Tuberculous pericarditis: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
Tuberculous pericarditis develop from lymphatic spread from peritracheal, peribronchial or [[mediastinal lymphnodes]] or by contiguous spread from a focus of infection in lung or pleura. This causes acute inflammation of pericardium with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may lead to [[pericardial effusion]] and fibrinous change of pericardium. There are four pathologic stages observed:<ref name="pmid18610109">{{cite journal| author=Peel AA| title=TUBERCULOUS PERICARDITIS. | journal=Br Heart J | year= 1948 | volume= 10 | issue= 3 | pages= 195-207 | pmid=18610109 | doi= | pmc=PMC481044 | url= }} </ref><ref name="pmid4050698">{{cite journal| author=Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J| title=Primary acute pericardial disease: a prospective series of 231 consecutive patients. | journal=Am J Cardiol | year= 1985 | volume= 56 | issue= 10 | pages= 623-30 | pmid=4050698 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4050698  }} </ref><ref name="pmid16330703">{{cite journal| author=Mayosi BM, Burgess LJ, Doubell AF| title=Tuberculous pericarditis. | journal=Circulation | year= 2005 | volume= 112 | issue= 23 | pages= 3608-16 | pmid=16330703 | doi=10.1161/CIRCULATIONAHA.105.543066 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16330703  }} </ref>
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 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 change of pericardium. There are four pathologic stages of involvement:<ref name="pmid18610109">{{cite journal| author=Peel AA| title=TUBERCULOUS PERICARDITIS. | journal=Br Heart J | year= 1948 | volume= 10 | issue= 3 | pages= 195-207 | pmid=18610109 | doi= | pmc=PMC481044 | url= }} </ref><ref name="pmid4050698">{{cite journal| author=Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J| title=Primary acute pericardial disease: a prospective series of 231 consecutive patients. | journal=Am J Cardiol | year= 1985 | volume= 56 | issue= 10 | pages= 623-30 | pmid=4050698 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4050698  }} </ref><ref name="pmid16330703">{{cite journal| author=Mayosi BM, Burgess LJ, Doubell AF| title=Tuberculous pericarditis. | journal=Circulation | year= 2005 | volume= 112 | issue= 23 | pages= 3608-16 | pmid=16330703 | doi=10.1161/CIRCULATIONAHA.105.543066 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16330703  }} </ref>


:'''Stage 1:''' Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium
:'''Stage 1:''' Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium
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:'''Stage 3:''' Absorption of effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.
:'''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. Pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue.
:'''Stage 4:''' Development of [[constrictive pericarditis]]. 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 constriction.  
Effusive [[constrictive pericarditis]] may be seen in some patients. The visceral pericardium thickens with fibrin deposition (changes of [[constrictive pericarditis]]) and concomitantly there is a pericardial effusion which may present as [[cardiac tamponade]]. In this scenario, the [[diastolic pressure]] continues to be elevated after pericardiocentesis due to persistent constriction.


==Diagnosis==
==Diagnosis==

Revision as of 18:56, 27 June 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Varun Kumar, M.B.B.S.

Overview

The incidence of tuberculosis caused by Mycobacterium tuberculosis and its complications has significantly decreased in developed nations while it remains high in developing countries. Approximately one third of the world population is believed to be infected with tuberculosis(TB)[1]. In 2006 WHO estimated the global prevalence of active TB[2] to be 14.4 million cases. TB accounts for 1.7 million deaths worldwide. One of the important complications of TB is pericarditis which is the inflammation of pericardial sac that encases heart.

Epidemiology and demographics

Tuberculous pericarditis is found in approximately 1-2% of patients with pulmonary tuberculosis[3][4]. It is the most common cause of pericarditis in Africa and other developing countries where TB is a major public health problem[5]. The incidence is increasing rapidly in presence of HIV[6].

In a study at Western Cape Province of South Africa, tuberculous pericarditis was noted in 69.5% of patients who were referred for diagnostic pericardiocentesis and one half of the patients were infected with HIV[7]. In contrast, the incidence of tuberculous pericarditis is 4% in developed countries[8].

Natural history and complications

Tuberculous pericarditis often has a complicated course and poor clinical outcomes. It can lead to pericardial effusion and subsequently, cardiac tamponade which may require urgent intervention including pericardiocentesis. The mortality rate of tuberculous pericarditis in the preantibiotic era was 80-90%[9]. The mortality rate in the modern era is currently 8-17%[10][11] and is 17-34% if the TB is associated with HIV[12].

Tuberculous pericarditis can also cause heart failure as observed in Eastern Cape and Zimbabwe where it is a common cause, but less common than rheumatic heart disease and more common than hypertensive heart disease and cardiomyopathy[13][14]

Constrictive pericarditis is another complication of tuberculous pericarditis occurring in 30-60% of patients despite prompt antituberculosis treatment and the use of corticosteroids[15][8]

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 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 change of pericardium. There are four pathologic stages of involvement:[16][17][18]

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 effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.
Stage 4: Development of constrictive pericarditis. 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 a pericardial effusion which may present as cardiac tamponade. In this scenario, the diastolic pressure continues to be elevated after pericardiocentesis due to persistent constriction.

Diagnosis

Tuberculous pericarditis has a variable clinical presentation and should be considered in the evaluation of all cases of pericarditis without a rapidly self-limited course[8].

References

  1. Lönnroth K, Raviglione M (2008). "Global epidemiology of tuberculosis: prospects for control". Semin Respir Crit Care Med. 29 (5): 481–91. doi:10.1055/s-0028-1085700. PMID 18810682.
  2. WHO. Global Tuberculosis control. WHO/HTM/TB/2008.393. Geneva: World Health Organization; 2008. Available online at http://www.who.int/tb/publications/global_report/2008/en/index.html (Accessed June 27, 2011)
  3. Fowler NO (1991). "Tuberculous pericarditis". JAMA. 266 (1): 99–103. PMID 2046135.
  4. Larrieu AJ, Tyers GF, Williams EH, Derrick JR (1980). "Recent experience with tuberculous pericarditis". Ann Thorac Surg. 29 (5): 464–8. PMID 7377888.
  5. Mayosi BM, Volmink JA, Commerford PJ. Pericardial disease: an evidence-based approach to diagnosis and treatment. In: Yusuf S, Cairns JA, Camm AJ, Fallen BJ, eds. Evidence-Based Cardiology. 2nd ed. London: BMJ Books; 2003: 735–748.
  6. Cegielski JP, Ramiya K, Lallinger GJ, Mtulia IA, Mbaga IM (1990). "Pericardial disease and human immunodeficiency virus in Dar es Salaam, Tanzania". Lancet. 335 (8683): 209–12. PMID 1967676.
  7. Reuter H, Burgess LJ, Doubell AF (2005). "Epidemiology of pericardial effusions at a large academic hospital in South Africa". Epidemiol Infect. 133 (3): 393–9. PMC 2870262. PMID 15962545.
  8. 8.0 8.1 8.2 Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J (1988). "Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment". J Am Coll Cardiol. 11 (4): 724–8. PMID 3351140.
  9. Harvey AM, Whitehill MR. Tuberculous pericarditis. Medicine. 1937; 16: 45–94
  10. Desai HN (1979). "Tuberculous pericarditis. A review of 100 cases". S Afr Med J. 55 (22): 877–80. PMID 472922.
  11. Bhan GL (1980). "Tuberculous pericarditis". J Infect. 2 (4): 360–4. PMID 7185934.
  12. Hakim JG, Ternouth I, Mushangi E, Siziya S, Robertson V, Malin A (2000). "Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive tuberculous pericarditis in HIV seropositive patients". Heart. 84 (2): 183–8. PMC 1760932. PMID 10908256.
  13. Strang JI (1984). "Tuberculous pericarditis in Transkei". Clin Cardiol. 7 (12): 667–70. PMID 6509811.
  14. Hakim JG, Manyemba J (1998). "Cardiac disease distribution among patients referred for echocardiography in Harare, Zimbabwe". Cent Afr J Med. 44 (6): 140–4. PMID 9810393.
  15. SCHRIRE V (1959). "Experience with pericarditis at Groote Schuur Hospital, Cape Town: an analysis of one hundred and sixty cases studied over a six-year period". S Afr Med J. 33: 810–7. PMID 14443596.
  16. Peel AA (1948). "TUBERCULOUS PERICARDITIS". Br Heart J. 10 (3): 195–207. PMC 481044. PMID 18610109.
  17. 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.
  18. Mayosi BM, Burgess LJ, Doubell AF (2005). "Tuberculous pericarditis". Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.