Robbins GI Morphology intestinal/colon/rectosigmoid

Question 1

Although the colon is the most common site of gastrointestinal ischemia, mucosal and mural infarction may involve any level of the gut from stomach to anus. The lesions can be continuous but are most often segmental and patchy ( Fig. 17-24 A ). The mucosa is hemorrhagic and may be ulcerated ( Fig. 17-24 B ). The bowel wall is also thickened by edema that may involve the mucosa or extend into the submucosa and muscularis propria.

Answer 1

Although the colon is the most common site of gastrointestinal ischemia, mucosal and mural infarction may involve any level of the gut from stomach to anus. The lesions can be continuous but are most often segmental and patchy ( Fig. 17-24 A ). The mucosa is hemorrhagic and may be ulcerated ( Fig. 17-24 B ). The bowel wall is also thickened by edema that may involve the mucosa or extend into the submucosa and muscularis propria.

Question 2

Substantial portions of the bowel are generally involved in transmural infarction due to acute arterial obstruction. The demarcation between normal and ischemic bowel is sharply defined and the infarcted bowel is initially intensely congested and dusky to purple-red. Later, blood-tinged mucus or frank blood accumulates in the lumen and the wall becomes edematous, thickened, and rubbery. There is coagulative necrosis of the muscularis propria within 1 to 4 days, and perforation may occur. Serositis, with purulent exudates and fibrin deposition, may be prominent.

In mesenteric venous thrombosis, arterial blood continues to flow for a time, resulting in a less abrupt transition from affected to normal bowel. However, propagation of the thrombus may lead to secondary involvement of the splanchnic bed. The ultimate result is similar to that produced by acute arterial obstruction because impaired venous drainage eventually prevents oxygenated arterial blood from entering the capillaries.

Microscopic examination of ischemic intestine demonstrates the characteristic atrophy or sloughing of surface epithelium ( Fig. 17-24 C ). In contrast, crypts may be hyperproliferative. Inflammatory infiltrates are initially absent in acute ischemia, but neutrophils are recruited within hours of reperfusion. Chronic ischemia is accompanied by fibrous scarring of the lamina propria ( Fig. 17-24 D ) and, uncommonly, stricture formation. In both acute and chronic ischemia, bacterial superinfection and enterotoxin release may induce pseudomembrane formation that resemblesClostridium difficile– associated pseudomembranous colitis (discussed later).

Answer 2

Substantial portions of the bowel are generally involved in transmural infarction due to acute arterial obstruction. The demarcation between normal and ischemic bowel is sharply defined and the infarcted bowel is initially intensely congested and dusky to purple-red. Later, blood-tinged mucus or frank blood accumulates in the lumen and the wall becomes edematous, thickened, and rubbery. There is coagulative necrosis of the muscularis propria within 1 to 4 days, and perforation may occur. Serositis, with purulent exudates and fibrin deposition, may be prominent.

In mesenteric venous thrombosis, arterial blood continues to flow for a time, resulting in a less abrupt transition from affected to normal bowel. However, propagation of the thrombus may lead to secondary involvement of the splanchnic bed. The ultimate result is similar to that produced by acute arterial obstruction because impaired venous drainage eventually prevents oxygenated arterial blood from entering the capillaries.

Microscopic examination of ischemic intestine demonstrates the characteristic atrophy or sloughing of surface epithelium ( Fig. 17-24 C ). In contrast, crypts may be hyperproliferative. Inflammatory infiltrates are initially absent in acute ischemia, but neutrophils are recruited within hours of reperfusion. Chronic ischemia is accompanied by fibrous scarring of the lamina propria ( Fig. 17-24 D ) and, uncommonly, stricture formation. In both acute and chronic ischemia, bacterial superinfection and enterotoxin release may induce pseudomembrane formation that resemblesClostridium difficile– associated pseudomembranous colitis (discussed later).

Question 3

Morphologically, angiodysplastic lesions are characterized by ectatic nests of tortuous veins, venules, and capillaries. The vascular channels may be separated from the intestinal lumen by only the vascular wall and a layer of attenuated epithelial cells; limited injury may therefore result in significant bleeding.