Department of Pharmacy, Vanderbilt University Medical Center, Nashville, TN, USA.
WI Poison Control Center, Milwaukee, WI, USA.
Clin Toxicol (Phila). 2023 Jul;61(7):536-542. doi: 10.1080/15563650.2023.2227998. Epub 2023 Jul 10.
Management of patients with salicylate toxicity frequently requires urine alkalinization to enhance excretion of salicylate. One strategy for determining when to stop urine alkalinization is to wait for two consecutive serum salicylate concentrations to be less than 300 mg/L (2.17 mmol/L) and declining. When alkalinization of the urine ceases, a rebound in serum salicylate concentration can occur from tissue redistribution or delayed gastrointestinal absorption. Whether this can lead to rebound toxicity is not well understood.
This was a single-center, retrospective review of cases with a primary ingestion of acetylsalicylic acid reported to the local poison center over a five-year period. Cases were excluded if the product was not listed as the primary ingestion or if there was no serum salicylate concentration documented after discontinuation of intravenous sodium bicarbonate infusion. The primary outcome was the incidence of serum salicylate rebound to a concentration greater than 300 mg/L (2.17 mmol/L) after discontinuation of intravenous sodium bicarbonate infusion.
A total of 377 cases were included. Of these, eight (2.1%) had a serum salicylate concentration increase (rebound) after stopping the sodium bicarbonate infusion. All these cases were acute ingestions. Five of the eight cases had rebound serum salicylate concentrations that were greater than 300 mg/L (2.17 mmol/L). Of these five patients, only one reported recurrent symptoms (tinnitus). Prior to stopping urinary alkalinization, the last or the last two serum salicylate concentrations were less than 300 mg/L (2.17 mmol/L) in three and two cases, respectively.
In patients with salicylate toxicity, the incidence of rebound in serum salicylate concentration after cessation of urine alkalinization, is low. Even if serum salicylate rebounds to supratherapeutic concentrations, symptoms are often absent or mild. Routine repeat serum salicylate concentrations after urine alkalinization is stopped may be unnecessary unless symptoms recrudesce.
治疗水杨酸毒性患者常需要碱化尿液以促进水杨酸排泄。停止尿液碱化的一个策略是等待两次连续的血清水杨酸浓度低于 300mg/L（2.17mmol/L）且呈下降趋势。当尿液碱化停止时，由于组织再分布或延迟胃肠道吸收，血清水杨酸浓度可能会反弹。这种情况是否会导致反弹毒性尚不清楚。
这是一项为期五年的单中心回顾性研究，纳入了当地中毒中心报告的主要摄入乙酰水杨酸的病例。如果产品未被列为主要摄入物，或在停止静脉注射碳酸氢钠输注后未记录血清水杨酸浓度，则排除病例。主要结局是停止静脉注射碳酸氢钠输注后血清水杨酸浓度反弹至大于 300mg/L（2.17mmol/L）的发生率。
共纳入 377 例。其中，8 例（2.1%）在停止碳酸氢钠输注后血清水杨酸浓度增加（反弹）。所有这些病例都是急性摄入。8 例中有 5 例反弹的血清水杨酸浓度大于 300mg/L（2.17mmol/L）。这 5 例患者中，只有 1 例报告出现耳鸣等复发症状。在停止尿液碱化之前，3 例和 2 例患者的最后一次或最后两次血清水杨酸浓度分别小于 300mg/L（2.17mmol/L）。
在水杨酸毒性患者中，停止尿液碱化后血清水杨酸浓度反弹的发生率较低。即使血清水杨酸反弹至治疗范围以上，症状通常也不存在或轻微。除非症状再次出现，否则停止尿液碱化后常规重复检测血清水杨酸浓度可能没有必要。
