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The main pathophysiological feature of sepsis is the uncontrollable activation of both pro-and anti-inflammatory responses arising from the overwhelming pro-duction of mediators such as pro-and anti-inflammatory cytokines. Such an uncontrollable inflammatory response would cause many kinds of metabolic derangements. One such metabolic derangement is hyperglycemia. Accordingly, control of hyperglycemia in sepsis is considered to be a very effective therapeutic approach. However, despite the initial enthusiasm, recent studies reported that tight glycemic control with intensive insulin therapy failed to show a beneficial effect on mortality of patients with severe sepsis and septic shock. One of the main reasons for this disappointing result is the incidence of harmful hypoglycemia during intensive insulin therapy. Therefore, avoidance of hypoglycemia during intensive insulin therapy may be a key issue in effective tight glycemic control. It is generally accepted that glycemic control aimed at a blood glucose level of 80-100 mg/dL, as initially proposed by van den Berghe, seems to be too tight and that such a level of tight glycemic control puts septic patients at increased risk of hypoglycemia. Therefore, now many researchers suggest less strict glycemic control with a target blood glucose level of 140-180 mg/dL. Also specific targeting of glycemic control in diabetic patients should be considered. Since there is a significantcorrelation between success rate of glycemic control and the degree of hypercytokinemia in septic patients, some countermeasures to hypercytokinemia may be an important aspect of successful glycemic control. Thus, in future, use of an artificial pancreas to avoid hypoglycemia during insulin therapy, special consideration of septic diabetic patients, and control of hypercytokinemia should be considered for more effective glycemic control in patients with severe sepsis and septic shock.
The main pathophysiological feature of sepsis is the uncontrollable activation of both pro-and anti-inflammatory responses arising from the overwhelming pro-duction of mediators such as pro-and anti-inflammatory cytokines. Such an uncontrollable inflammatory response would cause many kinds of metabolic derangements However, despite the initial enthusiasm, recent studies reported that tight glycemic control with intensive insulin therapy failed to show a beneficial effect on One of the main reasons for this disappointing result is the incidence of harmful hypoglycemia during intensive insulin therapy. Therefore, avoidance of hypoglycemia during intensive insulin therapy may be a key issue in effective tight glycemic control. It is generally accepted that glycemic control aim ed at a blood glucose level of 80-100 mg / dL, as initially proposed by van den Berghe, seems to be too tight and that such a level of tight glycemic control puts septic patients at increased risk of hypoglycemia. Therefore, now many now suggest less strict glycemic control with a target blood glucose level of 140-180 mg / dL. Also specific targeting of glycemic control in diabetic patients should be considered. Since there is a significantcorrelation between success rate of glycemic control and the degree of hypercytokinemia in septic patients, some of countermeasures to hypercytokinemia may be an important aspect of successful glycemicmia may be an important aspect of successful glycemicmia may be an important aspect of successful glycemicmia may be an important aspect of successful glycemicmia may be an important aspect of successful glycemicmia may be an important aspect of successful glycemicmia during beating hypoglycemia during insulin therapy, special consideration of septic diabetic patients, and control of hypercytokinemia should be considered for more effective glycemic control in patients with severe sepsis and septic shock.