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.

• Tuberculous pericarditis is the result of hematogenous or lymphatic spread of mycobacterium tuberculosis to the pericardium.^[1][2][3][4]
• This causes acute inflammation of the pericardium.
• We may have polymorphonuclear (PMN) and leukocytes infiltration in the pericardium.
• Pericardial vascularization may happen as well.
• This may lead to pericardial effusion and fibrinous changes of the pericardium.
• Effusive constrictive pericarditis may be seen in some patients.
• The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis).
• 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.

The development of tuberculous pericarditis is not the result of any genetic mutation.

Conditions associated with tuberculous pericarditis include:

• Pulmonary TB
• HIV
• Malignancy
• Chemotherapy
• 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.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology