Svensson Robert, Hahn Robert G, Zdolsek Joachim H, Bahlmann Hans
Department of Anesthesiology and Intensive Care, Linköping University, Vrinnevi Hospital, Norrköping, Sweden.
Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Intensive Care Med Exp. 2022 Dec;10(1):36. doi: 10.1186/s40635-022-00464-5. Epub 2022 Aug 29.
Hyperchloremic metabolic acidosis that develops during the treatment of diabetic ketoacidosis is usually attributed to the chloride content of resuscitation fluids. We explored an alternative explanation, namely that fluid-induced plasma volume expansion alters the absolute differences in the concentrations of sodium and chloride (the Na-Cl gap) enough to affect the acid-base balance. We analyzed data from a prospective single-center cohort study of 14 patients treated for diabetic ketoacidosis. All patients received 1 L of 0.9% saline over 30 min on two consecutive days. Blood gases were sampled before and after the infusions.
The initial plasma volume was estimated to be 25 ± 13% (mean ± SD) below normal on admission to the intensive care unit. At that time, most patients had an increased actual Na-Cl gap, which counteracts acidosis. However, the correction of the plasma volume deficit revealed that these patients would have had a decreased Na-Cl gap upon admission if they had been normovolemic at that time; the estimated "virtual Na-Cl gap" of 29 ± 5 mmol/L was significantly lower than the uncorrected value, which was 39 ± 5 mmol/L (P < 0.001). On Day 2, most patients had a decreased actual Na-Cl gap (33 ± 5 mmol/L), approaching the corrected value on Day 1.
The hyperchloremic acidosis commonly seen in diabetic ketoacidosis may not be primarily caused by the chloride content of resuscitation fluids but, rather, by the restoration of plasma volume, which reveals the hidden metabolic acidosis caused by a decreased Na-Cl gap. Trial registration Clinical Trials Identifier NCT02172092, registered June 24, 2014, https://www.
gov/NCT02172092.
糖尿病酮症酸中毒治疗期间发生的高氯性代谢性酸中毒通常归因于复苏液中的氯含量。我们探索了另一种解释,即液体诱导的血浆容量扩张改变了钠和氯浓度的绝对差值(钠-氯间隙),足以影响酸碱平衡。我们分析了一项针对14例接受糖尿病酮症酸中毒治疗患者的前瞻性单中心队列研究的数据。所有患者连续两天在30分钟内输注1升0.9%生理盐水。输注前后采集血气样本。
重症监护病房入院时,初始血浆容量估计比正常水平低25±13%(平均值±标准差)。当时,大多数患者的实际钠-氯间隙增加,这抵消了酸中毒。然而,血浆容量不足的纠正显示,如果这些患者当时血容量正常,入院时他们的钠-氯间隙会降低;估计的“虚拟钠-氯间隙”为29±5 mmol/L,显著低于未校正值39±5 mmol/L(P<0.001)。在第2天,大多数患者的实际钠-氯间隙降低(33±5 mmol/L),接近第1天的校正值。
糖尿病酮症酸中毒中常见的高氯性酸中毒可能并非主要由复苏液中的氯含量引起,而是由血浆容量的恢复导致,血浆容量恢复揭示了因钠-氯间隙降低而隐藏的代谢性酸中毒。试验注册 临床试验标识符NCT02172092,于2014年6月24日注册,https://www.CLINICALTRIALS: gov/NCT02172092。