PATHOLOGICAL SOCIETY OF LONDON.
2
72 Medical Societies. PATHOLOGICAL SOCIETY OF LONDON. Multiple Cavernons Angiomata.-Melanotic Tumour of Breast.-() Recoverv from Tubercular J.7J1eningitis.- Ra1/naud’s Disease and Peripheral Neuritis.-Rupture of Syphilitic Cardiac Aueurysm. pture of THE annual general meeting of this Society was held on Tuesday last, Dr. J. S. Bristowe, F.R.S., president, in the chair. The list of officers and Council for the ensuing year is appended to this report. The vote of thanks to the retiring President was proposed by Dr. T. Barlow, seconded by Mr. James Black, and carried by acclamation. The vote of thanks to Mr. Butlin, proposed by Dr. Goodhart and seconded by Mr. R. W. Parker, was also warmly received. Mr. F. S. EvE showed a specimen of Multiple Cavernous Angiomata of Leg. They were distributed along the internal and external saphenous veins, chiefly subcutaneous, but some were lying deeply in the popliteal space. On three of the digits were calcified enchondroma ; exostoses were found on each end of the tibia. A sarcomatous tumour sprang from the back of the tibia and included an angioma. Spaces bound with connective tissue were seen under the micro- scope, and these spaces could be injected from the vein. The sarcoma was a round-celled one. The tibia was bowed backwards, and showed a defect in organisation of osseous tissue. Phleboliths were contained within the angiomata. In Billroth’s last edition some mention was made of mul- tiple angiomata. Dependence of tumours on defective development was illustrated by the present case.--Mr. C. J. SYMONDS said Mr. Howse had recorded a similar case in the Guy’s Hospital reports. Mr. H. T. BuTLIN showed a Melanotic Tumour of the Breast taken from a woman aged sixty-four, who was first operated on in 1880. The tumour was of seven months’ duration. There were no adhesions, no enlargement of glands, no retraction of nipple, and no peculiar colour of skin. The breast was removed. Recurrence took place, and a fresh operation was performed in 1882; from beneath the scar the recurring tumour was removed. In 1884 a third tumour from the same situation was excised; and recently another tumour was cut away. There was no sign of disease of any internal organ. The section was brittle and rendered microscopic preparations difficult. There were many tiny, very bright nsevoid spots in the skin that were considered to suggest carcinoma. He believed it was a sarcoma with a distinct alveolar structure. There was a similar case in a woman aged sixty-eight in Billroth’s article on the Breast in the Deutsch. Chirurg. Gross allowed of melanotic car- cinoma, but not sarcoma. The melanotic granules appeared to be in the intercellular substance in the fibroid bands.- Mr. A. A. BowLBY said that there were many small pigmented spots. The growth was exceedingly friable. He did not think there was true melanosis. He concluded that it was a sarcoma from the distribution of the blood- vessels.-Mr. D’ARCY PowER said that the structure was peculiar; a base of connective tissue existed on which filaments sprouted, as happened in the growth of some fungi.-Mr. BuTLIN wished to have the specimen submitted to the Morbid Growths Committee. Dr. CARRINGTON read a case of old Phthisis and recovery from Tubercular Meningitis. He admitted that the case was open to criticism, but, inasmuch as it must have occurred to most to have at least suspected meningitis in cases that eventually recovered, he thought that any post-mortem evidence bearing on the point was worthy of discussion by the Society. The patient was a boy aged sixteen, a clerk. Three sisters had died in infancy, but the family history was otherwise good. On July 4th he was knocked down by a tricycle, which struck him on the right knee, but he only kept his bed for a week. Still, however, the knee continued to swell, and in the course of a year movement became much impaired. Fifteen months after the accident the left knee became affected, and eventually this joint also became to a degree fixed. The boy improved under treat- ment, but on Jan. 26tb, 1886, he was readmitted with psoas abscess on the right side. He again improved by treatment, and was discharged on April 24th, but was readmitted on Oct. 2nd with another abscess on the left side; he gradually sank and died. After death the pi-arachnoid was found to be generally thickened, and the sulci were matted to- gether. The membranes were granular, and exhibited small yellow tubercles, as was confirmed on microscopical examination. There was meningitis, probably of more recent origin, of the lower third of the cord; the brain and cord were healthy, except that the latter was softened. At the apex of each lung there were old phthisical lesions. The fourth and fifth lumbar vertebrae were carious, and the right knee-joint completely disorganised. With the excep- tion of lardaceous disease of the spleen and small intes- tine, the other viscera were healthy. As regards the tubercular nature of the old meningitis, Dr. Carrington was inclined to lay much stress upon the concomitance of old tubercular phthisis, old cerebral meningitis, caries of the spine, and chronic joint disease, as evidence of the tubercular nature of the meningitis, which he believed had been recovered from, but he thought the naked-eye and micro- scopical appearances were equally distinctive. The spinal meningitis was probably of more recent origin, and due directly to the cause. If the origin of the disease was claimed as due to the accident, it was curious that the second knee was not affected until fifteen months after- wards, and there certainly could not have been any cerebral meningitis at the time, for the man only kept his bed for a week, and then went to his work as a clerk. On the whole, he suggested that there was evidence of bygone tubercular meningitis, probably approaching in date the old phthisis.-Mr. S. G. SHATTOCK suggested that the meningeal appearances were somewhat like those of periarteritis, as shown by Dr. C. Turner.-Dr. J. S. BRISTOWE raised the question whether the nodules of tubercles were necessarily ancient.-Dr. CARRINGTON said that the tubercles were yellow and caseous, and adherent by fibrous tags. He felt sure that they would be found to have no connexion with the arteries.-In reply to a question, Mr. TARGETT said the intellect was unclouded. ’ Dr. COUPLAND showed for Dr. Wiglesworth specimens of Peripheral Neuritis in Raynaud’s Disease, the subject being a female inmate of RainhiIJ Asylum, aged twenty-six, who suffered from chronic Bright’s disease and dementia, with epilepsy. Before her admission in December, 1884, she had sustained amputation of several of the fingers and toes for gangrene, and whilst under observation she suffered from ulceration of these extremities, and in January, 1886, the terminal phalanx of the fourth left finger became gangrenous and required amputation. The patient died suddenly in May, 1886, after an epileptic fit. The kidneys were markedly granular. The spinal cord and several of the nerve trunks of the limbs were examined microscopically. In the cord the chief change was in the posterior vesicular column of Clarke, where the cells were rounded, their processes being ill-defined; and the neuroglia of the white substance appeared slightly thickened. In the nerves there was an overgrowth of the fibrous elements, with atrophy and degene- ration of the nerve fibres--e.g., the left posterior tibial nerve presented thickening of the epineurium, perineurium, and endoneurium, with atrophy of the nerve tubules. Similar changes oscured in other nerves, and were better marked in those of the left limbs than in those of the right. The changes were more marked at the peripheral than in the larger rerve trunks. Dr. Wiglesworth left the question open whether the change was primarily a chronic interstitial inflamma- tion invading the nerve bundles and causing their atrophy, or whether it was a primary degeneration of nerve tubules with secondary hyperplasia of the fibrous framework; but he considered that the case removed Raynaud’s disease from the category of neuroses, and showed that structural lesions of the peripheral nerves underlay it.- Mr. A. A. BOWLBY had examined the nerves, and found indentical changes. He thought it was very likely to be a disease dependent on lesions in the peripheral nerves; the stiffening of the joints pointed in the same direction. M. Pitres had recorded a similar case.-Dr. THOMAS BARLOW said similar cases had been recorded by Pitres and Mount- stein of Strasburg, but the changes were not so extensive as in Dr. Wiglesworth’s case. Though important contributions, they did not solve the difficulties. Raynaud’s disease was divisible into several classes. There were chronic cases like Dr. Wiglesworth’s, and the genuine or paroxysmal cases, which were as fit-like as a rigor in an attack of ague. The occurrence of paroxysmal haemoglobinuria and attacks of amblyopia and jaundice seemed to show that there must be a wider pathology than a peripheral neuritis. It seemed as
Transcript of PATHOLOGICAL SOCIETY OF LONDON.
72
Medical Societies.PATHOLOGICAL SOCIETY OF LONDON.
Multiple Cavernons Angiomata.-Melanotic Tumour ofBreast.-() Recoverv from Tubercular J.7J1eningitis.-Ra1/naud’s Disease and Peripheral Neuritis.-Rupture ofSyphilitic Cardiac Aueurysm.
pture of
THE annual general meeting of this Society was held onTuesday last, Dr. J. S. Bristowe, F.R.S., president, in thechair. The list of officers and Council for the ensuing yearis appended to this report. The vote of thanks to the
retiring President was proposed by Dr. T. Barlow, secondedby Mr. James Black, and carried by acclamation. The voteof thanks to Mr. Butlin, proposed by Dr. Goodhart andseconded by Mr. R. W. Parker, was also warmly received.Mr. F. S. EvE showed a specimen of Multiple Cavernous
Angiomata of Leg. They were distributed along the internaland external saphenous veins, chiefly subcutaneous, butsome were lying deeply in the popliteal space. On three ofthe digits were calcified enchondroma ; exostoses were foundon each end of the tibia. A sarcomatous tumour sprang fromthe back of the tibia and included an angioma. Spacesbound with connective tissue were seen under the micro-scope, and these spaces could be injected from the vein.The sarcoma was a round-celled one. The tibia was bowedbackwards, and showed a defect in organisation of osseoustissue. Phleboliths were contained within the angiomata.In Billroth’s last edition some mention was made of mul-tiple angiomata. Dependence of tumours on defectivedevelopment was illustrated by the present case.--Mr. C. J.SYMONDS said Mr. Howse had recorded a similar case in theGuy’s Hospital reports.Mr. H. T. BuTLIN showed a Melanotic Tumour of the
Breast taken from a woman aged sixty-four, who was firstoperated on in 1880. The tumour was of seven months’duration. There were no adhesions, no enlargement ofglands, no retraction of nipple, and no peculiar colour of skin.The breast was removed. Recurrence took place, and a freshoperation was performed in 1882; from beneath the scar therecurring tumour was removed. In 1884 a third tumourfrom the same situation was excised; and recently anothertumour was cut away. There was no sign of disease ofany internal organ. The section was brittle and renderedmicroscopic preparations difficult. There were many tiny,very bright nsevoid spots in the skin that were considered tosuggest carcinoma. He believed it was a sarcoma with adistinct alveolar structure. There was a similar case in awoman aged sixty-eight in Billroth’s article on the Breastin the Deutsch. Chirurg. Gross allowed of melanotic car-cinoma, but not sarcoma. The melanotic granules appearedto be in the intercellular substance in the fibroid bands.-Mr. A. A. BowLBY said that there were many small pigmentedspots. The growth was exceedingly friable. He did notthink there was true melanosis. He concluded that itwas a sarcoma from the distribution of the blood-vessels.-Mr. D’ARCY PowER said that the structure waspeculiar; a base of connective tissue existed on whichfilaments sprouted, as happened in the growth of somefungi.-Mr. BuTLIN wished to have the specimen submittedto the Morbid Growths Committee.
Dr. CARRINGTON read a case of old Phthisis and recoveryfrom Tubercular Meningitis. He admitted that the case wasopen to criticism, but, inasmuch as it must have occurred tomost to have at least suspected meningitis in cases thateventually recovered, he thought that any post-mortemevidence bearing on the point was worthy of discussionby the Society. The patient was a boy aged sixteen, aclerk. Three sisters had died in infancy, but the familyhistory was otherwise good. On July 4th he was knockeddown by a tricycle, which struck him on the right knee, buthe only kept his bed for a week. Still, however, the kneecontinued to swell, and in the course of a year movementbecame much impaired. Fifteen months after the accidentthe left knee became affected, and eventually this joint alsobecame to a degree fixed. The boy improved under treat-ment, but on Jan. 26tb, 1886, he was readmitted with psoasabscess on the right side. He again improved by treatment,and was discharged on April 24th, but was readmitted onOct. 2nd with another abscess on the left side; he gradually
sank and died. After death the pi-arachnoid was foundto be generally thickened, and the sulci were matted to-
gether. The membranes were granular, and exhibited smallyellow tubercles, as was confirmed on microscopicalexamination. There was meningitis, probably of more recentorigin, of the lower third of the cord; the brain andcord were healthy, except that the latter was softened.At the apex of each lung there were old phthisical lesions.The fourth and fifth lumbar vertebrae were carious, and theright knee-joint completely disorganised. With the excep-tion of lardaceous disease of the spleen and small intes-tine, the other viscera were healthy. As regards thetubercular nature of the old meningitis, Dr. Carrington wasinclined to lay much stress upon the concomitance of oldtubercular phthisis, old cerebral meningitis, caries of thespine, and chronic joint disease, as evidence of the tubercularnature of the meningitis, which he believed had beenrecovered from, but he thought the naked-eye and micro-scopical appearances were equally distinctive. The spinalmeningitis was probably of more recent origin, and duedirectly to the cause. If the origin of the disease wasclaimed as due to the accident, it was curious that thesecond knee was not affected until fifteen months after-wards, and there certainly could not have been anycerebral meningitis at the time, for the man only kept hisbed for a week, and then went to his work as a clerk. Onthe whole, he suggested that there was evidence of bygonetubercular meningitis, probably approaching in date the oldphthisis.-Mr. S. G. SHATTOCK suggested that the meningealappearances were somewhat like those of periarteritis, asshown by Dr. C. Turner.-Dr. J. S. BRISTOWE raised thequestion whether the nodules of tubercles were necessarilyancient.-Dr. CARRINGTON said that the tubercles wereyellow and caseous, and adherent by fibrous tags. He feltsure that they would be found to have no connexion withthe arteries.-In reply to a question, Mr. TARGETT saidthe intellect was unclouded.
’ Dr. COUPLAND showed for Dr. Wiglesworth specimens ofPeripheral Neuritis in Raynaud’s Disease, the subject beinga female inmate of RainhiIJ Asylum, aged twenty-six, whosuffered from chronic Bright’s disease and dementia, withepilepsy. Before her admission in December, 1884, she hadsustained amputation of several of the fingers and toes forgangrene, and whilst under observation she suffered fromulceration of these extremities, and in January, 1886, theterminal phalanx of the fourth left finger became gangrenousand required amputation. The patient died suddenly inMay, 1886, after an epileptic fit. The kidneys were markedlygranular. The spinal cord and several of the nerve
trunks of the limbs were examined microscopically. In thecord the chief change was in the posterior vesicular columnof Clarke, where the cells were rounded, their processes beingill-defined; and the neuroglia of the white substance
appeared slightly thickened. In the nerves there was an
overgrowth of the fibrous elements, with atrophy and degene-ration of the nerve fibres--e.g., the left posterior tibialnerve presented thickening of the epineurium, perineurium,and endoneurium, with atrophy of the nerve tubules. Similarchanges oscured in other nerves, and were better marked inthose of the left limbs than in those of the right. The changeswere more marked at the peripheral than in the larger rervetrunks. Dr. Wiglesworth left the question open whetherthe change was primarily a chronic interstitial inflamma-tion invading the nerve bundles and causing their atrophy,or whether it was a primary degeneration of nerve tubuleswith secondary hyperplasia of the fibrous framework;but he considered that the case removed Raynaud’sdisease from the category of neuroses, and showed thatstructural lesions of the peripheral nerves underlay it.-Mr. A. A. BOWLBY had examined the nerves, and foundindentical changes. He thought it was very likely to be adisease dependent on lesions in the peripheral nerves; thestiffening of the joints pointed in the same direction.M. Pitres had recorded a similar case.-Dr. THOMAS BARLOWsaid similar cases had been recorded by Pitres and Mount-stein of Strasburg, but the changes were not so extensive asin Dr. Wiglesworth’s case. Though important contributions,they did not solve the difficulties. Raynaud’s disease wasdivisible into several classes. There were chronic cases likeDr. Wiglesworth’s, and the genuine or paroxysmal cases,which were as fit-like as a rigor in an attack of ague. Theoccurrence of paroxysmal haemoglobinuria and attacks ofamblyopia and jaundice seemed to show that there must bea wider pathology than a peripheral neuritis. It seemed as
73
though there were vascular storms, perhaps dominated byvaso-motor centres of the cord.-Dr. HAiunNGTON SAINS-BURT asked whether there was any Bright’s disease, andwhat the condition of the peripheral vessels was. --Dr. J.A. ORMEROD said that in these cases there were not thesymptoms of peripheral neuritis. He had recorded in theSt. Bartholomew’s Hospital Reports some paroxysmal dis-orders that seemed to be dependent on mild neuritis : loss ofpower, with pains, and the backs of the hands swelled. Itwould be interesting to associate such conditions with otherparoxysmal ones like Raynaud’s disease.
112r. WITHERS GREEN showed a specimen of RupturedAneurysm from a barrister, aged thirty, who had drunkhard, but there was a clear history and evidence of syphilis.The patient died suddenly. The pericardium was distendedwith black clot, and a soft fawn-coloured bulging of auri-cular shape, the sac of an aneurysm of the wall of the rightventricle. A yellowish-white gummatous-looking swellingwas seen around the aneurysm. The clear dependence ofthe ruptured aneurysm tm syphilis was the great interestof the case.The following card specimens were shown: —Mr. Butlin
for Dr. Davies: Maternal Impressions; Purpura of Handsand Face in a New-born Child, who died in three hours. Themother was said to have been strongly impressed by thesight of a case of hasmorrhagic purpura one month beforeher delivery. Mr. Targett: Congenital Deformity of Legand Foot. Mr. Eve : (1) Multiple Painful Lipomata ofthe Arms: (2) Diffuse Unilateral Papilloma of the Tongue.Mr. Charters Symonds: Hydatid of the Breast. Mr. J. R.Lunn: Tumour of the Clavicle displacing the Larynx. Dr.Drewitt: Aneurysm of Mitral Valve. Dr. Sainsbury:Haematoma of Dura Mater. Dr. G. N. Pitt: Carcinoma ofthe Spine and Liver, with Deposit in Douglas’s Pouch.(Recent specimen.)The following is a list of office-bearers for the ensuing
year:-President: Sir James Paget, Bart., D..C.L., LL D.,F.R.S. Vice-Presidents : Drs. Henry Charlton Bastian, SyerBristowe, T. H. Green, Douglas Powell, Sir Joseph Lister,Bart., D.C.L., LL.D., F.R.S., Messrs. Morrant Baker, SydneyJones, and T. P. Pick. Treasurer: Mr. John Wood. HonorarySecretaries: Dr. Sidney Coupland, Mr. Rickman Godlee.Council: Drs. Robert Edmund Carrington, Henry RadcliffeCrocker, David White Finlay. James Kingston Fowler, JamesFrederic Goodhart, Walter Baugh Hadden, Arthur EdwinTemple Longhurst, Norman Moore, Joseph Arderne Ormerod,Felix Semon, Messrs. A. A. Bowlby, II. Butlin, W. Cheyne,Frederic S. Eve, H. Golding-Bird, J. R. Morgan, S. G. Shat-tock, J. B. Sutton, Charters J. Symonds, Frederick Treves.
EPIDEMIOLOGICAL SOCIETY OF LONDON.
Typho-malarial Fevr/’.AT a meeting held on Dec. 8th, Dr. W. Dickson, R.N.,
President, in the chair,Dr. J. E. SQUIRE read a paper on the above subject, of
which the following is an abstract. When observing thefever which occurred amongst the troops round Suakimduring the campaign last year, Dr. Squire realised thatthere were two diseases present, both possessing similarsymptoms, which led to their being diagnosed as entericfever. Post-mortem examination showed the diagnosis tobe correct for some of the cases, but in others, similar as tosymptoms, the absence of the enteric lesions which wereexpected to be present proved that these latter were notenteric fever. The definition of the term "typho-malarialfever" requires to be agreed upon before proceeding, foropinions differ as to its signification. The College of 1’hy-"icia.ns, following the opinion expressed bv the InternationalMedical Congress at Philadelphia in 1870, places the nameas a subdivision of enteric fever and describes it as a "com-bination of malarial and enteric fevers" -in other words, acompound fever resulting from the simultaneous action oftwo distinct poisons. A somewhat similar view was upheldbefore this Society in 1881 by Dr. E. G. Russell, who speaksof typho-malarial fever as an example of the parallelogramof forces, it being, as he considers, the resultant of the twopoisons of malarial and enteric fevers. Dr. Woodward, whogave us the name, considers it a hybrid between these twodiseases. Against these views the writer protests and givespreference to the opinion that typho-malarial fever is not a
result of the enteric fever poison, but a form of malarialfever, and he gives as a definition that " typho-malarialfever is an expression of the malarial poison (or a malarialfever) in which intestinal and adynamic symptoms areprominent, causing the illness to simulate enteric fever."The College of Physicians, in saying that typho-malarialfever is a combination of malarial and enteric fevers, pro-bably intend to signify that the one is modified by the other;not that a distinct disease --a hybrid, in fact-is produced,as would be suggested by Dr. Russell’s simile of the paral-lelogram of forces. The belief in hybrid diseases should bepassed for ever. A specific poison produces a specific diseasewith certain pathological results. The symptoms may bemodified by a variety of causes within or external to thepatient; or two poisons may enter the system at the sametime, and one may then delay or modify the manifestationof the other, but no new disease is thereby produced. Ifthe term " typho-malarial fever" expresses nothing to men’sminds beyond a modification of enteric fever, or a hybriddisease, it is not worthy a place in our nomenclature. Butif a poison absolutely distinct from that which producesenteric fever, and with a different pathological manifesta-tion, may, under certain conditions, cause symptoms closelyresembling enteric fever, and an illness often mistaken forthis disease, then we have a morbid state of much interestand of great importance, and one which has a claim tospecial recognition. This would appear to be the case withregard to the subject of this paper. The term "typho-malarial fever," having at length been included in ournomenclature, should remain; but it should be trans-ferred from its present position under "enteric fever,"and be placed as a subdivision of malarial fever. Thepathological signs, rather than the symptoms, serve toshow the differences between typho-malarial and en-
teric fevers ; and where the necropsies disclose thePeyerian ulceration of enteric fever, the latter disease is indi-cated. Dr. Squire’s experience at Suakim showed thatbesides cases of true enteric fever, verified post-mortem, therewere other cases diagnosed as such in which the necropsyshowed an absence of ulceration in Peyer’s glands, even afterthree weeks’ illness, and only a general congestion of theintestinal mucous membrane. Other instances were referredto, especially an outbreak of fever in two regiments in theBengal Presidency, recorded in the Army Medical Reportfor 1879, in which similar experience showed the existenceof enteric fever side by side with cases closely resemblingthis disease, but in which the intestines were unaffected.The course of typho-malarial fever is thus described: Ton-sillitis may occur as a premonitory sign. The onset is some-times more sudden than that of enteric fever, and biliousvomiting is often an early and persistent symptom. Diarrhoea.is frequently, but not invariably, present, the stoolsbeing greenish or resembling those seen in entericfever. Congestion may extend along the whole lengthof the alimentary canal, causing nasal catarrh, or
symptoms resembling dysentery. Later on the tonguebecomes dry and brown, and sordes appear. -Itental apathygives place to low muttering delirium, with subsultus andother signs of the typhoid condition ; and death may resultfrom exhaustion, or a prolonged convalescence keeps thepatient in hospital for weeks or months before ths absenceof diarrhoea and evening fever allows of dismissal from
, hospital. The temperature, though often resembling thatof enteric fever, reaches a high point earlier in the illness,and the daily range is greater. The absence of rose spots isinvariable. The symptoms being thus so similar to those of
I enteric fever, we must turn to the pathology of the disease, to see the great distinction between the two, their differen-
tiation being of importance from the differences in etiology.Speaking generally, the difference is found in this: that
, whereas cell-proliferation and subsequent ulceration inPeyer’s patches and the solitary glands of the ileum is the
i pathological sign of enteric fever, such ulceration is rarely,if ever, found after death from typho-malarial fever. As in
, other malarial fevers, ulceration may be found in the intes-,
tines in typho-malaria, but it does not select, and is not. confined to, Peyer’s patches and the solitary follicles. TheseI ulcers may be found in any part of the alimentary canal,I and may be of any shape and of almost any size. The otherI pathological signs are those of malarial fevers: congestionI and ecchymosis of the intestinal mucous membrane,I especially in the duodenum and upper jejunum, enlargementI of the spleen and of the mesenteric glands, and congestion, of the liver. Among the complications met with, htemor-
