Singh Mallika, Bloom Joshua, Howland Mary Ann, Biary Rana, Su Mark
Emergency Medicine, Jamaica Hospital Medical Center, Richmond Hills, USA.
Health and Mental Hygiene, New York City Poison Control Center, New York, USA.
Cureus. 2025 Aug 8;17(8):e89613. doi: 10.7759/cureus.89613. eCollection 2025 Aug.
Salicylate toxicity usually occurs as a result of elevated serum salicylate concentrations. Salicylate concentrations can be measured in cerebrospinal fluid (CSF), but the interpretation of these values is less well understood. Two phenomena believed to be associated with salicylate toxicity are neuroglycopenia and salicylate-induced coagulopathy, but these cases are typically not well-characterized. We report a case of delayed diagnosis of salicylate toxicity that was complicated by coagulopathy and had a quantifiable CSF salicylate concentration. An 18-year-old female patient presented with abdominal pain and an altered mental state; she had previously presented at another hospital one day prior. She did not initially report salicylate overdose. A lumbar puncture was performed 4.5 hours after emergency department (ED) presentation to rule out meningitis. Due to additional history, a serum salicylate concentration obtained at 25 hours led to a result of 48.8 mg/dL (therapeutic range: 15-30 mg/dL). Hemodialysis (HD) was performed 37 hours after ED presentation due to the altered mental state. Prior to HD, the patient had a prothrombin time of 63 seconds (reference range: 11-13 seconds), international normalized ratio of 5.52 (reference range: 0.8-1.1), and activated partial thromboplastin time of 40.2 seconds (reference range: 25-35 seconds). After the case conclusion, waste CSF was tested and the CSF salicylate concentration was 23 mg/dL; the corresponding CSF and serum glucose concentrations were 60 mg/dL (reference range: 50-75 mg/dL) and 87 mg/dL (reference range: 70-99 mg/dL), respectively. This is a case of delayed diagnosis salicylate poisoning complicated by coagulopathy, without neuroglycopenia. Although we do not recommend routine CSF testing in salicylate toxicity cases, analysis of CSF could shed insight into salicylate-induced encephalopathy. This case illustrates that prompt recognition and treatment of toxicity is key, as delayed diagnosis can increase morbidity and mortality.
水杨酸盐中毒通常是血清水杨酸盐浓度升高所致。可在脑脊液(CSF)中测量水杨酸盐浓度,但对这些值的解读尚不太清楚。两种被认为与水杨酸盐中毒相关的现象是神经低血糖症和水杨酸盐诱导的凝血病,但这些病例通常特征不明显。我们报告一例水杨酸盐中毒延迟诊断病例,该病例并发凝血病且脑脊液水杨酸盐浓度可量化。一名18岁女性患者出现腹痛和精神状态改变;她一天前曾在另一家医院就诊。她最初未报告水杨酸盐过量。在急诊科就诊4.5小时后进行腰椎穿刺以排除脑膜炎。由于补充病史,在25小时时测得血清水杨酸盐浓度为48.8mg/dL(治疗范围:15 - 30mg/dL)。由于精神状态改变,在急诊科就诊37小时后进行血液透析(HD)。在HD之前,患者的凝血酶原时间为63秒(参考范围:11 - 13秒),国际标准化比值为5.52(参考范围:0.8 - 1.1),活化部分凝血活酶时间为40.2秒(参考范围:25 - 35秒)。病例结束后,对废弃的脑脊液进行检测,脑脊液水杨酸盐浓度为23mg/dL;相应的脑脊液和血清葡萄糖浓度分别为60mg/dL(参考范围:50 - 75mg/dL)和87mg/dL(参考范围:70 - 99mg/dL)。这是一例并发凝血病但无神经低血糖症的水杨酸盐中毒延迟诊断病例。虽然我们不建议在水杨酸盐中毒病例中常规进行脑脊液检测,但脑脊液分析可能有助于深入了解水杨酸盐诱导的脑病。该病例表明,及时识别和治疗中毒至关重要,因为延迟诊断会增加发病率和死亡率。