Mucosal and mural infarctions by themselves may not be fatal. However, these may progress to more extensive, transmural infarction if the vascular supply is not restored by correction of the insult or, in chronic disease, by development of adequate collateral supplies.
Chronic ischemia may masquerade as inflammatory bowel disease, with episodes of bloody diarrhea interspersed with periods of healing.
Fig. 15.20 Ischemia.(A)Characteristicattenuatedandpartiallydetachedvillousepitheliuminacutejejunalischemia.Notethehyperchromaticnucleiofproliferatingcryptcells.(B)Chroniccolonicischemiawithatrophicsurfaceepitheliumandfibroticlaminapropria.
Cytomegalovirus (CMV) infection causes ischemic gastrointestinal disease as a consequence of the viral tropism for and infection of endothelial cells. CMV infection can be a complication of immunosuppressive therapy (Chapter 9).
Radiation enterocolitis occurs when the gastrointestinal tract is irradiated. In addition to epithelial damage, radiation-induced vascular injury may be significant and produce changes that are similar to ischemic disease.
Necrotizing enterocolitis is an idiopathic disorder of the small and large intestines that can result in transmural necrosis. It is the most common acquired gastrointestinal emergency of neonates, particularly those who are premature or of low birth weight. Its occurrence is often associated with initiation of oral feeding (Chapter 7). Although pathogenesis of necrotizing enterocolitis is not defined, ischemic injury is thought to contribute.
Angiodysplasia, characterized by malformed submucosal and mucosal blood vessels, occurs most often in the cecum or right colon, and usually presents after the sixth decade of life. Although it affects less than 1% of the adult population, angiodysplasia accounts for 20% of major episodes of lower intestinal bleeding.
Hemorrhoids are dilated anal and perianal collateral vessels that connect the portal and caval venous systems to relieve elevated venous pressure within the hemorrhoid plexus. Thus, although hemorrhoids are less serious than esophageal varices, the pathogenesis of these lesions is similar. They are common, affecting about 5% of the general population. Common predisposing factors include constipation and associated straining, which increase intraabdominal and venous pressures, venous stasis of pregnancy, and portal hypertension.
Collateral vessels within the inferior hemorrhoidal plexus are located below the anorectal line and are termed external hemorrhoids, while those that result from dilation ofthesuperiorhemorrhoidalplexuswithinthedistalrectum are referred to as internal hemorrhoids. On histologic examination, hemorrhoids consist of thin-walled, dilated, submucosal vessels beneath anal or rectal mucosa. These vessels are subject to trauma, which leads to rectal bleeding. In addition, they can become thrombosed and inflamed.
Hemorrhoids often manifest with pain and rectal bleeding, particularly bright red blood seen on toilet tissue. Hemorrhoids also may develop as a result of portal hypertension, where the implications are more ominous. Hemorrhoidal bleeding generally is not a medical emergency; treatment options include sclerotherapy, rubber band ligation, and infrared coagulation. In severe cases, hemorrhoids may be removed surgically by hemorrhoidectomy.
Intestinalischemiacanoccurasaresultofeitherarterial or venous obstruction.
Ischemicboweldiseaseresultingfromhypoperfusionismostcommonatthesplenicflexure,sigmoidcolon,andrectum; http://ebooksmedicine.net thesearewatershed zones wheretwoarterialcirculationsterminate.
Systemicvasculitidesandinfectiousdiseases(e.g.,CMVinfection)cancausevasculardiseasethatisnotconfinedtothegastrointestinaltract.