Tuberculous pericarditis

Tuberculous pericarditis

Tuberculous pericarditis is increasing in incidence in certain regions as a result of human immunodeficiency virus epidemic. The estimated number of new cases of tuberculosis was 8 million worldwide in 1997 and 8.3 million in 2000. In autopsy series, tuberculous pericarditis was noted in 1% of cases of tuberculosis. Tuberculous pericarditis was the etiology of pericardial effusion in about 70% of cases of evaluated pericardial effusion in developing countries while it was only 4% in developed countries.

Four pathological phases have been described in the evolution of tuberculous pericarditis. Initial phase is characterised by fibrinous exudation. The second phase is that of pericardial effusion which can sometimes be hemorrhagic. Third phase is that of absorption of the effusion with organization of granulomatous caseation and pericardial thickening. The fourth phase is that of constriction due to pericardial scarring.

Pericardial effusion of tuberculous origin can occur with or without manifestations of tuberculosis elsewhere. Chest pain, cough and breathlessness may be noted. Elevated jugular venous pressure, pulsus paradoxus and dullness beyond the apical impulse are useful findings of significant pericardial effusion. Pericardial friction rub may also be heard in some cases. Kussmaul’s sign and a normal cardiac size are noted in the constrictive phase. Features of venous congestion will dominate in those cases, with hepatomegaly, ascites and peripheral edema. ECG will show low voltage complexes and chest x-ray will show enlargement of the cardiac outline. Rapid increase in the cardiac size in serial X-rays is quite suggestive of pericardial effusion.

Echocardiography is the most important diagnostic tool to confirm pericardial effusion. Pericardial fluid is seen as echo free space around the cardiac chambers. Diastolic collapse of the right sided chambers would suggest cardiac tamponade. In constriction there is a rapid initial relaxation of the posterior wall of the left ventricle on M-Mode followed by a flat tracing. Respiratory variation of pulmonary venous flow or mitral inflow of more than 25% is also a useful finding. Plethora of the inferior vena cava, that is, absence of the normal inspiratory collapse, and traffic jam sign indicated by randomly moving spontaneous echogenic sources, are other features seen in constrictive pericarditis.

The definitive diagnosis is by aspirating the fluid and demonstrating tubercle bacilli or by histological section of the pericardium removed at surgery. Pericardial aspiration can be done therapeutically in case of large effusions. A pigtail catheter can be left in situ for a few days under aseptic coverage for repeated aspirations if there is rapid recollection of fluid. In regions with high prevalence of tuberculosis, a pericardial effusion is often considered to be of tuberculous origin if other etiologies are not evident.

Anti tuberculous therapy is useful in the resolution of most cases. Some cases may proceed to the constrictive phase even with successful chemotherapy. The role of corticosteroids in preventing this outcome is not well proven. Significant constriction is indication for surgical pericardiectomy, which is done better in the early phase of constriction than late. In late phases of constrictive pericarditis with calcification, surgical risks are high. Certain cases with features of both effusion and constriction are termed effusive constrictive pericarditis.