Etiology

• The epiploic foramen is a channel through which the greater and lesser omental sacs communicate (it is a 4-6 cm slit-like opening).
• It is bounded dorsally by the liver and caudal vena cava and ventrally by the hepato-duodenal ligament, the pancreas and the hepatic portal vein.
• EFE most commonly occurs in a left-to-right direction; occasionally the right-to-left form may be seen.
• Entrapment of the intestinal loop most frequently results in a strangulating obstruction of small intestine.
• The hernia may involve ileum or jejunum alone or both. 
• Up to 18 m of small intestine may be involved.

Predisposing factors

General

• Age - there is dispute as to whether older animals are predisposed to EFE (see above).

Pathophysiology

• Epiploic foramen entrapment consists of passage of a section of bowel through the epiploic foramen.
• Pain results due to stretching of the obstructed bowel, mesenteric traction, bowel compromise, toxin leakage and intestinal distension proximal to the obstruction.
• The circulatory effects of bowel compromise due to intestinal strangulation result from bacteria and toxins entering the blood stream; collapse and death due to endotoxemia can occur.
• Passage of food into an incarcerated section of gut can cause a build up of pressure, and this, together with increased tightness of the edges of the foramen around the gut loop contribute to pathology of an entraped bowel loop, particularly at the points where it enters and leaves the hernia.
• Reduced blood supply to the incarcerated section of bowel results in devitalization of the bowel wall. This can be very mild, resulting merely in release of toxins and inflammatory mediators, or may be more serious  → bowel compromise and necrosis.
• Effects on the blood supply of the bowel cause systemic signs, via the following process:
  • Venous drainage of the area is impaired resulting in swelling, edema, and congestion.
  • There may be 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.
  • Protein rich fluid leaks into the gut lumen and the peritoneal cavity.
  • Endotoxins and bacteria may 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 may develop.
• Partial obstruction of the gut lumen also results in pathology due to stretching and hypertrophy of the bowel proximal to the lesion - see Pathophysiology of ileal impaction Ileum: impaction.
• Pathology due to vascular compromise (where it exists) is, however, more serious; the severity depends on the extent of vascular compromise.
• 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) may be seen, and metabolic acidosis can occur causing tachypnea.
• Where gut compromise is severe, peritoneal fluid may become serosanguinous, to turbid in appearance.
• In some cases the clinical indicators of bowel and circulatory compromise are minimal, this may be due to the ischemic potion of bowel being effectively walled off within the omental bursa.

Timecourse

• This depends on the degree of vascular obstruction; some cases may take a chronic course over several days, but in rare cases where severe circulatory compromise is present, bowel wall damage can → endotoxic shock, and death can follow within hours.