Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, CO, USA.
Rocky Mountain Poison and Drug Center, Denver, CO, USA.
Clin Toxicol (Phila). 2020 Jan;58(1):16-19. doi: 10.1080/15563650.2019.1593432. Epub 2019 Mar 22.
: Salicylate toxicity is a common cause of morbidity and hospitalization. Animal and human studies suggest that salicylates cause a dose-dependent inhibition of the activation of factors 2, 7, 9, and 10. However, limited reports of coagulopathy or major bleeding from salicylate toxicity exist.: This is a retrospective study examining subjects from January 1, 2001 to December 31, 2011 in whom at least one serum salicylate concentration was measured above 30 mg/dL. Cases were patients with elevated salicylate concentration and coagulopathy (INR > 1.5). Major bleeding cases were those with elevated salicylate concentration who developed hemorrhagic death; or bleeding from an intracranial, intraspinal, intraocular, retroperitoneal, pericardial, intramuscular site; or hemoglobin decrease of >2 g/dL, or transfusion of at least 2 units of packed RBCs during hospitalization.: Twelve percent of all cases of elevated salicylate concentration developed coagulopathy, 6% developed major bleeding, and 3% died. In a multivariate model, duration of elevated salicylate concentration and renal impairment were associated with coagulopathy and no variable was associated with major bleeding. Patients were more likely to develop major bleeding if they had coagulopathy, but not all cases of major bleeding had coagulopathy.: Coagulopathy and major bleeding during salicylate toxicity has been underrecognized. Renal impairment and duration of salicylate elevation contribute to the risk of coagulopathy, but no factors predict major bleeding. Patients with coagulopathy have a high risk of bleeding but some bleeding occurs without coagulopathy, suggesting that other factors, such as platelet dysfunction, may play a role. Coagulopathy and major bleeding develop in a clinically relevant percentage of cases of salicylate toxicity.
: 水杨酸盐毒性是发病率和住院率升高的常见原因。动物和人体研究表明，水杨酸盐会导致因子 2、7、9 和 10 的激活受到剂量依赖性抑制。然而，有关水杨酸盐毒性引起凝血功能障碍或大出血的报道有限。: 这是一项回顾性研究，纳入了 2001 年 1 月 1 日至 2011 年 12 月 31 日期间至少有一次血清水杨酸盐浓度高于 30mg/dL 的患者。病例为水杨酸盐浓度升高且伴有凝血功能障碍（INR＞1.5）的患者。大出血病例为水杨酸盐浓度升高并发生出血性死亡的患者；或发生颅内、椎管内、眼内、腹膜后、心包内、肌肉内出血的患者；或血红蛋白下降＞2g/dL，或住院期间至少输注 2 个单位的浓缩红细胞的患者。: 所有升高的水杨酸盐浓度的患者中，有 12%出现凝血功能障碍，6%出现大出血，3%死亡。在多变量模型中，水杨酸盐浓度升高的持续时间和肾功能不全与凝血功能障碍相关，没有变量与大出血相关。如果患者有凝血功能障碍，则更有可能发生大出血，但并非所有大出血病例都有凝血功能障碍。: 水杨酸盐毒性导致的凝血功能障碍和大出血一直被低估。肾功能不全和水杨酸盐升高的持续时间增加了凝血功能障碍的风险，但没有任何因素可预测大出血。有凝血功能障碍的患者有发生出血的高风险，但有些出血发生时无凝血功能障碍，这表明其他因素（如血小板功能障碍）可能起作用。在有临床意义的水杨酸盐毒性病例中，会发生凝血功能障碍和大出血。
