Introduction

We describe the case of a 19-year-old male patient who presented with an idioventricular rhythm after a honeybee sting. The literature review has shown that the venom content of Apis mellifera can cause from local non-allergic to anaphylactic shock reactions.

Case presentation

A previously healthy 19-year-old man was admitted to our emergency department with generalized paresthesias, dyspnea, facial edema, and a rash in his neck and both upper extremities. On arrival, the patient was conscious and able to move his extremities.

Patient history before admission

Our patient had been stung by a honeybee in the neck 30 min before admission; he reported a previous anaphylactic shock following a bee sting 7 years earlier. On admission, his blood pressure was 60/40 mmHg, his pulse was regular at a rate of 40 beats/min, and his temperature was 37°C and pulse oximetry in 92%.

Hospital management

The patient’s airway was inspected and secured. An electrocardiogram (EKG) tracing taken on admission revealed idioventricular rhythm at a rate of 41 beats/min (Fig. 1). Oxygen was administered, an intravenous (IV) access was established, and the transcutaneous pacemaker leads were placed on the chest of the patient; then, atropine was administered at a dose of 0.5 mg IV, producing a change in the EKG tracing, which showed P waves and a heart rate of 65 beats/min. Two liters of normal saline, hydrocortisone, ranitidine, and chlorpheniramine were also administered intravenously. After these, the 12 lead EKG showed normal sinus rhythm at a rate of 65 beats/min (Fig. 2) and blood pressure rose to 120/70 mmHg. Blood test results were all within the normal range. The patient remained under observation for 24 h, after which he was uneventfully discharged home.

Figure 1 Admission electrocardiogram. It shows an idioventricular rhythm at 41’ bpm. 

Figure 2 Post-treatment electrocardiogram. After administration of 0.5 mg intravenous of atropine, it is seen a normal sinus rhythm with 65’ bpm. 

Discussion

Honeybee (Apis mellifera) venom can cause a variety of reactions ranging from local non-allergic reactions (pain and erythematous lesions) to anaphylactic (laryngeal edema, bronchospasm, and hypotension)¹ or in some rare cases toxic reactions (myocardial infarction, acute renal injury, and encephalopathy)², the local effects are due to the toxic component of the venom, while the most severe reactions are related to an allergic systemic response³. In the United States, hornets, bees, and wasps are the cause of 70% of all venomous animal-related fatalities, causing an average of 48 deaths/year⁴. In Mexico between 1998 and 2009, there were 480 deaths associated with bee stings⁵. Cardiovascular events after bee stings have mostly been described in relation to anaphylactic shock, although several reports have underlined the relevance of the direct action of the venom on the heart and the coronary circulation, even causing myocardial infarction⁶-⁹.

Honeybee venom is composed of a mix of peptides, amines, and enzymes that include apamin (a small neurotoxin that blocks Ca²⁺ dependent K⁺ channels)¹⁰, adrenaline, noradrenaline, histamine, serotonin, and tertiapine, which may provoke myocardial ischemia and intense hypotension¹¹. It could also be the cause of an allergic or non-allergic local reaction, anaphylaxis, or a systemic toxic reaction such as vomiting or edema¹².

Animal studies have proven that on the injection of bee venom, an intense bradycardic response is elicited which, at least in part, contributes to the fall in blood pressure that characterizes anaphylaxis. This response is probably related to the direct effect of toxins on the pacemaker of the heart and is transitory and fully reversible¹³. In small concentrations, bee venom caused a decrease in the heart rate of an isolated toad heart and elongation of the PR interval, with marked electrocardiographic changes that included depression of the ST segment, atrioventricular conduction disturbances, and atrial arrhythmia¹⁴.

Bee stings usually cause temporary electrocardiographic changes, given the local vasoactive, cardiotoxic, or anaphylactic effects contained in their venom⁶.

The clinical manifestations of bee stings can be local or generalized. Local reactions mainly include pain, swelling, and pruritus at the site of the sting and are self limiting¹⁵. Generalized reactions, including anaphylactic shock and cardiovascular effects, usually present within the first 30 min after the sting and can cause urticaria, rash, breathlessness, wheezing, airway edema, weakness, anxiety, and confusion¹⁶.

Treatment

Recommendations for the treatment go from the inspection of the site to remove any residue as they can form a portal for entry of germs and bacteria, cold ice, or compresses which should be administered to control the local reaction, as well as the administration of oxygen and fluids intravenously to avoid shock and hypotension¹⁷. The antihistaminics and epinephrine should be administered; in case, the patient has a known allergy. Some patients have required permanent pacemaker after a bee sting¹⁸. In the case of our patient, atropine was administered initially to treat the rhythm abnormalities observed in the EKG tracing, with successful results. Continuous observation for 24 h revealed no further EKG abnormalities and the rest of the manifestations caused by the bee sting resolved after the administration of histamine receptor blockers. It is important to know that bee stings can present with idioventricular rhythm.

Conclusions

Although bee stings are seldom lethal, they represent the first cause of death from venomous animal exposure in the United States. A full and prompt cardiovascular evaluation should be performed in all patients presenting to the emergency department after a bee sting, and published guidelines regarding the management of bradycardia and anaphylaxis should be followed to achieve successful outcomes.