Extended hospitalization is associated with varying degrees of malnutrition. Since the observation that length of ICU stay correlated with transplant liver function, i.e., a longer stay adversely affects function, attention has focused on nutritional support of the donor. In the catabolic, brain-dead patient receiving inadequate nutritional support hepatic glycogen stores are rapidly depleted. Glycogen represents the only fuel available for ATP generation during anoxic cold storage. ATP depletion renders the liver more susceptible to ischemic damage during an-oxic storage and reperfusion injury following revascularization. Numerous animal and some clinical studies support the administration of glucose to replete glycogen stores with improvement in posttransplant hepatocellular function. In practice, repletion of glycogen stores requires 24-48 hours, therefore a major limitation to this approach is time. Donor instability often precludes such an approach.
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