Peritonitis pathophysiology: Difference between revisions
No edit summary |
No edit summary |
||
| (10 intermediate revisions by the same user not shown) | |||
| Line 2: | Line 2: | ||
{{Peritonitis}} | {{Peritonitis}} | ||
{{CMG}}; {{AE}}{{SCh}} | {{CMG}}; {{AE}}{{SCh}} | ||
==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. | |||
==Secondary peritonitis== | |||
Bacteria and digestive enzymes act on the peritoneal serosal surface leading 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== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
Latest revision as of 03:19, 31 January 2017
|
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.
Secondary peritonitis
Bacteria and digestive enzymes act on the peritoneal serosal surface leading 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.