Watershed zones refers to intestinal segments at the end of their respective arterial supplies that are particularly susceptible to ischemia. These zones include the splenic flexure, where the superior and inferior mesenteric arterial circulations terminate, and, to a lesser extent, the sigmoid colon and rectum where inferior mesenteric, pudendal, and iliac arterial circulations end. Generalized hypotension or hypoxemia can therefore cause localized injury at these sites, and ischemic disease should be considered in the differential diagnosis for focal colitis of the splenic flexure or rectosigmoid colon.
Patterns of intestinal microvessls. Intestinal capillaries run alongside the glands, from crypt to surface, before making a hairpin turn at the surface to empty into the postcapillary venules. This configuration leaves the surface epithelium particularly vulnerable to ischemic injury. Thus, surface epithelial atrophy, or even necrosis and epithelial sloughing, with normal or hyperproliferative crypts constitutes a morphologic signature of ischemic intestinal disease.
MORPHOLOGYDespitetheincreasedsusceptibilityofwatershedzones,mucosal and mural infarction mayinvolveanylevelofthegutfromstomachtoanus.Involvementisfrequentlysegmentalandpatchy,andthemucosaishemorrhagicandoftenulcerated.Thebowelwallisthickenedbyedemathatmayinvolvethemucosaorextendintothesubmucosaandmuscularispropria.Withseveredisease,pathologicchangesincludeextensivemucosalandsubmucosalhemorrhageandnecrosis,butserosalhemorrhageandserositisgenerallyareabsent.Damageismorepronouncedinacutearterialthrombosisandtransmural infarction. Blood-tingedmucusorbloodaccumulateswithinthelumen.
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Coagulativenecrosisofthemuscularispropriaoccurswithin1to4daysandmaybeassociatedwithpurulentserositisandperforation.
Microscopicexaminationofischemicintestinedemonstratesatrophy or sloughing of surface epithelium (
Fig.15.20A ).Bycontrast,cryptsmaybehyperproliferative.Inflammatoryinfiltratesareinitiallyabsentinacuteischemia,butneutrophilsarerecruitedwithinhoursofreperfusion.Chronicischemiaisaccompaniedbyfibrousscarringofthelaminapropria(
Fig.
15.20B )and,uncommonly,strictureformation.Inacutephasesofischemicdamage,bacterialsuperinfectionandenterotoxinreleasemayinducepseudomembraneformationthatcanresembleClostridium difficile–associatedpseudomembranouscolitis(discussedlater).
Ischemic bowel disease tends to occur in older adults with coexisting cardiac or vascular disease. Acute transmural infarction typically manifests with sudden, severe abdominal pain and tenderness, sometimes accompanied by nausea, vomiting, bloody diarrhea, or grossly melanotic stool. This presentation may progress to shock and vascular collapse within hours as a result of blood loss. Peristaltic sounds diminish or disappear, and muscular spasm creates boardlike rigidity of the abdominal wall. Because these physical signs overlap with those of other abdominal emergencies, including acute appendicitis, perforated ulcer, and acute cholecystitis, the diagnosis of intestinal infarction may be delayed or missed, with disastrous consequences. As the mucosal barrier breaks down, bacteria enter the circulation and sepsis can develop; the mortality rate in these cases may exceed 50%.
The overall progression of ischemic enteritis depends on the underlying cause and severity of injury: