Tuberculous Pericarditis

Tuberculous pericarditis
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Author
Jason Stout, MD
Section Editor
C Fordham von Reyn, MD
Deputy Editor
Elinor L Baron, MD, DTMH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2015. | This topic last updated: Jan 05, 2015.
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 "Diagnosis of pulmonary tuberculosis in
HIV-uninfected patients" and "Epidemiology, clinical manifestations, and diagnosis of tuberculosis in HIV-infected
patients" and "Treatment of pulmonary tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary
tuberculosis in the HIV-infected patient".)
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 developing countries with a high prevalence of HIV, 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 HIV-infected patients
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 tuberculosisendemic 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 be inapparent.
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 tuberculoprotein. 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.
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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,
degree of extrapericardial tuberculous disease, and degree of pericardial involvement.
Patients 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
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].
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 [19]. In advanced disease, signs of heart failure may be
observed [20]. 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
"Diagnosis and treatment of pericardial effusion" and "Constrictive pericarditis" 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 HIV-negative individuals; further study is needed to clarify
this potential finding [21].
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", section on 'Physical examination'.)
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
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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 [22]. (See
"Differentiating constrictive pericarditis and restrictive cardiomyopathy" and "Constrictive pericarditis", 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 [23]. 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 'Physical findings'.)
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) [24].
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. A tuberculin skin test (TST) and/or
interferon gamma release assay (IGRA) may or may not be helpful. 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 72 percent of cases [3,16,19,25]. 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 [3,25].
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Interpretation of chest radiography in the setting of tuberculosis is discussed further separately. (See "Diagnosis of
pulmonary tuberculosis in HIV-uninfected patients", section on 'Chest radiography'.)
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 "Diagnosis and treatment of pericardial effusion".)
A thorough evaluation for tuberculosis should also include evaluation for presence of acid-fast bacilli in the sputum
smear and culture; positive results have been observed in 10 to 55 percent of cases [3,26]. Alternative approaches
include AFB smear and culture of gastric washings (in children) and urine [12].
CT and/or MRI of the chest can demonstrate pericardial effusion, pericardial thickening, and lymphadenopathy [27].
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 "Clinical presentation and diagnostic evaluation of acute
pericarditis", section on 'Electrocardiogram' and "Diagnosis and treatment of pericardial effusion", section on 'ECG
findings'.)
Tuberculin skin tests and interferon gamma release assays are useful for detecting TB infection but do not
distinguish between latent TB infection and active TB disease. The tuberculin skin test is positive in most
immunocompetent patients with tuberculous pericarditis (85 percent of cases) [4,28]. In contrast, the tuberculin skin
test is often negative in patients with HIV infection and tuberculous pericarditis [4].
Data on use of interferon gamma release assays 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 [29]. (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 [19]. 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 [30,31]. 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) [30]. The percentage of lymphocytes in the pericardial fluid is characteristically lower in patients with
HIV infection than in HIV-negative patients (36 versus 52 percent) [30]. Lights criteria for exudative pleural effusions
may also be used to establish the presence of pericardial exudate [32,33]. (See "Diagnosis and treatment of
pericardial effusion" and "Diagnostic evaluation of a pleural effusion in adults: Initial testing".)
Acid-fast bacilli are seen on smear of pericardial fluid in 40 to 60 percent of patients with tuberculous pericarditis; the
yield is increased by culture [16,19,30]. 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 [30]. In individual
patients with tuberculous pericarditis, the diagnostic tools available may be positive singly or in combination.
Polymerase chain reaction (PCR) for mycobacterial DNA in pericardial fluid may also be useful for diagnosis of
tuberculous pericarditis [30,34-36]. 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
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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 [37].
GeneXpert may be a useful adjunctive diagnostic but will not replace mycobacterial culture or histopathology in
diagnosis of tuberculous pericarditis. (See "Diagnosis of pulmonary tuberculosis in HIV-uninfected patients", section
on 'Culture' and "Diagnosis of pulmonary tuberculosis in HIV-uninfected patients", section on 'Nucleic acid
amplification'.)
Measurement of pericardial adenosine deaminase level can be useful for diagnosis of tuberculous pericarditis
[30,36]. 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 [38]. Another study noted a positive correlation between high
pericardial ADA levels and subsequent development of constrictive pericarditis [39]. Lower ADA levels have been
observed in HIV-infected patients with severe CD4 lymphocyte depletion [26]. 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 [30]. The mean
interferon-gamma concentrations in HIV-negative tuberculous effusions, HIV-positive 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 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 [40]. 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 [19]. Histology appears to be most important for cases in which no pericardial fluid can be obtained
[41].
Tissues obtained by biopsy should be stained with acid-fast reagents and examined for histological evidence of
granulomatous inflammation. The sensitivity of pericardial biopsy for diagnosis of tuberculous pericarditis ranges
from 10 to 64 percent [39,40]. 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 [42]. 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) [43]. 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).
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Patients with both tamponade and inflammation have a greater likelihood of tuberculosis infection than patients with
either tamponade or inflammation alone [44]. 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 [45,46]. 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 [31] down to 8 to 17 percent among HIV-negative individuals [20,47]
and 17 to 34 percent among HIV-infected individuals [48]. 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 [17,49].
Antituberculous therapy The approach to antituberculous therapy for treatment of tuberculous pericarditis is
generally the same as that for pulmonary tuberculosis (TB) [50,51]. 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 pulmonary tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in the
HIV-infected patient" and "Diagnosis, treatment, and prevention of drug-resistant tuberculosis".)
For patients in areas where TB is endemic 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
[52].
Role of corticosteroids Routine use of adjunctive corticosteroids in patients with HIV infection is not warranted
but may be appropriate if there is a perceived high risk to progression to constrictive disease. 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 [53]. 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) [19,36,48,54-58].
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 [53]. 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 [54]. 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
HIV-seropositive patients with 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 [19,48,54,57,58,60,61].
This approach is in disagreement with the 2003 guidelines issued by the American Thoracic Society, Centers for
Disease Control, and Infectious Diseases Society of America which favor use of corticosteroids for treatment of all
patients with tuberculous pericarditis [54]. Prior to the 2014 study, evidence favored corticosteroid use, but the topic
was controversial [19,36,48,54-57]. The available data suggested a trend toward reduction in mortality, but none of
the results was statistically significant. In addition, corticosteroids do not appear to affect the likelihood of pericardial
effusion reaccumulation [58]. Older studies of corticosteroid therapy were conducted prior to widespread HIV
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infection [19], 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 [5,36]. Some favor pericardiectomy for all
patients with constrictive pericarditis once antituberculous therapy has been initiated [62], 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 [49]. Earlier intervention is warranted for patients with
pericardial calcification, a marker of chronic disease. (See "Constrictive pericarditis", section on 'Chronic constrictive
pericarditis'.)
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Beyond the Basics topics (see "Patient information: 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,
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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 "Diagnostic evaluation of a pleural effusion in adults: Initial testing".)
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 pulmonary
tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in the HIV-infected patient"
and "Diagnosis, treatment, and prevention of drug-resistant tuberculosis".)
For patients with constrictive pericarditis and patients at high risk of constrictive tuberculous pericarditis, we
suggest administration of corticosteroids (Grade 2B); dosing is outlined above. For HIV-infected patients with
tuberculous pericarditis that is not constrictive, we recommend not administering corticosteroids (Grade 1B).
For HIV-uninfected patients with tuberculous pericarditis that is not constrictive, we suggest not administering
corticosteroids (Grade 2C).
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Topic 8002 Version 17.0
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GRAPHICS
Electrical alternans
Sinus tachycardia with electrical alternans which is characterized by

beat-to-beat alternation in the QRS appearance (best seen in leads V2
to V4). These findings are strongly suggestive of pericardial effusion,
usually with cardiac tamponade. The alternating ECG pattern is related
to back-and-forth swinging motion of the heart in the pericardial fluid.
Courtesy of Ary Goldberger, MD.
Graphic 72525 Version 4.0
Normal ECG
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Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR

interval of 0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75.
Courtesy of Ary Goldberger, MD.
Graphic 76183 Version 3.0
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Disclosures
Disclosures: Jason Stout, MD Nothing to disclose. C Fordham von Reyn, MD Nothing to disclose. Elinor L Baron, MD, DTMH Nothing to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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Tuberculous Pericarditis

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Tuberculous pericarditis

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Topic 8002 Version 17.0

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Sinus tachycardia with electrical alternans which is characterized by

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Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR

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