Spontaneous bacterial peritonitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
SBP is a result of culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped.[1]
Pathophysiology
SBP is a result of culmination of the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped. Following steps may explain the underlying process in a comprehensive way:
- Spontaneous bacterial peritonitis is thought to result from a combination of factors related to cirrhosis and ascites such as:
- Prolonged bacteremia secondary to compromised host defenses
- Intrahepatic shunting of colonized blood and
- Defective bactericidal activity within the ascitic fluid.[2] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[3][1]
With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.[4]
As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[5] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[6] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[4]
References
- ↑ 1.0 1.1 Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
- ↑ Runyon BA, Hoefs JC (1984). "Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis". Hepatology. 4 (6): 1209–11. doi:10.1002/hep.1840040619. PMID 6500513.
- ↑ Runyon BA (1988). "Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis". Hepatology. 8 (3): 632–5. doi:10.1002/hep.1840080332. PMID 3371881.
- ↑ 4.0 4.1 Alaniz C, Regal RE (2009). "Spontaneous Bacterial Peritonitis: A Review of Treatment Options". P T. 34 (4): 204–210. PMC 2697093. PMID 19561863. Unknown parameter
|month=ignored (help) - ↑ Runyon BA (1986). "Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis". Gastroenterology. 91 (6): 1343–6. PMID 3770358. Unknown parameter
|month=ignored (help) - ↑ Runyon BA, Morrissey RL, Hoefs JC, Wyle FA (1985). "Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis". Hepatology. 5 (4): 634–7. doi:10.1002/hep.1840050419. PMID 4018735.