Equis ISSN 2398-2977

Gastrointestinal: small intestine - intussusception

Contributor(s): Peter Rakestraw

Introduction

  • Small intestinal intussusception is a cause of abdominal pain in the horse, in one survey it accounted for approximately 0.5% of colic cases seen by a first opinion practice.
  • As the gut lumen becomes obstructed by one section of bowel telescoping into another, obstruction of part of the blood supply also occurs.
  • Signs: intermittent mild bouts of abdominal discomfort to severe abdominal pain with circulatory compromise.
  • Diagnosis: clinical signs, rectal and ultrasound laparotomy findings.
  • Treatment: resection of affected bowel and anastomosis, although in some cases the telescoped section of bowel can be teased apart at surgery.
  • Prognosis: guarded to good, with surgical treatment.

Pathogenesis

Etiology

  • Etiology is usually unknown, however a variety of factors can predispose to the development of intussusceptions.
  • The disease appears to follow changes in gastrointestinal activity, that involve a reduction in the production of co-ordinated smooth muscle activity.
  • Tapeworm presence, or recent tapeworm treatment is a possible predisposer, as is the presence of diarrhea - particularly in foals.

Predisposing factors

General
  • Abnormal gut motility, the cause of this is usually unknown, but hypermotility is thought to be involved. Drinking large amounts of cold water straight after exercise may cause abnormal motility and act as a predisposing factor.
  • Causes of small intestinal obstruction, such as impactions   Ileum: impaction  , and internal hernias   Gastrointestinal: epiploic foramen hernia  can cause secondary hypermotility and thus predispose to volvulus.

Pathophysiology

  • Telescoping of a section of small intestine into itself   →   partial obstruction of the bowel lumen, and partial occlusion of the blood supply to sections of bowel.
  • Pain results due to mesenteric traction of the intussuscepted section of bowel, stretching of the more proximal gut, and, potentially, to bowel compromise and toxin leakage.
  • Bowel compromise due to ischemia is rarely a sequel, but can occur   →   circulatory compromise via release of bacteria and toxins into the bloodstream. Bacteria and toxins can also be released into the peritoneum   →   fluid and white blood cell sequestration to this area. Hypovolemic and endotoxic shock result. Collapse and death due to endotoxemia or gut rupture can follow.
  • More commonly, the disease takes a chronic course, and pathology is largely related to the presence of a partial bowel obstruction.
  • Abnormal intestinal motility results in the telescoping of one section of bowel, and it's attached mesentery and thus blood supply, into another.
  • This results in acute abdominal pain, due to mesenteric traction and devitalization of the intussuscepiens.
  • Devitalistation of the telescoped section of bowel   →   reduction in pain sensation. The associated circulatory and peritoneal pathology that one would expect to occur (see Pathophysiology of small intestinal volvulus   Gastrointestinal: small intestine - torsion  ), is rarely a problem, since it is contained within the intussuscepiens.
  • Chronic intermittent pain usually follows the initial acute stage, and this is mostly due to partial obstruction of the intestinal lumen which can cause pathology due to stretching of the bowel proximal to the lesion (see Pathophysiology of ileal impaction   Ileum: impaction  ).
  • More serious pathology due to vascular compromise can, however occur, and is characterised by the following process
    • Venous drainage of the area is impaired resulting in swelling, edema, and congestion.
    • There is progressive arterial obstruction   →   cyanosis and ischemia of the affected bowel, which contributes to proximal distension of bowel with accumulation of gas and fluid.
    • Intraluminal distension results in progressive ischemia and disruption of the mucosal layers, which leads to necrosis and cell sloughing.
    • Protein-rich fluid, endotoxins and bacteria leak into the gut lumen, and can also leak into the peritoneal cavity.
    • Hypovolemia, endotoxic shock   Endotoxemia: overview  , electrolyte and acid/base abnormalities may develop in such cases.
  • Pain due to the stretching of proximal bowel wall, as well as to gut and vascular compromise at the site of the lesion is continuous, and shows little, or only temporary response to analgesics.

Timecourse

  • Most cases are acute.

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.
  • Gold J R, Belgrave J L & Haldorson G J (2006)Congenital intestinal polyp associated with intussusception in a 3-day-old foal.Equine Vet Educ18(3), 116-119 VetMedResource.
  • Frankeny, R Let al(1995)Jejunal intusseption - a complication of functional and-to-end stapled anastomoses in two ponies.Vet Surg24(6), 515-517 PubMed.
  • McGladdery, A J (1992)Ultrasonography as aid to the diagnosis of equine colic.Equine Vet Educ4(5), 248-251 Wiley Online Library.
  • Greet, T R C (1992)Ileal intussusception in 16 young Thoroughbreds.Equine Vet J24(2), 81-83 PubMed.
  • Edwards, G B (1992)Equine colic - the decision for surgery.Equine Vet Educ3(1), 19-23 VetMedResource.
  • Proudman, C J (1991)A two year, prospective study of equine colic in general practice.Equine Vet J24(2), 90-93 PubMed.

Other sources of information

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


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