Fiordalisi Irma, Novotny William E, Holbert Donald, Finberg Laurence, Harris Glenn D
Section of Pediatric Critical Care, Department of Pediatrics, Brody School of Medicine at East Carolina University, Greenville, NC 27834, USA.
Pediatr Diabetes. 2007 Jun;8(3):142-9. doi: 10.1111/j.1399-5448.2007.00253.x.
During the late 1900s, raised intracranial pressure (ICP) during treatment of pediatric diabetic ketoacidosis (DKA) surfaced as the most important cause of morbidity and mortality in pediatric DKA. The contribution of fluid and electrolyte therapy to neurologic deterioration during treatment remains controversial.
We proposed a physiologic approach to treatment of DKA, incorporating the principles of rehydration of hypertonic states. Consecutive episodes of pediatric DKA were managed using continuous intravenous insulin, an individualized assessment of the degree of dehydration, and rehydration solutions of tonicity approximating that of the patient. Gradual replacement of the volume of deficit after correction of shock, if present, was planned over 48 h with special attention to changes in effective osmolality along with intensive cardiorespiratory, neurologic, and biochemical monitoring. Mannitol was given for signs or symptoms of raised ICP.
Six hundred and thirty-five consecutive episodes of pediatric DKA were treated from January 1988 to September 2005. Means +/- standard deviation (SD) for initial measured concentrations of total carbon dioxide, glucose, and urea nitrogen were 7.8 +/- 3.3 mmol/L, 602 +/- 271 mg/dL (33.4 +/- 15 mmol/L), and 21 +/- 1 mg/dL (7.4 +/- 3.6 mmol/L), respectively. Pretreatment blood gases were available for 477 episodes. The mean initial partial pressures of arterial and venous carbon dioxide +/- SD were 16.8 +/- 7 mmHg (kP(a)CO(2)= 2.24 +/- 0.93) for n = 308 and 26.6 +/- 7 mmHg (kP(v)CO(2)= 3.54 +/- 0.93) for n = 169, respectively. Although repair was planned to occur over 48 h, the mean time to achieve clinical rehydration and correction of DKA was 11.6 +/- 6.2 h. Mannitol was given in 35 (5.5%) episodes. There was no neurologic morbidity or mortality.
Management of pediatric DKA using this multifaceted physiologic approach and the principles of rehydration described is safe and appears to minimize the risk of brain herniation during treatment.
在20世纪后期，小儿糖尿病酮症酸中毒（DKA）治疗期间颅内压（ICP）升高成为小儿DKA发病和死亡的最重要原因。液体和电解质疗法在治疗期间对神经功能恶化的作用仍存在争议。
我们提出了一种DKA的生理治疗方法，纳入了高渗状态补液的原则。连续的小儿DKA发作采用持续静脉胰岛素治疗、对脱水程度进行个体化评估以及使用与患者张力相近的补液溶液进行治疗。如果存在休克，在休克纠正后计划在48小时内逐步补充缺失的液体量，特别关注有效渗透压的变化以及进行强化的心肺、神经和生化监测。对于ICP升高的体征或症状给予甘露醇治疗。
1988年1月至2005年9月共治疗了635例连续的小儿DKA发作。总二氧化碳、葡萄糖和尿素氮初始测量浓度的平均值±标准差（SD）分别为7.8±3.3 mmol/L、602±271 mg/dL（33.4±15 mmol/L）和21±1 mg/dL（7.4±3.6 mmol/L）。477例发作可获得治疗前血气分析结果。动脉和静脉二氧化碳的平均初始分压±SD分别为：n = 308时为16.8±7 mmHg（kP(a)CO(2)= 2.24±0.93），n = 169时为26.6±7 mmHg（kP(v)CO(2)= 3.54±0.93）。尽管计划在48小时内完成纠正，但实现临床补液和DKA纠正的平均时间为11.6±
