Resident: Joshua Pettengill MD, PGY-1 Emergency Medicine
Faculty: Alexis L Cates DO, Emergency Medicine / Medical Toxicology
The case…
A 20 year-old female with a complicated psychiatric history of anxiety, bipolar disorder, OCD, and self-injurious behavior presents to the emergency department with a friend after a reported suicide attempt. The patient discloses that she had consumed a sizable amount of yew berry leaves after reading about it online. The patient presents approximately four hours after ingestion. The patient feels generally unwell and flushed. Vitals in triage reveal a heart rate of 96 beats per minute, blood pressure of 78/41 mmHg. All other vitals are within normal limits. Shortly after triage, the patient has a generalized tonic-clonic seizure which is aborted after 3 minutes with 2 mg IV lorazepam (1).
Learning Point #1: A little about Yew
The Common Yew (Taxus baccata) also known as the English Yew or the European Yew, classified in the Taxaceae family, is a medium-sized, evergreen tree (5).
Yew plants represent a genus of plants known to be highly toxic, though lethal intoxication is rare. The majority of deaths in yew toxicity occur due to tree part ingestion leading to a cardiotoxic effect, mediated through generation of a number of fatal tachyarrhythmias and bradyarrhythmias. From the different species of Yew, several taxine alkaloids have been characterized, most common being taxine A and taxine B. Most of the toxic effects of yew are attributed to taxine B including its cardiotoxic effects. The toxic taxine alkaloids have been reported to be present in the foliage, bark, seeds of the plants, and roots, but not in the fleshy scarlet aril/berry (6, 8).
Figure 1. The Yew aril/berry and structures of taxine A and taxine B. (4)
Learning Point #2: Clinical manifestations
For a lethal dose, time from ingestion to death is approximately 2-5 hours. Onset of symptoms are documented to typically occur from 30 minutes to 1 hour following ingestion. Symptoms of ingestion are non-specific and can include nausea, vomiting, impaired color vision, abdominal pain or muscle spasms. Clinical findings include dilated pupils, dyspnea, tachycardia in the earlier phase followed later by bradycardia, tonic–clonic convulsions, somnolence and the patient may become obtunded.
Lab results are nonspecific but will often show metabolic acidosis, hypokalemia or hyperkalemia, and hyponatremia.
Electrocardiogram (EKG) changes may include multiple premature ventricular contractions at the early stages of poisoning, followed by persistent ventricular tachycardias and ventricular fibrillation. Dysrhythmias prior to death may include significantly widened QRS complexes with bradycardia. Terminally, electromechanical dissociation and asystole follows (5).
The Case Continued…
The patient’s initial EKG showed monomorphic ventricular tachycardia and shortly after the patient rapidly experienced a pulseless electrical activity (PEA) arrest. The patient underwent 1 minute of CPR prior to achieving return of spontaneous circulation (ROSC). The patient was intubated and sedated and started on vasopressors including norepinephrine and vasopressin for persistent hypotension. After the airway was secured and the patient was started on vasopressors, her cardiac rhythm showed narrow complex tachycardia with occasional wide complex dysrhythmia. The patient then experienced a monomorphic wide complex ventricular tachycardia with a rate of 80-120 bpm which is shown below (5).
Figure 2. EKG showing ventricular tachycardia with rate 120–150 bpm, AV dissociation and fusion beats. (1)
Learning Point #3: Taxine causes cardiotoxicity
The taxine alkaloids (taxine A and taxine B) are the more common symptomatic toxins within the yew. The presence of an unsaturated lactone group makes this group of alkaloids similar to digitalis and yew poisoning may be confused with digoxin toxicity (8). Primarily taxine B has been found to potentiate dysrhythmias which tend to be resistant to standard treatment. The taxines increase cytoplasmic calcium via a dose-dependent inhibition of both calcium channel and fast sodium channels in cardiac myocytes. Taxine B also appears to increase inotropy and QRS duration, while increasing AV conduction time resulting in heart block (1). The toxidrome of taxine can mimic calcium channel blocker (especially verapamil) and digoxin toxicity. The probable minimal lethal dose in humans of the yew plant is 0.6-1.3 g/kg, which equates to 3.0-6.5 mg/kg of taxine assuming 5 mg of taxine per gram of yew (8).
Figure 3. The cardiac myocyte. Taxine B primarily inhibits fast sodium channels and L-type calcium channels in cardiac myocytes.
Learning Point #4: Management of Yew poisoning
There is no known antidote for yew poisoning and hypothesized treatments have not been proven to be effective. These proposed and trialed treatments include interventions directed towards the patient’s presentation signs and symptoms. These may include: atropine, amiodarone, sodium bicarbonate, Digibind, lipid emulsion infusion, and lidocaine. Management includes early recognition of potential yew toxicity, anticipation of dysrhythmias, and prompt supportive treatment. Supportive care generally includes attention to airway, breathing, circulation, IV access with appropriate fluid resuscitation if needed, electrolytes, vasopressors, and advanced cardiac intervention if needed. Transvenous pacing or ECMO may be considered in the most critical of circumstances (7).
The Case Concluded…
The patient was given magnesium sulfate, calcium chloride, and lidocaine via infusion but unfortunately this was unsuccessful in breaking her dysrhythmia. Gastrointestinal decontamination was attempted via gastric lavage and secondarily activated charcoal through nasogastric tube. A small amount of green liquid and leaves were suctioned. At the advice of the local poison control center and toxicology consultation, the patient was given a total of 20 vials of Digibind and lipid emulsion therapy. This did not result in a return to normal circulation. Transvenous pacing was performed and control of the patient’s tachycardia was achieved, and ultimately decreased her vasopressor requirement.
The patient was admitted to the Cardiac Critical Care Unit where she began having increasing vasopressor requirements, further runs of ventricular tachycardia, and no responsiveness to transvenous pacing and antidysrhythmics. The patient ultimately died after the family asked for withdrawal of invasive measures and resuscitative efforts (1).
Figure 4. Needlelike objects found in the postmortem gastric contents, consistent with the leaves of Taxus baccata. (7)
Works Cited:
1) Alarfaj, Mohammad, and Ankur Goswami. “Cardiotoxicity in Yew Berry Poisoning.” The American Journal of Emergency Medicine, vol. 50, 2021, https://doi.org/10.1016/j.ajem.2021.05.043.
2) Du, Eric Y., et al. “Dying to Be with Yew.” Toxicology Communications, vol. 5, no. 1, 2021, pp. 109–111., https://doi.org/10.1080/24734306.2021.1918898.
3) Gupta, Abhinav. “(Don’t) Do the Yew.” ACEP Symbol, https://www.acep.org/toxicology/newsroom/feb2021/dont-do-the-yew/.
4) Photograph of the English Yew with Berry and Seed as Well as Chemical …https://www.researchgate.net/figure/Photograph-of-the-English-yew-with-berry-and-seed-as-well-as-chemical-structures-of_fig1_352204297.
5) Piskač, Ondřej, et al. “Cardiotoxicity of Yew.” Cor Et Vasa, vol. 57, no. 3, 2015, https://doi.org/10.1016/j.crvasa.2014.11.003.
6) Ray, Charles David. “Toxicity of Yew Wood and Roots.” Penn State Extension, 12 June 2022, https://extension.psu.edu/toxicity-of-yew-wood-and-roots.
7) Rutkiewicz, Aleksander, et al. “Yew Poisoning – Pathophysiology, Clinical Picture, Management and Perspective of Fat Emulsion Utilization.” Anaesthesiology Intensive Therapy, vol. 51, no. 5, 2019, pp. 404–408., https://doi.org/10.5114/ait.2019.89952.
8) Vališ, Martin, et al. “Common Yew Intoxication: A Case Report.” Journal of Medical Case Reports, vol. 8, no. 1, 2014, https://doi.org/10.1186/1752-1947-8-4.
9) Wilson, Christina. “Toxicity of Yew (Taxus Spp.) Alkaloids.” Veterinary Toxicology, edited by Stephen Hooser, Academic Press, 2007, pp. 929–935.
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