Poisoning due to consumption of horse chestnut seed.

Horse chestnut (Aesculus hippocastanum) is a common tree found on roads and parks. The shape of the fruit is very similar to that of the edible Korean chestnut (Castanea crenata); thus, people can eat it by mistake. However, reports of the side effects and toxicity from ingestion are very rare. A 46-year-old male who had no unusual findings in the past had eaten horse chestnut seed which he had mistaken to be Korean chestnut. He visited the emergency department (ED) with complaints of epigastric pain, nausea, and sweating. Blood tests showed a slight increase in the levels of liver enzymes, serum amylase, and pancreatic amylase. During the monitoring, he complained of palpitations, and electrocardiogram showed atrial fibrillation. On the following day after conservative treatment, blood testing and electrocardiogram showed normal findings. He was discharged from the ED as he did not complain of any further symptoms. When a patient who has eaten horse chestnut visits the ED, blood examination and electrocardiogram monitoring are needed, and conservative treatment is required.

Comparison of the therapeutic effect between sodium bicarbonate and insulin on acute propafenone toxicity.

PURPOSE: Unlike other sodium-channel-blocking antiarrhythmic agents, propafenone has ß-blocking effects and calcium-channel-blocking effects. Yi et al recently studied insulin's treatment effect on acute propafenone toxicity in rats. However, because the degree of effectiveness of insulin compared to the previously known antidote sodium bicarbonate (NaHCO3) was not studied, the 2 treatment methods were compared for propafenone intoxication in rats. METHODS: Rats received intravenous propafenone (36 mg/[kg h]) for 12 minutes. After the induction of toxicity, rats (n = 10 per group) received normal saline solution (NSS), NaHCO3, or insulin with glucose as treatment. Animals in the NSS, NaHCO3, and Insulin groups received an intravenous infusion of 36 mg/(kg h) propafenone until death occurred. For each animal, the mean arterial pressure (MAP, heart rate, PR interval, QRS duration, total hemoglobin, sodium, potassium, potential of hydrogen, bicarbonate, glucose, lactate, and central venous oxygen saturation (Scvo2) were measured and compared among the groups. RESULTS: Survival of the Insulin group was greater than that of the NSS group by log-rank test (P = .021). Sodium bicarbonate prevented the decline of MAP for 55 minutes. In comparison, insulin prevented the decline of MAP and heart rate, and the elongation of the PR interval and QRS duration for 55 minutes (P < .05). Propafenone toxicity led to decreased Ca(2+), potential of hydrogen, and Scvo2 and increased lactate levels. Insulin prevented the decrease of Ca(2+) and Scvo2, whereas NaHCO3 prevented the increase in lactate. CONCLUSION: Insulin treatment was more effective than NaHCO3 on acute propafenone toxicity in rat. Therefore, when propafenone-induced cardiotoxicity occurs, which is unresponsive to current treatment methods, glucose-insulin infusion may be considered.

Cardioprotective effect of glucose-insulin on acute propafenone toxicity in rat.

OBJECTIVE: We recently observed a case of propafenone self-poisoning in which the patient was initially unresponsive to conventional therapies such as sodium bicarbonate, dopamine, and norepinephrine but recovered with intravenous glucose-insulin infusion. We raised the hypothesis that insulin may have a cardioprotective effect in acute propafenone toxicity. METHODS: We evaluated the effect of glucose-insulin infusion on mortality and electrocardiographic abnormalities during acute propafenone toxicity in rats. After measurements of basal mean arterial pressure, heart rate, PR interval, and QRS duration, rats received intravenous propafenone (36 mg/kg per hour) for 12 minutes. Two minutes after the induction of toxicity, the rats (n=10 per group) received either normal saline solution (NSS) or insulin with glucose. Rats in the insulin-treated (Insulin group) and the NSS-treated (NSS group) groups received an intravenous infusion of 36 mg/kg per hour of propafenone until death occurred. Rats receiving only NSS intravenously without propafenone toxicity served as control (Control group, n=10). RESULTS: Insulin treatment improved survival and delayed the hemodynamic and electrocardiographic consequences of propafenone toxicity. Survival was significantly greater in the insulin group than that in the NSS group (P<.001). Insulin prevented the decline in mean arterial pressure and heart rate (P<.05). Insulin also prevented the increase of the PR interval and the QRS duration (P<.05). CONCLUSION: Glucose-insulin infusion delayed the abnormalities in cardiac conduction and improved rat survival after acute propafenone toxicity. These results suggest a cardioprotective effect of glucose-insulin in acute propafenone toxicity.