Peritonitis

ISSN 2398-2942

Contributor(s) :

Introduction
Pathogenesis
Diagnosis
Treatment
Prevention
Outcomes
Further Reading

Introduction

Peritonitis may be diffuse (when the whole of the peritoneal cavity is involved) or localized (where the process becomes walled-off, generally by the omentum).
Cause: usually the result of bacterial peritoneal contamination.
Signs: acute diffuse bacterial peritonitis may cause pyrexia, depression, pain, sometimes vomiting and will progress to septic shock with tachycardia and hypovolemia.
Diagnosis: palpation, radiography, ultrasonography and abdominocentesis.
Treatment: manage hypovolemia and endotoxic shock, then surgical exploration to address underlying cause.
Prognosis: guarded.

Print off the owner factsheet on Peritonitis Peritonitis to give to your client.

Presenting signs

Depression.
Vomiting Vomiting.

Abnormal pain (may adopt abnormal posture indicative of abdominal pain).
Abdominal distension.

Acute presentation

Hypovolemia shock Shock.
Death.

Pathogenesis

Etiology

Primary

Very rarely hematogenous in the dog.

Secondary

Septic

Gastrointestinal tract leakage secondary to:
- Gastrointestinal tract wound dehiscence following surgery (most common cause) .
- Foreign bodies that damage and devitalize intestinal tissue, especially linear FBs Intestine: linear foreign bodies .
- Non-steroidal anti-inflammatory drugs and/or corticosteroids that ulcerate gastric and small intestinal mucosa.
- Infiltrative and erosive neoplasms.
- Intussusception Intussusception.
- Intestinal/mesenteric volvulus.
- Penetrating abdominal wounds.
- Ischemic intestinal disease .

The risk of septic peritonitis following gastrointestinal surgery is greatest at 3-5 days post-operatively and careful monitoring is imperative during this time. Any signs of deterioration should be followed with thorough patient assessment to rule out septic peritonitis.

Bacterial contamination from ruptured urogenital tract (pyometra Pyometra, prostatic abscess ).
Migrating foreign bodies, eg ruptured sublumbar abscess.
Post-surgical infection following any abdominal surgery.

Aseptic

Bile from extra-hepatic biliary trauma or gall bladder necrosis.
Urine from urinary tract trauma Bladder: trauma rupture.
Pancreatic enzymes released in pancreatitis Pancreatitis: acute.
Particulate matter, eg talc or gauze fibers following surgical intervention , barium leakage from perforated bowel following a radiological study.
Migrating parasitic larvae.

Pathophysiology

Leakage of intestinal bacteria into the peritoneal cavity induces inflammation of the mesothelial cells lining the peritoneal cavity resulting in activation of pro-inflammatory mediators.
Consequent increased microvascular permeability to causes transudation of plasma protein, electrolytes and phagocytic cells. Excessive nitrous oxide release results in arteriovenous dilation and decreased systemic vascular resistance, systemic hypotension and compensatory tachycardia.
Bacteria or bacterial components, such as gram-negative lipopolysaccharide, may be absorbed resulting in bacteremia and potentially septic shock Shock: septic.
A systemic response due to inflammatory mediator release will then result in the release of catcholamines and adrenocortical hormones.
Exudation of fluid into the peritoneal cavity (third spacing) results in profound electrolyte derangements, hypovolemia and hypoalbuminemia.
Systemic inflammatory response syndrome Systemic inflammatory response syndrome (SIRS) , multiple organ dysfunction Multiple organ dysfunction syndrome, disseminated intravascular coagulation Disseminated intravascular coagulation → death.