Peritonitis
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
Learn what the condition is, how it may be detected early, how it is treated or managed, and which breeds or species are linked to it.
A concise guide to the condition’s pattern, detection, management and urgency.
This snapshot is a general guide, not a diagnosis or treatment plan. New, severe or worsening signs require veterinary assessment.
Peritonitis is inflammation of the membrane lining the abdominal cavity and covering its organs. It may be septic, involving bacteria or gastrointestinal contamination, or sterile after surgery or chemical irritation. Causes include intestinal rupture, penetrating wounds, foaling injury, uterine disease, abdominal surgery, abscess leakage and spread from another infected structure. Primary bacterial peritonitis can occur without an obvious perforation, but a source must be sought carefully.
Signs vary with cause and speed of development. Horses may show fever, depression, loss of appetite, colic, reduced gut sounds, rapid heart rate, diarrhoea, weight loss or reluctance to move. Severe contamination produces endotoxaemia, dehydration, abnormal gums and shock. Protein-rich fluid and inflammatory cells move into the abdomen, while ileus and adhesions impair intestinal function. A chronic localised infection may instead cause intermittent fever, recurrent mild pain and progressive loss of condition.
Peritonitis is not diagnosed simply because abdominal fluid has an increased cell count after surgery. Expected postoperative inflammation must be distinguished from degenerate neutrophils, intracellular bacteria, falling fluid glucose and other findings supporting sepsis. Conversely, a sample collected very early after perforation or trauma can initially appear less abnormal than the horse’s developing disease.
Outcome depends on the source, bacterial contamination, speed of control and whether intestine or another organ is damaged. A treatable primary infection can have a reasonable outlook, while widespread fecal contamination following intestinal rupture is often fatal. Complications include adhesions, abdominal abscesses, persistent ileus, laminitis and recurrent colic.
Contamination may follow bowel rupture, penetrating injury, reproductive-tract trauma or abdominal surgery, while some cases arise without an obvious source. A ruptured stomach or intestine releases feed and bacteria and carries a grave prognosis; localised infection caught earlier may respond. The distinction matters because analgesia can temporarily soften colic signs without stopping continued leakage into the abdomen.
Investigation begins with the history, including recent abdominal surgery, foaling, breeding procedures, penetrating injury and previous colic. Fever, worsening abdominal pain, incisional discharge or unexplained loss of condition deserves prompt examination. Any object penetrating the abdomen should be left in place for veterinary assessment rather than removed, because it may be limiting haemorrhage or contamination.
Abdominocentesis is central to diagnosis. The veterinarian evaluates fluid colour, turbidity, total protein, cell count and cytology, including whether neutrophils are degenerate or contain bacteria. Culture and susceptibility help guide antimicrobials but can be negative after previous treatment. Comparing blood and peritoneal glucose or lactate may strengthen evidence of septic inflammation. Serial samples are useful when early results conflict with clinical deterioration.
Blood counts, inflammatory markers, protein, electrolytes, kidney values and lactate assess systemic impact. Ultrasound identifies free fluid, fibrin, thickened intestine, abscesses or impaired motility and can guide sampling. Rectal examination and surgical exploration may be necessary to locate a leak or devitalised bowel. Monitoring must include digital pulses and hoof temperature because endotoxaemia creates significant laminitis risk.
Treatment has three linked aims: control the source, suppress appropriate infection and support circulation and intestinal function. Broad-spectrum intravenous antimicrobials are commonly started when septic peritonitis is suspected, then refined using culture, likely organisms and clinical response. Intravenous fluids, electrolytes, analgesia and anti-endotoxin care address shock and pain. Plasma support may be considered when protein loss is severe.
Abdominal lavage and drainage can reduce contamination in selected cases. Surgery is required when there is intestinal rupture, devitalised bowel, a foreign body, uncontrolled reproductive-tract injury or another correctable source. No antimicrobial regimen can compensate for an ongoing leak. Ileus may require gastric decompression, nutritional planning and prokinetic treatment. Laminitis prevention and repeated hoof assessment remain important during systemic inflammation.
Response is followed through temperature, comfort, appetite, gut sounds, blood values, ultrasound and repeat abdominal fluid when indicated. Antimicrobial duration should reflect source control and objective improvement rather than an arbitrary short course. Horses recovering from severe disease are refed gradually and monitored later for adhesions, abscess formation and recurrent colic. Prognosis is more favourable when contamination is limited and the source is corrected promptly; diffuse fecal peritonitis, persistent sepsis or major bowel injury carries a poor outlook.
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