Abstract：
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.
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.
摘要：
背景：患有哮喘状态（SA）的患者经常出现乳酸性酸中毒（LA）。我们的目标是使用Stewart物理化学模型确定该LA的性质，并确定SA儿童中与LA相关的独立因素。
方法：采用嵌套病例对照设计的回顾性队列分析研究。包括24名儿童的28次SA发作。连续招募了在9年内因SA进入儿科重症监护病房（PICU）的患者。使用Stewart模型和强离子计算器分析数据。使用描述性统计分析数据，并在一般线性模型中拟合回归模型。
结果：在18次发作（15例；62.5%）中观察到高乳酸血症（Lact[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异减少引起的。最初，pCO2较高（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--5.412]），并且在临床过程中都没有显着变化。没有必要确定丙酮酸,由于NUI正常，LA为B型（非低氧，乳酸/丙酮酸<25)。我们观察到LA与到达医院时肌内肾上腺素之间的相关性（p=0.023）。但不是在LA和累积剂量的雾化沙丁胺醇之间。
结论：大多数SA患者表现为LA。Stewart模型证实LA没有缺氧,可能是与拟交感神经相关的糖酵解.
方法：采用嵌套病例对照设计的回顾性队列分析研究。包括24名儿童的28次SA发作。连续招募了在9年内因SA进入儿科重症监护病房（PICU）的患者。使用Stewart模型和强离子计算器分析数据。使用描述性统计分析数据，并在一般线性模型中拟合回归模型。
结果：在18次发作（15例；62.5%）中观察到高乳酸血症（Lact[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异减少引起的。最初，pCO2较高（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--5.412]），并且在临床过程中都没有显着变化。没有必要确定丙酮酸,由于NUI正常，LA为B型（非低氧，乳酸/丙酮酸<25)。我们观察到LA与到达医院时肌内肾上腺素之间的相关性（p=0.023）。但不是在LA和累积剂量的雾化沙丁胺醇之间。
结论：大多数SA患者表现为LA。Stewart模型证实LA没有缺氧,可能是与拟交感神经相关的糖酵解.
