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糖尿病酮症酸中毒患儿脑水肿的机制

Mechanism of cerebral edema in children with diabetic ketoacidosis.

作者信息

Glaser Nicole S, Wootton-Gorges Sandra L, Marcin James P, Buonocore Michael H, Dicarlo Joseph, Neely E Kirk, Barnes Patrick, Bottomly Jenny, Kuppermann Nathan

机构信息

Department of Pediatrics, Division of Emergency Medicine, University of California, Davis School of Medicine, Sacramento, California 95817, USA.

出版信息

J Pediatr. 2004 Aug;145(2):164-71. doi: 10.1016/j.jpeds.2004.03.045.

Abstract

OBJECTIVES

Cerebral edema during diabetic ketoacidosis (DKA) has been attributed to osmotic cellular swelling during treatment. We evaluated cerebral water distribution and cerebral perfusion during DKA treatment in children.

STUDY DESIGN

We imaged 14 children during DKA treatment and after recovery, using both diffusion and perfusion weighted magnetic resonance imaging (MRI). We assessed the apparent diffusion coefficients (ADCs) and measures reflecting cerebral perfusion.

RESULTS

The ADC was significantly elevated during DKA treatment (indicating increased water diffusion) in all regions except the occipital gray matter. Mean reductions in the ADC from initial to postrecovery MRI were: basal ganglia 4.7 +/- 2.5 x 10(-5) mm(2)/s (P=.002), thalamus 3.7 +/- 2.8 x 10(-5) mm(2)/s, (P=.002), periaqueductal gray matter 4.3 +/- 5.1 x 10(-5) mm(2)/s (P=.03), and frontal white matter 2.0 +/- 3.1 x 10(-5) mm(2)/s (P=.03). In contrast, the ADC in the occipital gray matter increased significantly from the initial to postrecovery MRI (mean increase 3.9 +/- 3.9 x 10(-5) mm(2)/s, P=.004). Perfusion MRI during DKA treatment revealed significantly shorter mean transit times (MTTs) and higher peak tracer concentrations, possibly indicating increased cerebral blood flow (CBF).

CONCLUSIONS

Elevated ADC values during DKA treatment suggests a vasogenic process as the predominant mechanism of edema formation rather than osmotic cellular swelling.

摘要

目的

糖尿病酮症酸中毒(DKA)期间的脑水肿被认为是治疗过程中渗透性细胞肿胀所致。我们评估了儿童DKA治疗期间的脑水分布和脑灌注情况。

研究设计

我们在14名儿童DKA治疗期间及恢复后,使用扩散加权磁共振成像(MRI)和灌注加权磁共振成像进行成像。我们评估了表观扩散系数(ADC)以及反映脑灌注的指标。

结果

在DKA治疗期间,除枕叶灰质外,所有区域的ADC均显著升高(表明水扩散增加)。从初始MRI到恢复后MRI,ADC的平均降低值分别为:基底神经节4.7±2.5×10⁻⁵mm²/s(P = 0.002),丘脑3.7±2.8×10⁻⁵mm²/s(P = 0.002),导水管周围灰质4.3±5.1×10⁻⁵mm²/s(P = 0.03),额叶白质2.0±3.1×10⁻⁵mm²/s(P = 0.03)。相比之下,枕叶灰质的ADC从初始MRI到恢复后MRI显著增加(平均增加3.9±3.9×10⁻⁵mm²/s,P = 0.004)。DKA治疗期间的灌注MRI显示平均通过时间(MTT)显著缩短,示踪剂峰值浓度更高,这可能表明脑血流量(CBF)增加。

结论

DKA治疗期间ADC值升高表明血管源性过程是水肿形成的主要机制,而非渗透性细胞肿胀。

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