Tuberculous pericarditis overview

Tuberculous pericarditis Microchapters
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Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Tuberculous pericarditis from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Fahimeh Shojaei, M.D., Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852. Tuberculous pericarditis is the result of hematogenous or lymphatic spread of mycobacterium tuberculosis to the pericardium. This causes acute inflammation of the pericardium and we may have polymorphonuclear (PMN) and leukocytes infiltration in the pericardium. This may lead to pericardial effusion and fibrinous changes of the pericardium. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis). There are four pathologic stages of involvement: stage 1 is presence of diffuse fibrin deposition, granulomas and abundant mycobacterium. Stage 2 is development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells. Stage 3 is absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen. Stage 4 is development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue. Conditions associated with tuberculous pericarditis include pulmonary TB, HIV, malignancy, chemotherapy, and diabetes mellitus. On gross pathology, thickened pericardium, shaggy hemorrhage, and exudate are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, acid fast bacilli is characteristic findings of tuberculous pericarditis. The prevalence of tuberculous pericarditis is approximately 1-2% of patients with pulmonary tuberculosis. Patients of all age groups may develop tuberculous pericarditis. The incidence of tuberculous pericarditis increases with age. Tuberculous pericarditis commonly affects elderly. Tuberculous pericarditis usually affects individuals of the black race. Men are more commonly affected by tuberculous pericarditis than female. Since the prevalence of tuberculous pericarditis may follow tuberculosis prevalence, The majority of tuberculous pericarditis cases are reported in South Africa, Indonesia, Nigeria, Pakistan, India, and China. Patients with tuberculous pericarditis may have a positive history of pulmonary TB, HIV infection, any Immune system dysfunction, elderly, black race, male gender, and living/traveling to TB endemic areas. Common symptoms of tuberculous pericarditis include fever, weight loss, night sweat, cough, breathlessness, chest pain, malaise, and ankle edema. Patients with tuberculous pericarditis usually appear Cachectic. They may have fever, tachycardia, pulsus paradoxus, hypotension, tachypnea, JVP distension, kussmaul's sign, lymphadenopathy, ankle edama, pleura dullness, decreased breath sounds, pericardial knock, pericardial rub, fine/coarse crackles upon auscultation of the lung, hepatomegaly, ascites, distant heart sounds, displaced point of maximal impulse (PMI) suggestive of cardiomegaly, friction rub, and S4. A 2 months course of isoniazid, pyrazinamide, rifampicin, and ethambutol followed by 4months course of isoniazid and rifampicin is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in HIV infected patients. The mainstay of treatment for tuberculous pericarditis is medical therapy. Pericardiectomy is usually reserved for patients resistance constrictive pericarditis.

Historical Perspective

Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852.

Classification

There is no established system for the classification of Tuberculous pericarditis.

Pathophysiology

Tuberculous pericarditis is the result of hematogenous or lymphatic spread of mycobacterium tuberculosis to the pericardium. This causes acute inflammation of the pericardium and we may have polymorphonuclear (PMN) and leukocytes infiltration in the pericardium. This may lead to pericardial effusion and fibrinous changes of the pericardium. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis). There are four pathologic stages of involvement: stage 1 is presence of diffuse fibrin deposition, granulomas and abundant mycobacterium. Stage 2 is development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells. Stage 3 is absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen. Stage 4 is development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue. Conditions associated with tuberculous pericarditis include pulmonary TB, HIV, malignancy, chemotherapy, and diabetes mellitus. On gross pathology, thickened pericardium, shaggy hemorrhage, and exudate are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, acid fast bacilli is characteristic findings of tuberculous pericarditis. Pericardiocentesis is the gold standard test for the diagnosis of tuberculous pericarditis. Pericardial biopsy must be performed when we can't find acid fast bacilli in sputum or pericardial fluid. Finding acid fast bacilli on pericardiocentesis is confirmatory for tuberculous pericarditis.

Causes

Common cause of tuberculous pericarditis is lymphatic or hematogenous spread of mycobacterium tuberculosis to the pericardium.

Epidemiology and Demographics

The prevalence of tuberculous pericarditis is approximately 1-2% of patients with pulmonary tuberculosis. Patients of all age groups may develop tuberculous pericarditis. The incidence of tuberculous pericarditis increases with age. Tuberculous pericarditis commonly affects elderly. Tuberculous pericarditis usually affects individuals of the black race. Men are more commonly affected by tuberculous pericarditis than female. Since the prevalence of tuberculous pericarditis may follow tuberculosis prevalence, The majority of tuberculous pericarditis cases are reported in South Africa, Indonesia, Nigeria, Pakistan, India, and China.

Risk Factors

Common risk factors in the development of tuberculous pericarditis include immunodeficiency (AIDS, malignancy, chemotherapy, diabetes and elderly), TB exposure, male gender, and African-American race.

Screening

There is insufficient evidence to recommend routine screening for tuberculous pericarditis.

Diagnosis

Diagnostic Study of Choice

Pericardiocentesis is the gold standard test for the diagnosis of tuberculous pericarditis. Pericardial biopsy must be performed when we can't find acid fast bacilli in sputum or pericardial fluid. Finding acid fast bacilli on pericardiocentesis is confirmatory for tuberculous pericarditis.

History and Symptoms

Patients with tuberculous pericarditis may have a positive history of pulmonary TB, HIV infection, any Immune system dysfunction, elderly, black race, male gender, and living/traveling to TB endemic areas. Common symptoms of tuberculous pericarditis include fever, weight loss, night sweat, cough, breathlessness, chest pain, malaise, and ankle edema.

Physical Examination

Patients with tuberculous pericarditis usually appear Cachectic. They may have fever, tachycardia, pulsus paradoxus, hypotension, tachypnea, JVP distension, kussmaul's sign, lymphadenopathy, ankle edama, pleura dullness, decreased breath sounds, pericardial knock, pericardial rub, fine/coarse crackles upon auscultation of the lung, hepatomegaly, ascites, distant heart sounds, displaced point of maximal impulse (PMI) suggestive of cardiomegaly, friction rub, and S4.

Laboratory Findings

Laboratory findings consistent with the diagnosis of tuberculous pericarditis include mild anemia, normal leukocyte count, exudate pericardial effusion, mycobacterium tuberculosis bacilli in pericardial effusion, and positive HIV test.

Electrocardiogram

An ECG may be helpful in the diagnosis of tuberculous pericarditis. Findings on an ECG suggestive of tuberculous pericarditis include low voltage QRS, absence of ST segment elevation which we usually see in acute pericarditis, inverted T wave, atrial fibrillation, and electrical alternans.

X-ray

An x-ray may be helpful in the diagnosis of tuberculous pericarditis. Findings on an x-ray suggestive of tuberculous pericarditis include pericardial calcification, pericardial thickening, pericardial effusion, and evidence of pulmonary TB.

Echocardiography and Ultrasound

Echocardiography/ultrasound may be helpful in the diagnosis of tuberculous pericarditis. Findings on an echocardiography/ultrasound suggestive of tuberculous pericarditis include pericardial effusion, , pericardial thickening, increased right ventricular dimensions, decreased left ventricular dimensions, abnormal septal motion, flattening of the left ventricular posterior wall during diastol, dilated inferior vena cava, and dilated atrium.

CT scan

CT scan may be helpful in the diagnosis of tuberculous pericarditis. Findings on CT scan suggestive of tuberculous pericarditis include calcification of the pericardium, thickened pericardium, pericardial effusion, and back flow of blood into the IVC and hepatic veins (in contrast CT scan).

MRI

MRI may be helpful in the diagnosis of tuberculous pericarditis. Findings on MRI suggestive of tuberculous pericarditis include pericardial effusion, pericardial thickening, mediastinal and tracheobronchial lymphadenopathy (with hilar sparing), and bowing of the interventricular septum toward the left ventricle during diastole.

Other Imaging Findings

There are no other imaging findings associated with tuberculous pericarditis.

Other Diagnostic Studies

Other diagnostic studies for tuberculous pericarditis include PPD skin test, interferon-gamma assay, smear and culture of pericardial, sputum, and gastric fluid, pericardial biopsy, and lymph node biopsy.

Treatment

Medical Therapy

A 2 months course of isoniazid, pyrazinamide, rifampicin, and ethambutol followed by 4months course of isoniazid and rifampicin is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in HIV infected patients.

Surgery

The mainstay of treatment for tuberculous pericarditis is medical therapy. Pericardiectomy is usually reserved for patients resistance constrictive pericarditis.

Primary Prevention

There are no established measures for the primary prevention of tuberculous pericarditis.

Secondary Prevention

There are no established measures for the secondary prevention of tuberculous pericarditis.

References

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