Equis ISSN 2398-2977

Ileum: impaction

Introduction

  • Ileal impaction is a cause of abdominal pain that is seen in approximately 1-2% of colic cases.
  • Cause: simple obstruction occurs due to intra-luminal blockage of the small intestine with ingesta. Any diseases that cause narrowing of the ileal lumen can predispose to this.
  • Signs: abdominal pain that usually responds only temporarily to medication.
  • Diagnosis: rectal examination, or laparotomy may be necessary.
  • Treatment: includes use of analgesics, fluids and laxatives, as well as surgery.
  • Prognosis: guarded.

Pathogenesis

Etiology

  • Etiology is usually unknown, but predisposing factors for ileal impaction include causes of extra-mural compression, causes of ileal wall thickening, intramural abnormalities, abnormal gut motility, and abnormal character of ingesta.
  • Extra-mural compression can be due to:
    • Extra luminal masses such as pedunculated lipomata   Abdomen: lipoma - pedunculated  . Although these can cause strangulation, if they become wrapped around a section of bowel, they can also cause direct compression of adjacent bowel. These are particularly common in older horses.
    • Strictures or fibrous bands, that may follow previous surgery or may be congenital, can cause bowel compression as well as predisposing to internal hernias. These include remnants of the vitelline arteries/mesodiverticular bands, and Meckel's diverticulum can be involved.
    • Adhesions are a common consequence of previous colic surgery   Abdomen: adhesions  , and can cause loops of bowel to be connected together, or to other organs such as the spleen. They can be localized, or widespread, but can cause compression and kinking of the bowel, and can also predispose to intenal herniation and volvulus.
    • Mesenteric abcesses can occur, particularly following the septicemic spread of respiratory infections such as strangles. Loops of gut become adhered to abcesses in areas of localized peritonitis.
  • Causes of bowel wall thickening include:
    • Ileal muscle hypertrophy is a distinct clinical entity involving thickening of the ileal musculature. This can occur associated with the presence of tapeworms, and can also have neurogenic causes.
    • Hypertrophy of the musculature also develops proximal to any other cause of luminal narrowing, due to an increase in peristaltic tone locally to keep ingesta moving through the damaged area.
    • Intramural neoplasia or inflammatory disease also can cause bowel wall thickening. Lymphosarcoma is the commonest type of neoplasia   Gastrointestinal: neoplasia  in this area.
  • Intraluminal foreign bodies (especially in young horses) can also predispose to the development of impactions, as can the presence of large numbers of worms in the gut lumen (particularly roundworms in young foals). Intussusceptions (commonest in yearling Thoroughbreds) also cause partial blockage of the lumen.
  • Abnormalities in gut motility may be involved, a combination of hyperperistalsis with segmental atony can occur, and in some cases larval strongyle migration is implicated in this.
  • Other predisposing factors include poor quality food (and eating of bedding), inadequate mastication and water deprivation.

Predisposing factors

General
  • Narrowing of the small intestinal lumen can, in itself, increase the chance of an impaction, it also can cause muscular hypertrophy of the more proximal gut due to increase in peristaltic intensity required to propel food past the lesion. This muscular hypertrophy can also increase the chances of impaction formation.
  • Poor quality food.
  • Dental disease/inadequate mastication.
  • Worms - particularly tapeworms but also roundworms in young horses.
  • Water deprivation.

Specific

  • Ileal hypertrophy, particularly of the muscular wall of the terminal ileum. may be due to tapeworms   Tapeworm infection  , or may have neurogenic basis.

Pathophysiology

  • Impaction of the small intestine with food material can occur due to a combination of factors.
  • The ileum is a predeliction site for impactions because of its narrow lumen, and anything that causes further narrowing of the lumen such as strictures, extra-luminal masses or adhesions, intramural neoplasia, ileal hypertrophy and even presence of foreign bodies can all increase the chance of an impaction occuring. Poorly masticated, dry food material is also more likely to cause a blockage.
  • The presence of impacted food material causes local pressure and pain.
  • The consequent build up of fluid and gas in the more proximal intestines results in further stretching of the bowel with the progression of pain, bowel wall compromise, and secondary circulatory compromise.
  • Gut rupture can follow.
  • Obstruction of the intestine prevents the passage of fluid produced in the upper alimentary tract (the volume of which in the course of one day almost equals the extracellular volume of the horses at approximately 125 liters) from reaching the lower bowel from where it can be absorbed. This can result in fluid sequestration, nasogastric reflux, and dehydration.
  • This depletion of circulating fluid volume, and subsequently of cardiac output can result in the development of circulatory shock.
  • Simultaneously, stasis of intestinal fluid proximal to the obstruction results 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 occurs, 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 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 characterised by metabolic acidosis.

Timecourse

  • The more proximal, the faster the development of clinical signs.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references fromPubMedandVetMedResource.
  • Merritt A M, Burrow J A & Hartless C S (1998)Effect of xylazine, detomidine and a combination of xylazine and butorphanol on equine duodenal motility.Am J Vet Res59(5), 619-623PubMed.
  • White N A II & Dabareiner R M (1997)Treatment of impaction colics.Vet Clin North Am Equine Pract13(2), 243-259PubMed.

Other sources of information

  • Rose R J and Hodgson D R.Manual of Equine Practice.Saunders (1993) ISBN 0 7216 3739 6.


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