Tuberculous pericarditis

INTRODUCTION — Tuberculous pericarditis is an important complication of tuberculosis (TB); the diagnosis can be difficult to establish and is often delayed or missed, resulting in late complications such as constrictive pericarditis and increased mortality [1]. Options for management of advanced disease are limited.

Issues related to evaluation and management of tuberculous pericarditis will be reviewed here. General issues related to diagnosis and management of TB are discussed separately. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Diagnosis of pulmonary tuberculosis in adults".)

EPIDEMIOLOGY — Tuberculous pericarditis occurs in approximately 1 to 2 percent of patients with pulmonary tuberculosis (TB) [2]. In one series of 294 immunocompetent patients in Spain with acute pericarditis (in whom the cause was not apparent at initial evaluation), tuberculous pericarditis was diagnosed in 13 patients (4 percent of cases) [3]. Cardiac tamponade was observed in five patients, and constrictive pericarditis developed in six patients.

In countries with a high prevalence of human immunodeficiency virus (HIV) infection, there has been a dramatic increase in tuberculous pericarditis. In one 1994 series of Tanzanian patients with large pericardial effusions, for example, all of the patients with HIV infection were found to have tuberculous pericarditis [4].

The incidence of tuberculous pericarditis in the United States has declined with the concomitant decline in prevalence of TB [5-7]. However, in areas of the United States with large immigrant populations from TB-endemic countries, extrapulmonary TB, including tuberculous pericarditis, is still seen with some frequency [8-10].

PATHOGENESIS — Pericardial infection with Mycobacterium tuberculosis may occur via extension of infection from the lung or tracheobronchial tree, adjacent lymph nodes, spine, sternum, or via miliary spread. In many patients, tuberculous pericarditis represents reactivation disease, and the primary focus of infection may not be apparent.

Four pathological stages of tuberculous pericarditis have been described [11,12]:

●Fibrinous exudation with polymorphonuclear leukocytosis, abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells

●Serosanguineous effusion with lymphocytic exudate and high protein concentration; tubercle bacilli present in low concentrations

●Absorption of effusion with granulomatous caseation and pericardial thickening with subsequent fibrosis

●Constrictive scarring; fibrosing visceral and parietal pericardium contracts on the cardiac chambers and may become calcified, leading to constrictive pericarditis, which impedes diastolic filling.

Tuberculous pericarditis may progress from one phase to the next or any one or series of phases may be present without the others. Rarely, the initial phase is identified by biopsy or autopsy as isolated granulomas in the pericardium. In general, the earliest recognizable phase of pericardial infection is the second phase consisting of lymphocytic effusion; the inflammatory process likely reflects a hypersensitivity reaction to antigens present in the tubercle bacilli. The diagnostic yield of pericardial fluid and tissue for acid-fast smear and culture is generally highest in the effusive stage [13,14]. In the absence of treatment, resorption of the effusion with resolution of symptoms occurs over two to four weeks in approximately 50 percent of cases [15]. Subsequently, constriction may or may not occur; the course of disease is variable.

Effusive constrictive pericarditis may develop in some patients. This is characterized by concurrent pericardial effusion and pericardial constriction; diastolic pressure persists after removal of pericardial fluid because of persistent constriction. The mechanism consists of visceral pericardial thickening (due in part to healing with fibrosis and calcification), which leads to constriction, and the pressure of pericardial fluid may lead to cardiac tamponade. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy".)

CLINICAL MANIFESTATIONS

Symptoms — The symptoms of tuberculous pericarditis can be nonspecific; fever, weight loss, and night sweats generally precede cardiopulmonary complaints [1]. The nature of symptoms depends upon the stage of infection, extent of tuberculous disease outside the pericardium, and degree of pericardial involvement.

Adults with tuberculous pericarditis generally present with clinical findings typical of pericarditis or cardiac tamponade. In most cases, tuberculous pericarditis is insidious; the onset is acute in up to 25 percent of cases [11]. In one series, the following frequency of symptoms was noted [16]:

●Cough – 94 percent

●Dyspnea – 88 percent

●Fever – 84 percent

●Chest pain (often pleuritic) – 76 percent

●Night sweats – 56 percent

●Orthopnea – 53 percent

●Weight loss – 48 percent

However, the frequency of these symptoms is variable. In another report including 41 patients, only 40 to 50 percent had cough, dyspnea, or chest pain, while 70 percent had fever [17]. Right upper abdominal pain due to liver congestion has also been described [18]. Children with tuberculous pericarditis often present with nonspecific symptoms such as failure to thrive or cough [19].

A minority of patients present in the late stages of illness with findings typical of constrictive pericarditis. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy".)

Physical findings — Physical findings usually observed with tuberculous pericarditis include fever, tachycardia, increased jugular venous pressure, hepatomegaly, ascites, and peripheral edema [16]. A pericardial friction rub and distant heart sounds are often observed. Cardiac tamponade was present in 10 percent of patients with tuberculous pericardial effusion in a study conducted in South Africa [20]. In advanced disease, signs of heart failure may be observed [21]. However, these findings do not distinguish tuberculous pericarditis from other causes (infectious and noninfectious) of pericarditis. (See 'Differential diagnosis' below.)

Potential complications of tuberculous pericarditis include constrictive pericarditis, effusive pericarditis, and cardiac tamponade. The physiology of the various pericardial compressive syndromes is discussed in detail separately. (See "Pericardial effusion: Approach to diagnosis" and "Constrictive pericarditis: Diagnostic evaluation" and "Cardiac tamponade".)

Constrictive pericarditis — Constrictive pericarditis occurs in 30 to 60 percent of patients, despite prompt antituberculous therapy and use of corticosteroids [3]. Patients with HIV infection may be less likely to develop constriction in the setting of tuberculous pericarditis than patients without HIV infection; further study is needed to clarify this potential finding [22].

The physical examination may be notable for Kussmaul's sign (lack of an inspiratory decline in jugular venous pressure), elevated and distended jugular veins with a prominent Y descent (the second inward deflection of the internal jugular pulse due to diastolic inflow of blood into the right ventricle), and a pericardial knock (rare). (See "Constrictive pericarditis: Clinical features and causes", section on 'Key signs of constrictive pericarditis' and "Constrictive pericarditis: Clinical features and causes", section on 'Constrictive pericarditis'.)

Pulsus paradoxus (a decrease in systolic blood pressure by >10 mmHg on inspiration) is a sign of tamponade and does not indicate constrictive physiology, since, in the setting of constriction, the inspiratory decline in pressure is not transmitted to the right heart chambers. (See "Pulsus paradoxus in pericardial disease".)

Effusive constrictive pericarditis — Effusive constrictive pericarditis is characterized by pericardial constriction and pericardial effusion and has been studied most in southern Africa. The constrictive hemodynamics persist even after removal of the effusion. Effusive constrictive pericarditis can be difficult to distinguish from constrictive pericarditis; clinical clues include:

●Pulsus paradoxus

●Absence of a pericardial knock

●A less dominant Y descent than expected

●Frequent absence of Kussmaul's sign

The diagnosis of effusive constrictive pericarditis often becomes apparent during pericardiocentesis in patients initially thought to have tamponade. Despite lowering the pericardial pressure to normal, the elevated right atrial pressure persists in association with the development of Y dominance and impaired respiratory variation [23]. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy" and "Constrictive pericarditis: Clinical features and causes", section on 'Effusive-constrictive pericarditis' and "Constrictive pericarditis: Diagnostic evaluation", section on 'Effusive-constrictive pericarditis'.)

Myopericarditis — Many cases of pericarditis have concurrent myocardial involvement; this is referred to as "myopericarditis" when the predominant pathology is pericarditis. Myopericarditis in the setting of tuberculous pericarditis refers to pericarditis with concurrent abnormal cardiac ejection fraction and/or elevated serum levels of cardiac enzymes. In one study, myopericarditis among patients with tuberculous pericarditis was associated with HIV-related immunosuppression [24]. Electrocardiographic ST elevation may be observed, particularly when the peripheral CD4 count is low. However, it is challenging to distinguish myopericarditis due to tuberculosis from preexisting HIV-associated cardiomyopathy (which also occurs among individuals with low CD4 counts) in the absence of myocardial biopsy. The prognosis of patients with tuberculous myopericarditis did not appear to differ from those with tuberculous pericarditis without myopericarditis. (See "Myopericarditis".)

Cardiac tamponade — The physical examination in cardiac tamponade may demonstrate hypotension with a narrow pulse pressure, reflecting the limited stroke volume. Other findings include sinus tachycardia (permitting at least partial maintenance of cardiac output), elevated jugular venous pressure, pulsus paradoxus, and ascites. (See "Cardiac tamponade", section on 'Diagnosis'.)

Patients presenting with ascites in the absence of other findings may be erroneously thought to have cirrhosis. The main clue to the diagnosis of tamponade is elevation of jugular venous pressure, which is not seen in cirrhosis unless there is tense ascites (which may increase venous pressure slightly) [25].

DIAGNOSIS

General principles — Tuberculous pericarditis should be considered in the evaluation of patients with pericarditis who do not have a self-limited course, in the setting of risk factors for tuberculosis (TB) exposure [3]. The diagnosis is established by detection of tubercle bacilli in smear or culture of pericardial fluid and/or by detection of tubercle bacilli or caseating granulomata on histological examination of the pericardium [12]. Tuberculous pericarditis is considered likely in the setting of pericarditis with tuberculosis demonstrated elsewhere in the body, lymphocytic pericardial exudate with elevated adenosine deaminase (ADA) level, and/or clinical response to antituberculous therapy.

Initial evaluation — Initial evaluation consists of chest radiography, echocardiography, and evaluation of sputum for acid-fast bacilli (AFB) smear and culture. Additional studies may include computed tomography (CT) and/or magnetic resonance imaging (MRI) of the chest in areas where available to help resolve local anatomy and other possible organ involvement. A tuberculin skin test (TST) and/or interferon gamma release assay (IGRA) may or may not be helpful; a positive test result in a patient with TB risks may support the clinical impression. In many cases, pericardiocentesis is also warranted. (See 'Pericardiocentesis' below.)

The likelihood of detecting evidence of pulmonary tuberculosis on chest radiograph in the setting of tuberculous pericarditis is variable and ranges from 32 to 80 percent of cases [3,16,19,20,26]. Cardiac findings on chest radiograph in the setting of tuberculous pericarditis include enlarged cardiac shadow in more than 90 percent of cases; in the setting of chronic pericarditis, pericardial calcification may be observed. Pleural effusions may also be seen [3,26]. Interpretation of chest radiography in the setting of tuberculosis is discussed further separately. (See "Diagnosis of pulmonary tuberculosis in adults".)

Echocardiography is an accurate and noninvasive tool for establishing the presence of a pericardial effusion and to detect signs of tamponade (movie 1 and movie 2). The role of echocardiography in evaluation of pericardial effusion is discussed further separately. (See "Pericardial effusion: Approach to diagnosis".)

A thorough evaluation for tuberculosis should also include evaluation for presence of AFB in the sputum smear and culture; positive results have been observed in 10 to 55 percent of cases [3,27]. Alternative approaches include AFB smear, culture of gastric washings (in children) and urine [12], and examination for peripheral lymph nodes, particularly in children [19].

CT and/or MRI of the chest can demonstrate pericardial effusion, pericardial thickening, and lymphadenopathy [28]. Characteristic lymph node involvement is mediastinal and tracheobronchial (with hilar sparing) and >10 mm with hypodense centers and matting.

The electrocardiogram is abnormal in virtually all cases of tuberculous pericardial effusion, usually in the form of nonspecific ST-T wave changes. Electrocardiographic findings seen in pericarditis and pericardial effusion are discussed in detail separately (waveform 1). (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Electrocardiogram' and "Pericardial effusion: Approach to diagnosis", section on 'ECG findings'.)

TSTs and IGRAs are useful for detecting TB infection but do not distinguish between latent TB infection and active TB disease. The TST is positive in most immunocompetent patients with tuberculous pericarditis (85 percent of cases) [4,29]. In contrast, the TST is often negative in patients with HIV infection and tuberculous pericarditis [4].

Data on use of IGRAs in the setting of tuberculous pericarditis are limited, but, like the skin test, they do not distinguish between latent TB infection and active TB disease so are unlikely to be diagnostically helpful in TB-endemic areas [30]. (See 'Pericardiocentesis' below.)

Pericardiocentesis — Pericardiocentesis is warranted for routine evaluation of suspected tuberculous pericarditis; cardiac tamponade is an absolute indication for pericardiocentesis [15]. Open drainage (rather than pericardiocentesis) does not appear to influence need for pericardiectomy or reduce the likelihood of subsequent constriction or death [20]. The diagnostic yield of pericardial fluid is generally highest in the effusive stage [13,14]. (See 'Pathogenesis' above.)

The technique for pericardiocentesis is described separately. The fluid should be evaluated for cell count, protein concentration, lactate dehydrogenase concentration, acid-fast smear/culture, Gram stain and bacterial culture, adenosine deaminase concentration, and cytology. Tuberculous pericardial effusions are typically exudative and characterized by high protein content and increased leukocyte count, with a predominance of lymphocytes and monocytes [31,32]. In one study, a pericardial lymphocyte/neutrophil ratio ≥1.0 had high sensitivity, specificity, and positive predictive value for diagnosis of tuberculous cause of pericardial effusion (73, 79, and 86 percent, respectively) [31]. The percentage of lymphocytes in the pericardial fluid is characteristically lower in patients with HIV infection than in patients without HIV infection patients (36 versus 52 percent) [31]. Light's criteria for exudative pleural effusions may also be used to establish the presence of pericardial exudate [33,34]. (See "Pericardial effusion: Approach to diagnosis" and "Pleural fluid analysis in adults with a pleural effusion".)

AFB are seen on smear of pericardial fluid in 40 to 60 percent of patients with tuberculous pericarditis; the yield is increased by culture [16,20,31]. In one study including 162 patients with tuberculous pericarditis (half of whom also had HIV infection), pericardial fluid cultures were positive in 56 percent of cases [31]. In individual patients with tuberculous pericarditis, the diagnostic tools available may be positive singly or in combination.

Polymerase chain reaction (PCR) for mycobacterial deoxyribonucleic acid (DNA) in pericardial fluid may also be useful for diagnosis of tuberculous pericarditis [31,35-37]. However, most studies on the validity of PCR in the diagnosis of extrapulmonary tuberculosis have involved relatively small numbers of patients and have been performed in endemic areas; the utility of PCR in nonendemic areas has not been studied extensively. Data regarding the performance of the GeneXpert test for tuberculous pericarditis are limited; one study including 176 extrapulmonary specimens that included pericardial fluid demonstrated overall sensitivity and specificity of 52 and 100 percent, respectively [38]. GeneXpert may be a useful adjunctive diagnostic; however, it is not approved by the US Food and Drug Administration for use with pericardial fluid and would not replace mycobacterial culture or histopathology in diagnosis of tuberculous pericarditis. (See "Diagnosis of pulmonary tuberculosis in adults".)

Measurement of pericardial ADA level can be useful for diagnosis of tuberculous pericarditis [31,37,39]. Different cutoff levels for ADA activity have been suggested as indicative of disease, ranging from 30 to 60 units/L. In one study of 64 patients in South Africa with tuberculous pericarditis, the median ADA level was 72 units/L (range 10 to 304 units/L); this level was significantly higher than the ADA levels in patients with other etiologies of pericarditis. Using a cutoff ADA level of 30 units/L, the authors calculated a sensitivity of 94 percent, specificity of 68 percent, and positive predictive value of 80 percent [40]. Another study noted a positive correlation between high pericardial ADA levels and subsequent development of constrictive pericarditis [41]. Lower ADA levels have been observed in patients with HIV infection and severe CD4 lymphocyte depletion [27]. ADA testing is limited to specialized laboratories, and proper interpretation requires consideration of pretest probability for tuberculous pericarditis; in areas where the prevalence of tuberculosis is low, the utility of the pericardial ADA test is correspondingly low.

Data on use of interferon-gamma testing for evaluation of pericardial fluid are limited. In one study including 162 patients with tuberculous pericarditis in South Africa, the sensitivity of pericardial interferon-gamma was 73 percent; approximately half of patients had HIV infection, but test results were not affected by HIV status [31]. The mean interferon-gamma concentrations in HIV-uninfected tuberculous effusions, HIV-infected tuberculous effusions, and nontuberculous effusions were 781, 624, and 27 pg/mL, respectively.

Pericardial biopsy — The diagnosis may remain uncertain after evaluation, as described in the preceding sections, including evaluation for tubercle bacilli in sputum, pericardial fluid, and other body sites. In such cases, options for next diagnostic steps include right scalene lymph node biopsy (if lymphadenopathy is present) and/or pericardial biopsy. For patients in areas where TB is endemic and/or for whom clinical suspicion of tuberculous pericarditis is high, pericardial biopsy is not required prior to initiation of empiric antituberculous therapy. In areas where TB is not endemic, a pericardial biopsy is warranted for patients with duration of illness >3 weeks in the absence of definitive diagnosis via the other investigations described above [12]. (See 'Initial evaluation' above and 'Pericardiocentesis' above.)

Earlier studies suggested that tuberculous pericarditis was more readily diagnosed from pericardial biopsy than pericardial fluid alone [42]. Histology findings are frequently nonspecific; in one prospective series including 78 patients with tuberculous pericarditis, characteristic granulomatous changes on histopathology were observed in 53 percent of cases [20]. Histology appears to be most important for cases in which no pericardial fluid can be obtained [43].

Tissues obtained by biopsy should be stained for AFB and examined for histological evidence of granulomatous inflammation. The sensitivity of pericardial biopsy for diagnosis of tuberculous pericarditis ranges from 10 to 64 percent [41,42]. Therefore, a normal pericardial biopsy specimen does not exclude tuberculous pericarditis; in some cases, examination of the full pericardium is required to establish the diagnosis [44]. Culture of pericardial tissue provides some additional diagnostic yield over culture of pericardial fluid alone; in one study including 15 patients with tuberculous pericarditis, polymerase chain reaction testing for M. tuberculosis was more sensitive when performed on pericardial tissue than pericardial fluid (80 versus 15 percent, respectively) [45]. The diagnostic yield of pericardial tissue is generally highest in the effusive stage [13,14]. (See 'Pathogenesis' above.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of tuberculous pericarditis includes pericarditis due to other infectious etiologies (eg, viral, bacterial, fungal pathogens) as well as noninfectious entities including sarcoidosis, malignancy, radiation damage, trauma, and hemopericardium. The clinical approach to these diseases is discussed separately (see related topics).

Patients with both tamponade and inflammation have a greater likelihood of tuberculosis infection than patients with either tamponade or inflammation alone [46]. In endemic areas, tuberculous pericarditis is an important cause of heart failure; it is less common than rheumatic heart disease but more common than heart failure due to hypertension or cardiomyopathy [47,48]. The differential diagnosis of mediastinal lymphadenopathy includes lymphoma, malignancy, and sarcoidosis.

TREATMENT — Antituberculous therapy has been shown to dramatically reduce mortality among patients with tuberculous pericarditis, from 80 to 90 percent [32] down to 8 to 17 percent among individuals without HIV infection [21,49] and 17 to 34 percent among individuals with HIV infection [50]. Antituberculous therapy has also been shown to reduce the likelihood of constrictive pericarditis, from 88 percent down to 10 to 20 percent of treated cases [17,51].

Antituberculous therapy — The approach to antituberculous therapy for treatment of tuberculous pericarditis is generally the same as that for pulmonary tuberculosis (TB) [52]. The drug regimen varies with whether or not the patient has HIV infection or drug-resistant tuberculosis. These issues are discussed in detail elsewhere. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Treatment of drug-resistant pulmonary tuberculosis in adults".)

For patients in areas where TB is endemic and/or for whom clinical suspicion of tuberculous pericarditis is high, initiation of empiric antituberculous therapy is appropriate prior to establishing a definitive diagnosis. Among patients for whom diagnosis cannot be established based on bacteriology, histology, or pericardial fluid analysis, clinical response to antituberculous therapy serves as support for a diagnosis of tuberculous pericarditis [12]. In areas where TB is not endemic, antituberculous therapy should generally not be initiated empirically in the absence of definitive diagnosis unless clinical suspicion is high [53].

Role of corticosteroids — In general, we favor administration of corticosteroids for patients with constrictive tuberculous pericarditis and patients at high risk of constrictive tuberculous pericarditis. Administration of corticosteroids does not appear to be beneficial in the setting of tuberculous pericarditis that is not constrictive, particularly among patients with HIV infection [20,37,50,52,54-58].

This was illustrated in a randomized trial published in 2014 including 1400 adults with definite (approximately 25 percent) or probable tuberculous pericarditis in South Africa; approximately two-thirds had concomitant HIV infection. The trial demonstrated no significant effect of adjunctive corticosteroids on the primary composite efficacy outcome of death, cardiac tamponade requiring pericardiocentesis, or development of constrictive pericarditis [54]. However, the incidence of constrictive pericarditis was significantly reduced by adjunctive corticosteroids (4.4 versus 7.8 percent; p = 0.009), at the price of increased HIV-associated malignancy (primarily Kaposi sarcoma).

Another study including 143 patients in South Africa with tuberculous pericarditis and constrictive physiology randomized to receive prednisolone or placebo (in addition to antituberculous therapy) noted that corticosteroids hastened clinical improvement and reduced the need for pericardiectomy [59]. Other data suggest that corticosteroids can shorten the time to resolution of clinical symptoms and decrease reaccumulation of fluid [60].

Corticosteroids may play a role in preventing constrictive pericarditis; selective use in patients at highest risk for inflammatory complications may be appropriate [54]. Such patients may include those with large effusions, those with high levels of inflammatory cells in the pericardial fluid, or those with early signs of constriction. For adults, the regimen is prednisone 60 mg/day (or the equivalent dose of prednisolone) given for four weeks, followed by 30 mg/day for four weeks, 15 mg/day for two weeks, and 5 mg/day for one week [20,52,59]. A shorter course of 60 mg of prednisone daily, tapering by 10 mg/day each week over a six-week period, has demonstrated efficacy in patients with HIV infection and tuberculous pericarditis and is a reasonable alternative in such patients [61]. Children should be treated with doses proportionate to their weight, beginning with about 1 mg/kg body weight and decreasing the dose as described for adults [20,50,52,56,60-62].

Corticosteroids do not appear to affect the likelihood of pericardial effusion reaccumulation [56]. Older studies of corticosteroid therapy were conducted prior to widespread HIV infection [20], and the pathogenesis of tuberculous pericarditis may be different in patients with HIV infection since tuberculosis in such patients appears to induce relatively low levels of inflammation.

Pericardiectomy — Pericardiectomy is warranted in the setting of persistent constrictive pericarditis despite antituberculous therapy. The timing is controversial, and data are limited [5,37]. Some favor pericardiectomy for all patients with constrictive pericarditis once antituberculous therapy has been initiated [63], while others favor reserving pericardiectomy for patients who do not respond to antituberculous therapy [3,59].

In general, pericardiectomy is appropriate for patients with hemodynamics that fail to improve or hemodynamics that deteriorate after four to eight weeks of antituberculous therapy [51]. Earlier intervention is warranted for patients with pericardial calcification, a marker of chronic disease. (See "Constrictive pericarditis: Management and prognosis", section on 'Treatment of late (chronic) disease'.)

In one series including 50 patients with tuberculous pericarditis in the absence of HIV infection from South Korea, over 80 percent of patients with initial constrictive physiology had improvement in constrictive pericarditis with medical therapy alone [64].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Diagnosis and treatment of tuberculosis".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Tuberculous pericarditis occurs in approximately 1 to 2 percent of patients with pulmonary tuberculosis (TB). Four pathological stages of tuberculous pericarditis have been described: fibrinous exudation, lymphocytic effusion, absorption of effusion with granulomatous caseation, and constrictive scarring. The earliest recognizable phase of pericardial infection is the second phase, and the diagnostic yield of pericardial fluid and tissue for acid-fast smear and culture is highest in this stage. (See 'Epidemiology' above and 'Pathogenesis' above.)

●The clinical manifestations of tuberculous pericarditis can be nonspecific; fever, weight loss, and night sweats generally precede cardiopulmonary complaints, and the onset is usually insidious. Symptoms may include cough, dyspnea, chest pain, pleurisy, orthopnea, night sweats, and weight loss. Physical findings may include fever, tachycardia, pleural dullness, increased jugular venous pressure, hepatomegaly, ascites, and peripheral edema. (See 'Clinical manifestations' above.)

●Tuberculous pericarditis should be considered in the evaluation of patients with pericarditis who do not have a self-limited course, in the setting of risk factors for TB exposure. The diagnosis is established by detection of tubercle bacilli in smear or culture of pericardial fluid and/or by detection of tubercle bacilli or caseating granulomata on histological examination of the pericardium. Tuberculous pericarditis is considered likely in the setting of pericarditis with tuberculosis demonstrated elsewhere in the body, lymphocytic pericardial exudate with elevated adenosine deaminase level, and/or clinical response to antituberculous therapy. (See 'General principles' above.)

●Initial diagnostic evaluation consists of chest radiography, echocardiography, and evaluation of sputum for acid-fast bacilli smear and culture. Pericardiocentesis is warranted for routine evaluation of suspected tuberculous pericarditis; cardiac tamponade is an absolute indication for pericardiocentesis. (See 'Initial evaluation' above.)

●Pericardial fluid should be evaluated for cell count, protein concentration, lactate dehydrogenase concentration, acid-fast smear/culture, Gram stain and bacterial culture, adenosine deaminase concentration, and cytology. Tuberculous pericardial effusions are typically exudative and characterized by high protein content and increased leukocyte count, with a predominance of lymphocytes and monocytes. Light's criteria for exudative pleural effusions may also be used to establish the presence of pericardial exudate. (See 'Pericardiocentesis' above and "Pleural fluid analysis in adults with a pleural effusion".)

●For circumstances in which the diagnosis remains uncertain, options for next diagnostic steps include right scalene lymph node biopsy (if lymphadenopathy is present), and/or pericardial biopsy. For patients in areas where TB is endemic for whom clinical suspicion of tuberculous pericarditis is high, pericardial biopsy is not required prior to initiation of empiric antituberculous therapy. In areas where TB is not endemic, a pericardial biopsy is warranted for patients with duration of illness >3 weeks in the absence of definitive diagnosis via the other investigations described above. (See 'Pericardial biopsy' above.)

●The approach to antituberculous therapy for treatment of tuberculous pericarditis is generally the same as that for pulmonary tuberculosis. The drug regimen varies with whether or not the patient has HIV infection or drug-resistant tuberculosis. These issues are discussed in detail elsewhere. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Treatment of drug-resistant pulmonary tuberculosis in adults".)

●For patients with constrictive tuberculous pericarditis and patients at high risk of constrictive tuberculous pericarditis, we suggest administration of corticosteroids (Grade 2B); dosing is outlined above. For tuberculous pericarditis that is not constrictive among patients with HIV infection, we recommend not administering corticosteroids (Grade 1B). For tuberculous pericarditis that is not constrictive among patients without HIV infection, we suggest not administering corticosteroids (Grade 2C). (See 'Role of corticosteroids' above.)