions—(1) its power to raise the
arterial and lower the venous blood-pressure by increasing the
systolic output of the heart and causing splanchnic vaso-con-
striction, and (2) its power to decrease the pumping of blood
from the abdominal veins into the heart, and so raise the venous
and lower the arterial blood-pressure. There are, therefore,
three possible results, either of these two opposite effects may
preponderate or they may mutually counteract each other and
leave the circulation unaffected. There are some circulatory
disturbances, such as shock, and some cases of aortic disease in
which opium may be given with safety; there are others, such
as severe pericarditis and pericardial effusion, in which the
respiratory pump may be carrying on the circulation almost
single-handed and in which opium must be highly dangerous ;
there are many more in which the respiratory pump is helping an
overworked right side, and in which no one can prophecy with
absolute certainty what final effect even a small dose of opium
will have on the circulation as a whole, and herein lies its danger.
In a doubtful case it is safer to give morphia by the mouth than
hypodermically, and if given hypodermically, it would make it
safer to add atropine or caffein to the injection and give the
patient inhalations of oxygen.
A RESEARCH UPON
THE NITROGENOUS METABOLISM IN A
CASE OF BRIGHT’S DISEASE.
By J. A. BUTLER, M.B., B.S. Lond., AND Н. S. FRENCH,
B.A., B.M., В.Сн. Oxon.
(From the Physiological Laboratory, Guy's Hospital.)
INTRODUCTION.
(The Figures after Observers’ Names indicate the Numbers of
the References given at the end of the Paper).
As far as we have been able to discover, the only published
experiments upon the Nitrogenous Metabolism in Bright’s disease
have been continuous for but short periods. The longest we
have found is of twelve days’ duration, upon a man aged 47, with
chronic interstitial nephritis, by Prior (50) in 1891. The uric
acid, the total urinary nitrogen, and the fæces nitrogen were
estimated ; the food nitrogen was sometimes estimated, and some-
times calculated from diet tables, whilst the urea was not esti-
mated at all. Upon two other occasions Prior (50) estimated the
uric acid, the albumen, the urea, the total urinary nitrogen and
the feeces nitrogen, but each investigation lasted seven days only.
P. Müller (45), Van Noorden and Ritter (64), Mann (41),
50 A Research upon the Nitrogenous Metabolism in a
Kornblum (32), and Baginsky (8a), all publish researches
extending over periods of a few days. İn all the total nitrogen
output was determined, but in many the nitrogen in the food was
wholly or partly taken from diet tables, and in none was the
urea determined. Korkounov (31), Evdokimov (13), Garine (16),
and Grigoriev (18), have published researches upon the subject,
but their papers, which are in Russian, are not easily accessible,
and we have not been able to obtain full particulars of their
work.
The case we have investigated was one of subacute parenchy-
matous nephritis, in a boy aged seven, under the care of Dr.
Taylor and Dr. Fawcett, in John ward, Guy’s Hospital. The
research was continuous for forty-one days, and included a period
of mild uremia. The estimations carried out daily were: (1)
The total nitrogen in the urine. (2) The urea. (3) The uric
acid. (4) The coagulable proteid. (5) The total nitrogen in the
feces. (6) The nitrogen in the milk supply. From time to time
additional estimations were necessary, a8 other articles of food
were added to his diet.
No attempt was made to estimate the nitrogen loss by the
skin, because we felt that any method of doing so that we could
devise must be too inaccurate to correspond with the accuracy
we hoped to attain in our other work. The boy was suffering
from psoriasis, which may have made the skin loss more than
usual.
We have divided the report of our work into the following
sections :—
I. A clinical account of the case.
II. The methods we have used.
III. The detailed tables of our results.
IV. The urea.
V. The uric acid.
VI. The coagulable proteid.
VII. The “ other bodies."
VIII. The feeces.
IX. The unrecovered nitrogen.
X. General conclusions.
XI. References.
Case of Bright’s Disease. 51
SECTION I.
A Clinical account of the Case.
W. W., male, aged 7 years, was admitted under the care of
Dr. Fawcett, January 10th, 1901, for cough, dropsy, and albumin-
uria. He was the eighth child of a family of twelve, of whom
only two besides the patient were living.
There was a history of varicella three years previously, and
of attacks of psoriasis. There was no history of diphtheria or
scarlet fever. His present illness began about October, 1900,
and was attributed by his mother to getting his feet wet. His
feet began to swell about December 10th, and his eyelids
and face were swollen about December 27th. No history of
hematuria could be obtained.
On admission (January 10th), his pulse was 112, respirations
40 per minute, and temperature 100:4? F. He had a good deal
of bronchitis and general cedema. The cardiac sounds were
normal, and the pulse tension was not particularly high.
The urine had a sp. gr. of 1040, and contained about 12 parts
per 1000, of albumen (by Esbach). There was a large deposit
of urates.
He had numerous patches of psoriasis on the extensor surfaces
of his arms and legs, and some on the trunk. He was very
drowsy, and during the first two or three days in the ward he
slept much, and passed little urine.
Under treatment his condition improved, and on January 17th
he was passing much more urine, and had very little cedema.
After this his condition varied considerably. The albumen never
disappeared from the urine, and on several occasions as large a
proportion as 14 parts per 1000 (by Esbach) was recorded.
Granular and epithelial casts were found.
The research began on February 19th. For some days
previously his diet had been milk only. He had slight cedema
52 A Research upon the Nitrogenous Metabolism in a
of the feet and legs. The abdomen was large, but there was
no ascites. He had no bronchitis. The cardiac sounds were
normal. There were numerous patches of psoriasis on the legs,
arms and trunk; the face and scalp being free. He had a hot
bath every night and was taking the following drugs :—
(l. R Ferri et Ammonii Citratis da gr. vi.
Liquoris Arsenicalis . ә m iv.
Liquoris Ammonii Acetatis ... 5].
Potassii Citratis ... ə ə gr. X.
Syrupi Aurantii ... as Js 3 88.
Aquam ad ios 3].
The blur glven sitive times a day.
(2. R Pulveris Scammonii Compositi (B.P.) gr. x.
The powder given, in a cachet, once a day.
February 19th. Bowels Opened (— B.O.) 1.
" 20th. B.O. 2.
5 91st. В.О. 6.
2 22nd. The mixture (1) was omitted, and the following
given for the rest of the time :—
(3). R Potassii Citratis ... - “ gr. XX.
Aquam Menthe Piperite (B. P. ) ad 3].
The mixture given three times a day.
February 23rd. The powder (2) was not given to-day. B.O. 4.
„ 24th. B.O. 2.
j 25th. The patient vomited a very small amount of
clear watery fluid. B.O. 4.
A 27th. B.O. 5.
" 28th. The patient was drowsy. He slept about one
and a half hours during the daytime. The
powder (2) was again omitted. B.O. 1.
March Ist. A few patches of psoriasis appeared on the face,
and fresh patches on the trunk. B.O. 2.
R 2nd. The powder (2) was reduced by one-half, and
from this date he took 5 grains each night,
in a cachet, unless otherwise stated. He
vomited again to-day, a very small quantity
of clear fluid of acid reaction. Those who
March
”
"
"
3rd.
Ath.
oth.
6th.
7th.
8th.
9th.
10th.
11th.
12th.
Case of Bright’s Disease. 53
saw him agreed that he had become distinctly
uremic; it is not easy to bring this out
clearly in a short report, as the change was
gradual. But the amount of urine passed
fell markedly, and he took food very badly.
He was very drowsy and slept about three
hours in the daytime. He complained of
headache, and of feeling sick. He took food
badly. В.О. 1.
He vomited three times, all the vomits being
quite small. There was slight cedema of
the face. He slept about one and a half
hours during the morning, and took little
food all day. B.O. 5.
He vomited once. Some cedema of face.
(Edema of face less. Patient was brighter.
He vomited once, but took his food a little
better. B.O. 2.
Patient complained of headache , his psoriasis
was getting worse. The hot baths were
discontinued from this date. He vomited
once. B.O. 2.
The cedema of legs and feet was getting worse.
There was also slight cedema of the face.
B.O. 1. |
Patient complained of headache and feeling
sick. B.O. 6.
Patient vomited once, and took his food very
badly. There was a great deal of swelling on
both sides of the face, over the parotid glands.
The parotid swelling was less marked, and he
took food better. The powder was not
given. B.O. 4.
Much general cedema, and abdomen larger. He
complained of headache; vomited slightly
twice; and during the night passed urine
into the bed in his sleep. He took little
food. B.O. 2.
54
March
”
13th.
14th.
15th.
16th.
17th.
18th.
19th.
20th.
21st.
22nd.
23rd.
24th.
25th.
26th.
A Research upon the Nitrogenous Metabolism in a
(Edema less. He vomited once
Fair amount of general cedema. Face less
cedematous; abdomen very large. He com-
plained of slight headache. He began taking
his food better; and from his general con-
dition it was agreed that the uremic symptoms
had markedly abated
Headache. (Edema of face slight; but marked in
feet and legs. He took his food well. B O. 3.
Headache, and feeling of sickness. Marked
cedema of legs and feet. A fine red papular
rash appeared on the shoulders, and caused
irritation and itching.
Rash more marked. Vomited once. B.O. 4.
Patient was brighter and more cheerful, com-
plained of irritation from the rash; was
taking his food well.
Slept for one hour during morning. Some
cedema of face. B.O. 2.
Rash still present, but it caused less irritation.
A good deal of cedema of the face, loins,
legs and feet. B.O. 1.
(Edema about the same. Psoriasis getting
better and rash disappearing. B.O. 4.
(Edema about the same. B.O. 4.
(Edema slightly less; both the rash and the
psoriasis were disappearing. B.O. 5. Patient
did not sleep well during the night, but took
his food very well.
(Edema of feet, legs, and loins persisted ;
abdomen very large, but no ascites found.
The powder was not given. B.O. 3.
Patient vomited slightly once, but continued to
take food well. B.O. 3.
Patient was drowsy this morning. There was
some cedema of the face and eyelids. The
powders were discontinued from to-day.
B.O. 1.
Case of Bright s Disease. 55
March 27th. (Edema less. Patient brighter. B.O. 1.
| 28th. Only slight -cedema, of the feet and legs.
Psoriasis almost gone. Rash quite gone.
B.O. 1.
A 29th. В.О. 1.
" 30th. Some headache in the afternoon. Patient was
not quite so well and took less food. B.O. 2.
m ölst. Patient complained. of headache, was drowsy
and less well. He took less food, and
seemed to be entering upon a second attack
of uremia.
April 1st. End of period of observation. As nearly as
could be judged there was about the same
amount of cedema of the feet and legs as at
first. Güdema of legs and feet was present
all through, but has not been noted every
day. Although the abdomen became very
large at times, there was never any definite
ascites, nor were there any signs of fluid in
the chest.
The vomits recorded have always been very small, on no
occasion more than about 30 c.c., and generally much less.
The temperature was taken per rectum every four hours
throughout, at the same times the pulse and respirations were
counted. The highest temperature recorded was 99:4? This was
reached on seven occasions, namely :—
March 24th. 2 p.m. Pulse100 Respiration 30
» 25th. 6 p.m. 104 30
» 28th. 6 p.m. 96 34
„ 29th. 6 p.m. 104 90
„ 90th. 6 p.m. 96 28
» ӘДв6, 6 p.m. 100 28
The lowest temperature recorded was 96?, on March 16th, at
2 a.m., when pulse = 66, respiration = 15.
Except where otherwise stated, the patient slept well through-
out the night (ten to eleven hours). He took no exercise during
the period he was under observation, and except on a few occa-
sions when he was allowed to sit up for an hour or two, wrapped
56 A Research upon the Nitrogenous Metabolism in a
in a blanket, he was kept in bed the whole time. He never had
any hematuria.
SECTION II.
The methods we used.
* by one of us.
I. Superviston of the patient.
The patient was under the charge of two special nurses, of
whom one or other was always in attendance, day and night
Each period of twenty-four hours began at 9 a.m.
II. Administration and measurement of the food.
(a). Milk.—This formed the major part of the diet through-
out. The day’s supply, 2000 c.c. was measured out* at
9 a.m., with a litre flask, and stored in a clean dry Winchester
quart stoppered bottle. A sample of the same milk was taken
for analysis each day. The milk required by the patient
from time to time was taken, by the nurse, from the quantity
measured out; any portion unconsumed being at once returned
to the bottle. A special drinking vessel was used, which was
washed only at the end of each day. The quantity remaining
in the Winchester quart at 9 a.m. of the next day was drained*
into a graduated cylinder, and the amount read off. This,
deducted from the amount measured out, gave the milk
consumed.
The following articles were subsequently added to his:
diet :—
(b). Bread.—A quantity, free from crust, was placed in a
closely covered tin, and the tin and bread weighed together.*
The bread eaten by the patient was taken by the nurse from
this tin, and the remainder, with the tin, was weighed*
at the end of each day. The difference between the two
weighings gave the amount consumed by the patient. A
sample of the same bread was taken for analysis.
(c). Biscwit.—The dinner biscuits were small and dry, and
were weighed in the same manner as the bread. A sample
was analysed.
III.
Case of Bright’s Disease. 57
The Garibaldi biscuits were found to vary extremely little
in weight. The following are the weights :—
(a). Of sixteen biscuits together ion = 327-70 grms.
From which the average of each biscuit— 20:48 grms.
(3). Of single biscuits, taken at random :—
(i) = 20°50 grms.
(ii) == 20°30 grms.
(ii) = 20:40 grms.
(iv) = 20°53 grms.
The number of these biscuits consumed each day was
counted; and this, multiplied by the average weight of a
single biscuit, gave the quantity consumed. A sample was
taken for analysis.
(d). Liebig’s extract of meat.—A sample having been taken
for analysis, the remainder was weighed in the containing
jar. It was kept closely covered; a spoonful or more was
taken by the nurse as required; and, to ensure that it all
reached the patient, it was stirred into boiling water with
the same spoon, until dissolved. The jar with its contents
was weighed* each day, the successive differences giving
the daily consumption.
(e). Other artcles.—The drugs given to the patient are
mentioned in the clinical account. The amount of nitrogen
they contained was calculated to be so small, that we thought
it might be neglected.
Water, both plain and aérated, was supplied to the patient
when he asked for it; the quantity was only roughly
measured, by the nurse, in fluid ounces.
He was also allowed a few sweets (acid drops) during a
portion of the time. The nitrogen in these was practically nil.
The collection and measurement of the urine, feces and vomits.
(a). The wrine.—Previous to the beginning of the research,
the patient was trained by his nurses not to defecate without
having previously passed all his urine. Faces and urine
were thus collected quite separately. A special vessel,
washed only at the end of each day, was kept for his use ;
after each micturition the nurse poured the urine into a
58
IV.
A Research upon the Nitrogenous Metabolism in a
clean stoppered Winchester quart bottle, reserved for that
day's urine. At 9 a.m., the end of each day, the bottle
containing the whole quantity collected during the previous
twenty-four hours, was handed over to us.
The amount was measured* in a graduated cylinder, to
the nearest c.c., and a sufficient quantity of the mixed urine
taken for the different analyses.
The reaction to litmus paper was recorded,* and the
specific gravity read off on a urinometer. For the last
thirty-one days the specific gravity was also ascertained by
weighing a measured volume (vide albumen estimation).
(b). The feces.—Each motion was passed into a separate
porringer, and as many of these as had been used were
handed over to us at the end of each twenty-four hours.
The contents of the whole number were washed with a jet of
distilled water into a large weighed evaporating basin, and well
mixed with a glass rod, hydrochloric acid being added until
they distinctly reddened litmus paper. They were then put
into a hot water oven and kept at about 80°C., being stirred
from time to time until they appeared dry; this took from
twelve to thirty-six hours, after which they were further
dried for about six hours in a hot air oven, between 100° C.
and 110°C. They were allowed to cool in a desiccator over
strong sulphuric acid, and then weighed in the evaporating
basin, to the nearest decigram.
The dried feeces were powdered as finely as possible in a
mortar, and a sample kept for analysis.
(c). The vomits.—These were collected separately, ‘in
porringers. All were extremely small. Analysed sepa-
rately at first, they were found to contain so little nitrogen
that subsequent vomits were mixed with the feces, and
estimated with them. Further mention of this is made in
Section VIII.
The methods of analysts.
The pipettes and burettes used were carefully standardised
before the experimental work began. Several blank Kjeldahl
estimations were made, to determine the correction for the
apparatus.
Case of Bright’s Disease. 59
The Kjeldahl method, as described by Kossel (33), was
employed for the estimation of the total nitrogen in the milk;
bread; Garibaldi biscuit; dinner biscuit; Liebig; urine;
and feces. Two estimations of the milk, urine and feces
were made each day. The results of the analyses of the food
stuffs are given in Table II.
The urea was estimated by the Morner-Sjóquist (44)
process, in two 5 c.c. samples each day.
The uric acid was determined by Hopkins' (26) potassium
permanganate method, in two 100 c.c. samples each day.
The albumen was estimated by the trichloracetic acid
method from February 20th to 28th inclusive; for the
remainder of the time by a heat coagulation process. The
following are detailed descriptions of each :—
(a). The trichloracetic acid method.—To two 50 c.c. samples
of urine each day, an equal quantity of 10 per cent. trichlor-
acetic acid was added. After standing, the precipitate was
filtered off, and washed with a jet of hot 5 per cent. trichlor-
acetic acid, until the washings gave no reaction with sodium
hypobromite. The filter paper with the precipitate was
dried; first on a water bath below 60° C., until apparently
dry; then in a hot air oven at 90° C. to 120°C. for four
hours; and finally in a desiccator over strong sulphuric acid
for four days. It was then weighed, and the known weight
of the dry filter paper deducted. The percentage of nitrogen
in four samples of the precipitated albumen was determined
by Kjeldahl; and from this the nitrogen as albumen in each
day’s urine calculated.
(b). The heat coagulation process.—50 c.c. of urine were
run into an india-rubber corked flask, the weight of the cork
and flask being known. The urine, cork, and flask were
weighed; the difference gave the weight of urine taken, and
also its accurate specific gravity. The urine was then boiled,
and, while boiling, 5 per cent. acetic acid was added from a
burette until no further coagulation occurred. About 5 c.c.
was usually added in this way. The flask was corked,
allowed to cool, and again weighed.
VOL. LVI. 8
60 A Research upon the Nitrogenous Metabolism 4n a
The coagulated proteid was then removed by filtering,
and the filtrate tested with nitric acid to be sure that none
remained. The nitrogen in two 10 c.c. samples of the
proteid free urine was estimated by Kjeldahl.
But 10 c.c. of this boiled urine = 10 c.c. of the original
weight after boiling. Therefore the nitrogen found
urine X weight before boiling.
in 10 c.c. of boiled urine was multiplied by the factor:
weight before boiling
weight after boiling'
original urine freed from coagulable proteid. The total
nitrogen in the urine being known, the difference between
this and the nitrogen in the proteid free urine gave the
coagulable proteid nitrogen.
The greatest correction was—
50:462 (weight in grms. berate boiling) .
56:043 (weight in grms. after boiling) ”
usually it was much less.
to give the nitrogen in 10 c.c. of
SECTION III.
Tables of results.
Tables I. and II. give in extenso our experimental results and
calculations from them. They are referred to in the different
sections, and summaries are there made. The meaning of the
figures is explained by the headings of the columns.
The following are the notes we wish to make about these two
tables. l
1. When not otherwise specified, two estimations were made
in every case, and the mean taken. Whenever, in the following
notes, it is stated that the higher of the two values was taken,
this was because the difference between the two observations was
more than 1 per cent. from the mean.
2. The volume of urine.—The figures are for urine actually
` measured, except on :—
March 9th, when 285 c.c. was measured and nurse
reported 3i. (=28 c.c.) spilled.
March 12th, when 267 c.c. was measured, and nurse
reported ziii, (= 85 c.c.) passed into bed.
4.
e
THE
genous Metabolis
ABLE
Tue Nitrogen y L#HE URIC Асто
THE UREA NITROGEN
RELATION. RELATIONS.
The total
Nitrogen in
The total | the Urine,
The Ratio Nitrogen in | minus the
Uric Aci d The Ratio. the Urine Coagulable
| Nitrogen: Uric Acid being Proteid
in | Nitrogen in Ҹә ` | (as such) regarded as | Nitrogen
id Feeces. Total to 100, the being
Nitrogen in Urea ‚Urea regarded as
Urine (as such). | Nitrogen
equals :—
100, the
Urea
Nitrogen
equals :—
Case of Bright’s Disease. 61
March 25th, when 1490 c.c. was measured, and nurse
reported 3ii. (= 7 c.c.) spilled.
March 26th, nurse reported a small quantity spilled, for
which we made no allowance.
8. The specific gravity of the urıne—When no decimal place is
given, there was a urinometer reading only. Otherwise the
figure is calculated from the weight of a measured volume.
4. The milk.—March 3rd, nurse reported a small quantity
spilled. We did not correct for this, so that it was calculated as
having been taken by the patient.
One estimation only: February 19th, March 3rd, March 21st.
The higher value taken: March 19th.
5. The vomits.—All were extremely small. They were lost on
February 25th (1), February 28th (1), March 3rd (8). They were
separately estimated, and the nitrogen added to the fæces on the
following days :— | |
March Sth su ə = 0:0483 grms. nitrogen.
March 6th ды ə — 0:0406 ý
March 14th ... = = 00629 “
They were estimated along with the feces on March 10th,
12th, 17th and 24th.
6. The feces —On March 3rd the amount was so small, one
Kjeldahl only was made. There were three estimations February
20th, 22nd and 23rd.
7. Total nitrogen in urine.—
One estimation only on March 4th and 7th.
Higher value taken on March 3rd and 21st.
8. Urea nitrogen.—
One estimation only on February 25th, 26th and 28th ;
March 6th, 7th, 12th, 22nd and 29th.
Higher value taken on March 2nd, 5th, 11th and 28th.
9. Uric acid mtrogen.—
One estimation only on March 4th.
Higher value taken on February 21st, March 1st, 2nd, 12th,
19th and 22nd. |
10. Proteid free urine.—
No estimation at all on February 19th and March 6th,
62 A Research upon the Nitrogenous Metabolism in a
Higher value taken on March 9th, 10th, 21st and 25th.
The columns of the tables are arranged so as to correspond ;
the urine and feeces figures, for example, are for the day on which
the patient passed the urine and fæces , the milk figures for the
day on which he consumed the milk.
The total intake and the total output nitrogen for each day,
the progressive nitrogen deficit, and the patient’s weight for each
day, are represented graphically in the chart.
SECTION IV.
The Urea.
In Text-Books of Medicine (11) the statement is often met with,
that in Bright”s disease, and particularly in uremia, the urea is
diminished. Authors do not specify whether this diminution is
relative as well as absolute.
That the absolute quantity of urea excreted by a person with
ursemia should be less than that by a healthy individual, is to be
expected, because his food nitrogen is less. But he may be
excreting quite as large a proportion of urea as would a normal
person upon the same diet.
We have found no experiment in which a healthy boy, of the
same age as our patient, took exactly the same amount of food
nitrogen as he did. Therefore we cannot say whether a healthy
boy, and a boy with subacute Bright's disease, each having the
same quantity of food nitrogen, would excrete equal amounts of
urea, or not. But we can determine the percentage of the total
nitrogen in the urine which is in the form of urea; and thus find
out whether the proportion of urea is diminished in Bright's
disease and uremia, or not.
In the following table are summarised the results obtained by
different observers, in healthy persons. Few complete investiga-
tions by the Mórner-Sjóquist process have yet been carried out ;
we have, therefore, included some less recent figures, obtained
by modified hypobromite methods. In one case only was the
diet solely milk. In all cases, the total nitrogen was determined
by Kjeldahl :—
63
Case of Bright's Disease.
8-18 | #-96 | 9-19 |"
6.88 | Р-Ӱб | 9-08 |"
2-38 | — = |
1-96 | — == cn
9.48 | 0-66 | 2-78 ||"
0-78 | 8-68 | 9-02 ||”
8-06 | 1-66 | 9-28 | "
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T-08 | T-#8 | @-LL İF”
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64 A Research upon the Nitrogenous Metabolism in a
Referring to the results obtained by the Mörner-Sjöquist
process only, it will be seen that the percentage of the total
nitrogen in the urine which is present as urea nitrogen, may, in
health, be as low as 67:5 per cent., or as high as 96:4 per cent.
These are extreme variations. Hale White and Spriggs, in a
series of twenty-seven consecutive observations upon the same
person, found an average of 87:3 per cent.
The averages obtained by the other workers quoted, vary from
80:1 per cent. to 93:8 per cent.
In none of the metabolism experiments upon Bright's disease,
have we found the urea estimated at the same time as the total
nitrogen. Prior (50) gives figures for the urea, by Pflüger's
method, in some cases; but, when reduced to nitrogen, the urea
nitrogen and the total nitrogen are identical. P. Müller (45),
we believe, estimated the urea; but we have been unable to
obtain the inaugural dissertation which contains his researches.
Gumlich (20), in occasional samples of urine from patients
with chronie parenchymatous nephritis, estimated the urea as
nitrogen not precipitated by phosphotungstic acid; and found the
proportion of urea nitrogen to vary from 72:8 per cent. to 88:9
per cent. of the total nitrogen in the urine. He made no allowance
for the coagulable proteid nitrogen.
Our own results are given in detail in Table I. We have
calculated the percentage relation of the urea nitrogen both to
the total nitrogen in the urine, and to the urinary nitrogen
remaining after deduction of that present as coagulable proteid.
Below we give the results summarised :—
(1). For the whole period.
(2). For the period of uremia.
(3). For the non-ur®mic period.
(4). For the different diets.
Case of Bright’s Disease.
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66 A Research upon the Nitrogenous Metabolism in a
At first sight, the percentage of urea nitrogen appears distinctly
lower than in health; the average for the whole period being
75:6 per cent., as against 87:3 per cent. in Hale White and
Spriggs’ case.
But, when we deduct from the total nitrogen of the urine, that
of the abnormal constituent, coagulable proteid, the urea nitrogen
forms 83:4 per cent. of the remainder; the extreme daily varia-
tions being 71:8 per cent. and 94:6 per cent. Regarding the
coagulable proteid, in this way, as an accidental impurity, the
proportion of urea nitrogen, in our case, was, therefore, within
the limits found in health.
As regards the uremic period, the urea nitrogen formed, on an
average, 82:03 per cent. of the urinary nitrogen after deduction
of that in the coagulable proteid. This is slightly less than 84-49
per cent., the average proportion for the remainder of the time.
But in Section V. it is shown that the proportion of uric acid was
at its maximum during the uremic period; this will partly
account for the slightly lower proportion of urea nitrogen. In
our patient, therefore, the onset of uremic symptoms was
accompanied by no marked relative decrease in the urea nitrogen.
The urea in 100 c.c. urine, on the other hand, rose considerably
at this time. The average, for the uremic period, was 2:07 grms.
of urea in 100 c.c. urine; whereas, for the remainder of the time,
it was 1:01 grms. The reason of this was the smaller volume of
urine passed, and its consequent greater concentration.
The influence of the different diets is also little marked. It will
be seen, in Table IV., that the urea nitrogen formed a slightly
greater percentage of the whole when Liebig was given, than
without it; but, whether the coagulable proteid nitrogen be
reckoned, or be previously deducted, the variations caused by
diet were slight.
The conclusions, therefore, which we draw from this section
of our work are, that, in our patient with subacute nephritis :—
(1). There was no diminution of the proportion of urea nitrogen
to the total nitrogen of the urine, if the coagulable proteid be
regarded as an accidental body, and its nitrogen first deducted
from the total; but that, reckoning the nitrogen of this abnormal
Case of Bright's Disease. 67
body in the total, the proportion of urea nitrogen was about
10 per cent. below the normal.
(2). The proportion of urea nitrogen to total urinary nitrogen
was not appreciably lower when uremic symptoms showed
themselves, than at other times; the total urea nitrogen was less
during uremia, as the food was less; whilst the percentage of
urea in the urine rose considerably.
(3). The addition of bread, biscuit, or Liebig’s extract of meat
to a purely milk diet caused no corresponding alteration in the
proportion of the urea nitrogen.
SECTION V.
The Uric Acid.
In Osler”s Principles and Practice of Medicine, p. 409, there is
a quotation from Koliseh (30) to the effect that in nephritis the
uric acid is diminished, and the xanthin bases in the urine
increased. Tn his original paper Kolisch states that in nephritis
the total alloxuric bodies remain constant, but that there is an
increase in the xanthin bases (xanthin, hypoxanthin, paraxanthin,
adenin, guanin, carnin), at the expense of the uric acid. He
quotes Baginsky (3), who found that in children with nephritis
the xanthin in the urine increases.
Kolisch and Dostal (30) estimated the total alloxuric bodies by
the method of Kriiger and Wulff (34), the uric acid by the
Ludwig (38) Salkowski (58a) process. In health they give the
uric acid nitrogen A,
xanthin base nitrogen 1
and this is confirmed by Kossel’s pupils, quoted by Zuelzer (69),
whilst Weintraud (67) found $ and 1. In nephritis their analyses
showed for single day estimations with different patients :—
Uric acid nitrogen 724, 24, and 2
.
proportion :
{3 ?
Xanthin base nitrogen 1 ' 1
68 A Research upon the Nitrogenous Metabolism in a
The nitrogen of the total alloxuric bodies in these cases was 0:152
grms., 0:220 grms., and 0:312 grms. respectively, whilst in health
they found 0:260 grms. They draw the conclusion that one of
the functions of the kidney is to convert the xanthin bases
into uric acid, and that in nephritis this change does not take
place.
Frerichs (15), Bartels (5), Dickinson (10), Fleischer (14),
Wagner (66), and Rosenstein (51), using Heintz’s (23) method,
found the uric acid diminished in Bright’s disease. Géza Fodor
(17), by the Ludwig-Salkowski (53a) process, obtained similar
results to those of Kolisch and Dostal as regards xanthin bases
and uric acid, and further found that the fall of uric acid in the
urine of nephritis was unaccompanied by any rise of uric acid
in the blood.
On the other hand, many investigators have been unable to
demonstrate any such fall. Vogel (65), though he used Heintz’
method, found as much uric acid in acute nephritis as in health ;
and the following more recent workers, employing the Ludwig-
Salkowski or Hopkins (26) processes, confirm this (See Table V).
Zuelzer (69) further states that he never found the uric acid
in Bright’s disease less than the xanthin bases, his ratio—
Uric acid nitrogen "ng f 18, 85, со
> — to — to —;
Xanthin base nitrogen Ы " r” |
whilst Umber’s (62) figures, for healthy persons, show variations
between ot and 7
The following table shows the values for uric acid, in health,
obtained by modern methods. (See Table VI.)
It will be seen that there are very wide variations in the uric
uric acid
acid, even in health. The ratio in Table VI. varies
uric acid nitrogen
=” = —- IPOs to
total urinary nitrogen ә
from „ to x; and the ratio
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Case of Bright’s Disease. 71
as. In Table V., of Bright’s disease, the ratio ario sold ranges
uric acid nitrogen
total urinary nitrogen
Therefore Kolisch’s statement, quoted by Osler, is not supported
from xy to y; and from 757 to gg.
by the results of more recent analyses. `
Our own results are given in full in Table I. The most
remarkable point, perhaps, is the almost constant, and relatively
high ratio 75 acid
2nd to 13th inclusive. This ratio is quite as high, but slightly
less constant, during the last nine days of the experiment,
during the period of mild uremia, March
when Liebig’s meat extract was added to the diet. During the
remaining twenty days the ratio was very variable, and the
mean much lower, as shown in the following summary :—
TABLE VII.
Ratio of uric acid | Ratio of uric acid | Total daily uric
nitrogen to total | (as such) to urea acid,
nitrogen of urine. (as such). in grams.
For the whole experiment % 1 os | A riz zu | 48 “12 924
41 days.
For the uremic period | öy gy dg | oe ds ss | 29 “15 2
12 days.
For the remaining period 27 12 “18
without Liebig 20 days. Sr rv rh | dy rir d
For the remaining period 48 ‘31 39
with Liebig 9 days. E ar de ts
72 A Research upon the Nitrogenous Metabolism in a
uric acid nitrogen
total urinary nitrogen
uric acid
The ratio is more variable, and of less
value, than that of , on account of the varying quantities
of coagulable proteid in the urine.
The high ratio ин when Liebig was given,
total urinary nitrogen
corresponds to the results obtained by Strauss (60) and Smith-
Jerome (57) with meat extract feeding in the healthy subject.
We conclude that, in our patient suffering from subacute
nephritis :—
(1). The uric acid was not diminished out of proportion to the
other urinary constituents.
uric acid
urea
(2). The variations in the ratio are not greater than
those which occur in health.
(3). The ratio mie add became higher, and much more
constant, with advent of uremic symptoms.
(4). The addition of extract of meat to the diet produced, as
in health, both an actual and a relative increase in the uric acid.
SECTION VI.
The Coagulable Proteid.
Albumen is present in the urine of Bright’s disease in such
variable quantities that we have not much to say about it in the
present instance. Great care was taken in the estimation of the
coagulable proteid nitrogen, but the deductions we can draw
are few.
The results have enabled us, however, in Section IV., to deduct
albumen nitrogen from total nitrogen, and to find the relation of
the urea nitrogen to the remainder, and we concluded that the
Case of Bright’s Disease. 73
coagulable proteid might be regarded as a foreign or adventitious
substance.
We made no attempt to differentiate the varieties of coagulable
proteid present.
Van Noorden and Ritter (64), estimating the albumen by
Scherer’s method, conclude from figures tabulated on p. 223 of
their paper, that the kind of diet has little effect upon the amount
of albumen in the urine; but that when there is a change of diet
there is often an increase in the albumen for a few days after the
change. The following table is a summary of our results :—
TABLE VIII.
Per cent. of Nitrogen
Ni bl
protein 34 hours m s, cosspisble pro
: rogen in urine.
Average of whole period (41 days) 0:6536 9:948 per cent.
Average of 11 days in uremic 0:6085 11:640 per cent.
peri
(There was no estimation on
March 6th)
Influence of kind of diet :—
Average of 18 days milk only 0:7080 9:884 per cent.
Average of 12 days milk and bread 0°5700 10:680 per cent.
or biscuits
Average of 9 days milk, biscuit, 0°6375 7:184 per cent.
Liebig
Influence of change of diet :—
Average of last 2 days of milk, 0:5500 —
before bread |
Average of first 2 days of bread 0:4479 —
Average of last 2 days of milk, 0:5417 —
before Liebig
Average of first 2 days of Liebig 0:6948 —
74 A Research upon the Nitrogenows Metabolism in a
If any conclusions can be drawn at all, we should infer from
Table VIII. that the average daily output of coagulable proteid
in the urine was almost constant in the different periods; that
the addition of bread or Liebig to our patient’s diet did not
cause it to alter much; that in the ursemic period the average
total for each twenty-four hours was approximately the same as
the average for the whole period; and that the average daily
total was more constant than the average percentage relationship
to the total nitrogen in the urine.
It is true that when Liebig was added to the diet there was
an increase in the coagulable proteid for the first few days , the
last two days, with milk diet before Liebig was given, gave an
average of 0:5417 grms. nitrogen as albumen; the average of the
first two days of Liebig was 0:6948 grms. nitrogen. The average '
for the whole Liebig period (0:6375 grms.) on the other hand, was
less than the average for the whole period of milk diet (0:7080 grms.)
The change, however, from milk to milk and bread or biscuit
gave a, fall in coagulable proteid nitrogen from 0:5500 grms. to
0:4479 grms. We do not find, therefore, as Van Noorden (64)
did, that change of diet always caused an increase in the
albumen.
The detailed figures in Table I. show the coagulable proteid
nitrogen to have been highest on March 1st and 2nd, namely, on
the first day of distinct ureemia, and on the day before it, but this
may be mere coincidence. It is of interest to compare the
figures with the clinical account; it will be seen that the cedema
was, as far as we could judge, most marked about March 20th,
the coagulable proteid nitrogen was by no means at its maximum
at this time. The total amount of coagulable proteid in the
urine gave no close index of the cedema present.
Case of Bright’s Disease. 75
SECTION VII.
The nitrogen as “other bodies.”
No attempt was made to determine what the “ other bodies ”
were. They were calculated by subtracting the urea nitrogen,
the uric acid nitrogen, and the coagulable proteid nitrogen, on
the one hand, from the total nitrogen in the urine on the other.
The following table gives the average percentage relation of
“other bodies” nitrogen to total urinary nitrogen for the different
periods :—
TABLE IX.
Per cent. of “other bodies ”
nitrogen referred to total
urinary nitrogen as 100.
Whole period :—
February 19th to March 31st ... 18:88 per cent.
Uremic period :—
March 2nd to March 13th 14:52 per cent.
Non-uremic period :—
February 19th to March 1st and 757 14th
to March 31st 13:60 per cent.
Milk diet only :—
February 19th to March 4th Es mun pə
to March 22nd 14:08 per cent.
Milk and bread or biscuit :—
March 5th to March 17th 13°92 per cent.
Milk and biscuit and Liebig :—
March 23rd to March 31st 13:24 per cent.
We draw no conclusions from Table IX. The figures are
averages; the daily variations, which were considerable, are given
in Table II. It is of interest to note how the average proportion
of ““ other bodies”” nitrogen remains almost constant throughout,
in spite of alterations in the patient’s general condition, and in
his diet.
VOL. LVI. 9
76 A Research upon the Nitrogenous Metabolism in a
SECTION VIII.
The faces.
Part of the treatment of Bright’s disease is usually directed
towards increasing the intestinal elimination, with a view to
diminishing the work of the kidneys. Unfortunately it is not yet
possible to determine how much of the nitrogen in the fæces is
derived from food unabsorbed, and how much, if any, from
metabolic end products excreted into the bowel. Nevertheless it
is interesting to compare the nitrogen in the fæces of persons
suffering from Bright’s disease with that in the feces of healthy
people.
Some observers compare the faces nitrogen with the total
nitrogen intake, regarding the former as loss, the difference
between the two as the true intake, and the relation between the
two as an index of the assimilative power.
This can only be true if no nitrogenous bodies are excreted by
the bowel. Pregl (49) has shown that excretory products, such as
urea and ammonia, may be found in the intestinal secretion; it
seems, therefore, justifiable to compare the faces nitrogen with the
total output of nitrogen in the urine and feces together, as well
as with the nitrogen in the food intake; an additional argument
for so doing arises from the fact that in many cases the food
nitrogen has been calculated from diet tables, and therefore may
be less accurate than the figures obtained by direct Kjeldahl
estimations of the urine and feces. In the following tables both
relations are given.
In the first are the results obtained by different observers in
normal people. A very large number of fæces determinations
has been found in the literature; but for purposes of comparison
with our own, only those in which the diet has been chiefly milk
have been tabulated; and no case given in which the observation
extended over less than three days.
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A Research upon the Nitrogenous Metabolism in a
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Case of Bright’s Disease. 79
In one case of Rudenko's, as much as 24°7 per cent. of the
nitrogen of the intake was found in the fæces, but in no other
case are the figures so high. Including this exceptional instance,
the average results of 37 investigations upon different healthy
persons having a milk diet showed that for every 100 grms. of
nitrogen in the food there were 7:4 grms. of nitrogen in the feces ;
and for every 100 grms. of nitrogen in the urine and feces there
were 7:3 grms. of nitrogen in the faces, and the average daily total
nitrogen in the feces was 1:2 grms.
Camerer’s experiments alone were made upon boys and girls of
. an age similar to that of our patient, and the figures, an average
of five cases are as follows:—For every 100 grms. nitrogen in
the food there were 6-1 grms. in the feces; for every 100 grms.
nitrogen in the urine and fæces there were 5:7 grms. nitrogen in
the feces; the daily average total nitrogen in the feces being
0:6 grms.
In the next table the figures obtained upon persons suffering
from different forms of Bright’s disease are tabulated. In these
the diet was not always milk only, though it was always light,
and in some of them drugs were given (See Table XI.). |
It will be seen that Korkounov on one occasion found as
much as 74:2 per cent. of the nitrogen intake in the fæces; and
Grigoriev 43:9 per cent.; but these figures are very much above
the average. The lowest figures are also Grigoriev's, namely,
3 per cent. of the nitrogen intake, and 2'7 per cent. of the total
nitrogen in the urine and faces. |
The average of the whole thirty-two cases shows that for every
100 grms. of nitrogen in the food, there were 14:1 grms.
nitrogen in the feces; for every 100 grms. of nitrogen in the
urine and faces, there were 14:0 grms. nitrogen in the feces.
The average daily nitrogen in the fæces being 1:9 grms.
Baginsky's patients alone approach in age to ours, and the
average of his results for four observations are as follows: for
every 100 grms. of nitrogen in the food there were 9:4 grms.
nitrogen in the faces; for every 100 grms. of nitrogen in the
urine and feces there were 12:0 grms. nitrogen in the faces.
The average daily nitrogen in the fæces being 1:2 grams.
18M M A
A Research upon the Nitrogenous Metabol
80
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81
Case of Bright's Disease.
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82 A Research upon the Nitrogenous Metabolism in a
The table shows that very wide variations in the fæces nitrogen
in Bright’s disease may occur quite independently of the form of
kidney lesion.
Our own figures for each day are given in extenso in Table I.
On some of the days the patient vomited, and the nitrogen of the
vomit has been added to the fæces nitrogen. The vomits were
always very small, being chiefly saliva. On three days, they
were estimated by Kjeldahl and found to contain 0:0482 grms. ;
0:0407 grms.; and 0:0629 grms. nitrogen respectively. Being
so small, the vomit was therefore on other occasions added to the
daily faaces and the two estimated together.
The following is a summary of our results arranged as follows:
(1). For successive periods of five days each, the first day
being neglected.
(2). For the period of mild uremia.
(3). For the different diets the patient took.
(4). The average for the entire experiment.
TABLE XII.
f Percentage of
Nitrogen in Average Nit-
fæces referred rogen in Fæces
to Nitrogen in | per diem in
Percentage o
Nitrogen in
Feces referred
to Nitrogen in
Urine an ҹи
Food. ra 77
(1). Successive periods of 5 days—
(a). February 20th to Febru- |
ary 24th n 13:6 14:8 13
b). February 25th to March 1st 18:0 19:7 17
o. March 2nd to March 6th .. 14:0 12:4 0:8
, Thto „ 1lth.. 20:1 20:6 1:3
6) „ 12th to „ 16th .. 11:6 18:9 0:8
, Mih to , 2186 ... 14:0 14:7 1:3
, 22ndto , 26th... 11:3 18:2 18
(o. , 2166 to , Bist ... 11:3 11:4 1:2
(2). Period of mild uremia—
March 2nd to ә 13th
(12 days) 15:9 157 1:0
(3). Different diets—
(O) February 19th to March 4th
February 19th to March 4t
March 18th to March and | 149 155 13
(b). Milk and bread or biscuit—
March 5th to March 17th . 14:9 16:1 1:0
(c). Milk & biscuit and Liebig—
March 28rd to March 81st .. 10:9 11:8 1:2
(4). Average for entire ix ,
41 days 18:9 147 1:2
Case of Bright’s Disease. 83
Van Noorden and Ritter (64) concluded from their researches
that the fæces nitrogen might, in Bright disease, either be almost
normal or considerably higher, but that neither from the general
condition of the patient, nor from the variety of the kidney lesion
could it be decided beforehand whether high or normal figures
would be found; and that it could not be determined whether the
feeces nitrogen was due to non-absorption or to true secretion.
Our own conclusions are that, in our patient, suffering from
subacute parenchymatous nephritis, and treated with purgatives :
(1). The average daily faces nitrogen (1:2 grms.) is the
same as that found as the mean of thirty-seven investigations upon
healthy persons of all ages upon a milk diet.
(2). The average daily fæces nitrogen (1:2 grms.) is double
that found as the mean of five investigations by Camerer upon
healthy children of about the same age as our patient (0:6 grms.).
(3). The average daily feeces nitrogen (1:2 grms.) is less than
that found as the mean of thirty-two investigations upon patients
of all ages suffering from different kinds of Bright’s disease (1:9
grms.). |
(4). The average daily fæces nitrogen (1:2 grms.) is the same
as the mean of four investigations by Baginsky upon children
suffering from acute nephritis, at ages comparable to that of our
patient. |
(5). The fæces nitrogen for the whole period expressed as per-
centage of nitrogen in urine and faces (14-7 per cent.) is slightly
greater than that of four children with acute nephritis investigated
by Baginsky (12:0 per cent.) ; is more than twice as much as that
of thirty-seven different healthy persons upon milk diet (7:0 per
cent.) ; and nearly three times that of five healthy children upon
a milk diet, investigated by Camerer (5:7 per cent.).
(6). The influence of diet is little marked: with Liebig the
proportion of fæces nitrogen (11:8 per cent.) was somewhat less
than with milk alone (15:5 per cent.); or with milk and bread
(16:1 per cent.).
(7). That during the ureemic period the proportion of the fæces
nitrogen (15:7 per cent.) did not appreciably differ from that of the
whole experiment (14:7 per cent.).
84 A Research upon the Nitrogenous Metabolism in a
(8). The proportion of feces nitrogen was uniformly high ;
and did not at any time shew wide variations from the average.
Such high proportion, however, does not prove that the bowel
was excreting nitrogen and thus doing work that would otherwise
be done by the kidneys, since we have no conclusive evidence
that the whole of the fæces nitrogen may not have been due to
non-assimilation from the food. In our patient there were three
possible sources of feeces nitrogen, namely :—
(1). Non-assimilation of food.
(2). True bowel excretion.
(3). Inflammatory exudation from mucous membrane.
SECTION IX.
The Unrecovered Nitrogen.
Our patient’s weight was approximately the same at the end of
the experiment as at the beginning. Therefore, the loss of nitrogen
(20-7 grms.) in the six weeks may be due either to experimental
error, or to the sweat and shedding of hair, surface skin and
psoriasis scales. How much is due to the second factor we do
not know; in spite of every care, the sum of the experimental
errors of forty-one days cannot but be considerable; because milk
spilled makes the intake too high, urine spilled, the output too low.
Other workers have found wide differences. Referring only to
those metabolism experiments in which the diet was milk and the
person healthy, we find that Hofman (25) in a three days’ obser-
vation recovered 30:3 grms. more nitrogen than was in the food,
— Lapschinsky (35) at the opposite extreme, found in six days a
deficit of 45 grms. Most of the experiments are for short
periods only, and the variations are so great that no useful purpose
would be served by giving all the results here. They have been
summarised in tabular form by Atwater and Langworthy (2).
Tunnicliffe and Rosenheim’s experiments upon two healthy chil-
dren, whose diet was chiefly milk, are of longer duration, and
comparable with our own as regards the diet and the patients’ age.
Case of Bright’s Disease. 85
The daily nitrogen deficit is tabulated in their paper (614).
In case A, a child of 24 years, the deficit was 18:87 grms. in
twenty-five days, with an increase of 0:17 kg. in body weight. In
case B, a child of 5 years, it was 14:05 grms. in twenty-two
days, the increase in weight being 0°28 kg.*
Turning now to metabolism experiments in Bright’s disease, we
find even wider variations. Thus, Korkounov (81) recovered an
excess of 89:3 grms. nitrogen in a three days’ observation in one
case, while in another of the same duration his deficit was 39:4
grms.
Numerous researches, all quoted in our introduction, have
been made, but for comparatively short periods continuously.
Baginsky's figures alone are for children with acute nephritis on
milk diet; we give them in full.
TABLE XIII.
Daily loss or gain of nitrogen in Baginsky's metabolism experi-
ments upon children with acute nephritis. (3a.)
A. (girl 133 years.) | B. (girl 133 years.) C. (girl 5 years.)
Daily loss | Progressive | Daily loss | Progressive | Daily loss | Progressive
or gain. deficit. or gain. deficit. or gain. deficit.
İst day ...İ —3:043 3:043 +0:275 —Ü 275 — 258 5:258
2nd , ...| —4:405 1:448 —2°280 2°005 —3 “834 9:092
Ərd , ...| 4-0:090 7:358 —2-590 4:595 — 4:638 13:730
4th , ...| +2°467 4:891 —1:900 60:495 —4-679 18:409
oth , .. | —3:724 8:615 —1:220 7715 — 5'350 23-759
6h , .. — — — —0:831 24:590
Average 1-728 1-548 4-098
daily del No gain wks No gain дә 0-59 kg.
loss of weight. of weight. gained.
— Means deficit. + Means surplus over intake.
* In a paper published since this was written (Journal of Hygiene, vol. 1,
No. 8, July, 1901), Tunnicliffe and Rosenheim give the results of further
metabolism researches upon the same children. In these experiments, which
extended over twenty-eight days, the nitrogen deficits met with were :—
Child A, 27:58 grms. , child B, 40°97 grms.
86 A Research upon the Nitrogenous Metabolism in a
No experiments upon children with nephritis have extended over
a longer period. None have included a period of uremia.
Our own results both as regards the gain or loss of nitrogen
each day and the progressive deficit from the beginning are given
in full in Table I.
The average deficit of nitrogen per diem was 0:506 grms., which
is much less than Baginsky found in his cases. An examination
of the figures in conjunction with the clinical account, shows that
the deficit occurred almost entirely when the general condition of
the patient appeared best. When uremic symptoms were present,
the output of nitrogen almost invariably exceeded the intake. This
is very clearly illustrated by the curves in the chart.
Thus, by the end of the tenth day the nitrogen deficit was 8-07
grms. , for the next twelve days the output exceeded the intake,
so that on the twenty-second day the nitrogen deficit was only
2°48 grms. and the patient had gained 1:1 kg. in weight. While
this recovery of nitrogen had been going on the patient was dis-
tinctly uremic. On the twenty-third day his health improved
greatly, and he continued better until the thirty-ninth day ; during
this time the nitrogen deficit increased to 23°75 grms. and his
weight to 1:5 kg. more. than at the beginning. During the last
two days he became less well, and again excreted more nitrogen
than he took as food, so that the deficit fell to 20:75 grms. This
was the commencement of a second ureemic period. Unfortunately
we were unable to continue the work after March 31st, but we saw
the patient the following week and he was distinctly uremic.
We had intended to compare the nitrogen deficit for the period
(Feb. 19th to March 6th inclusive) when baths were given, with
that of the remaining time without baths. The average daily
deficit for the period of baths was 0:23 grms. nitrogen; for the
period of no baths was 0:68 grms. nitrogen. At first sight this
seems to shew less loss of nitrogen by the skin when baths were
given than without them ; but the figures will not bear this inter-
pretation for the following reasons :—
(1). The body weight did not remain constant.
Case of Brighi’s Disease. 87
(2). The amount of edema was variable and we had no means
of measuring it exactly and so determining how much of the
variation in body weight was due to water.
(3). The period of uremia supervened.
Tunnicliffe and Rosenheim (614) in their experiments on two
healthy children found an average daily deficit of 0°75 and 0:64
grms. nitrogen. There were, it is true, gains of weight of 0:17
and 0:28 kg. respectively, which, if entirely due to proteid, would
account for part of the deficit.
Supposing that every 100 grms. of increased body weight
meant 3:3 grms. of food nitrogen converted into living tissues,
there would still be 0:53 and 0:22 grms. nitrogen daily unaccounted
for. We will compare these figures with our own. Over the
whole experiment, we found an average deficit of 0:50 grms.
nitrogen daily.
This is less than the average figures in Tunnicliffe and
Rosenheim’s cases, if no account be taken of altered body weight.
In our case, the presence of a varying cedema vitiates allowances
for changes in weight. An increase in our patients’ weight was
certainly not all due to building up of nitrogen into living proteid.
For example, at the end of the twenty-second day the total
deficit was 2:484 grms. nitrogen; but the body weight had
increased by 0:85 kg. If the latter were entirely due to proteid
built up, it would contain 27:05 grms. nitrogen; so that 18:9
times our nitrogen deficit would be accounted for.
This is not probable. Even though we make no allowance for
altered body weight in our case, and yet concede that the gain in
weight in the healthy children was entirely due to proteid, we find
that our daily nitrogen deficit was less than Tunnicliffe and
Rosenheim’s in their longest experiment, though greater than that
in their other. Remembering that our patient was covered with
psoriasis, and that during the period when baths were given he
often perspired very freely, whilst urea has been found in the
sweat of uremic patients (61), we expected our deficit to be
greater.
88 A Research upon the Nitrogenous Metabolism in a
The conclusions which we draw from this section of our work
are therefore two, namely, that in our patient suffering from sub-
acute nephritis :—
(1). The uremic period was marked, not by a retention of
nitrogen, but by an output in the urine and feeces of more nitrogen
than was taken in the food, the reverse being true when he was
in better health.
(2). The excretion of nitrogen by paths other than the kidney
and bowel was not appreciably greater than it is in health.
SECTION X.
General Conclusions.
Our general conclusions are: That,in our patient, with subacute
parenchymatous nephritis :—
(1). The proportion of nitrogen excreted as urea was not less
than that found in healthy persons, if the coagulable proteid in
the urine be regarded as a foreign constituent, and not as a true
excretory produot.
If the coagulable proteid nitrogen be included, the proportion
of urea nitrogen was less than in health.
(2). The above statements held good noth for the uræmic and
for the non-uræmic periods.
(3). The uræmic period was marked by :
(a). An output of nitrogen in excess of the intake.
uric acid
^ urea `
(4). The fæces nitrogen constituted a larger proportion of
nitrogen output than has been found in healthy children on a
milk diet.
(5). The loss of nitrogen by other channels than the urine and
fæces was not apparently greater than in health.
We desire to express our gratitude to Dr. Spriggs for his advice,
and especially for his assistance during the illness of one of us.
We thank Dr. Taylor and Dr. Fawcett for permission to investigate
(5). A high, and almost constant, ratio
Case of Bright's Disease. 89
the case; Dr. Pembrey for the facilities he gave us in his
laboratory; and the Matron of Guy's Hospital, Sister Clinical
and her Nurses, without whose hearty co-operation the work
could not have been accomplished.
The expenses of the research were defrayed out of a grant from
the Scientific Grants Committee of the British Medical Association
to Dr. Pembrey.
mcm P DII
SECTION XI.
References.
Argutinsky, Arch. f. d. ges. Physiol. Vol. 46, 1890, p. 599.
Atwater and Langworthy, Bulletin 45, Dept. of Agricult., U.S.A., 1897.
Baginsky, Du Bois Reymond’s Arch. f. Physiol, 1884.
. Baginsky, Arch. f. Kinderheilkunde. Vol. 15, p. 161.
Bain and Edgecombe, Journ. of Physiol. Vol. 23, 1898, p. 499.
Bartels, Ziemmsen’s Handbuch, Nierenkrankheiten, 1877.
Bohland, Arch. f. d. ges. Physiol. Vol. 43, 1888, p. 30.
Camerer, Zeitsch. f. Biol. Vol. 18, p. 489.
Camerer, Zeitsch. f. Biol., 1896, pp. 139-155.
Camerer, Zeitsch. f. Biol., 1897, p. 276.
Dickinson, Diseases of the Kidney, 1877.
Dickinson, Clifford Allbutt’s Syst. of Med. Vol. 4, p. 370.
Dunlop, Journ. of Physiol. Vol. 20, 1896.
Evdokimov, Inaug. Diss. (Russian), St. Petersburg, 1887, Table 8.
Fleischer, Deutsch. Arch. f. Klin. Med., 1881.
Frerichs, Die Bright’scae Nierenkrankheit und deren Behandlung,
Braunschweig, 1851.
Garine, Inaug. Diss. (Russian), St. Petersburg, 1887, p. 47.
Géza Fodor, Jahresbericht iiber Thier. Chemie, 1895, p. 571.
Grigoriev, Inaug. Diss. (Russian), St. Petersburg, 1888, pp. 81-96.
Goodbody, Journ. of Physiol. Vol. 25, 1900, p. 399.
Gumlich, Zeitsch. f. Physiol. Chemie, 1893, p. 18.
Haig, Uric Acid in Causation of Disease, 1900, p. 541.
Hale White and Spriggs, Journ of Physiol. Vol. 26, 1901, p. 162.
Heintz, Halliburton's Chem. Phys. and Path., p. 807.
Herringham and Groves, Journ. of Physiol., 1891, p. 480.
Hofman, Zeitsch. Klin. Med. 7 Suppl., p. 18.
Hopkins, Journ. of Path. Vol. 1, 1892-3.
Hopkins and Hope, Journ. of Physiol. Vol. 28, 1898, p. 294.
Horton-Smith, Journ. of Physiol. Vol. 12, p. 60.
Joslin, Journ. of Experimental Med. Vol. 5, No. 5.
Kolisch and Dostal, Wiener Klin. Wochenschrift, 1895.
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Kornblum, Virchow's Arch. Vol. 127, pp. 416-440.
90
A Research upon the Nitrogenous Metabolism in a
Case of Bright’s Disease.
Kossel, Medicinisch-Chemische Curse, pp. 34-36, Berlin, 1898.
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ROENTGEN-RAY DIAGNOSIS OF
RENAL CALCULUS.
By E. W. H. SHENTON.
RADIOGRAPHER TO Guy’s HosPITAL.
Tue detection of renal calculus, at once the most difficult and
most useful branch of Roentgen-ray science, has not received
the amount of attention that its merits deserve.
This can be accounted for in two ways, firstly by the dread of
dermatitis, shared alike by patient and medical adviser, secondly,
by the disappointment arising from a haphazard way of taking a
skiagram of an abdomen and calling it an X-ray examination of
that part. The novice with improper apparatus is responsible
for the dermatitis in these days, and there are few branches of
medicine in which this well-meaning but incompetent person
would not be dangerous. That dermatitis is an accident, and
one that can and should be avoided, is proved by the records of
the Guy’s Hospital department, for during the years that this
. work has been carried on there has not been a single instance of
inflammatory reaction taking place after a photographic exposure.
Even in cases where the rays have been used for therapeutic
purposes, and exposures of ten minutes several times a week
have been given, there is not a single recorded instance of der-
matitis. Most examples of Roentgen-ray dermatitis, if the
history be carefully enquired into, prove to be due to want of
knowledge on the part of those utilizing the rays.
VOL. LVI. 10
92 Roentgen-ray Diagnosis of Renal Calculus.
The unsatisfactory results from carelessly taken skiagrams
will always be present, unless the fact becomes more generally
known that a renal examination with the X-rays is not merely
* photographing a patient's kidneys," a foolish and prevalent
expression; prevalent because of the want of knowledge gener-
ally among the profession of things pertaining to the rays;
foolish because it is rare in the skiagram of an abdomen to see
the kidneys, for, as a rule, the less that is seen of the kidneys
the more chance there will be of seeing & calculus. It is
certainly time that these fallacious ideas were dispelled and a
fair statement of Roentgen renal examination set forward, with
its successes and failures. Supposing, as it is fair to do, that
dermatitis is & preventable accident, there is surely no more
harmless system of examining the abdomen than that afforded
by Roentgen's discovery. A skiagram per se is unreliable in all *
but the most obvious cases and, as in other branches of diag-
nosis, it is only by a systematic routine of examination that the
percentage of failures can be reduced to a minimum. Mr.
Jonathan Hutchinson, in a recent paper upon renal subjects, in
which he deals with the uses of the X-rays in calculus cases,
merely speaks of the photographie aspect of the subject, indeed
he does not even state the possibility of the screen being of
service. That photography alone is likely to prove very
unsatisfactory, can be abundantly proved, for it is possible to
So arrange tube and patient, that an obvious calculus does
not show in a photographic plate, and this is the error that
care alone can exclude, and it is also possible for a calculus
to move so much with respiration that it leaves no trace upon
the plate.
To merely speak, then, of the photographic aspect of kidney
examination is to leave out perhaps the most valuable part of
the system. Examination for renal calculus must be divided
into two distinct parts, the fluoroscopic and the radiographic ;
what is seen upon the screen and what is discoverable upon
the skiagram. As in other diagnostic methods, itis of extreme
importance to have a confirmatory test, and radiography is
usually the confirmatory test of radioscopy. The operator
4
Roentgen-ray Diagnosis of Renal Calculus, 93
has first to make himself familiar with the radioscopic
appearance of the normal abdomen, before attempting to
give an opinion on a renal case. In this he will meet with
many difficulties. The various effects produced by changes
in the position of the tube are mystifying (to obviate this
difficulty it has been suggested that the tube should always
be put opposite a certain spot. This suggestion is ridiculous, as
it would take away at once the chances of finding a stone when
not situated within a small area). Then, again, the shadows of
vertebra and other opaque objects are at the best so very faint
that a considerable time must be expended before the organs
which they represent can be recognised with any certainty.
One might draw a parallel between these faint shadows and the
faint sounds heard in a stethoscope. To the untrained eye or
ear neither have significance, yet it is possible that a careful
study of these ghostly screen effects may lead to a more delicate
and perfect method of ascertaining the condition of the abdominal
organs, as a proper appreciation of the faint auscultatory sounds
have led to the perfection of chest diagnosis. However this
may be, the search for calculus is an established and compara-
tively simple process, and one which, whenever accuracy of
diagnosis is of moment, should never be omitted. The observer
has not to trouble about any refinements in the quality of the
shadow, but merely to convince himself that a shadow of an
abnormal constituent of the abdomen is present, and by its size
and position and the compatability of the symptoms to decide
whether this shadow is that of a calculus. By considering the
symptoms it will be at times sufficient to examine the patient but
once, for a good history and an obvious foreign body in the
particular renal region to which these belong, will be sufficient
evidence; but in the event of a very doubtful history and an
indistinct shadow, possibly caused by some intestinal contents,
it will be most advisable to examine again at an interval that mA
have allowed such foreign matter to pass away. š
It will be asked in what percentage of cases examined are the
rays successfully used both as positive and negative evidence.
This is a very pertinent question aud one about which observers
94 Roentgen-ray Diagnosis of Renal Calculus.
differ. Some X-ray workers naturally see much better than others
in an almost darkened room, and these people, as one would
expect, see more upon the screen. Others, who are not so
successful in the screen work, will read the skiagram with a degree
of ease that will appear astonishing. Again, one operator will
know the degree of penetration requisite in his tube to suit his
patient, and in consequence the percentage of his failures will be
lessened. Another will know how to make up in exposure what
he is unable to get in the penetrative quality of his tube. It
is, therefore, much more the personal equation than any fixed
standard of excellence in the apparatus that has to be considered.
I have come across some quite busy X-ray workers who admit
that they have never been able to demonstrate the presence
of a calculus upon screen or skiagram. This may at times be due
to inferior apparatus, but as often as not the cause is want of
observation. Speaking of the cases seen in the Guy's Hospital
radiographic department in the past two years, I can give details
which, without being regarded as statistics, will help the reader
to form his own opinion of the usefulness of this method of renal
exploration. It is most probable that with the improvements of
the future the percentage of failures will diminish, and certainly
the past year has shown a distinct improvement on the year
before, only three mistakes having been made against five in the
previous twelve months, although during the latter period many
more cases were examined. It is unlikely that absolute accuracy
will ever be obtained in this as in any other method of diagnosis.
Mention will only be made of the work done in the past two
years, for it is only in this period that the Roentgen light has
been produced in sufficient quantity to be thoroughly useful.
There have been cases in which the rays have shewn calculi to
be present where the clinical signs did not more than suggest the
possibility of this condition. There have been others where the
patients have had no symptoms that would in the least have
suggested calculus, and the examination has been almost acci-
dental. There have been cases, perhaps, more remarkable, where
the symptoms have been so strongly pointing to calculus, that
the exploration with the rays has been considered a waste of time,
Roenigen-ray Diagnosis of Renal Calculus. 95
and yet neither the rays nor the surgeon have been able to bring
to view a particle of calculus. There have been cases in which the
rays have shewn calculus, but the surgeon has not. The following
is a summary of the results obtained.
Cases examined, two hundred.
Cases in which the raye and surgeon found calculi, twenty-
eight.
Cases in which surgeon found calculi but the rays not, eight.
Cases stated not to have calculi by the rays, and operated ou
with negative results, eleven.
Number of cases in which the rays found calculi, but surgeon
did not, two.
Therefore, the number of cases in which the result obtained by
the rays has been proved to be correct amount to thirty-nine.
The instances in which they have been proved wrong are
eight. The one hundred and fifty-three remaining cases are
doubtful as they have not been operated upon, but in most
instances the negative evidence of the rays has peen confirmed by
subsequent history. |
It will-be seen, therefore, that the positive evidence is almost
perfectly reliable, the negative not absolutely, but should be
allowed to have weight when considered with other symptoms.
The errors occurred in stout people and in those who presented
abnormal opacity to the rays, or in cases where the stones were
very small, or where composed of uric acid or urates without
admixture of more opaque salts. Fig. 1 shows the relative
densities to the rays of the three most common salts.
The method of examination has been as follows :—
Position of the patient with relation to the tube, etc.—There
&re several reasons why the horizontal position of the patient is
best for abdominal examination. The tube should be beneath
and the screen above. The couch, the height of an ordinary
table, should have an X-ray transparent top of sailcloth. When
the patient lies upon his back the antero-posterior measurement
of the abdominal region are considerably reduced. If he lies
upon his face there is a still greater diminution of the depth, and
this reduction is in the highest degree important. The abdominal
96 Roentgen-ray Diagnosis of Renal Calculus.
region is so dense to the rays that every effort has to be made
to lessen this density. Having turned the patient upon his face
he should be told to place his arms above his head and lie as
flat as possible. It is as well to allow no pillow for the head,
as this does not add to the comfort and prevents the back from
being straightened. Every attempt should be made to get the
lumbar spine straight, even to the extent of placing a pillow
beneath the abdomen, care being taken to see that there is
nothing in the pillow to interfere with the transit of the rays.
The tube, which in the couch that I have specially designed for
this work can be moved by the operator into any position while
the screen effect is watched, is now brought to within about six
inches of the patient’s abdomen as he lies upon his face. This
measurement is only approximate and will vary with the con-
dition of the tube and the size of the patient. The screen is
placed upon the patient’s back. By this means it is impossible
for the patient to move into contact with the tube and the
chance of accidental shock is eliminated. The current is now
passed through the tube and the effect upon the screen noticed.
It is as well to place the tube at the commencement of the
examination beneath the upper part of the trunk to note how
well the chest, a more transparent region, is shewn upon the
screen. Then as the tube is gradually moved downwards
careful scrutiny can be made of the abdominal contents in the
order of their appearance. The various changes in the effect
as seen while moving the tube from the chest down toward the
pelvis are shown in the illustrations. Figs. 2, 3 and 4..
The organs which are at times visible are :—
Liver. Upper margin well defined, the lower seldom seen
clearly. Fig. 5.
Spleen at times seen, as in Fig. 5.
Stomach. Evident occasionally as a clearly outlined trans-
parent area. It is best seen when distended with gas. (Figs. 22
and 23).
Large intestine. This shews well when distended with gas.
The sacculated form is quite easily made out. (Fig. 23).
The small intestine is hardly ever visible.
Roentgen-ray Diagnosis of Renal Calculus. ` 97
Kidneys. These are at times visible when the surrounding
organs are filled with gas. The lower borders are usually the
only parts that can be made out (Fig. 28). The more flatulent
the patient, the more can be made out of the abdominal contents,
and for purposes of examining a stomach for chronic dilatation
the rays are extremely useful if means are adopted to procure the
gaseous distention of this viscus.
A calculus must be sought with the utmost care, and to do this
the tube must be moved continually. When any suspiciously
opaque mass comes into the field, it should be viewed from all
directions, and the tube stationed in that position in which the
object is the most visible, and a plate laid face downward upon
this part of the patient’s back.
During exposure, which, if the tube used is the right one,
should not exceed a minute, the screen can be laid upon the plate
and the picture watched. This will at once tell the operator
whether he has selected the right place, for it is wonderfully easy
to place the plate incorrectly.
It will be noticed in the examples of renal stone here depicted
(Figs. 6 to 22), that the tube must have been situated differently
for nearly every case , there are several examples where, had the
tube been otherwise placed, no calculus would have been visible.
These alone point to the importance of careful screen work.
There have even been cases where a stone has been clearly seen
upon the screen, and owing to respiration no photographic record
could be obtained. In conclusion, it is well to warn the reader
against the skiagram that is too good. The clearly defined spine,
darkly pictured upon an almost white background is, perhaps, the
least likely of all to show a renal calculus. The renal regions
should be grey, and show the utmost detail.
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Roentgen-ray Diagnos
Ето. 18.—A calculus in the right kidney.
FiG. 17.—A calculus in the left kidney.
Exposure 20 secs.
Exposure 30 secs.
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BACTERIA: IN THROMBI.*
By J. H. BRYANT, M.D.
Assistant PHYSICIAN TO Guy's HOSPİTAL.
During the last few years considerable attention has been drawn
to the influence of micro-organisms in the causation of thrombosis
by the works of Cornil, Widal, Vaquez, Welch, Flexner, Pakes
and others. Many thrombi, which formerly would have been
classed as marantic, must now, in the light of careful bacteriolo-
gical investigations, be looked upon as infective. Vaquez, in his
work on phlebitis, draws attention to the presence of bacteria in
these so called marantic thrombi and in the adjacent parts of the
vessel walls, and looks upon the cause of the thrombosis as a
primary phlebitis. One of the following cases appears to bear
out this view, the chronic ulcers on the legs affording a ready
access for the bacilli, and well accounting for a primary phlebitis
of the adjacent veins. The following is an account of the cases :—
CASE 1.— Wm. W. was admitted on January 1st, 1900, under
the care of Dr. Hale White, for dyspnm@a, cough, and cedema of
the legs. He was found to be suffering from mitral stenosis and
regurgitation, and tricuspid regurgitation. On May 28rd, he
became very cyanosed, gasped for breath, and had some hemop-
_tysis. He picked up a little after this, but died suddenly on
June 1st.
* A paper read before the Pathological Society of London at the Labora-
tory Meeting held at Guy’s Hospital on May 7th, 1901.
100 Bacteria in Thrombs.
The post-mortem examination was made five hours after death.
The body, legs and feet were markedly cedematous, and there was
a large unhealthy looking ulcer on the outer surface of the upper
third of the right thigh. The lungs were tough. On section it
was found that all the branches of the pulmonary arteries were
thickened, dilated and atheromatous. The branches of the pul-
monary artery in the lower lobes of both lungs were filled with
ante-mortem thrombi, which could be traced to the two main
branches, where they united and formed a large thrombus, which
filled the pulmonary artery itself, the end of the thrombus being
just above the pulmonary valves. There were several recent
infarcts in both lower lobes. The heart weighed 542 grammes.
The right ventricle was considerably hypertrophied. The mitral
orifice was much stenosed, its circumference being about twenty
millimetres. The lower third of the abdominal aorta was also
blocked by an old ante-mortem thrombus, which extended to the
iliac arteries, both of which were also thrombosed. The pul-
monary thrombosis had the appearance of having commenced in
the smaller branches, and of having gradually extended upwards
to the main branches.
The outside of one of the main branches of the pulmonary |
artery was carefully sterilized, and cut open with a sterilized
scalpel. Cultures and cover glass preparations were made from
the centre of the thrombus. The microscopical preparations
showed streptococci and staphylococci. The cultures also showed
streptococci and staphylococci. The staphylococcus was identified
by its cultural reactions as the staphylococcus albus.
CASE 2.—Emma G., set. 40, was admitted under the care of Dr.
Newton Pitt, into Mary ward, Guy’s Hospital, on March 22nd,
1900. She was suffering from cedema of the rightleg. The right
internal saphenous vein was thrombosed and felt hard and tender.
She made good progress until April 26th, when diarrhea and
vomiting commenced. She gradually became weaker and died.
on June 6th at 8:30 a.m.
The post-mortem examination was made twenty hours after death.
The right leg was cedematous. The right common iliac vein and
the lower part of the inferior vena cava were filled with an old
Bacteria in Thrombı. 101
thrombus which completely blocked the former. The right
internal saphenous and femoral veins were also thrombosed.
There was well-marked tuberculous peritonitis and peri-
hepatitis. The iliac vein was ligatured in two places and then
removed. The outer surface of the vein was carefully sterilized,
and .cut open with a sterilized scapel. Cultures on various
media and microscopical preparations were made from the centre
of the thrombus. The cover glass preparations showed a few
bacilli and a (?)diplococcus. One organism only was obtained
from the cultivations. It gave the following reactions. The
organism was a bacillus which was fairly motile and varied con-
siderably in length. It stained well with methylene blue, but did
not retain the stain after treatment by Gram’s method.
Cultures.
Broth.—In twenty-four hours the broth became quite turbid
and after six days gave an indol reaction.
Agar.—A thick, moist, profuse, slimy, translucent growth,
spreading all over the surface. It had a curious dull metallic
appearance.
Litmus Milk.— There was a distinct acid reaction at the end of
twenty-four hours. On the third day some coagulation had taken
place. |
Urine.— Was rendered universally turbid in twenty-four hours,
and there was a crystalline deposit. It had a strong alkaline re-
action. A microscopical examination of the Ы. showed them
to be triple phosphates.
Potato.—After forty-eight hours there was a buff-coloured, shiny-
looking growth.
Gelatin.—In the shake culture there was abundant gas- forma-
tion and liquefaction.
Blood-serum.—A moist grey growth which was followed by
liquefaction of the medium.
The organisms grew anerobically. It was identified as the
proteus vulgaris. | |
CASE 3.—Joseph L., et. 54, was admitted into Stephen ward,
Guy's Hospital, under my care on September 22nd, 1900, for
dyspnoea and swelling of the abdomen and legs. At the age of
102 Bacteria in Thrombi.
twenty-four he was severely kicked on the left | leg, and an ulcer
resulted which had persisted and was present when he was
admitted. He had first noticed the dyspnoea on exertion at the
beginning of August and about this time his abdomen began to
enlarge. Two days after the abdominal enlargement was noticed
his left leg began to increase in size, this date probably indicating
the time at which the veins became thrombosed.
On admission, he was found to be suffering from ascites. Both
legs were swollen and cedematous the left much more so than
the right. Both saphenous veins could be felt to be thrombosed.
A large chronic ulcer was present on the inner side of the lower
part of each leg and there was a good deal of pigmentary change
in the adjacent skin. He gradually wasted and became worse.
On November 13th, paracentesis abdominis was performed and
some blood-stained fluid was withdrawn. He suddenly became
worse and died on the following day at 11 a.m.
The post-mortem examination was made four hours after death.
Diffuse carcinoma of the stomach with secondary growths in
the pleura, pericardium, and peritoneum were found. Both
saphenous, femoral and iliac veins were thrombosed.
Microscopical preparations and cultures on broth and agar were
made from the left saphenous vein. The skin was sterilized for
some distance over the inner side of the thigh and was then
incised with a sterilized scalpel. The vein was exposed by a
dissection with sterilized instruments. The surface of the vein
was carefully sterilized and incised with a sterilized knife. The
microscopical preparations and cultures were made from the
centre of the thrombus. A portion of the right saphenous vein
was ligatured and removed intact. The outside of the vein was
then carefully sterilised and cut open and similar preparations
were made.
The microscopical preparations from the left saphenous vein
showed a few rather long bacilli which retained the stain well
after treatment by Gram’s method.
The cultivations from this vein showed only one organism.
The bacillus was large and was distinctly motile. It stained
Bacteria in Thromb. 103
well with carbol methylene blue and retained the stain after
being treated by Gram’s method.
The Cultures.
Broth.—Was rendered turbid in twenty-four hours and the
surface was covered with a distinct scum.
Agar.—A rapid, dry, yellowish, spreading growth with a
markedly wrinkled surface. |
Litmus milk.—Very little change in forty-eight hours. At the
end of four or five days there was still a blue colour and no
definite clotting was noticed.
Gelatin.—The stab culture showed at the end of forty-eight
hours considerable liquefaction at the surface, with a pale
yellowish growth in the depth. On the fourth day the top of
the liquefied gelatine was covered with a white scum.
The slant culture showed extensive growth and liquefaction at
the end of forty-eight hours.
Potato.—A profuse raised brownish growth with a wrinkled
surface.
The organisms also grew well under ansrobic conditions. The
organism was identified as the bacillus subtilis. The micros-
copical preparations from the right saphenous vein showed
cocci. No bacillus was found.
` Cultivations showed only one organism. The organism was a
coccus which stained well with methylene blue and retained the
stain after treatment by Gram’s method. It gave the cultured
reactions of the staphylococcus albus.
It will be seen from the above that the bacillus proteus vulgaris
in pure culture was obtained from Case 2, the bacillis subtilis ‘in
pure culture from the thrombosed left saphenous vein, and the
staphylococcus albus from the thrombosed right saphenous vein
in Case 3, and staphylococci and streptococci from Case 1.
These results confirm the observations of other workers in this
field, that bacteria are found not only in thrombi of infective
diseases, but also in those which occur in cachectic and ansmic
conditions and in cardiac affections. In the thrombi which occur
as complications of diseases which are due to a recognised micro-
organism, it by no means follows that the specific micro-organism
104 Bacteria in Thrombi.
of that disease will be found, for, frequently the presence of some
other organism, and especially the streptococcus pyogenes and
the bacillus coli communis may be demonstrated, indicating the
probability of a secondary infection.
A point of very great interest is the occurrence of not only these
well-known pathogenic bacteria, but also of organisms which are
usually looked upon as non-pathogenic. The question naturally
arises as to the relation these non-pathogenic micro-organisms
have to the thrombosis. Mr. Pakes has recently reported to the
Pathological Society a case of venous thrombus, in which the
bacillus proteus vulgaris was found in pure culture. He was of
opinion that there was an important causal relationship between
the bacillus and the thrombosis.
The possibility of accidental contamination may be raised as
an explanation of the presence of the bacillus subtilis, and possibly
of the proteus vulgaris in the thrombi. The most stringent pre-
cautions were, however, taken to prevent the possibility of an
accidental external contamination; and, further, the bacillus subtilis
has been found in the organs of the body after death by other
observers in cases where a post-mortem invasion was unlikely.
Taking into consideration the precautions which were taken to
prevent the possibility of external contamination when the
cultures were made, and the periods after death when the post-
mortem examinations were made, viz., five hours after death in
the first case and four hours after death in the third case, the
possibility of an external contamination or a post-mortem
invasion is improbable.
The mere presence of an organism in a thrombus does not
necessarily imply that it was the cause of the thrombosis. Slow-
ing of the circulation, an altered condition of the blood, such as
is associated with ansemic and wasting conditions, and the presence
of toxines, may all predispose to thrombosis; the bactericidal
power of the blood is probably much reduced under such con-
ditions, so that non-pathogenic organisms may flourish and become
relatively pathogenic. On the other hand, micro-organisms which
are found in thrombi may be found in the blood in cases
in which there are no thrombi in any part of the body; for
Bacteria in Thrombi. 105
example, I have obtained pure cultures of streptococci from the
blood in cases of infective endocarditis, puerperal septicemia,
pyemia, and diabetic coma; pneumococci from a case of general
pneumococcal infection, and the bacillus coli communis from a
case of typhoid fever, eto. | |
In the case of the pulmonary thrombus, which contained
staphylococci and streptococci, there must have been several
factors leading to the thrombosis, viz., slowing of the blood-
Stream, which was the primary state, an alteration of the con-
dition of the intima of the blood-vessels, and the presence of the
micro-organisms. That there was an ante-mortem invasion by
these miero-organisms I have no doubt, but whether it was the
actual determining cause of the thrombosis or whether the
thrombus was secondarily infected, I must leave an open question.
These organisms probably gained access to the blood through
the lungs. |
With regard to the case in which the bacillus subtilis was
found, there was & chronic ulcer, which was probably an important
factor in the causation of the thrombosis, by setting up a local
phlebitis, and was, further, the probable channel by means of
which the bacillus subtilis gained access to the veins.
The proteus vulgaris is found in the lungs and feces, and cases
of cystitis are described in which the organism has been isolated.
The channel of infection in the case just recorded may have been
the lungs or intestine, for there was no local external lesion, as
in the case of the bacillus subtilis infection.
I bring forward these cases to show the importance of making
bacteriological examinations, and leave the question of their exact
relationship to the thrombosis an open one.
At the time this paper was in the hands of the printer, I had
the opportunity of investigating another case of ante-mortem
thrombosis. The thrombus was situated in the apex of the
left ventricle, and as a result of embolism there were infarcts in
the kidneys. I obtained the proteus vulgaris bacillus in pure
culture from the thrombus and also from one of the infarcts in
the kidneys. I consider this case the most important of the four,
106 Bacteria in Thrombs.
as indicating an ante-mortem invasion of the organism. The
post-mortem was performed thirteen hours and a half after death
in cold weather, which makes a post-mortem invasion unlikely.
The precautions taken in obtaining the cultures precluded the
possibility of external contamination. The fact that the same
organism was found both in the thrombus and in the infarcts is
strongly suggestive of a causal relation between the organism
and the morbid conditions found.
CASE 4.—Thomas P., set. 68, was admitted into Philip ward,
Guy’s Hospital, under the care of Dr. Hale White, on Avgust
18th, 1901, for difficulty in talking and swallowing. He had
various indications of organic disease of his nervous system,
which were thought to be of the nature of bulbar paralysis.
On October 10th the second toe of the right foot was found to
be showing signs of gangrene. On October 13th the third
toe of the same foot was similarly affected. He died on
November 11th.
The post-mortem examination was made thirteen and a half
hours after death. The body was badly nourished. The brain
weighed 1380 grammes. The terminal ends of both internal carotids
were atheromatous, calcareous, and dilated. There was softening
in both cerebral hemispheres. The branch of the left coronary
artery in the anterior interventricular groove was atheromatous,
calcareous, and thickened, and the lumen was practically obliter-
ated. The apex of the left ventricle was dilated and contained a
large, organised, ante-mortem thrombus which was softening in
the centre, for on cutting into it a quantity of thick, sanguineo-
purulent looking fluid oozed away. The lower portion of the clot
was firmly adherent to the endocardium, and had a markedly
laminated appearance.
The endocardium covering the portion of the ventricle which
was dilated was very much thickened and was quite opaque. The
corresponding part of the myocardium was very much thinned
and had undergone marked fibrosis. At its thinnest part it was
no thicker than the wall of a normal right auricle. There was no
valvular disease.
Bacteria m Thromb. 107
There were several large hemorrhagic erosions in the stomach.
The large intestine was congested.
There was superficial scarring of the under surface of the right
lobe of the liver.
The right kidney contained two small recent infarcts. The
testes were not fibroid. |
Cover glass preparations from the thrombus and one of the
infarcts shewed a few short thick bacilli.
Cultures were made on agar from the thrombus and one of the
infarcts. A moist, translucent, spreading growth over the
surface of the agar resulted.
Gelatin plates were made, and in both cases, after twenty-four
hours, at 20? C., complete liquefaction from plates 1 and 2 resulted
and on plate 3,-small pale, yellowish white, liquefying colonies
were seen. Several tubes containing different media were inocu-
lated from these liquefying colonies.
Cultures.
Agar.—After twenty-four hours, at a temperature of 37? C., a
spreading pale, yellowish white translucent growth, which covered
the surface of the gelatin, resulted.
Litmus Milk.—Was rendered slightly acid after incubation for
twenty-four hours at 37? C. There was no clotting.
Urine.— Was rendered alkaline at the end of twenty-four hours
at 37°, it became turbid, and there was a deposit containing
crystals, which proved to be triple phosphates on microscopical
examination.
Blood serum.—On this medium there was a free growth, and
marked liquefaction at the end of twenty-four hours at 37° C.
Nitrate broth.—There was a good growth, and the broth became
turbid. A good nitrite reaction was obtained with phenyl
diamine.
Gelatin.—There was abundant gas-formation and liquefaction
in shake cultures.
Microscopical examination of the cultures shewed a bacillus,
which varied in size, and was motile. It stained well with
methylene blue, but did not retain the stain when treated by
Gram’s method. It was identified as the proteus vulgaris.
VOL. LVI. 11
A CASE OF SUPPURATIVE
PYLEPHLEBITIS.
By FREDERICK TAYLOR, M.D.
SENIOR PHYSICIAN To Guy's HOSPITAL.
SUPPURATIVE PYLEPHLEBITIS is so rare that any instance of its
occurrence is worthy of record, and I take the opportunity of
describing the following case all the more willingly, because in a
recent volume of these Reports! a valuable analysis is given
by Dr. J. H. Bryant of twenty cases occurring at Guy's
Hospital, scattered over a long period of years. The report is
from the notes of Mr. F. G. Gibson.
E. W., et. 28, was admitted under my care into Clinical ward
on February 17th, 1901.
She had measles, whooping cough, and scarlet fever as a child.
She has been strong since, and has suffered only some slight |
abdominal pains, and has taken laxatives and used a “hydrant ”
for constipation.
Since Christmas she has been unwell and has suffered from
boils on the neck and under the chin. On the 12th inst. she had
a bad headache, and pain in the abdomen , she vomited and felt
“ chilly.” She attempted to work but had to go to bed, and had
then ‘‘cramps in the stomach." On the 13th the temperature
1 Guy’s Hospital Reports, vol. liv., p. 77.
110 A Case of Suppurative Pylephlebitis.
rose to 105°, and she had more shivering, involving the whole
body, and this occurred four times. The fever and headache con-
tinued until her admission.
On admission.—A well-developed and well-nourished woman,
milliner by occupation and unmarried. She is excited rather than
drowsy and has some pain in the abdomen, which she does not
localise.
The tongue is furred. The abdomen is full, moves well on
respiration, and presents a few doubtful rose spots on the left
side. The margin of the liver can be just felt below the costal
margin ; it is not tender even to deep pressure. The spleen can
be felt projecting, on deep inspiration, an inch and a half into the
abdomen, and the splenic dulness is correspondingly increased.
In the left flank, close to the spine, the kidney can be felt on
bimanual examination. In the right iliac fossa there is marked
gurgling on pressure. No peritoneal rub can be heard over liver
or spleen.
The motions are of the colour and consistency of pea soup, and
are not offensive in odour.
The chest appears normal on auscultation and percussion, with
the exception of a few sibilant rhonchi in front at the upper part.
There is also slight cough, but no expectoration.
The heart is normal; pulse 124, regular and full. A blood-
count gives red corpuscles 4,670,000, leucocytes 10,500, heemo-
globin 56 per cent. The reflexes and special senses are normal.
The urine is of specific gravity 1020, acid in reaction, depositing
urates abundantly, and containing a trace of albumin, but no
blood, pus, or sugar.
The menses are generally regular, but on this occasion com-
menced ten days before the expected time.
Progress of case.—She had very much the appearance of a
patient with typhoid fever, and on February 21st the serum gave
Widal’s reaction, but on the 22nd she had two rigors, followed
by profuse sweating. On the 24th three rigors; no signs in the
chest; the spleen scarcely palpable; bowels opened at mid-day ;
patient not drowsy; feels comfortable except during the rigors. On
the 25th three rigors, followed by vomiting ; a small amount of
A Case of Suppuratwe Pylephlebitis. 111
blood was passed with the stools. On the 26th, epigastric pains ;
no signs in chest; no evidence of a source of pyeemia in bones
or limbs; the heart-sounds clear. Pulse 100 to 120, regular.
February 28th. Has occasional rigors, during which the
pulse becomes weaker, and the face dusky and pinched, the left
side more than the right.
March 7th. During the week there have been rigors as
follows: one on March 1st, three on the 2nd, one on the 5th, and
two to-day The motions have been frequent, on some days as
many as five, very fluid, olive green in colour, not offensive, and
containing no sloughs, but on the 5th a little blood. No cardiac
bruits, no adventitious sounds in chest. Spleen felt on deep
inspiration.
March 12th. Patient much thinner. Diarrhoea has been
profuse, and on the 9th there was rather severe hemorrhage.
A Widal reaction on the 8th was negative. To-day there is
pain in the legs and thighs, the calves and pads of the toes
on the right foot are tender; knee-jerks depressed. At 1 a.m.
she retched violently, and fell back in a faint, became dusky and
almost pulseless. The condition of collapse continued in spite of
stimulants and transfusion of saline solution, and she died at
6a.m. .
The treatment consisted of milk diet; salol internally; on the
24th, quinine in two-grain doses. After this, opium enemas
were used to check the diarrhoea, and brandy was administered
freely towards the end. The temperature, taken every four
hours, ranged irregularly between 98? and 104°, rising and falling
often more than once daily, without any reference to morning or
evening hours. It often reached 105? in the rigors, of which
there were sixteen recorded, and once 106°. The pulse was
always 100 or more, and at some part of every day was 120
or 130. The respirations were commonly from 24 to 32.
Post-mortem.—The inspection was made by Dr. Fawcett on
March 12th. On opening the abdomen, the omentum was found
to be adherent to the underlying coils of small intestine, and
these coils were united together by recent deposit of lymph. On
separating these coils a small abscess cavity was opened in the
112 A Case of Suppurative Pylephlebitis.
right iliac region internal to the lower half of the ascending
colon. The cavity was shut off by adhesions from the general
peritoneal cavity, and its walls were formed on the inner side
and in front by coils of small intestine, and above by the hepatic
flexure of the colon, which had been pulled down over it.
Opening into the cavity was a hole which led into a thickened
and ulcerated appendix cseci. The appendix came off from the
inner side, and was running upwards along the inner aspect of
the ascending colon, and then inwards.
At the root of the appendix a gangrenous process had super-
vened, and the sloughing base of it was found to open into a
ragged cavity measuring 7 cm. by 4 cm. situated behind the
ascending colon. The walls of this cavity were of a dirty
black-grey colour, and at the upper extremity there were several
small round openings into the ascending colon, at a distance of
6 cm. above the iléo-cæcal valve. The edges of these openings
were acutely inflamed.
At a position corresponding to the origin of the appendix was
the mucous membrane, of deep red colour, with grey membranous
patches upon it. The attached portion of the mesentery was
much thickened, and its veins were full of a blackish-grey,
purulent fluid. The other main branches of the portal system
were also affected in the same manner, the splenic vein and main
trunk of the portal vein being lined by a yellow membrane very
similar to that known as the pyogenic membrane of an ordinary
abscess. Apart from the above changes, the intestines, small
and large, were healthy.
The liver weighed 1432 grammes; it was dark red in colour
for the most part, with a few scattered, yellow areas varying in
size, which on section yielded pus. On section of the organ,
numerous abscesses varying in size from that of a pin’s head to
that of a pea or threepenny-piece, were seen scattered throughout.
(see plate.) The portal vein branches were full of blackish-grey,
purulent material. The hepatic veins and biliary ducts were
normal,
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A Case of Suppurative Pylephlebitis. 113
The spleen weighed 150 grammes, and contained an infarct.
The other organs were normal: the heart weighed 231 grammes
and the kidneys 250 grammes.
Bacteriological report.—Pus from abscesses in the liver, and
blood from the heart, taken eight hours after death. The blood
from the auricle contained a pure culture of bacillus coli com-
munis. The pus from the abscess in the liver also gave a pure
culture of bacillus coli communis.
The above is a good example of suppurative pylephlebitis, and
so far as the pathological and setiological conditions are concerned
it resembles many of the cases already recorded. Suppurative
pylephlebitis is, as the name implies, an inflammation of the portal
vein resulting in the formation of pus. It is due, practically in
every case, either to a lesion of some structure within the tribu-
tary area of the portal vein, or exceptionally to a lesion of the
liver itself, involving the hepatic distribution of the vein and not
of the trunk and tributaries. As a result of such lesions, in the
former case, septic organisms are conveyed into the portal vein,
thrombosis and septic invasion of the clot take place, and from
this again septic particles are conveyed in the portal vein distri-
buted throughout the liver so that numbers of minute abscesses
in this organ are the result. In the latter case the disease begins
in the hepatic branches of the portal vein, and if these are
moderately large the same dissemination of septic particles
through the smaller veins can take place as in cases where the
causative lesion is on the tributary side of the vein.
Every part of the portal area may be the seat of the lesion
which is the primary cause of suppurative pylephlebitis. In the
twenty cases collected by Dr. Bryant from the Guy’s Hospital
records, the causes were ulcers of the stomach, duodenum, colon,
or rectum, appendicitis, gall-stones, and suppurating gall-bladder,
pyosalpinx, and suppurating ovary, and abortion. From other
writers he notes in addition, sloughing of the cecum, suppuration
in the spleen or mesenteric glands or about the hemorrhoidal
114 A Case of Suppurative Pylephlebitis.
veins, inflammation of the umbilical vein in infants, and ‘the
implication of the mesenteric vein by a fish-bone.
Chvostek, in a very complete article,? published some years ago,
besides most of the above, mentions also suppurative pancreatitis,
abscess between the layers of the mesentery, localised peritonitis
from a fall, and hepatic abscess or hydatid cyst, involving the
hepatic branches of the porta] vein.
It is thus seen that no part of the abdomen, which drains its
blood into the portal area, is exempt from the liability to cause
suppurative pylephlebitis. The most frequent lesion is probably
appendicitis. Of the twenty cases recorded from Guy’s, it was
the cause in eight, and the present case adds another. Chvostek
also mentions appendicitis as the most frequent cause.
Dr. Bryant calls attention to one notable exemption, that is, the
absence among the Guy’s cases of any in which typhoid ulceration
was the cause. From this alone, seeing that the number of cases
is so small, perhaps not much can be said; but no doubt, as he
remarks, typhoid ulceration is the most common form in this
country. Chvostek also, does not appear to have found typhoid
as a cause. The explanation of this common exemption may be
found in the bacteriology of the disease. Streptococci, staphylo-
cocci, and the bacillus coli communis have been most often found,
the latter was present in my case. The typhoid bacillus may have
less facility for transmission in this particular way ; and yet it has
been found in the pus of abscesses resulting from periostitis after
typhoid fever, and more to the point, in the gall-bladder in typhoid
cholecystitis, I should still think it likely that cases will be, or
may have been already reported; but even then the occurrence
must be very rare, as compared with the position which appendi-
citis holds.
I now come to the question of symptoms and to their recogni-
tion clinically in different cases, t.e., to the diagnosis. Briefly
stated, the condition is one of pyeemia, with more or less
evidence of abdominal disease, which may be of two kinds, one the
2 Klinisehe Vortrige über die Krankheiten der Pfortader und der Lebervenen.
Wiener Klinik, 1882, pp. 67-106,
A Case of Suppurative Pylephlebitis. 115
original suppurative or ulcerating lesion, the other, the changes
in the liver which result therefrom.
In a typical case, therefore, one might expect to get, first, the
signs of the original local disease, whether it be appendicitis,
gastric ulcer, or pelvic inflammation, with such local pain, tender-
ness, and resistance to pressure as they may cause.
Secondly, the development of a definitely pyeemic condition as
shown by rigors, great oscillations of temperature, undue prostra-
tion, drowsiness, sallow tint of complexion, etc., and thirdly, the
evidences of hepatic disease, namely :— |
(a) Pain, tenderness, enlargement of the liver.
(8) Jaundice from pressure on the bile-ducts.
(y) Enlargement of the spleen, diarrhoea, and sometimes hemor- ~
rhage from pressure on the portal vein.
(ò) Possible extension of inflammation through the diaphragm
resulting in a right-sided pleurisy.
(e) Possibly peritonitis.
Towards the end the typhoid or pysemic condition becomes the
prominent feature; the patient is emaciated, sallow, drowsy, or
semi-comatose, occasionally delirious, with rapid, feeble pulse.
The diagnosis is admittedly difficult, and in a great number of
cases is not made during life. By a careful consideration of the
symptoms, and of their relative frequency, we shall see how this
is so. |
Chvostek mentions the following diseases as likely to be con-
founded with suppurative pylephlebitis: pysemia, septicemia,
typhoid fever, malaria, adhesive pylephlebitis, catarrhal and other
forms of jaundice, chronic catarrh of the bile-ducts, biliary
calculus and cirrhosis of the liver. Dr. Bryant points out that
his colleagues and predecessors at Guy’s have succeeded in adding
to that list catarrhal pneumonia, general septic pneumonia,
empyema, subdiaphragmatic abscess, spinal caries, and rupture
of a reduced hernia.
The frequency with which among the Guy’s Hospital cases a
pulmonary or thoracic lesion was regarded as the primary disease,
emphasises the fact that the hepatic inflammation tends to spread
to the chest, a fact to which Chvostek makes but little reference.
116 A Case of Suppuratiwe Pylephlebitis.
At the same time it suggests one great difficulty in the diagnosis
of this disease, namely, the frequent latency or slight clinical
importance of the primary abdominal lesion. It will be con-
venient to take seriatim the several features of the disease which
Chvostek regards as guides for diagnosis and compare them
with the facts of my case and of others.
1. Demonstration of a possible cause.—It is a familiar fact that
such abdominal lesions as are enumerated above, are either entirely
latent, or so little distinctive in their symptoms, as to make
their recognition a matter of great uncertainty. Appendicitis,
which is a very common cause of suppurative pylephlebitis, may in
its gangrenous form be entirely latent until an acute and probably
fatal peritonitis is set up. In the present case the illness com-
= menced, according to the patient, with abdominal pain, vomiting
and shivering five days before admission; on the following day
she had four rigors, and on admission the spleen was already
enlarged. The only sign here, which could be referred to appen-
dicitis, was some gurgling in the right iliac fossa; and this was
obviously more suggestive of typhoid fever than of appendicitis.
Not that I have much confidence in the value of this sign as a
diagnostic feature in typhoid fever, and there is no doubt that a
large proportion of typhoid cases do not show it. But, on the
other hand, it is not a characteristic feature of appendicitis, in
which a more or less firm resistance, with tenderness and loca-
lised dulness are the more common signs. What the conditions
of the right iliac fossa may have been prior to admission I have
no means of knowing, but it seems to me probable that the
recognised commencement of the illness was determined by the
pysemie infection, and not by the gangrenous change in the
appendix. This is, at any rate, in accordance with the experience
of the cases already referred to, in which the symptoms fatal in
two or three days are referable entirely to a general acute peri-
tonitis, and little, if at all, to the gangrene of the appendix,
which must have preceded it.
2. Excluston of causes of pyemia and septicemia in the systemic
circulation and of ulcerative endocarditis ; and
8. The existence of septic fever,
A Case of Suppurative Pylephlebitis. 117
These may be taken together, but in reversed order.
There is, of course, the old difficulty of the specific distinctions
of the various forms of pyrexia. The septic, or septiceemic, or
pyeemic character of the fever must be shown before a diagnosis
of such a rare complaint as this can be made. Every one of the
primary lesions, which may be the cause of it, is commonly accom-
panied by some degree of pyrexia. If such a lesion is recognised
by local evidence, pyrexia in some form is to be expected, and
there is no need to be alarmed as to the existence of pylephlebitis.
If a local lesion is not recognised, then for some days possibly
one will be led to discuss the toxic conditions or infectious fevers,
which may exist with a minimum or an entire absence of local
signs, such as typhoid fever, tuberculosis, or influenza. Typhoid
fever is extremely likely to be suggested from its frequency, from
the great variety in the mode of its occurrence, and from the large
proportion of cases in which local evidence of the disease in Peyer’s
patches is early wanting ; and in many cases a diagnosis of this
kind has been for a time made and entertained. In the present case
there were four points in favour of typhoid fever on her admis-
sion on the sixth day of the illness, namely, headache, some
spots on the abdomen admittedly not very convincing, enlarge-
ment of the spleen, and the gurgling in the right iliac fossa before
referred to. In addition to this we had diarrhoea and frequent
motions after the fourteenth day, a successful Widal reaction on
the tenth day, and hemorrhage from the bowels on the fourteenth,
twenty-second and twenty-sixth days of the illness, the last
severe. But the chief feature against typhoid fever was the early
appearance and the frequent occurrence of rigors , and these com-
bined with the sallow, earthy, and septic appearance of the patient
in the latter part of her illness, determined the exclusion of the
diagnosis of typhoid fever, and the recognition of the fact that she
was suffering from one or another form of pysmia.
Not, however, that rigors of themselves are unknown in typhoid
fever; they are very uncommon, but it is well known that they
occur. Two years ago I devoted some part of a clinical lecture
to rigors in typhoid fever, based on a case under my care,” and
9 Guy's Hospital Gazette, June 23rd, 1900,
118 A Case of Suppuratwe Pylephlebitis.
I was able to refer to other cases that I had seen. Professor
Osler also has written on this subject in one of his reports from
“Johns Hopkins Hospital," and in his series of two hundred and
“twenty-nine cases of typhoid fever, there were thirteen in which
rigors occurred. Constipation and acute local inflammation,
like pneumonia, are sometimes the cause, but occasionally they
occur for no obvious reason, and cease, without prejudicing the
patient in any way.
Another feature in the case opposed to typhoid fever
was the course of the temperature (see fig. 1), when we had
sufficient of it to know the general course it was taking I need
not discuss the well-known features of a, typical typhoid chart,
nor the frequency with which the course of temperature in
typhoid is not typical.
We come, then, to recognise that this patient was pysemic, and
to inquire for the source of the pyemia. Chvostek rightly sees
that a, process of exclusion may bring us to the diagnosis. If
the systemic circulation on the venous side (ordinary pysemia),
and the heart or cardiac valves (malignant endocarditis), can be
excluded, then a portal pysemia alone is left. Unfortunately,
experience tells us that it is very difficult to exclude malignant
endocarditis and it is well known that this form of pysmia
(arterial pysemia) may exist without any indication, by murmur
or by irregular action, or by altered position or impulse, that the
heart is the seat of such a serious and fatal lesion. Instances
could be easily multiplied of this occurrence, and the following
case, which occurred a few years ago under my care, is an
exceedingly good example. It is all the more interesting here,
because the medical man who sent her into the hospital believed
she had appendicitis; and had that view been maintained for
any length of time after her admission, we ought, proceeding on
the lines of Chvostek’s formule, to have further diagnosed the
occurrence of suppurative pylephlebitis.
The patient was a woman aged 50. She had been for years
subject to pains in the limbs; four and a half years previously
pain over the region of the liver for a fortnight; constipated for
4 The Johns Hopkins Hospital Reports, vol. v., p. 445.
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A Case of Suppurative Pylephlebitis. 119
the last twelve months; never jaundiced. For three or four
weeks she has had a cold and has felt unwell. On December
10th she woke up with a pain in the abdomen and headache.
She vomited three times a slimy fluid with no blood. She
seems to have improved somewhat, but the pain was continuous,
dull, sharper at intervals, and running through to the back. On
the night of December 15th she had a rigor, and on the following
morning she vomited green fluid.
The doctor who first saw her on the 10th, wrote: “ Her
symptoms were subacute, and the fever subsided quickly ; the
temperature was normal on the 13th and 14th, but lighted up
again suddenly on the night of the 15th; she looks very ill."
He regarded it as a case of acute appendicitis and sent her to
the hospital on December 16th.
She appeared well nourished, and her cheeks were of good
colour. She lay in bed, apparently in no great pain, but with
some shortness of breath. The pulse was 108, the respirations
32, and the temperature 99°.
The abdomen was not distended, and it moved with respiration.
There was no visible peristalsis, and there were no spots. On
deep palpation, resistance was met with at the junction of the
. epigastric and right hypochondriac regions, as well as in the
neighbourhood of the right kidney, and between the umbilicus
and the right iliac spine, about one inch from the latter. There
was also a little tenderness near the right eighth rib and the
right iliac spine. Nothing could be definitely felt. The liver
was not enlarged, nor was the spleen.
The impulse of the heart was normal, the heart-sounds were
faint, but no adventitious sounds were heard. The lungs
appeared to be healthy. The urine was light yellow in colour,
deposited urates on cooling, had a specific gravity of 1028, and
was free from sugar and albumin.
In the evening the temperature rose to 102°. On December
17th she had a rigor, the temperature rising to 101:6*. On the
19th she had two rigors, the temperature in the first reaching
104:27, in the second 102°8°. In the intervals it never fell below
99, On the 18th she had much pain in the right side, but was
120 A Case of Suppuratwe Pylephlebitis.
free from it on the 19th. She had rigors again on the 21st and
22nd.
The sclerotics were thought to be slightly yellow on the 21st,
but they were not so on the 28rd. On this last day the right
iliac fossa was quite supple, and the fingers could be pressed —
deeply into it, without discomfort. The temperature on this day
was between 100°4° and 102:6?, and on the 24th occurred another
rigor. |
The temperature reached 103% on the 25th, and gradually fell
during the next six days to 100-1019, after which it rose a little,
keeping an irregular course between 99° and 102°, with no very
extensive oscillations.
On December 28th there was a trace of albumin in the urine ;
the patient was flushed, but not jaundiced, and nothing could be
felt in the abdomen. An examination of the pelvic organs on the
24th revealed nothing abnormal. The bowels had been moved,
on an average, once a day, and there was nothing remarkable in
the motions.
On January 2nd, sibilant rhonchi were heard in the chest,
back and front; sonorous rhonchi towards the axille; and
‘mucous ráles in the second and third intercostal spaces.
On January 4th, she was slightly jaundiced, and she vomited
undigested food and bile. Rhonchi as before, crackling rales at
the bases behind, and some impairment of resonance over the
middle of the right lower lobe. She complained of no pain in the
abdomen, but in the shoulders and hips; also of prostration and
shortness of breath. The liver was felt two inches below the
right costal margin, and the spleen extended below the left ribs,
moving freely with respiration. On the following day the crack-
ling ráles extended to the axilla, and an area of broncophony
was found over the right scapula. The next few days there was
increasing distress, a sense of dyspnoea, twitching of the ale
nasi, dusky flush in the face, tremors of the hands, frequent
retching and occasional vomiting. The signs in the chest per-
sisted; nothing wrong was discovered over the heart. The
albumin found in the urine again disappeared, and the jaundice
subsided.
A Case of Suppurative Pylephlebitis. 121
On January 10th and 11th, the temperature was mainly below
101°; it ranged between 97° and 99:8? on the 12th. She was
now rapidly sinking, and she died on the 13th, the temperature
being 97-82. The pulse throughout had varied from 110 to 120,
the respirations from 26 to 36.
Post-mortem.—Septic endocarditis of the mitral valve was
found, with pneumonic foci, and a hemorrhage in the right lung, —
a large soft spleen, kidneys scarred by infarcts, and a small renal
calculus on the right side.
4. The evidence of suppurative hepatitis, e.g., local pain, swelling,
and especially the elevations due to abscesses. In my oase the
insignificance of any local signs of disease of the liver was very
interesting. Hepatic pain was certainly not a striking feature in
her case. On admission she had abdominal pain, which she could
not localise; later on she was entirely comfortable but for the
rigors. On another occasion there was epigastric pain, which
may, of course, have been due to the liver. Hepatic swelling
scarcely existed, certainly not to an extent which would compel
One to consider a suppurative hepatitis the most probable condi-
tion. On admission the “lower margin of the liver was just
felt below the costal margin; it was not tender on deep palpa-
tion.” The abdomen was, of course, frequently palpated after-
wards, and no serious enlargement was observed. Moreover,
after death the liver weighed only 1,432 grammes, that is, 50:5
ounces, surely not a great size for the liver of & medium-sized
female. Still the fact remains that the liver is often enlarged
somewhat in these cases, and a frequent observation in the cases
collected by Dr. Bryant is that the liver can be felt just beneath
the costal margin; but when the enlargement is so little the
value of the change must depend upon the association with other
symptoms, such as pain, tenderness and jaundice.
The prominences on the surface of the liver, to which Chvostek
refers, appears to be relatively infrequent.
It is important to note further that jaundice, which would
necessarily attract attention to the liver, is by no means neces-
sarily present. This is well recognised, but the proportion of
cases in which it is present is given differently by observers,
122 A Case of Suppurative Pylephlebitas.
working in all instances on small collections of cases. Chvostek
says it is common, and quotes Frerichs as finding in it 75 per
cent. of recorded cases, whilst Chvostek’s own cases gave six
out of seven, or 85 per cent. The Guy’s cases showed it in
only 40 per cent., and in 55 per cent. it was expressly stated to
be absent. The present case had no jaundice, and it is clear
that one must try to make a diagnosis without this factor.
5. Evidences of stagnation of blood in the portal vein district. —Of
the five signs under this head mentioned by Chvostek, three are
admitted by him to be rare, namely, hematemesis ; ascites (rarer)
and distension of the abdominal veins (rarest of all). The remain-
ing two signs are enlargement of the spleen and diarrhea. They
were both present in this case, and they are clearly not infrequent.
But unfortunately they are not distinctive, and they are even
misleading, since they are two out of the most trusted witnesses
to typhoid fever, a disease with which suppurative phlebitis is
very likely on other grounds to be confounded.
I know of no means by which the enlarged spleen of one of
these diseases can be distinguished from that of the other, unless
it be by the bacteriological examination of blood drawn from the
spleen for Eberth’s bacillus, a process which Dreschfeld* says
cannot be countenanced for this purpose. |
With regard to the stools, it is certain that in spite of the
full descriptions of what we are all inclined to regard as the
distinctive features of typhoid stools, their ochrey yellow colour,
pea-soupy appearance, the presence of sloughs, the alkaline
reaction, ‘‘ offensive ” odour, or rather peculiar odour to those who
cau distinguish it (for no stools can be called fragrant), it is
doubtful if any physician would stake his reputation on an absolute
diagnosis by the stools alone in every case. It isquite certain that
the physical characters of typhoid stools are very closely imitated
by those in other diseases, of which I may mention tubercular
disease of the bowels and ulcerative colitis ; but it is also certain
that the stools in typhoid fever, even when diarrhoea is present, are
not always ochrey, or yellow in colour, but may be green or
blackish-green. Here again bacteriology is suggested. Dresch-
5 Allbutt”s System of Medicine, vol. 1., p, 835.
A Case of Suppurative Pylephlebitis. — 123
feld* says with regard to the detection of typhoid bacilli in the
stools that their “isolation and distinction from the bacterium
coli take much time, and are processes too elaborate to be clinically
useful ; moreover, the bacilli have not been found in the stool
before the eighth or ninth day of the fever.”
As four years have elapsed since this opinion was published, I
have asked our bacteriologist, Mr. W. C. C. Pakes,’ to let me know
the present state of the question. He writes thus :—“ Although I
have succeeded in isolating the bacillus a few times, I have failed
many times, and I have certainly come to the conclusion that the
labour is so excessive in comparison with the paucity of results
that it is only in the really important cases that it is worth while
trying.” And he says: “It is all but impossible to isolate the
B. typhosus from fæces in which this organism is in great
numerical inferiority.” He agrees that they are unlikely to be
found before the eighth or ninth day, as they are probably only
yielded by the ulcerated surface.
He goes on to say: “ The cases, in which I think that the in-
vestigation would be useful, are those that are thought to be
enteric; but which remain doubtful clinically, or fail to give
Widal’s reaction. The isolation of the B. typhosus from the
stools would, in my opinion, clear up the diagnosis, the failure
to find them would, of course, leave the physician in statu quo."
The other three symptoms under the head of portal stagnation,
namely, hematemesis, ascites, and distension of veins, are all of
rare occurrence. The first two would certainly direct attention to
the liver, and even to the portal vein, without having pathogno-
monic value. The third might suggest compression of the
inferior vena cava, and thus only localise the disease deep in the
abdomen, without further distinctive assistance.
6. Local pain.—The value of this from a diagnostic point of view
is probably not very great. First, the pain may be very insigni-
ficant, and secondly, the relation of pain in particular situations
to the organs supposed to correspond to these situations is known
6 Loc. cit. p. 835.
7 Since this was written, Mr. Pakes has been appointed Bacteriologist and
Public Analyst to the Transvaal Colony.
VOL. LVI. u 12
124 A Case of Suppuratwe Pylephlebitss.
by experience to be variable. From a given pain in the right
side, appendicitis, gall-stone, and renal calculus may all be diag-
nosed by different physicians or surgeons; and pain in the right
flank, which is believed to be hepatic, may prove to result from
pleurisy or pneumonia. İt is very doubtful whether there is any
material difference between the pain which may result from
pleurisy, hepatic congestion, and distension of the colon. I am
quite sure that the pains of gastric distension, and of post-herpetic
neuritis may be indistinguishable to the patient. A definite
tenderness over the liver is probably of much more value, and
combined with enlargement of that organ, should draw sufficient
attention to the possibility of hepatic inflammation to bring one
very near to a diagnosis. In the present case it is expressly
stated that the liver was not tender, even on deep pressure. The
pain was sometimes “ not localised,’’ at another time it was “in
the epigastrium.”
1. Prostration and Emaciation.
8. Peritonitis.
Obviously these have no diagnostic value. The first are the
results of any sufficiently prolonged and severe infectious disease.
Peritonitis is a common result of any similar infection localised
in an abdominal organ.
The signs and symptoms selected by Dr. Bryant® as valuable
in the diagnosis of this disease may be seen to cover the same
ground as those of Chvostek, though more briefly stated.
o Pyrexia, rigors, sweating, rapid pulse, abdominal pain, and
tenderness in the right hypochondriac or the epigastric region,
together with uniform enlargement of the liver, and tenderness
of that organ, especially if associated with or following any
ulcerative lesion of the alimentary tract below the csophagus,
should suggest the possibility of suppurative pylephlebitis.”
That is practically the recognition of—
(a). A condition of pysemia.
(b). A source of infection in the abdomen , and
(c). The implication of the liver.
? Loc. cit., p. 88,
A Case of Suppurative Pylephlebitis. 125
But I have already shown how it may be difficult to establish
or easy to overlook the evidence with regard both to (5) and to (c);
and thus we may. be face to face with a simple pyemia. If no
eause can be found for this in the systemic circulation, and the
heart is shewn to be normal, then the abdominal or portal cir-
culation is alone left to supply the septic focus for the pysemic
condition.
This formula is seen to be practically the same as a statement
of Chvostek's second and third points (see p. 116) in inverse order,
namely, the existence of pysmia or septic fever which is due
neither to a lesion in the systemic circulation, nor to malignant
endocarditis. Confirmation would then come from such evidence
as could be found in the abdomen of the primary septic focus, and
of secondary implication of the liver.
Even this may fail us in every one of its three divisions, for
first, it is known that the only evidence of malignant endo-
carditis may be a cardiac murmur, and that a murmur
is sometimes wanting. Secondly, it is conceivable that a minute
lesion in the general circulation may be overlooked, though
sufficient to serve as a focus of pyeemic infection. Thirdly, that
the septic or pysemic nature of an infection in the sense here
meant cannot be safely inferred without the occurrence of rigors.
Now, rigors are not constant in suppurative phlebitis. Chvostek,
it is true, speaks of them almost as if they were. He says,’ “Fever
is constantly observed in this process, and it is quite analogous to
that which is observed in pyemia. Attacks of shivering occur
followed by heat and profuse sweating, of which the first according
to Frerichs, should indicate the formation of pus in the portal
vein.” He then points out that the attacks are not regular in
occurrence, but from their commencement quite irregular, some-
times at intervals of two or more days, at other times occurring
twice or even four times in the day. Later on he says, “In pro-
tracted cases it became a remittent fever with morning remissions
and severe exacerbations in the evening, and this usually passes,
with increasing weakness of the patient, into an intermittent
® Loc. cit., p. 94.
126 A Case of Suppurative Pylephlebstis.
fever, in which the attacks do not begin with shivering, but are
nevertheless terminated by profuse night sweats.”
In the Guy’s cases, however, Dr. Bryant found rigors were
noted in only 50 per cent. of the cases, and were stated not to
have occurred in 40 per cent. Some of these may have been in
the late prostrate condition referred to by Chvostek.
The fact remains, however, that rigors, which are regarded as
the distinctive feature of pysmie infection, are not always
present.
It may be said that few diseases have pathogenic features by
which we can recognise them, and that in most diseases an
analysis such as the above would show that there was nothing to
be absolutely relied upon, and yet they are frequently, nay
constantly, diagnosed with success. There is, of course, one
factor in diagnosis which is of great importance at all times, and
that is our acquaintance with the disease, and our knowledge of
its probability. Suppurative pylephlebitis is very rare. Dr.
Bryant shows that the post-mortem records of Guy’s Hospital
contain only eleven cases in twenty years. Under these circum-
stances the probability of suppurative pylephlebitis being present
in any given case of septic disease is very small, and even the
possibility of its occurrence may easily be overlooked.
Malignant endocarditis was, no doubt, at one time in the same
position. It is desirable when we have to do with an obscure
septic condition to remember that the cause may be in the portal
as well as in the systemic circulation. The chief aid to the
diagnosis of the disease is the knowledge that it may oecur.
BLUE URINE.
By A. P. BEDDARD, M.D.
SENIOR DEMONSTRATOR OF PHYSIOLOGY.
Ir is well known that when methylene-blue is taken by the mouth
it reappears in the urine, giving it a deep green or peacock-blue
colour, according to the dose. Occasionally, however, a green or
blue urine is passed by a patient who is not taking medicine in
any form, and whose occupation does not suggest any possible
means of obtaining methylene-blue. In such a case it becomes:
necessary to determine the nature of the pigment.
Morley Fletcher (Clin. Soc. Trans., vol. xxxii.), reported two
cases of an apparently spontaneous passage of methylene-blue in:
the urine, and the following is a similar case. A country labourer,
aged 30, came up to the out-patient department, complaining that
for several days he had been passing more or less discoloured
urine. He had taken no medicine nor pills of any kind, had
nothing to do with paints or dyes, and had neither sucked nor
swallowed any dyed material. He passed a, specimen of urine
with the following characters:—It was of a rich peacock-blue
colour, distinctly acid in reaction, and normal in all other respects.
The urine was placed in a bottle and corked, and on the next day
it was found that the blue colour had entirely disappeared, leaving
the urine of an ordinary yellow colour. On shaking it up with
air, however, the blue colour rapidly returned, and after the
addition of a few drops of formalin, has never again disappeared.
128 Blue Urine.
The power of living tissues to remove oxygen from methylene-
blue and convert it into a colourless compound is well known,
and in this case was exerted by a growth of bacteria in the urine.
In passing, attention may be drawn to the remarkable fact that
methylene-blue is apparently able to exist in the urine in contact
with the tissues of the bladder in its blue condition, and this is all
the more remarkable in that urine contains the merest traces of
oxygen.
When this urine was examined, it could be seen that the blue
pigment was present, partly in solution and partly as blue amor-
phous granules, and when filtered a blue deposit was left on the
paper, the filtrate being not blue, but green. The blue deposit
was soluble in water, producing a clear blue solution.
Green urine may be caused by the presence in the urine of
biliverdin, by carboluria, or by indigo-blue or methylene-blue
taken by the mouth. The first two can be readily recognised by
the ordinary tests, it only remains to distinguish between the two
latter.
Again, blue urine may be due to methylene-blue or indigo-blue.
So far as is known, methylene-blue cannot be manufactured in the
body, but must have been absorbed as such. Indigo-blue may be
either absorbed as such or derived from proteid decomposition in
the alimentary canal. In the latter case, usually not indigo-blue
itself, but its colourless chromogens indican or indoxyl glycuronate
are passed. More rarely, however, indigo-blue may be present in
the urine when passed; its presence is due to an alkaline fermen-
tation taking place in the renal passages and splitting off from
the chromogens the indoxyl, which becomes oxidised into indigo-
blue. Consequently, indigo-blue, unless it has been absorbed, is
only present as such in alkaline urines, although it has been
recorded in one instance in an acid urine.
To distinguish between indigo-blue and methylene-blue in urine
it is only necessary to examine the urine spectroscopically, for the
characteristic bands of the two substances are in such widely
different parts of the spectrum that the diagnosis can be made
with certainty with an ordinary pocket spectroscope. Both pig-
ments are extracted from urine by chloroform, and when present
Blue Urine. 129
in the urine in only small quantities it is well to examine a
chloroform extract. Indigo-blue gives a broad band lying on the
yellow sodium line D. Methylene-blue, on the other hand, gives
a much narrower and darker band in the extreme red end of the
field of an ordinary pocket spectroscope.
If a spectroscope be not available, the diagnosis is still possible
by noting the following points :— |
(1). The reaction of the urine. If a blue urine is acid when
passed, it is probably not coloured by indigo-blue. If alkaline, the
colour may be due to either substance.
(2). Extraction with ether. Although chloroform extracts both
of the pigments from urine, ether only takes up indigo-blue.
(3). Disappearance of the blue colour in a corked bottle and
reappearance on shaking with air. Methylene-blue in urine may
be reduced by the growth of bacteria in a single night to a colour-
less compound. Tndigo-blue may also be reduced to indigo-white
by bacteria, but the conversion takes much longer. Both blue
colours rapidly reappear on shaking the urine with air.
(4). Heating two specimens of the blue urine with strong
mineral acids, one with HCl, the other with HNO, and noting
their behaviour. With HCl the blue colour of methylene-blue
rapidly disappears, and if the urine be then shaken vigorously
with air, its blue or green colour reappears. The colour of indigo-
blue, on the contrary, is not discharged.
With HNO, exactly the opposite is true; indigo-blue is split up
into isatin, its blue colour is destroyed and will not reappear on
shaking with air. Methylene-blue, on the other hand, is unaltered.
These colour changes are, however, complicated by the fact that
urine frequently contains two chromogens, which, the heating
with mineral acids, converts into red pigments, namely urorosein
and so-called indigo-red. Hither may be present alone, or both
together. Urorosein may be distinguished from indigo-red by the
following reactions—it is taken up from its solutions by amyl
alcohol and not by chloroform or ether, it is rapidly decolorised
by alkalies, and gives a broad absorbtion band midway between
D and H.
130 Blue Urine.
It thus comes about that heating a blue urine with HCl in the
case of methylene-blue, may turn it pink or red, and in the case
of indigo-blue a mixture of red with the blue. Heating with HNO,
may turn an indigo-blue urine red, and a methylene-blue urine a
mixture of green or blue with red.
In the Lancet of June 1st, 1901, the case is recorded of a man
who on several occasions, for no known reason, passed either
peacock-blue or sage-green urine, which was acid and otherwise
normal. When corked the blue colour disappeared and returned
on shaking with air. The blue or green colour was considered to
be due to indigo-blue, because when the urine was heated with
HCl it turned pink, which was held to prove the presence of
indican, and therefore of the source of the indigo-blue. From
what has been said above, however, it may be concluded that this
case of blue urine was one of urine containing not preformed
indigo-blue, but methylene-blue absorbed from some unknown
source.
REDUCTION EN MASSE.
By R. P. ROWLANDS, F.R.C.S.
DEMONSTRATOR OF ANATOMY, Guy's HOSPITAL.
Ir is not common for a strangulated hernia to be reduced en
masse , during the last forty years only fifteen instances have
occurred at Guy’s Hospital. It is, however, an unfortunate and
grave accident that may be produced by anyone who tries to
reduce a strangulated hernia. It is an injury that should rarely
be inflicted by the medical man, yet it is he who usually inflicts
it. When it has occurred, it requires very prompt recognition
and treatment. There is so little said about it in the ordinary
surgical works that I have ventured to write this paper, which
is based upon one hundred cases collected from various sources.
I am much indebted to the surgeons of Guy’s Hospital for
allowing me to make use of their cases. I have arranged the
cases in a, tabular form, adopting the method employed by Mr.
Birkett in his paper. My own case I have reported in full
because of some interesting features which it presented.
132 Reduction en Masse.
Reduction en masse is commonest in cases of inguinal hernia,
it is much less common in femoral hernia, and extremely rare
in all other forms of hernia.
Two very doubtful cases of reduction en masse of ventral
hernia are mentioned by Blackman.
Saviard" was the first to draw the attention of the profession
to this interesting accident. He witnessed an operation at
which the surgeon, mistaking the sac for intestine, reduced it.
At the autopsy, Saviard found the sac lying in the subperitoneal
tissue and enclosing strangulated bowel.
Le Dran, thirty years later, published an interesting case.
The French surgeons of the time, however, were not convinced
of the possibility of the accident, and severely criticised Le
Dran’s account of it.
Sir Charles Bell? was the first English surgeon to publish a
case.
Luke? gave a systematic account of the condition in 1850.
Birkett‘ contributed a most valuable paper on the subject in
1859. Mr. Birkett collected and tabulated 37 cases, which have
been included in the tables which follow these observations.
Blackman’ also analysed the cases recorded before 1851.
In reduction en masse the hernial tumour has been reduced
from its usual position, but the intestine is still strangulated by
the neck of the sac. This definition is perhaps too comprehensive,
but it is founded on a clinical basis. Literally, the term should
be applied to only the first of the following varieties. Common
and long extension of the name to the other varieties, and espe-
cially the clinical similarity of these justify their inclusion under
the one term “ reduction en masse."
1 Obs. de Chir., Paris, 1702.
3 Lond. Med. Gazette, 1828, vol. i., p. 484.
8 Idem., 1850, p. 286.
4 Med. Chi. Trans., xlii., p 247.
5 Tracts, B. 839, 1851.
Reduction en Masse. 133
Varieties that may occur in inguinal hernia.
1, The hernial sac and its contents have been completely reduced
through the internal abdominal ring into the subperitoneal tissue.
(Vide fig. 1). At least eighteen instances of this occur in the
tables.
Fia. 1.—Complete Reduction en Masse.
mall intestine.
ac completely reduced.
eritoneum pushed up.
ransversalis fascia.
nternal abdominal ring.
nfundibuliform fascia.
xternal ring in external oblique.
nternal oblique.
ransversalis muscle.
liac fascia.
ə kt HH 02 02
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ҝә
B
H jl H H dH H H W H H H id
mos
to ES О 40 00 SID m
— =
<
£e
=
134 Reduction en Masse.
2. The intestine has been reduced from an inguinal sac into an
abdominal subperitoneal sac, This variety is much the com-
monest. Some of the sac still remains in the inguinal canal, or
even in the scrotum. The abdominal and inguinal sacs have a
common neck. The subperitoneal sac may be a portion of the
original inguinal sac, which has ascended with the intestine
during the taxis, or it may have been gradually formed previously.
(Vide fig. 2).
ip
Uu
4 uy Tili
o
/
Q
Fic. 2.—Incomplete Reduction en Masse.
— Small intestine.
= Sac.
= Peritoneum pushed up.
= Transversalis fascia.
= Infundibuliform fascia.
= External ring in external oblique.
= Internal oblique.
= Transversalis muscle.
= lliac fascia
= Skin.
1
1
= О Q О0 -1 Op i£ OG; bo =
Reduction en Masse. 135
3. The intestine has been reduced from the inguinal sac through
the internal abdominal ring and then through a laceration in the
neck of the sac. The intestine lies free in the subperitoneal tissue.
This form was considered by Mr. Birkett to be very common.
There are three excellent specimens of it in the Guy”s Museum.“
The rupture is usually on the posterior wall of the sac.
(Vide fig. 3).
Fic. 3.—Reduction by Laceration.
Small intestine.
Sac
Peritoneum pushed up.
Transversalis fascia.
Internal abdominal ring.
Infundibuliform fascia.
External ring in external oblique.
Iliac fascia.
Skin.
Vas,
bə pu ONS Ot im CO tO =
M ME
$ Specimens 1134, 1135, 1136,
136 Reduction en Masse.
4. The intestine has been reduced into the peritoneal cavity
where it lies still strangulated by a ring consisting of the detached
neck of the sac. This form is very rare. (Case 13, Table I).
(Vide fig. 4). I
Fic. 4.—Reduction by Detachment of the Orifice of the Sac.
Small intestine.
Peritoneum pushed up.
Internal abdominal ring.
Infundibuliform fascia.
External ring in external oblique.
Ring orifice of sac.
Iliac fascia,
Vas.
Ы О ONO Ot CO m
— =
Reduction en Masse. 137
5. The intestine has been reduced from a scrotal sac into the
inguinal portion of an hour-glass-shaped sac. The sac has, how-
ever, ascended to some extent generally. Some would exclude
this variety. It is, however, difficult to distinguish it clinically
from the other forms. (Vide fig. 5).
Ето. 5.— Reduction from one Compartment of a Congenital Sac
into another one.
1 = Small intestine.
2 = Sac.
= Infundibuliform fascia.
7 = External ring in external oblique.
10 = Iliac fascia.
138 Reduction en Masse.
6. The testicle has been reduced with the hernia into the sub-
peritoneal tissue. Case 10, Table I. (Vide fig. 6, a and b).
Fia. 6a.—Retraction of Testicle.
1
2
-8
4
5
6
7
8
9
Small intestine.
Sac.
Peritoneum pushed up.
Transversalis fascia.
Internal abdominal ring.
Infundibuliform fascia.
External ring in external oblique.
Testicle.
Cord.
Iliac fascia.
Skin.
10
12
Reduction en Masse. 139
Fia. 6b.—Reduction of the Testicle into the Subperitoneal Tissue.
Small intestine.
Sac completely reduced.
Peritoneum pushed up.
Transversalis fascia.
Internal abdominal ring.
Infundibuliform fascia.
External ring in external oblique.
Testicle.
QO -3 Cə Of co b2 =
MECHANISM.
In nearly all the cases the constriction is at the neck of the
sac, and all the cases in the present series are oblique
inguinal hernie. In the large majority the hernia is of long
duration, the average being sixteen years. In six cases the
hernia became strangulated on its first descent, and four of these
(and probably all) were vaginal. It is well known that the
orifice of the sac frequently gets contracted in old herni&, and
that the orifice is very small in hernia into the vaginal process,
from the beginning. The wearing of a truss for a long time
also causes some contraction of the neck of the sac. The
accident is therefore especially likely to occur in a hernia with
a very contracted and rigid orifice to the sac. A very tight stran-
gulation from any cause is another important factor.
The rings and inguinal canal are usually dilated in these
chronic cases, and they allow the ascent of a considerable elastic
VOL. LVI. 13
140 Reduction en Masse.
tumour along them. The taxis fails to reduce the intestine
through the very narrow and firm orifice of the sac, and the
pressure on the tense and semifluid scrotal tumour then produces
dilatation of the inguinal part of the sac. When no further
dilatation of the sac can occur in the rigid canal, the pressure
is almost entirely conducted up to the neck of the sac, which it
separates from the transversalis fascia at the internal ring. The
portion of the sac that now lies just below the orifice, placed
within the subperitoneal tissues, is left with very little external
support to counteract the fluid pressure within it. It therefore
dilates, and the more it dilates the more it drags upon the
inguino-scrotal sac, which therefore follows it. If the lower
part of the sac is firmly fixed to the surrounding structures, the
neck may rupture from over-distension, and allow the fluid and
intestine to escape into the subperitoneal tissue. The cord and
testicle may, however, accompany the sac, and even the scrotal
skin became invaginated in one case of Dupuytren’s. It follows
that laceration of the neck of the sac is particularly likely to
happen in cases of hernia into the vaginal process. Reduction of
the testicle oceurs in the congenital cases for the same reason,
namely, the attachment of the sac to the testicle and cord.
When the hernia has been reduced into the inguinal canal, it is
difficult to apply powerful taxis, and it therefore follows that the
cases of incomplete reduction en masse are by far the commonest.
For the same reason also reduction en masse is most common in
scrotal cases.
The abdominal sac may, in some cases, have been formed
gradually, as suggested by Mr. Cock’.
The repeated forcible reduction so frequently practised by the
patient may produce this gradual formation. In Case 80, Table
III., the sac was completely and gradually reduced in this way.
In Case 19, Table III., the sac had probably been partially reduced
in a similar way. The reduction was completed after the onset
of strangulation.
1T Guy's Hospital Reports, 1847.
Reduction en Masse. 141
The long wearing of a truss may cause the development of a
diverticulum from the neck of the sac by preventing the protru-
sion of the intestine into the lower part of the sac, while allowing
its entry into the upper part, which dilates. Case 12, Table III.,
may be an instance of this.
Mr. Birkett considered that a complete reduction en masse did
not occur in cases of inguino-scrotal hernia. His paper served
to draw the attention of subsequent operators to this point, and
since then several examples have been recorded (vide Tables).
Reduction en masse is much more common in large than in small
hernie. Although in most of the cases the force and duration of `
the taxis have been excessive, yet some of the accidents have
been produced by gentle taxis, and there is one instance of
spontaneous reduction recorded.®
Adhesion of the bowel to the sac may be a cause in rare cases.?
It is remarkable that one can find no case recorded in which the
sac contained large intestine, and it is very uncommon for it to
contain omentum. Mr. Birkett believed that reduction en masse.
was very much more common in hernia into the vaginal process ;
but out of the twelve inguinal cases which have occurred at
Guy’s Hospital since 1860, eight were acquired and only three
were congenital.
It is a curious thing that a scrotal sac can be detached and
reduced into the abdomen without causing any evident bruising
of the tissues of the scrotum and inguinal canal; but the hernial
sac has looser attachments than is generally supposed. This is
sometimes well seen at the operation for radical cure.
Cloquet was able to reduce the sac on the cadaver in twenty-
five cases. Some of these sacs were empty.
When the hernial sac is adberent to the skin, the latter may
become invaginated to follow the sac.
In two” of the inguinal cases the injury was inflicted at the
operation of herniotomy, by reducing the rupture without opening
the sac. This dangerous practice has been wisely abandoned.
8 Case 3, Table V.
9 Richeraud , Dict. dds Scienccs Med.
10 Case 11, Table I.
142 Reduction en Masse.
This accident is much more common in herntotomy for femoral!
hernia. The sac has generally been mistaken for the bowel, and
has been reduced sometimes easily, but usually with considerable
difficulty. The comparative frequency of this mistake in femoral
hernia is due to the peculiar difficulty of recognising the coverings
of this hernia, the fascia propria having been taken for the sac.
Another cause is the remarkable mobility of the sac in some of
these cases. The fatty subperitoneal tissue is not uncommonly
mistaken for omentum. The mistake can be avoided by reason-
able care and by passing the finger up the crural canal to make
sure that the intestine has reached the peritoneal cavity. It is
rare for a femoral hernia to be reduced en masse by taxis only.
The obturator case, placed at the end of Table V., was probably
reduced by muscular action of the obturator externus during
eversion of the thigh.
SYMPTOMS.
The general symptoms of strangulation may diminish for a time
after the apparent reduction, and this may be very misleading.
The constipation, however, remains absolute in almost all the
cases. (In a Richter’s hernia the bowels may be relieved
several times. Case 8, Table IV., is an example of this.) Soon
the symptoms return in an aggravated form.
The local signs. Out of the 78 cases of inguinal hernia
reduced by taxis there were local signs in 55. Probably they
were present also in some of the others, in which the reports
make no statement on the subject. There were no local signs
noticed in the herniotomy cases, nor in the femoral cases. The
commonest local indications are the following :—
1. An ill-defined swelling or fulness in the upper part of the
inguinal canal, or near the internal abdominal ring, or in the
iliac ‘fossa.
2. Pain and tenderness over the same regions.
8. Failure to reproduce the rupture by coughing and straining.
This may indicate the side involved when two ruptures co-exist.
4, Repeated reproduction of the tumour after taxis.
11 Tables IV. and V.
Reduction en Masse. 143
5. An unduly patent canal or external abdominal ring.
6. Retraction or disappearance of the testicle.
7. A small flaccid tumour, at the external ring, giving no
impulse on coughing.
8. À tumour may be felt in the inguinal canal by the finger
which has been introduced by invaginating the scrotum. This
tumour may or may not give an impulse. |
9. The failure to feel a scrotal sac in a case known to have
been one of scrotal hernia.
10. Gurgling over the inguinal region on palpation.
11. A pelvic tumour in some femoral and in obturator cases.
DIAGNOSIS.
When a strangulated hernia has been apparently reduced but
the general symptoms of strangulation persist, it is very probable
that a reduction en masse has occurred. Certain other complica-
tions and sequel® of strangulated hernia may be confused with
reduction en masse, and may cause considerable anxiety and
doubt in the diagnosis. Some of these are :—
1. Paralytic distension, or indentation of the properly reduced
intestines. |
2. Volvulus associated with an external hernia.
8. Strangulation by bands, and other forms of acute intestinal
obstruction, which may coexist with a hernia.
4. Peritonitis following the reduction of a strangulated hernia.
5. Strangulation of the intestine by an omental sac, which may
have been reduced from the sac of an external hernia.
In cases of enteritis there is usually severe diarrhosa to dis-
tinguish them. ;
Strangulation by an omental sac within the sac of a hernia is
very uncommon. Complete omental sacs are uncommon except
in umbilical hernia, in which reduction en masse, rarely if ever
occurs.
The omental sac is generally more or less adherent to the her-
nial sac; and its reduction out of the latter is thus rendered
unlikely. No local signs of reduction en masse exist in such a
13 Hewett , Med. Chi. Trans., 1884, Vol. xxvii.
144 Reduction en Masse.
case. When peritonitis follows upon the reduction of a strangu-
lated hernia and induces vomiting with constipation, the con-
stipation is rarely complete as regards both flatus and feces.
The great rigidity and uniformly tender abdomen, associated with
some fever usually render the diagnosis easy. In more localised
peritonitis adhesions and kinking of the intestine may, however,
occur, and simulate reduction en masse very closely. The
absence of any local indication of reduction en masse may be of
considerable importance in determining the nature of a difficult
case of this kind.
When internal obstruction coexists with an external hernia, if
the hernia can be easily reduced and reproduced, it is certain that
some internal variety of obstruction exists. The early and great
distension usually prominent in cases of volvulus may indicate the
nature of that obstruction. An incompletely reducible entero-
epiplocele, or an inflamed gland associated with a hernia and an
internal strangulation may mislead even the wisest. Mr. Cock
diagnosed reduction en masse in a case of volvulus which co-
existed with a hernia and an inflamed gland.
The coexistence of an internal strangulation by a band, and a
strangulated inguinal hernia is fortunately a very rare thing.
Mr. Adams” records a case in which, the strangulated hernia
having been reduced, and the symptoms persisting, the diagnosis
of reduction en masse was erroneously made. The persistence
of the symptoms was really due to strangulation by a mesenteric
band in the right iliac region. Case 17, Table III., is an instance
of the association of a reduction en masse with an internal
strangulation by a band. |
Paralytic distension of the intestine reduced from a strangulated
hernia may cause great difficulty in the diagnosis. They are
generally cases of long duration of strangulation. There are no
local indications of reduction en masse. In searching for these
indications, especially in femoral cases, the pelvis should be
explored from the rectum or vagina. Some flatus may be passed
in cases of paralytic distension. Mr. Davies-Colley' performed
18 A lams; Med. Times and Gazette, 1853, p. 148.
1 Davies-Colley”s Reporis, 1887, No. 144.
Reduction en Masse. 145
an exploratory laparotomy on a case of paralytic distension two
days after a kelotomy. In considering the diagnosis it is important
to remember that reduction en masse is most common in cases of
right, oblique, large inguinal hernia of long duration.
Out of sixty-six cases, the hernia was on the right in forty-five
cases, and on the left in twenty-one. The average duration was
sixteen years. It may, however, occur in a hernia on its first
descent. Nearly all the inguinal cases occur in men, and almost
all the femoral cases occur in women.
Out of the hundred cases in the following Tables, eighty are
inguinal, nineteen femoral, and one obturator. The patient's
conviction that the hernia has not been properly reduced should
not be ignored. In Case 8, Table IV., the hernia was of the
Richter variety, and the bowels were opened several times after
taxis had been used. The other symptoms of strangulation
persisted. A pelvic examination would probably have led to a
correct diagnosis in this, and also in the obturator case. In cases
of double hernia, the side may be determined by the history of a
difficulty in the reduction of one of the ruptures, and the failure
to reproduce it by straining. Pain along the inguinal canal may
also serve to indicate the side affected (Case 30, Table III).
Dupuytren, in one case, opened the right canal first, and found
the sac to be empty. He then opened the left canal, and found
the reduced sac, and the patient recovered (Case 2, Table II.).
A most careful search should be made for local indications when
the patient is under the influence of an anesthetic and everything
is ready for the operation.
PROPHYLAXIS.
It is clear that excessive taxis is the chief cause of this serious
accident. The manipulation may be too forcible or too prolonged ;
and it is especially dangerous when the patient is under the
influence of an anesthetic.
The patient has inflicted the injury in but a few of the cases.
In the following series of cases the medical man caused the
“reduction ” in sixty-three cases, and the patient caused sixteen
only. These figures contradict the general statement that the
patient has generally effected the “reduction.” In the days of
146 Reduction en Masse.
septic surgery, prolonged taxis may have been justifiable. There
is no excuse for it at the present day. It is rare for the patient
to derive much benefit from taxis applied for more than three or
four minutes. It is far better for him to undergo the operation
of herniotomy than to submit to the repeated taxis and the
deplorable delay which are still far too common in the treatment
of strangulated hernia. Reduction en masse is only one of the
many dangers of excessive taxis. Great care should be exercised
to find, and to always open the proper sac at the operation of
herniotomy. This is especially necessary in femoral hernia, in
which operation reduction en masse is commonest. The finger
should be passed up through the divided orifice of the sac to
make certain that the intestine has been properly reduced.
TREATMENT.
As soon as it appears probable that a hernia has been reduced
en masse an exploratory operation should be undertaken. Delay
is nearly always fatal, and it is very rare in reduction en masse
for an operation performed later than the fifth day of strangula-
tion to be successful. When local indications are evident, the
inguinal (or femoral) canal should be explored. This also seems
to be the best course to adopt in the few cases in which no local
signs can be discovered. Abdominal section has been proposed
and practised by some surgeons in these cases. Annandale and
Stokes have each recorded a fatal case treated by this method.
The main objections to the adoption of laparotomy instead of the
ordinary operation seem to be the following :—
1. The increased risk of peritonitis. It is not possible to
foretell the condition of the contents of the reduced sac; and
the operator, working in the dark, may unnecessarily divide the
stricture and induce peritoneal extravasation of pus, or of faces.
2. The more severe shock which such an operation may
inflict upon a patient already seriously exhausted by prolonged
vomiting.
3. A radical cure of the hernia cannot be performed.
4. The difficulty of reaching the stricture and of safely
dividing it from a laparotomy wound may be considerable. Mr.
Stokes experienced this difficulty in his case, Mr, Annandale,
Reduction en Masse. 147
however, was more fortunate, and was able to reduce the
intestine with ease without dividing the stricture.
This method ha3, however, some compensating advantages in
some obscure cases. It allows a free exploration of the ab-
dominal cavity, and this may be of great advantage in cases of
internal strangulation which may be mistaken for reduction en
masse or may complicate it. The internal strangulation can
thus be found and treated without delay. Sometimes a femoral
or inguinal exploration has failed to discover an existing
reduction en masse, and the upper of two sacs has been
mistaken for the peritoneal cavity. These mistakes could hardly
have occurred if a laparotomy had been employed in these cases.
The errors can be avoided also by making the inguinal incision
of a sufficient size, and the search a very thorough one, A
laparotomy might have saved the life of the above case of
obturator hernia reduced en masse. In patients known to suffer
from more than one hernia, difficulties have arisen on several
occasions. Two or more hernie may have been recently reduced
after the onset of intestinal obstruction; and either no local
signs may be present or there may be a misleading one. Dupuy-
tren must have had considerable confidence in his diagnosis,
when, having opened the right inguinal sac and found it empty,
he explored the left inguinal canal and found his hopes realised.
(Case 2, Table IT.)
The inguinal exploration.—The external ring should be exposed
by the usual incision. A sac may in some cases be discovered
at the external ring, and it may be possible, to pull down the
reduced portion of the sac, to open it, to divide the stricture and
reduce the intestine. A finger introduced into the inguinal canal
may feel the sac, which may be seized with forceps and drawn
down. It is generally necessary and always wise to open the
inguina] canal freely in order thoroughly to expose the sac. It may
be necessary to prolong the incision upwards and outwards through
the lower fibres of the internal oblique and transversalis muscles
before the sac can be discovered. The incision should be free enough
to allow of a proper exploration of the parts. The operation
is a difficult one even through a free incision, and it is disastrous
148 Reduction en Masse.
to attempt it through a small one. This false conservatism was
the chief cause of death in eleven out of the thirty-one fatal
cases following operation. (Table III.). The sac should be opened
with more than the usual precautions, because adhesion of the
intestine to it is not uncommon. The contained fluid should be
swabbed away because it is very liable to be infective. The real
orifice of the sac can be discovered by passing the finger upwards,
along the anterior surface of the mesentery. The stricture should
be divided with care and the bowel loop drawn down to examine
its neck. Ifa greyish patch be discovered, it should be protected
either by oversewing or by grafting a piece of the sac over it,
after the manner successfully adopted by Mr. Dunn. (Cases 85,
36, Table IT.)
The operation may be completed by performing a simple form
of radical cure if the condition of the patient permits the neces-
sary extension of the time.
When the intestine has been ruptured by taxis, or has
perforated into the sac, it may either be left in the sac,
or resected. Of the two the former is probably the safer
method of treatment for these patients, because they may
be too ill to survive an immediate resection. It may be
necessary to carefully incise the stricture to allow a free evacua-
tion of the contents of the distended bowel above, but the sac should
be thoroughly cleansed first. This seems to be of especial value
when the perforation is a small one located at the fundus of the
loop. The feces may then pass along the intestine instead of
through the perforation into the wound. This, I think, accounts
for the spontaneous closure of the fecal fistula in my case. A
risk of peritonitis attends this division of the stricture. The
stricture is, however, much tighter than that observed in: the
ordinary cases of strangulated hernia, Ifthe perforation is a large
one and the finger can be passed through it into the lumen of
the intestine above the structure, the latter may be left undivided.
There is little to gain by incising the stricture in such a case, and
the risk of peritonitis prohibits it. At a later date an opera-
tion will probably be necessary to close the fecal fistula.
Reduction en Masse. 149
It is extremely uncommon for recovery to occur without opera-
tion. Sanson?” has described a case which may possibly have
been an instance of this. His case was treated by repeated
enemata ; after several days the hernia re-descended. Case 2,
Table V. is another doubtful case in which a fecal fistula
followed a supposed reduction en masse.
In Case 22, Table II., the surgeon induced the patient to cause
a re-descent of a probable reduction en masse by straining and
coughing. The surgeon then secured a part of the sac with his
left hand, and reduced the bowel with the right. I am afraid
that such treatment is not likely to be often attended with success;
and it is not even by any means certain ee this case was
really one of reduction en masse.
PROGNOSIS.
The prognosis is very serious. Out of the one hundred cases
tabulated below there were fifty-nine deaths and forty-one
recoveries. Of the eighty inguinal cases, thirty-six recovered and
forty-four died. Thirty-five recovered after an operation, and
one without an operation. Thirteen cases died untreated by
operation, and thirty-one after an operation.
In nineteen femoral cases there were fourteen fatalities and
five recoveries. Six died, although an operation was performed,
and eight without operation. One recovered without operation,
and four after an operation. The only obturator case was fatal.
It will be noticed that the prognosis of femoral cases is more
grave than that of the inguinal. This is probably due to the
absence of local signs, or failure to recognise them, in femoral
cases. Delay in treatment is therefore more common, and the
operations are less thorough. It is almost certain that the
mortality is higher than the figures indicate, because only
the successful cases are often recorded. This seems to be clear
from the fact that, of fifteen previously unreported cases included
in the Tables, there were only five recoveries. One of the
fatalities was due to an accidental cause, however; and three of
the others were femoral cases. With a recognition of the facts that
the treatment must be prompt, and that the operation must be
15 Diet de Med. et de Chir, 57,
150 Reduction en Masse.
thorough to be successful, better results may be hoped for in the
future.
The commonest causes of death are peritonitis, exhaustion
from long continued strangulation, and septic infection of the
wound.
FuLL REPORT OF CASE 84.
E. L.,a man of 55 years, came into Bright ward on April
6th, 1898, suffering from thrombosis of the left internal sap-
henous vein. He also had an acquired right scrotal hernia,
which had first appeared six months before admission. An
inefficient truss had been used. The patient had experienced
great difficulty in reducing the hernia on several occasions.
During the night of April 10th, the hernia again descended and
became strangulated. The patient made several vain attempts
to reduce it. Next morning I reduced the hernia fairly easily.
The patient went home a few days later.
On May 8th, 1898, the hernia reappeared and became strangu-
lated. The patient repeatedly tried and failed to reduce it.
Next day a doctor failed to reduce it. On the 10th, after
prolonged and very painful taxis, the doctor reduted the rupture.
The patient, however, felt convinced that the reduction was not
satisfactory. The symptoms, although relieved for a time,
became worse. Vomiting became severe and frequent, constipa-
tion remained absolute, and the abdomen became distended.
Colicky pains worried the patient at short intervals.
- The man was admitted into Bright on May 11th, at 11 p.m
He then looked very ill and collapsed, with a pulse of 120 and
feeble. His face was pinched and leaden and the eyes sunken.
The abdomen was uniformly distended and tender. There was
an abnormal fulness over the right inguinal canal. A vague
tender swelling was felt above the internal abdominal ring,
which was much more distinct later under an anesthetic.
The external ring was large and well defined. The testicle was
not retracted. |
A.C.E. was at once administered. The inguinal canal was
opened freely and a sac was found high up in it. The sac was
Reduction en Masse. 151
Era. 7.—Hlustrating Case of E.L.
1 — Small intestine.
2 — Sac in subperitoneal tissue.
= Parietal peritoneum pushed up.
Transversalis fascia.
Internal abdominal ring.
External oblique with external ring.
Internal oblique.
= Transversalis.
9 = Infundibuliform fascia.
10 = Iliac fascia.
11 = Small sac in inguinal canal.
12 = Vas.
8
4
5
6
7
8
incised, allowing some gas and feecal fluid to escape. The sac
wall was very thick. On passing my finger upward 1 felt a tubular
constriction of the sac just within the internal abdominal ring.
The finger was passed through this constriction with difficulty
into another and much larger sac lying entirely above the internal
ring and containing strangulated small intestine. No attempts
availed to bring this sac down into the wound. The incision was
therefore extended upwards and outwards through the abdominal
muscles for two inches above the internal ring. The second sac
was thus partly exposed, and was incised. About six inches of
small intestine, much congested and covered with recent lymph.
were thus partly exposed. The intestine was adherent to the
sac in several places. The sac was well irrigated and dried with
iodoform gauze. The neck of the sac was then discovered near
the anterior abdominal wall three inches above the internal
152 Reduction en Masse.
ring. The constriction, which was a very tight one, was carefully
incised. No attempt to find the perforation was made, lest
extravasation of fæces into the peritoneal cavity should be induced.
The loop of intestine was left in the upper sac, and the lower sac
was removed. The lower part of the wound was sewn up with
catgut, and a gauze drain was left leading from the loop of
intestine into the upper end of the incision. Some fæces escaped
for about three days and the wound suppurated, but it
gradually healed. The patient was discharged six weeks after
the operation wearing a specially designed blade-truss. This he
has worn since.
He has remained quite well for nearly three years. At the
present time there is no evidence of the existence of a hernia of
any kind in the right inguinal region. The patient, however, tells
me that he has suffered from several mild attacks of intestinal
obstruction during the summer. He also says that in August he
had complete constipation for eight days. During this attack
there was some swelling, pain, and tenderness in the right
Inguinal region. The symptoms were relieved by the persistent
use of enemata.
This case seems to be worthy of publication for several
reasons :—
1. The intestine had probably been ruptured within the sac
during the taxis.
2. It is the only case I can find recorded where the stricture
has been divided and the ruptured intestine has been successfully
left in the retroperitoneal sac. This was considered to be better
than resection in this case. Resection and reduction of the
intestine would probably have caused peritonitis, for the sac con-
tained fæces, and was already suppurating. Moreover, the
patient was too ill to successfully undergo a resection at the end
of a tedious operation. That the fecal fistula should have
spontaneously healed was, of course, unexpected.
3. It would have been disastrous to have treated this case
through a laparotomy wound, and it indicates some of the evident
alvantages of the inguinal over the abdominal operation in these
cases.
nal Hernia, 1
| Survived this ` Anno. Reference.
| attack. |
i — " — —
|
eduction 6 monthm, contained | 1740 | Arnaud Diss. p. 387, Obs. ix.
ast severe attack,
days.
— ing, where it | 1818 | Scarpa Sullérnie, 2nd edit., p. 49.
1819
bout 8 days ..-com internal | 1828 | Sir Charles Bell. , Lon. Med.
Gazette, 1828, vol. i., p. 484.
— ән . | Idem | Idem.
— ə ..| 1834 | B. B. Cooper; Guy's Hosp. Rep.
| vol. IV., p. 331.
to 7 days es 2 | 1886 | Parish; Observ. on Strang.
| | Hernia.
,
x | 1840 | Langier : Bull. Chir., i., 363.
| |
| |
bout 4 days id - дә | 1842 | Banner; Prov. Med. and Surg.
| Journal, 1843.
bout 4 days 1844-5 | Blackman, p. 38.
ied third day o
btrangulation
ather suddenly.
--- | 1877 | Howse; Reports.
days ә “.48SU€ ..| 1880 | Clement Lucas; Reports.
.
.
——— — — M... I. __.-
days əş --dtumour was — McCarthy ; Trans. Path. Soc.,
| n the canal. 1881, p. 80.
= is “ed the sac had — Idem.
| ium. 1
-ҹ
ON ENTERIC FEVER:
BEING
AN INVESTIGATION INTO THE BACTERIOLOGICAL
CONDITION OF THE URINE, AND IN SOME CASES,
OF THE KIDNEY IN THIS DISEASE.
(THESIS FOR THE M.D. CAMBRIDGE.)
By STANLEY E. DENYER, C.M.G., M.A., M.D., B.C., D.P.H.,
From the Bacteriological Laboratory, Guy's Hospital.
:0
In bringing before-you this paper on the result of some investi-
gations into the bacteriology of the genito-urinary tract in enteric
fever, 1 will not venture to apologise for its shortcomings, nor for
its inadequacy, because of these I am fully conscious. The subject is
one which demands more attention than has hitherto been bestowed
upon it, both from a clinical, pathological, and public health point
of view. Very little help is to be obtained from the literature,
which at present is but scanty. The earlier publications are of
little use, since our bacteriological knowledge was not then suffi-
ciently advanced to satisfaetorily differentiate the micro-organism
found. Krogius, writing on the subject of bacteriuria, bases his
remarks upon eight cases, in which he examined the urine under
aseptic conditions. In each of these cases he states that he found
the bacillus coli communis. He has, however, given but scanty
proof of the identity of the organism found. For example, in
154 On Enteric Fever.
Observation II. his proof of the presence of the bacillus coli
communis is given in the following words: “ l’ensemencement
de l'urine sur des plaques de gélatine, donna lieu au développe-
ment d'innombrables colonies du bacterium coli commune,” and in
Observation III. “ Sur les plaques de gelatine, il se développeé
le bacterium coli commune en culture puré.” In none of the
cases can I find that he published any further proof of the identity
of the organism found, although he is quoted as having made most
careful bacteriological examinations. In another case, published
as late as 1898, in speaking of the bacillus coli communis, the
author says, ‘‘ the bacteria were motile and otherwise character-
istic." * The later publications seem to shew that the urine of
patients suffering from enteric fever contained the bacillus typhi
abdominalis in about twenty-five per cent. of cases. In the few
cases that I have examined, the results have shown a lower
percentage than this.
My own object has been to examine into the bacteriological
condition of the urine in enteric fever, from the earliest possible
period in the disease, to carry on this investigation during the
whole period that the patient remained in hospital under treat-
ment, and in cases where death has occurred, to make examina-
tions of the viscera as early as possible after death. Bacteriolo-
gical examinations were made of the heart-blood or spleen, the
kidneys, and the urine in the bladder. Sections of the kidneys
were also made and examined for micro-organisms, with the idea
of finding, if present, their position in these organs, and whether
in the tubules, glomeruli, or in both.
From the small number of cases that I have been able to
examine, I am afraid that any deduction would be presumptuous.
But I think, as far as it is possible, under the circumstances under
which these examinations can be made, that the few facts I have
gleaned are reliable.
1A. Krogius. Sur la bacteriurie, Annales des Organ, Gén-Urin., 1894,
p. 196, et seq.
3 Nathan, P. W. Bacillus coli communis in the urine, and its significance.
Med, Rec., New York, 1898, vol. liii., 83-86.
On Pateric Fever. 155
METHODS ADOPTED IN THE BACTERIOLOGICAL
EXAMINATION OF THE URINE, KIDNEYS AND OTHER
VISCERA, AND THE BLOOD, IN ENTERIC FEVER.
The Bacteriological Examination of the Urine.—In the case of
male patients the glans penis and meatus urinarius were washed
with a solution of mercuric chloride (1—2000), or with lysol 2
per cent. The urine was then passed (the first portion being
rejected, as likely to contain organisms that might be present in
the urethra) into a sterilized flask, which was immediately closed
with its sterilized plug of cotton wool.
In the case of female patients, the urine was drawn off by a
catheter, passed by a reliable nurse, the parts being first cleansed
with a solution of mercuric chloride (1—2000). Some of these
cathefer specimens obtained by the nurse in this way were found
to be quite sterile. I have mentioned this fact, in order to point
out that the specimens obtained in this manner can be relied
upon equally with those obtained from male patients.
In each case hanging drop examinations of the urine were -
made. 5 c.c. of the urine were pipetted, with a sterile pipette,
into tubes of broth and glucose-formate broth respectively.
An agar plate was made and some urine spread over the
surface, every means being adopted to prevent the entrance of
adventitious organisms. The glucose-formate broth tube was
incubated in every case ansrobieally, a Buchner's tube being
used.
All three media were incubated for twenty-four hours and two
days at 37°C. At the end of these times they were examined,
hanging drop preparations being made, and films being stained
with carbol-methylene blue, and if bacilli were found, by Gram-
Weigert’s method.
Agar plates were then made, and if more than one organism
was present, separation was thus effected. In some cases it was
found necessary to replate several times, in order to obtain the
organisms in pure culture.
VOL. LVI. 14
156 On Enteric Fever.
When micrococci only were found, they were not worked out.
When pure cultivations of bacilli were found, the organism was
worked out according to the following scheme :—
Description.— Whether coccus, bacillus, etc.
Motility.—Whether non-motile, slightly motile, very motile,
etc.
Spores.—Presence or absence of.
Staining reactions.— With carbol methylene blue, carbol fuchsin,
Gram- Weigert.
Pleomorphism.—Any signs noted.
Cultural reactions.—The growth of the organism in broth and
peptone water. These were examined at the end of five days for
the production of indol, recognised by the fact that when acted
upon by nitric acid in the presence of nitrites, a nitroso-indol
compound is produced, which has a very red colour. (By using
commercial nitric acid, which contains nitrous acid as an im-
purity, this experiment can easily be performed.)
The reactions of the organism when grown upon lactose broth,*
formate broth, dextrose broth, saccharose broth, glycerine broth,
nitrate broth, lead broth (for detection of sulphuretted hydrogen),
litmus milk, and glucose-formate broth grown anerobically.
The characters of the growth upon agar, blood-serum and
potato. All of the above were incubated at a temperature of
87°C. The growth of the organism upon gelatine (stab, streak,
and plates), at a temperature of 20°C., was also investigated, and
the presence or absence of gas-production, or of liquefaction
was especially noted.
All were examined at the end of twenty-four hours, and at the
end of two, three and five days. An examination was made
earlier than twenty-four hours, in dextrose broth cultures for
gas-formation, and motility, and later than twenty-four hours
in the case of milk for the occurrence of clotting.
Bacteriological examination of the kidney.—The following pro-
cedure was adopted in the bacteriological examination of the
8 Lactose broth, dextrose broth, formate broth, saccharose broth and
glycerine broth, as we!l as litmus m'lk, were coloured blue with litmus, any
formation of acid being ndicated by a change in colour.
On Enteric Fever. 157
kidney. The kidney was removed from the body as soon as
possible after death, the capsule was then stripped off, and the
surface of the kidney seared with a hot iron and thus sterilized ;
an incision was next made with a sterilized knife into the kidney
substance, and a scraping was taken with a sterilized platinum
wire loop, and planted in broth and glucose-formate broth, and on
sloped agar. Direct films were also made, stained, and examined
for micro-organisms. The media after inoculation were incubated
at 37° C. for twenty-four hours and then examined. Hanging
drop preparations were made and examined. Films were
stained with carbol-methylene blue, carbol-fuchsin, and by
Gram-Weigert’s method. :
Plate preparations on agar were now made, and if more than
one organism was found, separation was thus effected. The
same routine method of working out the organisms was adopted
in all the cases.
The bacteriological examination of the spleen was carried out
in a similar manner. |
In the bacteriological examination of the heart-blood, the
pericardium was opened, and the surface of the heart sterilized
with a hot iron. A sterilized pipette was plunged through the
wall of the ventricle, and some blood sucked into it. The fine
end was then hermetically sealed, until the blood thus obtained
was required for cultivation.
In the bacteriological examination of the urine from the post-
morten bladder, the surface of the bladder was sterilized with a
hot iron, an incision was then made into it, sufficiently large
for the introduction of a sterilized pipette, some urine being
withdrawn, collected in a sterilized flask, and examined as
described above. |
Histological examination of the kidney.—In each case the
kidney was examined as soon as possible after death, both to
avoid, as far as one could, the presence of micro-organisms due
to post-mortem changes, and the post-mortem changes in the
kidney cells.
A suitable portion of the kidney was hardened, by placing it for
twelve hours in a saturated solution of mercuric chloride. It
158 On Enteric Fever.
was then immersed in equal parts of spirit and water for a few
hours, then in spirit for a few more; after that it was dehydrated
with absolute alcohol, and cleared with xylol. From this it was
transferred to a paraffin bath, heated to 56° C. for twenty-four
hours. The portion of the kidney was then embedded in paraffin,
and sections were cut with a microtome. These were stained
with carbol-thionin blue, and examined carefully for micro-
organisms under a one-sixth inch lens and under a one-twelfth
inch oil immersion lens.
BACTERIOLOGICAL REACTIONS OF THE BACILLUS
TYPHI ABDOMINALIS.
The following reactions have been taken to indicate the presence
of the bacillus typhi abdominalis.
A bacillus, which is motile, which stains with carbol-methylene
blue, and which is decolorized by Gram-Weigert’s method.
Which gives no indol reaction when cultivated on broth and
peptone water, and tested with nitric acid in the presence of
nitrites.
Which gives rise to no gas-formation when grown in formate
broth, dextrose broth, lactose broth, saccharose broth, glycerine
broth, or glucose-formate broth; this last grown anerobically.
Which produces nitrites when grown in nitrate broth, as shewn
by producing a ruby-red colour when tested with metaphenylene
diamine.
Which produces neither gas nor liquefaction when cultivated
on gelatine; which, when grown on sloped gelatine, produces a
whitish semi-translucent growth, with dentate edges.
Which gives a whitish semi-translucent growth on agar.
Which produces slight acidity, but no clotting of milk. Which
produces no spores. The non-production of spores is proved by
exposing a twenty-hours’ broth culture to temperature 80° C. for
twenty minutes, and inoculating from this with a negative result.
Of which a twenty-four hours’ growth on broth becomes clumped
when examined with serum from a typhoid patient, which has
On Enteric Fever. 159
caused clumping of a known bacillus typhi abdominalis grown in
the same way. (Gruber’s reaction).
By an atypical typhoid bacillus is meant an organism which
differs from a typical typhoid bacillus in one principal reaction,
while agreeing in other respects.
By a para-typhoid bacillus, an organism which differs from a
typical typhoid bacillus, in two principal reactions, while agreeing
in other respects.
The bacilli described in this paper as atypical bacillus coli
communis and para-colon bacillus differ from the normal bacillus
coli communis according to the same rules.
BRIEF ABSTRACT OF CASES.
Fifteen cases of enteric fever were examined. In one of these
the kidney only was examined. In ten cases the urine only was
examined, several examinations being made in each case In three
cases in which death occurred, the kidney, spleen, or heart-blood,
and the urine from the post-mortem bladder were examined. In
one case the urine was examined during the period of convales-
cence only.
CASE 1.—F., 28 years. Signs: Fever, enlargement of spleen,
rose-red spots on abdomen, bronchitis, feeble pulse. Death seven
days after admission. No Widal reaction performed. Post-
mortem signs of enteric fever found. Kidney sterile. Histo-
logical examination, nil.
CASE 2.—M., 31 years. Bacteriuria occurred for ten months
after an attack of enteric fever; it was arrested by urotropin.
Four examinations of the urine were made during a period of
three months. The bacillus coli communis and an atypical bacillus
coli communis were found. After administration of urotropin,
the urine became sterile.
CasE 3.—F., 9 years.—Enteric fever with relapse. Signs:
Fever, enlargement of spleen, spots on abdomen, and a positive
Widal reaction. Urine examined on thirty-fifth day (eighth day
of relapse), sterile. Examined on thirty-ninth day, staphylococci.
160 On Entertc Fever.
CASE 4.—M., 21 years. The history points to the fever on
admission being due to relapse, after a primary attack of a fort-
night’sduration. Signs: Fever, diarrhea, and fulness of abdomen.
Widal's reaction present. Urine examined three times during first,
second, and fourth weeks. Staphylococci only on each occasion.
CASE 5.—F., 32 years. Signs: Fever, rose-coloured spots on
abdomen, diarrhoea, & palpable spleen, some signs of bronchitis
and a marked Widal reaction. Urine examined on five occasions,
on the twenty-fifth day (sterile), twenty-seventh day (staphylo-
cocci), thirty-fourth day (staphylococci), forty-first day (sterile),
fifty-fifth day (cocci).
CASE 6.—M., 27 years. Signs: Fever, diarrhosa, pain in head
and abdomen, rose-coloured spots, dicrotic pulse, signs of bron-
chitis, and a positive Widal reaction; urine examined twice
(during convalescence), staphylococci only found.
CASE 7.—M., 29 years. Signs: Fever, spots, and palpable
spleen. Death occurred from hemorrhage of the bowel during
a probable relapse. Widal’s reaction negative. The post-mortem
signs of enteric fever were found. Bacteriological examinations
were made of the spleen, kidney, and urine from the post-mortem
bladder. The bacillus typhi abdominalis was found in pure culture
in spleen. The kidney was sterile. The urine from the post-
mortem bladder contained only staphylococci.
CASE 8.—F., 4 years. Signs: Fever, diarrhoea, fulness of
abdomen, rose-coloured spots, and a positive VVidal reaction.
Five examinations of the urine were made (1) on the eighth day, a
para-colon bacillus, (2) on the fifteenth day, a bacillus resembling
in many respects the bacillus enteritidis of Gartner, (3) on the
twentieth day the bacillus typhi abdominalis, (4) on the thirtieth
day, the bacillus proteus vulgaris, (5) on the forty-seventh day,
both the bacillus coli communis and bacillus proteus vulgaris.
Case 9.—M., 16. Signs: Fever, typhoid spots, constipation,
spleen not palpable and a positive Widal reaction. Six examina-
tions of the urine were made, on the thirteenth, eighteenth, twenty-
first, twenty-fourth, twenty-seventh, and fortieth days. On five
occasions staphylococci were found, and on the sixth, cocci which
were arranged in pairs. i
On Enteric Fever. = 161
CASE 10.—M., 11. The temperature after being raised for three
weeks became normal, but a relapse occurred with pyrexia of
slight degree continuing for another three weeks. Spleen pal-
pable, spots present on abdomen. Widal’s reaction present.
Urine examined four times, on the twenty-fifth, twenty-ninth,
thirty-ninth, and forty-seventh days, respectively. Staphylococci
only were found.
CASE 11.—M., 25 years. Signs: Fever, diarrhoea, enlargement
of spleen, absence of spots, fulness of abdomen. Widal’s reaction
was present. Three examinations of the urine were made. On
the first examination a para-typhoid bacillus found, on the second,
staphylococci, on the third, a bacillus of the proteus group.
CASE 12.—F., 30 years.—Signs : General malaise, fever,
diarrhoea and constipation alternating, enlargement of spleen,
rose-coloured spots on abdomen. The blood was negative to
Widal’s reaction. Urine examined on four occasions: On
twentieth day bacillus typhi abdominalis with staphylococci ;
on forty-third day bacillus typhi abdominalis in pure culture;
on forty-seventh day cocci and some large bacillus, not the
bacillus typhi abdominalis; on fifty-first day bacillus typhi
abdominalis, with a proteus-like organism.
CASE 13.—M., 19 years; a severe case, with fever, headache,
delirium, fulness of abdomen, rose-coloured spots. The spleen
was not palpable. Widal’s reaction negative. Death occurred
from perforation. Bacteriological examination of the (post-
mortem) urine, spleen and kidney, showed the presence in each,
in pure, culture of a para-colon bacillus.
CASE 14.—M., 34 years. Signs: Fever, alternating diarrhoea
and constipation, palpable spleen, rose-coloured spots on abdomen,
Death occurred from hemorrhage. Urine from bladder (post-
mortem) was sterile. No satisfactory bacteriological examination
could be made of the spleen and kidney.
CASE 15.—M., 11 years. Signs: General malaise, fever,
slight fulness of abdomen, palpable spleen, and suspicious spots
on abdomen. Widal’s reaction present. Urine examined on
three occasions. Staphylococci only found. The blood was
examined bacteriologically and found to be sterile.
162 | On Enteric Feuer.
DISCUSSION OF CASES.
Forty-five complete bacteriological examinations of the urine
were made. Of these, forty-two were made from the urine
during life, and three were from the bladder after death.
The earliest examination of the urine was made on the eighth
day of the disease, the bacillus para-coli communis being found.
The earliest day on which the bacillus typhi abdominalis was
found in the urine, was on the twentieth day of the disease (in
two different cases of enteric fever, it was found on the
twentieth day). The latest recorded examination was made on
the fifty-first day of the disease, the bacillus typhi abdominalis
being found, together with an organism giving the reactions
of the proteus vulgaris. The latest day on which the bacillus
typhi abdominalis was found in the urine, was therefore the
fifty-first day of the disease. Since patients leave the hospital
during convalescence, no attempt has been made to discover the
period during which the bacillus typhi abdominalis may remain
in the urine. A glance at Case 2 will show, however, that bacteri-
uria (in this case due to the bacillus coli communis) may continue
for several months after the temperature has become normal.
The organisms found in the urine, in enteric fever patients,
include the following :—
No. of examina-
tions of urine in
which the organ-
ism was found.
Organism found.
Bacillus Typhi Abdominalis m
ӧ Para-typhi Abdominalis ...
v Coli Communis ...
` " (atypical) -
R Para-coli Communis “
A bacillus resembling in many respects the
Bacillus Enteritidis of Gartner.
Bacillis Proteus Vulgaris ze
Staphylococcus
Total ...
Go Go = ҺӘ > O = >
DO
n
нә
E
cr
No. of examinations in which urine was
found to be sterile.
On Enteric Fever. | 163
Note 1.—In some cases two different organisms were found in
the same specimen of urine.
Norte 2.—The condition of the urine showed in most cases but
little departure from the normal. At most but a
slight trace of albumin was present, and in all the
urine was acid.
In three cases, a bacteriological examination of the kidney was
made on post-mortem examination. |
In the first case (Case 1) the kidney only was examined, and
was found to be sterile.
In the second case (Case 7), the kidney was found to be sterile,
and the spleen contained the typhoid bacillus in pure culture.
The urine in this case was unfortunately not examined during life.
A specimen taken from the post-mortem bladder contained
staphylococci only.
In the third case (Case 13), the kidney and spleen, as well as a
specimen of the urine from the post-mortem bladder, were
examined. All contained the para-colon bacillus in pure culture.
The urine in this case had not been examined during life.
In fourteen cases bacteriological examinations were made of
the urine.
A.—In ten cases bacteriological examinations were made during
the course of the disease, or during the period of convalescence
immediately following :—
In the first case of this series (Case 3), two examinations were
made, the first on the thirty-fifth day (eighth day of relapse),
when the urine was found to be sterile; the second, on the thirty-
ninth day, when the urine was found to contain staphylococci.
In the second case (Case 4), three examinations were made
during the first, second and fourth weeks. Staphylococci only
were found.
In the third case (Case 5) five examinations were made, on the
twenty-fifth day, when the urine was found to be sterile, on the
twenty-seventh and thirty-fourth days, when staphylococci were
found, on the forty-first day, when the urine was found to be
sterile, on the fifty-fifth day, when cocci were found.
164 On Enteric Fever.
In the fourth case (Case 6), two examinations were made
during convalescence, in both of which staphylococci were found.
In the fifth case (Case 8), five examinations were made. The
first on the eighth day, on which the bacillus para-coli communis
was found. The second, on the fifteenth day, in which a bacillus
was found, resembling in many respects the bacillus enteritidis of
Gartner. The third, on the twentieth day, on which the bacillus
typhi abdominalis was found in pure culture. The fourth, on the
thirtieth day, when the bacillus proteus vulgaris was found. The
fifth on the forty-seventh day, when both the bacillus coli com-
munis, and the bacillus proteus vulgaris were found.
In the sixth case (Case 9), six examinations were made, on the
thirteenth, eighteenth, twenty-first, twenty-fourth, twenty-seventh
and fortieth days of the disease respectively. In the first five
examinations staphylococci were found; in the sixth, cocci,
chiefly in pairs.
In the seventh case (Case 10), four examinations were made,
on the twenty-fifth, twenty-ninth, thirty-ninth and forty-seventh
days of the disease respectively. On each occasion staphylococci
only were found.
In the eighth case (Case 11), three examinations were made.
At the first examination, made during the interval between the
primary attack and a relapse, the bacillus para-typhi abdominalis,
and also staphylococci, were found. At the second examination,
made on the day of the rise of temperature due to relapse, staphy-
lococci alone were found. At the third examination, made on the
eighth day of relapse, staphylococci and an organism of the
proteus group were found.
In the ninth case (Case 12), four examinations were made,
on the twentieth day, when the bacilus typhi abdominalis and
staphylococci were found, on the forty-third day, when the bacillus
typhi abdominalis was found in pure culture, on the forty-seventh
day, when cocci and some large bacilli (not the bacillus typhi abdo-
minalis) were found, and on the fifty-firs& day, when the bacillus
typhi abdominalis and a proteus-like organism were found.
In the tenth case of the series (Case 15), three examinations
were made during the third and fourth week of the disease.
Staphylococci only were found on each occasion.
On Enteric Fever. 165
B. In one case (Case 2) bacteriological examinations of the urine
were made only some months after the occurrence of the disease.—
Five examinations were made, the first seven months after the
attack, the bacillus coli communis being found in pure culture. .
The second a month later, when an atypical bacillus colicommunis
was found, also in pure culture. The third, a month after this,
when the normal bacillus coli communis was again found in pure
culture. The fourth, a month later (ten months after attack), when
the atypical bacillus coli communis was again found. After this
six ten-grain doses of urotropin were administered, three times a
day, for two days. The urine was examined twenty-four hours
after administration of the last dose of urotropin, and was found
to be sterile. There was no albumin in the urine at any time.
C. In three cases bacteriological examinations were made from
the wrine, obtained from the post-mortem bladder. Unfortunately
in neither of these cases had examinations been made during life.
In the first case (Case 7) staphylococci only were found. (The
kidney was sterile, the spleen showed the presence of the bacillus
typhi abdominalis in pure culture.)
In the second case (Case 13) the bacillus para-coli communis
was found in pure culture. (The kidney and spleen also showed
the presence of the bacillus para-coli communis in pure culture.)
In the third case (Case 14) staphylococci only were found.
(The kidney was sterile and the spleen showed the presence of
the bacillus typhi abdominalis in pure culture.)
Proportion of cases of enteric fever in which the bacillus typhi
abdominalis was found in the urine. Also the proportion of cases
of enteric fever in which some other organisms were found.
In fourteen cases of enteric fever, bacteriological examinations
of the urine were made, either during the fever, or during the
period following the fall of the temperature, in one case extending
to a period of ten months, or from a specimen of urine obtained
from the bladder at the post-mortem examination (three cases).
In two cases (14:28 per cent.) the bacillus typhi abdominalis
was found. In eight cases (57:14 per cent.) staphyloccci (alone)
were found. In eleven cases (78:57 per cent.) staphylococci alone,
or with some other organism, were found.
166 On Enteric Fever.
The large proportion of cases in which staphylococci were
found, lends colour to the suggestion of its being due to acci-
dental contamination, notwithstanding every precaution possible
being taken to obtain uncontaminated specimens. This is
noticeable in Case 10, a male patient, aged 11 years, where
foreskin was long and could not be drawn back, and which made
it impossible to cleanse the meatus properly. It was not thought
advisable to use a catheter. On reference to the table it will be
seen that staphylococci were present on every occasion.
In Case 15, a male patient, aged 16 years, the same condition
was present, and in this case also staphylococci only were present
at each examination.
The bacillus typhi abdominalis, therefore, was found in only 14
per cent. of cases, and in these only at intervals, other organisms,
closely approaching it in their bacteriological reactions, being also
‘found. Thus, on reference to Case 8, it is seen, that an atypical
bacillus coli communis was found on the eighth day of the
disease, that a week later another bacillus, somewhat resembling
the bacillus enteritidis of Gürtner, and that a week after this the
bacillus typhi abdominalis in pure culture was found.
Again, in Case 11, the bacillus para-typhi abdominalis was
found on one occasion, while on another a bacillus of the proteus
group was found. It would appear from this, that although the
bacillus typhi abdominalis is found in the urine of enteric fever
patients, that other organisnis, approaching it more or less
closely in bacteriological reactions, are also found, and in the
urine of the same patient. |
Arguing from these premises, I would suggest, that if the
organisms found in the urine of enteric fever patients be carefully
and fully worked out, the percentage in which the bacillus typhi
abdominalts is found, will be lower than that usually given.
In thirteen of the cases Widal's reaction was performed in the
ordinary course of hospital routine. The following method was
adopted. It is described by Mr. W. C. C. Pakes, Bacteriologist
to Guy's Hospital, to whom I am indebted for the notes of the
Widal reactions, and is to be found in an article entitled “ Widal's
Reaction," in Guy's Hospital Reports, Vol. LV. :—
| On Enteric Fever. 167
“The serum is collected in special pipettes, made so that when
the blood is collected, it can be allowed to coagulate in the middle,
so that the serum can separate, and run down into the finer part,
free from corpuscles.”
“ The dilution of the serum.—In order to dilute the serum, small
test-tubes, and small graduated pipettes are used. Ten cubic
millimetres of serum are pipetted into a small test-tube, and are
mixed with 90 cubic millimetres of broth, which is measured in a
second pipette. This gives a fluid containing 10 per cent. of serum :
10 cubic millimetres of this 10 per cent. serum, are all pipetted
into a second test-tube, and are mixed with 90 cubic millimetres
of broth. This gives a fluid containing 1 per cent. of serum.
Sterile broth is used instead of water to prevent the laking of the
red discs. It was shewn soon after the reaction was discovered
that the red discs contained more of the agglutinius than the clear
serum, and if sometimes laked blood is present, and at other times
no blood, the observations cannot be said to be made under
identical conditions, and the value of the reaction as a diagnostic
test will be impaired.”
“ The culture of the bacillus typhi abdominalis.—The bacilli are
inoculated on agar every fortnight, and grown at 20°C. As
cultures are required for the reaction, broth tubes are inoculated
from the most recent agar culture, about eighteen hours before
they are required, the broth tubes being incubated at 37°C.”’
“ Mixing the serum with the broth culture.— Three microscopic
examinations have been made latterly, the serum in the mixtures
being in the proportion of 50 per cent., 5 per cent., and 0:5 per
cent. İn order to do this a platinum loopful of the undiluted
serum is mixed upon a clean coverslip, with the same loop full of
the broth culture, thus making the ö0 per cent. dilution. One
loopful of the 10 per cent. serum, and of the 1 per cent. serum,
mixed with a loopful of the broth culture, form a 5 per cent. and
0:5 per cent. dilution respectively. Immediately after mixing, the
coverslips are inverted upon a hanging drop slide, and the time of
mixing noted. '
“ The reaction, and reaction time.— When judging of a reaction
it is necessary that practically the whole of the bacilli shall be
grouped together, leaving only single bacilli free in the field, If
168 On Enteric Fever.
there are a few small clumps, but the majority of the bacilli-are
either motile or free in the field, I have called this a half reaction,
‘4+.’ As regards the time, I have always been very rigid, and
have continued to adopt the time I suggested in 1897, viz., half-
an-hour. If there is not a complete reaction within half-an-hour,
even if it is complete within one or two hours, I have returned
the result as ‘4+,’ that is ‘no reaction.’ "
I have taken a serum clumping in 5 per cent. strength in half-
an-hour as being diagnostic of enteric fever as far as the reaction
itself is concerned.
VVIDAL”S REACTION.”
Reaction. oz 3 Š
o. ; Ls 29 Results of Urine Examination :
of İ 50per | 5 per | 05 per on > o Organisms found.
Case. | cent. | cent | cent. E
1 i| — — — | Yes | Yes
2 i. O O O — — | Bacillus coli communis: atypical
bac. col. com.
3 T F + Yes | Yes | Staphylococci.
4 + + O No | No | Staphylococci.
5 iiij — + = Yes | Yes | Staphylococci.
6 + + 4+ | No | Yes | Staphylococci.
7 O O O Yes | Yes | Staphylococci.
8 O + O No | Yes | Para-colon bacillus. A bacillus
resembling in many respects the '
bac. enteritidis of Gártner. The
typhoid bacillus. Bac. coli com.
ë and bacillus proteus vulgaris.
1 + + .
9 i| ppt. i + : 4 No | Yes | Staphylococci.
10 O + + Yes | Yes | Staphylococci.
11 + + + Yes | No | Bacillus para-typhi abdominalis.
Staphylococci.
io O O Bacillus typhi abdominalis. Sta-
12 ir O A+ Ö Yes | Yes phylococci. A proteus-like
: organism, etc.
13 i = i = No | Yes | Bacillus para-coli communis.
14 iv. — — — | Yes | Yes | Sterile (p-m.).
i| O O $+
li.) + O O
15 iii. ppt. | 4+ O Yes | Yes | Staphylococci (v.).
iv! + + O
V. bi ee
Nore i.—No Widal examination made in this case.
Norte ii.—This serum, although being completely negative in
all strengths to the bacillus typhi abdominalis, was
found to react fully to a twenty-four hours’ culture of
* I have to thank Mr. W. C. C. Pakes for his courtesy in allowing me to
publish these Widal reactions.
On Enteric Fever. 169
the bacillus para-coli communis, isolated from the
urine of the same case. Its reactions were 50 per
cent. = +, 5 per cent. = +, 0°5 per cent. = О.
NoTE iii.—In this case no Widal examination was made at
Guy’s Hospital, but a marked Widal reaction was
reported from the Jenner Institute.
Note iv.—No Widal examination made.
Norte v.—Finding that staphylococci were so often present, –
and bacillus typhi abdominalis much less frequently,
it occurred to me that the growth of the one might
inhibit the growth of the other. In order to find
out if such were the case, I inoculated three broth
tubes, one with the bacillus typhi abdominalis, one
with staphylococcus, and one with a mixture of the
two, and placed them under like conditions at 37° C.
After seven days’ growth, the bacilli were found to
be chiefly in evidence.
Bacillus typhi abdominalıs.—Broth, 37° twenty-four hours.
Turbid, slight sediment. H.D., slightly motile bacilli.
G.F.B., 37° twenty-four hours. Turbid, no gas.
Staphylococcus.—Broth, 37° twenty-four hours. Good growth,
turbid, slight sediment. H.D., cocci, chiefly in pairs.
G.F.B., 37° twenty-four hours. Turbid, no gas.
Bacillus typhi abdominalis + Staphylococcus.—Broth, 37°,
twenty-four hours. Good growth, turbid, slight
sediment.
G.F.B., 37° twenty-four hours. Turbid, no gas.
H.D. (broth), bacilli very much more in evidence
than cocci. H.D., seven days, bacilli chiefly in
evidence.
N.B.—A serum clumping with 5 per cent. in thirty minutes
(5 per cent. = +) is taken as alone being positive and diagnostic.
In Case 2 an interesting condition was observed. This case
was one in which the patient had had a typical attack of enteric
fever some eight months previously. The blood was not examined
for the Widal reaction during the attack. Hight months after the
attack, however, the serum, on being tested by Widal’s method,
170 On Enteric Fever.
with a twenty-four hours’ old culture of bacillus typhi abdomi-
nalis, was found to give a completely negative reaction in all
dilutions. (50 per cent. = О, 5 per cent. = O,°5 per cent. = O).
The urine of this patient contained at the time the bacillus para-
coli communis. This had been grown in pure culture on gelatine.
A broth tube was inoculated from the gelatine, and a twenty-
four hours’ old culture obtained. This was used with the serum
instead of bacillus typhi abdominalis, and was found to give a
positive result. 50 per cent. = +, 5 per cent. = +.. (Gruber”s
reaction).
This condition of the blood is, I think, worthy of note, being
negative when tested by Widal’s method with the bacillus typhi
abdominalis, but reacting well with the bacillus para-coli com-
munis, isolated from the urine of the same case.
The question arises whether these cases which are on the
borderland of enteric fever as regards their diagnosis, are really due
to the bacillus typhi abdominalis. Mr. W. C. C. Pakes, in his
article on Widal’s reaction,‘ in discussing the diagnosis, says, “ Pro-
visional diagnoses during the course of the disease have not been
accepted, unless the physician has been satisfied, after the termi-
nation of the case, that it was really enterica or was really not
enterica.” This excludes a great number of cases, which may
be said to be on the borderland of enteric fever. I should like to
raise the question, whether some of the so-called aberrant forms
of enteric fever, may not rather be due to a septicemia, similar
to enteric fever, but arising from an infection with bacilli, allied
to the bacillus typhi abdominalis, or to some organism of the coli
group. That an infection arising in the alimentary tract in this
way, may give rise to an abdominal condition, closely simulating
enteric fever.
In connection with this point, I would bring forward a remark
by Dr. Rolleston, in an article on enteric cases, in the Imperial
Yeomanry Hospital at Pretoria. He says,” “ It is noteworthy
that a positive reaction was obtained in only 64:5 per cent. of
cases clinically regarded as certainly enteric.”
4 Widal’s Reaction. By W. C. C. Pakes. Guy's Hosp. Rep. Vol. LV.
5 The Agglutination Reaction in Typhoid Fever. Memorandum by Dr. H.
D. Rolleston. B.M.J., Oct. 12, 1901, p. 1084.
On Enteric Fever. 171
Mr. W. C. C. Pakes, however, gives a much higher percentage,"
as also does Gwynn.’ In one of the cases, in which I made a
bacteriological examination of the heart-blood, kidney, and urine
from post-mortem bladder, I found the bacillus para-coli communis
in each in pure culture. This patient had died with the clinical
symptoms of enteric fever. On post-mortem examination, the
appearances were those seen in enteric fever. A positive Widal
reaction had been obtained on one occasion.
This, I think, is suggestive of an organism distinct from the
bacillus typhi abdominalis being concerned. I have not been able
to go into the subject, as it is outside the scope of my thesis, but
since my attention has been drawn to it in the course of my
work, I have ventured to raise the point.
The subject is one of much difficulty, owing to the want of a
proper classification of these allied groups of bacteria, and from
the fact that the clinical phases which occur in the disease
known as enteric fever, if not grouped together in such a
way that “enteric fever" can be diagnosed, are described as
* aberrant forms of enteric fever," or ‘‘ abortive forms of enteric
fever," or in some such way.
THE PATHOLOGY OF THE CONDITION.
The presence of the typhoid bacillus in the urine is difficult of
explanation. It does not seem to appear in the urine early, for
the earliest date on which I found the bacillus was on the
twentieth day of the disease. On the other hand, it seems to
continue until late in the disease, and in some cases the bacteriuria
due to the typhoid bacillus or some allied organism continues far
into convalescence (vide Case 2).
6 Guy's Hosp. Rep. Ibid.
7 “Positive results of Widal's Reaction in cases certainly typhoid 99:6 per
cent. Of all cases 981 per cent." A Study of the Widal Reaction in 265
cases of Typhoid Fever. By Norman B. Gwynn, M.B. The Johns Hopkins
Hospital Reports. Vol. viii.
YOL. LVI. 15
172 On Enteric Fever.
I have been unable to find the bacillus typhi abdominalis in
sections of the kidney, taken from post-mortem cases of enteric
fever, that I have examined. Neither have I been able to cultivate
the bacillus typhi abdominalis from the kidney on any media that
I have used. I have, however, cultivated the bacillus para-coli
communis from the kidney in one case, and in this case I also
found the same organism in the urine taken from the post-mortem
bladder. Both of these were in pure culture. On histological
. examination of the kidney, stained with carbol-thionin blue, I was,
however, unable to detect the presence of any organisms in the
substance of the kidney, either in the cortex or medulla. Unfor-
* tunately, in this case, no examination had been made of the urine
during life, and the fact that the bacillus para-coli communis was
found also in the heart-blood in pure culture rather lessens the
value of this case, as the possibility of the bacilli getting into
the blood after death has to be borne in mind.
That the condition is due to a stray bacillus getting into the
bladder from the blood through the kidney and multiplying there
has been suggested by Dr. Horton Smith, who discusses the
question under the following heads :—
1. Filtration from the blood.—Dismiss this as there is extreme
difficulty in finding bacilli in the blood during life, and the blood
has been examined bacteriologically, when bacilli have been swarm-
ing in the urine, and no bacilli found.
2. Suppuration in kidney.—This is very rare, bacilluria com-
paratively common.
3. Entrance of a stray bacillus into bladder from blood, through
the kidneys.—Dr. Horton Smith shews that of six specimens of
urine taken and inoculated with typhoid bacilli, and incubated at
37° С., four shewed general turbidity from growth of the micro-
organisms at the end of eighteen hours, while two did not. These
latter, however, shewed good growth in forty-eight hours.
If, as he contends, 25 per cent. of patients suffer from bacilluria
due to the typhoid bacillus in enteric fever, this explanation of the
pathology seems hardly to meet the case. The possibility of some
8 Goulstonian Lectures on the Typhoid Bacillus and Typhoid Fever.—
Lancet, 1900. Part I., p. 821, ct seq.
On Enieric Fever. 173
morbid condition in the kidney, allowing the passage of the bacilli
through it, is one to be considered.
The pathology of kidney disease is at present obscure, and
many points in this connection require to be cleared up. Any
case of damage to an organ, however slight, is sufficient to upset
its physiological equilibrium. It has been shewn that the staphy-
lococcus pyogenes aureus, injected into the circulation of a rabbit,
in most cases, will produce no ill effects upon the healthy heart,
but if the cardiac valves have been previously injured, an infective
endocarditis will result.” But it has been proved by Biedl and
Kraus,” that in some cases, bacilli may come through the normal
kidney, for they showed that micro-organisms which circulate in
the blood, can be excreted through the absolutely intact kidneys.
To demonstrate this, they chloroformed dogs, fixed a sterilized
cannula into the vena jugularis or femoralis, performed laparotomy
on the animals, inserted cannulas into the ureters, and examined
the urine thus obtained under all the necessary precautions, after
having injected the staphylococcus pyogens aureus, the bacillus
coli communis, and the bacillus anthracis into the veins. Cultures
made from the urine, shewed the micro-organisms which had
been injected; examination of the urine was negative as to blood
or albumin. They concluded that the normal kidney, through
its physiological function, is able to excrete the micro-organisms.
In discussing bacteriuria, Herman Goldenburg" says that the
bacteria enter the bladder, either by infection or auto-infection.
Quoting Ultzmann, he says, that bacteriuria is found in patients
with malaria, and in those who work in dissecting rooms, where
the infection takes place through the respiratory organs, and that
he treated a patient with bacteriuria, complicated by hematuria of
renal origin, general malaise, and emaciation due to malarial
infection, rapid improvement following the administration of quinine
and salol. Cases are more frequent in which bacteriuria is due to
9 Surgical Pathology and Morbid Anatomy. By Anthony A. Bowlby,
F.R.C.S., 4th Edit., p. 49.
1 Quoted from Herman Goldenburg's article on Bacteriuria. Med. Rec.,
New York, 1896, p. 228. |
11H. Goldenburg. Bacteriuria. Med. Record, New York, 1896, vol. 1.,
p. 228.
174 On Enteric Fever.
catheterisation with dirty catheters, and auto-infection takes place
from the intestines, either directly through contiguity, or indirectly
through absorption by the lymphatics. In connection with infec-
tion taking place through the respiratory organs, the following is
instructive: Pneumococci were found in the urine in the case of
a female patient, aged 60 years, who had an attack of croupous
pneumonia. On the seventh day she had pain on micturition, and
other symptoms of cystitis. On examination of the urine, Fren-
kel’s pneumococcus was found.”
Wreden demonstrated in the laboratory of Professor Nencki,
that after a slight artificial traumatism in the rectum of male
rabbits, the bacillus coli communis could be found in the urine of
the animals. He claimed from this, that bacteria enter the bladder
directly through the lymphatics, which connect bladder and
rectum. He demonstrated that in rabbits, after a superficial
erosion of the rectal epithelium, fatty substances, such as oil and
vaseline, which were introduced into the rectum, were found in
the urine.
The theory that bacteria enter the bladder in this way seems to
be highly probable. Morris“ states that “ the lymphatics of the
bladder pass partly backwards, beneath the peritoneum, to join
the rectal lymphatics, or the lymphatics of the uterus and vagina
in the female ; and partly forward to join the prostatic lymphatics
and the lymphatics of the vesiculse seminales.”
Sappey states,“ that the lymphatics of the bladder have not
yet been fully worked out in man, although he has demonstrated
their arrangement in the rabbit and dog.
That the lymphatics are enlarged during pregnancy is un-
doubtedly the case, and admitting that the bacilli gain admittance
to the bladder through the lymphatics, one would expect them
to get into the urine more easily, during pregnancy, or during
the puerperal state.
13Pneumococci in the Urine. By G. Munro Smith. Bristol Med. Chir.
Journ., 1895, vol. xiii., p. 115.
15 A Treatise on Human Anatomy, by various Authors. Edited by Henry
Morris, M.A., M.B.
14 Description et Iconographie des Vaisseaux Lymphatiques Considérés
chez L’Homme et les Vertebrés. Par Ph. C. Sappey, p. 124. Vaisseaux
lymphatiques de la vessic.
On Enteric Fever. 175
This is borne out by Case 12, in which the patient was a
woman aged 30 years, who two or three weeks before being
attacked by enteric fever, had been delivered of a child. In her
case the bacillus typhi abdominalis was found in the urine on the
twentieth day of the disease, when the first examination was
made. They were also present on the fifty-first day, when the
last bacteriological examination of the urine was made. That they
were present before the twentieth day is very probable.
GENERAL CONCLUSIONS OBTAINED FROM THE
INVESTIGATION OF THE ABOVE CASES.
1. That there is no definite evidence that the typhoid bacillus
comes through the kidney.
2. That sections of the kidney, appropriately stained, shewed
no evidence of any bacilli.
3. That the entrance of the bacilli into the bladder through the
lymphatics, is much more probable, and that Wreden’s experi-
ments are valuable in this direction.
4. That in the majority of cases of enteric fever the bacillus
typhi abdominalis is not present in the urine.
5. That when it is present it occurs late rather than early in
the disease.
6. That when it is present the urine is generally normal in
other respects, or contains only a trace of albumin.
7. That other micro-organisms, such as the bacillus coli
communis, and the atypical bacillus typhi abdominalis are some-
times present in the urine in cases of enteric fever, and during
the period of convalescence. |
8. That аз a rule when the bacillus typhi abdominalis is
present in the urine there are no local clinical symptoms.
9. That bacteriuria may continue far into convalescence.
10. That the action of urotropin is very effectual in freeing the
urine from bacilli.
176 On Enteric Fever.
11. That the bacteriological examination of the urine may be
useful in some cases for diagnosis.
12. That the patient should be warned as to the possibility of
spreading infection by the urine during convalescence.*
In conclusion, I wish to offer my thanks to the physicians and
assistant physicians for their kindness in allowing me to study
hese conditions of enteric fever, in their respective patients, in
the wards of Guy's Hospital.
I wish also to thank Dr. Bryant and Dr. Fawcett for so gener-
ously giving me the opportunity of working at the morbid
anatomy and bacteriology of the cases on which a post-mortem
examination was made. And finally to express my appreciation
of the kindness and courtesy of Mr. W. C. C. Pakes, in allowing
me the use of the Bacteriological Laboratory, and giving me so
many facilities for working, and to thank him for many valuable
suggestions in technique.
* In the base hospitals in South Africa it is the rule for the officers of the
Roya! Army Medical Corps to retain enteric patients for seven weeks after
the temperature has reached normal, on account of their spreading infection
in this way.
Enteric Fever.
REMARKS.
ade ... | None mac.
Five exan
1. Sev,
In this case the urine was examined some
months after the attack.
On Enteric Fever. 177
LIST OF CASES.
ABBREVIATIONS.
B.T.A. x Bacillus typhi abdominalis,
B.C.C. = Bacillus coli communis,
H.D. = Hanging drop.
C.M.B. ES Carbol-methylene blue.
C.F. = Carbol-fuchsin.
Gr.-W. = Gram-Weigert.
G.F.B. = Glucose-formate broth.
F. = Female.
M. = Male.
NoTE.—In every case when an organism has been obtained in pure culture,
this organism has been worked out according to a definite scheme,
similar reactions being carried out with each organism, and com-
parisons afterwards made.
CASE 1.—F., et. 28 years. Admitted into Miriam Ward under Dr. Wash-
bourn, on July 11th, 1901, for pain in abdomen.
Patient had been ill nine days before admission with severe headaches. She
had had one shivering fit, and pain in abdomen. On admission, temperature
105°, pulse 184. A few scattered spots were present on the abdomen, the
spleen was palpable, and rhonchi could be heard over both lungs. The motions
were of a light yellow colour. The pulse was weak and feeble. Stimulants
(strychnine, musk, digitalis, and champagne) were administered. The pulse,
however, became more feeble, she became cyanosed and died seven days
after admission from heart failure. The blood was not examined for
Widal’s reaction.
A post-mortem examination was made six and a-half hours after death.
The right lung was oedematous. Three feet from the cecum was a small
ulcer per'orating the mucous membrane of the small intestine, and affecting
the muscular coat. Below this were numerous raised infiltrating Peyer’s
patches, in a few of which ulceration had occurred; in the majority, however,
there was no ulceration. There was no perforation of the intestinal wall.
The pancreas was tough ; the spleen large and tough. Histological examination
of the kidney shewed the absence of any organisms.
Bacteriological Examination of the Kidney.
Broth, 37°C. Eighteen hours; four days, nil.
Agar, 37° C. Eighteen hours; four days, nil.
G.F.B. (anzrobically) 37? C. Eighteen hours, nil ; four days, nil,
Direct fim. C.M.B. Nil.
Gr.-W. Nil.
The kidney was sterile.
CASE 2.—M., æt. 31 years. This case is one in which a definite attack of
enteric fever, with pyrexia, severe headache, and extreme prostration and
feeble pulse, and rose-red spots, occurred seven months before the first ex-
amination of the urine was made. No Widal’s reaction was tried at the time,
178 On Enteric Fever.
but the test being performed nine months, after the temperature fell to normal,
gave a negative reaction (50 per cent. = О. 5 percent. = O. 0:5 per cent,
=0). When, however, the serum was examined, as in Gruber’s reaction, using
a broth culture made from a gelatine culture of an organism, obtained from the
urine of the same case (the bacillus para-coli communis), it was found to cause
clumping of the bacilli.
The notes recording this are as follows :—
Blood examination for Gruber’s reaction—
50 per cent. commenced clumping in five minutes, fully clumped
in twenty-five minutes.
50 per cent. slight signs of clumping in twelve minutes, fully
clumped in thirty minutes.
0:5 per cent. not clumped in thirty minutes.
50 per cent. = +. 5 percent. = +. 0:5 percent. = O,
There were no complications in this case. Five examinations of the urine
were made. Four of these were made before, and one after the administration
of urotropin. The quantity of urotropin given was sixty grains, in six doses
of ten grains each, administered three times a day over a period of two days.
After this the urine was found to be quite sterile. There was no albumin at
any time. The first examination of the urine was made seven months after
the temperature became normal, the final one three months after this,
SPECIMEN 1.— Urine.
Description.— A bacillus.
Motility.—In dextrose broth, after six hours” growth, very slightly motile.
Staining.—Stains with C.M.B. Decolorised by Gram-Weigert.
Broth (87° twenty-four hours).—Turbidity, white sediment; two days,
very slight trace of indol.
Peptone water (37° twenty-four hours).—Slight turbidity.
Formate broth (87° twenty-four hours).—Much gas formation, slight
turbidity.
Dextrose broth (87° twenty-four hours).—Much gas formation, turbidity.
Lactose broth (87° twenty-four hours).—Gas formation, turbidity.
Saccharose broth (37° twenty-four hours).—Much gas formation, turbidity.
Glycerine broth (87° twenty-four hours).—Much gas formation, turbidity.
Nitrate broth (37° twenty-four hours).—No gas; turbidity. Red colour
with meta-phenylene diamine = nitrites.
Lead broth (87° twenty-four hours).—
Gelatin stab (20° twenty-four hours).—White growth down stab; no
spreading on surface ; gas formation; no liquefaction.
Gelatin streak (20° twenty-four hours).—Well marked, raised, moist-
looking, white vigorous growth, no liquefaction.
Gelatin shake (20° twenty-four hours).—Slight turbidity, much gas, no
liquefaction.
Gelatin plates (20° two days).—Moist looking, small, white colonies, no
liquefaction.
Agar streak (37° twenty-four hours).—Well marked, raised moist looking
growth, gas formation.
Agar plates (87° thirty-six hours).—Large white moist-looking growths ;
raised ; large gas bubbles ; very vigorous growth.
Blood-serum (37° twenty-four hours).—Vigorous, moist-looking, white,
raised growth,
On Enteric Fever. 179
Litmus milk (37° twenty-four hours).—Acidity, milk entirely clotted.
Potato (37° twenty-four hours).—Raised, yellowish, dirty-looking, vigorous
growth.
Anerobic growth (37° twenty-four hours).—Gas, slight turbidity, slight
sediment.
Laevulose peptone (twenty-four hours). Much gas formation. Turbidity.
= Bacillus Coli Communis.
SPECIMEN 2.— Urine.
Description.—A bacillus.
Motility.—Very slightly motile (two days agar).
Staining.—With C.M.B. Decolorised by Gram-Weigert.
Pleomorphism.—Long and short bacilli.
Broth (87° twenty-four hours).—Turbidity, flocculence, sediment ; four days,
do., no indol.
Peptone water (37° twenty-four hours). — Slight turbidity, flocculence,
sediment; four days, do.; five days, no indol.
Formate broth (81? twenty-four hours).—Gas formation, slight turbidity ;
four days, slight scum, no gas.
Dextrose broth (37° twenty-four hours).—Gas formation, slight turbidity ;
four days, no gas, acid.
Lactose broth (87° twenty-four hours).—Gas formation, slight turbidity ;
four days, no gas, acid.
Saccharose broth (87° twenty-four hours).—Marked gas formation, slight
turbidity; four days, no gas, acid, sediment.
Glycerine broth (37° twenty-four hours).—Gas formation, slight turbidity ;
four days, no gas, acid.
Nitrate broth (37% twenty-four hours).—Turbidity, white sediment; two
days, red colour with metaphenylene diamine = Nitrites.
Lead broth (37° twenty-four hours).—Turbidity ; four days, very slight Н.Б.
Gelatin stab (20° twenty-four hours).—Whitish growth along stab, gas;
four days, no liquefaction; twenty-five days, gas, no liquefaction.
Gelatin streak (20° twenty-four hours).—Raised, narrow, whitish growth ;
four days, increased, no liquefaction ; twenty-five days, no liquefaction.
Gelatin shake (20° twenty-four hours).—Gas formation; four days, dotted
colonies on surface, slight turbidity; twenty-five days, no liquefaction.
Agar streak (37% twenty-four hours).—Well-marked, raised, moist-looking
growth, gas formation; four days, do.
Agar plates (37° three days).—Large white colonies; gas formation.
Blood-serum (37° twenty-four hours).—Spreading, white, dry, growth; four
days, do.
Litmus milk (37° twenty-four hours).—Marked acidity, marked gas, some
clotting; two days, marked clotting; four days, decolourised.
Potato (87° twenty-four hours).—Raised, white, dry growth; four days,
raised, marked, yellowish-brown growth.
Anerobic growth (37° twenty-four hours). — Gas formation; four days,
gas formation.
Laevulose broth 37° (twenty-four hours).—Marked gas formation, turbidity ;
four days, no gas, sediment.
= Atypical Bacillus Coli Communis (atypical because of no indol formation),
180 On Enteric Fever.
SPECIMEN 3.—Urine. Acid, no albumen.
Description.—Bacilli, rather short and thick.
Motility.—? Slightly motile, agar. Definitely slightly motile (Dextrose
broth six hours.)
Staining with carbol methylene blue. Decolorised by Gram-Weigert,
Broth (87° twenty-four hours).—Turbid, white sediment, flocculi, no gas;
four days, trace of indol; five days, trace of indol.
Peptone water (37° twenty-four hours).—Turbid, white deposit; thirteen
days, no indol,
Formate broth (87° twenty-four hours).—Turbid, flocculent deposit; four
days, turbid, no gas, slight sediment.
Dextrose broth (37° two days).—Much gas, acid.
Lactose broth (37° twenty-four hours). — Turbid, acid, much gas; four
days, no gas.
Saccharose broth (87° twenty-four hours).—Turbid, acid, plenty of gas; four
days, turbid, acid, no gas.
Glycerine broth (87° twenty-four hours).—Turbid, acid, no gas; four days,
turbid, acid, no gas.
Nitrate broth (87° twenty-four hours).—Turbid, sediment, no gas; four
days, good nitrites (with metaphenylene diamine),
Lead broth (37° twenty-four hours).—Slight H,8.; four days, good H3S. ;
thirteen days, good HAS.
Gelatin stab (20° twenty-four hours).—Small dotted colonies down stab,
growth on surface, no liquefaction ; thirteen days, no gas, no liquefaction.
Gelatin streak (20° twenty-four hours).—Good growth, raised, moist-looking
white; thirteen days, no gas, no liquefaction.
Gelatin shake (20° twenty-four hours).—Good gas bubbles all through
medium, slight turbidity; thirteen days, gas at bottom only.
Agar streak (37° twenty-four hours).—Good growth, raised, white, vigorous ;
gas formation in agar. Four days, increased.
Agar plates (37° twenty-four hours).—White colonies, gas; seven days,
large, yellowish white, moist-looking colonies.
Blood-serum (87° twenty-four hours).—Raised, very thick, yellowish white
growth; four days, increased; thirteen days, ditto.
Litmus milk (37% twenty-four hours).—Well-marked acidity, no clotting,
scum ; four days, completely clotted, decolorized ; thirteen days, do.
Potato (87? twenty-four hours).—Raised, yellowish-white, moist-looking
growth; four days, yellowish-brown, moist; thirteen days, very moist-
looking, dirty-white growth.
Anerobic growth (87° twenty-four hours).—Turbid, good gas; four days,
good gas.
= Bacillus Coli Communis.
SPECIMEN 4.—Urine (Acid. No albumin).
Description.—A short oval bacillus.
Motility.—Very slight motility (Dextrose broth).
Staining.—Faintly with C.M.B. Slightly with C.F. Decolourised by
Gram-Weigert.
Pleomorphism.—Some larger forms.
Broth (37° twenty-four hours).—Turbid, white deposit, fair gas; two days,
slight trace of gas; five days, no indol.
On Enteric Fever. 181
Formate broth (37° twenty-four hours).—Abundant gas; two days, alkaline,
no gas; four days, alkaline.
Dextrose broth (37° twenty-four hours).—Abundant gas; two days, acid,
no gas; four days, acid, no gas.
Lactose broth (87° twenty-four hours).—Abundant gas; two days, acid,
no gas; four days, acid, no gas. |
Saccharose broth (87° twenty-four hours).—Abundant gas; two days, acid,
good gas; four days, acid, no gas.
Glycerine broth (37° twenty-four hours).—Very good gas; two days, acid,
no gas; four days, acid, no gas.
Nitrate broth (87°.twenty-four hours).—Abundant gas, good nitrites with
metaphenylene diamine.
Lead broth (87° twenty-four hours).—Turbid, no H.S ; four days, good H.S.
Gelatin stab (20° twenty-four hours).—Slight growth, no gas, no liquefaction.
Gelatin streak (20° twenty-four hours).—Fair growth, no gas, no lique-
faction.
Gelatin shake (20° twenty-four hours).— Good gas bubbles, throughout
medium , no liquefaction.
Agar streak (87° twenty-four hours).—Vigorous, white, raised, growth, some
gas bubbles; two days, increased; four days, increased.
Agar plates (37° twenty-four hours).—VVhite colonies; six days, large
white colonies.
Blood-serum (37° twenty-four hours).—Dry, wrinkled-looking growth; four
days, increased.
Litmus milk (37° twenty-four hours).—Acid, entirely clotted ; two days, do,
decolourised ; four days, do.
Potato (87? twenty-four hours).—Dry, yellowish, raised dotted growth,
over whole surface; four days, growth much raised.
Anarobic growth (37% twenty-four hours). — Turbid, abundant gas; two
days, good gas; four days, good gas.
= Atypical Bacillus Coli Communis.
There is no Indol Reaction, differing thus from the typical Bacillus Coli
Communis.
SPECIMEN 5.—Urine. No albumin. Acid.
Examined after the administration of six ten-grain doses of urotropin given
three times a day for two days, and found to be sterile.
Broth 37° twenty-four hours, nil; two days, nil; four days, nil.
Glucose formate broth (ansrobically) 37° twenty-four hours, nil; two
days, nil; four days, nil.
CASE 3.—F. st. 9 years. Admitted into Mary Ward under Dr. Taylor,
on July 3rd, 1901, for headache and fever. Twelve days before admission
she had a sore throat and headache. The throat improved but the head-
ache continued, and she complained of pain in legs. She became very weak.
The motions were watery and yellow. She has became thinner, and has great
thirst. She has had fever five days. Condition on admission: Pulse 124,
temperature 102:69, respiration 28, urine 1024, acid; no albumin. Spleen
not palpable. The temperature became normal on the fifth day after ad-
mission, and continued normal until the seventeenth, when it rose to 108:27.
(Interval=fourteen days). On the eighteenth day Widal’s reaction was
present. On the twenty-second, spots appeared on the abdomen, this being the
182 On Enteric Fever.
sixth day after the temperature rose; the spleen becamie palpable; on the
twenty-third day more spots appeared. The temperature rose to 104:69, and
patient was sponged. On the twenty-fifth day, being the thirty-fifth day of
the disease, including relapse interval, the urine was examined bacteriologi-
cally, and also on the thirty-ninth day of the disease.
July 28th. There are over thirty spots to-day.
July 30th. Some of the spots have faded, but there are still a large number.
Bowels constipated. Glycerine enema.
August 1st. Most of the spots have faded. Temperature keeps below
normal.
August 5th. Urine 1020, faintly acid. “. blood and pus present,
Urotropin er bəh F gr. v.
Ammon. Beng.... des = gr. v.
Tinct. Hyoscyam. ... ee m x.
Sp. Chlorof. ... ER m m v.
Inf. Uve Ursi ad er ид z ss. bis die.
The urine unfortunately was not examined bacteriologically at this time.
August 8th. There are no spots. Temperature normal. The urine became
normal after the exhibition of urotropin. Glycerine enema.
August 10th. Patient is going on well; temperature has not risen above
99° for nine days. Pulse 60, respiration 20. There are no spots.
August 12th. Condition is improving. The bowels are rather constipated.
The urine is normal. Temperature 96:4?—98:6?. There are no spots.
August 21st. On full diet. Gets up after tea.
August 24th. Patient discharged.
July 12th. Widal reaction 50 per cent. = + 5 per cent. = + 05 per
cent. = +.
SPECIMEN 1.
G.F.B. 37? (anerobically). Two days, nil.
Gelatine plate. Nil.
Two broth tubes added to flask at 37%, Twelve hours, nil; three days, nil.
— urine sterile.
SPECIMEN 2.
Hanging drop. Nil.
G.F.B., 37°. Twenty-four hours ; turbidity.
Broth, 87”, Twenty-four hours; turbidity.
Agar plates, 37°, Twenty-four hours; a few white colonies.
C.M.B. Staphylococci only. |
Gram-Weigert. Staphylococci present.
Staphylococci only.
CASE 4.—M., æt. 21 years. Admitted into Philip Ward under Dr. Taylor,
on July 26th, for diarrhoea. .
For three weeks before admission he suffered from headache. He did his
work nevertheless. For seven days before admission patient was feeling very
weak, and for three days had suffered with diarrhea.
On admission, he was pale and drowsy, with signs of much weakness,
with a foul tongue and breath. The abdomen was full, but the spleen could
not be felt. There was an apical systolic bruit. There were no spots. The
urine was normal. There was diarrhoea, The blood gave the Widal reaction,
On Enteric Fever. 183
The pyrexia continued for rather over three weeks and then dropped to
normal, the patient being eventually discharged convalescent.
Three examinations of the urine were made, on each occasion stapbylococci
only were found,
July 27th. Widal’s reaction, 50 per cent. = +. 5 percent. = +. 0°5 per
cent. = + O.
H.D. Urine, nil.
Broth, 37°. Twenty-four hours ; cocci in pairs.
G.F.B., 27°. Twenty-four hours; no gas ; slight turbidity (anzrobically).
Agar plates, 37°. Twenty-four hours; large white colonies.
C.M.B. Staphylococci only.
Planted agar tube from agar plate. Twenty-four hours.
H.D. Cocci; C:M.B., staphylococci.
Gram-Weigert. Staphylococci (stain well).
Staphylococci only present.
SPECIMEN 2.
SPECIMEN 1.—Urine. No albumin.
H.D. Urine, nil.
Broth, 37”. Twenty-four hours, turbid , no gas.
G.F.B., 37%. Twenty-four hours; no gas; cloudy; slight white sediment.
H.D., cocci only. . :
Agar plate, 37°. Twenty-four hours; a large number of large and small
white colonies. G.M.B. Staphylococci only.
Staphylococci only present.
SPECIMEN 3.—Urine. No albumin.
H.D. Urine, nil.
Broth, 37°. Twenty-four hours; turbid; no gas; H.D., cocci only.
G.F.B., 31°. Twenty-four hours ; slightly turbid; no gas.
Agar plate, 57°. Twenty-four hours ; dotted white colonies.
C.M.B. Staphylococci only.
Staphylococci only present.
CASE 5.—F., æt. 32 years, married. Admitted into Miriam Ward under
Dr. Washbourn, for continued fever and diarrhcea, on August 15th, 1901.
Thirteen days before admission she was attacked with severe pains in
the abdomen, and vomiting. On the day following diarrhea set in, and
has continued since. She has also suffered from headache, pain in the back
and limbs, and weakness. On August 12th a specimen of her blood showed a
marked Widal reaction when examined at the Jenner Institute. On admis-
sion: Temperature 103:2%, pulse 124, respiration 36. Tongue furred, face
flushed, abdomen full, with a few faint rose-coloured spots. The spleen is
not palpable. Pulse rapid, small, soft, regular. Heart-sounds normal.
Many non-consonating ráles to be heard in the chest. The pulse became
rather feeble, and she was ordered brandy. On August 17th the spleen
could be felt. The pulse is still feeble. On August 18th a few fresh spots
were noticed on the abdomen. Diarrhoea continued, and Mist. Ори Acida was
ordered. |
The diarrhoea ceased, and patient gradually improved, and was discharged
convalescent on September 27th. Bacteriological examinations of the urine
were made on five occasions. On the twenty-fifth, twenty-seventh, thirty-
fourth, forty-first and fifty-fifth day of the disease. Twice it was found to be
quite sterile. On three occasions staphylococci only were found.
184 On Enteric3 Fever.
SPECIMEN 1.—Twenty-fifth day.
H.D., urine, nil.
Broth, 37° twenty-fours, nil. Four. days, nil.
G.F.B. (anzrobic growth) 37° twenty-four hours, nil, Two days, nil. Four
days, nil.
SPECIMEN 2.—Twenty-seventh day.
Broth, 87? twenty-four hours, nil. Turbidity.
Glucose formate broth 87? twenty-four hours, nil. Three days, turbidity.
Agar slope, twenty-four hours, nil.
C.M.B., staphylococci only present.
SPECIMEN 3.—Thirty-fourth day.
H.D., nil.
Broth, 37°, twenty-four hours, nil. Two days, white sediment, clear fluid.
G.F.B., 37°, twenty-four hours, nil. Two days, turbid.
Agar plate, 37°, twenty-four hours, nil. Two days, white colonies.
Planted agar plates from agar. Small round white and yellow colonies.
Staphylococci only.
SPECIMEN 4.—Forty-first day.
H.D., urine, nil.
Broth, 37°, twenty-four hours, nil. Two days, nil.
G.F.B., 37°, twenty-four hours, nil. Two days, nil.
Agar plates, twenty-four hours, nil.
The urine is sterile.
SPECIMEN 5.—Fifty-fifth day. Urine. No albumin.
H.D., urine, nil.
G.F.B., 37°, twenty-four hours. Turbid.
Broth, 37°, twenty-four hours. H.D. cocci.
Agar plate, 37°, twenty-four hours. White colonies. H.D. cocci.
Planted agar tube from agar plate. Twenty-four hours, very sticky growth
of small white dotted colonies; vigorous growth. H.D. nil. C.M B. nil.
Planted a broth tube from agar tube as this so sticky that no organisms would
adhere to cover slip. Planted gelatin stab 20?, three days. No liquefaction.
C.M.B. cocci only. H.D. cocci only, chiefly in pairs. Planted broth 37°,
seven days. H.D. cocci only.
CASE 6.—M., ext. 27 years. Admitted into Stephen Ward under care of
Dr. Pitt, on August 15th, 1901, for pain in the head and abdomen. For three
weeks previously he had suffered from pain in the head and the back of neck.
He was weak, and suffered from giddiness.
On admission, temperature 103:2?, pulse 72. There is diarrhoea. There
are two or three rose-coloured spots on abdomen which disappear on pressure.
The tongue and breath are foul. The spleen cannot be felt. There are a few
ráles and rhonchi to be heard in the chest.
August 16th. More spots appearing.
August 17th. Temperature 103°6°. Patient gradually improved and was
discharged convalescent on September 12th.
A bacteriological examination of the urine was made on two occasions. On
each occasion staphylococci only were found.
August 17th. Widal reaction.
50 per cent. = + 5 per cent. = + 0:5 per cent. = + 4.
On Enteric Fever. 185
SPECIMEN 1.
H.D. Urine, nil.
Broth, 37°.
G.F.B., 37%. Twenty-four hours; H.D., cocci only, in short chains.
Planted agar from G.F.B. Twenty-four hours; small white and yellow
colonies ; cocci only.
Centrifugalized some (original) urine; planted broth; twenty-four hours;
white sediment ; staphylococci only. I
Planted three gelatine plates from broth; twenty-four hours, nil; three
days ; staphylococci only.
Staphylococci only present.
SPECIMEN 2.
H.D. Urine, nil.
G.F.B., 27”. Twenty-four hours ; slight turbidity ; sediment; no gas; two
days, do.
Broth, 377. Twenty-four hours; turbidity , white sediment; two days, do.
Agar plate, 37°. Twenty-four hours; numerous small white colonies ;
H.D., cocci.
Stained G.F.B. and agar plate growths with C.M.B.=staphylococci only.
CASE 7.—M., æt. 29 years. Admitted into John Ward under Dr. Wash-
bourn on August 15th, 1901, for pyrexia and albuminuria.
Seven weeks ago he had severe diarrhcea, which lasted about a month.
The motions were green. He had also slight headache. He was kept on
milk and soda water for a fortnight, and after that on custards. He was told
that he had gastritis. He remained in bed for three weeks, and, after that
he did no work for three weeks as he felt very weak. A week ago he caught
a chill and went to see his doctor, who took his temperature and sent him to
bed. He was told he had a relapse, and he was sent to Guy's Hospital after
having been in bed again for a week, during which he felt weak, but was
otherwise feeling well.
On admission, the pulse was 108, temperature 100:27, A few raised rose-
red spots which fade on pressure are present on the abdomen. The heart is
normal. Räles and rhonchi can be heard in the chest. The abdomen is not |
distended. The spleen is palpable. The pharynx is injected and sore. Ton-
sils swollen and covered with mucus. No diarrhea. Urine 1015; Neutral;
albumin, phosphates, and urates present. The blood was negative to the
Widal reaction.
August 16th. The spots have disappeared. No suspicious new ones have
appeared. Stools liquid, brown, not offensive. Diet, milk and soda water,
brandy.
August 17th. A small quantity of blood in motions this morning.
August 18th. Temperature 103°, sponged.
August 19th. Pulse 120, regular, weak. No definite spots. Spleen
palpable.
August 23. Sponging does not reduce temperature. Quinine, grs. xx. This
had apparently a marked effect. A trace of blood in motions. The blood is
still negative to Widal's reaction. -
August 26th. Temperature 104% Great heemorrhages from bowels this
morning, and he was much paler. Morphia was administered, and later lead
186 On Enteric Fever.
and opium, and tannic acid, ice compresses to abdomen. "These had, how-
ever, no effect, and patient died.
Post-mortem examination.—Spleen much enlarged. Ulceration of small
and large intestine. Iron found free in liver.
August 16th. Widal reaction.
50 per cent. = 0. $ percent. = 0. 0:5 percent. = 0.
Spleen.
Description.—S8hort bacilli.
Motility.—Fair motility.
Staining.—Fairly well with C.M.B. Decolorised by Gram-Weigert.
Broth.—(37° twenty-four hours).—Turbidity, no gas; four days, no indol.
Peptone water (37° twenty-four hours).—Turbidity, no gas; four days, do. ;
five days, no indol.
Formate broth (37° twenty-four hours).—No gas; four days, no gas.
Dextrose broth (87° twenty-four hours).—Acid, turbid, no gas; four days, do.
Lactose broth (37° twenty-four hours).—No gas; four days, do.
Saccharose broth (87° twenty-four hours).—No gas; four days, do.
Glycerine broth (37° twenty-four hours).—No gas; four days, do.
Nitrate broth (37° twenty-four hours).—Turbid, sediment, no gas; two days,
abundant nitrites (with metaphenylene diamine).
Lead broth (37° twenty-four hours).—Turbidity, slight H3S.; four days, do.
Gelatin stab (20° twenty-four hours).—Growth along stab; four days, do.,
some slightly spreading growth on surface.
Gelatin streak (20° twenty-four hours).-—Slight greyish white growth; four
days, do.
Gelatin shake (20° twenty-four hours).—Turbid, no gas; four days, no gas.
Agar streak (37° twenty-four hours).—Slight, white growth; four days,
increased slightly but not vigorous.
Blood-serum (87° twenty-four hours).—Slight white growth ; four days, do.
Litmus milk (87° twenty-four hours).—Nil; two days, distinctly acid, no
clotting; four days do., no clotting.
Potato (37° twenty-four hours).— Moist-looking growth; four days, do.,
a transparent film.
Anerobic growth (37° twenty-four hours).—Turbid, no gas; four days, no
gas, slightly turbid.
Gruber's reaction.—50 per cent. = +. 5 per cent. = ++. ‘5 percent. = +.
Мотк.— Ехрегипепб done with a twenty-four hours’ broth culture grown
from gelatine, using a serum that had previously reacted perfectly with a
known bacillus typhi abdominalis.
= Bacillus Typhi Abdominalis.
Bacteriological examination of urine from post-mortem bladder.
In the examination of the urine from the post-mortem bladder, the surface
of the bladder was sterilized with a searing iron, and an incision made with a
sterile knife through the bladder wall. Some urine was now drawn up by
means of a sterilized pipette, and transferred to a, sterilized flask.
Broth, 37°. Twenty-four hours ; turbid ; flocculent.
G.F.B., 37”. Twenty-four hours ; turbid; flocculent.
Agar, 379. Twenty-four hours; small, white, colonies dotted over the
surface.
On Enteric Fever. 187
Staphylococci only were found in these.
Bacteriological examination of kidney.
Agar, sloped, 37°. Twenty-four hours, nil; two days, nil; four days, nil.
Broth, 37°. Twenty-four hours, nil; two days, nil ; four days, nil.
G.F.B,, 37°. Twenty-four hours, nil; two days, nil; four days, nil.
The kidney is sterile.
Histological examination of a section of the kidney stained with carbol
thionin blue shewed the absence of any organisms.
CASE 8.—F., æt. 3 years and 10 months. Admitted under the care of
Dr. Taylor, into Mary Ward, on August 26th, for diarrhoea. Four days ago
she was taken ill with diarrhea. There has been no vomiting. She
has been drowsy, and has not appeared to be in pain. On admission,
temperature 103°, pulse, 120, respiration 32. Heart-sounds normal. Lungs
normal. The abdomen is full and there are some raised spots upon it, There
ie diarrhoea.
August 27th. Temperature 104.4°. More spots have appeared on the
abdomen.
August 29th. Temrerature 103:6. The blood gives a well-marked Widal
reaction. 50 per cent. = О. 5 percent. = +. 0:5 per cent. = O.
September 2nd. Temperature 104°. Abdomen tense and rather full.
September 5th. Temperature 102:8”. Diarrhoea still continues. Abdomen
less distended. Spleen not palpable.
September 8th. Diarrhea less.
September 14th. Diarrhoea almost disappeared. Temperature 101:49,
September 18th. Patient much improved. Spleen not palpable.
October 1st. Bowels constipated. Enemata. Temperature 99°
October 3rd. Farinaceous diet.
Bacteriological examinations of the urine were made on five occasions, on
the eighth, thirteenth, twentieth, thirtieth, and forty-seventh days of the
disease respectively. The first examination shewed an atypical colon bacillus
to be present in pure culture. The second examination shewed the presence
in pure culture of a bacillus, similar to the bacillus enteritidis of Gärtner, but
differing from it in that no alkalinity of milk was produced. The third
examination shewed the presence of the bacillus typhi abdominalis in pure
culture. In the fourth examination staphylococci were found, and a bacillus
which was probably proteus vulgaris, as it caused liquefaction of gelatine
among other reactions, thus differentiating it at once from the typhoid and
coli groups. The fifth examination shewed the presence of the bacillus coli
communis and the bacillus proteus vulgaris.
SPECIMEN 1.—Urine. No albumin. Catheterized, with aseptic precautions.
Description.—A bacillus.
Motility.—Fair motility.
Staining with C.M.B. Decolorised by Gram-Weigert.
Broth (37° twenty-four hours).—Turbidity, no gas; two days, turbidity,
sediment, no gas; six days, good indol.
Peptone water (37° twenty-four hours).—Turbidity ; six days, good indol.
Formate broth (37° twenty-four hours).—Marked gas formation ; two days,
no gas, no colour change ; six days do.
Dextrose broth (37° twenty-four hours).—Good gas formation, acid; two
days, no gas, acid; six days, do.
VOL. LVI. 16
188 On Enteric Fever.
Lactose broth (87° twenty-four hours).—Good gas formation, acid ; two days,
no gas; six days, acid.
Saccharose broth (87° twenty-four hours).—No gas, no colour change,
slightly turbid.
Glycerine broth (37° twenty-four hours).—Nil; two days, good gas forma-
tion, slightly acid ; six days, no gas, acid.
Nitrate broth (37° twenty-four hours).—Marked turbidity, gas, good nitrites
(with metaphenylene-diamine).
Lead broth (37° twenty-four hours).—Marked turbidity, no H,S; two days,
slight H48; six days, do.
Gelatin stab (20° twenty-four hours).—Slight growth aloug stab, no gas ;
two days do.; six days, no liquefaction, growth on surface.
Gelatin streak (20° twenty-four hours).—Slight growth; two days, trans-
parent growth, irregular edges, no liquefaction ; six days do.
Gelatin shake (20° twenty-four hours).—Turbidity, some gas bubbles, no
liquefaction ; two days do. ; six days do., cloudy.
Agar streak (37° twenty-four hours).—Vigorous, spreading greyish white
growth; six days do.
Blood-serum (37° twenty-four hours).—Well marked, raised white growth ;
two days do; six days do.
Litmus milk (37° twenty-four hours).—Marked acidity, no clotting; six
days, no clotting; twelve days, no clotting.
Potato (379 twenty-four hours).—Very slight whitish growth; two days do. ;
six days, raised yellowish white growth.
Anerobic growth (37° twenty-four hours). — Turbidity, marked gas
production.
= Atypical bacillus coli communis.
Differs from bacillus coli communis in that it does not clot milk.
SPECIMEN 2.—Urine.
Description.—A bacillus.
Motility.—Very motile.
Staining.—Stains fairly with C.M.B. Decolorised by Gram-Weigert.
Pleomorphism.—Longer and shorter forms.
Broth (37° twenty-four hours).—Marked turbidity, white deposit on sides,
sediment, no gas; two days, do.; four days, no indol.
Peptone water (37° twenty-four hours).—Slight turbidity, sediment, no gas ;
two days, do.; four days, do.; ten days, no indol.
Formate broth (37° twenty-four hours), —Slight turbidity, sediment, marked
gas formation, no acidity ; two days, no gas, alkalinity; four days, do.
Dextrose broth (37° twenty-four hours). — Sediment, acidity, marked gas
formation; two days, no gas; four days, do.
Lactose broth (37° twenty-four hours).—Sediment, acidity, gas formation ;
two days, no gas; four days, do.
Saccharose broth (37° twenty-four hours).—No gas, no change; two days,
slight turbidity; four days, do.
Glycerine broth (37° twenty-four hours).—Distinctly acid, no gas; two days,
do.; four days, do.
Nitrate broth (37° twenty-four hours).—Turbidity, sediment, no gas; two
days, do., good nitrites with metaphenylene diamine.
Lead broth (37° twenty-four hours).—Turbidity, very slight H,S.; two days,
fair H3S. ; four days, good HS.
On Enteric Fever, 189
Gelatin stab (20° twenty-four hours).—Slight growth along stab none on
surface; four days’ growth spreading on surface.
Gelatin streak (20° twenty-four hours). — Semi-translucent growth with
irregular edge, no liquefaction; two days, do.; four days, good growth.
Gelatin shake (20° twenty-four hours).—Slight turbidity, good gas bubbles,
no liquefaction; two days, do.; note that gas bubbles are not within half an
inch of surface; four days, growth on surface.
Agar streak (37° twenty-four hours).—Vigorous, yellowish white growth ;
two days, do.; four days, spreading growth on surface.
Agar plates (37° twenty-four hours).—Whitish colonies.
Blood-serum (87° twenty-four hours). — Raised, yellowish white growth
two days, do.; four days, do.
Litmus milk (37° twenty-four hours).—Marked acidity, no clotting; four
days, no clotting; ten days, no clotting; thirty days, no clotting.
Potato (37° twenty-four hours).—Very slight growth; two days, do.; four
days, thick raised growth. |
Anerobic growth (37° twenty-four hours). — Turbidity, very marked gas
formation; two days, do.; four days, still some gas; ten days, no gas,
sediment.
This bacillus is similar to the bacillus enteritidis of Gärtner but differs
from it in that no alkalinity of milk is produced.
SPECIMEN 8.— Urine.
Description.—A short bacillus, slightly motile (agar).
Staining.—Stains faintly with C.M.B., well with C.F., decolorised with
Gram-Weigert. |
Pleomorphism.—Longer and shorter forms.
Broth (37° twenty-four hours).—Slightly turbid, no gas; three days do;
four days, no indol.
Peptone water (37° twenty-four hours).—No gas; three days, nil; six days,
no indol.
Formate broth (37° twenty-four hours).—Very slightly turbid, no gas;
three days, no gas, slightly alkaline; eight days do.
Dextrose broth (37° twenty-four hours).—Acid, no gas, slightly turbid
three days do.
Lactose broth (87? twenty-four hours).—Nil; two days, slightly red, no
gas; six days, acid, no gas.
Saccharose broth (37° twenty-four hours).—Nil, no gas; three days, nil
six days, nil.
Glycerine broth (37% twenty-four hours).—No gas; three days, nil, six
days, nil.
Nitrate broth (37° twenty-four hours).—Slight nitrites (with metaphenylene
diamine). |
Lead broth (87° twenty-four hours).—No HAS, three days, no HS; six
days, no HS; thirteen days, no H.S ; twenty-one days, no H.S.
Gelatin, stab (20° twenty-four hours).—Nil, no gas; six days, very slight
growth down stab ; ten days, no gas, no liquefaction.
. Gelatin streak (20° twenty-four hours).—Very slight growth ; six days do.,
no gas; ten days, no gas; no liquefaction.
Gelatin shake (37° twenty-four hours).—No gas, nil; six days, nil, no gas;
ten days, no gas, no liquefaction,
190 On Enteric Fever.
Agar streak (37° twenty-four hours).—Slight white growth, dotted colonies ;
six days, do.
Blood-serum (87° twenty-four hours).—Very slight growth, dotted colonies ;
three days, do; six days, do.
Litmus milk (87° twenty-four hours).—Acid, no clotting; six days, do. ;
eight days, no clotting ; twenty-one days, no clotting.
Potato (37° twenty-four hours).—Nil; six days, nil; eight days, very slight
growth.
Anerobic growth (87° twenty-four hours).—Slight turbidity, no gas; three
days, do; six days, clear, sediment.
= Bacillus typhi abdominalis.
SPECIMEN 4.—Urine. No albumin.
20th September, 1901. H.D. Urine, nil.
Glucose formate broth, 87°. Twenty-four hours; turbid, gas, white flocculi.
Broth, 37°. Twenty-four hours; turbid, no gas, flocculi.
Agar plate, 87”. Twenty-four hours; a few white colonies, and an uniform
growth spreading over plate.
23rd September, 1901. C.M.B. agar. Staphylococci only.
C.F. broth. Bacilli, many well stained. Made three agar plates from
broth.
24th September, 1901. Rather short bacilli, very motile, stained with
C.M.B.
Planted agar tube, 37°. Twenty-four hours; growth simulates that of
proteus.
Formate broth, 37°. Gas, slight acidity.
. Gelatin slope, 20°. Twenty-four hours; pure culture; liquefaction of
gelatin; this excludes the coli and typhoid groups. Probably proteus vulgaris.
The organism was not further worked out.
l SPECIMEN 5.— Urine.
Description.—Short thick bacilli.
Motility. —Slightly motile.
Staining.—Fairly stained with C.M.B., well stained with C.F., decolorised
with Gram-Weigert.
Pleomorphism.—Short oval bacilli, some longer forms.
Broth (87° twenty-four hours).—Turbid, sediment, no gas; three days, do. ;
five days, good indol.
Peptone water (87° twenty-four hours).—Turbid, no gas; two days, turbid,
no gas.
Formate broth (37° twenty-four hours).—Turbid, gas formation, not acid ,
two days, no gas; four days, turbid, alkaline; no gas.
Dextrose broth (37° six hours).—Acid, turbid, abundant gas; twenty-four
hours, no gas.
Lactose broth (37° twenty-four hours).—Acid, gas; two days, acid, no gas;
three days, acid, fair gas; four days, acid, no gas. :
Saccharose broth (87° twenty-four hours).—Slightly acid, no gas; two days,
acid, very slight gas ; three days, acid, very slight gas; four days, do.
Glycerine broth (37° twenty-four hours).—Turbid, no gas; two days, fair
gas; three days, good gas; four days, acid, good gas.
Nitrate broth (37° twenty-four hours).—Turbid, good nitrites (with meta-
phenylene diamine).
On Entertc Fever. 191
Lead broth (87? twenty-four hours).—Turbid, no H4S; five days, good
HS. *
Gelatin stab (20° twenty-four hours).—Slight growth down stab, some
spreading on surface, no gas, no liquefaction ; nine days, do.
Gelatin streak (20° twenty-four hours).—Some white growth, no gas, no
liquefaction ; three days, no gas, no liquefaction ; nine days do.
. Gelatin shake (20° twenty-four hours).—Three days, turbid, no gas, no
liquefaction ; nine days do.
Agar streak (37° two days).—Vigorous, raised, white growth.
Agar plates (37° two days).—White colonies.
Blood-serum (37° twenty-four hours).= Raised, whitish growth; two days,
increased.
Litmus milk (37% twenty-four hours).—Marked acidity, milk clotted ; two
days, marked acidity, milk entirely clotted ; three days, do.
Potato (37° twenty-four h urs).—Moist brownish growth; two days, moist
brownish growth ; four days, do.
Anaerobic growth (37° twenty-four hours).—Very abundant gas, turbid; two
days, turbid, gas; three days, turbid, no gas.
= Bacillus coli communis.
Gruber’s reaction.—This reaction was carried out with a twenty-four hours’
old broth culture grown from gelatin. The serum used gave the following
result when used with B.T.A. for Widal’s reaction :—
5 per cent.=+ +. 0:5 per cent.=+ +.
On carrying out Gruber’s reaction with the above organism, a completely
negative reaction was given. Thus :—
50 per сепб. = О. 5 рег сепб. = О. 0°5 per cent.= O.
SPECIMEN 5 (2).
Gelatin stab (twenty-four hours).—Proteus-like growth; two days, lique-
faction of gelatine.
Formate broth (twenty-four hours).—Good gas; four days, alkaline.
Litmus milk (twenty-four hours).—Acid; no clotting; three days, precipi-
tation of casein.
Agar (twenty-four hours).—Spreading ; greyish white growth.
= Bacillus proteus vulgaris.
CASE 9.—M., set. 16 years. Admitted into John Ward under Dr. Shaw, on
August 31st, for pyrexia and headache. ;
For a week previous to admission he had felt weak and giddy, and had
suffered from headache. He had kept at his work until three days before
admission. No epistaxis. No diarrhoea.
On admission. The abdomen was not distended, the spleen was not
palpable. There was no diarrhea, the bowels being rather inclined to be
constipated. Pulse 120. Heart and lungs normal. Temperature 108-2^.
September 3rd. A partial Widal reaction was obtained. 50 percent. = —.
9 per cent. = +3. ‘5 percent. = +4.
September 5th. A complete Widal reaction was obtained. 50 per
cent. = ppt. 5 per cent. = +. ‘5 percent. = +.
The temperature fell to normal at the end of the second week, and patient
made an uninterrupted recovery. m
192 ` On Enteric Fever.
A bacteriological examination of the urine was made on the thirteenth,
eighteenth, ‘twenty-first, twenty-fourth, twenty-seventh, and fortieth day of
the disease.
On each occasion cocci only were found, these in most instances being
staphylococci.
H.D. Urine, nil.
Broth, 37%. Twenty-four hours; white sediment; white growth along sides
of tube.
G.F.B., 372. Twenty-four hours; no gas; slight white sediment. H.D.,
cocci. | |
Agar plate, 37°. Twenty-four hours; white colonies ; cocci only, chiefly in
groups.
C.M.B. Staphylococci.
Staphylococci only present.
SPECIMEN 2.— Eighteenth day.
September 10th, 1901. H.D., nil.
G.F.B., 37°. Twenty-four hours, nil; two days, turbid; no gas; white
sediment.
Broth, 37°. Twenty-four hours, nil; two days, turbid; no gas; white
sediment.
Agar plate, 37°. Twenty-four hours, nil ; white colonies.
September 12th, 1901. G.F.B. H.D,, cocci.
Agar plate, C.M.B. Staphylococci only.
Staphylococci only.
SPECIMEN. 3—Twenty-first day. Urine. No albumin.
September 18th, 1901. H.D. Urine, nil.
G.F.B., 37? Twenty-four hours, turbid ; white deposit on sides and bottom
of tube.
Broth, 37°. Twenty-four hours, turbid ; white deposit on sides and bottom
of tube. H.D., cocci.
Cocci in short chains with C.F.
Planted agar tube. Twenty-four hours. H.D., cocci.
C.M.B. Staphylococci.
SPECIMEN 1.
Staphylococci only.
SPECIMEN 4.—Twenty-fourth day of disease. Urine, no albumin.
September 16th, 1901. H.D. Nil.
G.F.B., 37°. Twenty-four hours, nil; two days, turbid; no gas; cocci.
Broth, 37°. Twenty-four hours, nil; two days, turbid ; no gas.
Agar plate, 37°. Twenty-four hours, nil; two days, white colonies.
C.M.B. from agar plate. Staphylococci only.
Staphylococci only.
SPECIMEN 5.—Twenty-seventh day of disease.
September 19th, 1901. H.D. Urine, nil.
G.F.B., 379. Twenty-four hours, nil; two days, turbid ; slight gas.
Broth, 37°. Twenty-four hours, nil ; two days, turbid ; no gas.
September 20th. Agar plate, 37°. Twenty-four hours ; a few white colonies.
H.D. Broth; cocci only.
C.M.B. Staphylococci only.
Staphylococci only present.
On Enteric Fever. 193
SPECIMEN 6.—Fortieth day of disease. Urine.—Slightly acid; excess of
phosphates ; no albumin.
October 2nd, 1901. G.F.B., 37°. Twenty-four hours, clear; no gas. H.D.,
Cocci chiefly in pairs.
Broth, 37°. Twenty-four hours. Slightly turbid; no gas.
C.M.B. Cocci only.
H.D. Cocci only, chiefly in pairs.
Agar, 37°. Twenty-four hours, no growth ; thirty-six hours, nil.
October 4th. G.F.B. H.D., repeated ; cocci only, chiefly in pairs.
C.M.B. Cocci only.
CASE 10. M., et. 11 years. Admitted into Philip Ward under the care
of Dr. Taylor, on August 28th, 1901, for headache, weakness, and pain in
right groin. He was affected with headache for nine days before
admission.
On admission, temperature 100:2?, pulse 88, respiration 24. He is pale
and drowsy and lies flat on his back. Tongue clean in middle but furred at
edges. There is pain in the left groin, where the glands are enlarged. The
bowels are regular, there is no abdominal tenderness. The spleen is palpable.
A few rose-coloured spots are present on the right side of the abdomen.
Respiratory system normal. Circulatory system normal. Urine 1010, neutral,
otherwise normal.
August 30th. Patient feels well; spleen palpable.
September 10th. Temperature falling every day; the spleen is not palpa-
ble; no spots have been seen for a week.
September 16th. Temperature 103°, pulse 182, respiration 24. He
had pain in his abdomen yesterday, and again this afternoon.
September 17th. Pain in the abdomen immediately after taking milk. There
is no distension, and the abdomen moves well with respiration. The recti
contract well and without pain when patient moves.
September 21st. There is no abdominal pain; no distension.
September 24th. Patient improving, temperature 1009.
October 2nd. Temperature 99°4°; spleen not palpable. Urine 1014, neutral,
no albumin or sugar, no sediment, a little mucus.
October 4th. Temperature 99°.
October 7th. Farinaceous diet.
October 12th. Full diet.
The urine was examined bacteriologically on five occasions. On each
of these staphylococci only were found. The examinations were made on
the twenty-fifth, twenty-ninth, thirty-ninth, forty-seventh, and fifty-eighth
day of the disease.
October 16th. Widal reaction.
50 per cent. = O. 5 percent. = O. 0-5 percent. = O,
SPECIMEN 1.
12th September, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours; turbid; no gas; white deposit; cocci C.F.
Broth, 37°. Twenty-four hours; slight white sediment; no turbidity.
Agar p'ate, 37°. Twenty-four hours; small white colonies; H.D., Staphy-
lococci.
194 On Enteric Fever.
18th September. Planted agar plates from G.F.B. Two days, small,
round, raised white colonies on plates; H.D., cocci only.
C.M.B. Staphylococci only.
SPECIMEN 2.
16th September, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours; very turbid; very slight gas; H.D., cocci.
Broth, 37°. Twenty-four hours; very small white dotted colonies.
Agar plate, 37°. Twenty-four hours ; small white colonies.
C.M.B. Staphylococci only.
C.F. ‘Staphylococci only.
SPECIMEN 3.
26th September, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours; very turbid; no gas; white sediment.
H.D. Cocci only, in groups.
C.M.B. Staphylococci only.
Broth, 8979. Twenty-four hours; turbid; no gas.
Agar plate. Twenty-four hours; white colonies.
C.M.B. Staphylococci only.
SPECIMEN 4.
Urine.—Neutral, cloudy; no albumin; excess phosphates.
5th October, 1901. H.D. Urine, nil.
G.F.B., 37%. Twenty-four hours; turbid; flocculent deposit; no gas;
H.D., cocci only; C.M.B., staphylococci.
Broth, 37°. Twenty-four hours ; turbid ; yellowish white deposit; no gas
H.D., cocci only, in pairs and masses.
Agar plate, 37°. 'i wenty-four hours; small colonies; H.D., cocci only.
Staphylococci only.
SPECIMEN 5. Urine.—Acid, no albumin ; excess phosphates.
15th October, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours; turbid; no gas; H.D., cocci only in
groups; C.M.B., staphylococci only.
Broth, 37°. Twenty-four hours; turbid; no gas; H.D., cocci only, C.M.B.
Staphylococci only.
Agar, 877. Twenty-four hours; small white colonies; two days, increased ;
H.D., cocci only, in groups.
Staphylococei only.
Case 11.—M., æt. 25 years. Admitted on September 11th, 1901, into
Stephen Ward under care of Dr. Bryant, for diarrhosa.
One month previous to admission he complained of general lassitude,
headache, diarrhosa, and pain in right side of abdomen. He vomited once.
The diarrhoea continued in spite of treatment; the number of stools was six
or eight a day, in character they were liquid and light yellow. He quite
lost his appetite and has been taking milk only. He has been growing
steadily weaker and has lost flesh considerably.
On admission, temperature 98°, pulse 72, respiration 24. Patient is thin,
but the abdomen is moderately full. The spleen is palpable; the diarrhea
is continual. The abdomen is not generally tender, but there is tenderness
in one spot in the left iliac region. There are no spots. The tongue is clean
in middle but furred at the sides. The breath is not foul. There is a rough
On Enteric Fever. 195
systolic bruit over the mitral area. He has a slight cough. The urine
is normal.
September 17. The blood gives a good Widal reaction. He is much
better, the diarrhoea is less, temperature is normal.
September 20th. Temperature 100°2°.
September 22nd. Temperature 102:2°.
September 26th. He is suffering from a relapse; the temperature is
keeping up. The diarrhoea, however, has ceased.
September 27th. There is still a little fulness of the abdomen, which is
slightly tender on pressure, especially on the right side.
October 3rd. He is constipated but otherwise is going on very well.
Temperature 101°.
October 6th. Temperature 101°. He feels well; there are no spots.
October 8th. Temperature 99°. There is still constipation.
October 10th. Patient is going on very well.
September 17th, 1901.
50 per cent. = +. Spercent. = +. ‘5 percent. = +.
A bacteriological examination of the urine was made on three occasions.
On the first occasion staphylococci and para-typhi abdominalis bacilli were
found.
On the second occasion staphylococci only were found. On the third,
staphylococci and a bacillus approaching the bacillus proteus vulgaris in
reactions.
>
SPECIMEN 1.— Urine, normal.
H.D. Urine, nil.
G.F.B., 37°. Eighteen hours; turbid ; no gas; H.D., cocci in short chains;
bacilli, slightly motile.
Broth, 37°. Eighteen hours; turbid, flocculent growth on sides of tube;
no gas.
Agar plate, 37°. Eighteen hours; white colonies ; staphylococci only.
September 18th, 1901. Made three agar plates ; twenty-four hours; white
colonies.
September 19th. H.D. cocci; C.M.G., short bacilli; C.F., do.
Planted agar tube and glucose formate broth (ansrobically) from agar plate.
September 20th. Short bacilli and cocci in chains of three or four in
glucose formate broth.
Short oval bacilli in pure culture on agar; two small white colonies.
Staphylococci found plus bacilli.
These bacilli were planted on agar, and finally worked fully out as given
hereunder. |
SPECIMEN 1.— Urine (normal).
Description.—Short oval bacilli, thick, many in pairs jointed together.
Motility.—Slightly motile (agar), slightly motile (dextrose broth six hours).
Staining.—Stain well with C.M.B., faintly with C.F., decolorised by Gram-
Weigert.
Broth (37° twenty-four hours).—Turbid, no gas; three days, do, white
sediment; five days, no indol.
Peptone water (37° twenty-four hours).—Nil; three days, nil; five days,
scum on surface, slight turbidity ; twenty-one days, no indol.
Formate broth (37° twenty-four hours).—Slight turbidity, no gas, deposit,
bleaching, slight reddening; thres days, reddened, turbid, no gas; five
days, do.
196 On Enteric Fever.
Dextrose broth (87° twenty-four hours).—Two days, acid, no gas.
Lactose broth (87° twenty-four hours).—Turbid, no gas, bleaching; three
days, gas, acid, turbid; five days, do., no gas.
Saccharose broth (37° twenty-four hours).—Slightly turbid, no gas; three
days, acid, no gas; five days, do.
Glycerine broth (37° twenty-four hours).—Slightly turbid, no gas, bleaching,
streaks of blue; three days, almost colourless; five days, do.
Nitrate broth (37° twenty-four hours).—Turbid, no gas, no nitrites (with
metaphenylene-diamine).
Iron or lead broth (37° twenty-four hours).—Two days, good H8.
Gelatin stab (20° twenty-four hours).—Very slight growth, no liquefaction ;
three days, increased; no surface growth; five days, no gas; no liquefaction.
Gelatin streak (20° twenty-four hours).—Very slight growth, no liquefac-
tion ; five days, no gas; no liquefaction.
Gelatin shake (20° twenty-four hours).—Streaked turbidity, no gas, no
liquefaction ; five days, no gas, no liquefaction.
Agar streak (37° twenty-four hours).—Slight, white, spreading, growth ;
three days, increased ; five days, do.
Blood-serum (37° twenty-four hours).—Very slight growth; three days,
slight increase; five days, do.
Litmus milk (37° twenty-four hours).—No clotting, decolorised, yellowish
colour , three days, quite clotted; five days, do.
Potato (87° twenty-four hours).— Very slight, moist-looking growth;
five days, do.
Anerobic growth (87° twenty-four hours).—Turbid, no gas; three days,
turbid, no gas.
= Bacillus para-typhi abdominalis.
SPECIMEN 2.
September 19th, 1901. H.D. Urine, nil.-
G.F.B., 37% Twenty-four hours; turbid; white; flocculi ; H.D., cocci.
Broth, 37°. Twenty-four hours; turbid; no gas.
Made three agar plates ; small white colonies.
C.M.B. Staphylococci.
Staphylococci only found.
SPECIMEN 8.— Urine, no albumin.
September 26th, 1901. H.D. Urine, nil.
G.F.B., 37°, Twenty-four hours ; abundant gas; marked turbidity ; H.D. ;
cocci, and many motile bacilli.
Broth, 879. Twenty-four hours; turbid; white sediment; no gas; H.D.;
cocci and motile bacilli.
Agar plate. Twenty-four hours; many white colonies; C.F. ; staphylococci.
NorE.—Many cocci and few bacilli in broth, but many bacilli and few cocci
in glucose formate broth.
September 27th. Planted three agar plates from glucose formate broth.
Two organisms appeared to be present, one simulating proteus, and one
simulating an organism of the typhoid group.
Cultures were made from each on agar. They were not pure. Cultures
were now made from broth 26th September. Twenty-four hours. Turbidity ;
H.D. ; bacilli, some motile.
On Enteric Fever. 197
Three agar plates were made from this. These were replated twice, and
the organism simulating the bacillus typhi abdominalis on agar, was
eventually obtained in a pure condition.
This organism when worked out was found to be very like proteus in
its reactions.
SPECIMEN 3.— Urine, 26th September, 1901.
Description.—A bacillus.
Motility.—Slightly motile (agar twenty-four hours).
Staining.—Faintly with C.M.B., well with C.F. Decolorised by Gram-
Weigert.
Pleomorphism.—All forms are short bacilli; practically no pleomorphism.
Broth (87° twenty-four hours).—Turbid, no gas; two days, do.; five days,
no indol; eight days, no indol.
Peptone water (87° twenty-four hours).—Turbid, slight sediment, no gas;
two days, turbid, no gas; nine days, trace indol.
Formate broth (37° two days).—-Good gas, turbid, no colour hangs.
. Dextrose broth (37° twenty-four hours).—Fair gas, decolorised, slight acid;
two days, no gas, acid.
Lactose broth (37° twenty-four hours).—Slight turbidity ; two days, До. |
four days, do.
Saccharose broth (37° twenty-four hours).—Nil , two days, turbid.
Glycerine broth (37° twenty-four hours),—Nil , two days, turbid, slight acid,
no gas.
Nitrate broth (37° twenty-four ə — Turbid, good nitrites, with meta-
phenylene diamine.
Lead broth (37° twenty-four hours).—Turbid, good HS; two days, very
marked HAS ; three days, do.
Gelatin stab (20° twenty-four hours).—Very slight growth; two days, no
gas, no liquefaction, white growth on surface; three days, liquefaction at
surface ; nine days, liquefaction on surface only, horizontally.
Gelatin streak (20? twenty-four hours).—Very slight growth, no gas, no
liquefaction ; two days, no gas, liquefaction; three days, increased liquefac-
tion; nine days, entirely liquefied.
Gelatin shake (20° twenty-four hours).—A few very small colonies in sub-
stance, no gas, no liquefaction; two days, do.; three days, liquefaction on
surface; nine days, surface liquefied horizontally.
Gelatin plates (20° twenty-four hours).—Nil ; four days, no growth.
Agar streak (87° twenty-four hours).—Vigorous, raised, whitish growth ;
two days, do.; four days, increased.
Agar plates (37° twenty-four hours).—White colonies; four days, raised
white, moist-looking colonies.
Blood-serum (37° twenty-four hours).—White raised, moist-looking growth ;
two days, liquefaction ; three days, do.; six days, complete liquefaction.
Litmus milk (37° twenty-four hours).—Slight acid, no clotting; two days,
less acid, no clotting; three days, no clotting, commencing decolorisation ;
nine days, no clotting, decolorisation, complete precipitation of casein.
Potato (37° twenty-four hours).--Vigorous, yellowish brown, raised, spread-
ing, moist-looking growth ; two days, do.
Anaerobic growth (37° twenty-four hours).—Turbid, good gas; two days,
turbid, fair gas; three days, good gas.
Urine (37° twenty-four hours).—Nil; two days, turbid, no alkalinity.
Approaches bac. proteus vulgaris in reactions.
198 On Enteric Fever.
CASE 12.—F., se". 30 years. Admitted into Mary Ward on September 4th,
1901, under Dr. Hale-White, for general malaria and pyrexia. She was
delivered of a child one month ago. One month ago a lodger in her house
died of typhoid fever. She got up after her confinement about a fort-
aight ago, and caught cold soon after this, and then felt languid and weak
and unable to get about. She had a cough. She slept well, but her appetite
was bad. The bowels were regular. On September lst she sent for a
doctor who diagnosed enteric fever, and who told her that she had had it ten
days.
On admission, temperature 101:6, pulse 132. Tongue furred, abdomen
protuberant, walls flaccid, spleen palpable, a few spots on abdomen and lower
part of chest. Pulse weak. Heart dulness increased laterally, tick tack
rhythm at base of heart. A few rales at bases of lungs behind. Urine 1028,
reddish, urates, acid, albumin.
Septemberöth. Temperature normal. Milk diet. No appetite. Condition
unchanged.
September 7th. She feels better. A few fresh spots on abdomen,
Temperature 101:6? at night.
September 10th. Dr. Hale-White diagnosed enteric fever.
September 13th. The serum does not give the Widal reaction.
September 18th. Patient progressing favourably. No spots on abdomen.
Urine, thick with deposit of mucus. Reaction acid, 1020; no sugar or
albumin.
September 24th. Still progressing favourably. Temperature rose to
101:8? yesterday, for no apparent reason.
September 26th. Urine, 1012; cloudy, slight deposit of urates , acid; no
albumin.
October 2nd. She is going on well. Temperature 97°.
October 12th. She is still going on well. Temperature 984".
A bacteriological examination of the urine was made on four occasions. On
the first, bacillus typhi abominalis with staphylococci were found. On the
second, B.T.A. in pure culture. On the third, cocci and some large bacilli
not B.T.A. On the fourth, B.T.A. with a proteus-like organism.
Widal reactions :-—
September llth. 50 percent. = O. 5 percent. = O. :5 per cent.
September 20th. 50 per cent. = О. 5 percent. = ğ-. ‘5 per cent.
SPECIMEN 1.—No albumin.
September 20th, 1901. H.D. Urine; cocci and slightly motile bacilli.
G.F.B., 37°. Twenty-four hours, turbid ; no gas; flocculi. -
Broth, 37°. Twenty-four hours, turbid; white flocculi. H.D., slightly
motile bacilli.
Agnr plate. Twenty-four hours. Cloudiness on plate.
C.M.B. Bacilli (agar). C.F. (broth), Staphylococci.
September 23rd. Made three agar plates from agar growth. Nothing
grown.
September 25th. Planted three agar plates from broth tube. Twenty-four
hours; white colonies. C.M.B., short bacilli. H.D., Motile bacilli. Obtained
8 pure growth by replating.
Planted agar tube from agar plate.
The organism was worked out according to scheme given below.
O.
O.
On Enteric Fever. 199
SPECIMEN 1. 20th September, 1901.— Urine. No albumin.
Description.—A rather short bacillus.
Motility.—Fair motility.
Staining.--Well with C.M.B., fairly with C.F., decolorised by Gram-
Weigert.
Broth (87° twenty-four hours).—Turbid, no gas; two days, turbid; no gas ;
five days, no indol.
Peptone water (37° twenty-four hours).—Turbid, no gas; two n turbid,
white sediment, no gas; five days, no indol.
Formate broth (37° twenty-four hours).—No gas, slightly acid; two days,
slight turbidity, slightly acid, no gas; five days, do.
Dextrose broth (37° twenty-four hours).—No gas, acid; two days, no gas,
acid; five days, do.
Lactose broth (37° twenty-four hours).—No gas, no colour change; two
days, no gas, no colour change ; five days, slight turbidity only.
Nitrate broth (37° twenty-four hours).—Good nitrites (with metaphenylene-
diamine).
Lead broth (37° twenty-four hours).—No HS; two days, slight HS; three
days, good H.S ; five days, good H.S.
Gelatin stab (20° twenty-four hours).—Slight growth, no gas; two days,
increased ; five days, no gas, no liquefaction, growth down stab.
Gelatin streak (20° twenty-four hours).—Slight growth; two days, in-
creased ; five days, no gas, no liquefaction, increased growth.
Gelatin shake (20° twenty-four hours).—Turbid, no gas, no liquefaction ;
five days, turbid, no gas, no liquefaction.
Agar streak (37° twenty-four hours).—Fair, yellowish white, raised growth ;
five days, do., no spreading.
Blood-serum (87? twenty-four hours).—Raised, yellowish, moist-looking
growth ; two days, do, ; five days, do., drier.
Litmus milk (37° twenty-four hours).—Slightly acid, no clotting; three
days, do. ; five days, do.
Potato (37° twenty-four hours).—Moist-looking brownish growth; two days,
do. ; five days, do.
Anezrobuc growth (87° twenty-four hours).—Slightly turbid, no gas; two
days, slightly turbid, no gas.
Gruber’s reaction.—Experiment performed with a twenty-four hours’ broth
culture grown from gelatin slope culture, and with a serum that reacted fully
to a known bacillus typhi abdominalis :—
50 per cent.=+. 5 per cent.= +. ‘5 per cent.= +.
= Bacillus typhi abdominalis.
SPECIMEN 2, 6th October, 1901.— Urine, 8rd October, 1901. Acid, slight
excess phosphates, no albumin.
Description.—Short oval bacillus.
Motility.—Slight y motilé (dextrose two days).
Staining.—Fairly with C.M.B., weak with C.F., decolorized by Gram-
Weigert.
Broth (8? twenty-four hours).—Turbid, no gas; two days, do.; five days,
no indol.
Formate broth (37° twenty-four hours).—Acid, no gas; two days, acid, no
gas; three days, less acidity,
200 On Enteric Fever.
Dextrose broth (87° twenty-four hours).—Acid, turbid, no gas; two days,
acid, no gas; three days, do.
Lactose broth (37° twenty-four hours).—Turbid, not reddened, no gas; two
days, no gas, no colour change; three days, very slightly alkaline.
Glycerine broth (37° twenty-four hours).—Turbid, not reddened, no gas;
two days, do.
Nitrate broth (87° twenty-four hours).—Turbid, no gas, good nitrites (with
metaphenylene diamine).
Lead broth (87° twenty-four hours)..—Good HS.
Gelatin stab (20° twenty-four hours).—Hardly perceptible growth, no gas,
no liquefaction ; three days, no gas, no liquefaction.
Gelatin streak (20° twenty-four hours).—Very slight growth no gas, no
liquefaction, spreading opaque growth.
Gelatin shake (20° twenty-four hours).—Very slight turbidity, no gas, no
liquefaction ; three days, do.
Agar streak (37° twenty-four hours).—Raised, not very vigorous, greyish
white growth; three days, increased.
Agar plates (37° twenty-four hours).— White colonies.
Blood-serum (87° twenty-four hours).—Raised white growth ; two days, do. ;
three days, increased; eight days, do.
Litmus milk (37° twenty-four hours).—Very slightly acid, no clotting :
three days, acid, no clotting; eight days slightly acid, no clotting.
Potato (37° twenty-four hours).—Slight, moist-looking growth; two days,
do.; three days, growth spreading over surface.
Anerobic growth (37° twenty-four hours).— Slightly turbid, white deposit,
no gas; two days, do., no gas; three days, do.
Gruber’s reaction.—This experiment was performed with a twenty-four
hours’ broth culture grown from a gelatin slope culture, and with a serum
which reacted fully to a known bacillus typhi abdominalis.
50 per cent.=4. 5 percent. =+. °5 per cent. =+.
= Bacillus typhi abdominalis.
SPECIMEN 3.— Urine, acid, no albumin.
October 7th, 1901. H.D. Urine. Large bacilli; motile.
G.F.B., 37°. Twenty-four hours; turbid; no gas; H.D.; cocci in short
chains.
Broth, 37°. Twenty-four hours; turbid ; no gas.
Agar plate 37°. Twenty-four hours; growth spreading over plate.
October 8th. Made three agar plates from G.F.B.
October 9th. Planted agar tube from agar plate. Twenty-four hours;
greyish white growth of small dotted colonies; H.D.; masses of cocci only;
C.M.B.; staphylococci.
In this specimen of urine some large well staining bacilli were seen, but
they did not grow—they were much too large for typhoid bacilli. Staphylo-
cocci only grew.
SPECIMEN 4.— Urine, acid, no albumin.
October llth, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours ; turbid; sediment; no gas; H.D., slightly
motile bacilli.
Broth, 37°. Twenty-four hours; turbid ; sediment ; no gas.
Agar plate 37°. Twenty-four hours; spreading growth on plate; H.D.
slightly motile bacilli.
On Enteric Fever. ' 901
October 12th. Made three agar plates from G.F.B.
Two days. (1) Proteus-like growth not worked out; (2) White colonies ;
H.D., motile bacilli; C.M.B., bacilli fairly stained.
October 14th. Planted from white colony.
Broth, 37°. Twenty-four hours; very turbid; no gas; H.D., motile bacilli.
Agar, 37°. Twenty-four hours, greyish white growth ; H,D., motile bacilli ;
C.M.B., well-stained bacilli.
G.F.B., 37°. Twenty-four hours; slight turbidity ; H.D., motile bacilli.
The organism having been obtained pure, was worked out from agar
culture.
SPECIMEN 4. 15th October, 1901.— Urine, 11th October, 1901. Acid.
No albumin.
Description.—A short bacillus.
Motility. —Fair motility (agar twenty-four hours).
Staining.—Well with C.M.B., faintly and irregularly with C.F., decolorised
by Gram-Weigert.
Broth (37° twenty-four hours).—Turbid, no gas; two days, do. ; three days,
do.; five days, no indol; six days, no indol.
Peptone water (37° twenty-four hours).—Turbid, no gas; two days, do. ,
five days, no indol.
Formate broth (37° twenty-four hours).—Slightly acid, no gas; two
days, do.
Dextrose broth (37° twenty-four hours).—Marked acidity, no gas; two
days, do.
Lactose broth (37° twenty-four hours).—No gas; two days, do., slightly
turbid, no colour change ; four days, no gas, no colour change.
Saccharose broth (37° twenty-four hours).—Slight gas, turbid; two days,
turbid ; three days, turbid.
Glycerine broth (37° twenty-four hours).—No gas; two days, do., turbid,
no colour change; three days, do.
Nitrate broth (37° twenty-four hours).—Good nitrites (with metaphenylene-
diamine).
Lead broth (37° twenty-four hours).—Turbid, very slight H,S; two days,
good HS; three days, very good Н.Б.
Gelatin stab (20° twenty-four hours).—Very slight growth along stab, no
gas, no liquefaction; three days, do. ; four days, increased growth, no gas, no
liquefaction.
Gelatin streak (20° twenty-four hours).—Very slight growth, no gas, no
liquefaction; three days, do.; four days, spreading growth, no gas, no
liquefaction.
Gelatin shake (20° twenty-four hours).—Turbidity, no gas, no liquefaction ;
two days, do.; four days, do.
Agar streak (37% twenty-four hours).—Semi-translucent, whitish, raised
growth, regular edges; two days, vigorous growth.
Blood-serum (37% twenty-four hours) —Yellowish, raised, moist-looking
growth; two days, do.
Litmus milk (87° twenty-four hours).—Acid, no clotting; two days, do. ;
five days, do.
Potato (87° twenty-four hours).—Moist, yellowish, brown growth; two
days, do. ; three days, do.
202 On Enteric Fever.
Anerobic growth (37° twenty-four hours).—No gas formation; two days,
do.; three days, do.
Gruber’s reaction.—This experiment was done with a twenty-four hours’
broth culture growth from a gelatin slope culture, and with a serum which
reacted fully to a known bacillus typhi abdominalis.
50 per сепб. = О. 5 percent.=+. *5 per cent.=4+.
= Bacillus typhi abdominalis.
CASE 13.—M., sat, 19 years. Admitted into Stephen Ward on August 19th,
under the care of Dr. Fawcett, for pain in the back of the head.
About three weeks ago he began to feel overtired, and had a bad head-
ache on rising; at night time he experienced pain all down his spine. For
the past week he has been sweating profusely, and the pain has been much
worse, with pain also over the abdomen. He has never at any time lost
consciousness, but has been drowsy and apathetic. He has not vomited.
The bowels have acted normally. He has had no trouble with micturition.
He has seen no spots on his body. He kept at work during the firat week of
his illness, but then had to give up. He has since gone back to work but
could not continue.
On admission, temperature 104:29, pulse, 116, respiration 24.
He lies in bed with his eyes half closed, and with a very drowsy appear-
ance. He very frequently mutters. The lips are cracked, the gums con-
jested, the teeth foul, tongue thickly furred, breath very foul. The abdomen
is full but not distended, is rigid but resonant all over. The liver and spleen
cannot be felt. The whole abdomen is very tender to pressure.
The pulse is soft, full, regular, dicrotic, the artery easily compressible. The
heart is normal. Respiratory system normal. Urine, 1025; urea, 2:5 per
cent., acid, normal.
August 20th. He is wandering in his mind to-day and is very drowsy.
He does not complain of abdominal pain to-day. Chloralamide gr. xxx. in
brandy.
August 21st. He is drowsy.
August 22nd He is drowsy, he cannot give a connected answer.
Mist. Chloral et Pot. Brom. Urine 1028, acid, high colour, normal.
August 23rd. He answers questions rationally. Splenic dulness enlarged.
Abdomen still rigid, but not tender. Tr. Opii. m x. statim.
The serum did not react in any dilution to the Widal reaction.
August 24th. He has had a better night; three typhoid spots on left
side of abdomen, two or three on chest.
August 26th. Temperature lower; clot of blood passed.
August 29th. Another specimen taken for Widal reaction. =
August 30th. Urine, 1030; acid, area 3 per cent.; no albumin. The
temperature has varied between 100-104° during last four days. Delirium
slightly worse. Abdomen less distended.
September 3rd. He is very restless and delirious, temperature 98°-102°4°.
September 10th. He is better this morning; tongue very furred.
September llth. Urine 1024 alkaline; mucus; no sugar or albumin;
mentally weaker; temperature 108:49,
September 12th. Abdomen rigid though resonant ; pain in back and lower
limbs.
On Enteric Fever. 203
September 14th. Mental condition slightly improved.
September 16th. Very noisy during night; cough bad; wandering in
mind.
September 17th. Still very noisy; sweats profusely; rhonchi in chest;
heart rapid; abdomen still rigid. Brandy and I.M.H.
September 18th. He commenced vomiting: keeps nothing down;
champagne by mouth; food by rectum; still noisy. Patient died at
6.20 p.m.
Post-mortem examination.—Made 20 hours after death.
Heart. Some recent vegetations on the valves. Otherwise normal.
Lungs. Extensive broncho-pneumonic changes, especially at the right base.
Liver and kidneys normal. Spleen enlarged,-some recent capsulitis.
Intestines. Perforation in ileum, six feet from ileo-ceecal valve. Severe
ulceration of small intestine, especially near ileo-cecal valve. Ulcer in
cecum. |
The urine of this case was not worked out during life. After death a
bacteriological examination was made of the heart-blood, kidney and the
urine from bladder. In all of these the bacillus para-colon communis was
found in pure culture.
This bacillus differed in its bacteriological reactions from the bacillus
coli communis only in the fact that it caused no clotting of milk.
Widal Reaction.
1. August 20th, 1901.
50 percent.=O. 5 рег сепб, = О. "Ə pet сепб, = О.
2. August 30th, 1901.
50 per cent. = О. 5 per cent. = +. *5 per cent. = O,
Heart-blood.
Description.—Short thick bacilli.
Motility.—Slightly motile (agar).
Staining.— With C.M.B. and C.F.; decolorised by Gram-Weigert.
Broth (87°. twenty-four hours).—Turbid, good gas; two days, turbid, very .
slight gas ; six days, good indol.
Peptone water (37° twenty-four hours).—Turbid, no gas; two days, turbid,
no gas; six days, good indol.
Formate broth (8? twenty-four hours).—Turbid, very good gas; two days,
turbid, very slight gas.
Dextrose broth (37° twenty-four hours).—Turbid, good gas ; two days, turbid,
acid, no gas.
Lactose broth (37° twenty-four hours).—Turbid, good gas; two days, acid,
no gas. :
Saccharose broth (37° twenty-four hours).—Turbid, gas; two days, good gas.
Glycerine broth (37° twenty-four hours).—Turbid, no gas; two days, no gas.
Nitrate broth (87° twenty-four hours).—Turbid, good gas, good nitrites (with
metaphenylene diamine).
Gelatin stab (20° twenty-four hours).—Fair growth along stab, no gas,
no liquefaction.
Gelatin streak (20° twenty-four hours). — Fair growth.
Gelatin shake (20° twenty-four hours). — Turbid, good gas bubbles,
throughout.
VOL. LVI. 17
204 On Enteric Fever.
Agar streak (87° twenty-four hours).—Vigorous, yellowish white growth,
regular edges; two days, increased.
Agar plates (37° twenty-four hours).—Large white colonies.
Litmus milk (87? twenty-four hours).—Acid, no clotting; two days, no
clotting ; eight days, no clotting.
Potato (87° twenty-four hours).—Moist brownish growth; two days, in-
creased ; eight days, increased.
Anaerobic growth (37° twenty-four hours).—Turbid, very abundant gas; two
days, very good gas.
= Bacillus para-coli communis.
This organism differs from the bacillus coli communis in that it does not
clot milk and gives no gas with glycerine.
Gruber's reaction.—This reaction was carried out with twenty-four hours’
old broth culture grown from gelatin. The serum used gave the following
result when used with B.T.A., for Widal’s reaction :—
5 percent. = + +. 0:5 percent. = + +.
On carrying out Gruber’s reaction with the above organism a completely
negative result was given, thus :—
50 per cent. = O. Spercent. = O. 0:5 percent. = O.
Urine from p.-m. bladder.
Description.—Short oval bacilli.
Motility.—Slightly, but definitely motile (agar).
Staining. — Stains with C.M.B., well with C.F., decolorised by Gram-
Weigert.
Pleomorphism.—Some short forms ; ; short, thick, oval bacilli; longer thick
bacilli (C.F.).
Broth (87° twenty-four hours).—Turbid, no gas; three days, do.; seven
days, very good indol.
Peptone water (37° twenty-four hours).—Turbid, no gas; three days, do. ;
seven days good indol.
Formate broth (37° twenty-four hours).—Good gas, turbid, no colour change;
three days, very slight gas.
Dextrose broth (37° twenty-four hours).—Good gas; three days, no gas.
Lactose broth (37° twenty-four hours).—Turbid, acid, no gas; three days,
acid, no gas, turbid.
Saccharose broth (37° twenty-four hours).—Turbid, no gas; three days, do.
Glycerine broth (37% twenty-four hours).— Turbid, no gas; three days,
turbid, good gas.
Nitrate broth (37° twenty-four hours).— Turbid, good gas, good nitrites
(with metaphenylene diamine).
Gelatin stab (20° twenty-four hours).—Good growth along stab, none on
surface, no gas, no liquefaction; five days, do.
Gelatin streak (20° twenty-four hours).—Good growth, gas on surface, no
liquefaction; five days, do.
Gelatin shake (20° twenty-four hours).—Scum on surface, good gas bubbles
in medium quarter of an inch below surface to bottom of tube; five days, do.
Agar streak (37° twenty-four hours).—Vigorous, raised, yellowish white
growth no gas; three days, increased.
Agar plates (37° twenty-four hours).—Two days, large, round, white colonies.
On Enteric Fever. 905
Litmus milk (37° twenty-four hours).—Acid, no clotting; three days, no
clotting ; thirteen days, no clotting.
Potato (37° twenty-four hours).—Slight, brownish, moist-looking growth ;
three days, increased.
Ancrobic growth (37° twenty-four hours).—Turbid, very good gas; three
days, turbid, slight gas.
= Bacillus para-coli communis.
This differs from bacillus coli communis only in the fact that it does not
cause clotting of milk, and gives no gas with lactose broth.
Gruber's reaction.—This reaction was carried out with a twenty-four hours’
old broth culture grown from gelatin. The serum used, gave the following
results when used with B.T.A. for Widal’s reaction :—
Š percent. = ++. 0:5 percent. = ++.
On carrying out Gruber’s reaction with the above organism, a completely
negative reaction was obtained. Thus—
50 per cent. = О. 5 percent. = O. 0°5 percent. = О.
Kidney.
Description.—Short, thick, oval bacilli.
Motility.—Slightly motile, agar two days.
Statning.—Slightly with C.M.B., well with C.F., decolorised by Gram-
Weigert.
Pleomorphism.—Short, thick, oval bacilli, some longer forms, some almost
like cocci (C.F.)
Broth (87° twenty-four hours).—Turbid, no gas; three days, do.; seven
days, good indol.
Peptone water (37° twenty-four hours).—Turbid, no gas; three days, do. ;
seven days, very good indol.
Formate broth (37° twenty-four hours), —Fair gas, no colour change ; three
days, no gas.
Dextrose broth (37° twenty-four hours).—Good gas, acid, turbid; three
days, do.
Lactose broth (37° twenty-four hours)-—Acid, turbid, no gas; three
days, do.
Saccharose broth (37° twenty-four hours).—Turbid, no gas, purple colour ;
three days, do.
Glycerine broth (37° twenty-four hours).—Turbid, no gas; three days, acid,
good gas.
Nitrate broth (87° twenty-four hours).—Turbid, good gas, good nitrites
(with metaphenylene diamine).
Gelatin stab (20° twenty-four hours).—Good growth down stab, very slight
on surface, no liquefaction.
Gelatin streak (20° twenty-four hours).—Whitish growth, no gas, no
liquefaction.
Gelatin shake (20° twenty-four hours).—Turbid, gas, no liquefaction, gas
not near surface.
Agar streak (87° twenty-four hours).—Well marked, vigorous, yellowish
white growth, regular edge; three days, increased.
Agar plates (37° twenty-four hours).—Round, white, large raised colonies.
Litmus milk (87° twenty-four hours).—Acid, no clotting; three days, do
nine days, no clotting, acid.
206 On Enteric Fever.
Potato (37° twenty-four hours).—Moist, raised, brownish yellow growth;
three days, increased ; nine days, increased.
Anaerobic growth (37° twenty-four hours).—Very good gas formation.
= Bacillus para-coli communis.
This bacillus differs only from bacillus coli communis in that it does not
cause clotting of milk, nor the formation of gas with lactose and saccharose
broth.
Gruber's reaction.—This reaction was carried out with a twenty-four hours’
old broth culture grown from gelatin. The serum used gave the following
result when used with B.T.A. for Widal’s reaction :—
5 per cent.=+ +. 0:5 per cent.= + +.
On carrying out Gruber’s reaction, with the above 0 a completely
negative result was obtained :—
50 per cent.=O. 5 per cent.=O. 05r per cent. — O,
CASE 14.—M., set. 24 years. Admitted into Stephen Ward under the care
of Dr. Perry, on September 14th, for slight pain in the &bdomen and general
malaise.
He has been a heavy drinker. His occupation consists mostly of working
in drains, and at the time of his illness he was engaged in repairing drains
condemned by the sanitary authorities.
Fourteen years ago he had an attack of rheumatic fever, which was
followed by another attack five years later.
On August 2öth he felt great pain and stiffness in all his limbs, and on
leaving work he went to bed. On the next day he saw a doctor, who
gave him medicine. On August 27th he went to work, but on August 28th
feeling worse he remained in bed. On August 29th he again went to work,
and remained at work until September 11th, when he saw his doctor, who
told him he had enteric fever, and he was sent into Guy’s Hospital. He has
suffered a deal from headache and slight giddiness. Until September 11th
he had been taking solid food. The bowels have been irregular, at one timo
being loose, at another constipated, the motions yellowish in colour.
On admission, temperature 102°, pulse, 92, respiration 20. The abdomen
moves well on respiration, no spots are to be seen. The spleen is just pal-
pable. Circulatory system: There is & systolic bruit at the apex. Second
sound very distinct in the aortic area. Urine, 1025, acid, nothing abnormal.
September 17th. A rose-red spot appeared to-day over right hypochondriac
region.
September 18th. He vomited to-day.
September 19th. Four more spots appeared on the abdomen. Another
severe attack of vomiting last night.
September 20th. Dr. Perry thought that the systolic bruit was due to an
old heart lesion.
September 22nd. He had severe hemorrhage from the bowel.
September 23rd. Patient had more hemorrhage and he died at 2 a.m. No
Widal's examination was made.
Post-mortem examination.—Lungs congested. Old pleuritio adhesions.
Heart. Old thickening of aortic valves.
Kidneys normal. Liver normal. Spleen enlarged and firm.
Intestines. Ulceration of ileum for about two feet above ileo-ceecal valve.
No ulceration of colon. No perforation.
On Enteric Fever. 207
Bacteriological examination of the urine :—
Glucose formate broth, 37°. Twenty-four hours, nil; two days, nil,
Broth, 37°. Twenty-four hours, nil; two days, nil.
Agar plate, 37°. Twenty-four hours, nil; two days, nil.
The urine is sterile.
Bacteriological examination of kidney and spleen.—No satisfactory ex-
amination could be made of the kidney, for in spite of all methods of
cultivation being employed, no growth could be obtained with enough vitality
to bear transplanting. They all died out, both in the kidney and the spleen.
Histological examination of the kidney, stained with carbol thionin blue,
shewed no organisms to be present when examined with both one-sixth inch
and one-twelfth inch oil immersion lenses.
CASE 15.—M., æt. 16 years. Admitted into Stephen Ward, under the
care of Dr. Bryant, on September 9th, 1901, for cough and pain in the
abdomen.
He has had cough, together with pain in the abdomen and back; he
has been listless and drowsy, and has had shivering fits. On the day before
admission he became feverish and lost his appetite.
On admission, temperature, 100:4?; pulse, 100; respiration, 24. He
appeared drowsy and inclined to sleep. He complained of pain in the
abdomen.
There is a localised apical systolic bruit, otherwise the heart is normal.
The spleen is palpable. The abdomen is slightly distended, and there are
two or three suspicious spots present. The lungs are normal. Urine 1010,
acid ; albumin present in small quantity. Diazo reaction obtained.
September 20th. The blood gave a partial Widal reaction.
September 24th. Blood does not react completely to 5 per cent., not at
all to “5 per cent. in the Widal reaction.
September 26th. He developed a sore throat last night, the fauces
and uvula being red and inflamed, but no membrane being present. A
cultivation was taken, but no Klebs-Loffler bacilli were found. He has fits
of coughing and there are ráles and ronchi in chest.
September 28th. The blood gives the Widal reaction in 5 per cent., but
not in *5 per cent.
October lst. Temperature, 100:8”. Urine normal.
October 6th. Temperature, 98:6? in morning, 102? in evening. He
feels comfortable.
October 8th. Temperature, 97:8? to 101:6”.
October 10th. Spleen felt below costal margin on inspection. It feels
rather hard. The throat has cleared up. Temperature 108:89,
October 14th. He feels better this morning. Temperature 101:8*.
Spleen still palpable below costal margin.
Widal reaction, 5 per cent. = + +. ‘5 percent. = + +.
October 15th. Urine, 1008; no sugar or albumin; acid, urea, 1:2 per cent.
Evening temperature 104°.
A bacteriological examination of the blood was made on one occasion. It
was found to be sterile.
A bacteriological examination of the urine was made on three occasions,
and on each of these it was found to contain only staphylococci.
208 On Enteric Fever.
Widal examinations.
1. 11th September, 1901—
50 per cent. = O. 5 percent. = O. "5 per cent. = $+.
2. 17th September, 1901—
50 per cent. = +. 5 per cent.
8. 24th September, 1901—
50 per cent. = ppt. Ö percent. =4+. *5 percent. = O.
4. 26th September, 1901—
50 per cent. = +. 5 per cent.
5. 17th October, 1901—
50 per cent. = . 5 per cent. = ++. “Ö per cent. = ++.
SPECIMEN 1. Urine.—No albumin.
September 26th, 1901. H.D. Urine, nil.
G.F.B., 37°. Twenty-four hours, turbid; no gas. H.D., coccionly, chiefly
in pairs and groups. C.M.B., cocci in pairs and groups.
Broth, 37°. Twenty-four hours, turbid; no gas.
Agar plate, 37%. Twenty-four hours. A few white colonies.
C.M.B. Staphylococci only.
SPECIMEN 2. Urine.—Acid, slight albumin.
September 28th 1901. Broth, 37°. Three days, turbid.
Agar plate, 37°. Three days, nil.
October 1st. Planted broth, 37°. Twenty-four hours, turbid; no gas.
H.D., cocci only, chiefly in pairs.
October 3rd. Planted three agar plates from G.F.B. Twenty-four hours;
dotted white colonies. H.D., cocci only.
C.M.B., Staphylococci only.
SPECIMEN 8.— Urine. Acid, slight trace albumin.
G.F.B., 37° twenty-four hours. Slightly turbid, no gas. H.D. cocci only,
in pairs.
Broth, 37° twenty-four hours. Turbid, no gas. H.D. cocci, chiefly in
pairs.
Agar, 87? twenty-four hours. Small white colonies. H.D. cocci only.
C.M.B., staphylococci only.
O. "5 per cent. = О.
+. '5 per cent. = O.
10.
11.
12.
13.
14.
On Enteric Fever. 209
BIBLIOGRAPHY.
Krogius, A, Sur la bacteriurie Annales des Organ. Gén.-Urin., 1894,
p. 196, et seq.
Nathan, P. W. Bacillus Coli Communis in the Urine, and its Signifi-
cance. Med. Rec., New York, 1898. Vol. liii., p. 83-86.
Pakes, W. C. C. Widal’s Reaction. A Critical Examination of 326
Cases in which the Reaction has been tried. Guy’s Hospital
Reports. Vol. lv.
Ibid.
Rolleston, H. D. The Agglutination Reaction in Typhoid Fever.
Memorandum. B.M.J., October 12th, 1901, p. 1084.
Pakes, W. C. C. Ibid.
Gwynn, Norman B. A Study of the Widal Reaction in 265 Cases of
Typhoid Fever. The Johns Hopkins Hospital Reports. Vol. viii.
Horton Smith, Dr. The Goulstonian Lectures on the Typhoid Bacillus
and Typhoid Fever. Lancet, 1900. Part I., p. 821, et seq.
Bowlby, Anthony A., F.R.C.S. Surgical Pathology and Morbid
Anatomy. Fourth Edition, p. 49.
Goldenburg, Herman. Bacteriuria Med. Rec., New York. 1896,
p. 228.
Ibid.
Smith, G. Munro. Pneumococci in the Urine. Bristol Med. Chir.
Journ. 1895, vol. xiii., p. 115.
A Treatise on Human Anatomy by Various Authors. Edited by Henry
Morris, M.A., M.B.
Sappey, Ph. C. Description et Iconographie des Vaisseaux Lymphati-
ques Considérés Chez l'homme et les Vertebres, p. 124. Vaisseaux
lymphatiques de la Vessie.
A CARDIOGRAPHIC TRACING,
SHOWING ASYNCHRONOUS ACTION
OF THE VENTRICLES.
By THEODORE FISHER, M.D.
PATHOLOGIST TO THE BRISTOL ROYAL INFIRMARY.
`
THE accompanying cardiographic tracing has been lying amongst
my notes for some years. It has always seemed to me to possess
features of considerable interest, but since the tracing is accom-
panied by very incomplete notes of the case from which it was
taken, I have not deemed it worthy of being brought before the
notice of others. Yet, meagre though the facts connected with
it may be, the rarity of such a tracing I trust will be thought
sufficient to justify its publication.
When I was taking the work of Dr. Michell Clarke at the
Bristol General Hospital, during his summer holiday in 1896,
a woman, aged 25, was admitted suffering from cardiac disease.
There was cedema of the legs, and the liver was several inches
below the ribs. The heart was enlarged, and the apex was
apparently in the fifth intercostal space, one inch external to
the nipple line, but the special features of interest were in the
character of the impulse. My notes thus describe it :—“ The
impulse 4s well marked, and is visible and palpable over the greater
part of the cardiac area. At the apex there is a short presystolic
thrill, but the most noteworthy feature 1s the double character oy
the impulse. There is a distinct double shock, and a striking point
is the fact that the second impulse as very well-marked between the
212 A Cardwgraphic Tracing, showing Asynchronous
apex and the sternum. The rise at the apex ts first seen, then a
rise nearer the sternum. In both places a double shock is felt by
the hand, but the earlier shock is most marked at the apex, and the
second nearer the sternum.”* Tracings were taken by means of
Marey’s cardiograph, which clearly illustrated the movements
felt and seen. The button of the tambour of one lever was placed
at the apex and the button of the tambour of the other was
placed at a spot one inch from the left border of the sternum,
also in the fifth interspace. Simultaneous tracings of the move-
ments at these two points were thus obtained, and a reproduction
of these tracings is shewn in the accompanying illustration. The
upper tracing is from the apex, the lower from the point near the
sternum. It will be noticed that the higher waves in the tracing
from the apex are not situated immediately over the high waves
of the tracing from the point near the sternum. There are other
details of interest, but this is the most striking characteristic of
the tracing.
We may reasonably, I think, attribute the undulations of the
upper tracing to movements of the left ventricle, and at least
the higher waves of the lower tracing to movements of the right
ventricle. I am aware that the power of the right ventricle to
give rise to a tracing has been doubted, and it is possibly true
that most tracings obtained from the surface of the right ventricle
merely indicate transmitted movements of the left ventricle. In
mitral stenosis, of which disease this case was an example, there
is, however, often considerable hypertrophy of the right side of
the heart. But although there was not an opportunity of dis-
covering that an amount of hypertrophy of the right ventricle
existed in this case which could easily have given rise to a
tracing, it cannot be supposed that the left ventricle was capable
of producing at one time a high wave outside the nipple line and
at another a similar wave close to the sternum. If the tracing
from the apex indicated movements of the left ventricle, then the
other tracing must have recorded movements of some other
1 It may be of interest to add that the patient was conscious of a peculiar
cardiac action, and stated that it had commenced a few days before admission,
during a severe thunderstorm.
Action of the Ventricles. 213
contractile body, which in this instance could have been nothing
else but the right ventricle. This seems to be indisputable so
far as the higher elevations are concerned, but it is possible that
the minor curves record impulses transmitted from the left
ventricle If this be considered to be the most reasonable
explanation of the minor curves, the tracing becomes still more
interesting, because we shall then have to believe that the right
ventricle intermitted while the left was contracting. Putting on
one side, however, the question of the mode of production of
these minor curves, examination of the tracing from the apex
shows that a comparatively forcible systole of the left ventricle
alternated with one much more feeble, and on comparing the
tracing with that taken near the sternum it will be noticed that
a strong contraction of the underlying ventricle generally took
place about the same time as the weaker contraction of the left
ventricle. At one spot the left ventricle apparently intermitted
when the right ventricle was contracting, and towards the end of
the tracing four strong systoles of the right ventricle have
occurred to two of the left.
Unfortunately I have lost my record of the cardiac sounds. I
must have examined the case on several occasions, since I have
several pulse-tracings taken at different times, both from the
radial and the carotid arteries, and also other tracings from the
heart. Not only have my notes been mislaid, but I regret to say
that I have no recollection of what was heard. Brief notes occur
on one of the cardiographic tracings, but they occur at a time when
the curious impulse had disappeared, and have evidently been
made there as a memorandum of the fact that the cardiac sounds
had altered. The date of the disappearance of the abnormal im-
pulse was six days after the first tracing had been taken. The apex-
beat then presented nothing especially noteworthy, and the sounds
heard there, were a ‘systolic murmur, loud second sound, with
a rumbling and blowing diastolic murmur.” At the point close to
the sternum where the second tracing was taken the sounds were
a ‘systolic murmur, loud second sound, and a diastolic sound."
That is to say, what some would describe as a false reduplication
of the second sound was associated with the systolic murmur, A
214 A Cardiographic Tracing, showing Asynchronous
subsequent note also shows that the general features were merely
those of the failing heart of mitral stenosis, The double action
is mentioned as absent and “a thrill and short shock ” as being
felt. The sounds are also described as resembling—
therr dup durr
(Systolic murmur. n sound. | ast murmur,
occasionally varied with a “ rapid, rolling action,” represented by
““ therrop, therrop, therrop." It should be mentioned that when
the double cardiac action was present, only one of the two beats
was felt at the wrist. The pulse was then slow, from forty-four
to fifty-two to the minute, but when the curious cardiac rhythm
disappeared it rose to ninety-two to the minute. The accompany-
ing tracings, taken from the right carotid artery—one at the time
the anomalous cardiac action was present, and the other after it
had passed off—give some idea of the alterations in the pulse-
rate. The first tracing also shows that only the stronger of the
two contractions of the left ventricle made itself felt in the arteries.
- Although I have no record of the sounds of the heart when
the double impulse was present, it may be safely asserted that
they did not appear to me to throw light upon the question of
the causation of reduplication of the first sound. At that time
I was interested in reduplication of the first sound, and in the
bruit de galop, and shortly after wrote a paper on the bruit
de galop (American Journal Med. Sciences, Sept., 1896). Had
the cardiac sounds in this case manifested features bearing
upon the subject, I should have remembered what was present.
It is possible, however, that the fact that the first sound was
replaced by a systolic murmur, and that a presystolic murmur
was associated with it, may have made it difficult to appreciate
lessons which might otherwise have been taught.
In cases of well-marked reduplication of the first sound and of
the bruit de galop, a double shock is easily felt by the hand
placed over the impulse. This doubling of the impulse can be
recorded by means of the cardiograph, but it is not always easy
to obtain a tracing, partly because the impulse is generally feeble
and diffuse, and partly because very slight pressure depresses or
obliterates the first of the two waves, J have sometimes found
Action of the Ventricles. 915
Dudgeon’s sphygmograph give a better idea of the movements
felt by the hand than Marey’s cardiograph.
A few tracings are given to illustrate the features of the impulse
associated with a bruit de galop and a reduplicated first sound.
Other tracings accompany those taken from the same cases at
times when the bruit de galop or reduplicated first sounds were
absent. In the tracing from the case of a bruit de galop, a high
wave is seen to precede the ventricular systolic wave, and a
broader wave occupies the same position in the tracing from the
case of a reduplicated first sound. In the case of reduplication
of the first sound, there are tracings taken at two positions, one
at the apex, the other in the fourth space one inch nearer to the
sternum. It is interesting to note that in the tracing taken
internal to the apex, the situation of the two waves is reversed.
— At the apex the second wave is the higher, but towards the
sternum the first wave rises above the second. What this
indicates it is difficult even to suggest. It has not been intended
to discuss the causation of reduplication of the first sound.
These tracings have been brought forward merely to show that
a doubled impulse is present in cases in which a bruit de galop,
or a reduplicated first sound is heard. It may be stated, however,
that it has in the past not seemed to me necessary to think that
the general condemnation of the view, which attributes redupli-
cation of the first sound to asynchronism of the ventricles, has
been a faulty judgment. In my paper upon the bruit de galop,
which bruit it is scarcely necessary to remark is very closely
related to reduplication of the first sound, I have attributed the
high wave that precedes the ventricular systolic wave to systole
of the auricles. The subject, however, presents many difficulties,
and it is one upon which one cannot dogmatise. The abnormal rise
in the tracing from a case of reduplication of the first sound,
cannot I think be attributed to systole of the auricles. A possible
explanation of the tracing would be that asynchronism was
present in the contraction of the ventricles, and that the higher
part of the doubled wave was produced by the left ventricle
at the apex, but by the right ventricle nearer the sternum. It
may be remarked that if this explanation be allowed, the case
216 <A Cardiographic Tracing, Showing Asynchronous
lends support to Dr. Gibbes’s (Lancet, vol. i., 1901, page 1601),
theory of the causation of the presystolic murmur, which theory
attributes the murmur to partial asynchronous action of the
ventricles. When the patient, a girl uged twenty, was first seen,
a rumbling presystolic murmur, associated with a thrill, was
audible at the apex. Three days later, when an abnormal impulse
which felt “ like two waves passing under the hand in quick
succession," was found to be associated with a reduplicated first
sound, the presystolic murmur had disappeared. Adopting the
theory of Dr. Gibbes, we may suppose that at first there was
sufficient asynchronism to give rise to a thrill and a presystolic
murmur, and that later, when the asynchronism increased, the
thrill became analysed into a double impulse, and the presystolic
murmur differentiated into one sound and part of another. Un-
fortunately for this theory, however, the tracings taken before the
reduplication of the first sound shewed itself, and also after it had
disappeared, give little indication of asynchronism of the con-
traction of the ventricles; yet possibly, one tracing in places may
be thought to slightly suggest it.
Whatever may be one’s view of the causation of a reduplicated
first sound it seems to me that writers upon the subject go too
far when they strongly assert that asynchronism of the ventri-
cular contractions is not possible. Mackenzie, in his able and
comprehensive paper upon the liver and venous pulses (Journal
of Pathology, vol. ii., 1894, pages 112 and 318), gives tracings
which seem to prove conclusively that such asynchronous action
can occur. He has taken tracings simultaneously from the
internal jugular vein and from the carotid artery in a large number
of cases, and one tracing shews pulsations in the jugular vein
of ventricular type continuing while the carotid pulse intermits,
and another reveals remarkable discordance of the two sides
of the heart.
The first tracings which accompany this paper seem to me also
to prove conclusively that asynchronism may be present at least
in the force of the contractions of the two ventricles.
Action of the Ventricles. 217
Fig. 1.
Tracings taken with Marey's cardiograph simultaneously at the apex in the 5th
intercostal space one inch outside the nipple line, and at a point one inch from
the left border of the sternum, also in the 5th intercostal space. The high curves
on the lower tracing do not underlie the higher undulations on the upper tracing.
Fig. 2.
Pulse tracing from the right carotid artery when the double impulse was present.
It gives some idea of the slowness of the pulse, and shows that the alternating
character of the cardiac contraction was not communicated to the arteries.
Fig. 3.
Pulse tracing taken from the same artery seven days later, when the unusual
features of the impulse had disappeared. The pulse, when this tracing was
taken, had nearly doubled in frequency.
918 A Cardiographic Tracing, Showing Asynchronous
Fig. 4.
il
Tracing of heart impulse taken with Dudgeon”s sphygmograph when
a bruit de galop was present. Respiratory undulations are also
present. A high pointed curve precedes the broader undulation due
to systole of the ventricles.
Fig. 5.
ne UU
Tracing from the same heart; but the breath held, and the paper
running more slowly.
Fig. 6.
Tracing taken five months previously with Marey's cardiograph
when no bruit de galop was present.
Action of the Ventricles. 219
Fig. 7.
Tracing taken at the apex in the 5th interspace, 34 inches from
the left border of the sternum, in a case of reduplication of the
first sound.
(Marey’s cardiograph.)
Fig. 8.
Tracing from the same case taken in the 4th inter-space one inch
nearer the sternum.
(Marey’s cardiograph.)
Fig. 9.
Tracing from the same case taken at the apex when the reduplication
of the first sound had disappeared.
(Marey’s cardiograph.
Fig. 10.
Tracing from the same case taken at the apex with Dudgeon’s
sphygmograph when the eduplication of the first sound was present.
Fig. 11,
A
Tracing taken with Dudgeon’s sphygmograph three days previously.
at the apex when the reduplication was absent, but a presystolic
murmur was audible, |
VOL. LVI. 18
ON ACUTE SEPTIC INFLAMMATION
OF YOUNG BONE GROWING FROM
CARTILAGE.
By R. LAWFORD KNAGGS, M.C. CANTAB,
ASSISTANT SURGEON TO THE LEEDS GENERAL INFIRMARY.
THERE are few diseases more perplexing to the student than those
connected with septic inflammation of bone. The subject is
usually split up in such a way that the learner often fails to per-
ceive that any very definite connection exists between conditions
which are in reality the various complications or results of a
single disease. He may indeed be pardoned if he finds it im-
possible to unravel the true story from the articles prepared
for his consumption under such headings as ‘‘ Acute Diffuse
Periostitis,” “ Acute Infective Osteomyelitis,” “ Acute Necrosis,”
“ Acute Epiphysitis,” ‘‘ Acute Arthritis," and “ Acute Arthritis of
Infants.” Nor are his difficulties made easier by the fact that the
most recent editions of the leading text-books are not all up to
date. |
Much of the haze which surrounds the subject is due to a slavish
adherence to the lines upon which it was formerly taught. But
by degrees well known conditions have been traced back to their
source, and now that the cause is found to be the same in all, the
time has surely come to study the disease as a whole by following
it from its commencement to its terminations,
222 On Acute Septic Inflammation of Young Bone
This is the object of the present paper. The writer does not
claim to say anything new, though he may hope here and there
to bring into prominence certain facts which have not as yet
received adequate recognition, and above all to simplify what is
admitted to be, a very difficult subject. |
The title adopted is necessarily comprehensive, but at the same
time a limiting one. The conditions dealt with always occur
in young people before ossification is complete, and take their
origin at some spot where cartilage is being transformed into
bone. Consequently septic inflammation of bone in adults is
not within its scope, and will only be referred to incidentally
or for purposes of contrast.
BACTERIOLOGY.
Though this portion of the subject has not been investigated
by the writer, it should be mentioned that the disease is generally
believed to owe its origin to pyogenic organisms. Of these
the most common is the staphylococcus pyogenes aureus, but
further information on this point may be found in the text-
books of Erichsen (vol. ii., p. 278), and Rose and Carless, and in an
experimental paper by Tubby in the Guy's Hospital Reports for
1890 (vol. 47, p. 85).
It 1s probable that in some instances the micro-organisms find
an entrance into the blood through some skin lesion, but the
respiratory and alimentary tracts are also open to them, so that
it is not surprising that the source of the infection is not always
obvious.
The Primary Focus.
In the long bones this is situated in one of two places;
either— |
(1) On the diaphysial side of the epiphysial line, or of the
cartilaginous epiphysis; in other words in the juxta-epiphysial
region (Figs. 2 and 3) ; or
(2) At the edge of an ossifying centre in the cartilaginous
epiphysis (Fig. 19).
In the small cancellous bones it occurs—
(3) At the periphery of the centre of ossification (Fig. 1).
On Acute Septic Inflammation of Young Bone
Growing from4 Cartilage.
Fic. 1.—From O. L. S., et. two months,
admitted with an acute abscess in the neigh-
bourhood of the ankle-joint, and who died in
hospital from convulsions. The photograph
shows a cartilaginous astragalus, containing an
abscess cavity, in which the necrosed centre of
ossification lies loose.
. Gy d.
Fic. 2.
Fic. 2.—Letitia G., st. 16. Sub-periosteal abscess of tibia. Pyemia.
Death. A vertical antero-posterior section has been made through the upper
part of the tibia. The epiphysis is almost completely united to the diaphysis;
but a small portion of the epiphyseal cartilage still persists on either side.
Beneath the anterior portion a small abscess cavity is seen, which communi-
cated with the sub-periosteal abscess on one side of the tubercle of the tibia.
The insertion of the ligamentum patelle is seen above it, and is suggestive of
the part that structure may have played in the production of the disease.
Growing from Cartilage. 223
In one instance it was found beneath the articular cartilage of
the acetabulum (Fig. 22), but as the child was only six months
old the small abscess cavity at that spot was really at the advanc-
ing edge of the enlarging ossific centre.
In every instance in which the writer has had the opportunity
of examining bones the subject of this disease, either in conse-
quence of death or after amputation, the starting point of the
mischief was discovered, or could with certainty be inferred when
the changes were not too far advanced for it to be demonstrated ;
and in no case was there the least reason to suppose that the
periosteum had played any other than a secondary part. It is,
however, important that the bone should be examined soon after
removal, as a small patch of suppurative osteitis which could not
possibly be overlooked when the surrounding cancellous tissue
is of the usual red colour, soon becomes difficult to distinguish
when the fluids, in which the bone is preserved, have decolourized
the specimen.
PREDISPOSING AND Ехстттма CAUSES.
These may be divided into two groups. In one may be included
such conditions as the patient’s general health, or his power to
resist infection, the local lesion from which the blood infection
takes place, the more general pyeemic state of which, in some
cases, the bone lesions may be expressions, and the proneness of
the highly vascular growing tissue at the juxta-epiphysial
region to become the seat of inflammatory changes. These will
not be discussed. |
The other comprises certain local anatomical and surgical con-
ditions, which have a very direct influence upon the production
of the disease. They are :—
l. The juxta-epiphysial region.
2. The influence of ligament and tendon strain.
3. Traumatic separation of an epiphysis.
1. The juxta-epiphysval region.—In the long bones the junction
of the diaphysis with the cartilaginous epiphysis, or with the line
of cartilage which is interposed for a number of years between
the largely ossified epiphysis and the diaphysis, is so well known
to be a weak spot in the continuity of the bone that it hardly
224 On Acute Septic Inflammation of Young Bone
requires a reference to the frequency with which separation of
the epiphysis is met with in children to emphasize it. This line
of weakness, and of cleavage in cases of separation, is not the
actual epiphysial line, but the soft, spongy layer of bone uniting
the diaphysis with the conjugal cartilage. It has already been
alluded to as the juxta-epiphysial region.
Injuries of an indirect nature, such as ricks, twists and sprains
in which leverage comes largely into play, but in which the force
is insufficient to cause fracture, or separation of the epiphysis, are
more likely to lead to traumatism at this spot than at any other
part of the bone.
Into the epiphysis are inserted ligaments and strong tendons,
which, when put upon the stretch by strain or muscular action,
serve to fix it, so that the stress of the injury falls upon the bone
between the points of application of the force and counter-force,
and the juxta-epiphysial region, in consequence of its weakness,
being less able than any other part of the bone to withstand the
tearing force brought to bear upon it, is prone to suffer.
2. The influence of ligament and tendon strain.—In many of the
illustrations accompanying this paper there is much that is ex-
tremely suggestive of the part played by ligaments and tendons
in the production of the initial lesion.
Thus, Fig. 22 shows a small abscess cavity just below the
insertion of the ligamentum teres into the acetabulum. Another
photograph (Fig. 5) shows the epiphysial cartilage separated (by
suppuration) from the lower end of the diaphysis of the tibia on
that aspect which is enclosed by the anterior and posterior inferior
tibio-fibular ligaments, and the separation is just below the tibial
insertion of the inferior interosseous ligament. In Fig. 2 the cavity
of a small abscess which led to acute periostitis is situated just
underneath the anterior extremity of an epiphysial line which is
completely ossified in its central portion. The ligamentum
patellee, which is also shown, would so obviously pull upon
and tend to strain the weak spot, that the influence it probably
exerted in the production of the disease can be appreciated at a
glance.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Frc. 3,
Fig. 3.—R. G., æt. 13, six days before admission was kicked behind the
right knee, and in trying to save himself he jerked his knee. There was
acute subperiosteal abscess of the femur and acute arthritis of the knee-
joint. Pyeemia, appeared within a few hours of the incisions. The right
hand specimen shows a small abscess cavity (bristle) at the juxta-epiphyseal
line, and an indistinctness in the cartilaginous disc in its vicinity. In the
left hand specimen the way in which the pus found its way beneath the
periosteum of the diaphysis on the posterior surface is seen (bristle). Areas
of osteitis are present in the diaphysis, the most marked being in direct
contact with the abscess. The attachment of the posterior ligament of the
joint to the epiphysis is also shown.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 4.
Fic. 4.—Alfred P., et. 16. Admitted with a history of five weeks’ illness,
and a sub-periosteal abscess, and acute arthritis of the left knee. The limb
was eventually amputated. The specimen shows necrosis of a portion of
compact bone and of a certain amount of cancelloustissue. The chief disease
is on the posterior surface and in close proximity to the epiphyseal line,
with which the disease was in direct contact in the other half of the bone.
The epiphyseal line cannot be traced in its posterior half in the photograph
as it was softened and had lost the appearance of cartilage. The outline of
the periosteal abscessis seen, and also some erosion of cartilage on the condyle.
On Acute Septic Inflammation of Young Bone
„Growing from Cartilage.
Етс. 5. Fic. 6.
Fic. 5 and Fic. 6.—Ambrose H., et. 10. Death from pyemia. The
photographs show, the lower extremity of a tibia. The mischief has begun at
the outer part of the juxta-epiphyseal line in the immediate vicinity of the
inferior tibio-fibular joint and the inferior interosseous ligament. Pus has
tracked upwards, and led to a sub-periosteal abscess of the diaphysis, and
downwards beneath the articular cartilage of the inferior tibio-fibular joint,
entering the ankle-joint, and causing suppurative arthritis.
(By permission of Dr. CHURTON).
Growing from Cartilage. 225
The frequency with which the bones which enter into the knee-
joint are attacked in this disease would seem to indicate the
existence of conditions favourable to its development. Now, the
knee can be fully flexed upon the thigh without putting its liga-
ments unduly upon the stretch, but extension is checked by all
the ligaments except the patellar. Especially may be mentioned
the posterior crucial and the posterior ligament of Winslow, and
with them may be included the tendon of the semi-membranosus,
and the two heads of the gastrocnemius. All these are inserted into
the two epiphysis entering into the knee-joint, and when put
upon the stretch in over extension the tendency of their pull is to
tear apart the epiphysis and the diaphysis of one or other bone
at its posterior aspect.
All the information that can be gathered from the specimens
here figured, points strongly to the belief that the primary focus
about the knee is produced through these agencies, and if so, it
explains why it is that the common place for necrosis in the lower
end of the femur is behind, in the triangular flat space above the
condyles.
3. Traumatic separation of the epiphysis.—If injuries to the
epiphysial line short of separation are frequent exciting causes
of the disease, it might be expected that actual separation would
also figure in that capacity. Fig. 7 is taken from a specimen in
which traumatic separation of the lower epiphysis of the ulna no
doubt determined suppuration, and other examples may be found
among the cases recorded in Mr. Poland’s work on Traumatic
Separation of the Epiphysis.
THE COMPLICATIONS OR CONSEQUENCES.
The initial lesion whose causation and situation have been
discussed, is a small suppurating focus of a more or less intensely
irritating character. The conditions to which it may give rise
depend upon the place where it forms, and upon the direction,
or directions, in which the pus may extend. The latter is
influenced by the nature of the tissues by which the abscess
is bounded, and also by the virulence of the poison.
226 On Acute Septic Inflammation of Young Bone
The conditions which may directly result from acute septic
inflammation of bone growing from cartilage are these :—
1. Acute subperiosteal abscess l
Acute osteomyelitis . | of the diaphysis.
Necrosis.
Separation of an epiphysis.
Acute septic arthritis.
Acute deep-seated abscess.
0
I. ACUTE SUBPERIOSTEAL ABSCESS.
In the long bones the deep or fibrous layer of the periosteum
is attached to each epiphysial line, and also to the articular
cartilages at both ends. It is possible, therefore, for pus to
accumulate under the periosteum covering the diaphysis, or under
that portion of it which overlies an epiphysis. An acute sub-
periosteal abscess of the epiphysis does occur, but is probably
never recognised clinically, for in addition to its small size it is
under cover of tendons and ligamentous expansions, and the pus
tracking towards the joint, lifts up the articular cartilage, bursts
into the joint and leads to arthritis (Fig. 16).
The subperiosteal abscess (acute infective periostitis) which is
so well known, is situated under the periosteum of the diaphysis.
When this is uncomplicated the original focus will frequently be
found just at that portion of the juxta-epiphysial line which
abuts upon the surface of the bone, usually, in the case of the
knee, the posterior surface (Fig. 8).
In these cases the juxta-epiphysial strain is probably received
during hyperextension, and the situation of the initial lesion is
explained by the fact that the maximum injury will be at that
part of the line which is first exposed to the tearing strain. The
pus, therefore, has not far to travel before it reaches the under
surface of the periosteum. Here it finds an easy path of least
resistance, and the periosteum, irritated by its virulent character,
becomes secondarily inflamed, and no doubt is responsible for a
very large proportion of the pus which is evacuated when the
abscess is incised.
As the implication of the bone in the vicinity of the conjugal
cartilage may under such circumstances be very trifling, these
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fia. 8.
Fic. 8.—A diagram to represent
what is probably a not uncommon
situation of the primary focus at the
posterior part of the juxta-epiphyseal
region of the head of the tibia. The
writer has seen several instances of
this lesion ; but the changes due to
preservative fluids have spoilt the
specimens for photographic purposes.
Such specimens are, as a rule, only
obtained after death from pysemia, as
the bone lesion is too trivial to neces-
sitate amputation.
Ето. 7,
Fia. 7.—A boy received an obscure injury to his wrist from a fall. A sub-
periosteal abscess developed in a few days. The elbow-joint became involved,
and eventually amputation was necessary. The specimen shows that the
original injury was a separation of the lower epiphysis of the ulna. New
periosteal bone is seen reaching down to, and helping to fix the epiphysis.
The elbow-joint was implicated by the pus tracking between the insertion of
the brachialis anticus and the origin of the flexor carpi ulnaris.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 9.
Ето. Y.—Upper portion of a tibia sawn open—from a leg amputated for
suppurative arthritis and its consequences. The central portion of the
epiphyseal disc has been destroyed. From this point the inflammatory
process has extended in all directions leading to absorption of cancellous
tissue and small areas of necrosis. (The soft granulation tissue has been
carefully removed). The epiphysis has heen invaded, and the process has
extended through the bone until the articular cartilage has been reached and
the joint involved. The upper end of the diaphysis has suffered considerably
and the medullary cavity has just been reached. In the left hand specimen
a glass rod shows a connection between the large central cavity and a cavity
in the epiphysis, and another shows the track along which the disease has
extended to the medulla. In the right hand specimen the process shows more
lateral extension, but no subperiosteal abscess was formed. The infection
has evidently not been of the most virulent type for the extension of the
disease has been retarded long enough to ensure the removal of a good deal
of bony tissue, and the medulla, though reached, was not obviously affected.
(By permission of Mr. W. H. Brown).
Growing from Cartilage. 227
cases may clear up, if an early incision is made, without any
obvious indication of necrosis; any small area of bone that may
die coming away as granular debris or being absorbed by the
resulting granulation tissue.
2. AcuTE OSTEO-MYELITIS.
If this term is applied to an acute inflammation of the peri-
pheral extensions of the medullary tissue that fill up the spaces
in the cancellous ends of the diaphysis, or of the soft tissue of the
cancellous spaces of the epiphysis, then no doubt acute osteo-
myelitis is present in every case to some extent, but always
extending from the initial lesion. But acute suppurative inflam-
mation of the medullary cavity is one of the least common of
the sequele of the inflammation of growing bone. Only one of
the specimens that the writer has had the opportunity to dissect
(Figs. 10 and 11) illustrates this condition ; but another specimen
(Fig. 9) shows how it is brought about, and why it is not
common.
The acute inflammatory process, as it extends from the central
point of primary infection, meets with different tissues, which
oppose varying degrees of resistance to its progress. At last the
suppurative process opens up a space in which the resistance is
comparatively trifling, and immediately extension takes place
rapidly in this direction, and a relief is afforded by which exten-
sion in other directions is brought practically to a standstill.
Thus, as the area of purulent infiltration increases, it may
reach either the surface of the bone under the periosteum, and
give rise, as already stated, to acute subperiosteal abscess, or it
may open up the joint and give rise to acute arthritis, or it may
extend to and infect the medullary cavity. Now, unless the
infection is exceedingly virulent, the medullary cavity is in many
cases the most difficult of the places for the process to extend to,
because the developed cancellous bone is less easy of solution
than the zone of growing tissue below the conjugal cartilage, or
than the cartilage itself, and an opposing barrier is more readily
formed. Consequently, either acute subperiosteal abscess or
acute arthritis is apt to develop before the medulla is invaded, and
228 On Acute Septic Inflammation of Young Bone
the tension of the inflammatory products within the bone being
relieved, extension towards the medulla is checked.
The nearer the centre of the juxta-epiphysial region the
primary seat of infection is situated, the greater is likely to be
the progress towards the medullary cavity. This is well
exemplified in Fig. 9; and another specimen, already alluded
to (Figs. 10 and 11), in which the central medulla was infiltrated
with pus throughout, confirms it. The bone, for which the
writer is indebted to the kindness of his colleague, Mr. Little-
wood, shows, on longitudinal section, that the whole of the
central part of the upper epiphysial disc has been destroyed, and
that there has been extensive necrosis of the cancellous tissue
extending towards the medulla, yet the small size of the periosteal
abscess and the persistence of the peripheral parts of the cartila-
ginous disc indicate the late arrival of the pus beneath the
periosteum and the freedom of the peripheral parts of the
cartilage from inflammatory softening.
But in those cases in which the primary lesion abuts on the
surface of the bone, the pus is quickly discharged beneath the
periosteum, and extension towards the central parts of the bone
can hardly be said to take place at all. Now, as the peripheral
part of the juxta-epiphysial line is very commonly affected, and
in cases of strain or injury the most likely place to suffer, the
infrequency of suppuration of the central medulla is not a matter
for astonishment.
Though these points are of considerable interest in connection
with the development or prevention of suppuration in the central
medulla, there is one other that transcends them all in import-
ance, viz., the degree of virulence of the infection. As in other
infections, the more virulent the poison the less able are the vital
powers of the patient to offer opposition to its spread. The
difference in virulence can best be illustrated by comparing the
effects produced in two cases— 3
Specimen 1218F in the Royal College of Surgeons' Museum is
the lower half of the right femur of a girl of eleven, who was
admitted into a hospital with a large abscess at the lower end of
the right thigh. The bone was found to be acutely inflamed, and
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 10. Eid; 11.
Fic. 10 and Fig. 11.—W. H., æt. 15, a labourer, had a subperiosteal abscess
opened a fortnight after a kick at football, which had led first to swelling
and then to very severe pain in the leg and constitutional disturbance.
Abscesses subsequently formed about the ankle, and amputation was
performed.
Fig. 10 is an antero-posterior section of the bone. The central medullary
cavity was infiltrated with pus throughout. Below the upper epiphysial disc
a very considerable area of the cancellous portion of the diaphysis was
necrosed and partially separated. "This necrosed portion did not reach to the
peripheral extremities of the conjugal cartilage. The destruction of tissue
seen in the photograph below this was due partly to a fracture caused in
sawing open the bone, and partly to the gouging of the bone when the peri-
osteal abscess was opened. The primary focus was probably near the centre
of the juxta-epiphysial area, and infection had spread rapidly towards the
central medulla and involved it before pus reached the surface of the bone
and led to the subperiosteal abscess, whose small size is well shown in
Fig. 11.
(By permission of Mr. LITTLEWOOD.)
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Era, 13;
Fic. 12.—Acute osteomyelitis of the tibia of a boy about twelve years old.
Amputation.
The most pronounced changes are at the upper extremity of the diaphysis,
which is completely separated from the epiphysis and necrosed. The
medulla was infiltrated with pus, and the juxta-epiphysial region at the
lower end of the diaphysis had been reached, and separation of the lower
epiphysis was in progress. The limits of the subperiosteal abscess beginning
at the upper end are seen about half way down the shaft, but suppuration
about the ankle in connection with the extension of the disease from the
lower end of bone was beginning.
(By permission of Mr, WARD.)
Growing from Cartilage. 229
immediate amputation was followed by a good recovery. In the
specimen the medulla and cancellous tissue of the diaphysis are
infiltrated with yellow foci of suppuration, and the outline of a
large subperiosteal abscess is seen on the surface of the bone.
Ulceration of the bone has occurred in the usual place poster-
iorly (viz., at the juxta-epiphysial line), but is not extensive.
The joint was not implicated.
The small amount of destructive bone change at the juxta-
epiphysial region, coupled with the nature of the wide spread
implication of the medullary tissue and the periosteum, justified
the assumption that the poison must have been of an intensely
septic character, and this was confirmed by Mr. Edmund Owen,
by whom the specimen had been presented, and who in answer
to an enquiry has written that the girl would have died of acute
septic intcxication if amputation had not been performed.
The description of this case may be contrasted with the speci-
men illustrated in Fig. 9, in which the medulla has been spared
in consequence of the slow progress that the suppurating process
has been able to make.
3. NECROSIS.
On this subject there is little left to say that is not found in
the text-books. Resulting always from subperiosteal abscess or
osteomyelitis, it is open to question if it should not have been dealt
with under those headings. Convenience, as well as precedent,
however, justify its separate treatment.
Only a few points call for comment here.
(1). Necrosis of compact tissue.— Though in extreme cases the
whole diaphysis or considerable portions of it may die, especially
at that end at which the primary focus is situated, yet the form
most commonly met with is necrosis of the compact tissue.
This form of necrosis is probably due to suppurative inflamma-
tion taking place in the vascular channels of the compact bone.
Direct infection of the superficial layers of bone is very liable to
1 Since this was written a se ond specimen of acute osteomyelitis of the
central cavity has come under the writers’ observation. It confirms much that
has been said with reference to the specimen illustrated in Figs. 10 and 11.
À detailed description is appended to its photograph (Fig. 12).
230 On Acute Septic Inflammation of Young Bone
occur when it is covered with pus under considerable tension.
But necrosis, though a usual result of acute subperiosteal abscess, is
not by any means a necessary one, and this fact shows that the
interference with the blood-supply from a stripping up of the
periosteum is not a sufficient explanation of it.
Necrosis rarely extends beyond the compact bone when the
infection is from the surface.
Those large cavities filled with granulation tissue and contain-
ing eroded fragments or plates of compact bone, which are
so commonly seen in sequestrotomy of a bone such as the
tibia, would seem to suggest that the necrosis had involved a large
portion of the shaft, and that the compact tissue by reason of its
density, was the only portion that had not been absorbed.
In view, however, of the infrequency of suppurative inflamma-
tion of the central medulla, the more probable explanation is that
the compact tissue alone perishes at the time of the formation of
the subperiosteal abscess, but the cancellous tissue in its vicinity
is gradually destroyed by the rarifying osteitis through which the
separation of the sequestrum is brought about.
(2) Migration of sequestra.—If a sequestrum forms in the
vicinity of the growing end of a long bone, it may in the course
of years, if not removed by natural or artificial means, be carried,
in consequence of the growth taking place at the epiphysial line,
a, considerable distance away from it.
Thus, Fig. 13 shows a strip of compact tissue which had under-
gone necrosis at the age of 2. It can be recognised as belonging
to the lower portion of the early shaft, and when the leg was
amputated ten years later, it was found quite two inches distant
from the epiphysial disc.
(8) The importance of removing sequestra when loose.—The
same case illustrates an exceptional danger that may result from
the neglect to remove a loose portion of dead bone. The seques-
trum in the course of years, and in consequence of its migration
and its gradual action upon the enclosing bone, had come to lie
almost transversely, transfixing the shaft of the femur. The end
that protruded upon the inner side had ulcerated into the femoral
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Ето. 13.
Ето. 13.—John W., et. 11, had an abscess in the lower part of the thigh
` at the age of two, and ever since there had been sinuses. Admitted for
hemorrhage of a serious character from the sinuses. The limb was ampu-
tated. The specimen shows a considerable sequestrum, representing a
vertical portion of the compact tissue of the early diaphysis. This lies
obliquely and its ends project through apertures on either side of the femur.
On the inner side it has ulcerated into the femoral artery, and the circle of
fishing gut seen on the left side passes round a rod lying in the artery at the
point where it is exposed by the hole in the vessel. In consequence of the
growth that has taken place at the lower epiphysis the sequestrum has been
displaced upwards for at least two inches and has also come to lie obliquely.
The front of the bone has been chiselled away to expose the sequestrum.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Ето, 14. Ето. 15.
Fic. 14.—From a boy. Subperiosteal abscess, suppurative arthritis, separation of
epiphysis. Amputation. Before amputation there was considerable deformity of the
joint simulating sub-luxation, but in reality due to displacement backwards of
the leg and the attached epiphysis of the femur. The lower end of the diaphysis
lay bare in the suprapatellar pouch of the joint. The specimen shows that suppura-
tion and destruction of bone has taken place over the whole juxta-epiphyseal area,
The lower end of the diaphysis is much eroded and also the surface of the compact
tissue for some distance. The limit of the subperiosteal abscess is evident.
Ето. 15.—From a child two years old. On incising a subperiosteal abscess, the
lower epiphysis of the femur was found separated. There was no history of injury.
Joint not involved. On re-admission for sequestrotomy, this skiagram was taken.
It shows displacement backwards of the lower epiphysis. This is united to the new
bone thrown out by the periosteum, which has retained its attachment to the
epiphysis. The joint could be placed in the position of genu recurvatum.
Growing from Cartilage. 231
artery, and led to severe recurring attacks of hemorrhage, for
which the limb was amputated.
4. SEPARATION OF AN EPIPHYSIS.
Separation of the epiphysis may result from suppuration
extending transversely over the whole juxta-epiphysial area.
Such a condition is shown in Fig. 14, and similar specimens
are not rare. Many of these cases end in amputation, but under
favourable circumstances it is possible for an epiphysis separated
in this way to unite. This actually occurred in the case from
which the skiagram (Fig. 15) was taken, but as a sequestrum is
still present, and the limb assumes the position of genu recur-
vatum, the patient cannot be regarded as having completely
recovered.
5. ACUTE Septic ARTHRITIS.
When this occurs as a consequence of inflammation of growing
bone it is brought about in one of several ways.
(1). From anatomical predisposttion.—In the case of certain
joints their implication is very largely dependent upon the
anatomical relations of the epiphyses forming part of them.
Thus the hip-joint is almost certain to suppurate when the
disease originates at the upper epiphysial line of the femur,
because the head and a large part of the neck lie practically
within the joint. And if the primary focus is situated at the
ossifying edge of the cartilage forming the acetabulum (Fig. 22),
it is impossible to conceive any other outlet for pus except into
the articulation.
The elbow is another joint that may suffer in consequence of
the position of the upper epiphysis of the ulna. This, after the
tenth year, is only a small disc situated at the extremity of the
olecranon process and the chief part of the great sigmoid fossa
is fashioned from the upper end of the diaphysis, consequently
the attachment of the deep layer of periosteum to the epiphysial
line cannot, in the case of the ulna, act as an outlying barrier for
the protection of the joint from the extension of a subperiosteal
abscess. In the case from which Fig. 7 was taken, suppuration,
which began at the lower epiphysial line after a separation of
the epiphysis, stripped up the periosteum along the whole length
232 On Acute Septic Inflammati.n of Young B ne
of the bone and found an entrance to the joint on the inner side
of the insertion of the brachialis anticus tendon.
(2) As a consequence of subperiosteal abscess of the epiphysis.—
Suppuration commencing as usual at the juxta-epiphysial line
may lead to an acute abscess beneath the periosteum covering
the epiphysis. This is necessarily so small as to be incapable of
recognition clinically. The pus strips up first the periosteum
and then the articular cartilage, and finally finds its way into the
joint. Itis not easy to understand how it finds its way under
this portion of the periosteum, for according to ordinary anato-
mical arrangements it would be expected to find an outlet under-
neath that membrane where it covers the diaphysis. This it
does in the very large majority of cases, but that it may take the
unusual course here stated is shown by the specimen depicted in
Fig. 16. Possibly it may find an easy passage along the course:
of one of the vessels which according to Poland? sometimes
perforate the epiphysial disc, or possibly the conjugal cartilage
may be softened by the inflammation and permit the passage of
pus through it, as later on it will be shown to do under other
circumstances.
(3) From direct extension of the suppurative process through the
epiphysis.—Suppuration of a joint not infrequently depends upon
the inability of the conjugal cartilage to withstand the softening
effects of the acute inflammatory process going on just beneath
it. It loses over a varying area its characteristic appearance, and
in the specimen is found to be converted into a soft, washleather-
like tissue, or even granulations.
By the destruction of a part of this barrier, the pus finds an
entrance to the epiphysis proper, and eventually reaches the joint
in one of two ways :—
(a) Hither it tracks round the circumference of the ossified
portion of the epiphysis, separating it from its as yet cartilaginous
periphery, until it reaches the articular cartilage, and breaks
through into the joint (Fig 17), or
(5) It may extend through the cancellous tissue of the epiphysis
as an acute osteo-myelitis. (Fig. 9).
2 Poland, Traumatic Separation of Epiphysis, p. 20.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
E15. 15.
Fig. 16.—The head of the tibia from a boy aged about 13. The leg was
amputated for profuse suppuration among the calf muscles following acute
arthritis of the knee. There had been no subperiosteal abscess of the
diaphysis, but the pus extending from the primary focus in the juxta-
epiphysial region had emerged on the surface at the crack seen in the
photograph below the patch of bare bone which corresponded with the
situation of the insertion of the semimembranous tendon. It had found
its way under the periosteum covering the epiphysis and had stripped up the
articular cartilage before opening into the joint, leaving & considerable
portion of the articular surface of bone bare.
On Acute Septic Inflammation of Young Bone
Growing from Cartilaye.
Fic. 17,
Fia. 18.
Fie. 17 and Етс. 18.—Photographs of the tibia from the amputated leg
of a young boy. There had been acute arthritis of the knee, and sub-
periosteal abscess of the tibia.
Fig. 17.—Antero-posterior section.—Only the lateral terminations of the
conjugal disc are seen, but in the specimen it could be recognised by a soft,
wash-leathery line, except in some places where it had completely disappeared.
On either side are marked changes. A large portion of the epiphysis is
necrosed and is separated from its cartilaginous periphery over a very con-
siderable area. This separation, by interfering with the blood-supply, is
probably responsible for the necrosis. In the diaphysis the carious and
necrotic changes are limited to the portion just below the epiphysial line, the
greater extension on the right of the right hand specimen being due to the
prolongation of the epiphysis downwards in the tubercle of the tibia. The
subperiosteal abscess has arisen in connection with this part of the mischief.
The suppurative process starting in the juxta-epiphysial region has softened
and permeated the conjugal cartilage and found an easy path round the
periphery of the bony epiphysis until it has reached the articular cartilage
and opened into the joint. On the side of the diaphysis it has evidently
extended more deeply into the bone, yet extension has taken place more
rapidly laterally where the cancellous tissue is of more recent formation.
Fig. 18 shows the articular surface, and a glass rod indicates the position
in which pus has found its way to the joint.
(By permission of Mr, TEALE,)
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 19. Fic. 20.
Fic. 19 and Fic. 20.— The two illustrations show the cause of suppuration in both
knee-joints of a boy st. four weeks. ,
Fig. 19 shows an abscess in the cartilaginous epiphysis which contained a, small
cretaceous mass. This abscess had opened into the joint. The diaphyseal side of the
cartilage is seen to be uninjured.
Fig. 20 shows an abscess in the juxta-epiphyseal area, which has hollowed out the
diaphysis more than the cartilage. This also had opened into the joint. These photo-
graphs serve to illustrate the different positions in which the primary focus originates,
viz., at the centre of ossification and at the juxta-epiphyseal region.
(By permission of Sir THOMAS SMITH).
FIG: 91. Fig. 22,
Fic. 21.—The head of the left femur of a congenital syphilitic infant, who had
suppuration of three joints, and died at twelve months of age. This abscess ‘ was
situated partly in the ossifying cartilage and partly in cancellous bone,’’ and opened on
the neck of the femur, close to the digital fossa.
(By permission of Sir THOMAS SMITH, figs. 19, 20 and 21 are taken from his article
on ““Acute Arthritis of Infants," (Cases 2 and 3,) in St. Bartholomew’s Hospital
Reports, vol. 10, p. 192).
Fra. 22.—Olive —, st. six months. Acute suppuration of the right hip-joint,
erysipelas, purulent peritonitis. Death. An aperture was found in the acetabulum,
leading through the articular cartilage to a small abscess cavity. In the photograph
the acetabulum is seen divided across, so as to show the abscess. In the upper half a
glass rod marks the track from the abscess cavity to the interior of the joint, and below
it a bristle is inserted into the cavity itself. In the lower half a piece of glass rod has
been laid laterally in the abscess cavity, which is situated between the articular
cartilage and the bone. The abscess is close to the origin of the ligamentum teres.
Below the glass rod is a pin.
Growing from Cartilage. 233
In either case, necrosis of the epiphysis, more or less complete,
results, and as the articular cartilage is usually largely destroyed,
the necrosed surface lies exposed in the joint.
In these cases, a study of the specimens leads to the belief that
the focus of the disease is situated near the central portion of the
juxta-epiphysial region, and not near the periphery. The disease
has usually led to considerable mischief below the epiphysial
line, and has probably penetrated it and got well started in the
epiphysis before it reaches the periphery, and leads to a sub-
periosteal abscess, which, in the majority of cases, even though
the joint is affected, is the condition which is most obvious when
the patient comes under surgical treatment.*
(4). In consequence of the cartilaginous nature of the epiphysis
in early infancy. ““ Acute Arthritis of. Infants."—In very young
infants, where the epiphyses are almost entirely formed of car-
tilage, the readiness with which the young cartilage disappears
before the suppurative process gives a very different character to
the disease. Abscesses develop in the soft cartilage whether the
primary focus happens to be at the juxta-epiphysial line or in
connection with an ossifying centre, and their cavities are
frequently found to open directly into joints.
This condition has been carefully described by Sir Thomas
Smith in his well-known paper on Acute Arthritis of Infants,
(St. Bart.’s Hospital Reports, vol. x., p. 192), and the writer is
indebted to him for permission to reproduce three photographs
from that paper, which seem clearly to suggest the positions
in which the mischief begins, and to illustrate the peculiar
features which acute septic inflammation of growing bone assumes
at a very early age in consequence of the difference in nature,
and possibly of texture, of the tissues at that period (Figs. 19,
20, 21).
6. DEEP-SEATED ABSCESS.
This complication, apart from necrosis and periosteal abscess,
does not seem to have received any attention in the text-books,
although it cannot fail to be familiar to most surgeons.
$In a discussion on this paper, at the Leeds and West Riding Medico-
Chirurgical Society, Mr. Littlewood referred to a case in which it was easily
demonstrated that infection had reached the joint along the popliteus tendon.
234 On Acute Septic Inflammation of Young Bone
The origin of acute abscesses beneath the deep fascise is often
very obscure. Glandular or lymphatic suppurations probably
account for many cases, but another large group undoubtedly
originates in connection with growing bone. There are a con-
siderable number of situations, apart from the epiphysial ends of
the long bones, where, during childhood and youth, cartilage is
being transformed into bone. The epiphysis of the great and
small trochanters of the femur, and of the coracoid process of the
scapula, the sacro-iliac synchondrosis, the cartilaginous bond of
union between the rami of the pubes and ischium, and the small
cancellous carpal and tarsal bones which possess centres of ossi-
fication, are a few that may be mentioned. The three first
exemplify the fact that these subsidiary epiphyses often serve for
the origin or insertion of powerful muscles, and are consequently
likely to experience occasionally some of the ill effects of strain
and tendon pull.
The small area covered by some of these epiphysis enables the
pus quickly to find a way to the surface of the bone, and the
periosteum is in many cases soon penetrated, possibly because it
is thin or because the origins of muscles have rendered it firmly
adherent. An abscess among the muscles results. There is
frequently hardly any stripping of periosteum, and necrosis may
or may not follow, and when it does it is often trivial. Conse-
quently many of these acute abscesses clear up without trouble
after incision, and unless the source of the mischief is found by
careful search, their real character may be missed. Further, it
will be seen from the cases that follow, that when inflammation
of bone originates at one of these somewhat inaccessible growing
spots it may prove a fruitful source of difficulty in diagnosis, or
of error.
CASE 1.—A boy, aged 6, was admitted to the Fever Hospital
for (?) typhoid, and in a few days was transferred to the Leeds
General Infirmary for an acute abscess in the adductor region.
The hip was unaffected. The abscess was opened and a small
area of bone was found bare and rough at the junction of the
rami of the pubes and ischium: a small transverse notch
indicated where the cartilage had probably been eroded. The
abscess healed quickly without any exfoliation of bone,
Growing from Cartilage. 235
CASE 2.—A youth of 15 had been in the medical wards for
two or three weeks with a high temperature, and pain about
the right hip. The joint was evidently unaffected. No diagnosis
was made. The development of a swelling in the right iliac fossa
led to the writer being asked to see him. A fluctuating tumour
could be felt, from the rectum, to lie over the sacro-iliac joint.
The condition was obviously acute and not tubercular. A
diagnosis of suppuration‘ originating at the sacro-iliac joint in
connection with growing bone was suggested. The case was
transferred to Mr. Littlewood, who opened the abscess, and after
a patient search found a small patch of bare eroded bone just
at the edge of the synchondrosis. No necrosis resulted and
the abscess healed without trouble. |
CASE 3.—A boy of 12 developed a very acute abscess about the
left shoulder two or three days after being pushed against by a
schoolfellow. It was opened in the axilla and the finger passed
between the two pectoral muscles to the coracoid process, which
was quite bare. This process necrosed and came away before the
resulting sinus healed.
CASE 4.—Specimen 1218 in the Royal College of Surgeons
Museum, is a scapula from a boy of 12, who died of pyemia after
a fall on the shoulder ten days before. -
The root of the coracoid epiphysis is denuded of its periosteum,
and the intervening cartilage is in great part destroyed. A sub-
periosteal abscess occupies the dorsal and ventral surfaces of the
scapula, and these communicate freely above the neck of the
bone. A full description of this case is given by Poland in
Traumatic Separation of the Epiphysis, p. 160.
Case 5.—-An infant, two months old, was admitted with an
acute abscess about one ankle. This was incised. The child
subsequently developed erysipelas and died of convulsions. The
cause of the abscess was necrosis of the centre of ossification of
the astragalus. (Fig. 1.)
OToRRHGA AND MASTOID ABSCESS.
Before this portion of the subject is dismissed, attention may
be directed to suppuration arising in connection with the temporal
bone.
VOL. LVI. 19
236 On Acute Septic Inflammation of Young Bone
“ Mastoid abscess ” is generally looked upon as secondary to a
chronic aural discharge, resulting from an otitis media. It is
admitted that an otorrhosa and a mastoid abscess may be due to
a primary disease of the bone, but so far as the writer can learn,
this primary disease has usually been regarded as tuberculous.
It is probable, however, that not a few of these primary bone
inflammations resulting in abscess are, in their pathology, iden-
tical with the acute periosteal abscesses which arise in connection
with the inflammation of growing bone. From this point of view
the development of the temporal bone is of interest.
Of its three portions the squamosal and the tympanic are formed
in membrane, and it may be noted in passing that this acute
infective disease rarely, if ever, attacks these or any other of the
membranous bones. The petrosal, from which the mastoid is
subsequently developed, arises by four centres in cartilage. The
growth of these bony centres is so rapid during the later months
of foetal life, that at birth all that remains of the cartilage is a
thin intervening plate at the squamo-petrosal suture, and this
becomes completely ossified during the first year. (Fig. 28 shows
the squamo-petrosal suture). So long as it exists it is, in effect,
an epiphysial disc where growth is taking place, and is no doubt
as prone to be attacked by suppurative organisms under favouring
conditions as conjugal cartilages elsewhere.
. Fig. 24 shows well the ridge on the squamosal at birth which
marks the squamo-petrosal suture and the position of the conjugal
cartilage. It lies immediately over the tympanum, and any
abscess originating in connection with growing bone at the
uniting cartilage would be almost certain to find its way into the
upper part of the tympanum. Not only would gravity favour
this, but the difference in tension between the middle ear and the
intracranial contents, as well as the firmer attachment of the
dura mater on the upper surface of the bone, would no doubt
tend in the same direction. |
The following case, which Mr. Nunneley has permitted the
writer to make use of, and from which the specimen shown
in Fig. 23 was prepared by Mr. Secker Walker, is very probably
an instance of this mode of origin of a mastoid abscess. Like
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 23.
Fic. 23.—The temporal bone of W. H. B., xt. three months, shows the
line left after suppuration and maceration have removed the cartilage at the
petro-squamosal suture. A portion of the squamous bone has been broken
in preparation.
(By permission of Mr. SECKER WALKER).
Fra. 24.
Fic. 24.—The squamosal portion of the temporal bone at birth. The ridge
which unites with the petrous portion at the petro-squamosal suture is well
shown, and the situation of the conjugal cartilage with respect to the middle
ear can be readily appreciated.
(Figs. 23 & 24 are from specimens prepared by Mr. SECKER WALKER).
Growing from Cartilage. 237
many cases of otorrhcea supposed to be due to primary disease
of bone, it occurred in the first year of life before the petro-
squamosal cartilage had disappeared.
VV. H. B., aged 3 months, had a purulent discharge from the left
ear for some time before admission, and facial palsy supervened.
There had been no exanthem or other serious illness except
occasional convulsions before the aural discharge. The mastoid
process was found soft and carious and the antrum filled with
soft caseating material. The child lived a week after the opera-
tion, during which there was general rigidity but no convulsions.
Post-mortem.—A few tubercles upon the surface of the spleen.
No tubercle in the lungs. Brain.—Increased arachnoid fluid, but
no distension of ventricles; the left half of the cerebellum was
softer than the right and easily broke down.
The condition in the left half of the cerebellum, the absence
of tubercular meningitis, and the specimen itself, are all more
in favour of an acute infective inflammation of growing bone
than of tubercle. The notes suggest that tubercle was the
dominant idea throughout the case and possibly explain the
description of the spleen.
A specimen, belonging to Mr. Arthur H. Cheatle (No. 618,
Catalogue of the Otological Museum—6th International Otological
Congress, 1899) is also suggestive. f
It is the ‘‘left temporal bone of a child aged one year who
died of suppurative meningitis. Membrane intact and bulging—
middle ear full of muco-pus containing streptococci and staphy-
lococci; lining membrane thick and congested looking; veins
from middle ear to the petro-squamosal sinus marked—roof of
middle ear was intact.”
238 On Acute Septic Inflammation of Young Bone
APPENDIX.
To prevent confusion, certain unusual and interesting cases are
dealt with here, apart from the main plan of this article, whilst
some other conditions are alluded to chiefly for the sake of
comparison.
TUBULAR OR PYRAMIDAL ABSCESS OF BONE.
There is a very unusual form of abscess in bone whose mode
of origin is somewhat doubtful. The abscess is tubular or pyra-
midal in shape, with its base resting upon a line corresponding
to the situation of the conjugal cartilage, and its apex directed
towards the medullary cavity. It runs a chronic course.
In the two specimens referred to below, the abscess was
situated in the lower part of the diaphysial portion of the femur,
and in both a sequestrum was or had been present. The speci-
mens suggest that a suppurating inflammation of bone, resulting
in necrosis, has occurred in the neighbourhood of the conjugal
cartilage, and that the abscess has been walled up by a sclerosing
osteitis around it, extension taking place directly upwards towards
the medulla, probably because the density of the bone in this
direction was least.
But the difficulty of accounting for suppuration taking place in
this situation arises from the ages of the patients.
In both the conjugal cartilage should have been completely
ossified years before the first signs of trouble showed themselves,
and yet the position and peculiarities of the abscesses give rise to
a strong impression that they originated from a portion of the
epiphysial cartilage that had failed to disappear.
Fig. 25 is a photograph of a specimen which was taken from a
leg amputated by Mr. Mayo Robson. In the lower part of the
abscess cavity there was found a small sequestrum lying vertically,
and since lost.
The patient was a woman of 35, in whom the first signs of the
disease had appeared five years before.
No. 1247 a in the Royal College of Surgeons’ Museum is a. very
similar specimen from a man of 46, whose illness began nine
years before amputation. A sequestrum was removed.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 25.
Fic. 25.—Tubular or pyramidal abscess of bone. The upper part of the
abscess sac has been laid open to show the glass rod, which is better seen in
the basal portion of the cavity.
(By permission of Mr. Mayo Rosson).
Growing from Cartilage. 239
~
Туо-Еог,о INFECTION.—ACUTE INFECTIVE INFLAMMATION OF
BONE ASSOCIATED WITH TUBERCULOUS SYNOVITIS.
The following case is of considerable interest :—
J. H. G., a boy, set. 11, whilst playing cricket was ‘seized with
sudden pain in the right knee. Till that moment he had been
quite well. The next day he had to lay up, and in due course an
abscess formed, which at the end of three weeks was incised, and
a pint of pus let out. Ten months later he was admitted to the
Leeds General Infirmary. The knee had all the characteristics
of a tuberculous knee-joint, which had gone on to subluxation.
There was also a good deal of thickening about the lower end of
the femur, and a sinus opened on the outer side. Excision of the
knee was performed. The joint was in that stage of pulpy disease
in which the condition was going on to repair. The granulation
tissue was largely transformed into fibrous tissue, and the patella
was ankylosed to the femur. In the lower part of the femoral
diaphysis a large abscess cavity was found containing a sequestrum
of the compact tissue two inches long by one inch broad. This
cavity communicated by the sinus with the exterior, but was
completely separated from the sawn surface of the epiphysis by
the healthy conjugal cartilage. Good union took place.
Here, in close proximity, there existed two distinct diseases—
a suppurative inflammation of growing bone speedily resulting in
abscess and necrosis, above the epiphysial line, and a tuberculous
and non-suppurative inflammation of the synovial membrane of
the knee-joint, involving the lower epiphysis of the femur,
below it.
The history of the onset of the former was readily forthcoming,
but the tuberculous state had come on gradually and unnoticed.
All that the patient or his friends could say was that the knee
had been quite well and like the other before the acute condition
set in.
It may be presumed, therefore, that the two diseases originated
at the same time, or that the tuberculous state became grafted
240 On Acute Septic Inflammation of Young Bone
upon a simple inflammatory synovitis, induced by the acute
suppuration in the vicinity of the joint.
NECROSIS IN THE FULLY ÖSSIFIED Lona BONES.
Necrosis which is neither traumatic, tuberculoüs, nor syphilitic,
is occasionally met with as a result of an apparently spontaneous
acute inflammation affecting a portion of a long bone.
Such cases are rare, and whatever their true pathology may be,
it is clear the inflammation does not originate where cartilage is
being transformed into bone. The inflammatory focus is, on the
other hand, probably a considerable distance from the vicinity of
an epiphysis.
The following case illustrates this and forms an excellent con-
trast to the conditions so frequently occurring in children and
young adolescents.
W. B., et. 43, a robust man, had been out on strike six weeks
when his right forearm began to swell for several inches above the
wrist. In a few days it was incised, and it continued to discharge for
three years, when the writer removed two sequestra—one of com-
pact bone, and the other of cancellous tissue as big as a marble—
from a, cavity surrounded [by sclerosed bone. This cavity was
quite one and a-half inches from the wrist, and a considerable
distance from the ordinary level of the epiphysial line. No history
of injury or of probable tubercle could be obtained, nor had the
patient suffered from want of food when on strike.
THE Immunity or MEMBRANF-BONES. |
One exceedingly interesting point in connection with the subject
of this paper is the immunity which bones developed from mem-
brane possess in regard to acute infective suppuration.
The writer has never seen an instance in which suppuration
or necrosis about the skull or face or lower jaw could be attributed
to the acute infective suppurative disease of bone which is so
very common in bones growing from cartilage before ossification
is complete; nor has he been able to find in three museums
(Hunterian, Guy's, and Leeds) a single specimen of cranial
necrosis which could with any probability be referred to that
disease.
On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
Fic. 26.
Ето. 26.—Matthew W., æt. 26. Chronic suppurative osteomyelitis of the
whole frontal bone ; showing his present condition.
Growing from Cartilage. . 241
The most likely explanation of this immunity is the absence of
a conjugal disc, and of the weak and vulnerable juxta-epiphysial
region. In the long bones the epiphysial disc and the juxta-
epiphysial region introduce not only a place of least resistance
but certain anatomical peculiarities, which are of considerable
importance in determining the various complications of infective
suppuration. This predisposing factor is absent in the membrane
bones and with it the typical complications by which the disease
is readily recognised.
Necrosis, other than syphilitic, is usually the result of direct
injury, but the bone is generally in contact with a septic wound,
and the inflammatory process which leads to its death is doubtless
secondary, and is speedily limited.
. Osteo-myelitis is also met with, for portions of the whole thick-
ness of a bone will necrose. Yet osteo-myelitis is rarely extensive
and is a part of the general osteitis associated with the septic
wound. The following case of an osteo-myelitis which involved
the whole diploe of the frontal bone, might at first sight very
possibly be thought to be an instance of the acute infective
variety, but the gradual way in which by successive extensions,
once connected with fresh injury, the condition spread during a
period of years, makes it present a very different clinical picture
to the acute osteo-myelitis which leads to necrosis of the diaphysis
in the long bones. In this instance there was no necrosis of the
inner or outer table but only of the diploe.
Matthew W., set. 26, ten or twelve years before his final admission
to the Leeds General Infirmary in 1898, received a scalp wound
over the left eye, which was stitched up. Some weeks later he
came under Mr. R. N. Hartley, at the Leeds Public Dispensary,
for a tender swelling at the outer side of the orbit. The outer
plate of the frontal bone was gouged through, and a small area of
diseased cancellous bone was scraped away. This relieved his
pain, but the disease continued to extend and reached the situation
of the frontal sinuses. At intervals four more similar operations
were performed, including drainage of the frontal sinuses.
Sinuses and offensive discharge persisted, and in 1896 he was
kicked on the head by a horse, and admitted under Mr. Robson
42 On Acute Septic Inflammation of Young Bone
Growing from Cartilage.
into the Infirmary. From this time onward the writer had
opportunities of seeing the patient when he made occasional
reappearances, and his condition became more and more dis-
tressing in consequence of the amount and foul odour of the
discharge. In January, 1898, he removed, at two operations, a
large horse-shoe of the outer table. This table was half an inch
thick and very dense, and between it and the inner table a quantity
of foetid granulation tissue, containing innumerable small can-
cellous sequestra, was found. After this had all been cleaned
away, the cavity between the two plates was found to extend over
the whole frontal bone. The patient made a satisfactory recovery,
and is now quite well, except that the prolongation of the frontal
sinus over the right orbit has not yet completely filled up.
(Fig. 26).
SOME NOTES ON THE ZTIOLOGY
OF STRABISMUS.
By ARTHUR W. ORMOND, F.R.C.S.
ASSISTANT SURGEON, ROYAL Eye HOSPITAL, SOUTHWARK.
OPHTHALMIC REGISTRAR AND Tutor, Guy’s HosPITAL.
THE Zütiology of Strabismus is a matter over which ophthalmo-
logists have long contended, and one which even now has many
points still unproved. There are, however, cases, perhaps the
majority, that may be satisfactorily explained, and it is my
object in this paper to record the notes of a selected number of
these cases, taken mainly from the out-patient department of
Guy's Hospital, and compare the various theories explaining
strabismus with the actual facts.
By strabismus, or squint, I mean the condition in which the
visual axis of one eye deviates from the visual axis of the other,
the axes not meeting at the object looked at, the angle of
deviation remaining the same, in whichever position the eyes
are turned. This excludes all those cases of deviation of the
visual axis of one eye from that of the other, due to paralysis
or paresis of one of the extrinsic muscles of the eye.
Strabismus manifests itself early in life, the patient squints if
he or she has the conditions necessary for its manifestation
in the majority of cases from the third to the fifth year of life,
244 Some Notes on the twlogy of Strabismus.
but a, concomitant squint may appear at any age, since, as I
shall point out later, a latent squint may become manifest if the
visual acuity of one eye should become seriously depressed below
that of the other; but convergent concomitant squints generally
manifest themselves before the tenth year. Consequently we
have to look for the cause of squints among conditions existent
in the eye during the early months of life.
According to Fleichsig, the formation of medullary sheaths to
the fibres of the optic nerves has commenced at birth, but has
not extended centripetally to the cortical area, consequently we
may assume that at birth there is no isolated conduction along
the fibres of the optic nerve to the brain.
Further, in order to correctly appreciate the appearance of
objects in space, as to form, colour, etc., the centres of the other
sensory organs must be developed and the transcortical fibres
connecting these with the visual centres must be also developed.
Probably a period of some two or three years is passed during
childhood before the centres and their communications one with
another are fully matured.
Baumgarten asserted some years ago, and experience confirms
his observation, that a newly-born infant saw merely light, and
that only quantitatively. We all know the vacant stare of very
young children, the inability to fix the eyes for more than the
shortest time, and the isolated movements of one eye and often
of one lid.
In the Philosophical Transactions of 1728, Cheselden reports a
case of a young man receiving sight after couching of the
cataract in each eye, he previously having been able only to
see light and discern colour in mass. In this case, and in others
that have been published since, we have the statement of
intelligent adults on the gradual development of vision in their
own eyes.
* When he first saw he was so far from making any judgment
about distances that he thought all objects whatever touched his
eyes (as he expressed it) as what he felt did his skin, and thought
no objects so agreeable as those: which were smooth and
regular, he knew not the shape of anything nor auy one thing
Some Notes on the Astiology of Strabismus. 245
from another, however different in shape and magnitude. Upon
being told what things were, whose form he before knew from
feeling, he would carefully observe, that he might know them
again, but having too many objects to learn at once he forgot
many of them, and (as he said) at first he learned to know,
and again forgot a thousand things in a day. One particular
only (tho’ it may аррзаг trifling) I will relate. Having often
forgot which was the cat and which the dog, he was ashamed to
ask, but catching the cat (which he knew by feeling) he was
observed to look at her steadfastly, and then setting her down
said, “ So, puss, I shall know you another time.” He was much
surprised that those things which he had liked best did not
appear most agreeable to his eyes, expecting those persons would
appear most beautiful that he loved most, and such things to be
most agreeable to his sight that were so to his taste. We
thought he soon knew what pictures represented, which were
shewed to him, but we found afterwards we were mistaken, for
about two months after he was couched, he discovered at once
they represented solid bodies, when to that time he considered
them only as party-coloured planes, or surfaces, diversified with
variety of paint, but even then he was no less surprised, expect-
ing the pictures would feel like the things they represented, and
was amazed when he found those parts, which by their light and
shadow appeared now round and uneven, felt only flat like the
rest, and asked which was the lying sense, feeling or seeing.
At first he could bear but very little light, and the things he
saw he thought extremely large, but upon seeing things larger,
those first seen he conceived less, never being able to imagine
any lines beyond the bounds he saw, the room he was in he said
he knew to be but part of the house, yet he could not conceive
that the whole house could look bigger. Before he was couched
he expected little advantage from seeing worth undergoing an
operation for, except reading and writing, for he said he thought
he could have no more pleasure in walking abroad than he had
in the garden, which he could do safely and readily. And even
blindness, he observed, had this advantage, that he could go
anywhere in the dark much better than those who can see, and
246 Some Notes on the Aitiology of Strabismus.
after he had seen he did not soon lose this quality, nor desire a
light to go about the house in the night. And now being
lately couched of his other eye, and looking upon the same
object with both eyes, he thought it looked about twice as large
as with the first couched eye alone, but not double that we can
anyways discover.”
The ability to use both eyes together is peculiar to man and
some of the higher vertebrates, but in no animal is the function
of binocular vision so highly developed and so essential as in
man, a function by no means present at birth, but acquired by
subsequent development. The appreciation of colour also is not
demonstrable before the sixth month, and that of different
colours is obtained by a gradual development, those nearer the
red end of the spectrum being appreciated first.
In view of these facts we must consider the visual power as
being gradually developed, the newly-born child starting with an
“organ possessing only the potential faculty of perfect vision, and
not more power probably than mere perception of light. This
is not strange, for we know that animals living in the dark have
only rudimentary organs of vision, consequently we should be
surprised if the newly-born infant possessed the power of seeing
and discriminating before the brain and the other sensory organs
were in a, position to assist the eye, to an intelligent appreciation
and discrimination of what was seen.
Donders’ theory that squint was due to an abnormal relation
of the power of convergence and accommodation, is not sufficient
to explain all the cases of squint that present themselves to us,
and the theory of amblyopia ex anopsia is quite untenable in the
face of many of the facts which are at hand to-day.
Donders points out that hypermetropes of moderate degree
have, in order to focus an object clearly, to use their accom-
modation in order to correct the static refraction of their eyes.
In the normal condition of an emmetropic eye a certain
amount of accommodation entails a certain amount of converg-
ence, and we generally say that an emmetrope accommodating
one diopter converges one metre angle, two diopters two metre
angles x diopters metre angles; consequently a hypermetrope
Some Notes on the Ætiology of Strabismus. 247
with a defective static refraction cannot conform to this con-
dition but accommodates in excess of his converyence, or
converges in excess of the proximity of the image looked at.
Hence one of two things must happen. The accommodation
being used to bring the object into focus clearly, the visual axes
of the two eyes do not meet at the object, but between the object
and the observer, the image of the object falling on non-corres-
ponding points of the two retina, diplopia or double vision
ensuing. The other alternative is single but misty vision.
In myopia the converse is the case, the accommodation being
weak or unnecessary. Convergence is in excess and an effort to
relax the convergence produces a tendency to divergence and
eventually divergent squint. Although it is unsafe to argue
that the relation of convergence to accommodation is the same
in ametropia as in emmetropia, still this theory of Donders’ is
no doubt true in a large number of cases but it is not sufficiently
explicit.
A choice has therefore to be made between double sight and
misty sight, that is to say, if the visual axes fall on the object
the image will be out of focus; if, on the other hand, the object be
focussed accurately double vision inust ensue.
On which of these alternatives the choice will fall depends on
the condition of the eyes. If, owing to any cause, such as a high
degree of ametropia, opacity of the refractive media, etc., clearness
of vision is impossible, then no squint will develop, the patient
giving up clear vision in order to preserve single vision ; on the
other hand, if the object can be seen clearly, then clear vision is
preferred and the diplopia overcome, according to Donders, by an
active supression of the image in the squinting eye.
We undoubtedly have power to neglect the image in one eye.
In gazing through a telescope, or an ophthalmoscope, or better
still a microscope, with both eyes open, many people have the
power of entirely neglecting the retinal picture in one eye. The
images are of course absolutely different, and no effort is made to
fuse them. By an effort, rendered easier by moving the micros-
cope slide, we can perceive one image only.
248 Some Notes on the .Etwl»gy of Strabismus.
We do not apprehend all we see, that is to say, a very small part
of what we see, the image of which falls on the retina, ever reaches
the state of consciousness, consequently it does not seem to me a
matter of very great surprise, that in order to avoid a most
annoying and muddling diplopia, a child should learn to neglect
the image falling on one retina entirely.
But now arises an interesting question, Can this suppression of
an image in consciousness lead to a condition of amblyopia such
that the patient cannot, even by an effort, with the good eye
covered, command good vision ?
I believe, that if the amblyopia were due solely or mainly to an
active suppression, that the patient would be able to command
full vision again; but that we are in reality dealing with an
amblyopia which depends for its existence upon some cause
apart from the squint, and existing previous to the squint, so that
the amblyopia is the cause of the squint rather than the squint
the cause of the amblyopia. The condition of the amblyopic eye
should be considered carefully in relation to this point.
When looked at from outside, or ophthalmoscopically, the
amblyopic eye is apparently healthy. Whatever change is present
is beyond the power of inspection or ophthalmoscopic examina-
tion to reveal.
The majority of cases show that one eye alone is involved, the
other eye showing, as a rale, no evidence of a similar defect of
visual acuity. The shape of the cornea, or refractive power of
the media is different from that of the other eye, both eyes having
an error of refraction, the higher error is usually in the amblyopic
eye.
I have found cases in which the refractive error by retinoscopic
examination was equal in the two eyes, but I do not remember
seeing a case where the amblyopic eye had the lower error of
refraction. |
We may find that correcting glasses improve the visual
acuity somewhat, or we may find that no improvement at all
takes place with any glass; but if improvement does take place
it is at the most partial only. |
Some Notes on the Etiology of Strabismus. 249
Colour vision is often unaffected, and although exceptions are
found, the field of vision is generally complete ; sometimes indeed
scotomata, central or peripheral, may be demonstrated.
The presence of indirect vision renders the eye of great service
to the possessor, even although the visual acuity may be less
than one-sixtieth of the normal standard.
On questioning the patient, if old enough and sufficiently intelli-
gent to understand, one is told that objects appear unreal, shadowy,
blurred, or sometimes unsteady, as if they were vibrating.
The degree of amblyopia is not proportional by any means
either to the length of time that the squint has lasted, or to the
degree of error of refraction present.
The effect upon the squinting and amblyopic eye of covering
the sound, non-squinting eye, for a prolonged period may be
nil, or, on the other hand, may lead to a slow but real improve-
ment, but not, however, to complete restoration of full acuteness
of vision. Such an improvement is doubtless due to certain
additional factors influencing the vision of the amblyopic eye.
Since the eye has not been used for fixation, binocular vision
being defective or absent, no effort to focus objects accurately
has been made; and further, the object looked at having been seen
indistinctly, we should expect a certain awkwardness to exist on
first employing functions which have been for a longer or shorter
time in abeyance—a sort of left-handed condition noticed in
right-handed people, when owing to some injury the right hand
is placed hors de combat. The improvement noticed in squint-
ing eyes, on covering the sound eye for long periods is probably
due to this awkwardness being gradually overcome.
_ If the amblyopia of the squinting eye were, due to the effect of
the suppression of the image of that eye we should expect the
prolonged covering of an eye would lead to defective visual acute-
ness, and that in those cases where the eye has been bandaged
for a long time, or owing to persistent blepharospasm the lids
have been kept closed, that a permanent defect of vision would
ensue, but this is only found to be the case where the affection
ensued before full and complete development of the visual
acuity had taken place. Tn adults this is not the case, since cases
250 Some Notes on the Etiology of Strabismus.
of cataract developing during childhood obtain full vision after
operation where the cataracts have existed for several years.
On the other hand, one can quite understand that any inter-
ference with the passage of light to the retina may have an
effect on the proper development of the macula, but this inter-
ference must exist at birth or very shortly after ; the macula being
once normally and completely developed is not permanently
depressed by the exclusion of light.
“ The excitation of light," says Dr. Steffan, “ is sufficient to
develop the functional activity of the eye; under its influence the
formation of the medullary sheath gradually extends in the optic
nerve from the periphery, and its forcing influence is such that
formation of the medullary sheaths takes place so rapidly in a
child born in the eighth foetal month that at the end of a month
the process is further advanced than it is in a child born at full
term.”
We see, therefore, that we have in the case of amblyopia in a
squinting eye a condition presenting no visible change to the naked
eye, a subjective rather than an objective change, accompanied,
however, by many associated conditions, such as abnormalities
in the shape of the eye or in the condition of the refractive media,
sometimes areas of blindness in the field of vision, and always by
a, defect of acuteness of vision of a varying but unalterable degree.
This defect has no relation to the duration of the squint, or to the
age of the patient. Further, the same condition is not uncommonly
found in cases in which there is not, and has never been, any
squint. For these reasons it is impossible to believe that the
amblyopia of the squinting eye is due to the squint.
We have, then, to ask ourselves the question, What is the cause
of this amblopyia? and that question cannot at present be satis-
factorily answered.
As I have already pointed out, the non-squinting eye does
not participate in the defect incident to its fellow. The non-
squinting eye has full visual acuity, full field of vision with
normal colour and light sense. Hence the lesion must be in
front of the chiasma, since no lesion behind that point would
give us clinically defective vision confined to one eye only,
Some Notes on the ZEtiology of Strabismus. 251
without ophthalmoscopic signs. Any theory advanced must
explain the main facts found in association with this amblyopia,
viz., the unilateral lesion, absence of ophthalmoscopic signs, the
higher error of refraction, the normal colour sense and field of
vision, the fixed degree of amblyopia, the existence of the same
kind of amblyopia without squint, and its occurrence at an early
stage of life.
Vision in the new-born being limited, as already expressed, to
quantitative perception of light, a very slight eause affecting the
vision of one eye may lead to the whole of the effort to cerebrate
being confined to one eye. In other words, that the image in one
eye being better than that of the other, the child develops and
unconsciously cerebrates the image formed on that retina only.
The amblyopic eye then develops normally, but the image is not
received into consciousness except when the retina receives
impressions not received by the good eye, that is, in the field
of vision peripherally. The function of binocular vision, then,
is either developed imperfectly or not at all, and as the extent
to which attention is paid to the image of either eye varies, so
conversely would the amount of amblyopia. The non-develop-
ment of the power to cerebrate the image in one eye as fully
as that in the other, leads to the loss of power to do so
even at will, with only one retina in use. There is no
evidence that any actual structural defect exists, since micros-
copical examination of an amblyopic eye must certainly be rare,
as such eyes are seldom, if ever, removed, except for other
reasons, accidents, etc.
Consequently, any cause acting in the first months of life, and
rendering the image in one eye less perfect than the other may
lead to amblyopia of that eye.
Schleich examined one hundred and fifty newly-born infants
and found in forty-nine cases (seventy-eight eyes) retinal heemor-
rhages besides a few other changes.
Naumoff (Archiv. of Ophthal., xxxvi., 8 p. 180), in 1890,
examined forty-seven infants at full term and found pathological
changes in twelve pairs, due he considered to increase of inter-
cranial pressure during labour.
VOL. LVI. | i 20
252 Some Notes on the Ltiology of Strabismus.
Hsmorrhages of this nature would be absorbed and leave no
trace behind.
The presence of a degree of astigmatism higher in one eye
than another, due to a badly-shaped cornea or globe, early
inflammation, blepharospasm, ulcers, or injuries, may depress
the visual acuity for a longer or shorter time during the
critical period of the development of the vision and so lead to
amblyopia.
This theory, then, would explain the unilateral change, and
also another fact not often noticed, viz., that the good eye, in
spite of comparatively big errors of refraction develops more than
usually acute vision, six-fifths being read quickly and easily, due
of course to the undivided effort to appreciate the image in that
eye; further, the existence of higher errors of refraction in the
amblyopic eye, the absence of ophthalmoscopic signs, the presence
of normal colour sense, the absence of any improvement by treat-
ment and the occurrence at an early period of life.
Whether strabismus will develop or not depends on the
existence of other factors which may be present; such as defects
of accommodation or convergence, muscular abnormalities, etc.
We find strabismus present in patients who have no
amblyopia; who possess eyes with some considerable, or, on the
other hand, some slight error of refraction, but with good visual
acuity in each, and we must consider why these patients squint,
knowing as we do that the majority of patients with errors
of refraction and good visual acuity in each eye do not squint.
In these cases we have undoubtedly another factor of normal
vision either wanting or defective, viz., the power of binocular
vision or the power of receiving in consciousness theimage in each
eye in such a manner that the object looked at is seen by both
eyes, and the resultant perception is due to a fusion of both
images in consciousness.
By the arrangement of the optic nerve fibres, all objects seen
on our right side are perceived by the left cerebral hemisphere,
consequently binocular vision is possible in those cases only
where complete decussation of the fibres does not take place.
Some Notes on the Attwlogy of Strabismus. 253
We find in fishes that the two optic nerves cross entirely to the
opposite side, no fibres remaining on the same side. The same is
true of amphibia and birds, but as we pass higher in the scale we
find that a larger and larger number of fibres do not decussate,
and finally in man the eyes are placed in the frontal plane and
about two-fifths of the fibres do not cross; that proportion, then,
of the field of vision is therefore involved in binocular vision,
the extent to which decussation does not take place, denoting
the degree of binocular vision possible.
This functidn of binocular vision is not present at birth, but the
conditions for its development being present, the function is
acquired during early life.
Undoubtedly in a large number of squints binocular vision is
either very imperfect or absent. By imperfect I mean that by
displacing the image of one eye above that of the other diplopia
is not obtained or obtained with difficulty. Often further efforts
must be made to separate the images, as by putting a red glass in
front of one eye and keeping the prism moving in front of the
other before the two images can be recognised. If the visual acuity
of one eye is much below that of the other, binocular vision will,
of course, be bad, but one finds in certain cases defective binocular
vision with good visual acuity in each eye. By means of this
binocular or stereoscopic vision (as well as by other means) we
appreciate the third dimension. If, then, this power in a certain
case is not present there is a very much lessened stimulus for the
two eyes to work together in a sort of double harness, but each
will work irrespective of the other, and it is quite clear that no
diplopia will be complained of.
Further, in the treatment of squint, the presence or absence
of binocular vision materially affects the prognosis. If present,
the chance of good recovery is infinitely greater than if absent.
We also find, in some cases, that binocular vision is not
present over the whole field, but only over a very small
portion, and this area may, by proper means, be considerably
extended. Binocular vision may be possible at a distance, but
owing to the presence of a divergent squint, associated with
detective convergence, on approximating the object looked at, is
954 Some Notcs on the Ætiology of Strabismus.
not obtained, and vice versd. The function may be entirely
absent, possibly due to a non-development of the power from
birth.
In some cases of squint in children diplopia is complained of,
and in these cases binocular vision is, of course, present ; but the
absence or diminution of this function explains the fact that
diplopia is so seldom recognised.
Undoubtedly, as Donders first pointed out, ametropia is present
in cases of strabismus in the vast majority of cases, and when
ametropia exists, the usual relationship of convergence to
accommodation is altered; for it is not accurate to argue that
the relation between accommodation and convergence which is
developed in emmetropia in consequence of daily practice exists
for all conditions of refraction. That the ciliary muscle is
affected by the refraction is well known, a larger development
of fibres taking place in hypermetropia than in emmetropia, and
a smaller number in myopia. Besides, a far larger number of
cases with errors of refraction do not squint, and taking cases
of squint alone, we do not find that even here the majority
show errors of refraction only, the two eyes being normal in
every other respect. Certainly, a fair number of cases, where
the relationship of accominodation and convergence satisfactorily
account for the squint exist, but other causes are more frequent.
Great defects of converging power in cases of emmetropia or
small degrees of astigmatism, are sometimes found among our
out-patients where not the slightest movement is made by the
visual axes to converge when an object is approximated to the
eyes, one or other eye fixing, whilst the other diverges. Binocular
vision in these cases is, of course, defective, since the two eyes
can never be directed towards an object close to them, but only
when the object is far off.
The lesion in these cases is probably nuclear, and binocular
fixation being impossible for most of the functions of life, bino-
cular vision is weak and generally divergent squint develops.
This defect leads us to another undoubted cause, the existence
previously of latent squints. Many of those cases of squint
noticed in cases where for some reason blindness or severe
Some Notes on the Ætiology of Strabismus. 955
impairment of vision has occurred in one or both eyes, are due
to this cause. The tendency for divergence to occur, as adoles-
cence is reached, accounts for the spontaneous cure of some
cases of convergent squint, and also cases where tenotomy having
been performed early in life and parallelism maintained for some
time, subsequent divergence ensues.
The majority of latent squints are due to insufficiency of the
internal recti, but a preponderance of these same muscles may
also occur and a latent convergent squint exist. The reason these
squints do not become manifest, is because good binocular vision `
exists and a most annoying diplopia would result if & constant
effort did not keep the visual axes directed, so that the two
images are superimposed, and one image received into conscious-
ness; if, however, the image in one eye is displaced vertically,
then the diplopia is readily recognised. Consequently, if from
any cause this objectionable diplopia ceases to exist, owing to
the acuteness of vision being severely diminished in one or both
eyes, then the eyes will take up the position of equilibrium due
to the muscular defect and a convergent or divergent squint
ensues, as the case inay be.
The notes of a case where fusion was impossible owing to
the existence of an altitudinal squint in addition to divergence
are recorded lower down. |
Paralysis or weakness of accommodation may also possibly
lead to a development of squint, owing to the absence of the
stimulus to convergence that the accommodative act usually
involves. The frequency with which some illness precedes the
manifestation of squint in children lends some colour to this idea,
since the intrinsic muscles of the eye may suffer in the general
debility during convalescence following one of the exanthemata.
A case of divergent squint with diplopia, in a boy of eleven,
following a severe illness, has recently come under my notice.
This patient has complete paralysis of accommodation.
In conclusion. Strabismus of the concomitant kind is due in
the majority of cases to absent or defective binocular vision.
The greater number of cases have defective binocular vision
because the visual acuity of one eye is very defective. This defect
955 Some Notes on the Etiology of Strabismus.
again is in a large number of cases due to amblyopia. No
satisfactory explanation of this amblyopia is at present known
to us.
The view that appears therefore to be most satisfactory is, that
in consideration of the condition of the eyes, as regards vision at
birth, a very slight interference with one eye may lead to a
deterioration of the image formed in that eye. This having
occurred, the better image alone is appreciated and developed
into consciousness, the other eye only being used to extend the
field of vision, and never being appreciated in consciousness to
the same degree. This function being undeveloped during the
developmental period is permanently lost. The degree of ambly-
opia depends on the extent to which the image of the eye has
been received into consciousness, that is, the extent of its
contribution to the single image seen binocularly.
Other causes leading to defect of visual acuity of one eye, lead
also to defective binocular vision, such as opacities of the
media, fundus changes, anisometropia, etc.
Other causes of squint are numerous, but errors of refraction,
abnormalities of the extrinsic muscles, or of the power of con-
vergence or accommodation, will explain most of the cases
remaining.
Some Notes on the Attiology of Strabismus. 257
CASES OF SQUINT SELECTED FROM THE OUT-PATIENTS OF GUY'S
HosPITAL DURING THE LAST TWO YEARS,
Cases where the squint was primarily due to impaired binocular
vision.
A. B., æt. 18.—Convergent concomitant strabismus noticed for many years.
Movement of eyes good, laterally, can fix with either eye. Has no binocular
vision. Refraction under atropine.
+1:5 +2:5
+2:5 +2:5
With correction vision is $ in both eyes.
E. T., et. 15.—When this patient gazes steadily in the distance, the right
eye is noticed to diverge, the action being recognised by the patient, she stating
that she knows some change has taken place.
Binocular vision obtained only with difficulty by means of prism and red
glass ; either eye will diverge when the other is covered.
Converging power good f +1.5
Refraction under atropine B.E. A) —-
+1:5
VE.E.=$
N. Y., æt. 15.—Convergent concomitant squint, angle about 45°. Can fix
with either eye. Convergence good. Vision with glasses § with each eye.
Has no binocular vision. Low degree of hypermetropic astigmatism.
Cases due to defective binocular vision associated with large
errors of refraction.
L. F. B., æt. 23.—Had convergent concomitant squint when a child, and
for this was operated on. When examined this year some divergence was
present. |
Binocular vision obtained with difficulty.
Crossed diplopia, Grefe's test with dot and line showed inability to obtain
two dots on one line.
V.R.E. cum. + 2-5 cyl. vert. = $.
V.L.E. cum. + 2:25 cyl. vert. = $"
F.B., et. 21.—Divergent concomitant squint noticed since birth. Can fix
with either eye.
Faint binocular vision obtained.
Convergence fair.
R.E.V. cum. — 6'5 sph. = ,§.
L.E.V. cum. — 4:5 sph. — — 2 eyl. axis 10° = $.
Only uses one eye at a time.
258 Some Notes on the Aitiology of Strabismus.
A. G., eet. 22.—Divergent concomitant squint. No binocular vision.
V.R.E. = «f$; cum. — 9 = x.
V.L.E. = ед, cum. — 18 = дӱ.
E. F., æt. 10.—Convergent concomitant squint. Can fix with either eye,
prefers to fix with left. Alternating squint, more marked on convergence,
almost parallelism at distance.
B.E. cum + 8.5 D sph.
+BDoyl. vert. ^?
Cases with amblyopia of one eye and defective binocular vision.
S. O., st. 18.—Convergent concomitant squint, noticed many years. Fixes
with left eye, can fix with the right eye. No binocular vision. No fundus
change. Both eyes have five diopters of hypermetropia.
V.R.E. cum. + 5 = ед.
V.L.E. cum. + 5 = $.
F. C., et. 15.—Divergent concomitant squint. No binocular vision. Move-
ments good. Fixes with the right eye. Tenotomy five years ago.
V.R.E. cum. + 1 = $. V.L.E. fingers at 5 feet.
+1 +1
Atropine ———— R.E. lənə dom
41 +15
Fundi normal.
G. F., æt. 13.—Convergent concomitant squint. Can fix with each eye
centrally, but always fixes with the right eye.
Field of vision is defective at outer part of left eye, which is amblyopic.
R.E.V. cum. + 5 = $. L.E.V. cum. + 5 = fingers at 1 foot.
Atropine +5
B.E. —..—
+55
Bad binocular vision, only obtained with difficulty.
Cases having gross fundus lesions of one eye, or opacities of
the transparent media, with defective binocular vision,
A. L., æt. 8.—Convergent concomitant strabismus. Appearing since in-
flammation of right eye. Fixes with the left eye.
V.R E. cum. + 3 = s has corneal nebula.
V.L.E. cum. + 3 = $.
W. P., æt. 7.—Divergent concomitant squint. Fixes with right eye. No
binocular vision.
R.E. + 75 = $. L.E, <, not improved.
The fundus of the left eye shows extensive choroidal atrophy.
S.C., et. 30. —Divergent concomitant squint. The vision of the right eye
has been known to be defective since the patient was twelve years old.
R.E. < ib, not improved. Large central patch of choroidal atrophy.
L.E.V. cum. + 1 = 6.
Some Notes on the Aitiology of Strabismus. 259
F No binocular vision. Movement good. Fixes onlyywith left eye.
F. L., et. 10. Convergent concomitant strabismus. Fixes with the left
eye. Squint more marked during convergence. Parallelism at distance.
Noticed since birth. No binocular vision.
By retinoscopy,
+ 45 N "Í + 65
B.E.
Z
R.E. fingers at 2 feet,”not further improved.
L.E. cum. + 4 _
+ z oyl. 1855 = $ some.
Fundus changes in the right eye. Along course of superior nasal artery
numerous patches of choroido-retinitis, looking like remains of old hemorr-
hages, disturbing deep parts of retina.
Cases with good vision in each eye. Binocular vision present,
and ametropia.
K. D., et. 40.—Divergent concomitant squint. Fixes with either eye,
usually the left. Has binocular vision.
R.E.V. cum. + 1:5 sph. =
+ 1-5 cyl. vert.
L.E.V. cum. + 1:5 sph. =$
+ 1:5. oyl. vert.
B. K., æt. 64.—Convergent concomitant squint. Noticed when two years
old.
+6 +6
+6 +6
V. cum. 5 D sph. = § each eye.
H. P., æt. 27.—Divergent concomitant squint. Fixes usually with left eye,
can fix with right. Has binocular vision for distance and near work.
V.R.E. cum. — 13 = $. V.L.F. cum. — 7 = 4.
Squint noticed since eight years old.
E. M., et. 18.—-Divergent concomitant strabismus. Complains of diplopia
and difficulty in reading. Convergence moderate when effort is made.
Divergence takes place usually when reading. Fixes with either eye.
R.E. —3:5 —3°5
= —2:5
R.E. cum. — 4 D sph.
— 8D sph.
ка = me. L.E. cum. — —— £ = f som
— 1 eyl. vert. sone TM Xod
— 1 horiz.
260 Some Notes on the /Ettology of Strabismus.
Cases of strabismus associated with anisometropia.
C. M. G.. et. 13.—Divergent concomitant squint. Fixes usually with
left eye, can fix with either. Has binocular vision. Convergence weak.
R.E.V. cum — 4 D sph.
— 85 eyl. O- 7 8
L.E.V. cum — 1 D sph. = $
E. W., et. 15.—Convergent concomitant squint. Fixes with left eye
usually. Can fix with either. Has good binocular vision.
R.E.V. cum. + 2°25 sph. zu
| + 2:25 cyl. vert. — 1?
L.E.V. cum. + “75 cyl. vert. = $.
M. M., æt. 9.—Divergent concomitant strabismus. Fixes with the right
eye usually. Can fix with either. Has binocular vision.
V.R.E. cum. — 1:5 sph.
— 2:5 eyl. horis. - $
V.L.E. cum. — 4 D sph. =
— 2°5 cyl. horiz.
Cases with defective convergence.
M. C., æt. 34.—Divergent squint, noticed since childhood. Has no binocular
vision. No effort made to converge when reading, sewing, or looking at near
objects.
V.R.E. = $. V.L.E. = $. A small degree of hypermetropic astigmatism
present in both eyes.
E. F., et. 29.—Divergent concomitant squint. Can fix with either eye.
Has faint binocular vision. Convergence very defective. An advancing
object towards patient, either eye fixes, the other rolling out.
4:25 +1
+ 2:25 +1
R.E. cum. + 2 eyl. vert. = $. L.E. cum. + 1 sph = 4.
H. A., et. 12.—Divergent concomitant squint. Can fix with either eye,
but never together. Noticed sincebirth. Slight nystagmic movements when
eyes are directed to extreme right or left side.
V.E.E. = 44. Abouttwoof hypermetropicineacheye. No binocular vision.
No fundus lesion.
Cases of latent squint.
A. H., æt. 21.—Complains of difficulty only on reading.
V.E.E. = $. Hm. = 5.
Has insufficiency of the internal recti. Cannot get the two dots on the
line. At any distance, slight divergence noticed on covering one eye. Has
crossed diplopia with prism vertical and red glass. à
M. D., æt. 30.—Complains of difficulty with reading.
V.R.E. = $. V.L.E. = $. Both eyes have some small degree of hyper-
metropic astigmatism.
With Grefe’s dot and line, homonymous diplopia is produced, the two
dots only being on the line when at a distance of ten inches.
Some Notes on the Aitiology of Strabismus. 261
W. Ross, set. 34.—Divergent squint noticed six months. V.R.E. fingers at
five metres. Left eye shadows at three inches. Fixes with right eye. Optic
atrophy, B.E. i
M. T., æt. 11.—Paralysis of accommodation. Complains of diplopia.
Divergent concomitant squint. Divergence not marked. Crossed diplopia,
with Maddox rod.
V.R.E. = fy, cum. + 1 = 8. V.L.E. = *, cum. + 1 = Reads J 1
cum. + 5 D sph. at six inches.
Pupils react very slightly to convergence. States that he had an illness
last March, and dates all his trouble since then. Under a mydriatic he has
about 1:5 hypermetropia.
H. S., et. 14.—Convergent concomitant squint.
R.E.V. = < é; cum. — 8D sph. = partly.
L.E.V. = $ cum. — 7 D sph. = 4$ partly.
Internal rectus of right eye, and subsequently of left eye, divided about
two years ago. When seen last the condition was one of divergence.
Atropine —10 —6
—10 —6
R.E. cum. — 11 = j£. L.E. cum. — 5:6 = $.
Binocular vision only at distance. No convergence for near. _
P. H., æt. 31.—Divergent and altitudinal squint. States that when he was
five years old he rememberes being taken to Dr. Walker, of Edinburgh, on
account of seeing double, and he believes he has had the trouble all his life.
Used to be teased at school about it.
—1\ /€I15 : + 25 /-—'5
R.E.V. = & s L.E.V. = "x
ZEN *Е
N
R.E. cum. —1 sph. =$ L.E. — ‘5 sph. ` .
— “5 eyl. 609 — — 2:5 eyl. axis. 309 `
Patient has no power of fusing one image with the other.
By means of prisms with apex down in front of the left eye about three
inches the images are level, and by using prisms horizontal, the images are
approximated but cannot be fused and held as one, since they appear to
oscillate when they get close together.
This case, then, is one where the visual activity remained during the early
period of life equal in the two eyes. Binocular vision normally developed,
but fusion of the two images prevented by the presence of an altitudinal
squint which he was not able to overcome by any effort.
W. H. N., et. 31.—Had a convergent concomitant squint when a child,
and was operated on, tenotomy being performed. The left eye was always
defective, the right eye being good until the accident.
During August, 1900, he received a blow on the right eye from a cork of an
exploding soda water bottle, and in consequence of this accident lost the sight
of the right eye entirely, baving only P. L. Since that time he has been
under observation, and as his sight in the left was very indifferent he was
obliged to change his occupation.
26? Some Notes on the Astrology of Strabismus.
The vision of the left eye in August, 1900, was ,$. Within afew davs a
marked improvement took place he seeing yz w.th a + cl. in the vertical.
Over twelve months has now elapsed. and on examination 14th October, 1901,
the vision of the left eye is nowise improved, in spite of the patient
saying that he could get along better with it.
The power of accommodation, however, was better, for in 1900 he could
only read Jeger 16 with his glass, whilst in 1901 he could read Jeger 8. The
improvement consequently is accounted for by his making better and more
effective effort to use his accommodation. The visual acuity remaining
practically the same.
M. M., et. 8.—Congenital amblyopia of both eyes. Has no central fixation.
Is not improved with glasses. Sees better with the right eye than the left.
R.E. -1 | +1
Atropine ——-|-—— —-
+15 | + 2°5
Vision of each eye less than yx. Convergent concomitant squint. Move
ments of muscles defective, especially upward movements. Some small
pigment dots in the macula region of the left eye, otherwise the fundi are
normal in appearance. Nystagmus of both eyes. Is being educated as a
blind child.
Notes of congenital amblyopia, affecting the greater number of
the members of a family.
M. H., æt. 40.—Has had defective sight all her life, and attended the
hospital (Moorfields) for a prolonged period without any benefit.
V.R.E. = ib. V.L.E. = if.
Not further improved with glasses. No fundus lesion. Has seven children
living, the eldest :—
1. D. H., et. 18.
R.E.V. = 44 cum. — 5 sph.
— 2cyl. O.
L.E.V. = $ cum. — 5:5 sph.
— 350.
Has binocular vision, and good convergence.
2. Child not seen. Does not wear glasses. Said to see well.
8. L. H., set. 94.
+ 1-5
V.E.E. = ff, unimproved. B.E. -—I-—
+ 1-5
4. I. H., et. 8.
V.E.E. = s. Retinoscopy under atropine.
— *75
Some Notes on the Aitiology of Strabismus. 263
V.E.E. cum. — 2 eyl. О = ££.
5. N. H., set. 6.
V.R.E. = $. Not improved. Emmetropic.
— 5
= EM tes cum. — 4sph _
V.L.E. = фу _3 — 2eyl.0 ` de
6. O. H., set. 43.
E.E. vision = & cum. — 8 D sph. = Z.
7. Æt. 8. — Vision, as far as could be discovered, good.
No gross fundus lesion in any of these cases.
SPECIMENS RECENTLY ADDED
TO THE PATHOLOGICAL MUSEUM.
By LAURISTON E. SHAW, M.D.,
AND
E. COOPER PERRY, M.D.
PERICARDIUM.
S. 137 Sarcoma of the Pericardium.
A heart divided to shew its ventricles encased in an
envelope of soft material, in some places an inch in thick-
ness, which consists of the pericardium infiltrated by a
vascular new growth. There is a similar layer around the
right auricle, the cavity of which is invaded and its wall
almost entirely replaced by the deposit. The glands in the
mediastinum are greatly enlarged, and the right bronchus is
narrowed. Histologically the growth is a small round-
celled sarcoma. The heart with its investment weighs
about 30 ounces.
Presented by Mr. W. F. CLowes, 1892.
S. 869 Localised Fibroid Pericarditis.
. A portion of a right auricle and ventricle shewing a
thickened and wrinkled condition of the epicardium
covering the former, whilst on the latter are two fibroid
patches somewhat resembling cheloid. Histologically the
266 Specimens recently added to the Pathological Museum.
fibroid tissue of which the patches consist is seen to
infiltrate the myocardium.
From a man who died in a tramcar on his way from an infirmary
which he had just left, contrary to the advice of the medical officers.
At the autopsy the heart was found to weigh 193 ounces. The mitral
valve was contracted and the myocardium fibroid. There was circum-
scribed pericardial adhesion over the lower part of the left ventricle.
The liver was nutmegged and the kidneys were granular. See Insp.,
1894, No. 298.
S, 161 Fibroid Nodules on the Pericardium.
A portion of the pericardium covering the right auricle
with the corresponding part of the parietal layer of the sac.
The epicardium of the auricle is roughened and rugose,
whilst upon the surface which was in apposition to it is
seen a cluster of flattened nodules elevated about y of an
inch above the surrounding surface, and each measuring a
line in diameter. Histologically these nodules have a
fibrous structure.
Augustus B., set. 30, was admitted under Dr. Goodhart for
hemoptysis, and died about three months later from phthisis. At the
autopsy both pleurse were found to be firmly adherent, and the lungs were
affected with extensive tuberculous disease. See Insp., 1892, No. 272.
8. 489 Acute Pericarditis. Epithelioma of (Esophagus.
A heart with the great vessels and portions of the
trachea and cesophagus. The interior of the pericardial sac
is seen to be covered with a thick deposit of recent lymph.
At the lower end of the cesophagus is a deep epitheliomatous
ulcer from the base of which two rods have been passed,
one into the right bronchus and the other into the peri-
cardial cavity close to the right auricle. The right lung,
which is adherent to the csophagus, is infiltrated by
growth.
Mary Ann M,, et. 60, was admitted under Dr. Shaw for dysphagia,
having suffered from severe pain in the chest for four months. She
died six days after admission, and at the autopsy patches of broncho-
pneumonia were found in the right lung, and there were secondary
deposits of growth in the mediastinal glands. See Insp., 1895, No. 178.
S. 627 Pericardium invaded by Sarcoma.
A heart with the great vessels and lower end of the
trachea mounted to show the pericardial sac invaded and
Specimens recently added to the Pathological Museum. 267
partially destroyed by a ragged.growth, apparently arising at
the lower part of the anterior mediastinum. The epicardium
is roughened and shaggy. On the reverse of the specimen
the superior vena cava is seen to be occluded by a thrombus
which extends into the right auricle. The lungs are ad-
herent to the pleural surface of the pericardial sac. Histo-
logically, the growth is a round-celled sarcoma.
Maria M., et. 71, was admitted into the Poplar and Stepney Sick
Asylum for rheumatism. Three days later oedema of the face and
arms suddenly came on, associated with cyanosis. The cardiac dulness
was found to be increased and there was a systolic murmur audible
over the whole of the precordial area. The patient died about six
weeks from the onset of acute symptoms.
Presented by Mr. CHARLES SPURRELL, 1896.
0.8. 642 Hydro-pericardium. |
A pericardial sac, from which the heart has been removed.
The sac is uniformly dilated, measuring seven inches from
above downwards and five inches transversely. In the
recent state it contained a pint and a-half of clear serum.
The wall is thin, and presents no evidence of old or recent
inflammation. |
John R., æt. 39, was admitted under Dr. Goodhart with general
dropsy due to aortic incompetence. The cardiac impulse was felt two
inches outside the nipple line, and there was considerable increase of
præcordial dulness. The patient died one month after admission and
at the autopsy the aortic valves were found to be thickened and rigid.
The heart weighed 22 ounces. Both pleural cavities contained serum.
See Insp., 1889, No. 246.
S. 662 Adherent and Calcareous Pericardium.
À heart divided by a frontal section, and seen from behind
to be enveloped in & rough fibrous membrane representing
the thickened and adherent pericardium. In the groove
between the right auricle and ventricle, and partly embedded
in the wall of the latter, is a calcified gumma measuring
rather less than half an inch in diameter. In the neighbour-
hood of the gumma and elsewhere the thickened pericardium
contains calcareous plates. The exterior of the sac shows
adhesion to the lungs, and there is a mass of fibro-fatty
tissue uniting it to the diaphragm. The heart is of normal
size ; the valves and myocardium are healthy.
VOL. LVI. 21
968 Specimens recently added to the Pathological Museum.
Thomas B., et. 27, was admitted under Dr. Pye-Smith for dyspnea,
cyanosis and cedema. Five years previously he is said to have had
rheumatic fever, followed four months later by bronchitis, hemoptysis
and jaundice. Subsequently he was on three occasions tapped for
ascites. A month after admission he died from cardiac failure, and at
the autopsy the peritoneal cavity was found to contain several pints of
fluid, the membrane itself being thickened and the mesentery shortened.
The pleure were universally adherent, and the tissues of the mediastina
were thick and fibrous. See Insp., 1896, No. 471.
S, 717 Chronic Pericarditis.
The base of a heart, seen from behind, and mounted to
show at the reflection of the pericardial sac several irregular
fibrous tags, the largest measuring an inch in length. The
pericardium over the left auricular appendix is thickened.
On the reverse of the specimen recent vegetations are
seen upon the aortic valves. There is mitral stenosis and
the left auricle is hypertrophied.
Hilda F., æt. 23, was admitted under Dr. Hale White with chronic
valvular disease of the heart, from which, on the following day, she died.
At the autopsy the heart was found to weigh 21 ounces, and there
were recent vegetations on the tricuspid and mitral valves. The
patient had been in the hospital suffering from acute pericarditis about
three years before her death. See Insp., 1897, No. 216.
0.8. 781 Acute Pericarditis.
A heart exposed in its pericardial sac to shew both serous
surfaces to be covered by a rugose layer of recent lymph.
In the fresh state the sac contained 16 ounces of blood-
stained fluid. Around the great vessels and at the bifurca-
tion of the trachea the lymphatic glands are seen to be very
greatly enlarged by a deposit which histologically consists
of small round cells and numerous giant cells with a few
foci of caseation.
Mary Ann T., et. 34, was admitted under Mr. Jacobson for a
swelling on the right side of her neck, which had been slowly
increasing in size for the preceding nine months. On admission, she
was found to be suffering from pericardial effusion, for the relief of
which her chest was twice aspirated. She died a week after admission,
and at the autopsy the cervical and mediastinal glands were found to
be enlarged, and there was considerable serous effusion into the pleural
and peritoneal cavities. See Insp., 1690, No. 101.
0.8.
0.8.
6. 2
Specimens recently added to the Pathological Museum. 269
859 Sarcoma of the Pericardium.
A heart shewing beneath the epicardium on the front
of the right ventriele a flattened nodule measuring a third
of an inch in diameter.
Robert R., æt. 54, was admitted under Dr. Hale White for malignant
growth of the liver secondary to a sarcomatous tumour which had
been excised from the right arm six months previously. He died one
month after admission, and at the autopsy secondary deposits were
found in the lungs, liver, spleen and peritoneum. See Insp., 1890,
No. 329; and Prep. 1525.
914 Adherent Pericardium. Chronic Endocarditis.
A heart the surface of which shews numerous flocculent
tags left after the partial removal of the adherent parietal
pericardium, a portion of which is still seen attached over
the right auricle. The aortic, mitral and tricuspid valves
are fibrous and stenosed.
Alice L., xt. 18, was admitted under Dr. Shaw for ascites and
dyspnoea due to heart disease. She had had numerous attacks of
chorea since the age of four, and one attack of acute rheumatism. She
died about four months after admission, and at the autopsy the heart
was found to weigh 16 ounces, and the lungs were splenised. The liver
was cirrhotic, the spleen enlarged, and the kidneys were indurated.
See Insp., 1890, No. 474.
HEART.
Perforation of Mitral Valve. Ulcerative Endocarditis
A portion of a heart mounted to shew a small perfora-
tion close to the free border of the anterior flap of the
mitral valve. Hanging immediately above it is a pendulous
mass of fibrinous deposit attached to one of the aortic
cusps. Similar smaller masses adhere to the other cusps,
which are in parts destroyed by ulceration, and elsewhere
thickened by chronic endocarditis. On the reverse of the
specimen the perforation is seen to be surrounded by a
raised ring of vegetations.
John P., set. 29, was admitted under Dr. Hale White with fever and
the physical signs of disease of the lungs and heart. He had had
acute rheumatism six months previously, and had recently suffered
from hemoptysis. He died eight days after admission, and at the
autopsy the heart was found to weigh 19 ounces, and both sides
were hypertrophied and dilated. There was a cavity at the apex of
270
S. 8
Specimens recently added to the Pathological Museum.
the left lung, and tubercle bacilli were found in the caseous material
lining its wall. The sp:een weighed 15 ounces, and contained a
large infarct. See Insp. 1891, No. 282.
Calcareous Yegetations on the Mitral Valve.
A mitral valve, thickened but not contracted, and mounted
to shew upon the auricular aspect of its posterior curtain
a cluster of fibro-calcareous vegetations, measuring an inch
and a half in length, and projecting half an inch into the
auriculo-ventricular orifice. The mass has a cauliflower-
like surface and is free from recent deposit.
Jane P., æt. 38, was admitted under Dr. Pitt a week after her con-
finement, for cardiac palpitation and dyspnosa. There was a systolic
murmur at the apex of the heart, associated with a diastolic thrill.
The patient died suddenly four days after admission, and at the
autopsy the heart was found to weigh 23 ounces, and the left
pleural cavity contained about a pint of serum. The right lung
contained a large infarct, and the liver was nutmegged. See Insp.
1891, No. 256.
S. 97 Incomplete Septum Yentriculorum.
A heart mounted to shew a small opening in the septum
ventriculorum, immediately below the right semilunar
valve. This valve is considerably thickened, and at the
bottom of the pouch which it forms with the aorta there
is a second opening close to the first, and, like it, com-
municating with the right ventricle. As seen from the
right ventricle, the second opening is situated in the centre
of a pouched membranous diaphragm, and corresponding
with the point on which the refluent blood-stream would
impinge is a fibrous thickening of the endocardium of the
ventricle.
John L., st. 15, was admitted under Dr. Hale White with
symptoms of chronic cardiac failure of about four months’ duration,
which proved fatal fourteen days after admission. At the autopsy the
heart was found to weigh seven and a half ounces, and the kidneys
and liver were congested. The lungs contained ““ apoplexies,” and
there were patches of recent lymph upon the pleura. See Insp. 1892,
No. 112; and Trans. Path. Soc., 1892, p. 34.
S. 186 Rupture of the Left Yentricle.
A heart shewing upon its anterior surface close to the
septum ventriculorum, an oblique rent three quarters of an
Specimens recently added to the Pathological Musewm. 271
inch in length which communicates with the left ventricle.
Immediately above it a smaller superficial rent is seen.
There is a considerable excess of fat upon the surface of the
organ. The coronary arteries are slightly atheromatous.
S. 194 Fibroid Endocardium.
A portion of a right ventricle shewing over many of the
columns carnes a white fibrous thickening of the endo-
cardium. The fibrous material is seen on section not to
penetrate the deeper layers of the muscle.
Joseph D., set. 42, was admitted under Dr. Hale White for hemop-
tysis, due to phthisis, from symptoms of which he had suffered for
seven years. Ascites and cedema of the lower extremities had existed
for six months. The abdomen was tapped twenty-seven times before
his death, which occurred eleven months after his admission to the
hospital. Whilst under observation a systolic bruit developed, which
was best heard between the apex of the heart and the sternum. At
the autopsy, both lungs were found to be affected with fibroid phthisis ;
there was general chronic peritonitis, and the liver was nutmegged.
. The heart weighed 19 ounces, and the left ventricle was of normal
size. The pulmonary artery was atheromatous. See Insp., 1893, No.
16; and Trans. Path. Soc., 1893, p. 24.
S. 197 Polypus in the Left Auricle.
A left auricle laid open to shew upon the inter-auricular
septum, above the situation of the fossa ovalis, a, smooth
rounded polypus measuring a quarter of an inch in diameter.
Histologically it consists of a hyaline matrix containing
blood-vessels and much brown pigment. On the reverse of
the specimen ante-mortem clot is seen in the right auricular
appendix.
Mary L., et. 68, an enormously fat woman, was admitted under
Mr. Symonds with a strangulated umbilical hernia, for the relief of
which herniotomy was performed. The patient died twenty-four
hours later. See Insp., 1893, No. 18.
S. 262 Partial Laceration of the Left Yentricle.
A heart divided, to shew in the interior of the left
ventricle towards the apex, a laceration of the muscle
which extends to, but does not perforate the epicardium.
Richard H., set. 48, was admitted, under Mr. Howse, for injuries
caused by some deal planks falling on him. He died about twenty-four
hours after the accident, and at the autopsy the sternum and three of
272 Specimens recently added to the Pathologt al Museum.
the ribs on the left side were found to be fractured. Blood was extrav-
asated into the tissue of the parietal pericardium and the anterior
mediastinum. There was a large ecchymosis on the surface of the
heart, corresponding to the laceration. There was no blood in the
pericardial sac. See Insp., 1893, No. 265.
S. 293 Atheromatous Coronary Arteries.
A heart with the first part of the aorta laid open to shew
the interior of the vessel extensively affected by atheroma.
The orifices of the coronary arteries are narrowed, the left
being almost entirely occluded. On the reverse of the
specimen, the arteries which have been laid open are seen
to be atheromatous, but in a much less degree than is the
aorta. The aortic valves are somewhat thickened but
appear to have been competent. Histological examination
of the myocardium shows that many of the fibres have
undergone fatty and hyaline degeneration.
James C., set. 59, was admitted under Dr. Washbourn for dyspnea,
for the relief of which paracentesis thoracis was performed He had
been attending as an out-patient for many months, suffering from
angina pectoris. At the autopsy the heart, which was below the
average weight, showed slight dilatation of the left ventricle. The
arch of the aorta was dilated. The orifice of the coeliac axis was
obliterated by calcareous deposit. There was chronic interstitial
nephritis, the renal arteries being atheromatous. See Insp., 1894.
No. 4.
S. 328 Punctured Wound of the Right Yentricle.
A heart shewing upon its anterior surface about the
middle of the right ventricle a linear wound measuring
three-eighths of an inch in length, which penetrates the
wall. Corresponding in position there is a small superficial
cut in the interventricular septum.
From a boy, æt. 11, who, while playing with a pocket knife, stabbed
himself in the preecordial region, and died in three minutes.
Presented by Mr. KNYVETT, 1894.
0.S. 358 Suppurative Myocarditis.
The heart of a child mounted to shew the cut surface of
the muscle of the left ventricle to have a somewhat mottled
appearance, the muscle in parts being replaced by a soft
white material, The valves and epicardium are normal.
Specimens recently added to the Pathological Museum. 273
Histologically the myocardium is seen to be in a condition
of diffuse purulent infiltration.
From a child st. 34 years who died in the Evelina Hospital with
symptoms of nephritis one month after the onset of an attack of
scarlet fever. At the autopsy the cavity of the left ventricle was found
to be somewhat dilated, and its wall very much thickened by a diffuse
infiltration of pus. There was no lymph on the surface of the valves
or pericardium. The kidneys were affected by tubal nephritis. See
Trans. Path. Soc., 1880, p. 70.
Presented by Dr. GOODHART.
S. 366 Hypertrophy and Dilatation of the Heart.
A heart with its cavities laid open to show the left
ventricle enormously dilated, whilst its wall is of about the
normal thickness. In the recent state the heart weighed
32 ounces, and the hypertrophy and dilatation affected both
sides equally. On the reverse of the specimen the epicar-
dium is seen to be free from adhesion, opaque and thickened.
Histological examination shews that the muscle of the left
ventricle is normal.
Robert L., a painter, was admitted under Dr. Taylor for
dyspnoea and attacks of faintness, from which he had suffered at
intervals for two years. There was a history of gout and lead
poisoning, but none of syphilis or rheumatism. On admission, there
were physical signs of great enlargement of the heart, without bruit or
albuminuria. Three days after admission the patient died, and at the
autopsy 50 ounces of serous fluid were found in the right pleural
cavity and 30 ounces in the pericardial sac. The valves of the heart
were normal and the aorta was not atheromatous. The kidneys were
healthy. See Insp., 1894, No. 272.
S. 447 Mitral Stenosis. Thrombus in Auricular Appendix.
A section through a heart shewing the mitral valve to be
funnel-shaped, and so narrowed as barely to admit the tip
of the little finger. The left auricle is dilated and slightly
thickened, and its appendix is distended with ante-mortem
thrombus.
Edith P., æt. 26, was admitted under Dr. Galabin in order that
labour might be induced for the relief of the symptoms of chronic
cardiac failure, which had gradually been increasing during her
pregnancy. She had suffered from chorea every year from the age of
7 to 14. Labour was induced three days after admission, and the
patient died four days later. At the autopsy the heart was found
to weigh 17 ounces, both pleural cavities contained serum, and there
were several recent infarcts in the base of the right lung. The kidneys
were scarred. See Insp., 1895, No. 127, | |
274 Specimens recently added to the Pathological Musewm.
E. 464 Ulcerative Endocarditis. Aneurysms of the Heart.
A portion of a heart mounted to shew extensive fibro-
calcareous changes in the aortic valve. There is a large
laceration in the free edge of the right anterior cusp,
surrounded by vegetations. There are small aneurysms
between the two anterior cusps and between the posterior
and left anterior cusp.
Nathaniel F., æt. 59, was admitted under Dr. Goodhart with
apoplectic symptoms, and died in a comatose condition fourteen hours
after admission. At the autopsy there was an aneurysm of the right
middle cerebral artery at its main bifurcation, together with a large
hemorrhage in the substance of the brain. The heart weighed 163
ounces. See Insp. 1894, No. 469.
0.S. 472 Aneurysm of the Heart.
A heart divided to shew the left ventricle converted into
an aneurysmal cavity, which measures five inches in its
longest diameter, and is almost filled with adherent
thrombus. The muscle of the interventricular septum is of
normal thickness, but elsewhere the myocardium is greatly
thinned, and at the apex of the heart is entirely replaced
by fibrous tissue. The epicardium, which is very thick, is
everywhere roughened by old adhesions.
From Thomas O., set. 42, who was found dead in the streets He
was said to have had syphilis, and to have been an in-patient in the
London Hospital two or three years before his death. At the autopsy
the heart was found to weigh 18 ounces; there was a scar upon
the glans penis, and one of the testes was fibroid. See Insp. 1888,
No. 287.
0.S. 479 Mitral Stenosis. Thrombus in the Auricle.
The base of a heart with the left auricle laid open to
shew a ragged mass of clot, almost entirely filling the
cavity and continuous with firmer thrombus distending the
appendix. The mitral orifice is contracted so as barely to
admit two fingers.
Sarah P., æt. 50, was admitted under Dr. Pavy for palpitation of
the heart and dyspnea, having three weeks previously suffered from
hsematemesis. On admission, the heart's action was noticed to be `
irregular, and a presystolic bruit was heard at the position of the
cardiac impulse. The patient died three weeks later, and at the
autopsy the heart was found to weigh 14 ounces and the kidneys
were scarred. See Insp. 1888, No. 307.
Specimens recently added to the Pathological Museum. 275
8.500 Dilatation of Left Ventricle.
A child's heart mounted to shew acute dilatation of the
left ventricle. The valves and pericardium are normal.
Histological examination shews the muscle of the left
ventricle to be healthy. In the recent state the heart
weighed three ounces.
William J., st. 4, was admitted under Dr. Shaw for tetanus,
following & punctured wound of a toe, and died six days after the
onset of symptoms. See Insp. 1895, No. 196.
S. 532 Hypertrophy of the Heart. Myocarditis.
A heart, which in the recent state weighed 18 ounces,
mounted to shew considerable hypertrophy of its walls with
some enlargement of the right side. The valves are healthy
and the aorta is free from atheroma. Histological examina-
tion of the left ventricle shews that the muscle fibres are
swollen, have lost their striation, and are separated from
each other by small-celled infiltration.
Thomas S., æt. 49, was admitted under Mr. Howse with pyrexia and
cedema of the lungs. A fortnight previously he had been in the
hospital for & few days with & contused wound of the scalp and
symptoms of concussion. After leaving the hospital he had been
drinking heavily, and on the day following his re-admission he became
delirious. Two days later, whilst straining at stool, he fell back and
died instantly. At the autopsy patches of softening were found in the
cerebral cortex, the liver was nutmegged, and the kidneys, which
weighed 16 ounces, were in & condition of cyanotic induration. See
Insp., 1895, No. 350.
S. 881 Aneurysms of the Heart.
A portion of a heart mounted to shew two sacculated
aneurysms, the orifices of which are situated just below the
two extremities of the posterior aortic cusp. The one on the
right admits the tip of the little finger, and the overhanging
right semilunar cusp has a wide perforation, through which
the regurgitant blood-stream apparently impinged upon the
wall of the sac. On the left side an oval opening three-
quarters of an inch in diameter leads into a sac about as
large as a walnut, which bulges into the left auricle. The
aortic valves are calcareous, distorted, and perforated in
several places. The mitral valve is somewhat thickened,
and there are fibroid patches in the myocardium,
From the Dissecting Room, 1889,
276 Specimens recently added to the Pathological Museum.
0.8. 566 Atrophy of the Heart.
A heart, which in the recent state weighed four and a-half
ounces, mounted to shew the atrophy of the organ associated
with chronic wasting diseases. There is a moderate deposit
of fat on the surface of the right ventricle.
William S., et. 94, was admitted under Mr. Durham for a psoas
abscess, having suffered for five years from symptoms of spinal caries.
He died about three months after admission, and at the autopsy the
liver, kidneys, epleen and intestines were found to be affected with
lardaceous disease. The liver, which weighed 68 ounces, was
very fatty. See Insp., 1889, No. 28.
S. 600 Aneurysm of the Mitral Valve.
The left ventricle of a heart, laid open to shew at the
upper part of the aortic cusp of the mitral valve a pouch,
which admits the tip of the middle finger and projects some-
what into the auricle. A little above the aneurysm is seen
a second slightly larger sac, caused by a protrusion of one of
the sinuses of valsalva. The aortic valves are thickened,
and were incompetent. The ventricle is dilated.
William C., set. 44, was admitted under Dr. Pye-Smith, for cardiac
pain and palpitation, from which he had suffered at intervals for three
years. On admission physical signs of enlargement of the heart were
detected, associated with a loud to-and-fro aortic bruit. The patient
became delirious, and died ten days after admission. At the autopsy,
the heart was found to weigh 293 ounces and many of the arteries were
atheromatous. See Insp., 1896, No. 66.
0.8. 624 Lacerations of the Left Yentricle.
A heart, in the dilated left ventricle of which are seen
two ragged lacerations extending about a third of an
inch into the cardiac muscle. One of them is situated
at the lowest part of the interventricular septum, and the
other, which is somewhat higher, crosses the base of the
papillary muscle arising from the anterior wall. On the
exterior of the heart, corresponding closely to this latter
laceration, is a rent with gaping edges about an inch in
length, in the upper margin of which is seen the torn end
of a coronary vein.
Jacob N., set. 35, was admitted under Mr. Howse, having been struck
by the pole of a van on the left side of the chest. About five hours
later he died, and at the autopsy several ribs were found to be fractured, `
and there were about 14 ounces of unglotted blood in the pericardium,
See Inap,, 1889, No. 202,
Specimens recently added to the Pathological Museum. 277
0.S. 654 Sarcoma of the Heart.
A portion of the right side of a heart mounted to shew
an oval mass of growth about an inch in length, situated
beneath the epicardium at the base of the right ventricle.
The growth, which projects as a convex nodule from the
surface of the heart, infiltrates the superficial layers of the
cardiac muscle. It has the histological structure of a round
and oval-celled sarcoma.
Michael S., et. 60, was admitted under Dr. Pitt with the physical
signs of a malignant growth of the mediastinum and effusion into
the left pleural cavity. He died a fortnight after admission, and at
the autopsy sarcomatous deposits were found in the thoracic glands
and in the liver and kidneys. See Insp., 1889, No. 288. “
0.8. 689 Atrophy of the Heart.
A heart weighing six ounces and mounted to shew the
condition of general atrophy. The epicardium is wrinkled,
and the coronary arteries are prominent. In the recent
state there was oedema of the epicardial connective tissue
with an almost total absence of fat.
Joseph T., æt. 55, was admitted under Dr. Perry with symptoms of
cancer of the stomach, having suffered from gastric symptoms for
three years. (Edema of the extremities supervened, and the patient
died eleven weeks after admission. At the autopsy the body was
emaciated, and the liver, which weighed only 28 ounces, contained
numerous small secondary deposits. See Insp., 1889, No. 387.
S. 703 Pysmic Abscesses of the Heart. Perforation of
Mitral Valve.
A portion of a heart mounted to shew two small round
patches of sessile vegetations upon the ventricular surface
of the posterior flap of the mitral valve. In the middle of
the larger patch is seen & perforation through which a blue
rod has been passed, traversing the valve and entering a
small abscess cavity in the wall of the ventricle immediately
beneath the aortic orifice. The cut surface of the ventricle
presents several other small points of suppuration.
Thomas R., st. 18, was admitted under Dr. Pye-Smith with
symptoms of pyemia, and died thirty-six hours after admission, on
the ninth day of hi« il'ness. At the autopsy a collection of pus was
f.und separating the periosteum from the neck of the right femur,
and the liver and kidneys contained numerous small abscesses. See
Insp., 1897, No. 106.
278 Specimens recently added to the Pathological Museum.
S. 715 Gumma invading the Right Yentricle.
A heart laid open to shew in the wall of the right
ventricle, immediately below the semilunar valves, a large
mass of gummatous material proyecting into the cavity of the
ventricle, and partially obstructing the pulmonary artery.
The deposit is continuous with a mass of fibro-caseous
material which surrounds and compresses the great vessels
at the base of the heart. The epicardium of the right side
of the heart is roughened, and was adherent.
From Hubert H., st. circa 80, who died quite suddenly. A few
weeks before his death he underwent an operation for piles, and was
then thought to be in good general health. At the autopsy all the
viscera with the exception of the heart were found to be normal.
Insp., 1897, No. 206.
0.8. 844 Thrombus in the Yentricles.
A heart with its ventricles laid open to shew in each of
them a considerable deposition of thrombus amongst the
meshes of the columns carnes. In the left ventricle the
thrombus presents numerous polypoid excrescences, somé
of which shew central excavation. On the right side,
where the clot is less abundant, a cylindrical mass is seen
adherent to the apex of the ventricle. The heart weighs
16 ounces. The valves are normal, and there is no clot in
the auricles.
Jane H., æt. 27, was admitted under Dr. Shaw for cedema of the
legs and of the left arm. She had been confined six week previously,
and on admission the precordial dulness was found to be increased to
the right of the sternum. Six days later she died, and at the autopsy
a large infarct was found in the anterior edge of the right lung, with
emboli in the spleen and kidneys. There was thrombosis of the
axillary, brachial and jugular veins on the left side. See Insp., 1890,
No. 293.
0.8. 871 Endocarditis of the Aortic Valves.
A portion of a left ventricle laid open to shew the aortic
valve affected by chronic and acute endocarditis.
cusps are thickened and their free borders are rounded, that
of the posterior cusp being capped by a row of minute
vegetations. Similar vegetations are seen along the line of
contact of the other cusps.
Specimens recently added to the Pathological Museum. 279
Thomas H., set. 22, was admitted under Dr. Shaw on the fifth day
of an attack of acute rheumatism, with a systolic bruit at the apex of
the heart. The patient subsequently developed physical signs of
pleurisy, pericarditis and double pneumonia, and died nineteen days
after admission. At the autopsy the heart was found to weigh
17 ounces, and the pericardial sac was obliterated by recent adhesions,
There were vegetations on the mitral valve. See Insp., 1890, No. 367.
0.S. 954 Aneurysm of the Heart.
A heart, at the apex of which is seen a thin-walled
globular sac, measuring an inch and a half in diameter, and
communicating with the left ventricle by a narrow opening.
The walls of the sac are formed of fibrous tissue, to which
the parietal pericardium is, in part, adherent. The endocar-
dium of the ventricle is much thickened. Histological.
examination of the muscle in the neighbourhood of the
apex shews fibroid change. The aorta is roughened by
atheroma.
Richard W., æt. 28, was brought in dead. He was said to have been
under treatment for syphilis. While following his occupation as a
labourer he attempted to lift a heavy load, and immediately expired.
At the autopsy, the heart was found to weigh 16 ounces, and the
pericardial sac was distended with 21 ounces of fluid and clotted
blood, which had escaped from & small V-shaped laceration of the
aneurysm. Both testes were fibroid. See Insp., 1891, No. 72; and
Trans. Path. Soc., 1891, p. 61.
0.8. 981 Thrombosis of the Left Auricle.
A section through the left auricle and ventricle, shewing
the cavity of the auricle to be almost filled with a laminated
and convoluted thrombus which is adherent to the wall at
its upper part. Smaller masses of clot are seen in the
appendix, and between the thrombus above mentioned and
the mitral valve. The valve is fibrous and greatly con-
tracted. The wall of the auricle is hypertrophied.
Robert C., set. 45, was admitted under Dr. Perry with a presystolic
bruit and signs of fluid in the right pleural cavity. Eight days later
he died, and at the autopsy an infarct was found in the right lung,
and the viscera were congested. The heart weighed 14 ounces,
and the tricuspid valve was somewhat contracted. There were small
thrombi in the right auricular appendix. See Insp., 1891, No. 149.
0.8. 982 Aortic and Mitral Incompetence.
A portion of a heart, laid open to shew the aortic valve
affected by chronic inflammation. The cusps are thickened,
280 Specimens recently added to the Patholoytcal Museum.
rigid and deformed; they are partially coherent to each
other, and between the posterior and left cusps is seen a row
of minute vegetations. The mitral valve is greatly thickened,
and was incompetent.
JohnO., et. 37, was admitted under Dr. Goodhart, with signs of chronic
cardiac failure. He had had rheumatic fever eight years previously.
On admission, a systolic bruit was heard at the apex of the heart, and
there was an inconstant diastolic bruit at the base. The patient died
from lobar pneumonia about six weeks after his admission. At the
autopsy the heart was found to be hypertrophied and dilated, weighing
24 ounces. The pericardium was adherent. The liver and kidneys
were congested. See Insp., 1891, No. 139.
0.8. 984 Endocarditis in Lobar Pneumonia.
An aortic valve mounted to shew upon the corpus arantii
of the right cusp a prominent vegetation about the size of
a swan shot. The cusps are otherwise normal.
Joseph R., æt. 50, was admitted under Dr. Perry on the fifth day
after the onset of symptoms of acute pneumonia with the physical
signs of consolidation of the right apex. A fortnight after admission
he became delirious, and a' week later he died. At the autopsy the upper
part of the right lung was found in & condition of acute interstitial
pneumonia, and there was early suppurative meningitis. Pneumo-
cocci were found in the lung, meninges, and in the aortic vegetations.
See Insp., 1891, No. 164.
S. 98/46 Atheroma of Aorta and Aortic Valves.
A portion of a left ventricle with the first part of the
aorta mounted to shew the vessel and the cusps of the
aortic valve affected by atheroma. In the aorta the disease
is limited to the first inch and a half of the vessel, the wall
being thickened and presenting a rough calcareous surface.
The cusps are deformed, stretched and thickened, and one
of them is partially torn from its attachment.
Henry R., et. 38, was admitted under Dr. Pye-Smith with signs of
heart disease. Nine weeks before admission, whilst at work, he was
suddenly seized with dyspncea and symptoms of cardiac failure. On
admission, there were physical signs of aortic regurgitation, and of
hypertrophy and dilatation of the heart. The left pleural cavity was
thrice aspirated. The patient died three weeks after admission, and
at the autopsy the heart was found to weigh 24 ounces. The lungs
were compressed, the liver nutmegged, and the kidneys indurated. See
Insp., 1898, No. 251.
Specimens recently added to the Pathological Museum, 281
S. 98/47 Melanotic Sarcoma of the Heart.
A heart divided to shew in the anterior wall of the left
ventricle a wedge-shaped mass of black growth, the base
being towards the epicardium and measuring three quarters
of an inch in diameter. There is a small similar deposit
beneath the endocardium of the right auricle. Histolo-
gically the growth is a sarcoma the cells of which are round
and oval and contain much pigment.
Eliza, W., set. 54, was admitted under Dr. Goodhart with symptoms of
cerebral tumour Five years previously Mr. Davies-Colley had removed
a growth from the lower jaw which recurred two years after operation.
The patient died seven days after her admission, and at the autopsy
deposits of melanotic growth were found in the brain, lungs, jejunum
and in the mesenteric glands. See Insp., 1898, No. 262.
S. 99/30 Mitral Stenosis. Dilatation of the Auricles.
A heart mounted to show great dilatation of the auricles
resulting from mitral stenosis and tricuspid regurgitation.
The left auricle measures six inches in its longest diameter,
and its walls are slightly thinner than normal. The mitral
valve is fibrous, and barely admits the tip of the index finger.
On the reverse of the specimen the right auricle is laid open,
and measures four inches in its longest diameter. The tri-
cuspid orifice admits four fingers, and the valve has a
thickened and rolled edge. The aortic and pulmonary
valves are healthy. The right ventricle is hypertrophied
and dilated, the left being somewhat below the average size.
Mary R., æt. 47, was admitted under Dr. Pitt with signs of heart
disease, having occasionally suffered from dyspnoea and cedema of the
ankles for fifteen years. Systolic and diastolic murmurs were heard
at the apex and a systolic murmur in the aortic area. The patient
died eight days after admission and at the autopsy the heart was found
to weigh 16 ounces and the kidneys were scarred. See Insp., 1899,
No. 83. ”
S. 99/87 Pouching of the Inter-auricular Septum. Patent
Foramen Ovale.
A heart which weighed 24 ounces, and presents general
hypertrophy and dilatation without valvular lesion. In
the right auricle is seen a finger-like membranous pouch,
measuring about two inches in length and an inch in width,
282 Specimens recently added to the Pathological Museum.
and having at its apex a circular opening a third of an inch
in diameter. An inspection of the left auricle shows that
the pouch is formed by a protrusion of the portion of the
inter-auricular septum, forming the fossa ovalis.
From a woman, xt. 55, who presented the physical signs of enlarge-
ment of the heart, and died from chronic cardiac failure. At the
autopsy, the right kidney, which was granular, was found to weigh
7$ ounces, the left being represented by a small mass of fibrous tissue
containing & few cysts. The liver was nutmegged, and there was
effusion into the pleural and peritoneal cavities.
Presented by Dr. CLAUDE TAYLOR, 1899.
LIST OF SPECIMENS ADDED TO THE
DENTAL MUSEUM.
By J. LEWIN PAYNE.
DENTAL SURGERY SECTION.
I. IRREGULARITIES OF THE TEETH :—
A. Number.
B. Size.
C. Form or structure.
D. Position.
A. NumBer.—tThirty-two teeth being the normal number for
man any excess or diminution constitutes an irregularity; both
of these forms are fairly common, but of the two one more
frequently meets with the excess in number.
Excess in number.—Any teeth in excess of the normal may be
spoken of as supernumerary ; but when they differ in no respect
from the members of the series in which they are situated they
are called supplemental teeth. =
Supplemental.— For example, increased number of lateral
incisors, either upper or lower; excessive number of bicuspids ,
cases have also been recorded of supplemental molar teeth.
1. Model of the maxillə taken at the age of 24 years, showing
a supplemental right temporary lateral incisor.
Presented by Mr. TRAER HARBIS.
2. A similar condition seen in a model taken at the age of 44
years.
VOL. LVI. 29
284 List of Specimens added to the Dental Museum.
3. Model of the upper jaw of a child, aged 7 years, in which
three right temporary incisors are seen; on the left side the tem-
porary incisors are gone, but it was stated that the teeth were
quite normal.
Presented by Mr. W. H. Morris.
4. Model of a mandible of a girl, aged 8 years, presenting five
permanent incisors.
Presented by Mr. A. V. BRIMMER.
5. A supplemental tooth—one of five lower incisors; three-
quarters of the root was exposed on the labial side and its position
was apparently that of a lower lateral incisor on the right side.
Presented by Mr. E. C. CLAYTON.
6. Model of the upper jaw, showing a supplemental left upper
lateral (chipped). i
Presented by Mr. F. NEWLAND-PEDLEY.
7. Models of a mouth showing a supplemental lateral behind
the left central incisor, which it has rotated and thrust forward.
Presented by Mr. W. A. Macas.
8. Model showing a supplemental upper lateral incisor on the
right side.
Presented by Mr. E. Hutson.
9. A supplemental left upper lateral incisor.
10. Model of the maxille with supplemental incisors situated
behind the centrals, which are slightly displaced. `
Presented by Mr. J. L. PAYNE.
11. Models of a mouth showing a small supplemental bicuspid
on the left side of the lower jaw.
Presented by Mr. W. A. Macas.
12. Model of a mandible with three bicuspids on each side of
the jaw.
Presented by Mr. R. UMNEY.
13. Model showing five lower bicuspid teeth on the left side
(Duplicate of one in the Museum of the Victoria Dental Hospital,
Manchester).
Presented by Mr. D. HEADRIDGE.
14, A remarkable model of the maxille with six bicuspids
on the left side, a pyramidal shaped supernumerary tooth behind
the central incisors, and another supernumerary gemminated to the
right lateral,
List of Specimens added to the Dental Museum. 285
15. Two models of maxillee each having a supernumerary molar
situated on the buccal side.
Irregular supernumerary teeth.—These are more common.
Characteristics.—(i.) The lingual and labial surfaces have not
necessarily any difference in form. (iH. The enamel is said to
terminate in an even line around the neck of the tooth (generally
this is so; but it is not always true). (iii. Roots are single (with
very rare exceptions).
T'ypes.—Conical, pyramidal, and molariform.
16. Model of the upper jaw showing a deciduous supernumerary
on the right premaxilla. Miss Y., aged 8.
17. Eight conical supernumerary teeth, some being remark-
ably small and very imperfectly formed, found in the front of the
mouths of different individuals.
Presented by the late Mr. JosePH Fox.
18. A progressive series of ten supernumerary teeth com-
mencing with the simple conical type and becoming more
complete as the series continues, the last showing an attempt at
the formation of cusps. (The root of the third shows signs of
absorption.)
Presented by Mr. F. NEWLAND-PEDLEY.
19. Three conical supernumerary teeth.
20. Model of upper jaw showing two conical supernumerary
teeth behind the right central incisor, causing displacement of the
central and canine. |
Presented by Mr. F. NEWLAND-PEDLEY.
21. A series of four models (a, B, y, à), of maxille, showing
conieal supernumerary teeth in the incisor region, in most cases
displacing central incisors.
22. Model showing a supernumerary in the place of the upper
left central incisor, conical in form.
Presented by Mr. G. O. RICHARDS.
23. Conical-shaped supernumerary projecting anteriorly
hetween the upper central incisors.
Presented by Mr. M. F. Hopson.
e
286 List of Specimens added to the Dental Museum.
24. Three models (a, 6, y) showing conical supernumerary
teeth in the median line; a, the dental arch is contracted giving
the appearance of a high vault. y. The cutting edge of the
tooth is grooved by attrition of the lower incisors.
25. A model of 2 conical supernumerary teeth situated behind
the right and left centrals respectively.
Presented by Mr. F. BLEwrrr.
26. A similar model in which the upper centrals and laterals
have been displaced.
Presented by Mr. F. E. LAMBEBT.
27. Another model in which a supernumerary tooth has
displaced a right upper lateral.
Presented by Mr. A. J. COLLETT.
28. A conical supernumerary tooth in the median line, causing
considerable irregularity and forming a, sort of central point
around which the upper central and lateral incisors are arranged.
Presented by Mr. S. R. APTHORPE, 1892.
29. Model of a lower jaw with a supernumerary tooth
situated in front of the left central incisor.
Presented by Mr. W. R. BUTLER.
30. Three supernumerary teeth in the palate, two being conical
and one having three cusps.
Presented by Mr. G. O. RıcHARDS.
31. Three supernumerary teeth, one with a cruciform crown
and the others having a triangular masticating surface.
Presented by Mr. F. TA'Bors.
32. Three molariform supernumerary teeth from the back part
of the jaws.
33. Model showing two supernumerary teeth of the bicuspid
type, in the median line, which are separating the upper central
incisors. The crowding has brought about caries in the left
canine.
Presented by Mr. F. V. MACEENZIE.
34. Two models of maxille, showing cubical-shaped super-
numerary teeth, situated behind the incisors.
Presented by Mr. T. S. DAVIDSON.
35. Cubical-shaped supernumerary tooth in median line,
causing displacement backwards of the right lateral.
List of Specimens added to the Dental Museum, 287
96. Two models, showing large, cubical-shaped supernumerary
teeth in the posterior incisive region , in one case the left upper
central is displaced forwards.
37. Model of two supernumerary teeth of cubical form,
occupying the position of the upper central incisors, the left
central seems about to erupt; the right central did erupt, but was
so loose that the patient removed it. Patient aged 19 years.
Presented by Mr. A. V. BRIMNER.
38. Model of the maxilla, with a supernumerary tooth in the
region of the third molar.
Presented by Mr. K. GOADBY.
Deficiency.—Deficiency in the number of the teeth may be due
to one of two causes :—
(a) Tooth quite unformed.
(6) Tooth, though developed, remaining unerupted.
VVhile in very rare cases there is a total congenital absence of
teeth, one not infrequently meets with patients in whom a large
number are missing.
Deficiency is more commonly observed in the permanent than
in the temporary series, the teeth most often absent being the
upper laterals, the third molars, and the second lower bicuspids.
Diminution in number resulting from extraction is not, of course,
included under this heading.
39. Model showing the absence of a left upper lateral incisor,
associated with the presence of a diminutive lateral on the right
side.
Presented by Dr. J. W. PARE.
40. A model showing a similar condition.
Presented by Mr. J. L. PAYNE.
41. Model with both upper laterals absent, and having the
canine teeth in close proximity to the central incisors on each
side. The persistent temporary canines are situated immediately
behind the permanent ones.
Presented by Mr. A. E. BAKER.
42. Model of the maxille with both lateral incisors missing,
and the temporary canine persisting behind its permanent suc-
cessor on the right side. Patient aged 25 years.
Presented by Mr. E. MORGAN.
288 List of Specimens added to the Dental Museum.
43. A similar model, in which the persistent temporary canine
is situated in front of its successor on the left side. Patient aged
24 years.
44. The model of the maxille of a girl, aged 14 years, showing
absence of the first and second left incisors, and having the left
temporary canine retained with its permanent successor in front
of it. No history of injury or extraction.
Presented by Mr. J. M. C. Jacoss.
45. The left half of an adult mandible, found in the grounds
of Guy’s Hospital during building operations, which shows the
second temporary molar persistent and moderately well implanted,
whilst a section of the bone beneath it demonstrates the absence
of any sign of a successional tooth. :
Presented by Mr. G. S. H. BARNETT.
46. A case of non-eruption of a, left upper central incisor in
a boy aged 12 years, apparently due to the persistence of a
temporary incisor root.
Presented by Mr. C. J. HINCHLIFF.
47. Singular models of upper and lower jaws taken from the
mouth of a patient aged 29 years, and showing total absence of
bicuspid teeth; the patient stating that she was quite certain
none had at any time been erupted or extracted. In the maxilla,
both the second temporary molars are standing, while an
interspace exists on the right side between the canine and
lateral; in the mandible, wide spaces are seen between the
canines and molars and also between the canines and laterals
on each side.
Presented by Mr. J. L. PAYNE.
48. Models from the mouth of a boy aged 13 years, the third
out of five children, there being nothing unusual in the dentition
of the other members of the family and no signs of rachitis or
syphilis in him. The father stated positively that no teeth had
been extracted. All the molars (except one lower temporary),
the second bicuspids, and the left lower central incisor are absent,
and the lower right central incisor is quite diminutive.
Presented by Mr. W. A. Maaas.
List of Specimens added to the Dental Museum. 289
49. Models of the upper and lower jaws, shewing unusual
deficiency ; in the mandible there are only four cone-shaped teeth
on each side in front of the mouth and two roots posteriorly ;
in the maxillə, there are but five teeth on either side, and a apace
exists on the left side of the median line.
Presented by Mr. J. H. Bapcock.
90. Models of the maxille and mandible having only four
teeth below and six teeth above; of the four lower teeth, two have
cone-shaped crowns, one is irregular, and the fourth molariform :
of the six upper teeth five are conical.
Presented by Mr. G. H. Morris.
51. Models of the maxilla and mandible presenting only six
teeth above (a canine and two bicuspids on each side) and four-
teen lower teeth (one incisor, a canine, one bicuspid, and two
molars on each side), the front teeth are conical, the molars
dwarfed and none had been extracted.
Presented by Mr. W. A. Maaas.
B. Sıze.—The teeth in the permanent series which are most
frequently abnormally large are the central maxillary incisors and
the second lower bicuspids, whilst diminution in size occurs more
often in the lateral incisors and the third molars in the maxilla.
Too large.
52. A large temporary molar with long roots.
53. Models showing large central and lateral incisors causing
irregularity in both upper and lower jaws. The upper laterals
were removed to make room for the other teeth.
Presented by Mr. H. P. TAYLOR.
54. A large left lower lateral incisor with flexuous root.
Presented by Mr. F. NEWLAND-PEDLEY.
55. A long upper right canine whose length has been partially
increased by exostosis.
56. Four large lower canine teeth, one of which has a bifur-
cated root. |
57. Two upper molars with very large crowns, in one, part of
the crown has been destroyed by caries, in the other, the com-
plexity may possibly be due to the fusion of a supernumerary tooth
with a molar of ordinary size.
Presented by Mr. F. NewLAND-PEDLEY.
290
58.
59.
60.
61.
62.
63.
List of Specimens added to the Dental Museum.
A large upper molar with four roots.
Presented by Mr. E. AsHBY.
Four large upper molars.
Two lower molars, with long roots.
Too small.
A tiny supernumerary tooth.
Five stunted central incisor teeth.
Presented by Mr. F. V. MACKENZIE.
A pair of upper central incisors with short roots and
crowns, and having stomatitic markings.
Presented by Mr. J. PAYNE.
64. Model of a lower jaw, showing a dwarfed central incisor.
Presented by Mr. J. M. C. Jacoss.
65. Three stunted upper bicuspid teeth.
66. Models showing small but perfectly shaped second upper
bicuspids ; in the lower jaw a diminutive left lateral is seen, while
the bicuspids are normal.
Presented by Dr. J. W. PARE.
LIST
OF
GENTLEMEN EDUCATED AT GUY’S HOSPITAL
WHO HAVE PASSED THE
EXAMINATIONS OF THE SEVERAL UNIVERSITIES, COLLEGES,
&o., &c.,
IN THE YEAR 1899.
Wnibersity of Oxford.
Examination for the Degree of Doctor of Medicine.
HARRY COOPER.
Final Examination for the Degrees of Bachelor of Medicine and
Surgery.
F. O. STOEHR.
Ülnifrersity of Cambridge.
Degree of Doctor of Medicine.
A. P. BEDDARD.
Final Examination for the Medical and Surgical Degrees.
Part I.
A. H. Davies. J. A. Glover. J. G. Taylor.
C. H, Glenn. T. E. Holmes. D. B. Watson.
L. Wilkin.
Part II.
A. C. Fry | H. A. Gaitskell. | F. Shufflebotham.
D. P. Watson.
Second Examination for the Medical and Surgical Degrees.
Part II. .
8. Child. | H. A. Cutler.
| H. P. Wiltshire.
299 Gentlemen admitted to Degrees, £c., in the year 1899.
First Examination for the Medical and Surgical Degrees.
Part IT.
B. H. Stewart.
Examination in Sanitary Science.
Parts I. and II.
S. Copley. C. A. Lumley. A. E. Porter.
J. H. Godson, E.L. Parry-Zdwards. | H.J. Spon.
C. M. Vernon.
Unibersity of London.
Examination for the Degree of Doctor of Medicine.
R. H. Ashwin. A. J. Cleveland. R. W. Mayston.
H. W. Bruce. C. R. Hodgson. H. J. Starling.
Examination for the Degree of Master in Surgery.
W. S. Handley. | W. T. Milton.
Examination for the Degree of Bachelor of Surgery.
First Division.
P. Turner.
Obtained Honours.
Second Division.
A. H. Carter. J. Howell. W. G. Stewart.
C. T. Hilton. G. N. Meachen.
Examination for the Degree of Bachelor of Medicine.
May.
First Division.
A. H. Carter.
Second Division.
F. J. H. Cann. | A. E. Clarke. | H. E. C. Fox.
P. McK. Wilmot.
October.
First Division.
H. L. Eason.
C. T. Hilton.
Obtained Honours in Medicine and Forensic Medicine.
Second Division.
G. N. Meachen. | P. Turner.
Obtained Honours in Forensic Medicine.
E. S. Hall. H. M. Reeve. W. G. Stewart.
A. G. Osborn. J. Robertson.
Gentlemen admitted to Degrees, &c., in the year 1899.
G. T. Collins.
W. J. Davies.
H. A. Ehrlich.
G. Evans.
S. J. Ormond.
D. Forsyth.
E. T. Jensen.
Intermediate Examination in Medicine.
January.
Entire Examination.
Second Division.
| H. B. Foster. | Н. С. Keates.
Excluding Physiology.
First Division.
M. A. Collins.
Second Division.
A. C. H. Gray. R . Robson.
. Trail.
Us
E
C. B. Penny.
E. F. Reeve.
Physiology only.
First Division.
| A. Pearson. | A. C. Ransford.
Second Division.
O. Marriott. M.
T. A. Matthews. D
J. Rees.
. W. Smith.
July.
Honours Examination.
W. H. Bowen.
293
Obtained Honours in Anatomy, Physiology and Histology, Materia Medica
M. Coplans.
H. W. Brown.
M. W. Cohen.
J. T. Hicks.
J. Evans.
M. A. Collins.
and Pharmaceutical Chemistry.
| A. E. H. Pakes. | L. E. Stamm.
Obtained Honours in Physiology and Histology.
Entire Examination.
Second Division.
N. N.A. Houghton. F.
W. G. Parker. A.
C. H. Robertson.
3
homas.
. Wall.
mb
td
Excluding Physiology.
Second Division.
| D. S. Graves. | H. K. Lacey.
F. C. Wetherell.
Physiology only.
Second Division.
| W J. Davies. | A.C. H. Gray
W. M. Robson.
294 Gentlemen admitted to Degrees, £c., in the year 1899.
Preliminary Scientific (M.B.) Examınatıon.
January.
Entire Examination.
First Division.
D. Isaacs.
Biology.
P. A. 8. Dyson. | P. A. Peall. | G. H. Rees.
July.
Entire Examination.
Second Division.
R. P. Rowlands. | G. Russell. | G. W. Smith.
Chemistry and Experimental Physics.
G. Hamilton. | A. M. Roome.
Biology.
A. E. F. Kynaston. | J. O. Musson. | C. H. Reinhold.
R O. Williams.
Intermediate Examination in Science.
E. H. B. Milsom.
Intermediate Examination in Science and Preliminary Scientific
Examination conjointly.
Second Division.
. Carter. R. Felton. M. G. Louisson.
H.H
J. H. Clatworthy. A. Leeming. A. P. Piggott.
Anibersity of Burham.
Examination for the Degree of Doctor of Medicine.
C. H. Bryant.
Examination for the Degree of Doctor of Medicine for Practitioners
of Fifteen Years’ Standing.
R. H. Browne. | J. S. Hooker. | W. Makeig Jones.
Alexander Lane.
Gentlemen admitted to Degrees, éc., in the year 1899. 295
Final Examination for the Degrees of Bachelor of Medicine and
Surgery.
R. Tilbury Brown. | H. W. Dudgeon.
Bachelor in Medicine.- -Third Examination,
H. Braund.
Bachelor in Medicine.—Second Examination.
8. G. Clapham. | M. C. Wetherell.
Bachelor in Medicine—First Examination.
Chemistry and Physics and Elementary Anatomy and Biology.
C. M. Anthony. B. Glendining. M. C. Wetherell.
J. W. Caton. C. B. Travers.
Chemistry and Physics only.
S. C. Clapham. | H. O. Sturdy. | G. W. Smith.
Royal College of Physicians of London.
Admitted to the Membership.
F. E. Fremantle. R. O. Moon. E. Tvens Spriggs.
L. C. Panting. | T. F. Ricketts. D. W. Samways.
Final Examination for the License.
January.
H. M. Berncastle. | A. Evans. F. J. Nicholls.
F. W. Brook. | Evan Evans. R. J. Pritchard.
A. H. Carter. J. H. Jones. F. L. Rae.
A. E. Clarke. A. H. B. Kirkman E. W. S. Rowland.
V. J. Crawford. T. H. W. Landon F. D. Turner.
P. J. Curtis. J. Matthews H. S. Turner.
J. T. Dunston. | W. T. Milton. F. E. Walker.
April,
W. L. Baker J. W. Ensor. A. A. Miller.
E. H. Cragg J. Howells. J. H. H. Parsons.
H. S. Crapper A. D. Lewis. J. H. Roberts.
E. B. Dowsett J. T. M. McDougall. H. C. Sturdy.
W. H. Edwards G. N. Meachen. O. C. Worthington.
July.
G. Beley. A. R. McLachlan. A. R. Thomas
V. T. C. Bent C. D. Outred. C. B. Thomson
W. R. Cazenove. H. M. Reeve. T. M. Walker.
H. R. H. Denny. S. A. Ruzzak. J. B. Walters.
E. A. Evans. G. S. Bimpson. C. F. Watson.
W. B. Hope. J. G. Taylor.
October.
G. M. Brown. R. Michell. J. L. Payne
T. W. S. Browne D. 7, Munro. A. W. Penrose.
W. W. Harrison. J. F, Northcott. E. R. Row.
P. C. P. Ingram, A. H, Palmer. W. G. Stewart.
H. Leader, E, E. Parrett. D. P. Watson,
L. Wilkin.
296 Gentlemen аатаиеа to Degrees, £c., ün the year 1899.
Royal College of Surgeons of England.
Final Examination for the Fellowship.
S. Copley. | J. Howell. F. W. Robinson.
First Examination for the Fellowship.
W. H. Bowen. A. C. H. Gray. F. H. Parker.
F. Curtis. L. Gifford Nash. O. W. Richards.
M. A. Collins. N. P. Blake Odgers, C. Tessier.
F. L. Thomas.
Final Examination for the Membership.
January.
H. M. Berncastle. A. Evans. F. J. Nicholls.
F. W. Brook. Evan Evans. R. J. Pritchard.
A. H. Carter. J. H. Jones. F. L. Rae.
A. E. Clarke. A. H. B. Kirkman. E. W. S. Rowland.
V. J. Crawford T. H. W. Landon. F. D. Turner.
P. J. Curtis. J. Matthews. H. S. Turner.
J. T. Dunston. W. T. Milton. F. E. Walker.
April.
W. L. Baker J. W. Ensor. A. A. Miller.
E. H. Cragg J. Howells. J. E. H. Parsons.
H. S. Crapper A. D. Lewis. J. H. Roberts.
E. B. Dowsett J. T. M. MeDougall. H. C. Sturdy.
W. H. Edwards G. N. Meachen. O. C. Worthington.
July.
G. Beley. A. R. McLachlan. A. R. Thomas.
V. T. C. Bent. C. D. Outred. C. B. Thomson.
W. R. Cazenove. H. M. Resve. T. M. Walker.
H. R. H. ə S. A. Ruzzak. J. B. Walters.
E. A. Evans G. S. Simpson C. F. Watson.
W. B. Hope. J. G. Taylor
October
G. M. Brown. R. Michell J. L. Payne.
T. W. S. Browne. D. J. Munro A. W. Penrose.
W. W. Harrison. J. F. Northcott. H. R. Row.
P. C. P. Ingram. A. H. Palmer. W. G. Stewart.
H. Leader. E. E. Parrett. D. P. Watson.
L. Wilkin.
Royal College of Surgeons of Edinburgh.
Examination for the Fellowship.
C. W. Booker. | R. B. Stamford.
Society of Apothecaries of London.
Final Examination for the License.
G. H. Bedford. H. M. Hardy. R. G. W. Saint-Cedd.
L. D. B. Cogan. H. C. Holden. T. J. Vick.
A. G. C. Davies. E. McD. Judge. C. C. Worts.
F. Golaing-Bird. S. H. Longhurst. H. B. Yorath,
Medallists and Prizemen. 297
MEDALLISTS AND PRIZEMEN.
JULY, 1900.
Open Scholarships in Arts.
Frank Thomas Herbert Wood, Roan School, Greenwich, £100.
Herbert Stanley Knight, Bancroft’s School, Woodford Wells, £50.
Herbert Andrew Watney, Trent College, Derbyshire, Certificate.
Dental Students.
Osborne Black, Foyle College, Londonderry, £30.
Open Scholarships in Science.
Henry Francis Bell Walker, Stockport Grammar School, and private
study, £150.
John Hunter Clatworthy, Guy’s Hospital, £60.
Gerald Russell, Guy’s Hospital, Certificate.
Harry Hunter Carter, Guy’s Hospital, Certificate.
Scholarship for University Students.
Paul Norman Blake Odgers, Lincoln College, Oxford, £50.
Greer Edmond Malcomson, Owen's College, Manchester, Certificate.
Frederick Henry Parker, Pembroke College, Cambridge, Certificate.
Junior Proficiency Prizes.
Percy Reginald Bolus, £20.
Edwin Henry Britton Milsom, £12 10s. | al
Neville Ivens Spriggs, £12 10s. ed ums
Kenneth Black, Certificate.
Reginald Larkin, Certificate.
Alexander Moxon Webber, Certificate.
The Michael Harris Prize for Anatomy.
Alexander Moxon Webber, £10.
Reginald Larkin, Certificate.
William Leigh Maule Day :
Lionel Henry Moiser | equal Certificate.
The Wooldridge Memorial Prize for Physiology.
Percy Reginald Bolus, £10
Neville Ivens Spriggs, Certificate.
Edwin Henry Britton Milsom, Certificate.
The Hilton Prize for Dissection (1899).
Haroid Tipping, £2 10s. T
Alfred Herbert Edwin Wall, £2 10s. | 2498--
298
Medallists and Prizemen.
The Arthur Durham Prizes for Dissection.
First Year's Students.
Edward Crosby Peers, £5.
Sentor Students.
Alexander Moxon Webber, £15.
Geoffrey Carlisle, Certificate.
Frederick Rogerson, Certificate.
Dental Prizes.
First Year's Students
Gerald Hamilton Morris, £10.
Samuel William Isles, Certificate.
Second Year's Students (1899).
John Black, £15.
27:07 Ы equal Certificates.
Practical Dentistry Prize.
Gerald Hamilton Morris, £5 aal
Arthur Henry Clogg, £5 em
Senior Proficiency Prizes.
Graham Scales Simpson, £20.
Edward Cohen, Certificate.
The Treasurer's Gold Medal for Clinical Surgery.
Graham Scales Simpson.
The Beaney Prize in Pathology (1899).
Caleb Thomas Hilton, £34.
Frank Shufflebotham, Certificate.
The Richard Bredin Prize for Clinical Study.
Caleb Thomas Hilton, £25.
Hospital Appointments held in the year 1899. 299
PHYSICAL SOCIETY.
Honorary President.—Sın SAMUEL WILEs, Bart., M.D., LL.D., F.R.S.
Secretaries.—Mr. Bellingham Smith and Dr. Beddard.
Presidents.
A. H. Davies, B.A., C. T. Hilton, M.B., B.S., A. H. B. Kirkman,
F. Shufflebotham, M.A., M.B., B.C., F. O. Stoehr, B.A., M.B., B.Ch., R. H. J.
Swan, M.B., B.S., P. Turner, M.B., B.S., B.So., F. G. Gibson, M.A., F. G.
Cross, H. S. French, B.A., F. E. Walker.
PRIZEMEN FOR THE SESSION 1899-1900. |
The Society's First Prize of £10 was awarded to Mr. F. G. Gibson for his
paper on “ The ZEtiology and Prognosis of Epithelioma of the Tongue,” and
Mr. F. Cross obtained the Second Prize of £5 for his paper on “ Abdominal
Injuries.”
CLINICAL APPOINTMENTS HELD IN THE
. E. Fremantle.
. Jephcott.
E15
F. S. Batchelor.
R. Balderston.
H. W. Bruce.
VOL. LVI.
. E. C. Handson.
YEAR 1899.
HOUSE PHYSICIANS.
M. F. Brickdale.
J.
E. W. S. Rowland.
W.H.
M. Telling.
HOUSE SURGEONS.
W. T. Milton.
G. C. Owsley.
W. L. Baker.
K. B. Alexander.
T. P. Berry.
A. H. B. Kirkman.
F. W. Brook.
A. R. Thomas.
S. E. Denyer.
P. Turner.
T. P. Berry.
A. H. M. Saward.
ASSISTANT HOUSE SURGEONS.
R. T. Fitz-Hugh.
K. B. Alexander.
F. E. Walker
F. D. Turner
A. H. M. Saward
H. L. Eason.
A. H. Carter.
G. N. Meachen.
J. T. Dunston.
RESIDENT OBSTETRIC ASSISTANTS.
A. J. Cleveland.
H. Leader.
W. J. Lindsay.
23
300 Hospital Appointments held in the year 1899.
pi z nip tU gi gg
CLINICAL ABSISTANTS.
W. H. M. Telling.
T. P. Berry.
F. D. Turner.
W. L. Baker.
A. E. Clarke.
D. P. Watson.
L. Wilkin.
J. F. Northcott.
3
B
. Handson.
iylor.
"Te
BE
HU
aitskell.
Qn
Z O p mb Obie
р E
QE E
E
eachen.
CLINICAL ASSISTANTS IN THE MEDICAL WARDS.
. Durbridge.
. E. Clarke.
. C. Mullins.
. G. Stewart.
. H. Brailey.
. B. Thomson.
2
F. O. Stoehr.
J. H. Roberts.
A. Fraser.
A. H. Davies.
T. 7. VVright.
F. VV. Brook.
H. A. Gaitskell,
G. M. Brown.
F. Shuffiebotham.
H. N. Clarke.
CLINICAL ASSISTANTS IN THE SURGICAL WARDS.
A. E. Cawston.
. H.
. B. Carr.
. V.
. H. Brailey.
. Northoott.
kins.
. Barron.
hen.
. Kelly.
. Lewis.
. Mitchell.
. Cross.
. Greenfield.
o
. Mandy.
. Fawley.
. Reeve.
Een
8
ar
. L. Camps.
earson.
. Morgan.
. B. Dobson.
Tacher.
. B. Hammond.
. Trubshaw.
. Smith.
rg
Qaya Sd dd HE E E S P d E n
577
7
. F. Hardenberg.
, Graham Smith.
T. J. Wright.
C. D. Bryan.
P. W. L. Camps.
SURGEONS' DBESSERS.
F. J. Felix Jones.
E. H. Felton.
H. A. Higgens.
T. P. Thomas.
tu
o
à
SUP RE
P
3
>
cD. Parrott.
mg
à
, Loo osely.
per.
. Ransford.
. Gibson.
, Robinson.
. Welchman.
. Bridger.
Beavers.
. Hodgson.
. F. Ticehurst.
. Bentley.
Hi Uo El SAME pe bima im:
oD o o m
J. Matthews.
W. H. Brailey.
A. C. Ransford.
. Lewis.
oC. Dallas.
. Miller.
, Hunter.
. Foster.
. S. "Perkins.
aser.
. Holmes.
. Ker.
. Glover.
Johnson.
WE. Whatley.
. R. Beale Browne.
Mua Hua n
ик ə:
cA
G. Clarke.
E. Shelton Jones.
E. G. Wales.
8. J. Ormond.
P. T. Manson.
H. Davies-Colley.
Hospital Appointments held in the year 1899. 301
. Greenfield.
. Brydone.
. Kelly.
. Whatley.
. Segreda.
. Cragg.
. Attwood.
, Curtis.
. Moon.
. D. Welch.
. Pern.
ор” ЕЗЕФ
. Smith.
, Matthews.
. Wood.
'acher.
. French.
. Manser.
. Collins.
'hompson.
. Wallis.
. Stamm.
20:
Faaa aa E инни акр
Beton 2
Q
o
Ë,
=
а
es
. Howard.
. W. Brook.
. E. Parrett.
. H. Brangwin.
Ci pl ya
C. R. Howard.
H. McD. Parrott.
E. J. F. Hardenberg.
o
. D. Bridger.
. F. Ticehurst.
. 8.
———
. Claxton.
DENTAL SURGEONS’ DRESSERS.
H. R. H. Denny.
H. M. Hardy.
O. Marriott.
H. Braund.
Graham Smith.
ASSISTANT SURGEONS’ DRESSERS.
з
=
o”
. Hammond.
lt ton Jones.
. B. Dobson.
gov
m x
h
5.
о,
Reeve.
poo
. Butler.
. Ransford.
. Gibson.
avies-Colley.
entley.
. Trubshaw.
. Marshall.
. Lacey.
. Ommanney.
. Smith.
. Welchmann.
, Kitchen.
. T. Griffith.
.H. Shannon.
. Kempthorne.
. Ehrlich.
. Davidson.
5:
Q pi pri 92 Ed Һә Hd tJ FLEX 4 Br] ii dai bd 0014 41-63
td
dade usn
S. A. Ruzzak.
T. E. Holmes.
B. W. Moss.
CLINICAL ASSISTANTS IN MEDICAL OUT-PATIENTS.
. Tongue.
. Clark.
. Thomson.
Brangwin.
. Hilton.
. Barron.
J ensen.
. B. Kirkman.
. Attwood.
> jo O O ttg
PRƏKEHƏNƏ
G. N. Meachen.
E. E. Parrett.
E. J. Tongue.
H. B. Dismorr.
E. R. Row.
G. H. Bedford.
A. A. Ruzzak.
J. F. N orthcott.
H. McD. Parrott.
W. H. Edwards.
P. C. P. Ingram.
E. A. Miller.
E. H. Felton.
DRESSERS IN THE EYE WARDS.
L. Wilkin.
H. A. Gaitskell.
R. Michell.
J. Matthews.
P. C. P. Ingram.
H. A. Higgens.
H. T. Palmer.
G. Lewin.
J. L. Whatley.
302 Hospital Appointments held in the year 1899.
CLERKS IN THE EYE WARDS.
C. B. Sells. H. R H. Denny E. E. Parrett.
E. B. Dowsett. G. N. Meachen H. M. 7
H. M. Hardy. F. O. Stoehr. A. H. Carte
H. E. C. Fox. H. St. A. Alder T. H. W. Yd doli:
P. C. P. Ingram. W. B. Secretan R. W. B. Hall.
A. Densham. M. J. Rees. H. Bentley.
F. W. Brook. L. C. Martin C. H. Glenn.
J. B. C. Brockwell. G. T. Wrench L. Hirsch.
W. W. Harrison. M. W. Cohen H. Braund.
C. H. Robertson. J. C. Curtis. A. H. E. Wall.
C. B. Penny. H. T. Palmer. W. C. Lewis.
E. G. Andrew. B. W. Moss. F. L. Thomas.
J. A. Wood.
DRESSEBS IN THE THBOAT DEPARTMENT.
T. W. H. Landon. | F. 6. Batchelor. A. A. Miller.
G. E. Richmond. , A.H. B. Kirkman. E. W. 8. Rowland
H. C. Sturdy. | F. W. Brook. C. T. Hilton.
J. Matthews. | C. G. Osborn J. Harris.
R. B. Stamford. | A. D. Lewis E. A. Longhurst
A.R. McLachlan. . E. Cohen. J. G. Taylor.
C. R. Hodgson. | H. J. Starling. O. Marriott.
E. E. Parrett. H. R. H. Denny. C. E. Hicks.
CLERKS IN THE THROAT DEPARTMENT.
H. C. Sturdy. W. B. Hope H. Braund.
G. T. Willan. F. D. Welch C. B. Thomson.
W. O. Roberts. L. Pern.
MEDICAL WARD CLERKS.
A. C. Ransford. J. A. Butler. E. G. Allport.
D. Forsyth. F. G. Gibson P. W. L. Camps.
E. F. Reeve. R. S. Roper. A. Pearson.
J. A. Wood. G. 8. Graham Smith. H. Bentley.
K. V. Trubshaw. H. Davies-Colley. J. F. Robinson.
D. L. Morgan. N. F. Ticehurst. P. T. Manson.
J. E. Collins. S. Hodgson. M. D. Wood.
T. A. Matthews. E. G. Wales. H. K. Lacey.
R. Jimenez. H. D. Kempthorne. L. Hirsch.
P. J. Nash. F. M. M. Ommanney. | R. P. Marshall.
S. S. H. Shannon. D. W. Smith. A. C. Osburn.
H. Wacher. F. E. Welchman. F. VV. Smith.
J. A. B. Hammond. D. R. T. Griffiths. F. VV. Sime.
T. H. F. Roberts. S. J. Ormond. H. A. Ehrlich.
E. C. Bevers. V. M. Wallis C. B. Penny.
G. G. Davidson. G. Clarke. W. O. Roberts.
C. R. Howard. T. H. B. Dobson E. I. Claxton.
E. H. Kitchin. R. Thompson H. S. French.
A. Wylie. F. B. Manser E. F. G. Heap.
C. B. Penny. 8. J. Ormond R. D. Smedley.
G. T. Collins. A. Croneen. L. E. Stamm.
C. E. Gaitskell. F. Curtis. F. A. Beattie.
M. J. Rees F. D. S. Jackson. G. Evans.
J. F. Douse. D. H. Trail. H. C. Keates.
G. S. C. Hayes. J. Evans. S. C. H. Bent.
A. W. Soper. E. Roberts. A. W. Gater.
E. J. Crew. A. C. Nash. W. M. Robson
G. H. H. Manfield. H. J. Gater. L. J. Hughes
H. W. Brown. F. C. Wetherell. G. T. Wrench
A. C. H. Gray. M. A. Collins. W. J. Davies
C. Tessier. G. W. C. Hollist. H. A. Cutler
R. C. Lawry. F. Bigg. J. A. Andrews.
S. Child. | H. P. Wiltshire. O. W. Richards
Hospital Appointments held in the year 1899.
. Atkins.
. Cohen.
. C. Martin.
. G. Stewart.
. A. Alabone.
. H. Glenn.
. Morgan.
. Shelton Jones.
. B. Carr.
. C. Holden.
. W. Talbot.
. Stott.
. E. Holmes.
. C. Mullins.
. C. Lewis.
. D. Welch.
. P. Ker.
. G.
ds
. T.
. E.
арын
Cross.
Felix Jones.
Jensen.
L. Bates.
7V“7vVvVv7Ü71(7v7v7
kı.
, F. Roberts.
. Davidson.
hompson.
He.
ichmond.
. Douse.
. Gaitskell.
. Trail.
. Gater.
. Soper.
. Gater.
. Bowen.
ssier.
, Faulks.
. Smith.
z zao mi
<
55517”
+
©
. G. Stevens.
plans.
. E. Wall.
. Grommitt.
. О. О. Bradb
. À. Ehrlich. >
oS ner her
uc i
PH
B
. Collins.
. Gater.
. Welch.
. Wetherell.
. Barron.
imi p» Ed hd iii
. Thomas.
. Robertson.
. Penny.
ӧлрновоожр-
ео
Griffiths.
. E. Kennard.
Mar 23398:
3
. Cawston.
stone.
raund.
. Foster.
. S. Perkins.
. Glover.
. Mitchell.
. Goadby.
. Whatley.
. Greenfield.
HUMmgEÁMIBEUPPEROUBHUuoOz
2 a dar
Wht
755
T. R. Beale Browne.
W. H. Loosely.
G. T. Willan. |
SURGICAL WARD CLERKS.
W. O. Roberts.
H. S. French.
E. H. Kitchin.
F. C. Wetherell.
. T. Heap.
. Collins.
. S. Jackson.
. H. Bent.
. C. Hollist.
. Crew.
. Manfield.
. Collins.
. Hughes.
. Lawry.
. Andrews.
. Richards.
. Graves.
. Curtis.
oir.
_W. Cohen.
57:
izi
"i
EB
grops
ORO DOS 11-11
SIDA
G. F. Humphreys.
H. Barber.
E. Malcomson.
C. B. Penny.
ASSISTANT SURGEONS’ CLERKS.
E. T. Jansen.
. Lewis.
EXTERN OBSTETRIC ATTENDANTS.
E. A. Miller.
G. Shorland.
G. S. Simpson.
D. P. VVatson.
VV. B. Secretan.
E. G. Andrew.
. Densham.
. J. Wright.
. Davies.
. Higgens.
, Felton.
. Northcott.
. Thornas.
ewin.
. Attwood.
. Kelly.
. Segreda.
[cD. Parrott
. Reeve.
. Brydone.
epi pid HE HE E He
prod rn E
aa UE
E. I. Claxton.
C. R. Howard.
R. D. Smedley.
E. Bigg.
A. Croneen.
G. Evans.
H. C. Keates.
. E. Wetherell.
. H. Gray.
. Cutler.
. Palmer.
ild.
. Wiltshire.
. F. Churchill.
. Miles.
. Turner.
. Collins.
. Parker.
. Parker.
. Soper.
Oh > a pe mm imt
255
a
oper.
eattie.
usins.
iles.
J
. Soper.
. Pakes.
Pooxuməmn
Ed x pri Q Z > 24)
Mags
p
a
303
304 Hospital Appointments held in the year 1899.
AURAL SUBGEON’S DRESSERS.
A. H. Carter. A. Reid. C. F. Watson
L. Wilkin. W. B. Hope. H. C. Sturdy
E. E. Parrett. H. M. Hardy. E. Cohen.
F. Shufflebotham. H. 8. Turner. H. B. Dismorr
J. Harris. H. A. Gaitskell. F. E. Fremantle
A. R. McLachlan. F. W. Sime.
OBSTETRIC DRESSEBS.
O. Marriott. J. T. Dunston. C. Edwards.
D. J Munro. H. Leader. J. B. C. Brockwell
A. G. Osborn. T. M. Walker. C. B. Sells.
A. A. Miller. C. R. Cazenove. C. B. Thomson
E. G. Andrew. A. Densham. E. E. Parrett
W. K. Wills. F. A. Beattie. A. W. Penrose
E. W. Goble. A. R. Thomas. E. Cohen.
J. M. Brydone. R. Tilbury. R. Braund
C. H. Brangwin. F. A. Segreda. F. O. Stoehr
J. S. S. Perkins. H. Durbridge. L. Pern.
W. M. Thomas. B. Muir.
ASSISTANT PHYSICIANS’ CLERKS.
W. H. Loosely. B. Muir. P. S. Mandy.
F. D. Welch. G. T. Willan. W. Johnson.
E. P. Mitchell. A. Moon. K. W. Goadby.
E. G. Andrew. J. D. Bridger. L. Pern.
H. G. Rashleigh T. B. Fawley. J. E. Collins.
R. Jiminez. E. G. Wales. H. Wacher.
T. A. Matthews. P. J. Nash. 8. S. H. Shannon
J. F. Robinson. L. Hirsch. R. P. Marshall.
F. W. Sime. J. D. Kempthorne. J. H. F. Roberts.
E. H. Kitchin. A. R. Thompson. D. R. T. Griffiths.
E. Bevers. E. I. Claxton V. M. Wallis.
H. S. French. A. C. Nash. E. Roberts.
P. A. Beattie. H. C. Keates A. Croneen.
G. T. Collins. M. J. Rees. O. W. Richards
A. O. H. Gray.
CLERKS IN THE SKIN DEPARTMENT.
C. H. Brangwin. F. J. Nicholls. E. J. Tongue.
H. B. Dismorr. A. R. McLachlan. F. D. Welch.
J. E. Collins. H. Braund. W. H. Brailey.
T. E. Holmes.
POST-MORTEM CLERKS.
C. H. Brangwin. H. R. H. Denny. H. Braund
A. Densham. H. M. Reeve. O. Marriott
J. D. Bridger. B. W. Moss. E. A. Miller
A. R. McLachlan. G. M. Brown. D. P. Watson
P. C. P. Ingram. T. E. Holmes. W. M. Thomas.
A. Wylie. H. K. Lacey. R. D. Attwood
T. B. Fawley. P. J. Nash. D. W. Smith.
R. P. Marshall. F. W. Sime. A. C. Osburn.
CLERKS IN THE ELECTRICAL DEPARTMENT.
H, Braund. | D, L. Morgan,
Hospital Appointments held in the year 1899. 305
. Dismorr.
Rowland.
aker.
. Stewart.
. Cawston.
‘arriott.
. Watson.
. Stoehr.
. Roberts.
. Holman.
Wrench.
hen.
. Jensen.
. Rae.
. Segreda.
. Osburn.
eele Perkins.
tkins,
Anne
= рә
sp iii gge Pa
5O:
p
. Shillingford.
.A.
, B. Kirkman.
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CLERKS TO ANZESTHETISTS.
A. Fraser.
A. Reid.
H. Braund.
W. H. Edwards.
H. W. Fox.
, VV. Goble.
. Secretan.
. Hardy.
arrison.
. Miller.
. Glenn.
wards.
. Brangwin.
. Penrose.
. Greenfield.
. Ommanney.
. Welch.
. Whatley.
. Lewis.
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. Holmes.
. Worts.
. Northcott.
. D. Bryan.
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. Longhurst.
. Simpson.
. Martin.
. Brailey.
. Wright.
. Moss.
irsch.
. Bubb.
. Sime.
, Ormond.
. Bagshawe.
. Barron.
. Ker.
. Lacey.
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DENTAL SCHOOL.
APPOINTMENTS HELD DURING THE YEAR 1899.
DENTAL HOUSE-SURGEONS.
. G. Plumley. P. 8. Campkin.
| P. H. Hayes Palmer.
A.G E. N. Mason.
S. H. Olver. A. E. Rowlett.
ASSISTANT DENTAL HOUSE-SURGEONS.
P. H. Hayes Palmer. A. E. Rowlett. J. Black.
H. T. Campkin. F. W. Garman. R. B. Recordon.
J. Bennett. H. N. Hillier.
DEMONSTRATORS IN THE CONSERVATION BOOM.
J. Black. A. M. Gabriel. H. Maurice.
F. W. Garman. F. J. Pearce. R, B. Recordon,
R. C. G. May. H. N. Hillier. J. Bennett.
S. L. Pallant J. H. Greenwood. W. R. Searle.
S.L. Prall. A, W. Aldis. G. W. Ray.
E. W. Corfe. T. Walkington.
ASSISTANT DEMONSTRATOR OF DENTAL MICROSCOPY.
R, B. Recordon.
306 Hospital Appointments held in the year 1899.
un
. Morris.
Shapland.
7
Aylen.
man.
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. Pallant.
cher.
alkington.
ewitt.
. Lowe.
, Dignum.
, Ross.
Dent.
. Jimenez.
. B. W. Rust.
. W. Bromley.
. W. Green.
. H. Solomon.
. Black.
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Whittington.
Pollitt.
. Garman.
. Green wood.
. Recordon.
. Shepherd.
. В. "Morris.
. Couchman.
. Maurice.
Fragman”
. H. Furnivall.
. W. Corfe.
. VValkington.
. Drewitt.
, E, Pedler,
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TR.
. H. Tattersfield.
Winckworth.
. Tattersfield.
N. P. Sheppherd.
W. R. Searle.
H. N. Hillier.
. Morris.
. F. Knowles.
. S. Wright.
. K. Perry.
, H. Drake.
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DRESSERS IN THE GAS ROOM.
. Searle.
. Shattock.
. Shelton.
. Steweni.
. C. Butler.
` G. Smith,
DRESSERS IN THE EXTRACTION ROOM.
A. M. A. Stevens.
A. W. Aldis.
G. H. Steweni.
` Pedler.
. Furnivall.
. Edwards.
eenwood.
. Smith.
. Witcombe.
. Webb.
. Iles.
, Bowle.
binson.
. Hinton.
. Ray.
. Meads.
. Wallis.
. Sams.
. А. Dennant.
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. Morrell.
. Drake.
. Allen.
. Longhurst.
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ennett.
. W. C. Jones.
. Wartski.
. Edwards.
. A. Stevens.
. Aylen.
cher.
. Prall.
. Ness.
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, St. H. Tweney.
Hospital Appointments held in the year 1899.
DRESSERS IN THE CONSERVATION ROOM.
A. H. Staple.
A. H. Saunders.
E. P. Uttley.
A. R. Cummings.
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. Chandler.
. Morris.
. Witcomb.
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. Wright.
. Knowles.
. W. Rust.
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. Jimenez.
. Bromley.
. Aylen.
. Ray.
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E. J. Gaffney.
G. W. Ray.
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. H. Morris.
H. N. Hillier. J. Milligan.
N. P. Shepherd. 8. L. Pallant.
J. Black. W. H. Tattersfield.
E. J. Gafiney. E. W. Corfe.
O. H. Dignum, D. H. Wallis.
F. VVarlov. S. E. Pedler.
J. S. Biss. E. B. L. White.
E. R. Howlett. G. H. Drake.
R. Peacock. S. H. Jones.
H. T. Campkin. J. A. Whittington.
W. W. C. Jones. W. A. Dennant.
J. H. Wilkes. H. L. Shelton.
A. Battersby. H. C. Winckworth.
G. P. Pollitt. P. Greenwood.
S. J. Tweney. C. F. Rose.
S. H. Longhurst. E. G. Walton.
P. P. Cole. C. H. Bubb.
J. B. Morrish. L. C. A. Knight.
H. R. Shapland. W. R. Searle.
A. Archer. W. E. Meads.
G. H. Steweni. S. C. Bowle.
A. W. Aldis. V. E. Turner.
K. C. Ness. P. E. Coish.
A. H. Smith. W. K. Perry.
C. Hickes. T. Walkington,
J. F. Rey. J. H. Hinton.
T. Robinson. C. R. Shattock.
C. S. Morris. VV. H. Solomon.
H. B. Ross. J. VV. Powell.
R. S. Witcomb. V. S. Sams.
A. C. Edvards. H. R. C. Butler.
VV. Jarvis. P. H. Furnivall.
A. M. A. Stevens. R. C. G. May.
C. Lee. A. L. Lamlbert.
G. VV. Badcock. VV. E. Love.
VV. Morgan. A. H. Clogg.
C. H. Mason. E. L. Davis
S. R. Lidiard. G. F. Sargood
J. S. Francis. O. Black.
JUNIOR DRESSERS IN THE CONSERVATION ROOM.
K. C. Ness. 8. Clifford.
. T. Walkington. S. E. Pedler.
J. F. Rey. E. W. Corfe.
R. S. Witcomb. H. B. Ross.
C. Hickes. P. E. Coish.
W. K. Perry. J. W. Powell.
N. W. Green. A. B. W. Rust
V. S. Sams. J. H. Hinton
W. E. Meads. O. K. Dignum
F. W. Bromley. H. J. Webb
H. S. Wright. V. E. Turner.
S. W. Iles. G. W. Badcock.
T. Robinson W. E. Lowe.
F. G. Day. O. Blac
W. Morgan. H. J. Corin.
S. R. Lidiard. E. L. Davis.
J. C. Holford. G. F. Sargood.
. Greenwood.
. Mitchener.
307
GUY'S
MEDICAL
HOSPITAL.
AND SURGICAL STAFF.
1901.
Consulting Physicians.—Sm SAMUEL Wings, Bart., M.D., LL.D.,
F.R.S.; F. W. Pavy, M.D., LL.D., F.R.S.; P. Н. PrEe-SMITH,
M.D.. F.R.S.: J. P. GoopHart, M.D., LL.D
Consulting Surgeons.—J. BIRKETT, Esq.; Tuomas Bryant, M.Ch.
Consulting Obstetric Physician.—H. OLDHAM, M.D.
Physicians & Assistant Physicians.
FREDERICK TAYLOR, M.D.
W. HALE Ware, M.D.
G. Newrox Prrt, M.D.
E. О. Perry, M.D.
L. E. SHaw, M.D.
J. W. WASHBOURN, M.D.
J. H. Bryant, M.D.
J. Fawcett, M.D.
Obstetric Physicians.
A. L. GALABIN, M.D.
P. Horrocks, M.D.
Assistant Obstetric Physician.
J. H. TanGETT, M.S.
Physician for Mental Diseases.
G. H. SAVAGE, M.D.
Aural Surgeon.
W. LAIDLAW PURVES, Esq.
Dental Surgeons.
P. NEWLAND-PEDLEY, Esq.
W. A. Maaas, Esa.
J. H. BADCOCE, Esq.
Medical Registrar and Tutor.
A. J. CLEVELAND, M.D.
Obstetric Registrar and Tutor.
G. BELLINGHAM SMITH, B.S.
Warden of the College.
Mr. DUNN.
Surgeons & Assistant Surgeons.
Н. G. Howsz, М.В.
R. CLEMENT Lucas, B.S.
C. H. GoLpmc-Biev, M.B.
W. H. A. Jacosson, M.Ch.
CHARTEBS J. SYMONDS, M.S.
W. ARBUTHNOT LANE, M.S.
L. A. рокн, M.S.
A.D. Fripp, M.S.
F. J. STEWARD, M.S.
Ophthalmic Surgeons.
C. HiGaGENS, Esq.
W. A. BRATLEY, Esq.
Instructor in Anzsthetics.
Tom Brrp, Esq.
Anesthetists.
G. ROWELL, Esq.
H. F. Lancaster, M.D.
C. J. OGLE, Esq.
W. S. HANDLEY, M.D.
R. H. J. Swan, B.S.
Surgical Registrar and Tutor.
G. S. Sımpson, Esq.
Ophthalmic Registrar and Tutor.
A. W. ORMOND, Esq.
Lying-in Charity.
Dr. Horrocks AND Mr. TARGETT,
Dean of the Medical School.
Dr. FAVOETT,
LECTURERS AND DEMONSTRATORS.
Clinical Medicine ... ... .. .. THE PHYSICIANS AND ASSISTANT PHY-
SICIANS.
Clinical Surgery ... ӧн ee THE SURGEONS AND ASSISTANT SUR-
GEONS.
Medicine ә e e 9 gə Da. TAYLOR AND DB. HALE WHITE.
Practical Medicine ... ... ... ... DR. CLEVELAND.
Surgery ... ә ә, e e иә MR. Howse AND MR. Lucas.
Operative Surgery ... ... ... ... Mh. FRIPP AND MR. STEWARD.
Practical Surgery... ... ... ... Mr. SIMPSON.
Midwifery and Diseases of Women... Dr. GALABIN.
Practical Obstetrics ... ... +. ... MR, TARGETT.
Mental Diseases... ... һә... ... DB. SAVAGE.
Ophthalmic Surgery... .. .. ... Mh, HIGGENS.
Dental Surgery ... ... .. .. ... MB. NEWLAND-PEDLEY.
Aural Surgery ... ... .. ... +... MR. LAIDLAW PURVES.
Diseases of the Skin ... ... ... ... DR. PERRY.
Diseases of the Throat... ... ... MR. SYMONDS.
Electro-Therapeutics... ... ... ... DR. BRYANT.
Anaesthetics... ... .. ә ... MB. Tom BiBD AND Mr. RowELL.
Hygiene and Public Health -. .. DR. SYKES AND MR. PAKES.
Pathology ... ә sso .. иә +... DR. PITT.
Morbid Anatomy °... ә DR. BRYANT AND DR. Fawcett.
Morbid Histology and Bacteriology... Mh. BELLINGHAM SMITH, MR. PAKES.
Medical and ә N
Classes... ... . DR. FAWCETT AND MR. STEWARD.
Bakery: дәк ән o o +... DR. VVASHBOURN AND MR. PAKES.
Forensic Medicine ... ... ... ... DR. STEVENSON.
Anatomy ... .. 6 vee e ә МВ. LANE AND MR. DUNN.
Practical Anatomy ... ... +... .. MR. FAGGE, MB. ROWLANDS AND
Mh. Swan.
Physiology ... ... e) eee c DR. WASHBOUBN AND DR. PEMBREY.
Practical Physiology ... ә se .. DB. PEMBREY, DR. BEDDARD AND
Dr. SPRIGOS.
Materia Medica and Therapeutics ... DB. PERRY.
Practical Pharmacy... ... ... .. THE HOSPITAL DISPENSER.
Chemistry ... sse .. ә. ..0. se MB. WADE.
Practical Chemistry ... ... ... ... MR. WADE, MR. RYFFEL AND MR. BALL.
Experimental Physics ... ... .. PROFESSOR REMmOLD, F.R.S., AND
Mh. BALL.
Biology... ... .. .. .. .. ... DR. STEVENS AND MR. Swan.
Psychology ... .. +.» «+ «se» ә DR, SAVAGE AND Dr. Hvsrop,
310 Scholarships and Prizes.
The Hospital contains 695 Beds, of which 554 are in constant occupation.
Special Classes are held for Students preparing for the University, and other
Higher Examinations.
APPOINTMENTS.
All Hospita] Appointments are made strictly in accordance with the
merits of the Candidates, and without extra payment. There are 28
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 recently
re-opened will provide additional accommodation for gynscological and
maternity cases.
ENTRANCE SCHOLARSHIPS.
YEARLY IN SEPTEMBER.
Two Open Scholarships in Arts, one of the 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 License in Dental Surgery.
NEW SCHOOL BUILDINGS.
The new Theatre and Laboratories, opened in June, 1897, by H.R.H. The
Prince of Wales, ufford every facility for practical instruction in Physiology.
COLLEGE.
The Residential College accommodates about 50 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. Fawcett,
Guy's Hospital, London Bridge, S.E.
THE STAFF OF THE DENTAL SCHOOL.
1901.
Dental Surgeons.
F. NEWLAND-PEDLEY, F.R.C.S., L.D.S.E.
W. A. Macas, L.R.C.P., M.R.C.S., L.D.S.E.
J. H. Вларсоск, L.R.C.P., M.R.C.S., L.D.S.E.
Assistant Dental Surgeons.
R. Wynne Rouw, L.R.C.P., M. F. Hopson, L.D.S.E.
M.R.C.S., L.D.S.E. J. B. Parrirr, L.R.C.P., M.R.C.S.,
H. L. PILLIN, L.D.S.E. L.D.S.E.
Demonstrators of Practical Dentistry.
J. L. PAYNE, L.R.C.P. M.R.C.S., * Р. S. CAMPKIN, L.D.S.E.
L.D.S.H. C. S. Morris, L.D.S.E.
E. B. Розтвктт, L.R.C.P., M.R.C.S., F. J. Pearce, L.D.S.E.
L.D.S.E.
Anesthetists.
F. W. Cook, M.D., M.S. W. S. Hanpury, M.D., M.S.
H. F. Lancaster, M.D. R. P. ROVLANDS,L.R.C.P.,F.R.C.S.
C. J. OGLE, M.R.C.S. R. H. J. Swan, M.B., B.S.
Lecturers.
Dental Surgery and Pathology.—Mr. NEWLAND-PEDLEY.
Dental Anatomy and Physiology.—Mr. Maaas.
Operative Dental Surgery.—Mr. Bapcock.
Dental Mechanics.—Mr. Wynne Rouw.
Practical Dental Mechanics.—Mr. PILLIN.
Dental Microscopy.—DB. BEDDARD AND DR SPRIGOS.
Metallurgy.—J. WADE, B.Sc.
Practical Dental Metallurgy.—Mr. Hopson.
Curator of Dental Museum.—Mr. Payne.
Dean.—Dr. FAWCETT.
GUY’S HOSPITAL REPORTS.
The Frfty-fifth Volume. Edited by J. H. Bryant, M.D.,
and F. J. Srewarp, M.S. Price to Subscribers, 6s.; to Non-
Subscribers, 10s. 6d. Postage free.
10.
11.
12.
CONTENTS.
. A Case of Cerebral Tumour in which the Skull was opened Four Times
for the Relief of Headache and Blindness. By W. Hale White, M.D.
, A Case of Calcification of the Arteries and Obliterative Endarteritis,
associated with Hydronephrosis, in a Child aged Six Months. By
J. H. Bryant, M.D., and W. Hale White, M.D.
Some Remarks on Transfusion and Venesection. By A. P. Beddard, M.D.
. Notes on Tubercular Disease of the Lymphatic Glands in the Neck.
By C. J. Harnett, M.D.
. Notes on the Setting-up and Working of an X-Ray Installation. By
E. W. H. Shenton.
. Functional Pulmonary Incompetence and Dilatation and Atheroma of
the Pulmonary Arteries, as Complications of Mitral Stenosis. By
J. Н. Bryant, M.D.
. Two Negele Pelves. By J. H. Targett, M.S.
. Widal’s Reaction: A Critical Examination of 326 Cases in which the
Reaction has been tried. By W. C. C. Pakes.
. Chronic Mercurial Poisoning, with Special Reference to the Danger in
Hatters’ Furriers’ Manufactories. By J. G. Taylor, B.A., M.B., B.C.
The Symptoms Immediately preceding Death from Exophthalmic Goitre.
By A. J. Cleveland, M.D.
Acute Intestinal Obstruction caused by the Ileum Becoming Adherent to
a Lithopedion. By J. H. Bryant, M.D.
On the Radical Operations for Uterine Cancer in Guy’s Hospital from
1886 to 1899. By T. G. Stevens, M.D.
List of Gentlemen Educated at Guy’s Hospital who have passed the
examinations of the several Universities, Colleges, etc., in the year
1898. |
Clinical Appointments held in the year 1898.
Dental Appointments held in the year 1898.
J €. A, CHURCHILL, Great Marlborough Street.
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Guy's Hospital.
Guy's Hospital reports
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