Alander S W, Dowd M D, Bratton S L, Kearns G L
Department of Pediatrics, Children's Mercy Hospital, Kansas City, Mo 64108, USA.
Arch Pediatr Adolesc Med. 2000 Apr;154(4):346-50. doi: 10.1001/archpedi.154.4.346.
To characterize demographic and clinical factors associated with pediatric acetaminophen overdose and identify risk factors for hepatocellular injury.
Retrospective 10-year chart review.
Two regional children's hospitals.
Records of patients examined because of acetaminophen ingestion from January 1, 1988, through December 31, 1997, were reviewed. Hepatocellular injury was defined as elevation of serum aminotransferase levels greater than 2 times the reference values. Severe hepatotoxic effect was defined as hepatotoxic effect with evidence of encephalopathy and/or coagulopathy.
Data from 322 patients (208 girls and 114 boys, aged 1-17 years) were obtained. Ingestions were intentional in 140 patients (median age, 14 years) and unintentional in 172 (median age, 2 years). Another 10 cases represented dosing errors with therapeutic intent (median age, 3.5 years). Twenty-seven patients had hepatocellular injury; of these, 4 had severe hepatotoxic effects and 1 died. Hepatocellular injury occurred in 10.0% of the dosing error group, 17.9% of the intentional group, and 0.6% of the unintentional group. No patients underwent liver transplantation. Hepatocellular injury was associated with presentation longer than 24 hours after ingestion (odds ratio [OR], 335.0; 95% confidence interval [CI], 40.8-275.0), age 10 to 17 years (OR, 36.9; 95% CI, 4.9-275.4), intentional overdose (OR, 37.2; 95% CI, 5.0-278.2), dose greater than 150 mg/kg (OR, 17.9; 95% CI, 2.3-139.2), and white race (OR, 2.8; 95% CI, 1.1-7.2).
Intentional and unintentional acetaminophen overdoses occurred with similar frequency. Therapeutic misadventure was relatively uncommon, as was hepatocellular injury. Practitioners should have greater suspicion of acetaminophen-associated hepatocellular injury in patients who present more than 24 hours after ingestion, older children, and those who have intentional ingestion.
描述与儿童对乙酰氨基酚过量相关的人口统计学和临床因素，并确定肝细胞损伤的危险因素。
回顾性10年病历审查。
两家地区儿童医院。
回顾了1988年1月1日至1997年12月31日因摄入对乙酰氨基酚而接受检查的患者记录。肝细胞损伤定义为血清氨基转移酶水平升高超过参考值的2倍。严重肝毒性效应定义为伴有脑病和/或凝血病证据的肝毒性效应。
获得了322例患者（208名女孩和114名男孩，年龄1至17岁）的数据。140例患者（中位年龄14岁）为故意摄入，172例（中位年龄2岁）为意外摄入。另外10例为有治疗意图的用药错误（中位年龄3.5岁）。27例患者出现肝细胞损伤；其中4例有严重肝毒性效应，1例死亡。肝细胞损伤在用药错误组中的发生率为10.0%，故意摄入组为17.9%，意外摄入组为0.6%。没有患者接受肝移植。肝细胞损伤与摄入后24小时以上就诊（比值比[OR]，335.0；95%置信区间[CI]，40.8 - 275.0）、10至17岁年龄（OR，36.9；95%CI，4.9 - 275.4）、故意过量摄入（OR，37.2；95%CI，5.0 - 278.2）、剂量大于150mg/kg（OR，17.9；95%CI，2.3 - 139.2）以及白种人（OR，2.8；95%CI，1.1 - 7.2）相关。
故意和意外对乙酰氨基酚过量的发生频率相似。治疗失误相对少见，肝细胞损伤也是如此。从业者应对摄入后24小时以上就诊的患者、年龄较大的儿童以及故意摄入者中与对乙酰氨基酚相关的肝细胞损伤有更高的怀疑。
