Etiology

• Etiology is usually unknown, but predisposing factors for ileal impaction include causes of extra-mural compression, causes of ileal wall thickening, intramural abnormalities, abnormal gut motility, and abnormal character of ingesta.
• Diet:
  • In areas of highest prevalence, diet appears to be the most common reason for development. In this region, Coastal Bermuda hay is believed to be cause. Many horses eat this hay with no problem, however, changes in quality can predispose. Additionally, horses that are abruptly switched to Coastal Bermuda hay from a different diet are also at higher risk for developing ileal impactions.
• Extra-mural compression can be due to:
  • Extra luminal masses such as pedunculated lipomata Abdomen: lipoma - pedunculated. Although these most typically cause strangulation, if they become wrapped around a section of bowel, they can also cause direct compression of adjacent bowel. These are particularly common in older horses.
  • Strictures or fibrous bands, that may follow previous surgery or may be congenital, can cause bowel compression as well as predisposing to internal hernias. These include remnants of the vitelline arteries/mesodiverticular bands, and Meckel's diverticulum can be involved.
• Causes of bowel wall thickening include:
  • Ileal muscle hypertrophy is a distinct clinical entity involving thickening of the ileal musculature. This can occur associated with the presence of tapeworms Tapeworm infection, and can also have neurogenic causes.
  • Hypertrophy of the musculature also develops proximal to any other cause of luminal narrowing, due to an increase in peristaltic tone locally to keep ingesta moving through the damaged area.
  • Intramural neoplasia or inflammatory disease also can cause bowel wall thickening. Lymphosarcoma Lymphosarcoma: overview is the commonest type of neoplasia Gastrointestinal: neoplasia in this area.
• Intraluminal foreign bodies (especially in young horses) can also predispose to the development of impactions, as can the presence of large numbers of worms in the gut lumen (particularly roundworms in young foals). Intussusceptions (commonest in yearling Thoroughbreds Thoroughbreds) also cause partial blockage of the lumen.
• Abnormalities in gut motility may be involved, a combination of hyperperistalsis with segmental atony can occur, and in some cases larval strongyle migration is implicated in this.
• Other predisposing factors include poor quality food (and eating of bedding), inadequate mastication and water deprivation.

Predisposing factors

General

• Narrowing of the small intestinal lumen can, in itself, increase the chance of an impaction, it can also cause muscular hypertrophy of the more proximal gut due to increase in peristaltic intensity required to propel food past the lesion. This muscular hypertrophy can also increase the chances of impaction formation.
• Poor quality food (especially round bale hay).
• Coastal Bermuda hay.
• Dental disease Teeth: dental disease - overview/inadequate mastication.
• Worms: particularly tapeworms Tapeworm infection but also roundworms in young horses.
• Water deprivation.

Specific

• Ileal hypertrophy, particularly of the muscular wall of the terminal ileum, may be due to tapeworms Tapeworm infection, or may have neurogenic basis.

Pathophysiology

• Impaction of the small intestine with food material can occur due to a combination of factors.
• The ileum is a predilection site for impactions because of its narrow lumen, and anything that causes further narrowing of the lumen such as strictures, extra-luminal masses or adhesions, intramural neoplasia, ileal hypertrophy and even presence of foreign bodies can all increase the chance of an impaction occurring. Poorly masticated, dry food material is also more likely to cause a blockage.
• The presence of impacted food material causes local pressure and pain.
• The consequent buildup of fluid and gas in the more proximal intestines results in further stretching of the bowel with the progression of pain, uncommonly bowel wall compromise, and secondary circulatory compromise.
• Gut rupture in ileal impactions is quite rare but can follow.
• Obstruction of the intestine prevents the passage of fluid produced in the upper alimentary tract (the volume of which in the course of one day almost equals the extracellular volume of the horses at approximately 125 liters) from reaching the lower bowel from where it can be absorbed. This can result in fluid sequestration, nasogastric reflux, and dehydration.
• This depletion of circulating fluid volume, and subsequently of cardiac output can result in the development of circulatory shock.
• Simultaneously, stasis of intestinal fluid proximal to the obstruction results in the multiplication of intestinal bacteria and the release of gas. Increased pressure within the bowel due to fluid and gas build up causes distension, which results in an increase in pain, as well as a decrease in peristalsis. The result is progressive filling and swelling of the gut, and atonia of the gut wall.
• Without treatment, progressive damage to the intestinal wall may occur.
• Endotoxemia Endotoxemia: overview may result, and this can cause further sensitization of the pain receptors. Electrolyte and fluid sequestration contribute to the development of circulatory collapse.
• In general, the more proximal the obstruction, the more acute the onset of signs, the more the pain, and the greater the volume of fluid buildup in the stomach. Large quantities of chloride are lost into the gastric fluid, and metabolic alkalosis can result.
• More distal obstructions tend to present more gradually, and tend to be characterized by metabolic acidosis.

Timecourse

• The more proximal, the faster the development of clinical signs.