Cardiac Tamponade with Nonhemorrhagic Pericardial Fluid Complicating Dressler's Syndrome

required. 1 The hematologic details of this second case are not given. Four survivors of pulmonary mucormy~ sis have been reported, 4 but in none of these was the underlying illness hematologic and in all, complete surgical resection was performed. Many factors acting in concert in this patient may have set the stage for fungal infections in general, including the presence of cigarette lung disease, chronic antibiotic treatment, and circulating immunologically abnormal cells. 5 In a large series of leukemic patients with mucormycosis, granulocytopenia, high dose prednisone therapy and hyperglycemia were prevalent. 6 No one of these particular parameters could be suggested as more important than the other two, and all three were present in this case. Amphotericin B was selected as a potentially useful antibiotic because some strains of mucormycosis have been sensitive to it in vitro. 3 While this drug is often used alone or as an adjunct to surgery in the rhin~ cerebral form of mucormycosis, no consistent clinical responses are noted. This may reflect irreversible host debilitation usually associated with diabetes. Alternatively, the drugs may fail to penetrate the infected tissue because the nourishing arteries are thrombosed and occluded by the proliferating hyphae. This same mechanism may ultimately limit the usefulness of 5-8uorocyt~ sine, although some strains of Mucor are sensitive to this antibiotic. 7 This patient's recovery, then, cannot be attributed with assurance to the amphotericin B therapy. That the blood disease could be better controlled was most important in this patient. An aggressive supportive course with respiratory care, around-the-clock nursing, blood products, and antibiotics was elected. In pursuit of a specific tissue diagnosis, open lung piopsy was performed. This encouraged the completion of a full course of amphotericin B, a potentially nephrotoxic drug, and discouraged therapy with other antibiotics. Finally, with better control of his blood disease and with attenuated steroid doses, his immune defenses may have improved. At best, it is difficult to evaluate the relative importance of these therapeutic maneuvers, but with this patient, we recognize -that pulmonary mucormycosis can be cured with prudent jpedical management without surgical resection. REFERENCES

1 Meyer RD: Mucormycosis-its changing status. Crit Rev Clin Lab Sci 4:21--51, 1973 2 Bogard BN : ·Pulmonary mucormycosis. N Engl J Med 286:606, 1972 3 Medoff G, Kobayashi GS : Pulmonary mucormycosis. N Engl J Med 286:86-87, 1972 4 Ga1e AM, Kleitsch WP: Solitary pulmonary nodule due to phycomycosis (mucormycosis). Chest 62:752-755, 1972 5 Dameshek W : Chronic lymphocytic leukemia-an accumulative disease of immunologically incompetent lymphocytes. Blood 29 : 566~, 1967 6 Meyer RD, Rosen P, Armstrong D: Phycomycosis complicating leukemia and lymphoma. Ann lnt Med 77:871-879, 1972 7 Bennett JE : Chemotherapy of systemic mycosis. N Engl J Med 290:30-32; 320-323, 1974

CHEST, 72: 1, JULY, 1977

Cardiac Tamponade with Nonhemorrhagic Pericardial Fluid Complicating Dressler's Syndrome* Franklin T. Tew, M.D.; John A. Mantle, M.D., F.C.C.P.; Richard 0. Rwsell, Jr., F.C.C.P.; and Charles E. Rackley, M.D., F.C.C.P.

A 39-year-old man developed cardiac tamponade witli Dressler's syndrome four weeks after an inferior myocardial lnfardion. Treatment of the tamponade by pericardiocentesls on two occasions produced serous Ouid. The pericardial effusion cleared with short-term therapy with corticosteroids and the prolonged use of indome~ acin. postmyocardial infarction syndrome, or Dressler's T hesyndrome, has been recognized since Dressler's reports in 19551 and 1956. 2 Pericardia! fiuid obtained at autopsy3 or at pericardiocentesis2 · ' in patients with Dressler's syndrome has varied from serous 2 to hemorrhagic. 2 - 4 Dressler2 reported that one patient with the syndrome who was receiving antico~t drugs died with hemorrhagic tamponade. 2 A second patient, who was not receiving anticoagulant drugs, may have been developing cardiac tamponade but improved symptomatically following withdrawal of 30 ml of "intensely hemorrhagic fiuid" by pericardiocentesis.• We have seen a patient at the University of Alabama Medical Center in Birmingham who had cardiac tamponade six weeks after an inferior myocardial infarction. Although the patient was receiving an anticoagulant drug, the pericardia! fiuid was serous in appearance. We believe that he represents the first reported patient with cardiac tamponade as a result of the postmyocardial infarction syndrome with nonhemorrhagic pericardia! fiuid.

CASE fu:roRT A 39-year-old white man had smoked 2l packs of cigarettes per day for 20 years and had a famUy history of premature coronary arterial disease. On July 2, 1975, he experienced the onset of acute chest pain, and an electrocardiogram in his local hospital's emergency room sho~ an inferior myocardial infarction. The patient suffered a cardiorespiratory arrest but was successfully resuscitated. On July 19, after an uncomplicated course of hospitalization, he was discharged on a regimen of diazepam, digoxin for possible con°From the Division of Cardiology, Department of Medicine, University of Alabama Medical Center; Birmingham. Supported in part by the Specialized Center of Research for Ischemic Heart Disease contract 1P17HL17667-02, the Cardiovascular Research and Training Center program project grant HL 11,310 (Division of Heart and Vascular Diseases, National Heart and Lung Institute), National Institutes of Health grant T01LM00154, and the Clinical Research Unit grant MO-RR00032-13 (General -Clinical Research Centers Program, Division of Research Resources, National Institutes of Health).

CARDIAC TAMPONADE 93

gestive heart failure, and warfarin ( Coumadin). Evidence of pericarditis by symptoms, signs, or ECG was not noted during that hospitalization. The patient convalesced uneventfully at home until Aug 8, 1975, when he experienced the onset of severe anterior chest pain that radiated to his neck, shoulders, and arms. Although the pain was constant, it was aggravated by inspiration and a supine position and required parenteral administration of narcotics for relief. Laboratory studies showed a white blood cell count (WBC) of 16,900/cu mm, with 92 percent polymorphonuclear leukocytes; a hematocrit reading of 45 percent; a prothrombin time of 24 seconds (with control being 13 seconds); normal levels of electrolytes, serum glutamic-oxa1oacetic transaminase (SGOT), lactic dehydrogenase, and creatine phosphokinase; and normal findings on urinalysis. The ECG showed low voltage, an old inferior myocardial infarction, and frequent premature ventricular contractions. The patient was treated with digoxin, warfarin ( Coumadin) , hydromorphone, indomethacin, and, in addition, procainamide hydrochloride for the frequent premature ventricular contractions. The dull, aching pleuritic pain continued for four days, when the patient developed shock with blood pressure of 90/70 mm Hg and pulse rate of 120 beats per minute; his skin was cool and clammy. Intravenous administration of metaraminol and fluids increased the blood pressure to 128/100 mm Hg. A determination for paradoxic pulse was not performed. The chest x-ray film revealed an enlarged cardiac silhouette. Pericardiocentesis produced 95 ml of straw-colored fluid, which showed no growth on routine culture but was not studied further. Immediately, the patient felt better, the blood pressure increased to 200/110 mm Hg, and therapy with metaraminol was discontinued. Three hours later, the blood pressure fell to 98/58 mm Hg, and again the patient had the appearance of shock. A repeat pericardiocentesis produced 230 ml of cloudy, nonbloody fluid and resulted in relief of the syndrome of shock. Again, the blood pressure increased, and the patient improved. He was referred to the Myocardial Infarction Research Unit at the University of Alabama Medical Center in Birmingham for further evaluation and treatment. Upon arrival, the patient was slightly cool and diaphoretic, with blood pressure of 100/80 mm Hg without paradox, pulse rate 80 beats per minute, respiratory rate of 18/min, and oral temperature 37•C (98.6•F) . There was no jugular venous distention at 30•, and bibasilar rales were noted. A two-component pericardia! friction rub was heard, without other abnormal sounds. Laboratory data included a WBC of 13,600/cu mm, with a slight leftward shift; hematocrit reading of 43 percent; prothrombin time of 20.8 seconds (with control being 10.3 seconds); SGOT level: 88 units/ ml; and a serum glutamic-pyruvic transaminase level SGPT of 105 units/mi. The results of his other laboratory studies, including levels of electrolytes, creatinine, glucose, calcium, and bilirubin, serum electrophoresis, antinuclear antibody test, lupus erythematosus preparation, VDRL, and urinalysis, were normal (a titer for antistreptolysin 0 was not performed). The ECG showed normal voltage, an old inferior myocardial infarction, and nonspecific ST-T wave changes. Echocardiogram revealed a posterior pericardia! effusion and normal movements of the mitral valve. Cardiomegaly with a "water-bottle" configuration was preSent on the chest x-ray film ( Fig 1 ) . ASwan-Ganz balloon flotation catheter was inserted, and the pulm9nary arterial pressure was found to be 19/ 14 mm Hg (mean, 16 mm Hg), with a mean right

94 TEW ET AL

FIGURE 1. Erect, portable six-foot posteroanterior chest x-ray film obtained on admission to University Hospital in August 1975. There is "water-bottle" configuration of heart. Cardiothoracic ratio is 0.60. atrial pressure of 9 mm Hg. &-Methylprednisolone 21-sodium succinate ( Solu-Medrol) was administered as a 100-mg intravenous bolus, and oral therapy with indomethacin ( 25 mg every six hours) and with prednisone ( 25 mg thrice daily) was begun. Vitamin K was administered intravenously to reverse the prolonged prothrombin time. The dosage of prednisone was gradually tapered over a ten-day period, but therapy with indomethacin was continued. The patient improved clinically, the pericardia! friction rub disappeared after one week, and the heart size decreased on the chest x-ray film. Right and left cardiac catheterization was performed on Aug 21, 1975, and the hemodynamic data, including cardiac output, were normal. On the biplane left ventricular angio-

-FIGURE 2. Routine posteroanterior chest x-ray film in December 1975. Lungs and heart appear normal. Cardiothoracic ratio is 0.47.

CHEST, 72: 1, JULY, 1977

gram, there was apical dyskinesis. Coronary arteriograms revealed three-vessel coronary disease. The patient was discharged on a regimen of indomethacin ( 25 mg every six hours) and quinidine gluconate ( 300 mg every six hours) for premature ventricular contractions. ,..If angina pectoris occurred, coronary arterial saphenous vein bypass grafting was to be considered. After discharge, and while receiving therapy with indomethacin, the patient had some recurrence of the pericardia! chest pain, which improved with short-term treatment with corticosteroids. In December 1975, the patient was asymptomatic, had returned to normal activity, and was taking only quinidine gluconate ( 330 mg thrice daily). Serial chest x-ray films in October and December have shown continued diminution in the heart size to a normal cardiothoracic ratio (Fig 2). Findings from the physical examination were unremarkable, and the patient was specifically without paradoxical pulse, murmur, rub, gallops, or pericardia! knock.

was nonhemorrhagic. Also, it is doubtful that therapy with procainamide hydrochloride was an etiologic factor, since the patient had received it for only four days after developing symptoms of pericarditis, and he had a negative antinuclear antibody test. Although the patient made a gratifying initial response to the intravenous administration of metaraminol and fluids, a more favorable hemodynamic response might have been expected if therapy with isoproterenol, in addition to intravenous fluids, had been used. 14 Prompt recognition and treatment of the tamp:made by the referring physicians was life-saving. Therapy with indomethacin and corticosteroids may have been of benefit in preventing a recurrence. ACKNOWLEDGMENTS: We would like to acknowledge Dr. R. T. Long and Dr. R. 0. Underwood fcx recognizing the initially treating and referring the patient to tamponade us.

ana

DISCUSSION

Dressler's syndrome, or the postmyocardial infarction syndrome, occurs in up to 3 to 4 percent of patients after myocardial infarction. 2 •5 •6 The syndrome includes any or all of the following: fever, pleuritis, pneumonitis, and pericarditis. It usually occurs at any time from two weeks to several months after acute myocardial infarction. 2 •1 • 8 Theoretic and investigative studies regarding the etiology of Dressler's syndrome have suggested that autoimmune mechanisms, with or without a latent or acute viral infection, are causative.9·13 The syndrome is usually benign, and its course is self-limited, although relapses may occur. 1 ·2,8 Therapy usually consists of administration of salicylates or indomethacin, with corticosteroids being reserved for severe or relapsing cases. We found no previous reports of cardiac tamponade developing in a patient with Dressler's syndrome who had a nonhemorrhagic effusion. We believe that our patient had Dressler's syndrome for the following reasons: (I) he had sustained a well-documented myocardial infarction four weeks previously; ( 2) there was no history suggestive of an antecedent viral illness; ( 3) the description of his chest pain in August was compatible with pericarditis, and it persisted for four days without electrocardiographic or enzymatic changes characteristic of a myocardial infarction; ( 4) the patient had no historical, physical, or laboratory evidence of any other cardiac or systemic disease; and ( 5) there was definite pericardia} effusion. The elevated right atrial pressure with normal jugular veins is difficult to interpret; this was not a single spurious measurement or technical error but was noted on several occasions. The presence of an elevated mean right atrial pressure and nondistended jugular veins illustrates a potential pitfall in reliance on observation of neck veins as a sign of elevated central venous pressure. The rales noted were most likely secondary to atelectasis or to pneumonitis, which is commonly seen in Dressler's syndrome. Support for the possibility of pneumonitis is suggested by review of the chest x-ray film on admission (Fig I). It is quite unlikely that administration of warfarin contributed to or caused the effusion, since the fluid

CHEST, 72: 1, JUlY, 1977

1 Dressler W: A complication of myocardial infarction resembling idiopathic, recurrent benign pericarditis. Circulation 12:697, 1955 (abstract) 2 Dressler W: The post-myocardial infarction syndrome: A report on 44 cases. Arch Intern Med 103:28-42, 1956 3 Levin EJ, Bryh D: Dressler syndrome (post-myocardial infarction syndrome) . Radiology 87:731-734, 1966 4 Dressler W, Yurkofsky GD, Starr MC: Hemorrhagic pericarditis, pleurisy and pneumonia complicating recent myocardial infarction. Am Heart J 54:42-4.9, 1957 5 Niarchos AP, McKendrich CS: Prognosis of pericarditis after acute myocardial infarction. Br Heart J 35:49-54, 1973 6 Das SK, Cassidy JT, Petty RE: The significance of heartreactive antibodies in heart disease. Chest 66:179-181, 1974 7 Likoff W: Pericarditis complicating myocardial infarction. Am J Cardiol7:69-72, I96I 8 Dressler W : Management of pericarditis secondary to myocardial infarction. Prog Cardiovasc Dis 3:134-139, 1960

9 Vender Geld H: Anti-heart antibodies in the post pericardiotomy and the post myocardial infarction syndrome. Lancet 2:617-618, 1964 10 Kaplan MH, Fringley JD: Autoimmunity to the heart in cardiac disease. Am J Cardiol24:459-473, 1969 11 Fowler NO: Autoimmune heart disease (editorial) . Circulation 44:159-161, 1971 12 Versey JMB, Gabriel R: Soluble-complex formation after myocardial infarction. Lancet 2:493-494, I974 13 Burch GE: Colcolough HL: Postcardiotomy and postinfarction syndrome: A theory. Am Heart J 80:290-291, 1970 14 Fowler NO, Holmes JC : Hemodynamic effects of isoproterenol and norepinephrine in cardiac tamponade. ·J Clin Invest 48:502-507, 1969

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