哮喘状态儿童的高乳酸血症。斯图尔特方法

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引用次数: 0

摘要

背景哮喘(SA)患者经常出现乳酸酸中毒(LA)。我们的目标是利用斯图尔特理化模型确定这种乳酸酸中毒的性质,并确定与哮喘儿童乳酸酸中毒相关的独立因素。研究纳入了 24 名儿童的 28 例 SA。连续招募了9年期间因SA入住儿科重症监护室(PICU)的患者。数据采用斯图尔特模型和强离子计算器进行分析。结果在 18 次病例(15 名患者;62.5%)中观察到高乳酸血症(乳酸[mM/L] = 3.905 [95% CI = 3.018-4.792])和酸中毒(pH = 7.294 [95% CI = 7.241-7.339])。根据斯图尔特模型,酸中毒是由强离子差下降引起的。最初,pCO2 偏高(pCO2[mmHg] = 45.806 [95% CI = 37.314-54.298]),但净未测量离子(NUI)成分正常(NUI = -4,461 [95% CI = -3.51 至 -5.412]),两者在临床过程中均无明显变化。由于 NUI 正常且 LA 为 B 型(非缺氧、乳酸/丙酮酸 <25),因此无需测定丙酮酸。我们观察到 LA 与到达医院时肌肉注射的肾上腺素之间存在相关性(P = .023),但 LA 与雾化沙丁胺醇的累积剂量之间不存在相关性。Stewart 模型证实,LA 并非缺氧,可能是由于拟交感神经相关的糖酵解所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyperlacticaemia in children with status asthmaticus. The Stewart approach

Background

Patients with status asthmaticus (SA) frequently present with lactic acidosis (LA). Our goal is to identify the nature of this LA using the Stewart physicochemical model and to identify the independent factors associated with LA in children with SA.

Methods

Analytical study of a retrospective cohort using a nested case-control design. Twenty-eight episodes of SA in 24 children were included. Patients admitted to a paediatric intensive care unit (PICU) for SA over a 9-year period were recruited consecutively. Data were analysed using the Stewart model and the Strong Ion Calculator. Data were analysed using descriptive statistics and regression models were fitted within the general linear model.

Results

Hyperlacticaemia (Lact[mM/L] = 3.905 [95% CI = 3.018–4.792]) and acidosis (pH = 7.294 [95% CI = 7.241–7.339]) were observed in 18 episodes (15 patients; 62.5%). According to the Stewart model, acidosis was caused by a decrease in strong ion difference. Initially, pCO2 was high (pCO2[mmHg] = 45.806 [95% CI = 37.314–54.298]) but the net unmeasured ion (NUI) component was normal (NUI = −4,461 [95% CI = −3.51 to −5.412]), and neither changed significantly over the clinical course. There was no need to determine pyruvate, as the NUI was normal and the LA was type B (non-hypoxic, lactate/pyruvate < 25). We observed a correlation (P = .023) between LA and intramuscular epinephrine administered on arrival at hospital, but not between LA and the cumulative dose of nebulized salbutamol.

Conclusions

Most patients with SA presented LA. The Stewart model confirmed that LA is not hypoxic, probably due to sympathomimetic-related glycolysis.

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