Grayanotoxins, a group of diterpenoid toxins found in death camas, azalea, Rhododendron spp, and mountain laurel, can become concentrated in honey made from these plants. Depending on the specific toxin, they variably open or close the sodium channel. In addition to causing bradycardia and hypotension, patients may exhibit mental status changes (“mad honey” poisoning) and seizures.2
Case Continuation
After rapid infusion of 1-liter of normal saline, the patient’s BP was 80/63 mm Hg and HR was 52 beats/minute. His wife arrived to the ED 30-minutes later with a plastic bag containing the red berries the patient had ingested. The emergency physician identified them as Taxus baccata, or more commonly, yew berries. The patient stated that he ingested both the red fleshy aril and chewed the hard central seed.
How is cardiotoxicity from yew berries treated?
Within hours of ingestion, toxicity progresses from nausea, abdominal pain, paresthesias, and ataxia, to bradycardia, cardiac conduction delays, wide-complex ventricular dysrhythmias and mental status changes.3 Although toxicity of Taxus has been known since antiquity, no antidote exists. Ventricular dysrhythmias causing hemodynamic instability should be electrically cardioverted, although there is no evidence to support the safety or efficacy of such therapy. Since the serum, and therefore cardiac concentration of taxine will be identical after cardioversion to its value prior, recurrent dysrhythmias are common.1 Sodium bicarbonate has been inconsistently effective in the treatment of wide-complex tachydysrhythmias,4 but its use seems counterintuitive for most cases. There may be merit to raising the sodium gradient on an already sodium overloaded myocyte, but short-term gain may lead to unintended consequences. Success with antidysrhythmics has been limited: although amiodarone is often used to treat wide-complex tachydysrhythmias, its efficacy in Taxus toxicity has been conflicting.4-6
There have been a few reported cases of yew alkaloid crossreactivity with digoxin assays, suggesting that digoxin-specific antibody fragments may bind taxine.7 There is no evidence, however, that cardioactive steroids are present in yew, and empiric use of antidigoxin Fab-fragments cannot be recommended. A single case report demonstrated that hemodialysis was ineffective in the removal of taxines, likely due to the toxin’s large volume of distribution.8 As a last resort, extracorporeal life support with membrane oxygenation is described favorably in two cases of yew berry poisoning refractory to conventional therapy.9,10
Case Conclusion
The patient’s ECGs showed a morphologically abnormal rhythm, possibly with a Brugada pattern, which are representative of the dysrhythmias caused by taxine’s inhibitory effects on the sodium and calcium channels. Despite an attempt at electrical cardioversion, the dysrhythmia persisted. He was given intravenous boluses of fluids and started on an amiodarone infusion. The patient’s BP gradually improved over the following 2 hours, and the dysrhythmia resolved with hemodynamic improvement. The amiodarone infusion was then discontinued, and he was admitted to the hospital for further testing. Echocardiography, electrophysiology studies, and cardiac catheterization were all normal. The absence of structural, dysrhythmogenic, and ischemic abnormalities supported the toxic etiology of his hemodynamic aberrations. He was discharged from the hospital 3 days later without report of sequelae.
Dr Nguyen is a medical toxicology fellow in the department of emergency medicine at New York University Langone Medical Center. Dr Nelson, editor of “Case Studies in Toxicology,” is a professor in the department of emergency medicine and director of the medical toxicology fellowship program at the New York University School of Medicine and the New York City Poison Control Center. He is also associate editor, toxicology, of the EMERGENCY MEDICINE editorial board.