Equis ISSN 2398-2977

Gastrointestinal: small intestine - obstruction

Synonym(s): Small intestinal obstruction

Contributor(s): Roberta Baxter, Alfred Merritt

Introduction

  • Small intestinal obstruction is a cause of abdominal pain in the horse. In one survey it accounted for 40% of all surgical colics.
  • Cause: cases can be divided into simple obstructions, eg due to feed impaction, or strangulating obstructions, the etiology of which involves vascular compromise.
  • Signs: moderate to severe abdominal pain, usually continuous rather than intermittent, which responds only temporarily to medication. If the affected section of bowel becomes totally necrotic, the pain may subside but the cardiovascular parameters will deteriorate.
  • Diagnosis: clinical examination, rectal examination, ultrasonographic examination, laparotomy.
  • Treatment: the use of supportive medical treatment, laxatives, surgery.
  • Prognosis: fair to poor, depending on the degree of vascular compromise and duration of the problem.

Pathogenesis

Etiology

  • Usually unknown.
  • Parasites.
  • Lipomas in older horses.
  • Consumption of chunks of feedblocks has been an identified cause.
  • Poor mastication of coarse hay.

Predisposing factors

General

  • Narrowing of the small intestine due to thickening of the wall, eg intramural neoplasia or inflammatory disease, extramural compression, eg lipomata or abcesses, adhesions, strictures and fibrous bands, which may be congenital or may result from previous surgery and can cause folding and kinking of the bowel. In addition, reactive hypertrophy of the bowel wall proximal to lesions can be a predisposing factor.
  • Intraluminal foreign bodies, eg roundworms in young horses Parascaris equorum infestation, tapeworms in older ones Tapeworm infection.
  • Abnormal bowel motility → intussusception - can be associated with tapeworms Tapeworm infection/larval strongyle migration Strongyle infestation: large or other neurogenic causes.
  • Local ischemia of the bowel wall, due to worms, torsion of the bowel/mesenteric root.
  • Consumption of abnormal ingesta which is insufficiently chewed.

Specific

Pathophysiology

Simple obstruction

  • Impaction of small intestine with food material/foreign body causes obstruction of lumen. This → local pressure and stretching of the bowel wall and pain Abdomen: pain - adult.
  • Vascular compromise is uncommon.
  • Accumulated fluid and gas proximal to the lesion cause further stretching and pain.
  • In cases where the vascular supply is compromised, the venous system may be obstructed first → intramural edema in the affected section, which causes serosal stretching and pain. Once arterial supply to that section is also cut off, the pain may subside because the tissue is totally dead.
  • The bowel wall associated with and proximal to the lesion becomes compromised resulting in more pain, leakage of bacteria and endotoxins and circulatory compromise.
  • Fluid produced in the upper gastrointestinal tract is prevented from reaching the lower gastrointestinal tract where it should be reabsorbed → dehydration and circulatory shock. Fluid and white blood cell sequestration occurs and hypovolemic and endotoxic shock result.
  • The edotoxemia and subsequent cardiovascular compromise will more likely be due to leakage of endotoxin and bacteria through mucosa than sequestration of fluid in the bowel.
  • Fluid accumulation within the proximal small intestine and stomach → progressive atonia of the affected intestinal wall which becomes increasingly compromised → more endotoxin release and more pain.
  • Fluid accumulation can → intestinal or gastric rupture with death a likely sequel.

Strangulating obstruction

  • The initial obstruction to the small intestine is caused by torsion of the small intestine, strangulation due to an extramural mass such as a pedunculated lipoma, the development of an intussusception Gastrointestinal: small intestine - intussusception, or an internal hernia/incarceration.
  • Circulatory compromise is one of the first effects due to constriction of the blood supply to the affected section of bowel wall which rapidly becomes ischemic. The result is a more rapid progression of circulatory abnormalities, hypovolemic and endotoxic shock.

Conclusion

  • In either case severe pain due to stretching of the bowel wall and tissue compromise develops rapidly and is unresponsive to, or only briefly responsive to, analgesics.
  • Large volumes of nasogastric reflux can usually be released on nasogastric intubation Gastrointestinal: nasogastric intubation; in some cases spontaneous nasogastric reflux occurs.
  • Peritoneal fluid aspiration Abdomen: abdominocentesis normally yields serosanguineous to turbid fluid with increased levels of protein and leukocytes.
  • Circulatory abnormalities include dehydration, increased capillary refill time with congestion or cyanosis of the mucus membranes, decreased pulse quality and tachycardia Heart: sinus tachycardia Heart: ventricular tachycardia.

Timecourse

  • The more proximal the obstruction, the more rapid the development of signs.
  • Within 4 h bowel wall damage can follow vascular compromise and death can result rapidly.

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 from PubMed and VetMedResource.
  • Freeman D E, Schaeffer DF J & Cleary O B (2014) Long-term survival in horses with strangulating obstruction of the small intestine managed without resection. Equine Vet J 46 (6), 711-717 PubMed.
  • Little D & Blikslager A T (2002) Factors associated with development of ileal impaction in horses with surgical colic: 78 cases (1986-2000). Equine Vet J 34 (5), 464-468 PubMed.
  • Mair T S (2002) Small intestinal obstruction caused by a mass of feedblock containing molasses in 4 horses. Equine Vet J 34 (5), 532-536 PubMed.
  • Morton A J & Blikslager A T (2002) Surgical and postoperative factors influencing short-term survival of horses following small intestinal resection: 92 cases (1994-2001). Equine Vet J 34 (5), 450-454 PubMed.
  • Grulke S, Gangl M, Deby-Dupont G, Caudron I, Deby C & Serteyn D (2002) Plasma trypsin level in horses suffering from acute intestinal obstruction. Vet J 163 (3), 283-291 PubMed.
  • Singer E R & Smith M A (2002) Examination of a horse with colic: is it medical or surgical? Equine Vet Educ 14 (2), 87-96 VetMedResource.
  • van den Boom R & van der Velden M A (2001) Short- and long-term evaluation of surgical treatment of strangulating obstructions of the small intestine in horess: a review of 224 cases. Vet Q 23 (3), 109-115 PubMed.
  • McGladdery A J (1992) Ultrasonography as an aid to the diagnosis of equine colic. Equine Vet Educ 4 (5), 248-251 Wiley.
  • Edwards G B (1991) Equine colic - the decision for surgery. Equine Vet Educ 33 (1), 19-23 VetMedResource.


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