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by the Grand Duchess Catherine, the aunt of the pre-sent Czar, which was most carefully administered, rigidantiseptic precautions being taken for three years, therewas no death from puerperal fever, whilst there was alarge mortality from that cause in the poor dwellings inthe immediate vicinity of the institution.-Dr. BARNESinsisted on the necessity of recognising more than onevariety of puerperal fever. Scarlet fever, erysipelas, andother affections, might all be merged and lost in thefever of the puerperal state. In illustration of this hereferred to a case which lie was sure had a zymotic origin,and, after some difficulty, a history of indirect contact witha scarlatinal case was clearly proved. He thought the valueof Dr. Smith’s research would be much increased if he gavethe history of the cases which had furnished him withmaterial. Dr. Priestley had alluded to two forms of thedisease, but he was sure there was an element in causationbefore either of these ; the patient might be poisoned byher own secretions. In general medicine something of thesame kind was known to happen-e.g., from the effect ofcold and damp in producing rheumatism. He referred tothe case of a woman who had not suckled her child, andwas more or less an invalid ; two months after her con-finement she developed acute rheumatism after exposureto cold. Had this illness occurred during childbedit might have been hard to differentiate it from puerperalfever. He felt sure that the whole subject of the origin ofthis disease would not be cleared up bv the discovery oforganisms.--Dr. HERMAN felt convinced that future in-vestigation would tend towards establishing the fact thatpuerperal fever owed its origin to micro-organisms, for allrecent statistics showed that in proportion to the diligencewith which antiseptics were used so the mortalitydiminished. In lying-in hospitals following rigidly theantiseptic system, if scarlet fever were introduced, thepatients who caught it suffered from scarlet fever andnothing else, and the same with erysipelas; neither the onenor the other, nor both, produced puerperal fever, andhe thought the evidence in this direction was over-

whelming. As to whether Di. Smith had succeeded inisolating the particular germ of this affection, he thoughtthat two cases were not sufficient to dogmatise upon.-Dr. ROUTH could not help thinking that the germ doctrine,when applied to puerperal fever, was being carried too far.Three varieties of this complex affection had already beenenumerated, and he would add two others, namely,puerperal peritonitis and the "sweating disease." Dr.Smith had brought forward no information with regard totreatment. It had been shown that many cases of diarrhceawere due to organisms, and administration of acids curedthe disease, the germs being unable to live in an acidmedium. Similarly great good would follow if Dr. Smithcould suggest some medicine to be given by mouth thatshould be capable of destroying the essential poison ofpuerperal fever.-Mr. WALTERS (Reading) confessed him-self a little sceptical with regard to the autogenetic originof puerperal fever. The method of conveyance of the poisonwas often ascertainable; for instance, it sometimes followedthe visits of certain nurses. He felt sure it was largelydependenton insanitary dwelling-houses, and the poison couldbe absorbed by the lungs; he quoted several cases showing theconnexion between defective drainage and the origin of thedisease.--Dr. GRIFFITHS said that, of Dr. Smith’s patients,one was from Queen Charlotte’s Hospital and the other fromSt. Bartholomew’s Hospital. Both, he thought, were isolatedcases, with absence of distinct history of cause.-Dr. WILLIAMDuNCAN found himself unable to assert dogmatically thatevery case must be of heterogenic origin, for he had seencases, and lie gave an account of one, which lie thoughtmust be autogenetic. He asked what was the evidence, incases like those of acute diffuse periostitis, that the micro-organisms came from without.-Dr. ANGEL MONEY saidthat undoubtedly micro-organisms might enter through thesmallest scratch on any part of the body.-Dr. SMITH, inreply, referred to the difficulty in finding suitable clinicalmaterial. The case at Queen Charlotte’s Hospital wastraced to be connected with a nurse who had attended somesimilar cases outside, and, if he remembered aright, theSt. Bartholomew’s case was one of the same class. Thesubject of treatment would be taken up afterwards, butnothing would contribute so much to the application ofrational treatment as a knowledge of the true causes of theaffection.A paper by Dr. SAMUEL WEST was then read on

Acetonuria and its relation to Diabetic Coma. The follow-

ing is an abstract. The relation of acetonuria to diabeticcoma had been investigated by experiment and by clinicalobservation, and this paper was a contribution to theclinical side of the problem. The results of experimentwere briefly referred to, and the conclusion to which theyled. Clinical observation was for a long time difficult fromthe want of trustworthy tests. A short account of the chiefones was given : 1. Lieben’s iodoform test. 2. Gunning’sand Le Nobel’s modification of it. 3. Reynolds’ test.4. Legal’s test with nitro-prusside of potassium. 5. LeNobel’s modification of it. 6. Penzold’s test. Legal’s testwas found to be the most convenient for use in the urinedirect, and Lieben’s in the distillate, but this reaction wasalso obtained if alcohol was present. But if the urine gaveLegal’s, and the distillate both Legal’s and Lieben’s tests, thepresence of acetone might be accepted. As control experi-ments two series of convalescent cases were examined. In thefirst thirty cases, a doubtful Legal’s reaction was obtainedin three. In the only one which was distilled neither testwas obtained in the distillate. In the second series of aboutthe same number no evidence of acetone was obtained inany. Of non-diabetic patients actually suffering fromillnesses at the time of examination, acetone was found infifteen cases. Acetonuria was therefore very rare inhealthy or convalescent persons, but common in variousforms of acute and chronic disease. Of diabetic patientsfourteen were examined, four being at the time comatose.In some of these cases the examination was continued formany days. The following conclusions were arrived at:-1. Acetonuria was common in diabetics without coma.

2. It was not constantly present in cases of diabetic coma.3. It varied greatly in the same case from time to timewithout definite cause. 4. It varied independently ofvariations in the amount of sugar, specific gravity, &c.5. It might even disappear when coma developed. The ironreaction showed also no relation either to coma or toacetone. Experiment and clinical observation thereforeled to the same conclusion-viz., that acetone couldnot be the cause of diabetic coma. Clinical observa-tion, however, seemed to show that acetonuria had a

clinical value as indicating that the patient was in a morecritical condition than when it was absent. The symptomsof diabetic coma depended, in all probability, upon acuteintoxication by some substance rapidly generated within thebody, but at present unknown. It might be that in theperverted chemical processes which developed it, acetoneand the allied body giving the iron reaction were produced,so that the presence of these bodies in the urine might serveas " danger signals."-Dr. MAGUIRE said that acetone wasevidently not the poison which produced diabetic coma;nevertheless, the condition was undoubtedly due to the

presence of a poison. The liver either might split it up or thekidneys eliminate it, so that, although it might be found inthe blood, serious symptoms might not develop. He lookedupon the presence of albuminuria as a valuable dangersignal when occurring in the course of diabetic coma, its

presence being probably due to renal irritation. In ever)’case he had examined, the kidneys had presented extremeparenchymatous inflammation, and such a condition couldbe brought about by the injection of diacetic ether or acetoneinto the blood. He thought that, if albumen were foundafter acetone had been ascertained to be present. the casewas graver than if acetone were found alone.-Dr. ANGELMONEY had on two occasions found hyaline necrosis in thekidneys from cases of diabetic coma. The iron reaction wasa sign of danger, and he had never failed to find it when theknee jerk was absent. Albumen was generally present infatal cases.-Dr. WEST replied that albumen, like acetone,

was by no means a constant phenomenon in fatal cases, and

therefore might or might not be a "danger signal."

CLINICAL SOCIETY OF LONDON.

Purulent Pericarditis; its Orgin, Symptoms, and Treatment.AN ordinary meeting of this Society was held on Nov. ?3rd,

Dr. W. H. Broadbent, F.R.C.P., President, in the chair.The announcement of the death of Dr. Greenhow, thepractical founder of the Society and its former treasurerand president, was received with signs of much regret.The meeting was most successful, and the audience verynumerous.

.

Dr. DICKINSON related a case of Purulent Pericarditissuccessfully treated by aspiration and drainage. A boy

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aged ten was brought to St. George’s Hospital, having hadsymptoms which Dr. Harris and Mr. Noad, both of Nor-wood, interpreted as pysemic. A large gluteal abscess wasfollowed by signs of pleural effusion and oedema of theface and chest. On admission, on June 15th, 1887, therewas evidence of effusion in the left pleura and in the

pericardium. The position of the heart was almost undis-coverable amid the dulness, which involved the left pleuraland precordial regions. There was much dyspncea, blue-ness, and irregularity of pulse. There was oedema more orless general, but especially marked about the thorax. Theliver was enlarged or depressed so as to reach the umbilicus.On the 18th the pleura was aspirated, and thirty-sevenounces of serum drawn off, which operation was repeatedon the 23rd, with the removal of thirty-two ounces. The

dyspncea, blueness, and oedema were but slightly and tem-porarily relieved by each operation, which had to be

repeated on the 25th and 28th, so great was the distressand so rapid the reaccumulation. On the 30th, the futilityof dealing with the pleura having become apparent, thepericardium was aspirated by Mr. Rouse, and one ounceof creamy pus withdrawn; the aspiration was repeatedwith more success on the 8th of July, and twelveounces of similar fluid withdrawn, and also on the 15th,with the withdrawal of nineteen ounces. The placeselected for puncture was on the right side close tothe edge of the sternum, in the fifth interspace. Theheart before each of these operations had been drawnto the left by a preceding evacuation of the pleura. Thelower part of the pericardium, where the swing of the heartwas greatest, and the right extremity of the cavity, fromwhich the heart was farthest removed, was obviously thepart which could be penetrated with the greatest safety.By July 22nd the pericardium was again as full as ever,and the general symptoms distressing. It was clearlynecessary to replace aspiration by a tapping opening.Mr. Rouse accordingly made an incision where the punctureshad been, and put in a tube. The aspiration was followedby some faintness and subsequently by great relief. Not tofollow the case in further detail, recovery, after some tem-porary drawbacks and three subsequent aspirations of thepleura, became complete. By the middle of September therewas no remnant of the pericardial puncture except a smallcicatrix, which moved with each beat of the heart. In thecourse of less than two months the chest had been puncturedsixteen times ; the pleura twelve times with the aspirator,and removal of serous fluid ; the pericardium four times,three times with the aspirator, and once so as to leave anopening and a constant discharge of pus. The nearly totalabsence of friction, which was recognised but on one occa-sion, was remarkable.Mr. PARKER related a case of extensive pyo-pericarditis

(associated with osteo-myelitis of the tibia) which he hadfreely incised. Death had occurred while irrigation wasbeing practised to wash out the thick membraniform puswith which the pericardium was distended. The patient wasa girl aged nine. She had been under treatment for acuteosteo-myelitis of the tibia, complicated with secondaryseptieasmic suppuration of the knee joint. The case wentfrom bad to worse, treatment and antiseptics notwithstand-ing. In the fifth week of the disease extensive pericardialeffusion supervened, and the girl’s position became des-perate. Tapping at first brought some relief, but as theeffusion recurred it was decided to incise the pericardiumand insert a drainage tube. When the pericardium hadbeen opened, the contained pus was found thick and tocontain large membraniform shreds, and so irrigation wasresorted to in order to wash them out, it being feared thatif left behind they would decompose and become a sourceof further danger. The already weakened heart was unableto bear this additional strain, and the child died. Afterrelating his case, Mr. Parker raised the question as to themode of causation of purulent pericarditis, and referred tothe usually accepted teacliing. He then discussed the mostappropriate treatment. Should free incision be advised ? Ifso, in what cases-in small as well as in large effusions ofpus ? Was spontaneous cure a clinical possibility ? Finally,as to the best place for making an opening. The author,from observations on the dead subject, recommended thefourth left intercostal space, close to the sternum. Anopening at this spot, he contended, would longest afford adirect communication with a gradually retracting peri-cardium, an important point in facilitating completedrainage. The author finished by advocating for pericardial

elusions the same line of treatment as had been so success-fully applied to pleural effusions, and emphasised, in thiseffort, the essential importance of aseptic conditions.

Dr. GOODHART related a case of pyo-pericardium occurringin a middle-aged woman, who had repeatedly suffered fromattacks of exhaustion and emaciation. The patient wasfirst seen by him a few days before her death, when thephysical signs of pericardial effusion were not remarkablyobvious; and though pyo-pericardium was suspected, yet onthe whole it was thought that a mediastinal tumour existed.The breathing in the left lung was much obscured. Thenecropsy proved that there was nothing else but a largepurulent effusion in the pericardium, which, however, hadaccumulated chiefly in the posterior region of the fibro-serous sac. In this case, as in others, friction sound wasabsent. The mode of onset and clinical course of pyo-pericardium were very insidious; the physical signs wereoften indefinite, so that a diagnosis could not be certainlyarrived at without the use of the exploring syringe.

Dr. SAMUEL WEST discussed the subject very fully.Rosenstein in 1881 first recorded a successful case ofpurulent pericarditus treated by incision and drainage underantiseptics, just as is so often done in empyema. Dr. West’scase, published in the Royal Medical and ChirurgicalTransactions, vol. lxvi., was the second on record, andDr. Dickinson’s the third. The most suitable place forpuncture is, as a rule, in the fifth left interspace close tothe sternum, but each case must be considered on its ownmerits. The best instrument for the puncture is a sheathedneedle or hollow needle, not the ordinary trocar and cannula,for the trocai had wounded the heart in one case at least,because it projected so far beyond the cannula. This puncturemust be made in order to detect the fluid and its nature;if found to be purulent, the fluid should be removed byincision and free drainage. As a method of exploration,Dr. West did not concur in Mr. Parker’s suggestion thatthe pericardium should be first exposed and then incisedwith a view to ascertain the presence and nature of anyfluid. Speaking of the site of puncture, he alhrded toRotch’s experiments, which consisted in injecting cacao

butter into the pericardium. These experiments were heldto prove by Rotch that dulness in the right fifth interspaceproved the presence of a pericardial effusion, and that sucha spot was the best for puncture. Dr. West asserted thatRotch stood alone in this belief. It was better not topuncture nearer the base or nearer the right side of theheart than could be avoided, because of the thinness of thewalls of the organ in these regions. The absence of frictionin cases of pyo-pericardium was remarkable, but well known,and was to be explained by the nature of the effusion. Asto the origin of purulent pericarditis, further informationwas required. That it arose in connexion with pypemia andempyema was certain, but some cases occurred in which thepericardium was the only seat of purulent effusion; perhapssuch were of bacillary origin. At all events, even in freshlydrawn pus from the pyo-pericardium the number of bacilliwas very remarkable, and Dr. West’s recent experienceconfirmed this. Again, pneumonia has been complicated bypurulent pericarditis, and Dr. Angel Money had noted casesof the kind. The symptoms of pyo-pericardium were some-times indefinite, and even a low temperature might prevailthroughout, just as had been noted in cerebral abscess.

Dr. ANGEL MONEY said that the remarks of the twoprevious speakers covered much of the ground for discus-sion, and his own experience generally accorded with theirobservations. He questioned whether mere pressure wouldalways account for the serous effusion in the left pleura incases of pyo-pericardium, because his recent experienceafforded two examples of cases of perinephric abscess in theleft side, and the pleura on the same side contained forweeks, in one case for months, a serous effusion. He related-a case of extreme pyo-pericardium which was diagnosedduring life as extreme empyema; the necropsy proved the-almost entire absence of the left lung, which formed merelya thin layer between the pyo-pericardium and the parietes,in this case the heart was beating almost in its naturalposition, and the fluid accumulated chiefly behind and to.the left side of it.

Dr. BARLOW referred to some experiments lie had madeto show the relationship of the heart to the surface of thechest wall; needles were inserted through the parietes intothe heart substance at various sites and different intervals;the experiments made on cases of pericarditis went to prove ethat the effusion had a great tendency to be stowed away in

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the posterior region of the pericardium, so as to leave the 4

heart near to the front surface. He confirmed Dr. Dickin- ison’s view of the mechanism of the pleural serous effusion Ion the experience that when the pleural cavity was inflamedthe nature of the fluid should be the same as in the peri- icardium.Mr. GODLEE drew attention to some anatomical features.

In children the left pleura so far covered the anterior surfaceof the pericardium that if the puncture were made an inchaway from the side sternal line the chance of the puncturinginstrument’s laying open the left pleura before it penetratedthe pericardium was very great, and pneumothorax might beadded to the list of symptoms from which a patient mightbe suffering. The internal mammary artery, too, ran soclose to the sternum in the fourth and fifth interspaces thatsufficient space between it and the sternum for the passageof the blade of a knife hardly existed. This would not beof much consideration in free incision, because the vesselwould be first secured and ligatured.

Dr. SIDNEY PHILLIPS believed that rheumatism couldcause purulent pericarditis. In the case of a female agedtwenty, admitted with all the symptoms of rheumatism,Jeath suddenly occurred, and a pyo-pericardium was foundat the necropsy.

Dr. DiCKlNSON, in reply, remarked that in one case a dis-tinguished surgeon thrust a very long aspirating needle intothe fourth left interspace a good distance away from thesternum, so as to avoid wounding the heart; the whole pro-ceeding suggested a bayonet thrust, and Dr. Dickinson wasrelieved as well as the patient when the needle was with-drawn. The patient’s relief proceeded from the circumstancethat the needle had gone through the pericardium into thepleura, and the pericardial effusion had emptied itself intothe p’eura. Dr. Dickinson’s relief proceeded from the circum-stance that he was mistaken in supposing that the suigeon’sneedle had entered the lieart-a suggestion which not

unnaturally presented itself from the escape of a jet ofblood through the needle immediately after its rapidinsertion.The following living specimens were exhibited :-Mr. H. BAKER: A case of Genu Recurvatum.Mr. CLUTTON : A case of Compound Dislocation of the

Elbow, with Complete Recovery of the Joint.Mr. T. SAVILLE: A case of Hystero-epilepsy and Func-

’tional Contraction.Mr. J. F. PAYNE : A case of Molluscum Fibrosum with

Multiple Neuro-fibromata.

MEDICAL SOCIETY OF LONDON.

Gov. —TraMMM’c -Poo-MH/eM. —VeMo-MUMCMZa Irrita--Resection of Inferior Maxillary Joint.-Ery-thema Gangrenosum.-Ectopia Vesicae.THE meeting of this Society on November 2Gth was a

clinical evening. The President, Sir William Mac Cormac,was in the chair.Mr. GEORGE STOKER read a communication on a case of

Goitre, illustrating a theory in reference to the function ofthe thyroid gland. He showed the patient, who came underhis care in April, 1888, with a hard, central, well-definedgoitre about the size of a small hen’s egg. He was giveniodide of potassium and fluoric acid internally, and externalapplications were made of a counter irritant and absorbentnature, but all without benefit. In June he had symptomsof chronic hypertrophic rhinitis, which caused muchinconvenience, the turbinated bodies being considerablythickened. The galvanic wire was applied in the usualway, the hypertrophied tissues being punctured andscarified; after the second or third application the goitrebegan to diminish; the cauterisation had been continuedat intervals of a fortnight up to the present time,and the goitre had quite disappeared. The medicinesand external applications were discontinued when thecauterisation was commenced. It seemed to him thatthe nasal treatment had produced reflex irritation ofthe vaso-motor nerves, causing constriction of the blood-vessels in the gland and diminution of the hypertrophy,illustrating the intimate connexion existing between thefunctions of the thyroid body and the vaso-motor system.There was, further, some pathological evidence in supportof the theory. Ziemssen reported eight cases in whichdegenerations were detected in the middle and inferior

cervical ganglia in association with thyroid disease, andanother case had been recorded by Dr. Shingleton. In hisown case lie thought the result had been brought aboutreflexly through the fifth nerve ; he had another case of thesame kind under similar treatment, in which the size of theneck had already diminished nearly an inch and a half.-Mr. LENNOX BROWNE referred to the cases of three youngmale patients, two of whom were exhibited. From two ofthem he had removed the isthmus, from the other theisthmus and right lobe, weighing 7 oz., and in each instancewith the result of giving complete relief to distressingdyspncea. He was disposed to think that the danger ofmyxoedema after entire removal had been exaggerated ; butseeing that it did exist, and that it was impossible toforetell the cases in which it might occur, he thought itbetter to do a partial operation. He had now removedeither the isthmus or the isthmus and one lobe in ten cases,and in all with a completely satisfactory result. Haemor.

rhage at the time of the operation was but slight,but in two instances there had been rather severe

secondary haemorrhage on the seventh or the eighth day.Mr. Browne showed the portions removed in the threecases, as well as photographs before and after operation.-Sir WILLIAM MAC CORMAC said that surgeons were justifiedin hesitating to remove the entire gland, which might befollowed by spurious cretinism, when a good result followedthe taking away of the isthmus alone.-Dr. HADDEN saidthat symptoms of spurious cretinism sometimes did followpartial excision, but that was perhaps because the part leftbehind was diseased. In some cases, where all the thyroidhad been removed and no myxcedema had followed,post-mortem examination had revealed hypertrophied accessorythyroids, which had carried on the work of the gland.--Mr. PiTTS had found the trachea altered in shape and flat-tened where dyspnoea was present. In all cases but one thecompression had been from side to side, but in one case atumour of the isthmus extending behind the manubriumsterni had caused antero-posterior flattening.-Mr. BERRY

inquired if the gland enlargement were local or general.Goitres often disappeared spontaneously, and he doubted theeffect of the cautery in Mr. Stoker’s case ; he was likewisesceptical as to the connexion between goitre and disease ofthe sympathetic nerve. He advocated an oblique incision inoperating on large goitres, and preferred to ligate vesselsseparately lather than tying the isthmus en masse.-Mr.STOKER replied that the cauterisation was very thorough,the enlargement of the gland was a local one, and hispatient exhibited many evidences of sympathetic disturb-ance.—Mr. LENNOX BROWNE said that in many cases thesymptoms were distressing from the dense character of thegrowth and its tendency to constrict the trachea ; he hadseen sympathetic disturbance without evidence of direct

pressure on the nerve, and lie preferred the vertical incisionas producing less disfigurement. In removing the wholegland, he tied the vessels separately, but transfixed and tieden 9)icisse when dividing or removing the isthmus.

Dr. C. E. BEEVOR showed a case of Polio-myelitis (?) frominjury. A boy, aged twelve, at the beginning of lastAugust fell on his left elbow in getting over a stile. Hewas unable to move the left arm after the accident, and itwas put in splints immediately after, there being fractureof the humerus. When the splints were taken off a monthlater, the left arm was found to be paralysed in certainmuscles, especially the supinator longus, biceps, brachialisanticus, deltoid, supra- and infra-spinati, and teres major,but there was no anaesthesia. At present he had paralysisin the above muscles, and they did not react to the faradaiccurrent, but showed the reaction of degeneration. Therewas some thickening about the lower end of the humerusand about its neck. The case, he considered, was eitherone of injury to the spinal roots (the fifth and sixthcervical), or a case of polio-myelitis. Owing to the absenceof any history of anaesthesia the latter was considered to bethe cause. An important symptom was the fact that thepatient was able to use the upper part (clavicular) of the

, pectoralis major in conjunction with the sternalpartinpress-ing the hands together and adducting the humerns, but hewas unable to throw the clavicular part into action in raisingup the arm when advanced (i.e., flexing the shoulder) wherethe muscle should act with the paralysed deltoid. It seemedthat in this case there was a muscle paralysed for one move-

; ment and not for another, and this would be in favour ofthe physiological functional grouping of muscles in thespinal cord.-Dr. SYDNEY PHILLIPS asked if any part of