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Stress Hyperglycemia

應激性高血糖血症

摘要


如第二型糖尿病患者,在胰島素阻抗狀態下,肝細胞葡萄糖輸出增加及周邊組織葡萄糖利用率下降,導致了危重病患的高血糖血症。這是應激性高血糖血症的核心機制。2001年之後,Van den Berghe G認為高血糖可以導致細胞能量代謝異常及後續器官衰竭,所以在病患進住重症加護病房幾天以後,發生併發症及死亡,可歸因於高血糖及感染性併發症的增加。所以積極使用胰島素,維持血糖濃度(140mg/dL-200mg/dL),是當前ICU照護的新策略。更複雜的事,是外源性營養素的投入,加劇了最初的問題:嚴格血糖控制或是否營養攝取達到預定目標。這是兩難的議題,因為長期低熱量餵養會導致病患營養不良。但急重病患可以容忍多長時間低熱量餵養,仍在辯論中。利用胰島素輸注控制血糖,看起來多麼簡單,但應激性高血糖血症的分子機制與臨床效益,仍需要進一步的探討。

並列摘要


Morbidity and mortality in Intensive Care Units (ICU) occurring beyond the first few days of critical illness are attributable to the increased susceptibility to infectious complications. As is the case in insulin resistance in type II DM, increase of hepatic glucose output and decrease of peripheral glucose utilization in critically ill patients resulting in high blood glucose are the core mechanisms of stress hyperglycemia. After 2001, Van den Berghe G considered that persisted hyperglycemia leads to the disturbance of cellular energy metabolism and subsequent organ failure. Maintaining glucose concentration (140 mg/dL-200 mg/dL) using insulin infusion aggressively is a new strategy of current ICU practice. The most complicated factor is exogenous nutritional inputs exacerbating the original problem: glucose control or targeting nutrition goal. It is still a subject of debate of how long hypocaloric feeding can be tolerated in acutely ill patients. Blood sugar control with insulin infusion seems to be simple and straightforward. The molecular mechanisms of stress hyperglycemia and clinical benefits of IIT need to be further studied.

被引用紀錄


黃惠敏(2014)。重症病患之血糖與C-反應蛋白值對呼吸器脫離的影響〔碩士論文,中山醫學大學〕。華藝線上圖書館。https://doi.org/10.6834/CSMU.2014.00041

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