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严重糖尿病酮症酸中毒时血糖校正后血清钠与神经状态的时间关系。

The temporal relationship between glucose-corrected serum sodium and neurological status in severe diabetic ketoacidosis.

机构信息

Evelina Children's Hospital, Guy's and St Thomas' NHS Foundation Trust, London, UK.

出版信息

Arch Dis Child. 2011 Jan;96(1):50-7. doi: 10.1136/adc.2009.170530. Epub 2010 Oct 4.

Abstract

OBJECTIVE

Cerebral oedema is a potentially devastating complication of diabetic ketoacidosis (DKA). The relationship between osmolar changes, acid-base changes and development of cerebral oedema during therapy is unclear.

DESIGN

Retrospective cohort study on 53 children with severe DKA (mean pH at presentation 6.92±0.08). Cerebral oedema was diagnosed using neurological status, response to osmotherapy, and neuroimaging, and classified as: early (occurring ≤1 h after presentation, n=15), late (1-48 h, n=17) or absent (controls, n=21). The temporal profiles for various osmolar and acid-base profiles were examined using a random coefficients fractional polynomial mixed model, adjusted for known risk factors.

RESULTS

The three groups could not be differentiated by demographic, osmolar or acid-base variables at presentation. All osmolar and acid-base variables showed non-linear temporal trajectories. Children who developed late onset oedema showed dramatically different temporal profiles for effective osmolality and glucose-corrected serum sodium (both p<0.001). Glucose-corrected sodium provided better qualitative discrimination, in that it typically fell in children who developed late oedema and rose in controls. The maximum between-group difference for both variables approximated the median time of clinical cerebral oedema onset. Blood glucose and acid-base temporal profiles did not differ between the groups. Late onset oedema patients received more fluid in the first 4 h, but this did not influence the osmolar or glucose-corrected sodium trajectories in a predictable fashion.

CONCLUSIONS

Glucose-corrected serum sodium may prove a useful early warning for the development of cerebral oedema in DKA.

摘要

目的

脑水肿是糖尿病酮症酸中毒(DKA)潜在的破坏性并发症。在治疗过程中,渗透压变化、酸碱变化与脑水肿发展之间的关系尚不清楚。

设计

对 53 例严重 DKA 患儿(就诊时平均 pH 值为 6.92±0.08)进行回顾性队列研究。脑水肿通过神经状态、对渗透压治疗的反应和神经影像学来诊断,并分为:早期(就诊后≤1 小时发生,n=15)、晚期(1-48 小时发生,n=17)或无(对照组,n=21)。使用随机系数分数多项式混合模型检查各种渗透压和酸碱剖面的时间曲线,调整已知的危险因素。

结果

三组在就诊时的人口统计学、渗透压或酸碱变量上无法区分。所有渗透压和酸碱变量均显示出非线性的时间轨迹。发生晚期水肿的患儿,有效渗透压和葡萄糖校正血清钠的时间曲线明显不同(均 p<0.001)。葡萄糖校正后的血清钠提供了更好的定性区分,因为它通常在发生晚期水肿的患儿中下降,而在对照组中上升。两组间最大组间差异接近临床脑水肿发作的中位数时间。血糖和酸碱时间曲线在各组之间没有差异。晚期水肿患者在头 4 小时内接受了更多的液体,但这并没有以可预测的方式影响渗透压或葡萄糖校正后的血清钠轨迹。

结论

葡萄糖校正后的血清钠可能成为 DKA 脑水肿发生的有用早期预警指标。

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