No. 4471.

MAY 8, 1909.

Lumleian LecturesON

RHEUMATIC FEVER AND VALVULARDISEASE.

Delivered before the Royal College of Physicians of London onMarch 23rd, 25th, and 30th, 1909,

BY NORMAN MOORE, M.D. CANTAB.,F.R.C.P. LOND.,

SENIOR CENSOR OF THE ROYAL COLLEGE OF PHYSICIANS OF LONDON;PHYSICIAN TO ST. BARTHOLOMEW’S HOSPITAL.

LECTURE IIL’ 1

Delivered on j!larch 30th.

PROGNOSIS AND TREATMENT.

MR. PRESIDENT, CENSORS, AND FELLOWS OF THE COLLEGE,-The book called Hpo-yvwo-,rLK6v in the Hippocratic writingsseems at its beginning to promise to treat its subject in thewidest sense in which the word can be used. T6v l7jTpÒV OOKÜL

poc flp,o-TOP eivac 7rpÓVOLav i7rLT7jOEÚo-LV. " He seems to me to bethe best physician who knows how to know beforehand whatwill happen. z’ "He will treat diseases best when he shall beable from knowledge of the patient’s actual state to foreseethe condition of the future." " These are sentences of the

preamble, but as the book goes on the subject is restricted toacute diseases and to a discussion of the interpretation ofsymptoms, not as bearing on particular maladies, but of themeaning of symptoms in relation to all forms of acutedisease. The famous passage on the Facies Hippocraticaoccurs in this book, and, well known as it is, I will ventureto quote it, since it is a perfect illustration of how thePrognosticon deals with its subject :-In acute diseases the physician should make the following observa-

tions : he should examine first of all the face of the patient and shouldnotice if his countenance is like that of men in health, but chiefly if itis like its own natural condition. This would be the most favourablecondition, and the more it seems to differ from that the greater thedanger. The features have attained the most extreme degree of altera-tion when the nose is pointed, the eyes sunken, the temples flattened,the ears cold and shrunken, the lobes of the ears prominent, the skin ofthe forehead dry, stretched, and rough, the skin of the whole faceyellow, or black, or livid, or leaden. If from the onset of the diseasethe countenance shows these appearances, and if other symptoms donot furnish sufficient suggestions, the patient should be asked if hehath long watched, if he has had a severe diarrhoea, if he has sufferedfrom hunger; the answer yes on one of these matters makes it rightto think of the danger as less imminent. Such a morbid state whenone of these causes has thus altered the countenance will be decidedwithin a day and a night. But if the patient remembers no such causeand if the disease does not come to an end within that time it must beknown that death is at hand.

Gnashing of teeth, movement of the hands, rapid breathing,sweats, the state of the hypochondrium, pulsations in thehypochondrium, dropsy, coldness of the hands and feet, sleep,the intestinal discharges, the urine, vomiting, expectoration,pains with fever, crises, pains in the head, sore throat,returns of fever-all these are discussed in their most generalapplication to acute disease. The only special applicationto any single morbid condition is in the remarks on pneu-monia and empyema. I may mention incidentally, becauseI do not remember to have noticed that it is pointed out inany of the commentaries, that Hippocrates here shows thathe knew that empyema sometimes follows pneumonia.Such is the Hippocratic treatise on prognosis, an attempt

to arrive at general laws upon the interpretation for good orevil of particular symptoms. At the present day the wordprognosis, I observe, generally suggests to the practiser orstudent of medicine a single inquiry and no more. Will thepatient live or die ? 1 A sounder use of the word is to includeunder it the whole probable future of the disease after thediagnosis has been made in each particular case. Theconstant practice of such a way of considering each case iscertainly to the advantage of the patient, for it cannot buthave an important effect upon his treatment. It is in thissense that I propose to apply myself to the consideration ofthe prognosis of rheumatic fever and of valvular disease.The first question to be discussed is the duration of

rheumatic fever. How long does the organism continue to1 Lectures I. and II. were published in THE LANCET of April 24th

(p. 1159) and May 1st (p. 1227), 1909, respectively.No. 4471

live on in the endocardium ? Does it after an attack die outof its condition of multiplication, so that we can say the’disease is absolutely at an end, as does the pneumococcus ofpneumonia ? Or does it, like the tubercle bacillus, live onindefinitely in the body, maintaining its lodgment, for a.

time not spreading, then again multiplying and doing more-injury, sometimes finally dying out ? Take the first ten casesyou meet of rheumatic fever, what light do they throw onthis question ? 1A girl, aged six years, had rheumatic fever in September, 1905, and’

was in St. Bartholomew’s Hospital for six weeks. She came in again.in December, 1905, for six weeks. She was an out-patient for six-months for her consequent valvular disease, mitral regurgitation, andduring these months occasionally complained of joint pain. Then camean interval in which she seemed well ; from August, 1907, onwards,till on Dec. 4th, 1907, she had definite rheumatic fever and was re-admitted to the hospital.

Is not the appearance of such a case as regards its lastingbut intermitting effects very like one of tuberculosis ? Wouldanyone doubt with such a history of manifestations in a caseof tuberculosis that the whole was due to the effects of the

original settlement of bacilli in the body ? Would the inter-mission of raised temperature and of other symptoms fromAugust to December in the second year give rise to any doubton the subject of the whole being one attack of tuberculosis ?A woman, aged 24 years, had well-marked rheumatic fever in July,

1908; in March, 1908, she had had an attack and had had one in 1904.

Supposing this patient had had haemoptysis in 1904 andwell-marked pulmonary symptoms in March and July, 1908,should we not have expected to find tubercle bacilli in hersputa in July, 1908, and should we not be certain that herillness began in 1904 ? 1A woman, aged 25 years, who came into St. Bartholomew’s on

account of palpitation and shortness of breath in January, 1908, hadmitral obstruction and regurgitation but no present pains in her jointsor fever. She had had rheumatic fever in 1899, and in 1904 had beenadmitted to St. Bartholomew’s Hospital for rheumatic fever and hadstayed in hospital for six weeks. She had had rheumatic fever again inOctober, 1906, and was in bed for ten weeks. Since then she had hadoccasional pains in the joints.

If this patient had bad dysentery in India in 1899, hadgot over it and had returned to England, and had beenadmitted to the hospital in 1904 with a chronic diarrhoea,with blood and mucus discharged from the bowel, andafter treatment had got well and left and had come backagain in October, 1906, with a similar diarrhoea, and if afterseeming to recover she had now and then passed a littleblood and mucus, would not much the most probableexplanation be that her Indian infection was the cause ofall the prolonged symptoms and that if she died we shouldfind imperfectly healed old ulceration with scar tissue nearit in the large intestine ? 1 Should we not venture to state aswe went round the ward that that anatomical change wasthen present in her intestine and that the whole dated fromher attack of dysentery in India in 1899 ? ’1A woman, aged 24 years, was admitted to one of my wards on

Oct. 3rd, 1908. with rheumatic fever, of which the pains had begun onSept. 21st. The pain and swelling of joints were well marked and shehad mitral regurgitation. In 1900 she had chorea which lasted for sevenmonths.

Might not this case be compared to that of a patient whohad an attack of pleurisy on the left side, the nature ofwhich was undetermined at the age of 16 years, and who haddeveloped well-marked tuberculosis of the lung on the leftside at the age of 24 years ? 1 Would it not be possible thatthe original infection had remained, that the pleurisy wasdue to a settlement of the tubercle bacillus which had sincebeen so inactive as to produce no symptoms noticed by thepatient, and which in 1908 under some favouring circum-stances had been able to grow and produce the tuberculosis ?If the original pleurisy had been shown to be tuberculousshould we not at once admit that the tubercle of the lungeight years later was a probable development of the sameinfection? 1 I have chosen this comparison because while wecannot be certain that an attack of chorea which we havenot witnessed was of the variety which undoubtedly belongsto the series of phenomena of rheumatic fever, the pre-sumption is strong that any chorea which occurred in theearly life of a young patient with rheumatic fever was of thatvariety.A woman, aged 24 years, was admitted to hospital on July 8th, 1908,

with valvular disease, mitral regurgitation and aortic obstruction andregurgitation, but without symptoms of rheumatic fever. She had hadrheumatic fever when aged eight years and had had 12 attacks since;he first. The last attack was some time before May, 1908, so that!he had 13 definite attacks in 15 years.

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In the absence of an exact history of each attack and ofthe intervals we can only apply our knowledge of the fre-quency with which some pains appear between seriousattacks, and the probability seems to be that this was onelong period of rheumatic fever-that is, not of continuousfever, but of continuous disease due to the original infection,and to the constant presence of the organism to whichrheumatic fever may be believed to be due.A ’woman, aged 18 years, was admitted to hospital with rheumatic

fever on August 24th, 1908. She had mitral obstruction and regurgita-tion. She had been admitted on three previous occasions with rheu-matic fever and had thus had it under observation in 1898, 1900, 1902,and 1908.

Here again, if the analogy of tuberculosis has any force itmay be applied to enable us to accept the probability that aparticular organism was present in her system, probably inher endocardium, for ten years. a

’A boy, aged 16 years, was admitted to hospital on April 24th, 1907,with rheumatic fever. He had at the time mitral regurgitation andaortic obstruction and regurgitation. In 1896, when aged five years, hewas in bed for six months with rheumatic fever; in 1897 he had choreafor seven weeks : in 1898 rheumatic fever; in 1899 rheumatic fever foreight weeks, and in 1904 another attack.

Supposing this boy had acquired the haematozoon of tertianague in a malarious region in 1896 and had soon after movedto a healthy part of England we should have had no difficultyin believing that a recurring tertian fever was due to theparasite. I have myself observed a case in which a tertianague continued at intervals for nine years, and have read oflonger liability to the fever. The possibility of obtainingthe hasmatozoon from the blood of course supplies a testof the continuity which must be absent while the micro-organism of rheumatic fever is unknown.,A boy, aged 12 years, was admitted to hospital with rheumatic fever

in January, 1907. He had mitral regurgitation. In the summer of1903 he had had an attack of rheumatic fever and since had had pains inhis joints with fever at intervals.A boy, aged 11 years, was admitted to hospital with rheumatic fever

and had mitral regurgitation. His present attack seemed to havebegun on Nov. 1st, 1906, and he had a similar attack three yearsbefore.A boy, aged nine years, was admitted to hospital with rheumatic

fever on Sept. 24th, 1904. He had disease of both mitral and aorticvalves. In 1903 he was in the hospital with rheumatic fever for nineweeks and was readmitted in May, 1904, and was under observation tillthe beginning of August.The history in this last case for more than a year was

nearly continuous, and in this, as in the former two, theanalogy of a development of the tubercle bacillus may beused to explain the course of a disease dependent on theorganism of rheumatic fever.

It would, of course, be easy to mention many more suchcases, but I have perhaps said enough to satisfy you thatthere is nothing unlikely in the view that the several attacksof rheumatic fever from which so many patients suffer arereally successive developments of an organism which remainsin the endocardium throughout the series of attacks. Thus,using the word rheumatic fever for the condition presentwhen this organism is in the system, whether developedor in a potential state of development, I arrive at the con-clusion that rheumatic fever has a variable duration. It

sometimes, though rarely, lasts two months and no more.It frequently lasts from three to ten years and may lastlonger still. A short attack is more probable after 30 yearsof age than before. A long attack is most likely to occurwhen the disease begins in early childhood.The answer to the question whether the patient will live

or die in the first attack must, of course, be that he will notdie in it. The cases of death said to be due to a first attackof rheumatic fever are generally diminished in numberwhen minutely examined. Thus, a woman, aged 26 years, inSt. Bartholomew’s Hospital, under the care of the late Dr.Reginald Southey, had a loud systolic murmur, plainest at theapex, and some swelling of the right knee and fever. Shehad been ill for seven days, and she died three days later.It was supposed that she had rheumatic fever, but the post-mortem appearances seemed inconsistent with this view,though the endocardium was affected, and there were no

signs of ulcerative endocarditis. The pericardium was

adherent and in one part was calcified. The whole heartwas dilated. The endocardium of the right auricle showed18 small white specks, circular and encircled by an area ofengorgement. These seemed on microscopic examination tobe localised haemorrhages of old standing, but what theirnature was not discovered. There were 250 in the rightventricle, some in- the left auricle, and many in the left

ventricle. The valves had no such specks on them, nor hadthey any recent growths on them, though both the tricuspidand the mitral were incompetent. There was a small patchof recent lymph on the wall of the left auricle. The peri-toneal surface of the intestines, the kidneys, and the livercontained similar specks, and it seemed possible that thedisease was, in fact, a pyaemia, and that these were minuteabscesses of various dates. As the post-mortem examinationwas made in 1879 the test of cultivation was not used.That the illness beginning with a first attack of rheumatic

fever will ultimately by the way of valvular disease be thecause of death is true of a large percentage of cases. In asmaller percentage the valvular disease, while not itself theimmediate cause of death, is a chief contributing cause insome such acute disease as pneumonia. In another group ofcases of valvular disease descended from an attack of rheu-matic fever, a pericarditis perhaps of the same infection,perhaps of a pneumococcus or other organism, is the cause ofdeath. In a small percentage again the rheumatic fever is aremote cause of death, since it has prepared the endocardiumto receive the infection of ulcerative endocarditis or ofinfluenza. In ten cases of ulcerative endocarditis an

endocardium damaged in long past attacks of rheumatic feverwas found in five. Thus rheumatic fever must be regardedas leading to a large sacrifice of life in at least four differentways of death. Will the endocarditis certainly leave per-manent damage to some valve or valves ? 7 To this the answeris that a small percentage of patients receive no permanentdamage, that a further small percentage receive damage,the signs of which after a lapse of time disappear, butthat a large proportion of patients do acquire permanentvalvular disease. It must be added that the proportion ofcases which do not end in permanent valvular disease maycertainly be increased by judicious treatment, just as

judicious treatment diminishes the mortality in entericfever, and that the commonest cause of a further continuanceof the disease is letting the patient get up too soon.The true result of an attack of rheumatic fever on the

valves of the heart cannot be determined till after thepatient has been up and about for some time and the tone ofthe myocardium has been completely restored. The injuryto the valves may then prove to be much less than was beforeexpected, and now and then it may prove to be unexpectedlygreater. The valvular damage can as a rule be accuratelydetermined three months after the patient’s convalescence.The commonest valvular lesion after rheumatic fever ismitral regurgitation. The more often the febrile attacks are

repeated the greater will be the degree of injury to thevalves. In every case of rheumatic fever it is safe to predictthat there will be no permanent damage to the joints. Theseare the chief points in the prognosis of rheumatic fever itself.The prognosis of the several forms of valvular disease may

properly begin with the general statement that death inmitral disease tends to occur gradually with long-precedingdropsy, and that in aortic disease, while the same method oftermination may occur, there is also the permanent risk ofa sudden termination of life.The post-mortem appearances of the heart in cases of

gradual death from valvular disease show that it is theenfeebled or degenerate condition of the myocardium whichis the cause of the general dropsy and of the patient’s death.The post-mortem appearances in cases of sudden death withdisease of the aortic valves sometimes include a degeneratemyocardium but in other cases show muscular tissue inwhich degeneration has not begun.The temporary recovery which patients make from a con-

dition of cardiac embarrassment, even if associated withextensive general dropsy, shows that an enfeebled myo-cardium may attain strength again and :be able for sometime longer to do its work. If at the supposed end of anattack of rheumatic fever a patient is left with distinct mitralregurgitation what will’be the effect of that lesion upon hisphysical future and in what ways is that future affected ? 7The first danger before him is that endocarditis is merelydormant, a danger to be met only by taking the fullest painsto ascertain that the attack is at an end. Further, rheumaticfever always means increased injury to the first affected valvewith the possibility of injury to other valves. Let us supposethat no further endocarditis occurs. The imperfection in thecirculation caused by the damaged valve is likely to beremedied by hypertrophy of the parts of the myocardiumaffected, of which the left ventricle is part. The apex beat,

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therefore, is found lower down and further to the left thanin a normal heart. The degree of hypertrophy of coursedepends on the difficulties to be overcome. To what extentwill it go ? 1The heaviest heart due to mitral regurgitation alone which

I have myself met with post mortem weighed 22 ounces. Itwas that of a man, aged 20 years, who had no chronic inter-stitial nephritis and no adherent pericardium or othervalvular lesion than mitral regurgitation. The degree ofhypertrophy in a man does not often make the heart exceed16 ounces in cases of mitral regurgitation. A patient, aged12 years, with mitral regurgitation may in the course of fromsix to eight years attain such a good working heart that heonly feels the presence of the valvular lesion after greatexertion. Alcohol will sometimes relieve the cardiacuneasiness which he feels after fatigue, and I have seen afew cases of chronic alcoholism which seemed traceable tothe endeavour thus to overcome the sensations produced byan overworked heart with mitral regurgitation. The heartthat has accommodated itself in course of years to a consider-able mitral regurgitation will go on working well for years,and even inco old age if it be not affected by fresh endo-carditis of any kind and is not exposed to unfavourable con-ditions, of which too great physical exertion and prolongedmental distress or anxiety are the most important, and thenext in importance such diseases as pneumonia and influenza.These are particularly dangerous to such hearts in two ways-the pneumococcus or the bacillus of influenza may attackthe old damaged endocardium or they may originatepericarditis ; and in either condition, besides the embarrass-ment due to it, considerable enfeeblement or further changein the myocardium must be expected and generally occurs.In this way such an attack is often fatal. Over-physicalexertion seems to strain the muscular tissue and thus leads togreat irregularity in the action of the heart, but rest andtreatment may restore the heart to its former condition.Prolonged mental distress seems to have even a more severeeffect on the condition of such a heart than too great physicalexertion, and the restoration in such cases is often a matterof extreme difficulty. The condition of the heart seems

directly traceable to the disturbance of the mind or of thefeelings, and as the illness goes on with these unrelieved thecondition of the heart itself seems to react on the mentalstate and to aggravate it. Such patients sometimes recoververy slowly ; sometimes the natural ultimate failure of a

damaged heart seems hastened and they die from dropsy, butI have seen several in whom an attack of pericarditis-notextensive or with great effusion-terminated life.

In mitral regurgitation aches are occasionally felt in theheart wall, not confined to one spot but extending from baseto apex. Very severe spasmodic pain is also sometimes feltwhich might be mistaken for angina pectoris, but whenwatched is seen to be different, in that it lasts a much

longer time, often several hours, and does not give any senseof actually impending death. The occurrence of simpleemboli and of right hemiplegia due to such an embolus areoccasional incidents of a case of mitral regurgitation as alsoof aortic valvular disease and add further to the long list ofthe consequences of rheumatic fever.

If instead of merely allowing regurgitation the mitralorifice is greatly narrowed by adhesion of the flaps of thevalve to one another, so that there is well-marked mitralstenosis, the patient will have a still less easy life, morepalpitations, a more frequent sense of cardiac irregularity,and less power of work, and will altogether be in a moredistressing condition, and one in which there are fewerpossibilities of improvement by way of hypertrophy or inany way. The patient with mitral regurgitation, as we allknow, may often live to old age ; the patient with mitralstenosis very rarely indeed. The narrower the orifice the fewerwill be the patient’s years. The heart may be capable ofvery nearly regular action in a few cases, but even in thesevery little extra exertion is sufficient to make it embarrassedand very irregular. The lungs are permanently engorgedand attacks of bronchitis are frequent. A distress whichrecurs after relief, and with each recurrence grows worse, ispain in the liver. The tenderness to the touch may beextreme and often there is a sense of stretching there whichamounts to acute pain as the patient lies still. Sometimesthere is a similar pain in the spleen. The urine becomesdiminished in quantity and albuminous. The general dis-comfort may be increased by piles ; ascites and anasarca of

the legs and arms appear, and a continued reduction in thequantity of the urine which diuretics affect but little pointsto the constant engorgement and gradual hardening of thekidneys. Treatment and rest give relief, but it is rarelylong-continued, and the patient’s life, even if carefullyregulated, consists of little more than longer or shorterintervals between painful attacks. At last the cardiac

irregularity and tumultuous action are incessant, the dropsybecomes inveterate, the engorgement of the liver cannot bediminished any more, constant cedema of the lower lobes ofthe lungs is present, the imperfect aeration of the bloodaffects the brain, and the patient has temporary delusionswhen awake and dreadful dreams during restless and ofteninterrupted sleep. Mitral stenosis is the most distressing ofall the common forms of valvular disease. It gives thepatient least ease and soonest terminates his life. If ithas begun in the girlhood of a woman she seldom lives

beyond 40 years of age if she is married and has children,or much later than 50 years if she lives unmarried under themost comfortable circumstances. I have seen very few menwith mitral stenosis who reached the age of 50 years. Ithink it is the cares of a household rather than childbearingwhich makes the lives of married women with mitral stenosisshorter than those of spinsters, for during pregnancy thepatient is often much less distressed by her heart than at anytime, though after childbirth she sometimes perishes owingto the onset of a fresh endocarditis. The addition of

tricuspid stenosis increases the obvious irregularity of theheart and adds to the distress and diminishes very much theduration of life. From each side of the heart simple embolimay be shot into the circulation and may produce haemoptysisor hasmaturia, while other hemorrhages may occur as resultsof venous engorgement.The hypertrophy produced by mitral disease seldom.

increases the heart to more than twice its natural weight.That produced by disease of the aortic valves often does so,and may be the origin of a hypertrophy reaching 30 or even38 ounces. It is important to bear this general fact in mindin cases in which the cause of a systolic murmur is difficultto determine. If there is very great hypertrophy (and noother present cause, such as adherent pericardium or chronicinterstitial nephritis), if with a heaving impulse the apexbeat is in the sixth space and beyond the nipple line, thenthat hypertrophy alone makes it probable that aortic diseaseis present. Such cases generally terminate in a sudden death,and of all causes of transition from what seems fair healthto immediate death aortic valvular disease is the most

frequent. This sudden death may be very long deferred.Thus a patient who probably acquired aortic valvular diseasein 1837, after a well-regulated life in which it rarely troubledhim, died suddenly from his aortic disease while dressing onemorning in 1900.Angina pectoris is to be regarded as a likely incident in

this form of valvular disease. Its occurrence at once, and

generally correctly, suggests a near termination, but some-times the patient goes on living a very long time. A man whoseaortic valves became diseased between 1877 and 1880 foundthat hard mental work affected his heart soon after 1890’when he was 43 years of age, and in 1898 he had definite

angina pectoris which never left him but continued for tenyears. I have met with several other instances where a manwho seemed likely to die very soon yet lived ten years undersimilar circumstances.Such are a few of the points of prognosis in rheumatic

fever and in valvular disease. They all involve a repeatedconsideration of the patient’s state and of his account of it.In receiving such accounts of past attacks and pains a literalinterpretation of words must not be used nor too muchinformation expected. Johnson in his noble poem on thedeath of Levett, as he repeated it to Boswell-

" In misery’s darkest caverns knownHis ready help was ever nigh,

Where hopeless anguish pour’d his groanAnd labour steals an hour to die "

-has a last line afterwards altered by him, which expresseswith the force of true poetry an observation on human lifemade among those who can but just earn their living, thejustice of which we, who have all of us known and respectedin the wards of our hospitals many such people, can confirm.How many a man and woman have we seen who seemed

barely able to spare the time to die and who had amidlaborious occupations neglected to record in the mind or to

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remember illnesses not great enough to prevent going towork.

There is another cause which obscures a man’s life-historyand which makes him subdue the sensation of cardiacirregularity and go on till the time for resting his heart isalmost past and degeneration of the myocardium has begun.Alcohol at this serious and fatal cost obscures his conditionfrom himself and keeps him going when he ought to be inbed. It does much to obscure the gradual, and often to berelieved, course of the valvular disease due to rheumaticfever and leads men to think symptoms sudden which arein reality but the last steps of a very gradual descent.Cases of this kind, of which there are very many, tend tospread the belief that death from valvular disease is a morerapid process than it really is.

Such are the points of prognosis which have struck memost.

The treatment of rheumatic fever proposed by Sydenhamwas based on the theory that it was an inflammation

supported by the observation that the blood drawn fromthe rheumatic patient presented the same appearances asthat drawn from one with pleurisy, a condition then

universally described under the pathological headinginflammation. His first proceeding was to order ten ouncesof blood to be taken from the arm on the side affected.The next day the bleeding was repeated ; after one or twodays there was a third bleeding, and after three or four daysmore a fourth bleeding, which was generally the last. A

cooling julep, which was little more than a draught ofsweetened water, was to be taken at the patient’s pleasure.The painful joints were to be relieved by a poultice of whitebread tinctured with saffron or by the repeated applicationof a cabbage-leaf. The diet was one of barley and oatmealbroth, all meat or meat broths being absolutely forbidden.The patient was allowed to drink small beer, everybody’sdaily drink at that time, or ptisans of barley, liquorice, orsorrel boiled in water. He was to keep some hours every

’

day out of bed. On the alternate days to the bleedingsenemata of milk with sugar were given and for eight daysafter the last bleeding. After that a purge was to be takenin the morning and the same evening a large dose ofdiacodium in cowslip water. Then the patient was allowedgradually to return to his wonted way of living with onecaution-that he should drink no wine and no spirits andshould avoid salted and spiced meats and anything difficultof digestion for a long time. "Pains," says Sydenham,"will thus be lessened, but will remain about for a longtime." "

Dr. Peter Mere Latham, who wrote in 1845 and whoseknowledge of the practice of his day went back to a fewyears before the battle of Waterloo, had seen rheumaticfever treated by bleeding, by opium (2 to 5 grains every24 hours), by calomel, by colchicum, and by drastic

purgatives. When he was a student at St. Bartholomew’s

Hospital from about 1810 to 1814 the treatment of rheumaticfever usual there was to give a dose of liquor ammoniasacetatis three times a day and an opiate at night-a humane method perhaps traceable to the practiceof the enlightened David Pitcairn. He himself thoughtbleeding expedient in many cases. His view about it in the- reign of Queen Victoria was much the same as that of

Sydenham in Charles II.’s. He had used opium with success,though as, unlike Sir William Gull, he had never thoughtit right to leave cases quite untreated, he had, he

admits, no sufficient standard of comparison to tell himwhether he had done more than relieve pain. On the whole,he thought that the best plan of treatment was that by large(10 to 20 grains) and repeated doses of calomel followed bypurgatives. I was a clinical clerk at St. Bartholomew’sHospital about a quarter of a century after the end ofDr. Peter Mere Latham’s active life in his profession, beyondwhich his honoured age lasted for many years. His method-was entirely obsolete and the general method of treatment ofrheumatic fever was by alkaline salts. This method andseveral others have since become obsolete, and for the pre-sent, so far as the Pharmacopoeia is concerned, it seems clearthat the salicylates are much more efficient than any remedyof past times. They lead to a rapid cessation of the painand swelling of the joints, and when continuously admini-stered in the dose proper to each patient over several weeksthey seem, so far as the temperature chart and the absenceof further symptoms enable one to judge, to prevent the

further development of the organism in the endocardium orto destroy it altogether. The difficulties of administrationwhich occur in particular individuals can generally be over.come by a little ingenuity in prescribing. A more rapidextermination of the organism is desirable, and for this wehave yet to seek a drug. For the present that which wehave does a good deal for the relief of the patient’s painswhile it is not inoperative in the process of terminating hismalady.We rightly regard the keeping the patient sufficiently

long in a condition of absolute rest in bed as one ofthe greatest modern improvements-as compared with thepractice of past times-in the treatment of enteric fever,and I think we may believe that there is no practiser ofmedicine in England who fails to carry it out thoroughly.I wish to urge the importance of a similar unanimity withregard to rheumatic fever. My experience leads me to thebelief that there is always fear of re-development of thedisease if the patient is allowed to leave his bed till his

temperature has been absolutely normal, without any risewhatever above the normal line, for three weeks at leastfrom the last rise. After this he ought long to be watchedday by day with the aid of a temperature chart; and if in theweek of his leaving bed or later any definite rise is observed,he ought to go back to bed for a further three weeks. If norise occur he ought still to continue under observation forthree months, if possible, taking salicylates or similar drugsin adequate but diminishing quantities, and all this time hislife should be so ordered that no strain is put upon hisheart. If he is a boy at school he is not to take part in gamesall this time. If he is at home he is to take carefullyregulated exercise and to have one rest or more in the day aswell as a long night.Perhaps in hospitals it may prove that three weeks of

normal temperature is not enough before allowing the patientto get up. This may be discovered when three weeks havecome to be generally adopted as a minimum period. I amcertain that an earlier day of getting up only leads to

prolongation of the disease.One point which I wish to urge about the valvular disease

due to rheumatic fever is the importance, when we see suchcases, of taking the temperature or asking for a temperaturechart. Thus only can we be certain that endocarditis is notpresent and that our treatment ought not to require that thepatient stay in bed. Most physicians have seen children whowalked to the hospital and who had the day before playedabout who, when examined, had raised temperature and suchmarked alteration of cardiac sounds that it was certain theyhad had endocarditis for several days. Arthritis was, ofcourse, present, but of some small joint and causing only alittle pain. Thus, when seeing a case of valvular disease ina young person, the first question to which the observer mustascertain the answer is not, when had he rheumatic fever,but has he got rheumatic fever at present. Thus the observerwill come to know whether he has to treat a condition ofacute endocarditis or one in which he is to try to relieve theheart in difficulties which it suffers from this or that simpleor complex valvular defect.As to this last part of the subject, it would be obviously

impossible within the limits of these Lumleian lectures todeal with it. If, like the accomplished Sir Charles

Scarburgh, versed alike in medicine, in anatomy, in Greek, andin mathematics, I were to hold the lectureship for 38 yearsI might perhaps, if I had his abilities as well as his time,exhaust all that there is to be said on valvular diseasein all its forms. Or if like the learned and judicious Dr.Richard Powell, the first describer of facial palsy, I were tohold the lectureship for ten years, I might make considerableprogress in the statement of sound principles of treatmentand the refutation of much that is foolish which has beensaid about it ; but my measure is smaller and my course oflectures is finished. Your time and mine will not have beenwasted if I have persuaded you, and through you our pro’fession at large, (I.) that rheumatic fever is a single definitedisease ; (II.) that endocarditis is always an essential part ofit ; (III.) that its duration may extend over many years,and that these circumstances, but half demonstrated as theynecessarily are at present, are still the safest indicationsof method in the treatment of the disease.Lord Lyndhurst, the Chancellor, once said in conversation,

.. I consider that the worst exaggerator is the person whounderstates." The remark was original and wise. It is

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ullustrated in the books of many writers on rheumatic fever.

They understate the conclusions which their own experiencewould allow. I have tried to avoid this fault and to staterthe conclusions to which my own experience has led mewithout abatement and without reservation. I have venturedto risk the censure which might attend such a course becauseI believe that the adoption of these opinions would notmerely lead to a saving of lives but also to the preventionof many of the fatigues, disappointments in work, checksin usefulness, and other inconveniences which follow thevalvular disease consequent on the endocarditis of rheumatic,fever.

An AddressON

GALL-STONES,Delivered before the South-West London Medical Society on

Jan. 13th, 1909,

BY HERBERT F. WATERHOUSE, M.D.,C.M. EDIN., F.R.C.S. ENG.,

SURGEON TO, AND LECTURER ON SURGERY AT, CHARING CROSS HOSPITAL ;SENIOR SURGEON TO THE VICTORIA HOSPITAL FOR SICK CHILDREN;

EXAMINER IN SURGERY AT THE UNIVERSITY OF LONDON.

GENTLEMEN,-When your President and Council did me-the honour to invite me to address you this evening I decidedthat I would choose as my subject "Gall-stones." " Amongthe reasons for my choice were the facts that gall-stonesconstitute one of the most frequent of all the many morbidconditions to which the human body is liable, that theirexistence and their causal relationship to many grave formsof disease remain in many instances unrecognised, at leastfor a considerable time, and my conviction that the aid of the:surgeon in cases of gall-stones, often sought too late, cannotbe summoned too early. Time will only permit me to dealauperficially with my subject, as it is too vast for adequatedescription in one address. I have no intention of describing’the technique of the various operations that may be

employed, as I have been informed that my audience is

,essentially composed of general practitioners, not of

,operating surgeons.Let me remind you that though biliary calculi are far

most frequently found in the gall-bladder, yet they may befound within the liver itself in one of the rootlets of the

,hepatic duct. Such hepatic stones, I believe, are rare,and are discovered on the post mortem, rather than,on the operating, table. I have been struck by the;fact that the size and number of biliary calculi bear norelation to the symptoms which they may produce. The

largest gall-stone that I have removed is this which I showyou (from a patient under the care of Dr. Arthur Farr).It measures two inches in length and three and a half inchesin circumference measured at right angles to its longdiameter. The smallest amount of concretion was repre-sented by half a saltspoonful of fine sand, and yet in thiscase the symptoms were so urgent that immediate removal ofthe gall-stones was recommended by Dr. A. H. Vassie andmyself. As to number, gall-stones may be solitary or very’numerous. Solitary gall-stones are by no means rare ; thethree that I now show you were removed by me during thepast year. They are all, as you will observe, pear-shaped oroval, and lack the facets so characteristic of multiple calculi.Biliary calculi are largely composed of cholesterin whichforms about 80 per cent. of their bulk, bilirubin andinsoluble lime salts, held together by an albuminoid- scaffolding.

Little is known of the mode of formation of gall-stones.The cholesterin may be derived from the bile by precipita-tion, as the latter contains only about 2 per cent. of-cholesterin, but it is now commonly believed that thecholesterin. the bilirubin, and calcium salts, and thealbuminoid framework, all owe their origin to catarrh of themucous membrane of the gall-bladder (lithogenous catarrh)commonly, if not invariably, of microbic origin. I believethat in all cases microbic infection of the mucosa of thegall-bladder is the chief causal agent in the production of:gall-stones. It acts by giving rise to inflammation of the

mucous lining of the gall-bladder and ducts, and thus formingmucoid masses around which are deposited cholesterin,bilirubin, and lime salts.

I am convinced that typhoid fever is a potent cause ofgall-stone formation. A history of typhoid fever has beenpresent in more than a quarter of the cases upon which Ihave operated. I have found typhoid bacilli in the gall-bladder three years after all symptoms of this disease hadceased, and have operated upon cases of typhoid chole-cystitis. If this be true of the bacillus typhosus, surely itis only reasonable to suppose that other microbes which maygain access to the interior of the gall-bladder, either by wayof the common bile-duct from the duodenum, or possibly bythe blood stream, may have the same power. It is by nomeans uncommon to find gall-stones apparently dating froman attack of gastro-duodenal catarrh. In nine out of ten of

my gall-stone cases in which a bacteriological examinationwas made, micro-organisms, chiefly bacillus coli, bacillustyphosus, and staphylococci, were found.

Gall-stones, as is well known, are more common in thefemale than in the male subject, and in those over 40 yearsof age, who are stout and indolent. The proportion of casesin private practice is far greater than among hospital patients,and among large eaters than among those who indulge freelyin alcohol. I have found gall-stones more frequently amongtotal abstainers than among those who drink alcohol, thereason being, I believe, that teetotalers are in general largeeaters. A statement which is undeniable is that biliary calculiare many times more frequent in women who have bornechildren than in those who are childless. Few medicalmen seem to recognise how common biliary calculi are.

From various statistics it is certain that they are found atnecropsies in 9 per cent. of all adults and in 27 per cent. ofwomen over 50 years of age. Though I have for many yearsbeen surgeon to a large children’s hospital, I have only oncefound gall-stores in a child under 12 years of age.

SYMPTOMS AND RESULTS OF GALL-STONES.

With these preliminary observations, allow me now to passunder review some of the symptoms and results of gall-stones. In the first place, let me say that though I am asurgeon I admit freely that in a considerable number ofcases gall-stones give rise to no symptoms, or perhaps Ishould say to none recognised by the medical attendant,and this especially in cases in which bile can pass easilyinto the intestine. How often has it happened thata necropsy has revealed a gall-bladder containing manycalculi, the presence of which has never been suspectedduring life. Such instances have, in my experience, mostlyoccurred in old patients. In many cases, however, stones inthe gall-bladder give rise to many and diverse symptoms,and not infrequently produce results of extreme gravity.Allow me to remark that there is no morbid condition of

equal frequency that is more commonly overlooked thancholelithiasis. When there are no symptoms whatever andthe patient enjoys freedom from discomfort, the non-recogni-tion of gall-stones is readily comprehended. But permitme to point out that we see many times a year cases ofgall-stones which cause symptoms and which ought to bediagnosed as such, but are not. The reason of this failure ofdiagnosis is that the patient refers all his, or her, pain anddiscomfort to the stomach and not to the gall-bladder orliver. The great majority of patients, possessors of gall-stones, have, I am convinced, been treated for months, andeven years, for dyspepsia, chronic gastric catarrh, pain re-ferred to the epigastrium, and flatulent distension of the

stomach-i.e., for the conditions of which they themselvescomplained, whereas the real cause of their sufferingand ill-health was the presence of calculi in the gall-bladder. How frequently has every surgeon known theold woman who has for years been treated for indiges-tion and wind on the stomach until some new sym-ptom drew attention to her gall-bladder, when thestones were removed, and all stomach troubles completelydisappeared. My firm belief is that the majority of flatulentdyspeptic women who attend the medical out-patient roomwith such wondrous regularity to receive their weekly bottleof medicine are really suffering from gall-stones. I do not

expect you to believe me, but I think that I am right and thatI have the high authority of Mr. Moynihan on my side. Manyof these patients, victims of unrecognised gall-stones, sufferfrom attacks of vomiting, many from pain in the right