Equis ISSN 2398-2977

Colon: infarction - non-strangulating

Synonym(s): Verminous arteritis Thromboembolic colic


  • Non strangulating infarction is a rare cause of colic.
  • Cause: often unknown but migrating larval strongyles may be implicated.
  • Signs: intermittent low grade colic and chronic wasting to severe and acute abdominal pain with cardio-vascular compromise.
  • The degree of clinical disease depends on the extent of gut that is affected, and the extent of collateral circulation to the area.
  • Diagnosis: requires laparotomy, although pain and edema of the affected bowel wall may be detectable on rectal examination.
  • Treatment: requires surgical resection of affected bowel in acute cases. Some chronic cases may be treatable medically.
  • Prognosis: guarded in surgical cases, but good in chronic low grade cases.



  • Inflammation and damage to the blood supply to the large bowel.
  • This may be due to larval strongyle migration, hence 'Verminous Arteritis'.

Predisposing factors

  • Strongyle infestation.


  • True non-strangulating infarction is uncommon.
  • Migrating strongyles   Strongylus spp    Strongyle infestation: large  are implicated in the cause of this disease, but their role is uncertain.
  • Localized areas of intestinal infarction cause bowel ischemia and necrosis.
  • Hypotension and circulatory shock may lead to hypoxemia and infarction.
  • Pathogenesis is very simmilar to that of strangulating obstruction.
  • Obstruction of the blood supply of a section of bowel due to infarction results in ischemia and necrosis of that section of bowel in the same way as vascular compromise due to intestinal volvulus causes these bowel changes.
  • The severity of pathology determines whether the disease presents as acute and severe or more chronic, depending on the extent of the vascular compromise, and involves:
    • Impaired venous drainage of the area results in swelling, edema, and congestion.
    • Arterial obstruction causes cyanosis and ischemia of the affected bowel, which causes gut spasm, and contributes to proximal distension of bowel with accumulation of gas and fluid.
    • Progressive ischemia leads to disruption of the mucosal layers, which causes necrosis and cell sloughing.
    • Protein rich fluid leaks into the gut lumen, as well as the peritoneal cavity.
    • Endotoxins and bacteria leak into the bloodstream and peritoneal cavity, causing damage to epithelial cells and platelets. Platelets release thromboxane and serotonin causing vasoconstriction. Endothelial cell damage causes the stimulation of neutrophils.
    • Hypovolemia, endotoxic shock, electrolyte and acid/base abnormalities develop.
  • Pain due to the stretching of proximal bowel wall, as well as to gut and vascular compromise at the site of the lesion can be continuous, and show no, or only temporary response to analgesics, however devitalization of affected bowel can lead to loss of sensation.
  • Cardiovascular compromise is reflected by tachycardia, a decrease in pulse quality, mucous membrane congestion or cyanosis, and an increase in capillary refill time. Secondary increases in packed cell volume (PCV) and plasma proteins (TPP) are seen, and metabolic acidosis causes tachypnea.
  • Peritoneal fluid may be sero-sanguinous, and contain increased protein and leukocyte levels, as the disease progresses, these levels rise further, and the fluid takes on a turbid/opaque appearance.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Van Loon G, Deprez P, Muylle E & Sustronck B (1995) Larval cyathostomiasis as a cause of death in two regularly dewormed horses. Zentralbl Veterinarmed A 42 (5), 301-306 PubMed.
  • Mair, T S & Pearson G R (1995) Multifocal non-strangulating intestinal infarction associated with larval cythostomiasis in a pony. Equine Vet J 27 (2), 154-155 PubMed.