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Abdomen: peritonitis

pequis

Introduction

  • Peritonitis is defined as inflammation of the peritoneal lining.
  • It can be diffuse or focal and can cause acute or chronic disease.
  • Cause: mechanical, infectious or chemical irritation of the peritoneal lining.
  • Signs: abdominal pain, depression, pyrexia, diarrhea and weight loss.
  • Diagnosis: is based on the confirmation of abnormal peritoneal fluid.
  • Treatment: antibiotics, NSAIDs, and (potentially) abdominal lavage depending on underlying cause.
  • Prognosis: guarded. Can be life-threatening.

Pathogenesis

Etiology

  • Peritonitis can be defined as primary or secondary, septic or non-septic, diffuse or focal and acute or chronic.
  • Primary peritonitis may occur in the absence of peritoneal damage or an obvious source of infection. The precise etiology is not fully understood, but some impairment of peritoneal defenses (immunodeficiency or suppression) may be involved. It is often difficult to identify the cause of peritonitis.
  • Secondary peritonitis may occur secondary infectious (bacterial, viral, parasitic or fungal) or non-infectious (chemical, neoplastic or toxic) stimuli. The most common causes include colic, when ischemia of a section of bowel allows the leakage of toxins and bacteria, or gut rupture may occur. Peritonitis has rarely been reported secondary to viral disorders such as influenza, EVA, EIA and African Horse Sickness. Urogenital injuries can also result in chemical or bacterial peritonitis, as can the spread of infection from other areas such as the liver, kidneys or internal abscesses and the spread of internal parasites.
  • Iatrogenic peritonitis can occur following gross contamination of a laparotomy site at surgery, abdominocentesis Abdomen: abdominocentesis with accidental enterocentesis, liver biopsy Liver: biopsy, castration or grade 3 or 4 rectal tears Rectum: tear.
  • Blunt or penetrating trauma to the abdomen can result in hemoabdomen or septic peritonitis if the peritoneal lining is disrupted.
  • Most cases in the horse are secondary, acute, diffuse and septic or primary, acute, diffuse and non-septic.
  • A variety of bacterial species have been isolated from septic peritonitis cases, eg B. fragilisActinobacillus equuli Actinobacillus equuliE. coli Escherichia coliS. zooepidemicus Streptococcus sppStaphylococcus spp Staphylococcus sppR. equi Rhodococcus equiClostridium spp Clostridia spp, etc. Mixed infections are common.

Predisposing factors

General

  • Severe colic that involves bowel ischemia/rupture.
  • Laparotomy, abdominocentesis, liver biopsy, castration.
  • Trauma to abdominal wall or urogenital organs.
  • Parasitic migration.
  • Viral infection.

Pathophysiology

  • Damage to viscera in the peritoneal cavity can allow the leakage of cells and bacteria into the peritoneal cavity. Alternatively, bacteria may arrive in the peritoneum in the absence of visceral damage where impairment of the peritoneal defenses has occurred. In either case, inflammation of the peritoneum occurs.
  • Inflammation of the peritoneum is characterized by an increase in peritoneal fluid, and an increase in cellularity and protein content of the fluid. In addition, the peritoneum also becomes more permeable, allowing the entry of more toxins and bacteria to the peritoneal cavity.
  • Inflammation of the peritoneal cavity can result in impairment of organ function, as well as loss of appetite and pain.
  • The severity of the disease is related to a number of factors including the underlying cause, the nature of the infectious agent(s), the resistance of the host, speed of recognition and intervention, and the response to initial therapy.
  • Inflammation of the mesothelial lining of the peritoneal cavity results in an increased blood supply and peritoneal effusion and fibrin deposition. The peritoneum also becomes more permeable, an increase in cellularity of peritoneal fluid occurs with chemotactic phagocytosis, but leakage of toxins and bacteria also becomes increased.
  • Leukocytes and immunoglobulins are mobilized by the inflammatory response.
  • Re-distribution of proteins, fluid and electrolytes from the plasma also occurs.
  • Absorption of pathogen associated molecular patterns (PAMPs), eg lipopolysaccharide (endotoxin) can result in systemic inflammatory response syndrome (SIRS). This can lead to marked hypovolemia and cardiovascular compromise and is associated with mortality.
  • Normal peritoneal fluid suppresses fibrin precipitation. Inflammation, however, depresses fibrinolytic activity and fibrin precipitates. This aids confinement of an area of contamination and infection, but ultimately is a cause of adhesion formation and pain, as well as potentially compounding the processes that result in hypovolemia, hypoproteinemia Hypoproteinemia and also the development of ileus.
  • When ileus occurs, it leads to bowel wall ischemia and further peritonitis.

Timecourse

  • Timecourse varies from acute, for instance where gut rupture results in toxemia, circulatory failure and death within hours, to chronic, when low grade peritoneal inflammation manifests itself over several weeks to months.

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.
  • Dart A J & Bischofberger A S (2011) Peritonitis in the horse: A treatment dilemma. Equine Vet Educ 23 (6), 294-295 VetMedResource.
  • Tennent-Brown B S et al (2010) Common variable immunodeficiency in a horse with chronic peritonitis. Equine Vet Educ 22 (8), 393-399 VetMedResource.
  • Witonsky S (2010) CVID in a horse with chronic peritonitis: Case review and overview of other immunodeficiencies. Equine Vet Educ 22 (8), 400-402 VetMedResource.
  • Delgado M A, Monreal L et al (2009) Peritoneal d-Dimer concentration for assessing peritoneal fibrinolytic activity in horses with colic. J Vet Intern Med 23 (4), 882-889 PubMed.
  • Henderson I S F, Mair T S, Keen J A, Shaw D J & McGorum B C (2008) Study of the short- and long-term outcomes of 65 horses with peritonitis. Vet Rec 163 (10), 293-297 PubMed.
  • Blikslager A T (2006) Peritonitis in the horse. Equine Vet Educ 18 (3), 143 VetMedResource.
  • Semevolos S A et al (2006) Perforating jejunal diverticulosis in 2 horses. Equine Vet Educ 18 (3), 139-142 VetMedResource.
  • Snalune K L & Mair T S (2006) Peritonitis secondary to necrosis of the apex of the urinary bladder in a post-parturient mare. Equine Vet Educ 18 (1), 20-24 VetMedResource.
  • Ragle C A (2006) Assessment of peritonitis in the complicated post partum mare. Equine Vet Educ 18 (1), 24-26 VetMedResource.
  • Browning A (2005) Diagnosis and management of peritonitis in horses. In Pract 27 (2), 70-75 VetMedResource.
  • Chase J P, Beard W L, Bertone A L & Goltz K (1996) Open peritoneal drainage in horses with experimentally induced peritonitis. Vet Surg 25 (3), 189-194 PubMed.
  • Hawkins J F, Bowman K F, Roberts M C & Cowen P (1993) Peritonitis in horses - 67 cases (1985-1990). JAVMA 203 (2), 284-288 PubMed.
  • Mair T S, Hillyer M H & Taylor F G (1990) Peritonitis in adult horses - a review of 21 cases. Vet Rec 126 (23), 567-570 PubMed.
  • Hinchcliff K W, MacWilliams P S & Wilson D G (1988) Seminoperitoneum and peritonitis in a mare. Equine Vet J 20 (1), 71-73 PubMed.

Other sources of information

  • Mair T S (1999) Peritonitis. In: Proc 38th BEVA Congress. pp 93-95.
  • Rose R J & Hodgson D R (1993) Manual of Equine Practice. Saunders. ISBN: 0 7216 3739 6.

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