Harris G D, Fiordalisi I, Yu C
Department of Pediatrics, East Carolina University School of Medicine, Greenville, North Carolina 27858, USA.
Life Sci. 1996;59(20):1695-702. doi: 10.1016/s0024-3205(96)00505-x.
Increased intracranial pressure (ICP) resulting in death or neurologic morbidity continues to complicate traditional management of diabetic ketoacidemia (DKA) in pediatric patients. When ICP or cerebrospinal fluid pressures have been measured, correction of hyperglycemia in animals and treatment of DKA in humans have consistently resulted in pathologic increases in ICP. We hypothesized that elevations in ICP can be minimized if changes in effective osmolality (Eosm) are controlled during treatment of DKA. During a six-hour study period, three groups of rabbits were studied: a normal control group of nondiabetic animals (Cnor, n = 10), a control group of animals with DKA (CDKA, n = 8), and an experimental group of animals with DKA (EDKA, n = 8). There was no significant difference between the two groups with DKA regarding pretreatment degree of dehydration, blood pressure, hyperglycemia, acidemia or ICP. During the treatment period, Cnor received maintenance fluids only. CDKA received insulin and an assumed volume of deficit (150 ml/kg) along with maintenance fluids and urinary output replacement with 0.45% NaCl. EDKA received insulin and one-half the volume of deficit calculated by the weight lost with 0.9% NaCl plus maintenance fluids. There was no significant difference between CDKA and EDKA regarding the rate at which DKA was corrected. While CDKA demonstrated a progressive and statistically significant increase in ICP, EDKA exhibited no such increase in ICP compared to normal, nondiabetic controls (Cnor) during treatment. Changes in Eosm during treatment in CDKA compared to Cnor and in CDKA compared to EDKA were significantly greater (p < .01), however, changes in EOSM in EDKA compared to Cnor were not significant. These data support the clinical observation that decreasing EOSM during treatment of DKA is associated with increased ICP and suggest that DKA can be treated effectively with i.v. fluids and insulin without increasing ICP.
颅内压（ICP）升高导致死亡或神经功能障碍，这仍然是小儿糖尿病酮症酸中毒（DKA）传统治疗中的复杂问题。当测量了ICP或脑脊液压力时，动物体内高血糖的纠正以及人类DKA的治疗一直导致ICP出现病理性升高。我们假设，如果在DKA治疗期间控制有效渗透压（Eosm）的变化，ICP的升高可以降至最低。在为期6小时的研究期间，对三组兔子进行了研究：非糖尿病动物的正常对照组（Cnor，n = 10）、患有DKA的动物对照组（CDKA，n = 8）和患有DKA的动物实验组（EDKA，n = 8）。两组患有DKA的动物在脱水程度、血压、高血糖、酸血症或ICP的预处理方面没有显著差异。在治疗期间，Cnor仅接受维持液。CDKA接受胰岛素和假定的缺水量（150 ml/kg），以及维持液，并使用0.45% NaCl替代尿量。EDKA接受胰岛素和根据体重减轻计算出的缺水量的一半，使用0.9% NaCl加上维持液。CDKA和EDKA在DKA纠正率方面没有显著差异。虽然CDKA的ICP呈现出渐进性且具有统计学意义的升高，但与正常非糖尿病对照组（Cnor）相比，EDKA在治疗期间ICP没有出现这种升高。与Cnor相比，CDKA治疗期间Eosm的变化以及与EDKA相比，CDKA治疗期间Eosm的变化显著更大（p < .01），然而，与Cnor相比，EDKA的EOSM变化不显著。这些数据支持了临床观察结果，即DKA治疗期间Eosm降低与ICP升高有关，并表明DKA可以通过静脉输液和胰岛素有效治疗而不增加ICP。
