Resuscitation and support

Acute intestinal ischemia involves loss of body fluids, the effects of bacterial invasion, and the absorption of toxic factors into the portal and systemic circulations.

Fluid loss initially consists of water, electrolytes, and protein. This results in hemoconcentration and a fall in circulating volume, leading to impaired flow to both the gut wall itself and the rest of the body. Replacement is guided by urine output, hematocrit, and central venous or pulmonary artery wedge pressure. Depending on the hemodynamic status, liberal quantities of balanced saline, colloid, or protein solutions are given until the patient is adequately resuscitated. Monitoring of cardiac output provides additional accuracy both before and during operation.

Bacterial invasion and toxemia clearly demand the use of antibiotics. In the necessary absence of laboratory control, the chosen regimen will often include an aminoglycoside, such as gentamicin, coupled with metronidazole to combat anaerobic organisms. Polymyxin B may have a specific protective effect against mucosal ischemia and endotoxemia. In fact, although antimicrobial therapy is logical, the acute and sporadic nature of these problems precludes controlled trials and there is no concrete evidence of any effect on mortality.

Metabolic acidosis is due to the combination of poor tissue perfusion, hemoconcentration, and absorption of the products of gut necrosis. To this is added a respiratory component, resulting from impaired respiratory movement and increased blood viscosity with intrapulmonary sludging. Measurements of PCO2 and arterial pH will guide the amount of support required.

Additional measures

Laboratory evidence suggests that a-blocking agents (phenoxybenzamine), b-stimulators (isoproterenol), and inotropic agents (dopamine and glucagon) increase flow in the mesenteric circuit and may preserve viability. Clinical information is not available, and it is doubtful whether, in the presence of a blocked superior mesenteric artery or massive shutdown of the minute vessels, they penetrate the gut wall. Additionally, the hypotension that these agents (particularly phenoxybenzamine) produce may be difficult to control.

The gut mucosa is uniquely rich in xanthine dehydrogenase which, in the circumstances of ischemia, converts to xanthine oxidase resulting in the production of toxic reactive oxygen metabolites including superoxide (O2-), peroxide (H2O2), and the hydroxyl radical (OH-). This oxidative tissue damage is particularly severe during reperfusion. The process can be mitigated by the use of superoxide dismutase which 'scavenges' oxygen, catalase which reduces H 2O2, and dimethylsulfoxide which scavenges OH-. Another agent which may be useful in the preservation of acute mesenteric ischemia is allopurinol which blocks xanthine oxidase. Laboratory results suggest that, to be effective, the therapy must be given before the ischemic injury occurs. Although no controlled information is to hand, it would seem a wise precaution to cover operations for elective reconstruction of the mesenteric arteries with superoxide dismutase and allopurinol.

Digitalis and other cardiac glycosides constrict the mesenteric vessels and can provoke intestinal necrosis ( BMlkIey.┬žnd.MMa,h.D 1988). Nonetheless, in the control of congestive heart failure and atrial fibrillation, their effect will be to raise cardiac output and improve mucosal flow.

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