Document 15e0j7yE7X96yZj1w6exGZwEq

u-l , O <a e u 3c 'n O' /t O' O 5c** * o~-* oqO**o^ * w SW 3"T 3S <3 I It 566182 PLAINTIFFS EXHIBIT I JXM-m.. tn b<^ 0(0 cnS g af s ** O o RAYMOND . FLAKE, M, JK VoL 261 No. 7 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 345 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL respirations 22. The blood pressure was 140 systolic, 85 diastolic. The urine gave a + + + test for albumin; the sediment contained 3 to 5 white cells and a moderate number of hyaline and coarsely granular casts per high-power field. Examination of the blood revealed a hemoglobin of 17.4 gm. per 100 ml. and a white cell count of 7400. The nonprotein nitrogen was 33 mg., the bilirubin 1 mg., the calcium 7.2 mg., Weekly Clinicopathological Exercises FOUNDED BY RICHARD C. CABOT Benjamin Castleman, M.D., Editor Betty U. Kibbee, Assistant Editor r* n / n r if'D I C CASE 45331 Presentation of Case A sixty-five-year-old retired asbestos worker entered the hospital because of dyspnea. Ten weeks previously he experienced a sudden episode of collapse, with dyspnea and weakness, that lasted for an hour. Two weeks later he noticed swelling of the legs, dyspnea on exertion and ano rexia. His physician prescribed a low-salt diet, and digitalis therapy was begun. One month before ad mission the edema and dyspnea increased and persisted despite Diamox therapy. During the two weeks before entry Mercuhydrin therapy was given, without effect. There was no chest pain or hemopty sis. The patient allegedly had rheumatic fever when he was twenty-four years old and was admitted to a hospital for three months. There were no known cardiac murmurs. His dental hygiene had been poor for many years. He had been an asbestos worker for thirty-five years, and had retired one and a half years before entry after sustaining accidental injuries. He was studied at a sanatorium two years before admission, and was told that he had fibrosis of the lung. Physical examination showed a slightly cvanotic man who was dyspneic after exertion. Clubbing was present The teeth were very carious. Examination of the chest revealed moist rales at both lung bases and dullness with diminished breath sounds at the right-lung base. The left border of cardiac dullness extended 3 cm. beyond the mid-clavicular line in the fifth intercostal space. The pulmonic second sound was greater than the aortic; no murmurs were audible. The abdomen was normal. There was + + + pitting edema of the legs and thighs. The temperature was 99F., the pulse 76, and the Fioure 1. Posteroanterior Film of the Chat, Showing Car diac Enlargement, Pulmonary Congestion and a Pleural Re action, Together with Fluid at the Right Base. the phosphorus 3 mg., the protein-bound iodine 6 microgm., and the total iodine 8.4 microgm. per 100 ml. The sodium was 136 milliequiv., the potas sium 4 milliequiv., the chloride 92 milliequiv., and the carbon dioxide 36 milliequiv. per liter. The prothrombin content was 65 per cent, and the alka line phosphatase was 7 units. The transaminase was 25 units. A sputum culture grew out a normal flora and a few colonies of pneumococci; cytologic ex aminations for malignant cells were negative. The tuberculin skin test (second-strength PPD) was posi tive. X-ray films of the chest (Fig. 1) demonstrated moderate, nonspecific cardiac enlargement; there was a moderate right-sided pleural effusion, with some pleural thickening around the lower portion of the thorax bilaterally, more pronounced on the right; the pulmonary vessels were congested; there was no hilar lymphadenopathy. An electrocardiogram (Fig. 2) showed low voltage and atrial fibrillation, with a very regular ventricular rhythm, probably of nodal origin; there were small Q waves in Leads 1 and aVL and a QS pattern in Leads V, through V3. DOW 05880 346 THE NEW ENGLAND JOURNAL OF MEDICINE Au*. 13, 1959 A thoracentesis on the right side yielded 1100 ml. An electrocardiogram on the first hospital day showed of amber fluid: it contained 500 white cells and no change from the previous tracing. On the next AVft 'Oo rLO If'i C> I-- oo V4 AVL \ts AVF V3* Fiouu 2. 7300 red cells per cubic millimeter; the specific gravity was 1.008; the total protein was 0.43 gm. per 100 ml.; cytologic examination for tumor cells was negative. Ammonium chloride therapy was begun. day there was marked diaphoresis. A protodiastolic gallop was present for several days. Three times the patient complained of generalized abdominal pain that occurred after a bowel movement and DOW 05881 Vol. 261 No. 7 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 347 lasted for one or two hours. The pain did not recur after ammonium chloride was stopped and calcium chloride was given orally. Two bowel move ments were normal, and a third stool was watery and gave a + + guaiac test. Physical examination at that time showed no change other than signs of sion persisted, although it was diminished. There was + + + edema of the legs and feet. A bariumenema examination was negative, and an upper gas trointestinal series was normal. Episodes of hemopty sis continued. Cytologic examinations of sputum for tumor cells were negative. An electrocardiogram on .,QQ/ QQQ0 I S Fiouaa 3. less fluid in the right pleural cavity. An electrocardio gram showed disappearance of the nodal rhythm, but atrial fibrillation persisted. X-ray films of the chest showed no change. With digitalis, Mercuhydrin, Diamox and calcium chloride therapy the patient lost 20 pounds in weight. There was_ an episode of hemoptysis. On the twelfth hospital day he coughed up thick, mucoid sputum; a smear for acid-fast bacilli was negative. The temperature remained normal. The right-sided pleural effu- the fourteenth hospital day (Fig. 3) showed a normal sinus rhythm, with a PR interval of 0.26 second: the P waves were prominent in Leads 2 and V,: Q waves were present in Leads 1 and aVL and V;: through V*. On the seventeenth hospital day, about fifteen minutes after a normal bowel movement, persistent, severe, generalized, nonradiating abdominal pain suddenly developed. There was no associated dyspnea. The patient vomited about 500 ml. of light-brown DOW 05882 STO566786 348 THE NEW ENGLAND JOURNAL OF MEDICINE Aug. 13, 1959 mucus, with a few small red blood dots. Physical 1 The aorta is tortuoiis, the hilar, vessels are prominent, examination showed the neck veins to be distended and the , prominence of the pulmonary vessels ex 5 cm. above the level of the clavicles when he Was tends well out into the lungs. The question of under raised 45. The skin was cold, clammy and; lying pulmonary fibrosis has been raised, but such dusky. The pulse was 88 and thready, and 'the: changes are minimal, if present, and I am unable blood pressure was unobtainable. .Theref were^ signsi > to make a positive statement in view of the pulmo of a pleural effusion on the right side and rales at nary congestion. , I see no evidence of a pulmonary both limg bases. The heart sounds were distant, infarct or other localized active process. The left ahd: there was a gallop arid a normal sinus rhythm. leaf of the diaphragm is elevated, but that is prob The abdomen was diffusely slightly tender and rigid, ably not a significant finding. V with hypoactive bowel sounds; there was no rebound ; In the films taken four days later, after the pa tenderness.. The femoral pulses were good. An elec* tient had received diuretic therapy, the pulmonary trocardiogram showed no change except for^ non--! vessels are definitely, less engorged. Although 1100 specific STjsegment changes. Despite Aramine and ml. of fluid had been removed from the right pleural Levophed given intravenously the blobd pressure^ cavity,; the, obliteration of the costophrenic angle remained unobtainable. .Ah kbdqminal paracentesis demonstrates that a fair amount remained. Trying yielded no fluid, and an x-ray film of the abdomen was again to answer the question of an underlying fibro normal. The patient died seven hours laterv^^.^-^'#', ^j. sis, I think that minimal discrete linear shadows may be present, but I cannot interpret them as frank Differential Diagnosis * fibrosis. The heart has not changed greatly in size. Overlying the left heart border I see a little area of Dr. Myles P. Baker* : tin suirimaryj this is'-the: calcification that intrigues me, and I wonder if it problem of a sixty-five-year-old man who entered might represent calcium in a coronary artery or even the hospital in congestive heart failure; . Treat in the wall of-the left ventricle. ment with the standard measures achieved some Dr.-Paul D. White : Is there a round shadow improvement, but the progress was punctuated by near thje right base? episodes of abdominal pain and of apparently small ^ . Dr. : Wyman : I think that is. an optical illusion, = hemoptyses, and was finally brought toanabrupt and is probably a superimposition of shadows. and disastrous close by severe abdominal pain and One more chest examination, done about ten days circulatory collapse. We must find the answers to later, shows. very: little alteration. The pulmonary several questions. Regarding the edologyof the heart vessels may be!a little, more engorged, but this change disease, is there evidence in support of pneumoconio- certainly minimal. -sis with chronic.cor pulmonale, rheumatic heart dis; ease or coronary thrombosis and myocardial infarc tion? Had there been pulmonary embolism and in farction? Finally, what explanation best fits the ter- Dr. Baker : The patient was in acute circulatory failure at that time. . Dr. Wyman: I see no evidence of pulmonary edema other than a very questionable little patch minal episode? "...-V-V. . - in the right-middle-lung field. This patient certainly had an occupational history Dr. White: Does the calcification remain in the suggestive of;, pneumoconiosis. He was exposed to same place? . the danger of pulmonary asbestosis, and puhnpnary fibrosis was : repotted on ah x-ray exaininatibn two years before admission to this hospital. However; the x-ray films obtained on entry apparently did DilWyman: The calcification is still present, overlying the left heart border. I wish I could say exactly where it lies, but I can't not indicate the type of pneumoconiosis that tends The films from the barium-enema and the gastro to be a precursor of right-sided heart failure be intestinal examinations were normal Those films of cause there is no menridh of large agglomerates with the pbdomeri that were taken just before the patient fuzzy borders, although pleural thickenings were died are poor because of his precarious condition. noted. I think that the x-ray examination has much The film taken with the patient in a supine position information to offer in this case, and I should like shows no significant; distention of bowel, and that to see the films now. taken with the patient lying on the left side with Dr. Stanley M. Wyman : On the films of the the right side elevated shows no free air in the ab- chest taken on admission (Fig. l) cardiac enlarge dominal cavity. ment can be fairly well seen, and the left ventricle Dr. Baker: I think die negative findings in the in particular seems prominent The right costo- x-ray films are most' important -- the absence of phrenic angle is obliterated, probably by fluid, al-" marked pneumoconiodc processes, of mitral config though there may be underlyingpleural changes. uration of the heart and of pronounced widening of the pulmonary conus. This man's pulmonary func *Phnician,.Munchtnetu General. Hiapiul; clinical eaodate in med icine, Harvard Medical School. tion could have been severely limited by pneumoconi- DOW 05883 L8L99S01S Vol. 261 No. 7 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 349 osis, although we have little evidence of pulmonary Dr. Baker: Will you comment on the height of emphysema in either the films or the physical findings, the P waves in Leads 2 and Vs? and there is no indication in the history that he had Dr. Keevil: The P waves in Leads 2 and V! are been a pulmonary cripple before the onset of his trou certainly large enough to attract attention, although bles two months before admission. However, he did they are not above 3 mm. They suggest atrial hyper have clubbing of the fingers, which is otherwise unex trophy, although they are not nearly as striking as plained, and a high blood carbon dioxide level, which those often seen in that condition. may accompany chronic pulmonary disease. Dr. Baker: They are not as high as the P waves Before attacking the problem of the structural that are sometimes seen in chronic cor pulmonale. nature of this patient's heart disease, we should note Dr. Keevil: The P waves in chronic cor pulmo that pulmonary and pleural tuberculosis were looked nale are often more peaked and prominent. for and within reason excluded, and also that bron Dr. Baker: The developments shown by the elec chogenic carcinoma was considered and not found trocardiograms, particularly the second tracing after to be the factor responsible for the bloody sputum the return to a normal sinus rhythm, impressed me and the pleural effusion. The findings pertinent with the likelihood of a previous anterolateral myo to the heart at the time of admission include its cardial infarction. If we accept this diagnosis we large size, atrial fibrillation and the absence of hyper must make the following assumptions: that the initial tension. The conspicuous absence of murmurs vir collapse, with dyspnea but no chest pain, ten weeks tually rules out rheumatic heart disease. The labora before admission was due to either pulmonary em tory data conformed to the usual pattern of con bolism or myocardial infarction, probably the former: gestive heart failure in a patient with pitting edema that congestive heart failure, both left-sided and of the legs, presumably a large liver, basal rales and right-sided, developed on the basis of coronary- a right-sided pleural effusion, although the electro artery disease, possibly triggered by pulmonary em lyte pattern was not as disturbed as one might ex bolism; and that the profuse sweating on the second pect in a waterlogged patient who had failed to hospital day was the expression of another vascular respond to treatment with diuresis in the previous* accident, probably myocardial infarction. The pro month. Indeed, the congestive heart failure did react longation of the PR interval that appears in the to standard therapy in a somewhat encouraging tracing made a few days before death I find more fashion, although the patient's legs apparently re difficult to explain on the basis of an infarct involv mained edematous. However, three threatening ing the lower part of the septum because such a symptoms intervened: profuse sweating on the second change ordinarily accompanies right-coronary-artery hospital day followed by a gallop rhythm, indicative occlusion. of a dilated heart; abdominal pain after defecation, We come to a consideration of the possible ex with a suggestion of gastrointestinal-tract bleeding; planations for the hemoptyses in this case. A chronic and the production of bloody sputum. Each of these bronchiectatic infection would account for the bloody new features has a bearing on the cause of this sputum in the absence of pleural pain, but we have no man's heart failure. reason to suppose from his symptoms before admis May we review at this time the electrocardiograms sion that this man had been suffering from bronchi that were taken on admission and two weeks later? ectasis. However, if repeated lower-lobe pulmonary Dr. Charles S. Keevil, Jr.: The initial tracing embolism and infarction had occurred, the infarcted (Fig. 2) shows low voltage in the limb leads. Atrial areas could easily have been tucked away behind the fibrillation and a regular ventricular rate are demon basal shadows, particularly in view of the probable strated, indicating complete atrioventricular block, fluid on the right side. Therefore, I am inclined to at with the ventricular rhythm of nodal origin. In tribute the hemoptyses to pulmonary infarction rather Leads I, AVL, V* and V, there are Q waves, which than to bronchiectasis, since the previous story did are suggestive of an anterior infarction, although of not point to infection and the x-ray picture was not uncertain age. In the electrocardiogram done on characteristic of diffuse, severe pneumoconiotic the fourteenth hospital day (Fig. 3) a normal sinus changes. One might consider the prominent P waves rhythm has appeared, with a prolonged PR interval, that appeared on the second tracing a straw of evi constituting evidence of first-degree atrioventricular dence in favor of right-sided heart strain in the block. In Lead V, there is a definite small R wave face of repeated pulmonary embolism. The char that becomes smaller in Lead V,, and gives way to Q acter of the pleural fluid, with the large number of waves in Leads V* through V. This pattern gives red blood cells, is also consistent with pulmonary additional weight to the possibility o an anterior infarction. infarction, although the changes between this and This line of thought is abruptly halted by the the initial tracing may be merely due to electrode development on the seventeenth hospital day of position and not necessarily the result of an exten severe abdominal pain, which is our next diagnostic sion of the process. problem. The studies done at the time of the ter- DOU 05884 350 THE NEW ENGLAND- JOURNAL OF MEDICINE : Aug. 13, 1959 ST0566788 | minal episode yielded no evidence of rupture of the world a case of "EMFj" as they call it, that resembled abdominal aorta intraperitonekllyj acute small-bowel the ;ones that I saw in'Kampala. However, that dis] obstruction, rupture of a viscus, abdominal aortic orderdoesproduceextensive myocardial disease, not dissection or a new myocardial injury. Therewere on-acorbnarybasis,with some calcification. Calcifi- no iiew signs of trouble in the chest. The distended cation is also seen with chronic pericardial disease, neck veins raise the question of cardiac tamponade but that diagnosis wouldn't be consistent with this from hemorrhage into the'pericardial sac,1 but this, patient's history.. The calcification in this case could condition would scarcely be compatible with the have been in' an area of myocardial infarction or abdominal pain, and the venous distention in the, . possibly in a coronary artery, j neck can equallywell beexplaihedbyleft-sidedand The electrocardiogram seems consistent with se- ! right-sided heart failure. The sudden character of vere myocardial disease of coronary origin, without | the pain suggests another embolism! The fact that theaddition of ^something" like cor pulmonale. The it again followed defecation implies that the lesser low voltage is prominent in the limb leads, a finding , attacks of similar pain that had been occurring for that is more common with extensive myocardial dis- i about two weeks were more Ominous than the ease due to coronary thrombosis than any other cramps of muscular irritability due* cause. One sees it sometimes with pericardial disease plained hypocalcemia, which apparently interested .. and with myxedema, but I think those conditions are the House Staff at the time. ; ; very unlikely in this case. The original attack ten Several explanations of the terminal episode weeks previously could have been a coronary attack | come 'to mind. First of Jail, was % rembolism of because most of the dues of painless coronary throm; the superior mesenteric artenV at firit with small bosis that I have seen have been associated with emboli and finally with either; a large embolus or collapse! Therefore, this wasn't necessarily pulmoI sufficient small onw to fh^ertollaterals ineffectual? " - nary: embolism, although embolism is a strong pos- In that event, symptomatic"infarction of the small, sibility; add for that reason IJ tried to find a small bowel either did result or .would have resulted if infarct in the lung.'.Dr. Wyman doesn't,agree, but the patient had lived longer. 'Tl^^iourice'Jof'. such.:1* still a little suspicious of that area.- I believe an embolus could have been either a mural" thrombus: that the terminal event was probably embolism, in the left ventricle. consequent-'toj the ^niyocMiiial''l!V-V:;`DiL: Casteeman: Dr. Hardy, will you comment infarct that I believe this patient bad, or the pre-t onthe{Possibility ofasbestosis? viously fibriliatii^'^^.:\lt;:u.'llUso^pbible,.tlutt `VDr. -HMHUfcT.-i* Hardy:' 'This "patient could have advent of abdomiinalf pain not` long after defecation had asbestosis, and yet not as a prominent part of was due to a smashing pulmonary-artery embolism. , thehospital episode. Asbestosis would account for Under such conditions no new signs in the chest the dubbed fiiigeri and the relatively high hemo- would be expected, the examination of the abdomen, globin.andcould even" have been responsible for might be undiagnostic, as in this case, and the signs the calcification because the inhalation of asbestos of.heart strain would be similar*'td' those-described.:duuactoisiically causes marked pleuritis and even It should be emphasized that the pain of lower-lobe calcification. In diis case there may have been some pulmonary embolism;* in particular, may be referred fibrosis that developed .over a long period and thus to the upper abdomen. ". ; wasn't remarkable on the x-ray films. Asbestos bodies | My diagnoses, therefore,' are coronary-artery dis-' . were probably present throughout the lung, but these ease, with myocardial infarction and congestive heart merely reflect asbestos exposure and are not corre- failure, pulmonary embolism and infarction, partic- lated with the pulmonary fibrosis of asbestosis, which ulariy of the right lower lobe; and terminal embolism' is disabling. Since this patient hyd a sedentary job he of the superior mesenteric artery. Some evidence ^ might well have had asbestosis that was of no imof pneumoconiosismayhavebeen found, but I. don't portance'in his clinical course, believe, that this man had chronic cor pulmonale. ' Dr. Castleuan: Dr. Wyman, do you think that Dr. Benjamin Castleman : Would anyone like ; streak bf dklcificRtim eodld be in the pleura? j to offer any comments?; 'v!'f ` ;jr.DR: Wyman: It's inanodd place to be construed Dr. White: I agree that this man-probably had as in the pleura. Calcification in the pleura would extensive myocardial disease, and ceitainly coronary- lie in a plane perpendicular to the x-ray and not artery disease is a more likely diagnosis than the tangential, and therefore wquld not cast a thin linear other rare conditions that might simulate it. I was shadow, as this does,: unless an anomalous fissure was recently in Africa, atndj saw1 someJ of the patients present. I'd like toagree with Dr. White and Dr. : with endomyocardialfibrosis, which 5: frequently! Baker about the probability of infarcts in this case, found in East Africa and can give rise to extra- butT just can't recognize any evidence for infarction j ordinary myocardial changes, abnormalitiea in the in \-iew of the manvpleural changes. ! electrocardiogram and even Calcification iii the myo- * ` Dr. 'Castleman : Is there considerable pleural | cardium, but I have'never seen in this part of the thickening?1 . j*',v '' dow 05885 Voi. 261 No. 7 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 351 Dr. Wyman: I think the changes are primarily due to pleural fluid, but it is impossible to differen tiate thickening in the presence of so much fluid. Dr. Richard A. Field: Dr. Hardy, is this case at all reminiscent of the man with asbestosis and a hidden carcinoma of the lung whom you reported?1 He ended up with cardiac involvement from car cinomatous infiltration into the interstices of the myocardium. Dr. Hardy: Yes, it is, and I committed myself in the record that even with a negative sputum ex amination we might find a carcinoma of the lung in this man. We have seen 5 patients with asbestosis at this hospital, and 3 of them have been examined at autopsy and found to have bronchogenic carcinoma. The present patient had the same history of ex posure as one of our patients. Dr. White: I thought of suggesting that a malig nant process in the heart must not be forgotten, but I don't believe that it would give this electrocardio graphic pattern. Dr. Hardy: Since Dr. White has brought Africa into the discussion, I might add that I've just been abroad and learned about a high incidence of pleural mesotheliomas in asbestos workers in Africa, a report of which is about to appear.1 Dr. Castleman: We have seen 1 asbestos worker who had a mesothelioma. Dr. Kurt J. Isselbacher: How extensive was the exposure of the patient under discussion? Dr. Hardy: This man worked with asbestos for three years in a shipyard down in the holds of ships, spreading asbestos powder in a paste to cover pipes. He had previously worked in a variety of companies applying mixtures of asbestos, magnesium and other ingredients as linings for the boilers of ships. The asbestos is dry and powdery, and is mixed by the worker when he is ready to apply it. The present patient worked with asbestos alone and in the mix ture described for thirty-five years, and since some of the work had been in confined spaces he certainly had been thoroughly exposed. Dr. Walter W. Point: Wouldn't it also be pos sible to explain terminal bowel infarction without im plicating an embolus in the superior mesenteric ar tery? It should be pointed out that some patients in failure have been examined at autopsy and found to have bowel infarction with no embolus at all -- merely arteriosclerotic narrowing. Dr. Castleman : That is the usual finding in patients in congestive heart failure. Dr. Kenneth T. Bird: From the pulmonary viewpoint, the persistence of a loculated right-sided pleural effusion, with apparent clearing of the peripheral edema, is certainly a reasonable indication for a needle biopsy of the pleura, particularly in view of the known high incidence of associated car cinoma of the lung with pulmonary asbestosis. This is an easy procedure, and I think it should often be employed in conjunction with the initial thoracente sis except in patients in overt congestive heart failure or with an obvious systemic disease causing a pleural effusion. When a pleural effusion persists in this age group one has to beware of an underlying carcinoma or even of a pleural membrane that has formed around a contracted lung, leading to the chronic re current effusion described by Stead et al.s In any event, a needle biopsy of the pleura in this patient might have been helpful. Dr. Baker: Would you do a needle biopsy even if the edema hadn't cleared up? Dr. Bird: Probably not, although the biopsy find ings might still be helpful in the management of the case. Dr. White: Of course, one has to remember that right-sided hydrothorax in congestive heart failure is the last congestion to clear. Dr. Bird: Yes, but I am impressed with the known association of asbestosis with carcinoma. Dr. John H. Knowles: As a matter of cold, hard fact, I did a pleural biopsy on this patient, al though with tongue in cheek. It was negative. From the time of admission he had a very loud, persistent diastolic gallop rhythm, and he was never free of congestive heart failure. I thought that the principal problem could be summed up purely on the basis of heart disease and not asbestosis or bron chogenic carcinoma, and pulmonary embolism seemed a useful way of explaining the terminal episode. Dr. John Denovian: Dr. White, isn't it unusual for a fibrillating heart in a patient in severe failure to revert suddenly to normal sinus rhythm? Dr. White: We frequently see paroxysmal fibrilla tion in a very sick patient, with a spontaneous return to a normal rhythm. Clinical Diagnoses Coronary-artery disease. Congestive heart failure. Infarction of small bowel. Dr. Myles P. Baker's Diagnoses Coronary-artery disease. Myocardial infarction. Congestive heart failure. Pulmonary embolism and infarction, particularly in right lower lobe. Embolism of superior mesenteric artery, terminal. ? Pneumoconiosis. Anatomical Diagnoses Coronary-artery disease, with myocardial infarct, old, left ventricle and interventricular septum. Mural thrombosis, left ventricle and atrium. OOU 05886 352 THE NEW ENGLAND JOURNAL OF MEDICINE Aug. 13, 1959 Endocardial fibroelastosis, left ventricle. Arteriosclerosis of aorta, severe, with mural throm bus occluding orifice of superior mesenteric artery. Infarction of small bowel, terminal. Pulmonary infarct, organizing, right lower lobe. Pulmonary asbestosis, with pleural and subpleural fibrosis, marked, and pulmonary fibrosis, slight. Cor pulmonale. Pathological Discussion Dr. Castleman: Professor Harrison, of the Post graduate Medical School in London, is pathologist pro tempore this week, and I have given him the assignment of explaining this case. Dr. C. Victor Harrison (London, England): This is a great privilege if a little of an embarrass ment. I will put up on the blackboard so that I don't stray from the trail myself the problems that I think ought to be answered. There was first of all the incident of ten weeks before admission, followed by congestive cardiac failure; then there were the pleural effusions, the hemoptyses and finally the fatal collapse. The final collapse was due to infarction of the small intestine. The patient had an infarct that started about 1 meter below the end of the jejunum and ended about 1 meter above the ileocecal valve. There was no embolus, but he had what must have been a fantastically rare lesion -- a dreadful athero sclerosis in the aorta with a mural thrombus on top of it that had grown and flapped over the origin of the superior mesenteric artery. A completely f^hnlmis i;hing, but there it was. I am a little disturbed because the extent of the infarction did not exactly correspond to the anatomical distribution of the whole of the superior mesenteric artery. It should have gone farther around, but possibly there was some collateral circulation through the inferior mesenteric artery. Histologically, the infarction was extremely fresh, fitting very well with the short dura tion of the final episode. The heart was not very heavy, weighing only 350 gm. The size was, I think, due very largely to dilata tion. Two possibly dissociated lesions were found -- a cor pulmonale, with a right ventricular hypertrophy up to about 6 mm. in thickness at the conus, as well as a big, dilated left ventricle with a magnificent endocardial fibroelastosis! Although this man had had rheumatic lever and was in the hospital for three months, it doesn't seem to have done him much harm because the chordae tendineae of the mitral valve were of decent appearance and were quite slender, and the commissures of the aortic valve were not fused. I think we can forget the rheu matic story. There was, however, a remarkable fibro elastosis, with dilatation and relative thinning of the left ventricular wall. Considering that the heart weighed 350 gm., there must have been considerable stretching to make the wall so thin. Among the columnae cameae were some ante-mortem thrombi. Histologically, elastic stains showed a greatly thick ened layer of fibrous tissue interlaced layer by layer with elastic tissue (Fig. 4). Presumably, it had been present quite a long time. I don't know the cause of the fibroelastosis, but it was associated with diffuse ischemic heart disease. This man had calcification with about 30 per cent reduction in the lumen of the right coronary artery. In the two left coronary arteries there was very gross narrowing producing "pinhole" lumens with 80 or 90 per cent reduction. Fiourx 4. A large area of scarring was irregularly distributed beneath the thickened endocardium. The precise cor relation of the chronic ischemic heart disease, the old myocardial infarct, the left ventricular dilatation and the fibroelastosis cannot be specified, but it is possible that they were related. An explanation of the cor pulmonale is equally difficult The right lung weighed 900 gm., and there was a fair bit of edema in it. Infarction of the greater part, nearly the whole, of the right lower lobe was found, as well as a reddish-brown thrombus in the lower-lobe arteries corresponding to it. The left lung had a few little scars, but no apparent ST0566790 DOW 05887 16 /Qocnic VoL 261 No. 7 CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL 353 infarcts. Both lungs were fairly firm to the touch, but the prosector did not describe any chronic inter stitial fibrosis of the type one would expect in asbestosis. About 1 liter of fluid was present in each pleural sac. The visceral pleura was considerably thickened, but showed only patchy adhesions to the fibrosis, which quite honestly I would not have rec ognized as due to asbestosis if I had not found the scanty asbestos bodies. When we examined sections of the lung, we found that the impacted embolus in the right lower lobe had organized to an appreciable depth. I think there is little doubt that the embolus had been there for some time, and it seems fair to say that the original attack ten weeks previously was due to this embolus (Fig. 5). The rest of the lung was macroscopically free from infarcts, and the vessels of dissectable size did not show emboli, but microscopically in a few arteries there were recently organizing emboli. Dr. White: Where did the pulmonary emboli come from? Dr. Harrison: The legs were examined as far as the popliteal space, Dr. White, but nothing was found. My own suspicion is that the source was in the calf because the pulmonary emboli were such little chaps. The only other findings were passive congestion of the liver, chronic cholecystitis with some calculi, and a little right adrenal adenoma. Dr. White: Did you find pulmonary or pleural calcification? Dr. Harrison : We found calcification, only in the coronary arteries. It is described as severe. Dr. White: That linear calcification shown in the x-ray film may have been in a coronary artery. Figure 5. parietal pleura on each side. I think we can assume that the pleural fibrosis was due to asbestosis. Micro scopically, we did find asbestos bodies, but they were not at all frequent -- they had to be looked for. There were also odd little spots of rather nonspecific References 1. liaelbacher, K. J.,, Klaus, H.t and Hardy, H. L. Asbestosis and bronchogenic carcinoma: report of one autopsied case and review of available literature. Am. /. Mtd. 11:721-732, 1953. 2. Johannesburg Conference on Pneumoconiosis, Johannesburg, South Africa, February, 1959, (in press). 3. Stead. W. W., Ekhenholx, A., and Stausi, H. K. Operative and pathologic findings in twenty-four patients with syndrome of idio pathic pleurisy with effusion, presumably tuberculous. Am. Rto. Thfierr. 71:473-502, 1955. DOW 05888 354 THE NEW ENGLAND JOURNAL OF MEDICINE Aug. 13, 1959 The New England Journal of Medicine Official Organ of The Massachusetts Medical Society Owned by the Society and Published Weekly under the Jurisdiction or the Committee on Publications Richard M. Smith, M.D., Ckairman Oliver Cope, M.D. James M. 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MicaoFU.it volumes available to regular subscribers through Univer sity Microfilms, 313 N. First Street, Ann Arbor, Michigan. Communications should be addressed to the New England /earns! of Medicine, 8 Fenway, Boston 15, Massachusetts. Telephone CO 6-7510 MEDICAL EDUCATION AND THE WMA The Second World Conference on Medical Educa tion, the first having been held in London in 1953, has already had a preliminary bout of advance pub licity in the Journal of April 16, 1959. In this second such conference to be held, after a decent interval of six years, medical educators and others interested in medical education from fifty countries are expected to join forces in Chicago's Palmer House from August 29 to September 4, under the sponsorship of the World Medical Association, the World Health Or ganization, the Council for International Organiza tions of Medical Sciences, and the International As sociation of Universities. President Eisenhower, who helped organize the National Fund for Medical Edu cation during his presidency of Columbia University, is not only patron of the Conference, according to a recent release, but has been invited to attend it. No fewer than 125 speakers are scheduled to par ticipate in the Conference, as are delegations from both the Union of Soviet Socialist Republics and Poland. Neither of these countries is represented in the World Medical Association. The Conference, which, through the wizardry of modem technics o ', communication, will be carried on simultaneously in English, French and Spanish, will be divided into four sections. Each section will devote two and a half days to its allotted subject -- Section I to Basic Clinical Training for All Doctors, Section II to Advanced Education for General and Specialty Practice, Section III to The Development of Teachers and Investigators, and Section IV to Continuing Medical Education. Various social events will reach their zenith, although presumably in the evening, at an official Conference dinner. The President of the Conference will be Dr. Ray mond B. Allen, chancellor of the University of Cali fornia in Los Angeles. He will be aided by two deputy presidents: Dr. Ray F. Farquharson, Sir John and Lady Eaton Professor of Medicine, University of Toronto, and Dr. Victor Johnson, director of the Mayo Foundation for Medical Education and Re search of the University of Minnesota's Graduate School of Medicine. According to Dr. Allen, "It is the purpose of this Second World Conference on Medical Education to pass on to the young in mind and heart the experience and learning of the ages" -- certainly a commendable objective. At the end of the Conference those who are capable of further intellectual absorption will move on to Montread, possibly by water, since the passage can now be accomplished without an overland portage, to reconvene as the Thirteenth General Assembly of the World Medical Association at the Queen Eliza beth Hotel, across the border. Here, on Monday afternoon, September 7, the Assembly will open with the tenth annual medical editors' conference, which ST0566792 DOW 05889