Spontaneous bacterial peritonitis pathophysiology
|
Spontaneous bacterial peritonitis Microchapters |
|
Differentiating Spontaneous bacterial peritonitis from other Diseases |
|
Diagnosis |
|
Treatment |
|
Spontaneous bacterial peritonitis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Spontaneous bacterial peritonitis pathophysiology |
|
Spontaneous bacterial peritonitis pathophysiology in the news |
|
Directions to Hospitals Treating Spontaneous bacterial peritonitis |
|
Risk calculators and risk factors for Spontaneous bacterial peritonitis pathophysiology |
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:
Natural barriers
Routes of infection
- Hematogenous
- Lymphogenous
- Transmural migration through an intact bowel wall from the intestinal lumen
- Bacterial translocation: Enteric bacteria from the bowel lumen → Mesenteric lymph nodes → Systemic circulation (via the thoracic duct)
- Enteric bacteria → Portal vein → liver / portosystemic shunts ( in portal hypertension) → Systemic circulation.
- Conn and Fessel postulated that organisms removed from the systemic circulation by the liver contaminate hepatic lymph and pass through the permeable lymphatic walls into the ascitic fluid
- Enteric bacteria may also gain access to the peritoneal cavity by traversing directly the intact intestinal wall.
Hypo-motility
- Distal propulsion of luminal contents by intestinal peristalsis is a critical factor in the inhibition of bacterial colonization and replication in the proximal gastro-intestinal tract, which leads to bacterial overgrowth.
Intestinal mucosal permeability
Altered microbial flora
Intestinal bacterial overgrowth
- Probably due to disturbances in the intestinal peristalsis, gastric acid and mucosal immunity in cirrhotic patients.
- Studies have shown that the incidenceof bacterial overgrowth in the small intestine was significantly higher in liver cirrhotic patients with history of SBP than in those without SBP (70% vs. 20%).
- Once bacteria reach a critical concentration in the gut lumen, they “spill over”, and escape the gut, “translocating” to mesenteric lymph nodes.Then they enter lymph, blood, and eventually ascitic fluid.[2]
Intestinal permeability
Hepatic Reticulo endothelial system activity
Porto-systemic shunting
Phagocytic response
Serum factors
Bacterial translocation
Routes of transmission
Reticulo endothelial dysfunction
Alterations in the systemic immune response
Ascitic fluid defense mechanisms
Cytokine response
-
- Prolonged bacteremia secondary to compromised host defenses
- Intrahepatic shunting of colonized blood and
- Defective bactericidal activity within the ascitic fluid.[3] 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.[4][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.[5]
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.[6] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[7] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[5]
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, Squier S, Borzio M (1994). "Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis". J Hepatol. 21 (5): 792–6. PMID 7890896.
- ↑ 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.
- ↑ 5.0 5.1 Alaniz C, Regal RE (2009) Spontaneous bacterial peritonitis: a review of treatment options. P T 34 (4):204-10. PMID: 19561863
- ↑ Runyon BA (1986) Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology 91 (6):1343-6. PMID: 3770358
- ↑ 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.