Tuberculous pericarditis pathophysiology

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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 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.

Pathophysiology

Pathogenesis

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

Genetics

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

Associated Conditions

Conditions associated with tuberculous pericarditis include:

  • Pulmonary TB
  • HIV
  • Malignancy
  • Chemotherapy
  • Diabetes mellitus

Gross Pathology Images

On gross pathology, thickened pericardium, shaggy hemorrhage, and exudate are characteristic findings of tuberculous pericarditis.


Microscopic Pathology Images

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

References

  1. Peel AA (1948). "TUBERCULOUS PERICARDITIS". Br Heart J. 10 (3): 195–207. PMC 481044. PMID 18610109.
  2. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J (1985). "Primary acute pericardial disease: a prospective series of 231 consecutive patients". Am J Cardiol. 56 (10): 623–30. PMID 4050698.
  3. Mayosi BM, Burgess LJ, Doubell AF (2005). "Tuberculous pericarditis". Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.
  4. Sagristà-Sauleda J, Angel J, Sánchez A, Permanyer-Miralda G, Soler-Soler J (2004). "Effusive-constrictive pericarditis". N Engl J Med. 350 (5): 469–75. doi:10.1056/NEJMoa035630. PMID 14749455.