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

• 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.