Benjamin W Hatten1, L Keith French2, B Zane Horowitz2, Robert G Hendrickson2. 1. Section of Medical Toxicology, Department of Emergency Medicine, University of Colorado School of Medicine, Aurora, CO, and the Rocky Mountain Poison and Drug Center, Denver Health and Hospital Authority, Denver, CO. Electronic address: benjamin.hatten@ucdenver.edu. 2. Oregon-Alaska Poison Center, Department of Emergency Medicine, Oregon Health & Science University, Portland, OR.
Abstract
STUDY OBJECTIVE: In cases of high-concentration peroxide ingestion reported to US poison centers, we describe medical outcomes, examine the role of hyperbaric oxygen, and review the use of endoscopy. METHODS: The study was a retrospective analysis of a structured database, the National Poison Data System. The chart for each poison center case of a high-concentration (>10%) peroxide ingestion was obtained and abstracted in a standardized fashion; 1,054 cases were initially considered and 294 cases met inclusion criteria. The primary outcome of possible embolic event was defined as seizure, altered mental status, respiratory distress, hypoxia, hemodynamic instability, ECG changes, radiographic evidence of cerebrovascular accident, focal neurologic deficit on examination, pulmonary embolism, cardiac emboli, elevated troponin level, physician bedside diagnosis, or rapid improvement after hyperbaric oxygen therapy. Both descriptive statistics and logistic regression models were used to analyze the data. RESULTS: In the 10-year study period, 41 of 294 patients (13.9%; 95% confidence interval 10.2% to 18.4%) with symptoms after high-concentration peroxide ingestion demonstrated evidence of embolic events, and 20 of 294 (6.8%; 95% confidence interval 4.2% to 10.3%) either died or exhibited continued disability when the poison center chart was closed. Improved outcomes were demonstrated after early hyperbaric oxygen therapy. Endoscopy revealed grade 3 or 4 lesions in only 5 cases. CONCLUSION: Symptomatic high-concentration peroxide exposures had a high incidence of associated embolic events in this cohort. Patients with evidence of embolic events had a high rate of death. Early hyperbaric oxygen therapy may be useful, but routine endoscopy is unlikely to be of benefit.
STUDY OBJECTIVE: In cases of high-concentration peroxide ingestion reported to US poison centers, we describe medical outcomes, examine the role of hyperbaric oxygen, and review the use of endoscopy. METHODS: The study was a retrospective analysis of a structured database, the National Poison Data System. The chart for each poison center case of a high-concentration (>10%) peroxide ingestion was obtained and abstracted in a standardized fashion; 1,054 cases were initially considered and 294 cases met inclusion criteria. The primary outcome of possible embolic event was defined as seizure, altered mental status, respiratory distress, hypoxia, hemodynamic instability, ECG changes, radiographic evidence of cerebrovascular accident, focal neurologic deficit on examination, pulmonary embolism, cardiac emboli, elevated troponin level, physician bedside diagnosis, or rapid improvement after hyperbaric oxygen therapy. Both descriptive statistics and logistic regression models were used to analyze the data. RESULTS: In the 10-year study period, 41 of 294 patients (13.9%; 95% confidence interval 10.2% to 18.4%) with symptoms after high-concentration peroxide ingestion demonstrated evidence of embolic events, and 20 of 294 (6.8%; 95% confidence interval 4.2% to 10.3%) either died or exhibited continued disability when the poison center chart was closed. Improved outcomes were demonstrated after early hyperbaric oxygen therapy. Endoscopy revealed grade 3 or 4 lesions in only 5 cases. CONCLUSION: Symptomatic high-concentration peroxide exposures had a high incidence of associated embolic events in this cohort. Patients with evidence of embolic events had a high rate of death. Early hyperbaric oxygen therapy may be useful, but routine endoscopy is unlikely to be of benefit.