The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children
The UK case-control study of cerebral oedema complicating diabetic ketoacidosis in children
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DOI：
10.1007/s00125-006-0363-8
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发表时间：
2006-09-01
期刊：
影响因子：
8.2
通讯作者：
Dunger, D. B.
中科院分区：
文献类型：
--
作者：
Edge, J. A.;Jakes, R. W.;Dunger, D. B.
目的/假设糖尿病酮症酸中毒（DKA）并发脑水肿仍然是1型糖尿病儿童发病和死亡的主要原因，但其病因尚不清楚。我们的目标是确定基线生化因素和治疗相关变量对DKA儿童发生脑水肿风险的影响。材料和方法这是一项英国国家病例对照研究。通过英国儿科监测单位，我们确定了43例脑水肿。通过平行报告系统，我们还确定了2,940例DKA发作，并根据可比的年龄、性别、新发或已知糖尿病病例数和入院日期选择了169例对照受试者。基线生化数据和治疗相关变量提取的情况下，对照subject.Results允许在年龄，性别和新的或已知的糖尿病的差异，在诊断DKA的情况下，更多的酸中毒（比值比[OR]的事件在最少的酸中毒与最酸中毒三分位数=0.02 [95% CI：0.002-0.15]，P < 0.001）。此外，病例基线时钾和尿素水平较高。计算的渗透压摩尔浓度和基线葡萄糖无显著差异。在考虑酸中毒的严重程度后，第一个小时内的胰岛素给药（OR 12.7 [1.41-114.5]，p=0.02）和前4小时内的液体给药量（OR 6.55 [1.38-30.97]，p=0.01）与风险相关。在最终的回归模型中，低基线血浆钠和升高的p（a）CO（2）也有助于风险。Biclitazone管理是不相关的事件的风险增加时纠正acidosis. Conclusion/interpretation在这种情况下，对照研究DKA，基线酸中毒和异常的钠，钾和尿素浓度是脑水肿的风险的重要预测因素。确定的其他风险因素是早期胰岛素给药和大量液体。在设计治疗方案时应考虑这些观察结果。
Aims/hypothesis Cerebral oedema complicating diabetic ketoacidosis (DKA) remains the major cause of morbidity and mortality in children with type 1 diabetes, but its aetiology remains unknown. Our objective was to determine the impact of baseline biochemical factors and of treatment-related variables on risk of the development of cerebral oedema in children with DKA.Materials and methods This was a national UK case-control study. Through the British Paediatric Surveillance Unit we identified 43 cases of cerebral oedema. Through a parallel reporting system, we also identified 2,940 episodes of DKA and selected 169 control subjects on the basis of comparable age, sex, numbers of new or known cases of diabetes and date of admission. Baseline biochemical data and treatment-related variables were extracted from the clinical notes of cases and control subjects.Results Allowing for differences in age, sex and new or known diabetes, cases were more acidotic at diagnosis of DKA (odds ratio [OR] for events in the least acidotic compared with the most acidotic tertile=0.02 [95% CI: 0.002-0.15], p < 0.001). In addition, cases had higher potassium and urea levels at baseline. Calculated osmolality and baseline glucose were not significantly different. After allowing for severity of acidosis, insulin administration in the first hour (OR 12.7 [1.41-114.5], p=0.02) and volume of fluid administered over the first 4 h (OR 6.55 [1.38-30.97], p=0.01) were associated with risk. Low baseline plasma sodium and an elevated p(a)CO(2) also contributed to risk in the final regression model. Bicarbonate administration was not associated with increased risk of an event when corrected for acidosis.Conclusions/interpretation In this case-control study of DKA, baseline acidosis and abnormalities of sodium, potassium and urea concentrations were important predictors of risk of cerebral oedema. Additional risk factors identified were early administration of insulin and high volumes of fluid. These observations should be taken into account when designing treatment protocols.