No. 4385.

SEPT. 14, 1907.

A LectureON

THE COÖRDINATION OF POST-MORTEMWORK AND CLINICAL OBSERVATION.

Delivered at the Post-Graduate Course, Leeds Public

Dispensary, on, June 14th, 1907,

BY E. F. TREVELYAN, M.D, B.Sc. LOND.,F.R.C.P. LOND.,

PHYSICIAN TO THE LEEDS PUBLIC DISPENSARY; LATE PROFESSOR OFPATHOLOGY, LATE YORKSHIRE COLLEGE (VICTORIA UNIVERSITY) ;

PHYSICIAN (WITH CHARGE OF OUT-PATIENTS) TO THELEEDS GENERAL INFIRMARY.

GENTLE11IEN,-A sound clinical knowledge of disease is

impossible without a sufficient knowledge of the pathologyof disease. Therefore the importance of bringing into closerelationship the pathological changes found in the post-mortem room and our observations of disease made duringlife is obvious. At a time when the great advances in sciencehave made it necessary that the teachers of pathology in ourmedical schools should give their whole time and attentionto their subject it becomes of greater importance than everthat the clinical element should be kept constantly in view inthe post-mortem room. For this reason I think it would bea misfortune if the post-mortem room were handed over tothe pathological specialist as it is eminently the groundwhich should be occupied by those in close touch withclinical work, for the clinician learns by daily experiencethe needs and wants of those training to be clinicians.Of course, the aid of the bacteriologist, morbid histo-logist, and pathological chemist will always be required tosupplement and confirm the post-mortem room findings.Such reports when received can be read out on a subse-quent occasion and the case recapitulated and reviewedin the light of any additional information obtained. Naked-

eye morbid anatomy as such can be learnt in the pathologicalmuseum now furnished with specimens which retain more orless perfectly their original colour, but morbid anatomy inrelation to clinical work can only be satisfactorily learnt inthe post-mortem room where the whole clinical and patho-logical aspects of disease can be coordinated. I decline tomake a post-mortem examination where there are no clinicalnotes available, as I look upon it as almost waste of time.Some 15 years’ experience of post-mortem work has led me

to adopt the following method of procedure. Before thepost-mortem examination is made the clinical report isabstracted and the abstract is written on the black-board in the post-mortem room. At the commencementof the examination this abstract is read out and themorbid changes which it is expected to find are outlined.The various morbid changes are then demonstrated andthis is followed by a commentary on the pathologicalfindings. Finally the symptoms are compared step by stepwith the pathological changes present. I need not say thatthe clinical diagnosis made during life is always regarded asthe best that could be made in the circumstances, so as topermit of the freest possible discussion of details bothclinical and pathological. Everybody with a tithe ofclinical experience appreciates to the full the diagnosticdifficulties that may arise in any case. Finally, it is almostneedless to add that each post-mortem examination shouldbe thoroughly made-that is, every organ examined, and forthis reason it seems to me impossible satisfactorily toconduct more than one or at most two examinations at atime. In this demonstration I shall follow the orderindicated above. Thus I shall first give a few clinical notesof the case. I shall then describe the specimens and makesome pathological comments upon them. Finally, I shallendeavour to coordinate the morbid changes found afterdeath with the symptoms present during life.L-SYPHILIS OF THE TRACHEA AND BRONCHI; STENOSIS OF

A BRONCHUS.The specimen came from a woman, aged 32 years, with an

enlarged thyroid. A month before death when I saw hershe had inspiratory and expiratory stridor, and diminishedmovement of the right side of the chest with a deficient airentry. Nothing abnormal was seen in the larvnx. A

diagnosis was made of pressure on the right bronchus,probably due to malignant di"ease. The specimen showsone large and several small ulcers in the lowest part of thetrachea. There is also ulceration in the uppermost part ofthe left bronchus. The right bronchus is stenosed for about.halt an inch at its origin where it will only admit a smallquill. The stenosis appears to be due to a sclero-gummatousprocess in the submucosa as no distinct evidence of pastulceration is visible. It does not therefore represent a moreadvanced stage of the ulceration seen in the left bronchus.The left lung was considerably larger in size that the rightowing to hypertrophy. The left lung did not present anyabnormal appearances. No evidence of syphilis was foundelsewhere in the body.

Syphilis of the trachea and bronchus is rare. I have norecollection of meeting it before in the post-mortem room.Unless in association with laryngeal syphilis its site of pre-dilection is in the lowest part of the trachea and upper partof the bronchi. If the ’disease extends to the bronchi itusually affects both of them. The reason of -this localisationis unknown to me. Tuberculosis more commonly gives riseto ulceration of the trachea than syphilis and is found almostexclusively in association with laryngeal tuberculosis. Therewas no evidence of tuberculosis in the above case nor did theulcers themselves appear tuberculous. The morbid changesmet with here explain all the symptoms and signs presentduring life-the stridor, deficient air entry, &c. Perhaps Iought to have made a more exact diagnosis during life, andno doubt it would have been wise to have given iodides in acase where the nature of the disease was involved in somedoubt.

II.-CASEOUS PNEUMONIA ; TUBERCULOUS LARYNGITIS.The specimens were obtained from a man, aged 25 years,

who also had spinal caries and paraplegia (see Spe-cimen VIII.). The pulmonary disease had lasted threemonths and was attended with cough and sputum, pyrexia,and some hoarseness. There were signs of consolidation atthe right apex.The right lung is solid almost throughout but the lesion

is more marked towards the base. A lobular distribution isclearly evident in parts and some tubercles are present inthe pleura. Scattered aggregated tubercles are seen in theopposite lung. The larynx shows a symmetrical ulcer onthe posterior part of both cords and there is early but distinctpachyderma affecting the posterior laryngeal wall.

Caseous pneumonia, or broncbo-pneumonia, represents oneof the acute forms of pulmonary tuberculosis. Its distribu-tion suggests very strongly an aerial infection. In this casethere was no older lesion from which tuberculous productscould have been aspirated as may happen in the more acutebasic infection of the lung in some cases of apical pul-monary tuberculosis. There was, however, a focus of diseasein the immediate neighbourhood-viz., in the tenth dorsalvertebra, and it is possible that the infection spread fromthis focus. It has been suggested, and I have seen at leastone instance which seemed to bear out the view, that thelung may be infected from caseous bronchial glands in itsneighbourhood without the latter directly communicatingwith the air passages. An interesting question might beraised as to the respective age of the laryngeal and pul-monary lesions in this case. The laryngeal disease certainlyhas the appearance of being the older but I have never yetseen a case of unmistakably primary laryngeal tuberculosis.The symptoms are sufficiently explained by the morbid

anatomy found, though here, as in many cases, the amount ofdisease present was much greater than might be anticipatedfrom the signs. The laryngeal lesion produced hoarsenessand if there had been any difficulty in the diagnosis of thenature of the pulmonary disease the examination of the

larynx would have cleared it up. This bears out the state-ment that in cases of doubtful pulmonary tuberculosis it iswell always to examine the larynx.

III.-MARKED ATHEROMA OF THE AORTA, CORONARYARTERIES, AND SPLENIC ARTERY ; GREAT HYPER-

TROPHY OF THE HEART WITHOUT VALVULARDISEASE OR RENAL DISEASE.

The patient, a man, aged 50 years, had rheumatism when24 years of age. He bad presented steadily increasingsymptoms of illness for the past seven years. (Edema ofthe legs appeared in August, 1906, and he gave up work inNovember. On admission in May, 1907, he was water-logged. The apex beat was displaced outwards but there

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was no murmur. His pulse was tense but there was noalbumin in the urine. The heart was greatly enlarged,weighing 30 ounces. The valves were competent to thehydrostatic test. The kidneys were quite competent organs.There was advanced atheroma of the aorta, also of thecoronary arteries and of the splenic artery. The left radialartery at the wrist appeared quite healthy. The liver showedmarked nutmeg change. There were infarcts in bothlungs.The chief pathological feature of this case was the con-

siderable cardiac hypertrophy due to vascular disease, thearterial disease being of the nature of atheroma (nodulararterio-sclerosis) of the aorta and some of the medium-sizedarteries. A complete examination of the arterial systemwas, unfortunately, not made, but I think the markedarterial disease was sufficient to explain the cardiac hyper-trophy. It has been stated that atheroma of the meflentericarea should be a very efficient cause of cardiac hypertrophy,but, unfortunately, only the splenic artery was examined inthis case. The anterior coronary artery was much affectedwith typical atheroma and the left ventricle was markedlyhypertrophied. The right coronary artery was similarlydiseased but only in its proximal part. I could not detect withthe naked eye any disease whatever in the cardiac muscle.The mode of production of the engorged pulmonary circula-tion, of the nutmeg liver, and of the dropsy is difficult ofexplanation unless there was functional regurgitation duringlife, yet neither the post-mortem appearances nor the clinicalsigns give any real ground for such an assumption. Themorbid appearances otherwise corresponded well to the

symptoms present during life. A long illness steadily pro-gressing to a fatal termination is explained by a slowlyprogressing arterial disease.

IV.-COLLOID CARCINOMA OF THE STOMACH.This specimen came from a woman, aged 40 years, who

had suffered from dyspepsia (pain after food relieved byvomiting, &c.) and wasting for six months and who presentedanomalous nervous symptoms during the last few days oflife. Death occurred in coma. The specimen shows a

large mass of colloid carcinoma surrounding the pylorus andextending along the lesser curvature. There were no

secondary deposits. The kidneys were healthy and the brainshowed no abnormality.

Colloid carcinoma of the stomach is no doubt a degenera-tive form of other growths such as columnar carcinoma. Ihave rarely met with this form of growth of the stomach inthe post-mortem room. There was no obvious explanationof the nervous symptoms present, so I suppose that theymust be attributed to an intoxication produced by the newgrowth.V.-CALCULOUS DISEASE OF THE KIDNEY ; ORBITAL AND

FRONTAL SINUS SUPPURATION ; LIMITEDSUPPURATIVE MENINGITIS.

A boy, aged 14 years, died from an acute illness lastingabout 12 days. It began with a swelling about the left eyeand then suppuration occurred in the orbit. The pus waslet out from the orbit and also from the frontal sinuses.Four days before death vomiting took place, then opticneuritis, and twitching of the left side of the face and con-vulsions. Death occurred in coma. There was a suppura-tive meningitis limited to the right hemisphere and havingits greatest intensity over the frontal pole and about theSylvian fissure. The base of the brain showed no change.Some pus was found in the orbit and also in the frontalsinuses. The ethmoid cells were healthy. The right middleear contained pus. The left kidney was small and the rightwas twice as large as the left. The pelvis and ureters ofboth kidneys were dilated and the bladder hypertrophied.(There was no stricture of the urethra.) There was a stonein the left kidney and a consequent destructive nephritis.The right kidney was hypertrophied but showed a slightdegree of hydronephrosis and the microscope revealed somedisease of the renal substance itself. Some pus was foundin the pelvis of this kidney. The surface of the stone wassmooth and its colour dark brown. It was very hard. Onsection it showed several concentric layers. It was thoughtto be a uric acid calculus but it did not give the murexidetest. It was not a xanthin nor yet a calcium oxalatecalculus. It contained a large amount of phosphate ofsodium and nothing else of importance has as yet beenfound in it.The exact path by which the meninges were infected was

not evident unless it took place from the right frontal sinus

yet there was no obvious disease in the right orbital plate ;indeed, the intensity of the disease was situated on the leftside where the orbital plate was thinned and discoloured. Idid not look upon the suppurative lesion in the ear as at alla probable cause of the meningitis.The urinary disease was an unexpected finding, the acute

illness having obscured its manifestations. These lesionswere assigned to calculous disease. Some time ago the leftkidney had become more or less disorganised as a result of itand the right kidney hypertrophied in consequence, but thiskidney did not escape from the effects of the calculousdisease. This patient must have suffered at some time fromcystitis, otherwise the thickness of the bladder walls couldnot be explained.VI.-TERMINAL TUBERCULOUS MENINGITIS; PULMONARY

,

AND GENITAL TUBERCULOSIS.A man, aged 24 years, was in a sanatorium under my care

five years previously. He then presented signs of a limitedlesion at the right apex and the disease had already lastedabout a year. He was discharged greatly improved. Hewas admitted into the Leeds Infirmary for a tuberculousepididymitis of six weeks’ standing and then the meningitissupervened and rapidly proved fatal.The brain showed the characteristic lesions of tuberculous

meningitis. The exudative element preponderated, butminute tubercles were visible. Limited tuberculous lesionswere found at the apices of both lungs of a quite chronicform with excavation. The rest of the lungs were healthywith the exception of one or two small recent tuberculousfoci. The connexion between genital tuberculosis and tuber-culous meningitis has been emphasised by some writers. Itoccurred only twice in 110 cases of tuberculous meningitisin the records in the Leeds Infirmary, but the vesiculasseminales were not by any means always examined. Tuber-culous meningitis is a distinctly rare complication in myexperience of pulmonary tuberculosis. This terminal

meningitis has usually been of much shorter duration thanthe ordinary typical case in the child and its symptomshave sometimes been considerably masked. The symptomsof the case were readily explained by the morbid lesionsfound.

VII.-APOPLECTIC CYSTS OF THE BRAIN.

(a) A cyst occupying the region of the right lenticulateMMCMS.—This specimen came from a patient, aged 32 years,who had diphtheria at the age of seven years, followed inthree weeks by a left hemiplegia. This hemiplegia wassaid to vary in degree. The cyst (1 inch by 2 inch byinch) was lined by a delicate cyst wall and containeda clear fluid. There was no pigment about it. The con-volutions and also the vessels of the left hemisphere were ofsmaller size than on the right side. There was old healedtuberculosis at both apices and some recent tuberculosis inother parts of the lungs. It is suggested that a blocking ofan artery occurred as the result of embolism. This wasfollowed by necrosis and afterwards a cyst formed. Embolismhas been known to occur after diphtheria. I have seen atleast one other example of a lesion in the neighbourhood ofthe internal capsule (but not involving it) produce a hemi-plegia. In a recent instance occurring in a girl, aged 14 years,who died in advanced pulmonary tuberculosis, the softeningwas limited to the middle third of the lenticulate nucleus. Anartery at the base of the brain was blocked. There weremarked aphasia, paralysis of the right arm, and paresis ofthe right leg. Possibly the variation in the degree of thehemiplegia may have been due to variation in the fluidcontents of the cyst.

(b) A cyst situated in the right half of the po?ts. -This camefrom a woman, aged 40 years, who died as a result of burns.It was stated that she had an apoplectic seizure some two orthree years before her death but it left no permanentparalysis. The cyst measures 7 millimetres by 5 millimetresby 4t millimetres and is multiloculated. There is no cystwall. The basilar artery is extensively diseased and the cystis believed to be the result of occlusion of a small branch ofthis vessel. It produced no definite symptoms during lifebeyond what is stated above.

VIII.-VERTEBRAL CARIES ; PARAPLEGIA ; CYSTITIS ; PYELO-NEPHRITIS ; CASEOUS PNEUMONIA ; TUBERCULOUS

LARYNGITIS (see Specimen II.).A man, aged 25 years, had constant pain in his back for

about 21 weeks before his death and for the last 18 weekshe was unable to work. About five weeks before death he

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had difficulty in micturition one evening and the next dayhe lost the power in his legs. On admission besides thepulmonary symptoms he had complete paraplegia. Therewas tactile anmsthesia up to the umbilicus with hyper-sesthesia above it. He had retention of urine with overflow.Defsecation was involuntary and unconscious. The cremas-teric reflex was present but the knee-jerks were absent.Babinski’s sign (extensor response) was present. The urinewas ammoniacal. There was much wasting of the limbs.The tenth dorsal vertebra was largely destroyed and a

sequestrum was present in it. External pachymeningitiswas present opposite to the diseased vertebra and it extendeddown for some three inches. The pia-arachnoid appearedquite healthy to the naked eye. Somewhat lower downthere was a distinct softening of the substance of the cordextending over about an inch, but even here the markings ofthe grey and white matter could still be made out. A micro-

scopical examination of the cord has not yet been made butthe cord, hardened in formol-bichromate solution, shows thefollowing changes when examined by the naked eye anda hand lens.The lumbar, sacral, and coccygeal regions appear to be

healthy with the exception of the lateral columns wherethere is a slight discolouration indicating some degeneration.In the lowest dorsal region no disease can be detected buta little higher up the markings become very indistinct andare finally not to be discerned. This extends for about three-quarters of an inch. Above this an ascending degenerationis distinctly visible and it gains in extent as the upper partof the dorsal and the cervical cords are reached.

In this case it is obvious that the disease commenced in thebody of the tenth dorsal vertebra. It produced an externalpachymeningitis. The disease spread, as it often does,through the pia-arachnoid without producing any veryobvious changes in it, and the spinal cord was ultimatelyinvolved, perhaps owing to the action of toxins upon itsstructure.This rough naked-eye examination shows that the motor

and sensory paralysis was due to actual disease within thespinal cord itself. It would explain the presence of thecremasteric reflex (L 1 and 2 intact) and the present butaltered plantar reflex (L 5 to S 2 intact together withdegeneration in the lateral columns), but it does not accountfor the disturbance of the vesical and rectal functions(S 4 and S 5 intact). No doubt the microscopical examina-tion will explain what the naked eye fails to detect.

In conclusion I hope that I have succeeded in emphasisingthe importance of studying morbid anatomy in close con-nexion with the signs and symptoms which it has producedduring life. In this way alone can the full advantage betaken of the abundant opportunities afforded by the post.mortem room to obtain a more intimate knowledge of disease.I have to thank Dr. T. Churton, Dr. T. Wardrop Griffith,Mr. H. Littlewood, Mr. B. G. A. Moynihan, and Mr. G.Constable Hayes for kind permission to use their clinicalnotes.

An AddressON

INHALATION.Delivered before the Midland Medical Society.

BY ARTHUR FOXWELL, M.D.CANTAB.,F.R.C.P. LOND.,

PROFESSOR OF THERAPEUTICS IN THE UNIVERSITY OF BIRMINGHAM,

GENTLEMEN,-Perhaps we prescribe few things moreignorantly than an inhalation ; the nature of the drug or Idrugs chosen we may take the trouble to indicate, but whoamongst us knows the strength of the actual inhalation orwhat change must take place in that strength ere it reach thelung alveoli. Moreover, our directions as to the method ofemployment are often vague: how much and how hotshould be the added water, how long should each treatmentlast, how often should it occur. The fact is, we are half-hearted in our belief of its efficacy and so take but littleinterest in its administration. I think the advent of thethroat surgeon is the chief cause of this ; we can see, withoutmuch thought, the result of his labours and so gladly hand

over to him conditions we previously treated by the slowerand more doubtful method of inhalation. If this were all Ishould not greatly complain. But unfortunately we handover not only the local but the constitutional treatment ;this means-and small blame to the surgeon-that the con-stitutional treatment is to a large extent neglected, withthe consequence that the patient remains for years in thehands of his local ameliorator till such time as his vis nat1l’l’aemay choose of herself to bring about a betterment of hisconstitution. For the greater proportion of these naso-pharyngo-laryngo-tracheal conditions are constitutional. Thelocal trouble is merely the maximum expression of a dyscrasiawhich exists throughout the body and can there be detectedby the painstaking physician, though the symptoms may beso vague and indefinite that they pass unnoticed by thepatient himself.The real source of the trouble is often not in the local

mucous membrane but in the nutriment supplied to this byblood and lymph ; perhaps these fluids are themselvesdeficient in nutriment, as in the anaemias, the goutydiathesis, or chronic renal disease; or, though not deficientin nutriment, they contain irritating material, as again ingout and renal disease or in gastro-intestinal catarrh, theseproducing a hyperplasia of connective tissue throughout thebody, one of its local expressions being hypertrophic rhinitis,pharyngitis, or laryngitis; or, though the fluids themselvesare fairly healthy, the vaso-motor control is imperfect andthe tissues lie too long soaked in venous blood and used-

up lymph; or, lastly, there is feeble action of the govern-ing system, there is nervous debility or acute prostration,the stimuli have lost their energy and directness of command,with a resulting inertness and flabbiness of the stimulatedtissue, a granular and oedematous pharyngitis resulting.The special surgeon may say that, while removing the localtrouble, he in no way forgets the constitutional dyscrasia andis as competent to treat it as the physician. He may be,though I do not think he is ; but whether he be so or not hispatient does not believe him to be so. Not seldom I havehad patients who have been to such a surgeon, have reapedmuch local benefit at his hands, have trusted greatly in him,and have persistently continued the local medicament he

prescribed, but have omitted altogether, or very soon, his

general treatment, supposing it was not likely to be of muchbenefit as it was " not in his line." This is one of the cursesof specialism.The layman supposes that if there is any local anatomical

abnormality then the local malfunction must necessarily bedue to this. Are we always careful to point out that thoughit may increase the malfunction it is very rarely its cause?Do we not too readily allow the sufferer, eager for relief, tosubmit to the removal of the abnormality with but atemporary improvement, perhaps none at all, or, may be,speedily followed by an exacerbation of his condition ? Dowe always insist upon explaining that his abnormalityexisted years before his malfunction, was perhaps even

congenital, and that if only the malfunction can be other-wise remedied he will again cease to observe it ?Yet I am convinced that in most of these cases the correcttreatment is to endeavour to relieve the constitutional con-dition which has caused the local trouble, and then, if youlike, remove the cause which has rendered the localitypeculiarly susceptible to the dyscrasia. And why ? First,because it is never right to allow a patient to continue withany dyscrasia if it can be remedied ; it is our duty to removehim from this danger zone, where he is constantly liable toattack, and place him in a condition of good natural resist-ance. Secondly, if an operation should then prove necessary,it is more likely to prove successful than if attempted whenhe is functioning badly. Even in war we try to remove ourwounded from the danger zone to the field hospital before weoperate, and, I understand, our civil surgeons prefer to waittill the patient be in the best possible condition physio-logically before they undertake a serious operation. Thirdly,we must remember that in most of these nasopharyngealoperations a raw surface is left bereft of mucous membrane.We hope that healthy mucous membrane will in time coverit. What chance is there of this if the neighbouring mucousmembrane be unhealthy ? If it should succeed in coveringit with unhealthy membrane like itself the old condition willsoon reassert itself, but more probably a scar tissue will be-left as after a skin burn and, like this, incapable of takingon healthy action, so that the result in either case is merelytemporary amelioration, the patient becoming a lifelongvisitor to his surgeon.

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