Stung to the Heart.

A 48-year-old woman with a history of scorpion sting was admitted with cardiogenic shock. Electrocardiogram showed ventricular tachycardia which reverted with magnesium sulphate after failed attempts with electrical cardioversion. Postcardioversion electrocardiogram showed Brugada pattern. (Level of Difficulty: Advanced.).

History of Presentation

A 48-year-old woman was stung by an Indian scorpion (Figure 1) while working in the paddy fields. She developed pain at sting site followed by profuse sweating and vomiting. She was admitted at an outside hospital where she received scorpion antivenom, intravenous fluids, and oral short-acting prazosin hydrochloride 500 μg every 3 hours. One day later she reported breathlessness and was transferred to our hospital. On arrival, she had a pulse rate of 200 beats/min and systolic blood pressure of 50 mm Hg. Her jugular veins were distended. Coarse crackles were heard in both the lung fields. Her skin was moist and her peripheral extremities were cold. Her electrocardiogram (ECG) showed regular wide complex tachycardia, left axis deviation with right branch block pattern in V1 consistent with origin of arrhythmia from the free wall of the left ventricle. The QRS duration was 240 milliseconds and the r to S wave nadir duration was 160 milliseconds, with a heart rate of 214 beats/min, positive concordance in V1 through V6, and AV dissociation, consistent with the diagnosis of ventricular tachycardia (VT) (Figure 2).

Figure 1

Venomous Scorpion (Mesobuthus Tamulus)

This is most lethal species of scorpion (Mesobuthus Tamulus).

Figure 2

Monomorphic Wide Complex Ventricular Tachycardia

Wide complex tachycardia, positive concordance in V1-V6 and atrioventricular dissociation (arrows) suggestive of ventricular tachycardia.

Learning Objectives

To identify cardiac manifestations of scorpion sting.

To review pathophysiology of ventricular arrythmia and Brugada phenocopy caused by scorpion sting.

Past Medical History

The patient was an otherwise healthy adult with no history of medication use. There was no family history of sudden cardiac death, and she denied any history of recurrent palpitations or tachycardia.

Differential Diagnosis

There is clear history of the scorpion sting. The scorpion was found and it was killed. Moreover, the clinical signs and symptoms of autonomic storm further confirmed the diagnosis of scorpion sting.

Investigations

Laboratory investigations showed elevated levels of troponin I 3.23 ng/dL (normal 0-0.02 ng/dL) and BNP 2,768.09 pg/mL (normal 0-100 pg/mL). Serum electrolytes were normal. Her echocardiogram and coronary angiogram were normal.

Management

Multiple attempts were done to electrically cardiovert her VT; however, all were unsuccessful. A bolus of amiodarone was administered, but with no success. However, the VT responded to an intravenous bolus of magnesium sulphate, which was then continued at 30 mg/kg as an infusion. Her vitals stabilized after chemical cardioversion. The ECG after cardioversion showed sinus rhythm, coved ST-segment elevation of >2 mm in V1-V3 leads, followed by a negative T-wave, consistent with Brugada pattern (Figure 3). A day later, her ECG showed rS in V1-V3 mimicking anterior myocardial infarction (pseudoinfarction pattern) and LAHB with QTc of 760 ms (Figure 4). The pseudoinfarction pattern reverted on subsequent ECG (Figure 5). She was observed in the intensive care unit where she received supportive treatment. She did not have any further arrhythmia episodes and was discharged a week later.

Figure 3

Left Anterior Hemiblock + Brugada Pattern

Sinus rhythm with coved ST-segment and T-wave inversion in V1-V3 suggestive of Brugada pattern.

Figure 4

Left Anterior Hemiblock + Pseudoinfarction Pattern

Sinus rhythm with left anterior hemiblock with rS pattern in V1-V3 (pseudoinfarction pattern) with prolonged QTc (760 milliseconds).

Figure 5

Pseudoinfarction Pattern Aborted

Discussion

Scorpion venom acts by activating neuronal sodium channels and inhibiting the calcium-dependent potassium channels. This causes sudden release of endogenous catecholamines resulting in an autonomic storm characterized by transient parasympathetic and prolonged sympathetic stimulation. Excessive catecholamines result in myocardial injury, which manifests as heart failure, cardiogenic shock, conduction abnormalities, QTc prolongation, and ventricular tachycardias as seen in our case. Scorpion venom delays the closing of neuronal sodium channels, resulting in autonomic storm. Poststimulation fatigue of cardiac sodium neuronal channels result in transient Brugada phenocopy (Figure 3).

The appearance of Brugada phenocopy after scorpion sting has been previously reported. It has been proposed that the intense and persistent depolarization of the autonomic nerves by the scorpion venom depletes the intracellular sodium, which manifests as Brugada phenocopy on the ECG.

Alpha receptor stimulation plays an important role in the pathogenesis of refractory pulmonary edema caused by a scorpion sting. Prazosin is a phosphodiesterase inhibitor and postsynaptic receptor blocker that acts as a physiological and pathological antidote to venom actions. Scorpion antivenin is a specific antidote to venom and it neutralizes the circulating and venom deposited at sting site. Thus, simultaneous administration of scorpion antivenom and oral prazosin hastened the recovery in severe scorpion sting.

Follow-Up

At a 2-week follow-up visit, the patient was completely asymptomatic and her ECG was normal (Figure 5).

Conclusions

A scorpion sting can cause life-threatening ventricular arrhythmias. Rarely, severe scorpion envenomation can unmask Brugada phenocopy. Hence, close follow-up is warranted.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the content of this paper to disclose.