What food/supplements cause GI symptoms and bradycardia?
April 19, 2024
A 50-year-old woman presents with complaints of weakness, abdominal pain, vomiting and diarrhea. VS: 95/65 mmHg; HR 35 bpm; temp 97.7; 100% on RA. EKG revealed scooped T-waves. Her husband had the same presentation 2 days prior which resolved during observation. Atropine was administered with transient improvement in HR but no change in blood pressure.
Two people in the same house with a similar clinical presentation makes one think of a common exposure like a food/supplement ingestion. Sinus bradycardia with a relative decrease in blood pressure, GI upset, and an EKG with scooped T- waves has to make one think of cardiac glycosides (such as digoxin), but if we are thinking of ingestion of food/supplements, one must consider yellow oleander, common oleander, and foxglove. These plants contain cardioactive steroidal glycosides. The seeds of yellow oleander, which are extremely toxic, look very similar to candlenut seeds-an innocuous plant whose seeds are ingested for weight loss.
Other differential diagnosis for the clinical presentation of GI symptoms with bradycardia;
“Mad honey” contains grayanotoxin which is derived from plants in the Rhododendron genus (family: Ericaceae). The toxin is extracted by bees from nectar and pollens of flowers and incorporated into the honey. Mad honey is used as an aphrodisiac and in alternative therapies. Grayanotoxin acts on sodium ion channels and muscarinic receptors, causing dysrhythmias such as bradycardia, atrial fibrillation, complete atrioventricular block as well as respiratory depression. Ingestion of mad honey was originally described in Turkey. Mad honey is now shipped around the world.
Camas roots, or death camas is a common plant (Zigadenus) in the lily family found throughout the United States. Its onion-like roots can be mistaken for an edible plant, although all parts of the plant, including the flowers, are toxic. The toxin is the steroidal alkaloid zygazine. Vagal stimulation may also occur. Fatalities have been reported following ingestion.
(Cholinesterase inhibitors such as organophosphates or carbamates must be considered, but these are primarily pesticides and it would be unusual for them to occur in high enough concentration in food to cause this syndrome)
Ciguatera toxins are produced by dinoflagellates (unicellular algae) which grow on coral reefs. These organisms are consumed by herbivorous fish which are in turn consumed by carnivorous fish. The toxins become more concentrated as they move up the food chain. Humans are affected when they ingest the flesh of the large fish. Cooking or freezing the fish does not reduce the toxin. The toxicity of ciguatoxin is due to its potent depolarizing action in the nerve cells and striated muscle. GI symptoms usually occur within 6-12 hour after ingestion and may last days. Neurologic symptoms include paresthesia, pruritis, dizziness and hot-cold temperature reversal. Ciguatoxin binds to cardiac sodium channels and has some cholinomimetic activity-thus the bradycardia. Treatment is primarily supportive.
Denouement: Both had eaten barracuda within the previous couple of days. Barracuda is a predatory fish (like grouper and snapper) that eats herbivorous fish.
And if you’re doubting, DOH testing was positive for ciguatoxin.
Question prepared by Donna Seger MD
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Donna Seger MD Professor Emerita
Dept of Medicine
VUMC