Pleural and pericardial effusions in a 50-year-old woman.

Abstract

HomeCirculationVol. 93, No. 12Pleural and Pericardial Effusions in a 50-Year-Old Woman Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBPleural and Pericardial Effusions in a 50-Year-Old Woman Eddy Barasch, Ramesh Hariharan, Ping Fai Wong and Kent A. Heck Eddy BaraschEddy Barasch From the Department of Internal Medicine (E.B., R.H., P.F.W.) and the Department of Pathology and Laboratory Medicine (K.A.H.), University of Texas Health Science Center at Houston. Search for more papers by this author , Ramesh HariharanRamesh Hariharan From the Department of Internal Medicine (E.B., R.H., P.F.W.) and the Department of Pathology and Laboratory Medicine (K.A.H.), University of Texas Health Science Center at Houston. Search for more papers by this author , Ping Fai WongPing Fai Wong From the Department of Internal Medicine (E.B., R.H., P.F.W.) and the Department of Pathology and Laboratory Medicine (K.A.H.), University of Texas Health Science Center at Houston. Search for more papers by this author and Kent A. HeckKent A. Heck From the Department of Internal Medicine (E.B., R.H., P.F.W.) and the Department of Pathology and Laboratory Medicine (K.A.H.), University of Texas Health Science Center at Houston. Search for more papers by this author Originally published15 Jun 1996https://doi.org/10.1161/01.CIR.93.12.2197Circulation. 1996;93:2197–2202Case Presentation (Ramesh Hariharan, MD)A previously healthy 50-year-old Chinese woman presented with a low-grade fever, a generalized headache, and chest pain of 2 to 3 weeks’ duration. She described intermittent sharp chest pain over the precordium that intensified when she lay down and shortness of breath after minimal exertion. Despite having lost her appetite, she had gained ≈10 pounds during the past month and had noticed ankle swelling. She denied having had arthralgia or skin rash and had not experienced any nocturnal dyspnea, wheezing, cough, expectoration, or hemoptysis. She had visited her relatives in the Middle East 6 months earlier, but her past medical history was uneventful. She had taken acetaminophen (Tylenol) tablets and a Chinese herbal preparation, but her symptoms continued.On physical examination, she appeared weak and ill. Her temperature was 36.7°C (98.0°F), and her pulse was 110 beats per minute, regular, and had normal volume and character. Her blood pressure was 115/70 mm Hg, which decreased to 90/70 mm Hg on inspiration; her respiratory rate was 22 breaths per minute. Carotid pulsations were normal. Jugular veins were distended to the angle of the mandible when the patient sat upright, but no further venous engorgement was noted on inspiration. There was mild mucosal pallor, but the oropharynx was otherwise normal. The first and second heart sounds were normal, and there were no clicks or gallops. A superficial scratchy systolic sound was heard intermittently over the left lower sternal region. Dullness to percussion, scattered inspiratory crackles, and diminished air entry were evident over both lung bases. Abdominal examination demonstrated a soft, tender liver palpable 2 cm below the right costal margin. Her pelvis and rectum showed no abnormality. A stool guaiac test was negative. Neurological examination was normal. There was moderate pitting edema below the level of the knees.Results of the initial laboratory studies appear in Tables 1 and 2, and the results of chest roentgenography, electrocardiography, and echocardiography are presented in the “Clinical Discussion.” A CT scan of the chest showed bilateral pleural effusions. An abdominal CT scan was normal.The patient was admitted to the coronary care unit and underwent diagnostic pleural aspiration and pericardiocentesis. One liter of amber-colored pericardial fluid was aspirated. Results of the analysis of pleural and pericardial fluid appear in Table 3. A diagnostic procedure was performed.Hemodynamic Measurements During Pericardiocentesis (Ping Fai Wong, MD)A radial arterial catheter and a balloon-tipped pulmonary artery catheter were placed for hemodynamic monitoring before pericardiocentesis. An arterial blood pressure tracing showed that blood pressure decreased from 155/75 to 125/55 mm Hg during inspiration, which corresponded to a pulsus paradoxus of 30 mm Hg (Fig 1). The pulmonary artery catheter was inserted via the right internal jugular vein. Pressure measurements were made in the right atrium, right ventricle, main pulmonary artery, and the pulmonary capillary wedge position while the catheter was being advanced. Right atrial pressure was elevated, with an a wave of 17 mm Hg, a v wave of 14 mm Hg, and a mean pressure of 14 mm Hg. Early diastolic y descent was absent. The right ventricular pressure tracing showed a respiratory variation ranging from 32/16 mm Hg during expiration to 40/18 mm Hg during inspiration. The mean pulmonary capillary wedge pressure was 18 mm Hg. After the pericardial catheter was successfully placed, the mean intrapericardial pressure measured 13 mm Hg. A simultaneous mean pulmonary artery pressure measured 15 mm Hg, nearly equivalent to the intrapericardial pressure. One liter of serosanguinous fluid was removed from the pericardial cavity. A subsequent blood pressure tracing showed resolution of the pulsus paradoxus, and the mean intrapericardial pressure fell to −4 mm Hg (Fig 2).Clinical Discussion (Eddy Barasch, MD)This was a middle-aged woman who presented to the hospital with cardiac tamponade and bilateral pleural effusions. She had low-grade fever, shortness of breath, and a pleuritic type of chest pain for several weeks before admission. The relevant blood laboratory data were hyponatremia, an abnormal albumin/globulin ratio, high haptoglobin, mild anemia with thrombocytosis, and a moderately elevated erythrocyte sedimentation rate. The serology report was notable for an antinuclear antibody titer of 1:80 with a speckled pattern, low total serum hemolytic complement, and negative anti-dsDNA antibody. The hepatitis B core antibody test was positive, and the hepatitis B surface antibody test was negative.The patient’s ECG showed sinus tachycardia and low-voltage QRS complexes in the standard leads, with diffuse, nonspecific ST-segment and T-wave changes. The chest roentgenogram revealed bilateral pleural effusions and cardiomegaly. Unfortunately, the first roentgenographic study was lost; Fig 3 shows the chest roentgenogram taken after pericardiocentesis. The fluid removed during pericardiocentesis had the characteristics of an exudate with lymphocytosis. A pleural tap was performed and revealed a transudate rich in lymphocytes.A transthoracic echocardiogram showed cardiac chambers of normal size and wall thickness. Global left and right ventricular systolic function was increased. A “swinging” heart movement resulted from a large amount of pericardial fluid (Fig 4). Numerous fibrinous strands were attached to the parietal pericardium. Early diastolic right ventricular collapse (Fig 5) and late diastolic right atrial free wall compression were observed. The inferior vena cava was dilated, and its diameter did not vary with respiration. On pulsed Doppler examination of the mitral inflow, a 40% inspiratory decrease of peak E-wave velocity with a corresponding 60% increase of peak E-wave velocity of the tricuspid inflow was detected. Hepatic vein flow showed only x waves during expiration and apnea. Together, these findings strongly suggest the presence of cardiac tamponade.Cardiac tamponade occurs when diastolic filling is impaired by an absolute rise in intrapericardial pressure. The diagnosis is based on clinical examination, which reveals elevated systemic venous pressure, tachycardia, dyspnea, and pulsus paradoxus. The presence of a paradoxical arterial pulsation is insufficient to diagnose cardiac tamponade, but its absence does not rule out the diagnosis. Pulsus paradoxus may be present in patients with chronic obstructive pulmonary disease, massive pulmonary embolism, constrictive pericarditis, or right ventricular infarction; these conditions may induce changes in both left and right ventricular filling that also depend on the respiratory phase. In the presence of cardiac tamponade, pulsus paradoxus may be absent if the patient (1) has severe left ventricular systolic dysfunction or severe aortic regurgitation in which left ventricular diastolic pressure may equal intrapericardial pressure, (2) has an atrial septal defect in which the respiratory changes in ventricular filling are significantly diminished, or (3) is being mechanically ventilated, in which the inspiratory increase in intrathoracic pressure may abolish the mechanism that gives rise to pulsus paradoxus.12The echocardiographic signs of cardiac tamponade are early diastolic collapse of the right ventricular free wall, late diastolic compression of the right atrium, and persistently dilated venae cavae. On pulse-wave Doppler, one can observe a decline on inspiration of ≈40% of peak early diastolic filling wave (E wave) velocity of the mitral inflow, an 80% increase in peak E-wave velocity of the tricuspid inflow, and an 85% increase in the isovolumetric relaxation time of the left ventricle. Furthermore, y waves may be absent from hepatic vein flow during apnea or expiration. Right ventricular hypertrophy, changes in the right ventricle and/or atrium compliance, or an increase in intravascular volume may abolish these Doppler echocardiographic signs.3 Low-pressure tamponade with hypovolemia and localized tamponade, especially in the period immediately after cardiac surgery, are distinct categories.The fluid in the patient’s pericardial and pleural spaces had probably been accumulating for several weeks before her admission to the hospital. Because of the amount of pericardial fluid, a recent acute event, such as an acute myocardial infarction with acute or subacute rupture of the left ventricular free wall, was unlikely. A slowly developing process is more likely to have enabled the accumulation of a large amount of fluid in the distensible pericardial sac while simultaneously producing the slow development of symptoms. Rapid accumulation of even 200 mL of fluid may produce cardiac tamponade. Other causes for tamponade, such as cardiac surgery, chest trauma, or the rupture of an ascending aortic aneurysm, were excluded by the patient’s echocardiographic data and medical history.A primary or secondary malignant process may induce the formation of a large pericardial effusion. However, primary pericardial malignant tumors are rare,4 and their solid or cystic structure was not identified by echocardiography in this patient. Lung, breast, or gastrointestinal carcinoma; melanoma; leukemia; and Hodgkin’s or non-Hodgkin’s lymphoma may involve the pericardium and are the most frequent causes of massive pericardial effusion.5 Lung carcinoma with pleural and pericardial involvement would already have been in an advanced stage, but the patient had no symptoms or signs of this disease. In addition, the chest roentgenogram did not disclose any pulmonary masses. The patient had no palpable breast lumps or axillary and/or supraclavicular adenopathy. The chest roentgenogram and negative CT scans of the chest and abdomen revealed no evidence of lymphomas. Because the patient was Chinese, hepatoma should be considered among the potential malignancies because of its increased prevalence, secondary to hepatitis B infection, among Asians. However, her symptoms and the results of her liver function tests made this diagnosis unlikely.Pericarditis is the presenting symptom in 6% of women with systemic lupus erythematosus (SLE).6 Except for serositis, however, no symptoms in this patient suggested SLE. In addition, the patient denied taking lupus-inducing drugs such as hydralazine or procainamide. Antinuclear antibodies are very sensitive but not specific for SLE; they may also increase with age or with viral or chronic infections. The patient’s speckled antinuclear antibody pattern reflected the presence of antibodies directed against non-DNA nuclear constituents. The anti-dsDNA antibody test, which is relatively specific for SLE, was negative. The anti–extractable nuclear antigen assay detects antibodies against two extractable nuclear antigens: the Sm and RNP antigens.7 Antibodies against the Sm antigen are characteristic for SLE, and a high titer of anti-RNP antibodies is the hallmark of mixed connective tissue disease, in which pleuropericardial involvement occurs in ≈25% of patients and pericarditis is the most common manifestation.8 Pericardial effusion is also found in 40% of patients with progressive systemic sclerosis,9 but no clinical or laboratory data support such a diagnosis in this patient. Other diseases in which pleuropericarditis may be a presenting symptom, such as rheumatic fever or rheumatoid arthritis, are also unlikely in her case. Metabolic disorders such as renal failure and myxedema, two potential causes of massive pericardial effusion, are essentially ruled out by the normal kidney and thyroid function tests.Could this woman have sarcoidosis? The disease is not prevalent among Asians, and the pericardium is rarely affected. Most patients are <40 years old, and the lungs are almost always involved. The patient also lacks the multisystem organ manifestations that are characteristic of this disease.The massive pericardial effusion in this patient may have been caused by an infectious agent. Viral infections, especially coxsackievirus B and echovirus 8, may cause pericarditis with clinical features that cannot be distinguished from idiopathic pericarditis. The diagnosis of viral infection is strongly supported by the greater than fourfold rise in serial neutralizing viral antibody titers during the initial 3 weeks of the illness. Pericardial effusion and constrictive pericarditis are potential consequences of such an infection. The symptoms of this patient, however, would be unusual in a benign viral infection. Pericardial effusion is one of the most frequent cardiac manifestations in AIDS patients, but the patient was HIV negative.Among fungal infections, histoplasmosis is most often associated with cardiac tamponade,10 but it usually resolves spontaneously within 2 weeks. The patient’s record does not indicate that she lived or traveled in an area where histoplasmosis is endemic, and her other symptoms and laboratory data do not support such a diagnosis. Other fungal diseases, such as blastomycosis, coccidioidomycosis, aspergillosis, and candidiasis, are usually lethal in a relatively short time.Tuberculosis is the cause of 7% of cardiac tamponade cases, and it should be considered in any case in which pericarditis is not rapidly self-limiting.11 In the United States, between 1985 and 1990 the tuberculosis case rate increased by 15.8%. A third of the world’s population is infected,12 and women are more frequently affected than men. Patients who have tuberculous pericarditis usually have a focus of infection elsewhere in the body. In a recent retrospective study, the main symptoms of tuberculous pericarditis were chest pain, dyspnea, cough, weight loss, and increased perspiration.13 The reported clinical signs, in order of decreasing frequency, were fever, pericardial friction rub, pericardial effusion, cardiac tamponade, and pleural effusion.Tuberculous pericarditis is associated with pleural effusion in 61% of patients.13 What suggested tuberculous pericardial effusion in our patient? The patient may have had a reactivated infection of tuberculosis contracted many years ago in China. She might also have contracted tuberculosis during her air travel or her stay in the Middle East. Transmission of Mycobacterium tuberculosis has been associated with air travel,14 and there has been a resurgence of tuberculosis in both the United States and the countries of the Middle East. The patient’s low-grade fever and loss of appetite and the laboratory data that suggest a chronic inflammatory or infectious process, together with the predominance of lymphocytes in both pleural and pericardial fluid, might point toward tuberculosis as the cause of her cardiac tamponade.Serum hyponatremia may result from low antidiuretic hormone secretion or adrenal involvement by the infectious process. A morning serum cortisol level should help to rule out adrenal insufficiency. The relatively high glucose concentration in both pericardial and pleural fluid is an unusual finding in tuberculosis. A purified protein derivative test was not done. The test is positive in 40% of patients with idiopathic pericarditis and negative in 25% of patients with tuberculous pericarditis.11 An adenosine deaminase level >45 U/L in both the pericardial and pleural fluids might suggest tuberculosis. False-positive results have been described in neoplastic pericarditis. In our patient, adenosine deaminase was not measured. Today, available polymerase chain reaction techniques have a 97% accuracy and enable a diagnosis of tuberculosis in 48 hours by amplification of DNA from as little as 1 μL of pericardial fluid1516 ; however, such a test was not done in our patient.Pericardioscopy and thoracoscopy followed by pericardial and epicardial biopsy are relatively new techniques for diagnosing the cause of pericardial effusion. Protuberances on the epicardium are specific for tuberculous pericardial effusion and neoplastic disorders. The pericardial fluid seldom yields tubercle bacilli during early phases of the disease: <50% of patients have positive acid-fast stains.1718 In nearly 100% of the cases in which tubercle bacilli are found in the pericardial tissue, tuberculosis is the diagnosis.1519 The presence of caseating granuloma is nonspecific, because it is also found in fungal infections.Because the incidence of constrictive pericarditis in cardiac tamponade cases is between 30% and 57% within 2 to 4 months of diagnosis, if the tamponade recurs after 4 to 6 weeks of therapy, pericardiectomy is indicated.1318 The use of corticosteroids is controversial and apparently does not decrease the incidence of constriction but was reported to decrease mortality by threefold, from 14% to 3%.20In summary, I believe that this patient had cardiac tamponade, probably caused by tuberculosis; a malignant process is a possible but less likely cause.Pathological Findings (Kent A. Heck, MD)The diagnostic procedure was a pericardial biopsy. The specimen consisted of small, irregular fragments of soft tissue that measured, in aggregate, 3.2 cm. The biopsy demonstrated marked thickening of the pericardium, with the innermost surface layered with extensive granulation tissue accompanied by lymphohistiocytic and plasmacytic infiltrates (Fig 6). Well-formed caseating granulomata occupied the central portion of the specimen (Fig 7). Special stains confirmed the presence of acid-fast organisms in peripherally localized histiocytes. The histopathologic features are indicative of granulomatous pericarditis secondary to acid-fast bacilli, consistent with Mycobacterium tuberculosis. Because microbiological cultures for Mycobacterium failed to grow organisms, further characterization of the subtype of Mycobacterium could not be established.Tuberculous pericarditis may be histologically classified into three stages: acute, subacute, and chronic. The histopathologic features in this patient correspond to the subacute stage, in which granulomatous inflammation is a predominant feature. Caseation necrosis is usually encountered and is surrounded by Langhans’-type histiocytes. Occasionally, caseous necrosis may be exuberant and cover the surface of the heart. Acid-fast stains and cultures are more likely to be confirmatory during the subacute stage. Constrictive pericarditis, which has an incidence of ≈30% in this disorder,21 may arise in either of the two latter stages.In one report, pericardial biopsy yielded positive results in 84% of patients with positive pericardial fluid microbiological cultures.20 Other reports record a lower diagnostic yield.1922 The differences between the results of these studies may be partially attributed to the stage at which biopsies were obtained. The efficacy of polymerase chain reaction for confirming tuberculous pericardial effusions is being investigated, and this test may serve as a further adjunct in diagnosis.Clinical Follow-upThe patient was treated with a combination of isoniazid, rifampicin, ethambutol, and pyrazinamide; she has nearly completed this antituberculous therapy. She improved significantly both subjectively and objectively and returned to her usual activities.Final DiagnosisTuberculous pericarditis.Download figureDownload PowerPoint Figure 1. Before pericardiocentesis: Marked variation of systolic blood pressure with respiration, indicating pulsus paradoxus. The mean pulmonary capillary wedge pressure and the mean intrapericardial pressure approached equalization of pressure at the end of the tracing. Upper tracing, Radial arterial blood pressure; middle tracing, pulmonary capillary wedge pressure; lower tracing, intrapericardial pressure.Download figureDownload PowerPoint Figure 2. After pericardiocentesis: Pulsus paradoxus resolved. The intrapericardial pressure fell to −4 mm Hg. Equalization of pressure disappeared.Download figureDownload PowerPoint Figure 3. A portable anteroposterior chest roentgenogram taken after pericardiocentesis shows an enlarged cardiac silhouette, pulmonary venous vascular congestion, and bilateral pleural effusions. A Swan-Ganz catheter and a catheter in the pericardial space can be seen.Download figureDownload PowerPoint Figure 4. Parasternal short-axis view below the level of the papillary muscles showing a massive pericardial effusion surrounding the heart, with fibrinous strand (arrow).Download figureDownload PowerPoint Figure 5. M-mode echocardiogram with the cursor at the level of mitral valve leaflets showing early diastolic collapse of the right ventricular free wall (thick arrow), which corresponds to the E-point on the anterior mitral leaflet opening (thin arrow).Download figureDownload PowerPoint Figure 6. Low-power (×100) hematoxylin-eosin–stained photomicrograph of markedly thickened and inflamed pericardium.Download figureDownload PowerPoint Figure 7. High-power (×400) hematoxylin-eosin–stained photomicrograph of central pericardium with granulomatous inflammation surrounded by Langhans’-type giant cells (arrow). Table 1. Blood Chemistry StudiesValueReference RangeSodium, mmol/L134135-145Potassium, mmol/L4.83.5-5.0Chloride, mmol/L9795-105Bicarbonate, mmol/L2324-32Blood urea nitrogen, mg/dL810-20Creatinine, mg/dL0.60.5-1.4Glucose, mg/dL9875-115Total protein, g/dL7.15.5-8.0Albumin, g/dL2.33.5-5.5Bilirubin, mg/dL1.00.3-1.0Aspartate aminotransferase, U/L830-35Alanine aminotransferase, U/L590-35Serum alkaline phosphatase, U/L20830-120Lactate dehydrogenase, U/mL43925-100Calcium, mg/dL8.59-10.5Phosphorus, mg/dL4.33-4.5Lipid profileNormalThyroid function testsNormal Table 2. Hematologic and Other Laboratory DataValueReference RangeHemoglobin, g/dL10.112-16Hematocrit, %32.137-48Leukocyte count, ×103/mm312.54.3-10.8Platelet count, ×103/mm3482130-400Prothrombin timeNormalPartial thromboplastin timeNormalErythrocyte sedimentation rate, mm/h600-30UrinalysisNormalBlood culturesNegativeSerologyRheumatoid factorNegativeAntinuclear antibodyPositive, 1:80 with a speckled patternAnti-dsDNA antibodyNegativeComplement, C3 and C4NormalCH100, U/mL38HIVNegativeHBcAbPositiveHBsAgNegativeCH100 indicates total hemolytic complement; HBcAb, hepatitis B core antibody; and HBsAg, hepatitis B surface antigen. Table 3. Analysis of Pleural and Pericardial FluidsPleural FluidPericardial FluidGlucose, mg/dL153128Total protein, g/dL2.95.1LDH, U/mL124488Cholesterol, mg/dL4956RBC/mm370015 500WBC/mm322002900Differential count, %Lymphocytes9084Histiocytes88Neutrophils28Gram stainNegativeNegativeAFB stainNegativeNegativeCultures of fungi and AFBNo growthNo growthCytologyNegativeNegativeLDH indicates lactate dehydrogenase; RBC, red blood cell count; WBC, white blood cell count; and AFB, acid-fast bacillus.Presented March 13, 1995, at the University of Texas Health Science Center Medical School at Houston. FootnotesCorrespondence to Eddy Barasch, MD, University of Texas Health Science Center at Houston, MSB 1.257, 6431 Fannin, Houston, TX 77030. References 1 Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol.1970; 26:480-489. CrossrefMedlineGoogle Scholar2 Reddy SP, Curtiss EL. Cardiac tamponade. Cardiol Clin.1990; 8:627-637.CrossrefMedlineGoogle Scholar3 Fowler NO. Cardiac tamponade: a clinical or an echocardiographic diagnosis? Circulation.1993; 87:1738-1741. CrossrefMedlineGoogle Scholar4 Pascual MA, Povar J, Munoz JR, Cabeza FG, Portoles A, Casado IL, Lore B, Ibbara F. Pericardial mesothelioma. Rev Esp Cardiol.1989; 42:559-561. MedlineGoogle Scholar5 Mukai K, Shinkai T, Tominaga K, Shimosato Y. The incidence of secondary tumors of the heart and pericardium: a ten-year study. Jpn J Clin Oncol.1988; 18:195-201. MedlineGoogle Scholar6 Fowler NO. The Pericardium in Health and Disease. Mt Kisco, NY: Futura; 1965. Google Scholar7 Fye KH, Sack KE. Rheumatic diseases. In: Stites DP, Stobo JD, Wells JV, eds. Basic and Clinical Immunology. Norwalk, Conn: Appleton & Lange; 1987:356-384. Google Scholar8 Prakash UBS, Luthra HS, Divertie MB. Intrathoracic manifestations of mixed connective tissue disease. Mayo Clin Proc.1985; 60:813-821. CrossrefMedlineGoogle Scholar9 Smith JW, Clements PJ, Levisman J, Furst D, Ross M. Echocardiographic features of progressive systemic sclerosis: correlation with hemodynamic and postmortem studies. Am J Med.1979; 66:28-33. CrossrefMedlineGoogle Scholar10 Wheat LJ, Stein L, Corya BC, Wass JL, Norton JA, Grider K, Slama TG, French ML, Kohler RB. Pericarditis as a manifestation of histoplasmosis during two large urban outbreaks. Medicine.1983; 62:110-119. CrossrefMedlineGoogle Scholar11 Permanyer-Miralda G, Sagristá-Salueda J, Soler-Soler J. Primary acute pericarditis: a prospective series of 231 consecutive patients. Am J Cardiol.1985; 56:623-629. CrossrefMedlineGoogle Scholar12 Daniel TM. Tuberculosis. In: Isselbacher KJ, ed. Harrison’s Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994:710-718. Google Scholar13 Sagristá-Salueda J, Permanyer-Miralda G, Soler-Soler J. Tuberculous pericarditis: ten years’ experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol.1988; 11:724-728. CrossrefMedlineGoogle Scholar14 Driver CR, Valway SE, Morgan M, Onorato IM, Castro KG. Transmission of Mycobacterium tuberculosis associated with air travel. JAMA.1994; 272:1031-1035. CrossrefMedlineGoogle Scholar15 Maisch B. Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology, new diagnostic imaging methods, and treatment. Curr Opin Cardiol.1994; 9:379-388. CrossrefMedlineGoogle Scholar16 Seino Y, Ikeda U, Kawaguichi K, Yamamoto K, Sekiguchi H, Nakayama T, Tkewaki S, Okubo A, Nagai R, Yyazaki Y, Schimada K. Tuberculous pericarditis presumably diagnosed by polymerase chain analysis. Am Heart J.1993; 126:249-251. CrossrefMedlineGoogle Scholar17 Fowler NO, Manitsas GT. Infectious pericarditis. Prog Cardiovasc Dis.1973; 16:323-328. CrossrefMedlineGoogle Scholar18 Fowler NO. Tuberculous pericarditis. JAMA.1991; 226:99-103. Google Scholar19 Rooney JJ, Crocco JA, Lyons HA. Tuberculous pericarditis. Ann Intern Med.1970; 72:73-78. CrossrefMedlineGoogle Scholar20 Strang JI, Kakaza HH, Gibson DG, Allen BW, Mitchison DA, Evans DJ, Girling DJ, Nunn AJ, Fox W. Controlled clinical trial of complete open surgical drainage and of prednisolone in treatment of tuberculous pericardial effusion in Transkei. Lancet.1988; 2:759-764. CrossrefMedlineGoogle Scholar21 Gleckman RA. Nonviral infectious pericarditis. In: Spodick DH, ed. Pericardial Diseases. Philadelphia, Pa: FA Davis; 1976:159-176. Google Scholar22 Hageman GH, D’Esopo ND, Glenn WL. Tuberculosis of the pericardium: a long-term analysis of forty-four proved cases. N Engl J Med.1964; 270:327-332. CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Schattner A (2021) Associated Pleural and Pericardial Effusions: An Extensive Differential Explored, The American Journal of Medicine, 10.1016/j.amjmed.2020.11.001, 134:4, (435-443.e5), Online publication date: 1-Apr-2021. Cherian G, Uthaman B, Salama A, Habashy A, Khan N and Cherian J (2016) Tuberculous Pericardial Effusion: Features, Tamponade, and Computed Tomography, Angiology, 10.1177/000331970405500410, 55:4, (431-440), Online publication date: 1-Jul-2004. June 15, 1996Vol 93, Issue 12 Advertisement Article InformationMetrics Copyright © 1996 by American Heart Associationhttps://doi.org/10.1161/01.CIR.93.12.2197 Originally publishedJune 15, 1996 KeywordsClinicopathological Conferencesechocardiographypericarditiscardiac tamponade Advertisement