Clinical outcome of massive acetaminophen overdose treated with standard-dose N-acetylcysteine.

BACKGROUND: Recent recognition of "massive" acetaminophen (APAP) overdoses has led to the question of whether standard dosing of N-acetylcysteine (NAC) is adequate to prevent hepatoxicity in these patients. The primary aim of this study was to evaluate the clinical outcome for patients with massive APAP overdose who received standard intravenous NAC dosing of 300 mg/kg over 21 h. METHODS: This was a single-center retrospective cohort study conducted by chart review of APAP overdoses reported to a regional poison center from 1 January 2010 to 31 December 2019. Massive APAP overdose was defined by single, acute overdose resulting in an APAP concentration exceeding 300 mcg/mL at 4 h post-ingestion. Standard univariate statistical analysis was conducted to describe the cohort, and a multivariate logistic model was utilized to calculate adjusted odds ratios for risk of hepatoxicity. RESULTS: 1425 cases of APAP overdose were reviewed. 104 cases met the inclusion criteria of massive APAP overdose. Overall, 79 cases (76%) had no acute liver injury or hepatotoxicity, and 25 (24%) developed hepatoxicity. Nine percent (n = 4) of cases receiving NAC within 8 h developed hepatotoxicity. Crude odds for hepatoxicity was 5.5-fold higher for cases who received NAC after 8 h. CONCLUSIONS: Standard NAC dosing received within 8 h prevented hepatoxicity in 91% (n = 40) of cases in our series of massive APAP overdoses. Additional data is needed to determine the clinical outcomes of massive APAP overdose using current intravenous NAC dosing.

Fatal pulmonary edema after acute occupational exposure to nitric acid.

BACKGROUND: Nitric acid (HNO(3)) is a solution of nitrogen dioxide (NO(2)) in water commonly used as an industrial chemical and cleaner. Oxides of nitrogen liberated as nitric acid interact with the environment to cause inhalation injuries. The coexistence of HNO(3) with varying oxides of nitrogen likely results in the large continuum of symptoms related to HNO(3) exposure and varying times of onset--acute, subacute, and delayed. Furthermore, dyspnea and evidence of acute lung injury may not occur for several hours after exposure and can lead to rapidly progressive acute respiratory distress syndrome (ARDS). OBJECTIVES: This case illustrates to physicians and occupational health personnel that HNO(3) inhalation may initially appear benign and that onset of severe effects may be delayed. CASE REPORT: A 66-year-old man developed delayed-onset pulmonary edema, ARDS, and fatal circulatory collapse 53 h after occupational exposure to HNO(3). CONCLUSION: This case serves to increase awareness among emergency physicians, as well as occupational health personnel, that patients exposed to HNO(3) may initially be asymptomatic. Patients should be evaluated and observed regardless of the severity or benign nature of symptoms, which occur immediately after exposure, as the most severe symptoms are often delayed in onset and rapidly progressive.