Equis ISSN 2398-2977

Gastrointestinal: stricture

Contributor(s): Peter Rakestraw

Introduction

  • Intestinal strictures are an uncommon cause of obstructive colic.
  • They may be congenital or acquired.
  • Signs: include symptoms of abdominal pain.
  • Diagnosis: requires laparotomy.
  • Treatment: may include sectioning of an external band, or resection and anastomosis may be necessary.
  • Prognosis: guarded to good depending on the exact cause.

Pathogenesis

Etiology

Congenital
  • Causes include congenital defects, and congenital remnants of the vitelline artery/mesodiverticular band.
  • Meckel's diverticulum may also be associated with stricture formation.

Acquired

  • These include intramural neoplasia and muscular hypertrophy of the terminal ileum (see Ileal impaction   Ileum: impaction  ).

Specific

  • Previous gastrointestinal surgery.

Pathophysiology

  • Presence of intestinal strictures causes obstruction to the intestinal lumen.
  • Disease develops due to an obstruction which is usually partial, but may be progressive.
  • In many cases partial stricture causes no clinical signs, or only very mild bouts of abdominal pain that may manifest as nothing more than intermittent inappetance. Such cases are unlikely to be diagnosed or treated. In rare cases where clinical signs do develop they may be related to partial luminal obstruction causing mild and intermittent bouts of abdominal pain (which may again go undiagnosed) or the development of more serious and severe signs as the degree of obstruction increases.
  • Most commonly partial obstruction of the intestines causes pathology via localized hyper-peristalsis and resulting muscular hypertrophy of the proximal intestine, as it works harder to advance ingesta.
  • Some swelling of the proximal portion also results.
  • Pain due to bowel swelling and hypermotility occurs.
  • The muscular hypertrophy of the proximal intestine can become a vicious circle since it causes further luminal narrowing.
  • This depletion of circulating fluid volume, and subsequently of cardiac output, can result in the development of circulatory shock.
  • Stasis of intestinal fluid proximal to the obstruction can result in the multiplication of intestinal bacteria and the release of gas. Increased pressure within the bowel due to fluid and gas build up causes distension, which results in an increase in pain, as well as a decrease in peristalsis. The result is progressive filling and swelling of the gut, and atonia of the gut wall.
  • Without treatment, progressive damage to the intestinal wall can occur, with degeneration, cell sloughing, and vascular compromise. Endotoxemia   Endotoxemia: overview  may result, and this can cause further sensitization of the pain receptors. Electrolyte and fluid sequestration contribute to the development of circulatory collapse.
  • In general, the more proximal and complete the obstruction, the more acute the onset of signs, the more the pain, and the greater the volume of fluid build up in the stomach. Large quantities of chloride are lost into the gastric fluid, and metabolic alkalosis can result.
  • More distal obstructions tend to present more gradually, and tend to be characterized by metabolic acidosis.
  • Rarely, if complete obstruction of the intestine develops, the passage of fluid produced in the upper alimentary tract (the volume of which in the course of one day almost equals the extra-cellular volume of the horses at approximately 125 liters) may be prevented from reaching the lower bowel from where it can be absorbed. This can result in fluid sequestration, nasogastric reflux, and dehydration.

Timecourse

  • Variable.

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 Jet al(1992)Resection and anastomosis of the small colon in four horses.Aust Vet J69(1), 5-7 PubMed.
  • Rose P Let al(1991)Surgical correction of strictures of the large colon in three horses.Vet Surg20(4), 260-263 PubMed.


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