Pericarditis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S.; Cafer Zorkun, M.D., Ph.D. [2]

Overview

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated.

Pathogenesis

  • Bacterial pericarditis results from:
  1. Contiguous spread of infection within the chest,[4][5] either de novo or after surgery or trauma.[6]
  2. Spread from infective endocarditis[7][8]
  3. Hematogenous spread of infection
  4. Direct inoculation as a result of penetrating injury or cardiothoracic surgery
  • Tuberculous pericarditis develops from lymphatic spread of peritracheal, peribronchial or mediastinal lymph nodes or by contiguous spread from a focus of infection in the lung or pleura. There are four pathologic stages observed:[9][10][11]
  • Stage 3: Absorption of 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.
These types of granulomatous pericarditis also occur with fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

Gross Pathology Images

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









Microscopic Pathology Images

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



Videos

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Acute Fibrinous Pericarditis

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References

  1. Ilan Y, Oren R, Ben-Chetrit E (1991). "Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients". Jpn Heart J. 32 (3): 315–21. PMID 1920818.
  2. Shabetai R (1990). "Acute pericarditis". Cardiol Clin. 8 (4): 639–44. PMID 2249218.
  3. Matthews JD, Cameron SJ, George M (1970). "Constrictive pericarditis following Coxsackie virus infection". Thorax. 25 (5): 624–6. PMC 472200. PMID 5489188.
  4. Klacsmann PG, Bulkley BH, Hutchins GM (1977). "The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients". Am J Med. 63 (5): 666–73. PMID 930941.
  5. Kauffman CA, Watanakunakorn C, Phair JP (1973). "Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era". Am J Med. 54 (6): 743–50. PMID 4200204.
  6. Rubin RH, Moellering RC (1975). "Clinical, microbiologic and therapeutic aspects of purulent pericarditis". Am J Med. 59 (1): 68–78. PMID 1138554.
  7. Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM (1985). "Pericarditis in infective endocarditis". Eur Heart J. 6 (11): 975–8. PMID 4076207.
  8. Roberts WC, Buchbinder NA (1972). "Right-sided valvular infective endocarditis. A clinicopathologic study of twelve necropsy patients". Am J Med. 53 (1): 7–19. PMID 4402567.
  9. Peel AA (1948). "TUBERCULOUS PERICARDITIS". Br Heart J. 10 (3): 195–207. PMC 481044. PMID 18610109.
  10. 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.
  11. Mayosi BM, Burgess LJ, Doubell AF (2005). "Tuberculous pericarditis". Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.

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