ABSTRACT
More recent studies have examined the effects of small intestinal intraluminal distention and decompression on the microvasculature. For example, distention of the jejunum to an intraluminal hydrostatic pressure of 25 cm H2O for 120 minutes resulted in a significant reduction in the number of perfused vessels in the seromuscular and mucosal layers, and vascular perfusion remained abnormal after decompression.1 Furthermore, during distention, blood flow to the intestine was reduced by 50%, and microvascular permeability increased after decompression, suggesting that reperfusion injury was occurring in
Simple Obstruction Simple obstruction of the intestinal lumen typically involves an intraluminal obstructive mass composed of ingesta or foreign material, such as bailing twine, a piece of hay net, or rubber fencing. Additionally, endogenously formed obstructive masses, specifically enteroliths, also cause simple obstruction. All of these obstructive masses block the passage of ingesta and secreted fluid, but they do not directly interrupt intestinal blood flow, at least during the early phases of obstruction. As simple obstructive masses persist, however, fluid, gas, and ingesta accumulate proximal to the mass, resulting in increased intraluminal pressure that ultimately compresses the intestinal intramural blood supply, resulting in the onset of localized intestinal ischemia.1,2 Furthermore, obstructive masses may ultimately directly compress the intestinal wall surrounding them, particularly as the masses are forced distally by propulsive intestinal motility into regions of the intestine having a smaller luminal diameter. For example, an enterolith formed in the distal aspect of the ascending colon may be small enough to reach the small colon, where it may fully occlude the lumen, and begin to induce mural-pressure necrosis, ultimately leading to intestinal rupture in some cases.3
