Peritonitis pathophysiology: Difference between revisions
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* The main causes of peritonitis are the acute inflammation of the abdominal viscera, discontinuity and increased permeability of their walls, open and closed traumas of the abdomen with the damage of viscera followed by microbial contamination of peritoneal cavity. | * The main causes of peritonitis are the acute inflammation of the abdominal viscera, discontinuity and increased permeability of their walls, open and closed traumas of the abdomen with the damage of viscera followed by microbial contamination of peritoneal cavity. | ||
* Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation. | * Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation. | ||
* Chronic peritonitis mainly | * Chronic peritonitis is caused mainly by extraperitoneal (lungs, lymph nodes) tuberculosis, entering the peritoneal cavity through hematogenous route.<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. | ||
=Secondary peritonitis= | ==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. | 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== | ==References== | ||
Revision as of 03:12, 31 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]
Overview
Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritants.Release of bile or gastric juices initially causes chemical peritonitis, infection occurs when bacteria enter and contaminate the peritoneal cavity.Bacterial peritonitis is usually caused by normal enteric flora like E.coli, Klebsiella. Inflammatory process causes shift of fluid into the peritoneal cavity(third spacing) which leads to hypovolemia, septicemia and multi-organ failure resulting in death of the patient if not adequately diagnosed and treated early.
Pathogenesis of peritonitis
- The main causes of peritonitis are the acute inflammation of the abdominal viscera, discontinuity and increased permeability of their walls, open and closed traumas of the abdomen with the damage of viscera followed by microbial contamination of peritoneal cavity.
- Despite the cause of peritonitis, the disease is characterized by a typical bacterial inflammation.
- Chronic peritonitis is caused mainly by extraperitoneal (lungs, lymph nodes) tuberculosis, entering the peritoneal cavity through hematogenous route.[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.