Acute mesenteric ischemia: pathophysiology, diagnosis, and treatment.

摘要: Ischemia has been traditionally defined as an insufficiency of oxygen delivery by the blood. Lately it become clear that such a view is too restrictive. Hypoperfusion may be caused both anatomic and functional impediments to either inflow or outflow from organ. Furthermore, pathophysiologic consequences are likely involve not only cellular hypoxia, but also restricted supply nutrients other important molecules, abnormal elimination physiologic wastes carbon dioxide. Acute mesenteric ischemia (AMI) is, therefore, severe limitation splanchnic circulation, resulting in dual defect intestinal hypoxia hypercarbia. It complex syndrome includes three related processes: occlusive ischemia, nonocclusive sepsis-induced ischemia. Acute local impairment blood flow. Arterial occlusion usually embolism rather than thrombosis. Mesenteric vein thrombosis responsible for 20% acute ischemia. This condition termed primary when no predisposing factors can identified. Secondary occur portal hypertension, intraabdominal infection, carcinomatosis (particularly gastrointestinal pancreatic). Nonocclusive nonobstructive reduction below critical level where consumption becomes dependent tissues resort anaerobic metabolism. Nonocclusive observed shock syndromes, low-flow states, drug-induced vasoconstriction, hypotension complicating vasodilator therapy, conditions. Preexisting vascular disease diabetes with small vessel arteriosclerosis will predispose ischemia. Visceral characterized synthesis acceleration catabolism adenosine triphosphate. finally occurs because reduced demand excessive, combination both. Depressed generally develops diminished delivery. consequence severely uptake, utilization apparatus. Excessive acid produced buffered, thereby generating CO2 anaerobically. The increase production, coupled removal due absent flow, forms basis cellular, tissue, venous Splanchnic flow sensitive numerous including autonomic nervous system, hormones, endogenous mediators, various drugs. Reperfusion injury secondary damage ischemic after reestablishment intense vasospasm mucosa. oxygen-derived free-radical-mediated damage. transformation provides rationale vasodilatory therapy ischemia. Sepsis intricately associated evolution AMI almost always complicated sepsis enteric organisms. Sepsis-induced tract dysfunction appears visceral probably uncontrolled inflammation. When AMI, marks point at which process acquires multisystemic dimension, heralding multisystem organ failure its dismal prognosis. The difficulty early diagnosis most cause high mortality, varies 60% 90%. particularly difficult elderly lack specificity paucity symptoms. must made on index suspicion. Clinical clues include nausea, vomiting, diffuse abdominal pain out proportion symptoms. The compounded revealing laboratory data, often nonspecific consist moderate leukocytosis, hyperamylasemia, lactic acidosis. Rarely, plain film abdomen suggest diagnosis. Angiography demonstrate vasospasm, arterial occlusion, obstruction. Other diagnostic modalities under investigation mucosal tonometry, ultrasonic duplex scanning, flexible endoscopy, laparoscopy, surface oximetry, infrared photoplethysmography, 31P magnetic resonance spectroscopy. Most cases diagnosed long episode started. treatment two major goals: prevention infarction forestallment failure. Management established involves treating well systemic consequences, sepsis. There types care: resuscitative, operative, nonoperative.