糖尿病酮症酸中毒性脑水肿引起的死亡可见于二种不同的情况,即昏迷病人及接受治疗的神智清醒的病人。 1936年Dillon等对8名脑水肿病人进行了观察,这些病人无感染,在酮症酸中毒1—3天后发生昏迷。当半数病人的高血糖和酸血症已得到改善后,一些病人却于2—24小时内死亡。临终前以休克和发热为特征,这些迹象通常于治疗开始后出现。所有病人脑毛细血管广泛扩张,内皮细胞变性,血管及细胞周围水肿。尸检时未发现其他死亡原因。Dillon等的结论为,毛细血管改变引起的脑水肿可使糖尿病昏迷病人发生休克和呼吸衰竭。 1948年Kety等对未经治疗的糖尿病昏迷病人进行了研究,他们的观察表明,这些病人常常发生脑血流调节紊乱,这可能反映出 Diabetic ketoacidosis Brain edema-induced death can be seen in two different situations, namely coma patients and treated sober patients. In 1936, Dillon et al. Observed 8 cerebral edema patients who had no infection and were unconscious after 1-3 days of ketoacidosis. When half of the patients have had their hyperglycemia and acidosis improved, some patients die within 2-24 hours. Pre-dying is characterized by shock and fever, and these signs usually appear after treatment begins. All patients with extensive expansion of the brain capillaries, endothelial cell degeneration, blood vessels and peripheral edema. No other cause of death was found at necropsy. Dillon et al. Concluded that cerebral edema caused by capillary changes can cause shock and respiratory failure in diabetic coma. In 1948, Kety et al. Studied untreated diabetic coma patients. Their observations showed that these patients often had disorders of cerebral blood flow regulation, which may reflect