Pericarditis pathophysiology: Difference between revisions
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{{Pericarditis}} | {{Pericarditis}} | ||
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}; [[Varun Kumar]], M.B.B.S. | ||
==Overview== | ==Overview== | ||
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Depending on the timing of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Clinically, acute pericarditis presents within 6 weeks of the disease onset; subacute pericarditis presents within 6 weeks to 6 months of the disease onset; and chronic pericarditis manifests after 6 months of the disease onset.[[Acute pericarditis]] is more common than chronic pericarditis, and often occurs as a complication of viral infections, immunologic conditions, or as a result of a [[heart attack]] ([[myocardial infarction]]). Chronic pericarditis is less common, which may manifest as scarring of the pericardium a condition known as [[constrictive pericarditis]]. | Depending on the timing of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Clinically, acute pericarditis presents within 6 weeks of the disease onset; subacute pericarditis presents within 6 weeks to 6 months of the disease onset; and chronic pericarditis manifests after 6 months of the disease onset.[[Acute pericarditis]] is more common than chronic pericarditis, and often occurs as a complication of viral infections, immunologic conditions, or as a result of a [[heart attack]] ([[myocardial infarction]]). Chronic pericarditis is less common, which may manifest as scarring of the pericardium a condition known as [[constrictive pericarditis]]. | ||
Cardiotropic viruses usually spread to the [[myocardium]] and [[pericardium]] hematogenously and cause acute inflammation with infiltration of [[polymorphonuclear]] (PMN) [[leukocytes]] and pericardial vascularization. This may cause [[pericardial effusion]] and fibrinous change of pericardium. Most patients with viral pericarditis recover completely with few developing recurrences<ref name="pmid1920818">{{cite journal| author=Ilan Y, Oren R, Ben-Chetrit E| title=Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients. | journal=Jpn Heart J | year= 1991 | volume= 32 | issue= 3 | pages= 315-21 | pmid=1920818 | doi= | pmc= | url= }} </ref><ref name="pmid2249218">{{cite journal| author=Shabetai R| title=Acute pericarditis. | journal=Cardiol Clin | year= 1990 | volume= 8 | issue= 4 | pages= 639-44 | pmid=2249218 | doi= | pmc= | url= }} </ref>. Some patients develop [[constrictive pericarditis]] which could be disabling<ref name="pmid5489188">{{cite journal| author=Matthews JD, Cameron SJ, George M| title=Constrictive pericarditis following Coxsackie virus infection. | journal=Thorax | year= 1970 | volume= 25 | issue= 5 | pages= 624-6 | pmid=5489188 | doi= | pmc=PMC472200 | url= }} </ref>. | ==Pathogenesis== | ||
*Cardiotropic '''viruses''' usually spread to the [[myocardium]] and [[pericardium]] hematogenously and cause acute inflammation with infiltration of [[polymorphonuclear]] (PMN) [[leukocytes]] and pericardial vascularization. This may cause [[pericardial effusion]] and fibrinous change of pericardium. Most patients with viral pericarditis recover completely with few developing recurrences<ref name="pmid1920818">{{cite journal| author=Ilan Y, Oren R, Ben-Chetrit E| title=Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients. | journal=Jpn Heart J | year= 1991 | volume= 32 | issue= 3 | pages= 315-21 | pmid=1920818 | doi= | pmc= | url= }} </ref><ref name="pmid2249218">{{cite journal| author=Shabetai R| title=Acute pericarditis. | journal=Cardiol Clin | year= 1990 | volume= 8 | issue= 4 | pages= 639-44 | pmid=2249218 | doi= | pmc= | url= }} </ref>. Some patients develop [[constrictive pericarditis]] which could be disabling<ref name="pmid5489188">{{cite journal| author=Matthews JD, Cameron SJ, George M| title=Constrictive pericarditis following Coxsackie virus infection. | journal=Thorax | year= 1970 | volume= 25 | issue= 5 | pages= 624-6 | pmid=5489188 | doi= | pmc=PMC472200 | url= }} </ref>. | |||
Bacterial [[pericarditis]] results from | |||
*'''Bacterial [[pericarditis]]''' results from | |||
#Contiguous spread of infection within the chest<ref name="pmid930941">{{cite journal| author=Klacsmann PG, Bulkley BH, Hutchins GM| title=The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. | journal=Am J Med | year= 1977 | volume= 63 | issue= 5 | pages= 666-73 | pmid=930941 | doi= | pmc= | url= }} </ref><ref name="pmid4200204">{{cite journal| author=Kauffman CA, Watanakunakorn C, Phair JP| title=Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era. | journal=Am J Med | year= 1973 | volume= 54 | issue= 6 | pages= 743-50 | pmid=4200204 | doi= | pmc= | url= }} </ref>, either de novo or after surgery or trauma<ref name="pmid1138554">{{cite journal| author=Rubin RH, Moellering RC| title=Clinical, microbiologic and therapeutic aspects of purulent pericarditis. | journal=Am J Med | year= 1975 | volume= 59 | issue= 1 | pages= 68-78 | pmid=1138554 | doi= | pmc= | url= }} </ref> | #Contiguous spread of infection within the chest<ref name="pmid930941">{{cite journal| author=Klacsmann PG, Bulkley BH, Hutchins GM| title=The changed spectrum of purulent pericarditis: an 86 year autopsy experience in 200 patients. | journal=Am J Med | year= 1977 | volume= 63 | issue= 5 | pages= 666-73 | pmid=930941 | doi= | pmc= | url= }} </ref><ref name="pmid4200204">{{cite journal| author=Kauffman CA, Watanakunakorn C, Phair JP| title=Purulent pneumococcal pericarditis. A continuing problem in the antibiotic era. | journal=Am J Med | year= 1973 | volume= 54 | issue= 6 | pages= 743-50 | pmid=4200204 | doi= | pmc= | url= }} </ref>, either de novo or after surgery or trauma<ref name="pmid1138554">{{cite journal| author=Rubin RH, Moellering RC| title=Clinical, microbiologic and therapeutic aspects of purulent pericarditis. | journal=Am J Med | year= 1975 | volume= 59 | issue= 1 | pages= 68-78 | pmid=1138554 | doi= | pmc= | url= }} </ref> | ||
#Spread from [[infective endocarditis]]<ref name="pmid4076207">{{cite journal| author=Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM| title=Pericarditis in infective endocarditis. | journal=Eur Heart J | year= 1985 | volume= 6 | issue= 11 | pages= 975-8 | pmid=4076207 | doi= | pmc= | url= }} </ref><ref name="pmid4402567">{{cite journal| author=Roberts WC, Buchbinder NA| title=Right-sided valvular infective endocarditis. A clinicopathologic study of twelve necropsy patients. | journal=Am J Med | year= 1972 | volume= 53 | issue= 1 | pages= 7-19 | pmid=4402567 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4402567 }} </ref> | #Spread from [[infective endocarditis]]<ref name="pmid4076207">{{cite journal| author=Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM| title=Pericarditis in infective endocarditis. | journal=Eur Heart J | year= 1985 | volume= 6 | issue= 11 | pages= 975-8 | pmid=4076207 | doi= | pmc= | url= }} </ref><ref name="pmid4402567">{{cite journal| author=Roberts WC, Buchbinder NA| title=Right-sided valvular infective endocarditis. A clinicopathologic study of twelve necropsy patients. | journal=Am J Med | year= 1972 | volume= 53 | issue= 1 | pages= 7-19 | pmid=4402567 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4402567 }} </ref> | ||
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#Direct inoculation as a result of penetrating injury or cardiothoracic surgery | #Direct inoculation as a result of penetrating injury or cardiothoracic surgery | ||
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. | |||
*'''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. 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> | |||
:'''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. | |||
*Pericarditis in '''renal failure''' is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins such as [[urea]], [[creatinine]], [[methylguanidine]]. | |||
==Gross Pathology Images== | ==Gross Pathology Images== |
Revision as of 16:41, 26 June 2011
Pericarditis Microchapters |
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Pericarditis pathophysiology On the Web |
American Roentgen Ray Society Images of Pericarditis pathophysiology |
Risk calculators and risk factors for Pericarditis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.
Overview
Pericarditis is inflammation of the pericardium, 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 inflammed as well. If the myocardium is involved in the inflammatory process, then this is called myopericarditis, and the CK and troponin may be elevated.
Classification
Pericarditis can be classified according to the composition of the inflammatory exudate or the composition of the fluid that accumulates around the heart.
Types include:
Acute Versus Chronic Pericarditis
Depending on the timing of presentation and duration, pericarditis is divided into "acute" and "chronic" forms. Clinically, acute pericarditis presents within 6 weeks of the disease onset; subacute pericarditis presents within 6 weeks to 6 months of the disease onset; and chronic pericarditis manifests after 6 months of the disease onset.Acute pericarditis is more common than chronic pericarditis, and often occurs as a complication of viral infections, immunologic conditions, or as a result of a heart attack (myocardial infarction). Chronic pericarditis is less common, which may manifest as scarring of the pericardium a condition known as constrictive pericarditis.
Pathogenesis
- Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may cause pericardial effusion and fibrinous change of pericardium. Most patients with viral pericarditis recover completely with few developing recurrences[1][2]. Some patients develop constrictive pericarditis which could be disabling[3].
- Bacterial pericarditis results from
- Contiguous spread of infection within the chest[4][5], either de novo or after surgery or trauma[6]
- Spread from infective endocarditis[7][8]
- Hematogenous spread of infection
- Direct inoculation as a result of penetrating injury or cardiothoracic surgery
- 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. There are four pathologic stages observed:[9][10][11]
- 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.
- Pericarditis in renal failure is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins such as urea, creatinine, methylguanidine.
Gross Pathology Images
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Fibrinous pericarditis: Gross, natural color, an excellent example of bread and butter appearance. Uremia, chronic glomerulonephritis and sepsis.
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Fibrinous pericarditis: Gross, a good example (bread and butter appearance).
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Fibrinous pericarditis: Gross, an excellent example.
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Fibrinous pericarditis: Gross, an excellent example, close-up view of fibrin.
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Fibrinous pericarditis: Gross, an excellent example, close-up view.
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Fibrinous pericarditis: Gross, an excellent example.
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Fibrinous pericarditis: Gross, external view of localized pericarditis over an acute infarction
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Fibrinous pericarditis: Gross, intact heart, good example
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Fibrinous pericarditis: Gross, good example, mild, with small amount of fibrin
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Fibrinous pericarditis: Gross, close-up, an excellent example of color and detail
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Fibrinous pericarditis: Gross, a good example
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Fibrinous pericarditis: Gross, a good example, very mild case
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Fibrinous pericarditis: Gross, an excellent example.
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Fibrinous pericarditis: Gross, a close-up view, an excellent illustration of fibrinous exudate.
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Pericarditis in uremia
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Fibrinous pericarditis: Gross, fixed tissue (note to color changes), a close-up view of fibrin on epicardial surface of heart. A typical example.
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Fibrinous pericarditis: Gross, natural color, large right atrial thrombus and fibrinous pericarditis. Normal tricuspid valve with some aging changes (good example)
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Fibrinous pericarditis: Gross, natural color
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Fibrinous pericarditis: Gross, natural color, an excellent example
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Fibrinous pericarditis: Gross, natural color, very close-up photo showing fibrinous exudate simulating frost (an excellent example)
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Rheumatoid fibrinous pericarditis: Gross, natural color, a typical lesion in 22 years old white female due to juvenile rheumatoid arthritis.
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Fibrinous pericarditis: Gross, natural color, close-up view of minimal fibrinous exudate on epicardial surface due to terminal renal failure
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Fibrinous pericarditis: Gross, natural color, anterior view of heart with mild fibrinous exudate over epicardium due to terminal renal failure
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Tuberculous pericarditis: Gross, natural color, shaggy hemorrhagic exudate. This case is much more hemorrhagic than the typical tuberculous pericarditis.
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Heart transplant: Gross, natural color, external view of heart. Two months after transplantation with fibrinous pericarditis
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Neoplastic pericarditis: Gross, natural color, shaggy pericarditis. Primer is adenocarcinoma of the lung.
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Heart: Septic pericarditis
Microscopic Pathology Images
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Tuberculous pericarditis.
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Tuberculous pericarditis.
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Tuberculous pericarditis: Micro oil acid fast stain. The organism easily seen.
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Tuberculous pericarditis: Micro oil acid fast stain. The organism easily seen.
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Uremic pericarditis: Micro med mag, H&E. A good example
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Tuberculous pericarditis: Micro med mag, H&E, a typical lesion
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Fibrinous pericarditis.
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Pericarditis fibrinosa (Fibrinous pericarditis).
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Malignant Mesothelioma, Biphasic Type: Pericardium: This tumor has epithelioid cells (lower half) surrounded by spindled cells. The patient was a 46-year-old woman with constrictive pericarditis; the pericardium was studded with coalescing tumor nodules.
- <Youtube v=AKS7kSl4x5k/>
- Acute fibrinous pericarditis
<Youtube v=5fz_W1YxbC8/>
- ↑ 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.
- ↑ Shabetai R (1990). "Acute pericarditis". Cardiol Clin. 8 (4): 639–44. PMID 2249218.
- ↑ Matthews JD, Cameron SJ, George M (1970). "Constrictive pericarditis following Coxsackie virus infection". Thorax. 25 (5): 624–6. PMC 472200. PMID 5489188.
- ↑ 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.
- ↑ 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.
- ↑ Rubin RH, Moellering RC (1975). "Clinical, microbiologic and therapeutic aspects of purulent pericarditis". Am J Med. 59 (1): 68–78. PMID 1138554.
- ↑ Ribeiro P, Shapiro L, Nihoyannopoulos P, Gonzalez A, Oakley CM (1985). "Pericarditis in infective endocarditis". Eur Heart J. 6 (11): 975–8. PMID 4076207.
- ↑ 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.
- ↑ Peel AA (1948). "TUBERCULOUS PERICARDITIS". Br Heart J. 10 (3): 195–207. PMC 481044. PMID 18610109.
- ↑ 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.
- ↑ Mayosi BM, Burgess LJ, Doubell AF (2005). "Tuberculous pericarditis". Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.