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ABSTRACT OF

Lettsomian LecturesON THE

TREATMENT OF SOME OF THE FORMS OFVALVULAR DISEASE OF THE HEART,

Delivered at the Medical Society of London, Jan. 8th, 1883,

BY A. E. SANSOM, M.D.LOND., F.R.C.P.,PHYSICIAN TO THE LONDON HOSPITAL, SENIOR PHYSICIAN TO THE NORTH-

EASTERN HOSPITAL FOR CHILDREN, ETC.

LECTURE I.

ENDOCARDITIS.

IN this course of lectures my plan will be to enunciatevery briefly the bases on which I believe our therapeuticsought to rest. These are, in my opinion : (1) The teachingsof morbid anatomy; (2) clinical observation of disease

processes and their correlations. Then I propose to review

(3) the lesson of the past as to treatment; and (4) to adducetowards the elucidation of the various problems the argu-ments from analogy afforded by experimental investiga-tion-a mode of inquiry rendered difficult, alas! by thestumbling-blocks which a false sentimentalism has placedin our way.

First, then, I will consider the teaching of morbid anatomyas to lesions of the valves of the heart. You will under-stand that I shall do this very briefly, for my object is

merely to note them in so far as they may afford a guide totreatment, and when I speak apparently dogmatically, I donot make an assertion ex cathedrd, but in the spirit of aninquirer after truth.We will first consider the disease which most commonly

affects the valvular apparatus of the heart and the adjacentendocardium - the disease known as endocarditis. Inbriefly reviewing its morbid anatomy, much will remainunsaid, but I shall treat it first from the standpoint of mereobservation, leaving all speculative questions. I wouldclassify the first changes in the endocardium which I shallnotice as exudative. The curtains or cusps of the valvesmay be seen to be slightly swollen, and the endocardium tocontrast by its dulness with the healthy portions adjacent.But the changes are most noticeable at the free edges of thevalves, where mav be seen isolated or agglomerated bead-like processes. Upon such processes may be observedsometimes little caps of fibrin. A thin section of a valvethus affected is seen under the microscope to differ fromhealthy valve structure in that its cellular elements aremore numerous, and, especially towards the free edge, areclosely aggregated. I wish to insist on the fact that in avalve so affected even the portions which seem to the nakedeye unaffected are really infiltrated with cells; only theaggregation is greater at the free edge, where such caps offibrin are often found attached. The beadlike eminencesobserved by the naked eye are, according to my view, indi-cations of a more widely-spread inflammatory change in thevalve than might be at first suspected.The second form of endocarditis, or properly-speaking

valvulitis, to which I shall call attention, is that which Iwould term the sclerous, or fibrotic form. Here the valve,and it is the mitral which is affected in by far the greatestfrequency, is thickened, but the thickening is not due toswelling of the soft tissue. It is felt to be hard and firm.The endocardium of the auricle, near the other valve, isfound to be dense and white. The valve-curtains, and oftenthe cords and fleshy columns, are more or less rigid. Apatch of the endocardium lining the left ventricle, and leadingup towards the aortic cusps, is sometimes also found whiteand thick, and the aortic valves themselves may be seen tohave undergone similar changes. In this form microscopicsection shows that there is a gradual fibrous transformationof the neoplasm resulting in the production of a quasi-cicatricial tissue.A third form of endocarditis which I think of practical

importance to distinguish is that which is secondary toendarteritis (atheroma). In this form it is the aortic valves

which are affected in a large majority of instances. Patchesof soft flabby swelling may be seen in the lining membraneof the aorta, close to the aortic cusps, involving them in thechange, and, perhaps, causing the inversion of one or more ;or yellowish patches may be observed, in some cases coveredby a soft pulpy material, the blood, perhaps, forcing its wayat some softened spot between or within the arterial coats ;or the root of the aorta may be bard and thick, the thicken-ing being of cartilaginous consistence, and in such thickeningthe cups of the valve may be involved ; or in like situation,and with like deformity of valves, there may be a bony orstony hardness, a calcareous change. The evidence ob-tained by microscopic investigation is to the effect that inthe swollen soft patches are abundant exudation cells with ahyaline or slightly fibrillar matrix. These occur mostly asswellings of the internal coat, but Dr. Wilks has observedthem in all the coats of the vessel. The yellow patchesshow fat granules and cholesterine crystals. There is evi-dently a fatty degeneration of the inflammatory neoplasm.In the fibrous or semi-cartilaginous variety there is morefibrillation and fewer cells, and in the hard and bony formthere is a deposit of earthy salts in the interstices of theflibrous tissue.The fourth form of endocarditis to which I shall call atten-

tion is that termed ulcerati’Je endocarditis. Swollen and dullportions of the endocardium of the valve may be seen to pre-sent here and there a yellowish or greyish discolouration, andto be covered by a finely granular debris. The superficialendocardium in such situations has become necrosed.Through such breach blood may find its way, and, spread-ing between the layers constituting the valve, may form ananeurism thereof ; or the ulceration extending through bothlasers the valve may be perforated. More commonly a con-siderable portion of the valve is eroded, and upon the erodedsurface fibrine is deposited in the form of single or multiplevegetations. The finger readily detaches these vegetations,and the surface below them is found to be covered by afriable material.

Secondly, the rise and progress of endocarditis as

evidenced by clinical observation. The fact which stands outpre-eminently in this connexion is the association with rheu-matism, acute and subacute. Amongst English observers(Fuller, Sibson, Budd, Latham, and others), the figuresapproximate tolerably closely and indicate that in acuterheumatism endocarditis becomes manifest in one out ofevery two or three cases. Continental observers, however,record a less proclivity, the figures of Bamberger, Lebert,Wunderlich, and Roth showing a proportion of one in five toeight cases. The statistics collated for me by Dr. Gabbettfrom the records of the London Hospital show that in 1880113 cases of valvular complications were noted in 244 casesof rheumatic fever-a proportion of 463 per cent., and in1881 170 in 295, or 60’6 per cent. The increasing proclivityto valvular complications with repeated attacks of rheumaticfever is well shown.The first sign by which endocarditis is rendered probable

is in my opinion a prolongation of the first sound ofthe heart, which may afterwards develop into a distinctsystolic murmur. Such murmur is, however, not absolutelypathognomonic, for it may be due to regurgitation fromadynamia of the left ventricle. Such modification is com-monly heard directly the patient comes under observation.I have observed also as indicating signs reduplication ofheart sounds, and in these cases a presystolic murmur sub-sequently develops. Rarely a diastolic aortic murmur is thedeclaratory sign. Endocarditis is by no means necessarilyattended with pyrexia, nor even by any sign or symptomwhatever referred to the heart.

I will now inquire concerning those cases of endocarditiswhich are not associated with a history of acute or subacuterheumatism. These may conveniently, for purposes of inves-tigation, be divided into two classes: (1) tho"e which areobserved in early life, and (2) those which develop aftermaturity. In the latter class are the cases of gradualonset which involve the aortic orifice, and sometimes themitral subsequently, which are traceable to sub-inflam-matory changes at the root of the aorta, and degenerationafterwards. In these cases the endocarditis and valvulitisare consecutive ; they have no necessary connexion withrheumatism, and their consideration may be convenientlydeferred. The study of endocarditis as it occurs in the earlyperiods of life is, I think, at the point at which our inves-tigation has hitherto been advanced, a matter of very greatimportance. Almost every practitioner is familiar with the

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fact that cases of disease of the valves present themselveswhich have shown evidence of such disease from manyyears, from very early periods of the life of the patient, andyet inquiry fails to elicit that the subject of such diseasehas ever suffered from rheumatism in any form. It is surelya matter of importance, therefore, that we should endeavourto learn how such disease originates in the period of child-hood. In acute and subacute rheumatism in the child theproneness to endocarditis is greater than in the adult.Typical rheumatic fever is much less common in the childthan in the adult; the articular manifestations are slighter,but I consider the morbility of the endocardium to begreater Of thirty-two cases of acute and subacute rheu-matism occurring in children under twelve years of ageadmitted into the North-Eastern Hospital during the pastthree years, twenty, or 62 per cent., presented signs of endo-cardial affection. The development of endocarditis, however,in the child has not so close a relation with the other phe-nomena of rheumatic fever as in the adult. It may precede,or may succeed even after long periods, the attack.But there are other diseases besides rheumatism in the

child with which endocarditis stands in close relation. Theseare chiefly scarlatina and measles. In relation with scarla-tina endocarditis may occur either with or without the inter-vention of articular symptoms. Post-scarlatinal rheumatismis well known, and bears a close similarity to ordinary rheu-matic fever ; associated endocarditis is, therefore, renderedprobable. But I have shown from recorded cases that suchendocarditis may become manifest after scarlatina, not onlywithout the intervention of articular phenomena, but longafter the period of fever has passed, and during a time whenthere is no elevation of the temperature of the body, no pyrexiawhatever. 1

Again, there is evident proof that endocarditis can arise inclose relation with nzcasles. I have recorded a case in whichboth pericarditis and endocarditis occurred a fortnight afterthe commencement of convalescence from measles. At thistime a perilous attack of chorea developed. There was hereno obvious manifestation of rheumatism nor hereditarytendency thereto. It appears to me that the influence ofmeasles in predisposing to endocarditis has been much under-rated, and a fortiori the frequent sequence of thesediseases as observed in children becomes an agency, andthat, as I think, very probable, not only to the productionof the endocardial disease, but to acute rheumatism itself.Excluding these causes, there yet remains a considerable

minority of cases of endocarditis in children in whom notraceable disease has led up to the valve deterioration. Thecondition is only betrayed by various morbid conditions, theresults or concomitants of the valvular disease. I havenoted twenty-seven of such cases. They have been markedby (a) disorders of the nervous system: hemiplegia, hemi-ansesthesia, epilepsy, chorea ; (b) disorders of nutrition:wasting, anaemia, &c.; (c) disorders of respiration or circula-tion : cough, dyspneea, or the usual phenomena of progressivecardiac failure. Sufficient is this evidence to prove, I think,that in the child endocarditis can arise and progress withoutspecial symptoms, without pyrexia, without the disturbinginfluence of any acute disease.

C3

As regards the pathogenesis of rheumatic endocarditis, Ido not think the evidence at all justifies the conclusion, thatits first cause is extrinsic to the body or that it is of malarialorigin and of the nature of an organised germ. On theother hand, there is much to prove that the "poison" isgenerated by a perverted metamorphosis, by retention ofeffete products in the blood. It is quite probable, I con-sider, that lactic acid is one, but not the only product capableof acting as the pathogenetic agent. Such agents may bemany, between fibrin on the one hand and the excreted morbidacid on the other. It is not proven, but yet not improbable,that disturbance of a tract of the spinal cord-a postulatedchemical coordinating centre-may be a mode in which thedisorder can be originated and prolonged, as Dr. P. W.Latham has argued.

I must now approach another part of my subject and in-quire concerning the efficacy of extant methods of treatmentin regard to rheumatic endocarditis. It has been claimed ofalmost all methods of treatment of rheumatism that have beenadvocated, thatthey have been instrumental in controlling orpreventing the cardiac complications of the disease. The in-dividual experience of observers has been cited again and againto point the efficacy of this or that remedy or method in miti-gating the chief danger of rheumatic fever. Yet proof of such

1 Lectures in Medical Timesand Gazette, Oct. 25th, 1879, p. 472.

vaunted efficacy has soon been found to be unsatisfactory,and it may be confidently asserted that no antidotal treat.ment is yet known-that we have, for instance, no drugwhich can influence endocarditis as quinine influences ague,or as mercury and iodide of potassium influence syphilis. Thediscussion so ably sustained in this Society during thelast session, which has been fully reported, has put theclaims of various forms of treatment of rheumatic fever to anumerical test. The results of treatment by rest and mint-water, by alkalies, by blistering, and by administration ofsalicin and its compounds were compared, and it is fair toassume that if any agent other than these had been efficientin the treatment of rheumatic fever or of endocarditisevidence would have made this apparent. The result of thediscussion, which it is unnecessary to epitomise,2 was to showa strong concurrence of testimony to the effect that theadministration of salicin or the salicylates very decidedlyreduced the suffering and the fever of rheumatism, but inno marked degree influence the development of endo-carditis and other cardiac complications. Primâ faciethis seems to be a strange conclusion, for one might imaginethat an agent that reduced in such marked degree the painand fever which must contribute to disturb the heart even ifit had no decided effect upon the rheumatic process withinthe heart, would with great probability influence for good theinflammatory process in pericardium as well as endocardium.The conclusion is forced home, howerer, alike by individualexperience, for we find that pericarditis and endocarditisare shown by physical signs to arise and progress in patientswho are fully under the salicin treatment, and by statisticalinquiry from large numbers of cases treated by the salicincompounds, compared with those treated in the presalicylicera, such as has been carefully followed out by Dr. GilbartSmith.3 3 Dr. Maclagan, to whom the profession and thepublic are indebted for the introduction of agents which

B have at any rate been proved to contribute to the comfort ofsuffering patients, himself allows that the hopes that theywould ward off cardiac complications have not been realised.I consider that there are strong reasons why a mode of treat.ment which is efficacious in rheumatic fever is powerless asregards cardiac complications. To put the matter clinicallyor practically. We observe, let us assume, a patient in afirst attack of rheumatic fever. He presents (1) a murmurindicating an endocardial complication. I think I musthave convinced you that such endocarditis may have arisennot during the attack from which he is at present suffering,but from the disease acquired insidiously at any time pre-viously. It is obvious that any remedy would fail to influ-ence the cardiac complication in such a cJas of cases. Or(2) a modification of sounds, or actual systolic murmur,developing at the apex, makes us suspect the present riseand progress of endocardial inflammation. But such mayhad its commencement long before the advent of the othersymptoms, for no sign will betray the gradual swelling of avalve. A swollen valve is not necessarily incompetent. Onthe other hand, a veritable systolic murmur at the apex is noconclusive proof of endocarditis, for it may be due to ady-namia of cardiac muscle. Here, then, is a double sourceof fallacy in the statistics of the cardiac complicationsof rheumatism. Or (3) the patient manifesting no evi-dence of valvular impairment is, at the termination of hisattack of rheumatic fever, discharged as free from cardiacdisease. I do not think that such conclusion is to be justi-fied. A valve may be inflamed and give no evidence ofincompetence, the patient may be discharged and show nosigns of cardiac trouble, but a slow process of shrinking or ofsclerosis may be going on; and when the patient next pre-sents himself there may be undoubted evidence of endo-cardial mischief. This is, I consider, by no means ofinfrequent occurrence; and this is one reason why a secondattack of rheumatic fever is attended with such notableevidence of a highly increased ratio of cardiac complications.For such reasons as these, I think it impossible-the

sources of error being so numerous-that we can get fromstatistical inquiry satisfactory evidence as to the efficacy ofdifferent plans of treatment in warding off endocardialdisease ; and I dissent from those who hold that a remedywhich is efficacious in the treatment of acute rheumatismought to show, on numerical inquiry, a favourable influenceon the correlated heart disease. I consider the treatmentby salicin and the salicylates, even though no favourable

results are manifest as regards cardiac complications, to be2 THE LANCET, Dec. 17th, 24th, and 31st, 1881 ; Jan. 7th and 28th, 1882.

3 Ibid., Jan. 28th, 1882, p. 135.

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the most favourable to the patient of all forms of treatmenthitherto known. In such cases it may be legitimately askedwhether I adopt an altogether pessimist view of the treat-ment of endocarditis. Can nothing be done ? My answeris, much ; but it must be in the direction of preventive treat-1Wfd..My own experience is strongly towards the con-

clu,,ion that endocarditis is more prevalent, as well as

more extensive and severe, among the poor than amongthe well-to-do. This question is one that might with

advantage be put to the numerical test ; we greatlywant the evidence of the family practitioner to com-

pare with that afforded by our hospital statistics. Thepredisposing causes to the advent of endocarditis, whichas I have shown can arise without the intervention ofobviously rheumatic phenomena, are most probably (1) ex-posure to vicissitudes of temperature, (2) and irregular andimproper dietary. These are the impulses to a pervertednutrition, resulting in the retention within the blood of thoseexcrementitious products which we may call "the rheu-matic poison. Attention to the clothing and proper feedingof infants and children constitutes in my mind, therefore,the treatment of the first importance as regards endocar-ditis. There is no need nowadays to insist on the importanceof preventive treatment as regards the zymotic diseases.This is well recognised. Is it not quite as important asregards the subtle disease we are considering ? I would,whilst recognising the difficulties of such proceeding, stronglyrecommend the periodic medical examination of children,even though they present no obvious signs of disease.Of no less importance is the treatment in regard to the

zymotic diseases which are correlated with endocarditis-viz., scarlatina and measles. The subject of an attack ofscarlatina should be watched with great care for long periodsafter convalescence. Moreover, the slightest sign of throatailment, especially with children, should be looked uponwith suspicion. I have no doubt whatever that in a largenumber of instances ulcerative tonsillitis of zymotic typeoccurs in children unnoticed and unknown, and that inmany such a renal complication is instituted which isalso neglected. The rise of endocarditis in such case is,as I have said, not during the period of fever. I do notrecognise the influence of morbid germs in direetly occasion-ing the inflammatory change in the valves. Such change is aconsecutive and secondary effect. The teaching I wouldenforce, therefore, is that the subject of scarlatina, or of theallied forms of throat affection, should be watched, protected,dieted, and treated for periods much longer than is nowusual. And as regards measles. There is, unfortunately,a widely-spread tendency to regard measles as a very slightailment that requires little or no treatment. Experiencetells, however, that it is not only the immediate pre-cursor of broncho-pneumonia frequently, and heart diseaseoccasionally, but that it effects a deleterious change uponthe powers of nutrition, which lasts, as in the case of scarla-tina, for long periods. The subsequent treatment, therefore,of the subjects of measles should, in my opinion, be muchmore protracted than it is at present. Such is an outline ofwhat I consider the common-sense treatment of the firstcauses of endocarditis. During its rise and progress in anattack of rheumatism, I prefer the treatment by salicin orthe salicylates in sufficient doses (usuallly twenty grainsevery four hours, till subsidence of the pain and pyrexia,and afterwards the same dose thrice or twice a day). From theevidence of Dr. Isambard Owen, there is a good case infavour of combining with this the administration of fulldoses of alkalies. 4 Vesication by the application of liq. vesica-torius in the left axilla, I think also of service.

It now only remains for me to allude to the clinical signifi-cance of ulcewitize endocarditis, with regard to indications fortreatment. It happens sometimes that this affection arisesand runs its course with little or no evidence that the endo-cardium is impaired. Such cases often present a strong re-semblance to typhoid fever. Here treatment is of no avail,the disease is uniformly fatal. By far the most frequentlythe diseae is engrafted, as it were, on chronic disease of thevalves. It appears to me that such cases can be dividedinto two classes, the infective and the non-infective. In theinfective cases there are extraordinary disturbances of tem-perature, multiple emboli and septicsemic signs or evenabscesses. It is in such that micrococci are discovered.They are, I believe, specific organisms, associated with somesubtle zymotic influence or virus, as in the puerperal cases.

4 THE LANCET, Jan. 28th, 1882.

It is not that the micrococci induce the endocarditis, but theycomplicate the already existing endocarditis by inducingnecrosis of the diseased tissue. In other cases, though nearlyall are characterised by embolism, the proof of infection,and, as I think, the probabilities thereof, are wanting. Ina case lately under my care in the London Hospital therewas no marked pyrexia whatever, the temperature neverexceeding 101° F., and for the most part keeping close to thenormal. I consider it most probable that in some suchcases the ulceration is induced by mechanical causes.

Drs. Wilks and Moxon have pointed out that a great massof vegetation may cause ulceration of the heart-wall bydirect pressure, or a fibrinous clot swinging in the blood-current coming sharply into contact with the muscle, mayby friction start an ulcer.5 In like manner I think it veryprobable that a weighty vegetation, or a mass of vegetation,upon a valve may, by agitation in the blood-current, so dis-turb the nutrition of the endocardium, which constitutes itsbase, as to start the process of necrosis. The treatment ofulcerative endocarditis, when once established, is hopeless,but the lessons taught by a study of the cases are, I con-sider : (1) that more than ordinary care should be exercised tokeep the subjects of valvular disease of the heart fronipossible sources of infection; (2) that any threatening ofendocarditis should be treated by the most perfect physio-logical rest attainable ; (3) that nutrition should be sustainedto the highest degree practicable.

FIBRINOUS COAGULA IN THE HEART ANDPULMONARY ARTERY.

BY SIR JOSEPH FAYRER, M.D., F.R.S.(Continued from p. 3.)

SOME of the m0st remarkable examples of this morbidcondition have occurred as sequels, if not direct results, ofinjuries, wounds, or surgical operations, not only in caseswhere pyaemia had supervened, but in others, in which

nothing indicated the approach of danger until the symptomsof obstructed pulmonic circulation had set in. It is mybelief that climatic influences, by deteriorating the blood-elaborating organs and by interfering with the due action ofthe trophic and vaso-motor apparatus, may determine theoccurrence of changes in the blood which render it prone tothe formation of these coagula, and in climates like that ofBengal, where all are more or less exposed to malarialinfluences, its greater frequency than elsewhere may be thusaccounted for. But thrombosis of the pulmonary artery andcardiac clot are neither confined to malarial climates nor totraumatic causes, for under certain conditions of disease andof septicaemia, whether traumatic or otherwise, it may occureverywhere, and notnerely as a process of the act of dis-solution, but as an independent cause of danger or deathwhich, without it, would not have happened.

I am aware that Dr. Richardson and others have long agopointed out the tendency of the blood to assume thisdangerous condition in certain diseases; but it is to the analo-gous condition when determined by malarial and spleniccachexia or by other conditions which induce leucocythsemia,and to that which results from wounds, injuries, and opera-tions (traumatism), that I now refer, and of which I expressmy belief that it is a more frequent cause of death than isgenerally supposed, especially after wounds, operations, orinjuries which involve removal of large parts of the body, ormuch loss of blood and great nervous disturbance ; and Iwoult, with much deference, suggest that some of the deathswhich have been ascribed to what appear insufficient expla-nations may have been due to this cause.Thirteen or fourteen years ago I wrote as follows in regard

to a case where death had resulted from this cause after acomparatively trivial injury, a contusion, which had causedsloughing of a small portion of integument on the leg:" There was not sufficient in this case to account for deathin an ordinary individual, but in a person suffering as he didfrom malarial poisoning and enlargement of the spleen, itwas more than sufficient." Probably in no condition ofdisease is the formation of fibrinous congula more likely to

5 Pathological Anatomy, 2nd edition, p. 120.