THE CASE
A 56-year-old physician (CUL) visited a local seafood restaurant, after having fasted since the prior evening. He had a history of hypertension that was well controlled with lisinopril/hydrochlorothiazide.
The physician and his party were seated outside, where the temperature was in the mid-70s. The group ordered oysters on the half shell accompanied by mignonette sauce, cocktail sauce, and horseradish. The physician ate an olive-size amount of horseradish with an oyster. He immediately complained of a sharp burning sensation in his stomach and remarked that the horseradish was significantly stronger than what he was accustomed to. Within 30 seconds, he noted an increased heart rate, weakness, and intense sweating. There was no increase in nasal secretions. Observers noted that he was very pale.
About 5 minutes after eating the horseradish, the physician leaned his head back and briefly lost consciousness. His wife, while supporting his head and checking his pulse, instructed other diners to call for emergency services, at which point the physician regained consciousness and the dispatcher was told that an ambulance was no longer necessary. Within a matter of minutes, all symptoms had abated, except for some mild weakness.
THE DIAGNOSIS
Ten minutes after the event, the physician identified his symptoms as a horseradish-induced vasovagal syncope (VVS), based on a case report published in JAMA in 1988, which his wife found after he asked her to do an Internet search of his symptoms.1
THE DISCUSSION
Horseradish’s active component is isothiocyanate. Horseradish-induced syncope is also called Seder syncope after the Jewish Passover holiday dinner at which observant Jews are required to eat “bitter herbs.”1,2 This type of syncope is thought to occur when horseradish vapors directly irritate the gastric or respiratory tract mucosa.
VVS commonly manifests for the first time at around age 13 years; however, the timing of that first occurrence can vary significantly among individuals (as in this case).3 The afferent aspect of a VVS episode is poorly understood, while the efferent aspect has been elucidated. A transient inhibition of the sympathetic nervous system results in vasodilatation, hypotension, and a temporary increase in vagal tone with bradycardia,4-7 which leads to cerebral underperfusion and loss of consciousness.
The loss of consciousness may be caused by an emotional trigger (eg, sight of blood, cast removal,8 blood or platelet donations9,10), a painful event (eg, an injection11), an orthostatic trigger12 (eg, prolonged standing), or visceral reflexes such as swallowing.13 In approximately 30% of cases, loss of consciousness is associated with memory loss.14 Loss of consciousness with VVS may be associated with injury in 33% of cases.15
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