Medicine, Owens College. RHIEUMATIC PERICARDITIS. G(ENTLEMEN,-We had recently in the wards a case of rheumatic pericarditis in a young man who had been the subject of acute rheumatism three years ago, and who had again suffered from slight arthritis of the knees about a fortnight before admission to hospital on November 17th last. fIe had gone about his work, however till November ioth. He did not seem to have had any chest pain till the gth, when he had severe pain on the left side, specially

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... n taking a deep breath, and he noticed that he was short of breath. He had had attacks of chorea at the ages of 8, 9, and iI respectively. There could be no doubt, then, that he was a thoroughly rheumatic subject, and had had endocarditis in all probability. When I examined him on November i8th, the day after admission, I was surprised to find, besides the physical signs of a moderate left pleural effusion, not so extensive as to prevent the left border of the cardiac dulness being defined so far, a huge precordial dull area, and such a dull area as would imply enormousl enlargement of the heart, were it due to the size of the heart, and of the shape that is assumed by a true cardiac dulness only in rare cases, as Sir William Gull long ago pointed out, of general dilatation of the heart, in which the dilatation of the left ventricle, and that of the right auricle and of the infundibulum of the right ventricle are all extreme. But this lad's history pointed to his cardiac disability being comparatively recent. When I listened over the heart what struck me most was the feebleness of cardiac sound of any kind. All I could make out, in fact, was the presence of a slight systolic murmur in the mitral and tricuspid areas. I could hear no friction. We had then a remarkable degree of silence over the heart, a greatly increased area of dulness, and a very feeble systolic murmur in the tricuspid and mitral areas. The natural inference to be drawn from this condition, of course, was that there was pericardial effasion. The absence of friction sound was of course remarkable, as there was every reason to believe that if pericardial effusion were present it was of inflammatory origin in view of the rheumatic but otherwise good history of the patient. It was on Saturday (November i8th, I899) that I examined the case with the result related. On the following Monday on my arrival I was informed that our resident medical officer, Dr. Melland, had detected pericardial friction sound, an observation most creditable to his acuteness of observation, because the sound, as some of you can bear me out in saying, was of the feeblest, and, moreover, was limited to a small area, I should think about an inch and a-half in its vertical and an inch in its transverse diameter. This area was situated at the left border of the lower part of the sternum. During the following couple of days the friction increased in loudness and extent of area of audibleness, and then it declined and ceased. But if any doubt had remained as to the diagnosis of pericardial effusion, it was soon dissipated by the rapid diminution of the precordial area of dulness till it approached practically normal limits. The pleuritic effasion-which in this case waas evidently genuine-moreover soon likewise receded. (You will see the meaning of my use of the word " genuine " later.) The mitral murmur remained, and became associated with a reduplicate diastolic sound. Evidently the murmur was old, and the result of the first rheumatic attack, or more likely of the earlier chorea. The tricuspid murmur was no doubt due to the debility of the cardiac muscle only. Unfortunately the patient absconded four days ago, but, to do him justice, he took this action in a good cause: to join his militia regiment. PERICARDIAL EFFUSION WITHOUT FRICTION. Sometimes, though rarely, you have to make the diagnosis 5 of pericardial effusion without any assistance whatsoever from auscultation, that is to say, pericardial friction may never be heardfrom first to last. Again, paradoxically, shall relate to you a case in which friction was audible over the heart, and yet in which it could hardly be said there was pericarditis present at all, so trivial evidently was the process that temporarily annulled the smoothness of the gliding surfaces. First, as to pericardial effusion without friction sound. When I was resident medical officer here, an old woman with chronic Bright's disease, but without any general dropsy, was admitted to the wards. It was noticed that she always sat up in bed, leaning forwards, and was evidently unable to lie down owing to the dyspncea it occasioned her. Percussion of the chest showed a precordial dull area of enormous size, extending upwards and to both right and left sides. The heart sounds were feeble, but there was neither friction sound nor murmur audible. There was no febrile disturbance. In a few days the dull area had become greatly diminished, while neither friction nor murmur had been heard. The patient could now lie down comfortably. Evidently this was a case of one of the copious effusions into sacs or loose tissues that are so apt to occur in the course of Bright's disease. So much for effusion into the pericardium without any evidence of inflammation whatsoever. I next relate to you a case to show that there may be severe pericarditis with great effasion and fibrinous exudation, and yet, again, there may be no friction sound audible throughout the period of observation, extending over weeks, while the debility of the heart muscle in consequence of the contiguous inflammation and the embarrassment of its movement occasioned by the effusion may determine the ordinary effects of heart failure on the general circulation. History.-Mrs. M. A. T., aged 27, was admitted to the Mat chester RoIal Infirmary on September 24th, x89I, suffering from dyspncea, dropsy of the lower extremities and of the right upper extremity, and from ascites. Her illness, which had commenced several weeks before admission, had followed recent conflnement. She had never had rheumatic fever or chorea. The temperature was moderately febrile. Condition on Admission.-The upper right extremity was found to be much swollen, and the swelling was stated to have been preceded by pain referred to the region of the corresponding clavicle and shoulder. The area of precordial dulness was enormously increased, but its extension upwards was proportionately less than that to the right and left sides, especially the latter, the left border of the dull area passing in a slanting direction across the axillary region, the base of theleft lung being at the time resonant. Both sounds of the heart were audible and free from murmur. There was no trace of friction sound. The liver was enlarged' and tender-no doubt from venous stasis-and there were moist sounds at the bases of the lungs. There was no albumen in the urine. The patient was aniemie and cachectic-looking. After-History.-Slight hiemoptysis occurred from time to time, and the pulmonary bubbling sounds became more abundant, while the bases of the lungs became impaired. Post-mortem Examination.-The pericardium was hugely distended with light amber-coloured fluid. Both the visceral and parietal layers were the seat of diffuse haemorrhagic fibrinous pericarditis. The heart itself had a patchy, shaggy, rough, brownish appearance, due to the irregularly deposited flaky lymph which, adherent below, had its upper layers blood stained. This lymph was deposited on both surfaces of the pericardium, and was particularly marked around the origin of the large vessels at the base of the heart aDd over the auricles and around the pulmonary veins. The fibrinous deposit was fairly firmly adherent and had evidently been of some standing. The heart was small and presented no valve lesion. There was some fluid in both pleurae and infarets in both lungs. The pelvic organs were matted together and surrounded by inflammatory material. Thrombi were found in several veins, including the right subclavian. The abdomen contained ascitic fluid, the liver was enlarged and presented appearance of well-marked passive congestion. Kidneys normal in size and general appearance, except for slight congestion. This case, then, was an instance of the fact that even fibrinous pericarditis may be present, run a subacute course, and occasion great effusion and yet be unaccompanied by any friction sound. In the case narrated the septicwemic source seemed to lie in the pelvis. The next fact with regard to pericarditis to which I wish to call your attention is that cases of the worst type of pericarditis not rarely run their fatal course without a trace of friction sound from first to last. I refer to suppurative cases of septieemie origin.