Yew tree poisoning: a near-fatal lesson from history (2)

Editor - Sandilands and Bateman raise an important point in regard to the safety of induced emesis and rightly remind us that it is no longer routinely recommended in cases of poisoning. It was not the intention of the previous report to advocate its use as a primary management step in cases of poisoning. Indeed, it can be seen from the case report that this was not part of the management strategy which was guided both by reference to the online TOXBASE and by discussion with the National Poisons Information Service. We concede that there is only anecdotal, dated and rather tenuous basis for the induction of emesis and perhaps the mention of induced emesis in the original report belongs in the same history books as those used by our patient to glean her knowledge of yew toxicity!

In cases of rare poisoning such as this there is little evidence on which to guide management. A review of 10 years' data from the American Association of Poison Control Centers Toxic Exposure Surveillance System revealed only four cases of life-threatening complications of yew ingestion.¹ TOXBASE lists only eight references on which it bases its guidance and information to emergency departments throughout the UK. All of the measures recommended on TOXBASE and highlighted by Sandilands and Bateman were attempted but none appeared to improve the clinical situation at the time.

Given this, it is worth reporting that the young lady described in the case report has presented once again with deliberate self-poisoning with yew foliage. She absconded from the supposedly secure psychiatric unit where she was an inpatient following her previous presentation. She made her way directly to where she knew the yew trees were growing and once again consumed a quantity of shoots and leaves which she washed down with a fizzy drink which she brought specifically for this purpose. Although she was apprehended quickly she was observed continuing to consume yew leaves even after apprehension having hidden some in the pockets of her trousers. She was brought immediately to the emergency department where, because she presented within 60 minutes of ingestion, she was given 50 g of oral-activated charcoal. Although she developed a marked sinus tachycardia, she remained clinically well with a blood pressure of 125/90 mmHg and peripheral oxygen saturations of 99% while breathing room air. She was discharged back to the psychiatric unit the following day. While induced emesis may not be recommended, she has, unintentionally, provided a single patient case-control ‘study’ into the effectiveness of the early use of oral-activated charcoal. The lack of effect seen from late administration of charcoal is in keeping with current guidelines and published studies showing a steady reduction in toxin absorption with time.²

Guha is right to mention the QT prolonging and proarrhythmic potential of amiodarone. While caution with the use of antiarrhythmic medications is certainly prudent, in this case amiodarone was given in the setting of a cardiac arrest with shock refractory ventricular tachycardia (VT) (and later repeated because of the apparent success of the initial administration) and is in keeping with current UK resuscitation guidelines to provide standard advanced life support if cardiac arrest occurs. TOXBASE already acts as a comprehensive database and we hope that publication of rare case reports such as this will help to inform future practice.

• © 2011 Royal College of Physicians