Tuberculous pericarditis pathophysiology


 * Associate Editor-In-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Pathophysiology
Tuberculous pericarditis develops as a result of lymphatic spread from peritracheal, peribronchial or mediastinal lymphnodes or by contiguous spread from a focus of infection in the lung or pleura. This causes acute inflammation of the pericardium with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may lead to pericardial effusion and fibrinous changes of the pericardium. There are four pathologic stages of involvement:


 * Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium


 * Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells


 * Stage 3: Absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.


 * Stage 4: 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.

Effusive constrictive pericarditis may be seen in some patients. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis) and concomitantly there is presence of pericardial effusion which may present as cardiac tamponade. In this scenario, the diastolic pressure continues to be elevated after pericardiocentesis due to persistent pericardial constriction.