ISSN 2398-2993      

Peritonitis

obovis
Contributor(s):

Ash Phipps

Mike Reynolds


Introduction

  • Cause:
    • Primary peritonitis is associated with systemic infection.
    • Secondary peritonitis occurs after an abdominal surgical procedure or as a consequence of a viscus perforation and abdominal contamination.
  • Signs:
    • Peritonitis is inflammation of the peritoneum accompanied by abdominal discomfort, pyrexia, +/-toxemia and alternation in fecal output.
    • Acute clinical disease is associated with characteristic clinical signs (abdominal pain, abdominal distension, anorexia, pyrexia, hypogalactia/milk drop, ileus, scleral injection, toxemia, dehydration, tachycardia, atonic rumen and scant feces).
    • Chronic clinical disease is associated with more non-specific clinical signs (mild recurrent abdominal discomfort, weight loss, ‘tucked-up’ appearance with diarrhea).
  • Diagnosis:
    • May be challenging, as the clinical presentation is similar to many other diseases.
    • Diagnostic procedures include; withers test, clinical pathology, abdominocentesis, ultrasonography, radiology, rectal palpation and exploratory laparotomy.
  • Treatment:
    • May depend on the underlying disease process.
    • General treatment consists of broad spectrum antimicrobials and anti-inflammatories. In severe cases, intravenous fluid therapy and abdominal lavage may be indicated.
  • Prognosis: The prognosis is likely to be guarded, but will depend on the underlying disease process and severity of the peritonitis.

Pathogenesis

Etiology

Pathophysiology

  • There are six factors that contribute to the clinical presentation of peritonitis in cattle;
    • Toxemia and septicemia - toxins produced by bacteria that have gained entry into the peritoneal cavity (through a perforating injury, impaired surgical hygiene or rupture of the gastrointestinal tract) are readily absorbed by the peritoneum and are responsible for the clinical illness observed. The degree of clinical illness observed will be dependent on the type of bacteria present and the type of toxins produced.
    • Shock and hemorrhage - if a large quantity of fecal matter or uterine fluid is deposited into the abdomen, shock and significant hemorrhage occurs.
    • Abdominal pain - often a variable sign in cattle. In severe cases, cattle may have a reduced response to pain stimuli. However, in less severe cases, cattle display abdominal discomfort when palpating the abdominal wall and often adopt a ‘tucked-up’ appearance.
    • Paralytic ileus - results due to the reflex inhibition of the alimentary tract (potential functional obstruction of the intestine) resulting in reduced fecal output.
    • Exudate - accumulation of large volumes of inflammatory exudate within the abdominal cavity (this may result in abdominal distension).
  • Adhesions - cattle respond to peritoneal trauma with the deposition of fibrin (thrombin converts fibrinogen to fibrin) which forms adhesions in an attempt to wall off and localize the infection within the peritoneal cavity .

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Hussain S A, Uppal S K, Sood N K, Randhawa C S & Prabhakar S (2011) Clinical, Haemato-biochemical findings and Therapeutic management of Peritonitis in Cattle. Intas Polivet 12 (2), 283-289.
  • Fecteau G (2005) Management of Peritonitis in Cattle. Vet Clin North Am Food Anim Pract 21, 155-171 PubMed.
  • Wilson A D, Hirsch V M & Osborne A D (1985) Abdominocentesis in cattle: technique and criteria for diagnosis of peritonitis. Can Vet J 26 (2), 74 PubMed.

Other sources of information

  • Radostits O M, Gay C C, Blood D C & Hinchliff K W (2006) Veterinary Medicine. A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 7th edn, Saunders, China, pp 282-287.
  • Parkinson T J, Vermunt J J & Malmo J (2010) Diseases of cattle in Australasia: a comprehensive textbook. New Zealand Veterinary Association Foundation for Continuing Education, Wellington, New Zealand, pp 123-125.

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