[Alterations of blood glucose homeostasis during septic or injury stress--hyperglycemia].

Le résumé fourni par la source

Claude Bernard in the late 19th century, was one of the first who recognized that acute injury was associated with the development of hyperglycemia. In 1942 David Cutherbertson introduced the terms ebb and flow to describe the phases of hypo- and hypermetabolism, which follow traumatic injury. Hyperglycemia during the ebb phase is promoted by hepatic glycogenolysis secondary to catecholamine release, as well as by direct sympathetic stimulation of glycogen breakdown. Hyperglycemia is a prominent feature of the flow phase in patients who sustain more severely injured or in whom septic complications develop. It results from augmented glucose production in the presence of insulin resistance in peripheral tissues. The flow phase is clinically expressed as a syndrome consisting of: hypermetabolism (manifested by hyperglycemia, hyperlactatemia and protein catabolism), hyperdynamic cardiovascular state and clinical manifestations of fever or hypothermia, tachycardia, tachypnoea and leucocytosis. The hypermetabolic response to stress may be prolonged when there is stimulus for continuous formation of mediators--a persistent focus of injury or infection. Three systems are responsible for translating the initial insult into the stress response: nervous, endocrine and humoral (cytokine). These systems are interrelated. Maximal metabolic response to stress requires the participation of all three systems. Although glycogenolysis increases hepatic glucose output during the ebb phase, this effect is transient because glycogen stores are rapidly depleted. In contrast, the flow phase is characterized by a sustained increase in gluconeogenesis, which in turn promotes hyperglycemia. Hyperglycemia is common following stress, despite the fact that many tissues exhibit increased cellular uptake and utilization of glucose. Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. In addition, hepatic insulin resistance also plays a role in the genesis of hyperglycemia during stress. In general, the degree of hyperglycemia and insulin resistance are directly proportional to the severity of the stress response. Hyperlactatemia and oxygen consumption also increase concurrently with the severity of stress. Modest hyperglycemia during stress may be of potential benefit by promoting cellular glucose uptake, however, severe hyperglycemia may be associated with complications, this in turn could result in organs dysfunction.

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