Case Report: Clinical Presentation of Toad Venom-Induced Cardiac Intoxication

Abstract

Six people made the mistake of eating toad soup, and one of them died before arriving hospital. Five patients presented conscious change, gastrointestinal upset, or bradycardia. We checked their blood and electrocardiography to monitor the cardiac intoxication from toad venom. This experience revealed that the serum level of digoxin does not indicate the severity of intoxication but has the diagnostic value. And, serum potassium level is useful to provide valuable therapeutic information.

Introduction

Toxins are produced by all toads, but the potency of toxins varies by species and by geographic location within individual species. 1 In Asia, dried venom from toad parotid glands is involved in a variety of diseases, including inflammation and antineoplastic activity. 2 Sebaceous glands secrete toxins, which include bufagenins and bufotoxins. Bufagenins have digitalis-like effects, 3 and bufotoxins can block sodium channels 4 and lead to inhibition of myocardial conduction and function and cause arrhythmia, of which bradycardia and ventricular tachycardia are the most common. Specific antidotes and detectors for toad toxins are not available. Therapy is directed at minimizing toxin absorption and controlling associated clinical signs.

Case Report

Six people believed they had eaten frog soup, but actually, they had eaten toad. Two hours after eating toad soup, they began to experience dizziness and gastrointestinal upset, and two of them experienced altered consciousness. The toad eaten was proved of the Bufo bankorensis species. One elderly male (case 1) died before arriving at a hospital, and five patients were sent to the emergency department at our hospital.

Patients’ information is shown in Table 1 , and electrocardiograms are shown in Fig. 1 . The worse survivor (case 2) ate soup and three toads 8 hours before admission. On arrival, the patient’s heartbeat was irregular, and an electrocardiogram showed atrial fibrillation with a slow ventricular response ( Fig. 1 A). We used a percutaneous pacemaker to save the patient from this deadly arrhythmia, and the patient was then transferred to the intensive care unit (ICU). In the ICU, one of the patients received an atropine pump instead of percutaneous pacemaker, and the total dose of atropine was used 10 mg. The patient was discharged on the seventh day. The other four patients received supportive care and were soon discharged.

Table 1 . Data from all 6 patients admitted with toad venom-induced cardiac intoxication .

^a The patient case 2 was admitted to the ICU for 3 days, with a temporary pacemaker. A few days later, the atropine pump instituted the pacemaker, then the patient was transferred to the ordinary ward. After more 4 days admission, he was discharged.

Characteristic		Case 1	Case 2	Case 3	Case 4	Case 5	Case 6
Age (years)		60	61	62	64	63	72
Sex		Male	Male	Male	Male	Male	Female
Amount (toads)		Unknown	3	5, peeled	2	3	4
Symptoms		Change in consciousness	Vomiting, change in consciousness	Dizziness, headache, diarrhea, vomiting, limb numbness	Dizziness, headache, nausea, vomiting, diarrhea	Nausea, vomiting, mild dyspnea	Dizziness, vomiting, epigastric pain
Heart rate (bpm)			49	47	66	88	68
ECG		Asystole	Af with SVR	SB	NSR	NSR	NSR
Digoxin (ng/mL)	Initial	NA	0.79	0.60	0.57	0.69	0.69
	Following	NA	0.45	0.23
K+ (mmol/L)		NA	6.2	4.3	4.4	4.4	4.0
Prognosis		Expired before admission	ICU a	Admission (5 days)	OB (18 hours)	OB (15 hours)	OB (20 hours)

Fig. 1 . Electrocardiograms from cases 2 and 3. Bradycardia was observed, which returned to normal as symptoms subsided. (A) The electrocardiogram from case 2 shows atrial fibrillation with a slow ventricular response. (B) The electrocardiogram from case 3 shows sinus bradycardia.

Discussion

There have been few reports of accidental human exposure to toad venom in the past. We collected information about toad toxin-induced cardiac intoxication. The diagnosis of toad-induced cardiac intoxication is clinically dependent on a combination of exposure history, clinical presentation, laboratory data, and electrocardiographic manifestation. Patient prognosis depends on the number of toads consumed. In our case report, the deceased patient ate the greatest number of toads out of all patients assessed. However, we cannot determine the degree of poisoning by identifying the number of toads consumed because toad toxins are partially dissolved in the soup. We know that the concentration of digoxin does not serve as a reliable indicator of the severity of symptoms and dysrhythmia. In the emergency department, elevated serum digoxin concentrations may confirm exposure but may not correlate with clinical manifestations of toxicity. Digoxin-induced hyperkalemia is a reliable reference for the severity of intoxication when digitalis-like toxin blocks the sodium–potassium pump 5 . Extracellular potassium increases, which is a reasonable indicator of cardiac intoxication from toad venom. Case 2 had hyperkalemia and bradycardia, and the patient needed intensive care. Digoxin-specific Fab fragments are beneficial in treating toad-induced cardiac toxicities in previous articles. 6 , 7 The antibody fragments bind with the digoxin molecules to form complexes and are then excreted in the urine. 1 However, there is no consensus on the instructions for digoxin-specific Fab fragments. The less controversial suggestion is to use the antidote in some situations, such as suspected or known digoxin toxicity with life-threatening arrhythmia, cardiac arrest, and hyperkalemia (potassium > 5.0 mmol/L). 8 - 10 We did not use digoxin-specific antibody fragments to treat the lethal arrhythmia. Because the condition of case 2 improved soon after undergoing percutaneous pacemaker intervention and atropine therapy in the ICU, in addition to the shortage of digoxin-specific antibody fragments, we preserved a few antidotes for possibly more critical cases. Although the patient potassium-lowering agents and calcium administration are controversial in digitalis intoxication treatment, 11 case 2 received single-dose calcium administration and other treatments for digoxin-induced hyperkalemia without adverse effects.

This report emphasizes the diagnostic role of serum digoxin and potassium levels in treating toad venom-induced cardiac intoxication in patients in the emergency department and shares our valuable experiences in treating poisoning from toad venom.