Hyponatremia Associated with Oleander Toxicity
Background: Oleander species contain cardiac glycosides: oleandrin and nerioside. Ingestions of significant amounts of oleander can result in vomiting and cardiac glycoside toxicity: conduction blocks, arrhythmias and hyperkalemia. Hyponatremia is not typically associated with oleander poisoning. We...
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Veröffentlicht in: | Clinical toxicology (Philadelphia, Pa.) Pa.), 2007-05, Vol.45 (4), p.343-343 |
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Sprache: | eng |
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Zusammenfassung: | Background: Oleander species contain cardiac glycosides: oleandrin and nerioside. Ingestions of significant amounts of oleander can result in vomiting and cardiac glycoside toxicity: conduction blocks, arrhythmias and hyperkalemia. Hyponatremia is not typically associated with oleander poisoning. We report a case of hyponatremia associated with oleander ingestion. Case report: A 66-year-old female presented to the Emergency Department two hours after intentionally ingesting an unknown amount of oleander leaves. She denied any medical conditions and was not taking any medications. Initial vital signs (VS) were: HR = 64 in sinus rhythm, BP = 155/78. The Poison Control Center (PCC) recommended single-dose activated charcoal (AC), electrolytes, cardiovascular monitoring and a digoxin level. On follow up 2.5 hours after ingestion the patient remained alert and oriented but vomited several times. Vital signs were HR = 51 sinus bradycardia, BP = 167/67. The digoxin level was 2.7 ng/mL, calcium 9.0 meq/L, sodium = 115 meq/L, potassium = 6.5 meq/L, blood urea nitrogen (BUN) =16 mg/dL, creatinine = 0.9 mg/dL. The PCC recommended digoxin-specific immune Fab (Digibind registered ), intravenous hydration, and serial electrolytes. Two hours post administration of ten vials of Digibind registered HR = 80-90 and potassium = 4.2 meq/L. Ten hours post ingestion the patient continued to vomit, HR = 50 in second degree atrialventricular (AV) block and systolic BP = 90-100. She was receiving 3% sodium chloride. A repeat dose of AC was recommended. Twelve hours post ingestion HR = 61, BP = 88/28, sodium = 122 meq/L, potassium = 4.9 meq/L, BUN = 13 mg/dL, creatinine = 1.0 mg/dL. Twenty hours post ingestion the patient developed third degree AV block with a rate of 30-40, BP = 90s/30s on 7 mcg/kg/min of dopamine and five additional vials of Digibind registered were administered. Twenty-seven hours post ingestion HR = 50-60 in first degree AV block, BP = 133/60, sodium = 128 meq/L, potassium = 3.4 meq/L, BUN = 12 mg/dL, creatinine = 0.9 mg/dL. Thirty six hours post ingestion vitals were: HR = 69 in sinus rhythm, BP = 145/47, sodium = 138 meq/L, potassium = 3.4 meq/L, BUN = 15 mg/dL, creatinine = 0.8 mg/dL. The patient remained clinically stable and was discharged four days post ingestion. Conclusion: We report a case of significant and prolonged hyponatremia as well as cardiac glycoside poisoning after ingestion of oleander leaves. With aggressive supportive care including AC, Dig |
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ISSN: | 1556-3650 |