Tuberculous pericarditis

Tuberculous pericarditis
Author
Jason Stout, MD
Section Editor
C Fordham von Reyn, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Disclosures
All topics are updated as new evidence becomes available and our peer review
process is complete.
Literature review current through: Mar 2013. | This topic last updated: Aug 22,
2012.

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-negative
patients" and "Epidemiology, clinical manifestations, and diagnosis of tuberculosis
in HIV-infected patients" and "Treatment of pulmonary tuberculosis in HIV-negative
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 tuberculosis-endemic countries,
extrapulmonary TB, including tuberculous pericarditis, is still seen with some
frequency [ 8-10 ].

PATHOGENESIS — Pericardial infection with M. 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.

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 (an 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
associated 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' .)

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) [ 23 ].

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 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
level, and/or clinical response to antituberculous therapy.

Initial evaluation — Initial evaluation consists of chest radiography,

echocardiography, and evaluation of sputum for 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
testand/or interferon gamma release assay 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 x-ray in the

setting of tuberculous pericarditis is variable and ranges from 32 to 72 percent of
cases [ 3,16,19,24 ]. Cardiac findings on chest x-ray 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 [ 3,24 ]. Interpretation of chest radiography in the
setting of tuberculosis is discussed further separately. (See "Diagnosis of
pulmonary tuberculosis in HIV-negative 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 1and 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 [ 3,25 ]. 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 [ 26 ]. 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 "Electrocardiogram in pericarditis and pericardial
effusion" .)

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) [ 4,27 ]. 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 [ 28 ]. (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 [ 29,30 ]. 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) [ 29 ]. 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) [ 29 ]. Light’s
criteria for exudative pleural effusions may also be used to establish the presence
of pericardial exudate [ 31,32 ]. (See "Technique of
pericardiocentesis" 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 [16,19,29 ]. 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 [ 29 ].
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 [ 29,33-35 ]. 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.
(See "Diagnosis of pulmonary tuberculosis in HIV-negative patients", section on
'Culture' and "Diagnosis of pulmonary tuberculosis in HIV-negative patients",
section on 'Molecular tests' .)

Measurement of pericardial adenosine deaminase (ADA) level can be useful for

diagnosis of tuberculous pericarditis [ 29,35 ]. Different cutoff levels for ADA
activity have been suggested as indicative of disease, ranging from 30 to 60 U/L. In
one study of 64 patients in South Africa with tuberculous pericarditis, the median
ADA level was 72 U/L (range 10 to 304 U/L); this level was significantly higher than
the ADA levels in patients with other etiologies of pericarditis. Using a cutoff ADA
level of 30 U/L, the authors calculated a sensitivity of 94 percent, specificity of 68
percent and positive predictive value of 80 percent [ 36 ]. Another study noted a
positive correlation between high pericardial ADA levels and subsequent
development of constrictive pericarditis [ 37 ]. Lower ADA levels have been
observed in HIV-infected patients with severe CD4 lymphocyte depletion [ 25 ].
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 [ 29 ]. The mean interferon gamma concentrations in HIV-negative
tuberculous effusions, HIV-positive tuberculous effusions, and non-tuberculous
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 [ 38 ]. Subsequently,
prospective data has shown that culture of pericardial fluid confirmed the presence
of tuberculous more often than pericardial histology [ 19 ]. Histology appears to be
most important for cases in which no pericardial fluid can be obtained [ 39 ].

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 [ 37,38 ]. 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 [ 40 ]. 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 non-infectious 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
[ 41 ]. 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 [ 42,43 ]. 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 [ 30 ]
down to 8 to 17 percent among HIV-negative individuals [ 20,44 ] and 17 to 34
percent among HIV-infected individuals [ 45 ]. 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 [ 17,46 ].

Antituberculous therapy — The approach to antituberculous therapy for

treatment of tuberculous pericarditis is generally the same as that for pulmonary
tuberculosis [ 47,48 ]. 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-negative
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 [ 49 ].
Role of corticosteroids — The benefit of corticosteroids in tuberculous
pericarditis is controversial [ 19,35,45,50-53 ]. Three clinical trials (with a total of
326 participants) have been performed to assess the effectiveness of adjunctive
steroids in management tuberculous effusion; two were performed in the pre-HIV
era [ 19,45,53 ]. The available data demonstrate that corticosteroids can shorten
the time to resolution of clinical symptoms and decrease reaccumulation of fluid
[ 54 ]. They also suggest 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 or progression to
constrictive pericarditis [ 55 ].

Corticosteroids appear to be most useful among patients with constrictive

pericarditis. Among 143 patients with tuberculous pericarditis and constrictive
physiology in South Africa randomized to receive prednisolone or placebo in
addition to antituberculous therapy during the first 11 weeks of treatment,
corticosteroids hastened clinical improvement, reduced the need for
pericardiectomy, and reduced mortality, although the findings were not statistically
significant [ 56 ].

We are in agreement 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 [ 52 ]. Use of corticosteroids is likely to be most beneficial for patients
with constrictive pericarditis. 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.
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.

Pericardiectomy — Pericardiectomy is warranted in the setting of persistent

constrictive pericarditis despite antituberculous therapy. The timing is controversial,
and data are limited [ 5,35 ]. Some favor pericardiectomy for all patients with
constrictive pericarditis once antituberculous therapy has been initiated [ 57 ],
while others favor reserving pericardiectomy for patients that do not respond to
antituberculous therapy [ 3,56 ].

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 [ 46 ]. 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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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 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/orclinical 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 "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-negative
patients" and "Treatment of pulmonary tuberculosis in the HIV-infected
patient" and"Diagnosis, treatment, and prevention of drug-resistant
tuberculosis" .)
 The role of corticosteroids in tuberculous pericarditis is controversial, and
data are limited. For patients with constrictive tuberculous pericarditis, we
recommend administration of corticosteroids ( Grade 1B ); for patients
with tuberculous pericarditis that is not constrictive, we suggest
administration of corticosteroids ( Grade 2C ). Dosing is outlined above.
(See 'Role of corticosteroids' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate, Inc. would like to

recognize Dr. G. Ralph Corey and Dr. Daniel Sexton for their contributions to
previous versions of this topic.