Purpose: This article reviews the pathophysiology, clinical relevance, and therapy of the catabolic response to surgical stress.
Principle Findings: The key clinical features of perioperative catabolism are hyperglycemia and loss of body protein, both metabolic consequences of impaired insulin function. Muscle weakness and (even moderate) increases in perioperative blood glucose are associated with morbidity after major surgery. Although the optimal glucose concentration for improving clinical outcomes is unknown, most medical associations recommend treatment of random blood glucose > 10 mmol·L(-1). Neuraxial anesthesia blunts the neuroendocrine stress response and enhances the anabolic effects of nutrition. There is evidence to suggest that the avoidance of preoperative fasting prevents insulin resistance and accelerates recovery after major abdominal surgery.
Conclusions: Current anticatabolic therapeutic strategies include glycemic control and perioperative nutrition in combination with optimal pain control and the avoidance of preoperative starvation. All these elements are part of Enhanced Recovery After Surgery (ERAS) programs.
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