Pyogenic liver abscess pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Development of pyogenic liver abscess is the result of infection through the following routes like portal vein (also from pylephlebitis of portal vein), hepatic arteries as metastatic abscesses, direct spread from nearby infection, trauma and retroperitoneal extension from appendix.[1][2][3][4]Ascending biliary infection is the most common source of pyogenic liver abscess.
Pathophysiology
- Development of pyogenic liver abscess is the result of extension of infection through the following:[1][2][3][4]
- Portal vein (also from pylephlebitis of portal vein)
- Hepatic arteries as metastatic abscesses
- Direct spread from nearby infection
- Trauma
- Retroperitoneal extension from appendix (suppurative appendicitis most frequent source of infection)
- Ascending biliary infection is the most common source of pyogenic liver abscess.
- Right lobe of liver is most commonly involved due to its greater blood supply than caudate and left lobes.
- Bacteria involved in pyogenic liver abscess include:
Pathogenesis
- In healthy patients the reticuloendothelial cells (kupffer cells) of liver control the transient portal bacteremia but in elderly and immunocompromised the bacteria can overwhelm the kupffer cells and lead to an abscess.[5]
Gross Pathology
- Single or multiple cavities, filled with fowl smelling, creamy yellow necrotic material, usually in right lobe of liver.
- The abscess may have fibrous capsule which is a centimeter or more thick and gradually merges into the liver parenchyma.
Microscopic Pathology
- Multiple neutrophilic abscesses with areas of necrosis are seen in the liver parencyma.[6][7]
- Suppuration, liquefaction with presence of fibrino-purulent debris, and fibrosis are seen depending on stage.
- The edges of the cavities are composed of a chronic inflammatory infiltrate consisting of lymphocytes, epithelioid macrophages, eosinophils, and neutrophils.
- Adjacent hepatocytes appear reactive.
References
- ↑ 1.0 1.1 Munro JC (1905). "VII. Lymphatic and Hepatic Infections Secondary to Appendicitis". Ann Surg. 42 (5): 692–734. PMC 1425980. PMID 17861705.
- ↑ 2.0 2.1 Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL; et al. (1996). "Pyogenic hepatic abscess. Changing trends over 42 years". Ann Surg. 223 (5): 600–7, discussion 607-9. PMC 1235191. PMID 8651751.
- ↑ 3.0 3.1 Rahimian J, Wilson T, Oram V, Holzman RS (2004). "Pyogenic liver abscess: recent trends in etiology and mortality". Clin Infect Dis. 39 (11): 1654–9. doi:10.1086/425616. PMID 15578367.
- ↑ 4.0 4.1 Lam YH, Wong SK, Lee DW, Lau JY, Chan AC, Yiu RY; et al. (1999). "ERCP and pyogenic liver abscess". Gastrointest Endosc. 50 (3): 340–4. doi:10.1053/ge.1999.v50.98065. PMID 10462653.
- ↑ Stain SC, Yellin AE, Donovan AJ, Brien HW (1991). "Pyogenic liver abscess. Modern treatment". Arch Surg. 126 (8): 991–6. PMID 1863218.
- ↑ https://librepathology.org/wiki/Liver_pathology Accessed on February 22, 2017
- ↑ Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin JI, Malech HL; et al. (2002). "Hepatic abscess in patients with chronic granulomatous disease". Ann Surg. 235 (3): 383–91. PMC 1422444. PMID 11882760.