The pathophysiology of intestinal damage: effects of luminal distention and ischemia.

Intestinal edema, luminal distention, and ischemia are common pathologic processes involved in producing the intestinal damage found during surgical exploration for acute abdominal disorders in the horse. The severity of intestinal edema depends on the degree of altered intravascular forces and changes in capillary permeability. Capillary hydrostatic pressure rises as the less pliable venules and veins become occluded during intestinal obstruction. Concurrently, the production of various endogenous products that damage the vascular wall leads to increases in capillary permeability and protein exudation, causing fluid movement into the interstitium and consequent tissue edema. The information presently available indicates that luminal distention does not produce the morphologic damage observed during natural conditions. However, slight intestinal edema was observed with experimental distention of the equine small intestine. Although the effects of increased luminal pressure appear minor, in the overall scheme of intestine damage, many processes are occurring together, and the luminal distention may be additive in the production of intestinal damage. The intestinal damage occurring during natural obstructions is most likely related to both the severity of the ischemia and the subsequent reperfusion injury. Experimentally, an ischemic insult produces a consistent sequence of mucosal alterations to both the equine small and large intestine. Severity of ischemia may be the limiting factor in determining the clinical outcome in cases in which the ischemic insult is irreversible; however, if the intestinal tissue survives the ischemia, the reperfusion injury may substantially increase the damage, producing an irreversible injury. The proposed mechanisms responsible for the reperfusion injury include the presence of highly reactive cytotoxic oxygen radicals. The intestinal epithelium and vascular endothelium are both capable of producing these unstable compounds. Secondly, the influx and activation of neutrophils may also release oxygen radicals. During experimental ischemia, neutrophils gradually move to the affected area; however, during reperfusion their numbers dramatically increase and may play a significant role in producing intestinal damage. Therapy for intestinal damage involves first determining the viability of the affected intestine. All nonviable bowel should be resected and viable intestine anastomosed. The care and maintenance of intestine of questionable viability are presently based on therapy in humans and experimental information concerning the pathophysiologic mechanisms of intestinal ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)