Suicidal bupropion ingestions in adolescents: increased morbidity compared with other antidepressants.

OBJECTIVE: Bupropion is often categorized as a newer generation antidepressant and assessed with serotonin reuptake inhibitors as a lower risk than older tricyclic antidepressants (TCAs). The objective of this study was to compare outcomes in adolescent suicide from ingestions between bupropion and TCA medications. STUDY DESIGN: An analysis of the National Poison Data System for exposures coded "suspected suicide" in adolescents (age: 13-19) was undertaken for the years 2013-2016 and included TCAs or bupropion. We compared clinical effects, therapies and medical outcomes. RESULTS: Over the four-year period there were 2253 bupropion and 1496 TCA adolescent suspected suicide calls. There was a significant linear increase in bupropion ingestions over the four years. Across all years, there were on average 189.2 (95% CI: 58.1-320.4; p = .01) more ingestions of bupropion than TCA. When comparing bupropion to a TCA, ingestions of bupropion were significantly more likely to be accompanied by seizure (30.7% vs 3.9%; p < .01), to be admitted (74.8% vs 61.6%; p < .01) and medical outcomes to be coded as a major outcome (19.3% vs 10.0%; p < .01). The number of cases with death or major clinical outcome for both increased over the four-year period. Ingestions of bupropion were less likely to have hypotension (2.7% vs 8.0%; p < .01) and less likely to be intubated (5.6% vs 16.4%; p < .01) as compared to ingestions of TCA. CONCLUSIONS: Adolescents who overdose on a single medication in a suicide attempt with bupropion have a statistically significant higher incidence of major outcomes and seizures. The risks of bupropion as a potential means of suicidal gesture by overdose must be considered, and weighed against its benefits and side effect profile when choosing an appropriate agent for the treatment of depression in adolescents.

Acute pneumonitis associated with nickel carbonyl exposure in the workplace.

BACKGROUND: We describe the clinical course of one industrial technician occupationally exposed to nickel carbonyl (NiC). CASE REPORT: A 50-year-old male industrial technician presented with complaints of nausea, myalgia, and cough to a local clinic after suspected occupational exposure to nickel carbonyl. He has no history of lung disease or smoking. His initial urine nickel concentration was 692 ug/L. He had infiltrates on the initial chest X-ray (CXR) and an oxygen saturation (O2) of 97% on room air. The patient was started on disulfiram 1 g by mouth (PO), 500 mg six hours after the first dose, then 250 mg twice daily for five days with prednisone 60 mg by mouth for five days. He presented 48 hours later with worsening respiratory symptoms. His O2 saturation decreased to 85% despite two days of oral steroids, and he was admitted to a hospital. He received prednisone 60 mg/day PO, 4 L nasal O2, and disulfiram 500 mg twice daily. He was discharged on day 7 post-exposure with disulfiram and prednisone. Case discussions: NiC is a severe respiratory irritant. Disulfiram was used off-label and was based on an established company protocol. CONCLUSIONS: Inhalation exposure to NiC resulted in a delayed respiratory dysfunction which responded to disulfiram treatment.

Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature.

INTRODUCTION: Ingestion of concentrated hydrogen peroxide (H(2)O(2)) has been associated with venous and arterial gas embolic events, hemorrhagic gastritis, gastrointestinal bleeding, shock, and death. Although H(2)O(2) is generally considered a benign ingestion in low concentrations, case reports have described serious toxicity following high concentration exposures. Hyperbaric oxygen (HBO) has been used with success in managing patients suffering from gas embolism with and without manifestations of ischemia. METHODS: Poison center records were searched from July 1999 to January 2010 for patients with H(2)O(2) exposure and HBO treatment. Cases were reviewed for the concentration of H(2)O(2), symptoms, CT scan findings of portal gas embolism, HBO treatment, and outcome. RESULTS; Eleven cases of portal gas embolism were found. Ages ranged from 4 to 89 years. All but one ingestion was accidental in nature. In 10 cases 35% H(2)O(2) was ingested and in 1 case 12% H(2)O(2) was ingested. All abdominal CT scans demonstrated portal venous gas embolism in all cases. Hyperbaric treatment was successful in completely resolving all portal venous gas bubbles in nine patients (80%) and nearly resolving them in two others. Ten patients were able to be discharged home within 1 day, and one patient had a 3.5-day length of stay. CONCLUSIONS: HBO was successful in resolving portal venous gas embolism from accidental concentrated H(2)O(2) ingestions.

Amanita smithiana mushroom ingestion: a case of delayed renal failure and literature review.

INTRODUCTION: In the Pacific Northwest a new pattern of mushroom ingestion has emerged, attributed to Amanita smithiana, in which renal failure has been the predominant manifestation. CASE REPORT: A 55-year-old male ate 3 raw wild mushrooms in a salad and had onset of severe nausea and vomiting within 6 hours. His vital signs were unremarkable. His labs were significant for a BUN of 14 mg/dL (5.0 mmol/L), and a creatinine of 1.0 mg/dL (88 umol/L), transaminases were elevated with an AST of 56 U/L (nl 9-40) and an ALT of 131 U/L (nl 14-72). Treatment was initiated with N-acetyl cysteine, penicillin, and milk thistle extract on the presumption that this was an amanitin-toxin containing mushroom. He developed acute renal failure that was not responsive to our treatment. Dialysis started on day 4 with a creatinine of 6.5 mg/dL, which peaked on day 7 at 10.2 mg/dL. We were able to obtain a positive mushroom identification by a mycologist as Amanita smithiana. The patient was discharged from the hospital for outpatient dialysis on day 10 and dialysis catheter was removed 39 days after ingestion with a creatinine of 1.4 mg/dL (123.8 umol/L). DISCUSSION: Amanita smithiana mushroom poisoning presents within 6 hours of ingestion with GI toxicity, and develops delayed onset of renal insufficiency over the first 1 to 4 days. The early hospitalization of this case allowed a profile of the onset of liver and renal injury. Mild elevation of hepatic transaminases occurred on presentation and peaked 24 hours after the ingestion. Renal injury was detected 1 day after presentation, and progressed to require hemodialysis by 4 days postingestion. This pattern of delayed-onset renal toxic mushroom ingestion is emerging among mushroom ingestions in Western North America.