目的:探讨糖尿病酮症中毒并发脑水肿的临床特征以及危险性。方法:随机选取50例患有糖尿病酮症酸中毒患者进行临床观察与分析,将并发脑水肿的患者分为研究组,未并发脑水肿的患者分为参考组,并对两组患者的临床资料进行比较。结果:50例患者当中,研究组患者即并发脑水肿患者例数为9例(18%),经过临床诊断后判定为重度的酮症酸中毒,与其他未并发脑水肿却同等酮症酸中毒情况的患者相比,研究组患者在接受临床治疗期间血钠提升的速度较为缓慢,个别患者还会出现降低的情况,尿素氮的水平较非研究组患者较高。在研究组9例患者当中,有5例患者进行了碳酸氢盐的应用,剂量大于参考组。结论:糖尿病在并发重度的酮症酸中毒时较为容易引发脑水肿,在临床当中对血钠变化、血尿素氮变化以及碳酸氢盐剂量的控制不合理,会使得脑水肿的危险性增加,进而造成严重的不良后果。 Objective: To investigate the clinical characteristics and risk of diabetic ketosis with cerebral edema. Methods: Fifty patients with diabetic ketoacidosis were randomly selected for clinical observation and analysis. Patients with concomitant cerebral edema were divided into study group, patients without concomitant cerebral edema were divided into reference group and clinical data of two groups Compare. Results: Among the 50 patients, the number of patients in study group was 9 (18%) with concurrent cerebral edema. After clinical diagnosis, severe ketoacidosis was found, which was the same as ketoacidosis without cerebral edema Patients in the study group had a slower rate of increase in serum sodium during their clinical course of treatment compared with patients in the study group. Some patients also experienced a decrease in blood urea nitrogen levels compared with those in the non-study group. Of the 9 patients in the study group, 5 patients underwent bicarbonate therapy at doses greater than the reference group. CONCLUSIONS: Diabetes mellitus is more likely to cause cerebral edema in patients with severe ketoacidosis. In clinical practice, it is not reasonable to control the changes of serum sodium, blood urea nitrogen and bicarbonate dosage, which will increase the risk of cerebral edema and further Causing serious adverse consequences.