Peritonitis overview: Difference between revisions

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==Pathogenesis==
==Pathogenesis==
=='''Secondary peritonitis'''==
*The virulence of the bacteria that cause peritonitis is enhanced when certain microorganisms are either combined intraperitoneally with substances such as mucus, enzymes, or hemoglobin or are combined with certain other microorganisms.
*Chemical peritonitis can be produced by escape of bile or of gastric or pancreatic secretions into the peritoneal cavity. When ''gastric acid'' escapes into the peritoneal cavity, there is an outpouring of serum protein and electrolytes from the blood into the peritoneal cavity. The acidity is neutralized quickly by these buffers and by diffusion of hydrogen ions into the body fluids. Widespread necrosis may result from enzymatic digestion after intraperitoneal spillage of potent pancreatic enzymes. Escape of ''bile'' into the peritoneal cavity is generally considered to be a grave, often fatal situation. *The severity of peritonitis after escape of these intestinal secretions results in subsequent bacterial peritonitis. *Bacteria may enter the peritoneal cavity with contaminated intestinal secretions through perforations in the gastrointestinal wall or by migration through the wall of the intact gastrointestinal tract in response to irritation of the serosal surface by bile and possibly other intestinal tract secretions.
*Establishment of an anaerobic infection requires a favorable environment. These requirements are usually met by tissue devitalized as a consequence of ischemia, trauma, or neoplastic growth. When proper conditions are obtained, anaerobic organisms can achieve doubling rates equivalent to rates seen with aerobic enteric bacilli. In vivo, the rapidly expanding bacterial and inflammatory cell mass, frequently accompanied by gas production, can interrupt the blood supply to the immediately surrounding tissue and cause further tissue necrosis.
*Gram-negative anaerobic cocci and bacilli (including B. fragilis) possess endotoxins, although with much weaker biologic activity in comparison with endotoxins extracted from their aerobic counterparts. In addition, anaerobes may be resistant to host defenses.


==Causes==
==Causes==

Revision as of 16:08, 5 January 2017

Peritonitis Main Page

Patient Information

Overview

Causes

Classification

Spontaneous Bacterial Peritonitis
Secondary Peritonitis

Differential Diagnosis

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 is defined as inflammation of the peritoneum (the serous membrane which lines part of the abdominal cavity and some of the viscera it contains). It may be localised or generalised, generally has an acute course, and may depend on either infection (often due to rupture of a hollow viscus) or on a non-infectious process. Peritonitis generally represents a surgical emergency.

Historical Perspective

Classification

Pathophysiology

Pathogenesis

Causes

Causes (Microbiology)

Differentiating Peritonitis from Other Diseases

Epidemiology and Demographics

Risk Factors

Patients with liver disease are at increased risk. Risk factors for liver disease include alcoholic cirrhosis and other diseases that lead to cirrhosis, such as viral hepatitis (Hepatitis B or C). Spontaneous peritonitis also occurs in patients who are on dialysis for kidney failure.

Screening

Natural History, Complications and Prognosis

Natural History

Complications

Prognosis

With treatment, patients usually do well. Without treatment, the outcome is usually poor. However, in some cases, patients do poorly even with prompt and appropriate treatment.

Diagnosis

Diagnostic Criteria

History and Symptoms

The main manifestations of peritonitis are acute abdominal pain, tenderness, and guarding, which are exacerbated by moving the peritoneum, e.g. coughing, flexing the hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits pain, but releasing the hand abruptly will aggravate the pain, as the peritoneum snaps back into place).

Abdominal pain and tenderness: The localization of these manifestations depends on whether peritonitis is localized (e.g. appendicitis or diverticulitis before perforation), or generalized to the whole abdomen; even in the latter case, pain typically starts at the site of the causing disease. Peritonitis is an example of acute abdomen.

Physical Examination

Laboratory Findings

A diagnosis of peritonitis is based primarily on clinical grounds, that is on the clinical manifestations described above; if they support a strong suspicion of peritonitis, no further investigation should delay surgery. Leukocytosis and acidosis may be present, but they are not specific findings. Plain abdominal X-rays may reveal dilated, oedematous intestines, although it is mainly useful to look for pneumoperitoneum (free air in the peritoneal cavity), which may also be visible on chest X-rays. If reasonable doubt still persists, an exploratory peritoneal lavage may be performed (e.g. in cause of trauma, in order to look for white blood cells, red blood cells, or bacteria).

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Surgery (laparotomy) is needed to perform a full exploration and lavage of the peritoneum, as well as to correct any gross anatomical damage which may have caused peritonitis.[1] The exception is spontaneous bacterial peritonitis, which does not benefit from surgery.

Prevention

References

  1. "Peritonitis: Emergencies: Merck Manual Home Edition". Retrieved 2007-11-25.


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