Equis ISSN 2398-2977

Cecum: torsion

Contributor(s): Peter Rakestraw

Introduction

  • Cecal torsion is a very rare cause of severe abdominal pain in the horse.
  • As the gut twists obstruction of both its lumen and its blood supply occurs.
  • Signs: severe abdominal pain and distension with circulatory compromise.
  • Diagnosis: clinical signs, rectal and laparotomy findings.
  • Treatment: resection of affected bowel and anastomosis.
  • Prognosis: guarded.

Pathogenesis

Etiology

  • Usually secondary to torsion of ascending colon.
  • The cause of primary cecal torsion is usually unknown.
  • Abnormal gut motility is usually thought to be involved.
  • Other possible factors are cecocolic fold hypoplasia and abnormal dorsal mesenteric attachments.

Predisposing factors

General
  • Dietary change.
  • Tympanitic colic - gas accumulation allows the cecum to 'float' into an abnormal position.
  • Pregnancy/parturition.

Pathophysiology

  • Torsion of the cecum causes blockage of both the lumen of the cecum, and its blood supply.
  • Pathology relates to both bowel and circulatory compromise.
  • Pain results due to mesenteric traction, stretching of the more proximal gut, and to bowel compromise and toxin leakage.
  • Bowel compromise due to ischemia can occur, particularly in cases of 360° torsion. It results in circulatory compromise via release of bacteria and toxins into the bloodstream. Although the lack of collateral circulation means that cecal wall compromise develops relatively early in the course of disease, signs take longer to develop than in similar cases involving the small intestine.
  • Bacteria and toxins can also be 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 or gut rupture can follow.
  • Obstruction of the intestinal lumen can cause pathology due to stretching of the bowel proximal to the lesion.
  • 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 resulting in swelling, edema, and congestion.
    • There is progressive arterial obstruction, which causes cyanosis and ischemia of the affected bowel, which causes gut spasm, and 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. 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, causing 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. Although pain often initially seems relatively mild, the course of disease means that more severe pain develops, and the pain is unremitting.
  • 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) and plasma proteins (TPP) are seen, and metabolic acidosis causes tachypnea.
  • 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.

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.
  • Suthers J Met al(2013)Survival of horses following strangulation large colon volvulus.Equine Vet J45(2), 219-223 PubMed.
  • Dart A J, Dowling B & Hodgson D R (1999)Caecal disease.Equine Vet Educ11(4), 182-188 VetMedResource.
  • Dabareiner R M & White N A II (1997) Diseases and surgery of the cecum.Vet Clin North Am Equine Pract13(2), 303-315 PubMed.
  • Dart A Jet al(1997)Cecal disease in the eqiuds.Aust Vet J75(8), 552-557 PubMed.
  • McGladdery A J (1992)Ultrasonography as aid to the diagnosis of equine colic.Equine Vet Educ4(5), 248-251 Wiley Online Library.
  • Proudman C J (1992)A two year, prospective study of equine colic in general practice.Equine Vet J24(2), 90-93 PubMed.
  • Edwards G B (1991)Equine colic - the decision for surgery.Equine Vet Educ3(1), 19-23 VetMedResource.
  • Walmsley J P (1991)Subacute colic caused by epiploic foramen incarceration of the small intestine in a horse.Equine Vet Educ3(1), 13-15 VetMedResource.
  • Foerner J J (1982) Diseases of the large intestine - differential diagnosis and surgical management.Vet Clin North Am [Large Anim Pract]4(1), 129-146 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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