Acute mesenteric ischemia: pathophysiology, diagnosis, and treatment.
Ischemia has traditionally been viewed as arising only from abnormalities of oxygen dynamics, namely the cellular hypoxia resulting from the imbalances between oxygen supply, consumption, and demand. Recently, it has become clear that such a view is too restrictive. Hypoperfusion may be caused by both anatomic and functional impediments to either inflow or to outflow from an organ. Furthermore, the pathophysiologic consequences are likely to involve not only cellular hypoxia, but also a restricted supply of nutrients and other important molecules and an abnormal elimination of physiologic wastes such as carbon dioxide. Hence the recommendation that ischemia be defined as a dual defect of oxygen deficit and carbon dioxide excess. AMI is, therefore, a severe anatomic or functional impediment to the splanchnic circulation, resulting in a dual defect of intestinal hypoxia and cellular hypercarbia. Although the functional and structural consequences of cellular hypoxia are well known, the pathophysiology of cellular hypercarbia has only begun to be explored. AMI syndromes include three related processes: occlusive mesenteric ischemia, nonocclusive ischemia, and sepsis-induced SI. Leakage of bacteria or bacterial toxins into the circulation during mesenteric ischemia forms the basis of the systemic components of this syndrome. Striving for an earlier diagnosis, treating the systemic (septic) consequences, and taking measures to promptly restore mucosal oxygen balance through aggressive pharmacologic and appropriate surgical intervention have significantly improved the prognosis. About 80% of patients with acute arterial embolism, 60% of those with nonocclusive ischemia, and only 20% of patients with arterial thrombosis are expected to live without significant residual nutritional deficits. The cause of death is usually sepsis and multisystem organ failure, and therefore, further reductions in mortality are likely to occur with the improved prevention and treatment of sepsis.
Benjamin
E
E
Mount Sinai School of Medicine, New York, New York.
Oropello
J M
JM
Iberti
T J
TJ
D000208:Acute Disease; D006801:Humans; D007511:Ischemia / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D008641:Mesenteric Vascular Occlusion / Q000209:etiology / Q000503:physiopathology; D008643:Mesentery / Q000098:blood supply*