Metabolic response to surgery: essentials

Abstract

Surgical trauma initiates a complex series of neuroendocrine responses which results in an immediate and profound change in the body's metabolic activity. The resultant metabolic response is intended to counteract the effects of the injury and ensure survival of the organism. If the individual survives the injury, the metabolic environment is further modified to permit an orderly repair. However, if the postoperative period is complicated by additional traumatic events or sepsis, there is continued neuroendocrine activity with a continuation of the adaptive metabolic environment. Over 50 years ago, Sir David Cuthbertson, a Scottish biochemist, described the metabolic response to injury in a systematic and quantitative fashion (Cuthbertson, 1932). He described the main features of this response, which evolve with time, and which he divided into two distinct phases. The initial 'ebb' phase develops immediately following injury, and arises l~rimarily because of a decreased cardiac output, which limits tissue perfusion. This phase persists for a short period of time and is characterized by a decreased oxygen consumption, lowered body temperature and lethargy. With successful resuscitation the 'ebb' gradually gives way to the 'flow' phase, which is characterized primarily by hypermetabolism. There is an increase in oxygen consumption, body temperature and protein breakdown, with a net loss of body nitrogen. In addition, there are significant alterations in the metabolism of carbohydrates, lipid and fluid and electrolytes. The therapeutic objective during the flow period is to provide sufficient substrate to meet the hypermetabolism associated with the heightened cardiovascular and metabolic activity.