Equis ISSN 2398-2977

Gastrointestinal: small intestine - torsion

Synonym(s): Twisted gut

Contributor(s): Peter Rakestraw

Introduction

  • Small intestinal volvulus is a cause of severe 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 twists obstruction of both its lumen and its blood supply occurs.
  • Signs: development of severe abdominal pain with circulatory compromise.
  • Diagnosis: clinical signs, rectal and laparotomy findings.
  • Treatment: resection of affected bowel and anastomosis.
  • Prognosis: fair to good.

Pathogenesis

Etiology

  • Etiology is usually unknown, however a variety of factors can predispose to the development of torsions.

Predisposing factors

General
  • Abnormal gut motility, the cause of this is usually unknown, but hypermotility is usually 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   Gastrointestinal: stricture  , such as impactions   Ileum: impaction  , intussusceptions, and internal hernias   Gastrointestinal: epiploic foramen hernia  can cause secondary hypermotility and thus predispose to volvulus.
  • Adhesions may also be involved   Abdomen: adhesions  .

Pathophysiology

  • Rotation of sections of small intestine through up to 180° along the long axis of the mesenteric root results in loss of blood supply to sections of bowel, as well as obstruction of the gut lumen.
  • Rotation of the mesenteric root itself causes obstruction and ischemia to the whole of the small intestine.
  • Pain results due to stretching of the obstructed bowel, to mesenteric traction, and, within hours, to bowel compromise and toxin leakage.
  • Bowel compromise due to ischemia results in circulatory compromise via release of bacteria and toxins into the bloodstream. Bacteria and toxins are also released into the peritoneum causing fluid and white blood cell sequestration to this area. Hypovolemic and endotoxic shock result.
  • Collapse and death due to endotoxemia   Endotoxemia: overview  or gut rupture   Stomach: rupture  can follow.
  • Obstruction of the intestinal lumen can cause pathology due to stretching of the bowel proximal to the lesion - see Pathophysiology of Ileal impaction   Ileum: impaction  .
  • Pathology due to vascular compromise is, however, more serious, and the severity depends on the extent of vascular compromise:
    • Venous drainage of the area is impaired   →   in swelling, edema, and congestion.
    • There is progressive arterial obstruction   →   cyanosis and ischemia of the affected bowel   →   gut spasm.
    • Intraluminal distension   →   progressive ischemia and disruption of the mucosal layers, which   →   necrosis and cell sloughing. Within 4-5 hours the mucosal epithelium is necrotic, after 6-7 hours the necrosis has extended to the external muscular layer.
    • Protein-rich fluid leaks into the gut lumen, as well as the peritoneal cavity.
    • Endotoxins and bacteria leak into the bloodstream and peritoneal cavity   →   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 is continuous, and shows no, or only temporary response to analgesics.
  • 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)   Blood: packed cell volume (PCV)  and plasma proteins (TPP)   Blood: biochemistry - total protein  are seen, and metabolic acidosis causes tachypnoea.
  • Peritoneal fluid is sero-sanguinous, and contains increased protein and leukocyte levels, as the disease progresses, these levels rise further, and the fluid takes on a turbid appearance.

Timecourse

  • This depends on the degree of vascualr obstruction, but within 2-4 hours vascular compromise will cause bowel wall damage, and endotoxic shock and death can follow within hours.

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.
  • Dabareiner R Met al(1993)Evaluation of the microcirculation of the equine jejunum and ascending colon after ischemia and reperfusion.Am J Vet Res54(10), 1683-1692 PubMed.
  • Dabareiner R Met al(1993)Evaluation of the microcccirculation of the equine small intestine after inraluminal distension and subsequent decompression.Am J Vet Res54(10), 1673-1682 PubMed.
  • Proudman C J (1992)A two year, prospective study of equine colic in general practice.Equine Vet J24(2), 90-93 PubMed.
  • McGladdery A J (1992)Ultrasonography as aid to the diagnosis of equine colic.Equine Vet Educ4(5), 248-251 Wiley Online Library.
  • Edwards G B (1991)Equine colic - the decision for surgery.Equine Vet Educ33(1), 19-23 VetMedResource.
  • Moll H D (1991)Small-intestinal volvulus as a complication of acquired inguinal hernia in two horses.JAVMA198(3), 153-156 PubMed.

Other sources of information

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


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