Peritonitis pathophysiology: Difference between revisions
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{{Peritonitis}} | {{Peritonitis}} | ||
{{CMG}}; {{AE}}{{SCh}} | {{CMG}}; {{AE}}{{SCh}} | ||
* Spontaneous bacterial peritonitis is thought to result from a combination of factors often related to Cirrhosis and | * Spontaneous bacterial peritonitis is thought to result from a combination of factors often related to Cirrhosis and preexisting ascites, such as: | ||
* In patients with diseased liver and altered portal circulation a defect in the usual phagocytic activity results in the hematogenous spread of organisms | |||
* prolonged [[bacteremia]] secondary to compromised host defenses | |||
* Intrahepatic shunting of colonized [[blood]] and | |||
* Defective bactericidal activity within the ascitic fluid<ref name="pmid3371881">{{cite journal| author=Runyon BA| title=Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis. | journal=Hepatology | year= 1988 | volume= 8 | issue= 3 | pages= 632-5 | pmid=3371881 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3371881 }} </ref><ref name="pmid4018735">{{cite journal| author=Runyon BA, Morrissey RL, Hoefs JC, Wyle FA| title=Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis. | journal=Hepatology | year= 1985 | volume= 5 | issue= 4 | pages= 634-7 | pmid=4018735 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4018735 }} </ref>. 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. | |||
* With respect to compromised [[immune system|host defenses]], patients with severe acute or chronic liver disease are often deficient in [[Complement system|complement]] and may also have malfunctioning of the [[neutrophil]]ic and [[reticuloendothelial systems]]. | * With respect to compromised [[immune system|host defenses]], patients with severe acute or chronic liver disease are often deficient in [[Complement system|complement]] and may also have malfunctioning of the [[neutrophil]]ic and [[reticuloendothelial systems]]. | ||
* 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<ref name="pmid3770358">{{cite journal| author=Runyon BA| title=Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. | journal=Gastroenterology | year= 1986 | volume= 91 | issue= 6 | pages= 1343-6 | pmid=3770358 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3770358 }} </ref>. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP. | * 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<ref name="pmid3770358">{{cite journal| author=Runyon BA| title=Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. | journal=Gastroenterology | year= 1986 | volume= 91 | issue= 6 | pages= 1343-6 | pmid=3770358 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3770358 }} </ref>. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP. | ||
Revision as of 19:27, 12 January 2017
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Peritonitis Main Page |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]
- Spontaneous bacterial peritonitis is thought to result from a combination of factors often related to Cirrhosis and preexisting ascites, such as:
- In patients with diseased liver and altered portal circulation a defect in the usual phagocytic activity results in the hematogenous spread of organisms
- prolonged bacteremia secondary to compromised host defenses
- Intrahepatic shunting of colonized blood and
- Defective bactericidal activity within the ascitic fluid[1][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.
- 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.
- 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[3]. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.
Secondary peritonitis
Bacteria and digestive enzymes act on the peritoneal serosal surface lead to enzymatic digestion and necrosis and an outpouring of serum protein and electrolytes from the blood to the cavity. There is formation of exudate rich in granulocytes, which may be diffuse or confined to an abscess. Systemically, there is paralysis of the bowel, hemoconcentration occurs, and alterations of the cardiac output due to the shift of fluids and later acidosis. Intrapulmonary shunting, hypo- or hypercapnia, hypoxemia, progressive azotemia, acute tubular necrosis, weight loss by protein consumption, fall of body temperature, loss of heat production, and exhaustion are other complications that may lead to the death of the patient, if the process is not interrupted.
References
- ↑ Runyon BA (1988). "Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis". Hepatology. 8 (3): 632–5. PMID 3371881.
- ↑ 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. PMID 4018735.
- ↑ Runyon BA (1986). "Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis". Gastroenterology. 91 (6): 1343–6. PMID 3770358.