Cardiac effects of “mad honey”: a case series

Background. Grayanotoxins (GTX), also known as andromedotoxins, are produced by plants of the Ericacae family. This toxin is responsible for “mad honey” intoxication, which can present with fatal cardiac bradyarrhythmias and circulatory collapse. GTXs lead to cardiac toxicity because they increase sodium channel permeability and activate the vagus nerve. Objective. We evaluated 42 patients (33 males) prospectively who had been hospitalized with diagnosis of “mad honey” intoxication in a state hospital setting. Methods and results. The median age of patients was 48.5 years and all patients were admitted with complaints of nausea, vomiting, dizziness, fainting, and sweating. Five of the patients had syncope before admission. On admission, the mean systolic blood pressure was 73.1 ± 12.7 mmHg, the mean diastolic blood pressure was 52.1 ± 11.3mmHg, mean heart rate was 38 ± 7 bpm. On initial electrocardiograms, 18 patients had sinus bradycardia, 15 patients had complete atrioventricular block, and 9 patients had nodal rhythm. All patients were monitored in a coronary care unit and treated sympomatically with atropine, intravenous fluids, and dopamine. None of the patients needed temporary pacing and all were discharged without complications. Conclusion. “Mad honey,” which is produced widely in northern parts of Turkey can be toxic. This intoxication should be considered in patients admitted to emergency department with bradycardia and hypotension especially in regions where this honey is produced.     

Mad honey: uses,intoxicating/poisoning effects,diagnosis, and treatment

Honey has been used as a folk medicine since 2100 BC; however, mad honey is different from normal natural or commercially available honey as it is contaminated with grayanotoxins, which leads to intoxication/poisoning upon consumption. Grayanotoxin is generally found in Rhododendron genus (family: Ericaceae) and is extracted by bees from nectar and pollens of flowers. Mad honey has been commonly used as an aphrodisiac (sexual stimulant), in alternative therapy for gastrointestinal disorders (peptic ulcer disease, dyspepsia, and gastritis), and for hypertension for a long time. Grayanotoxin acts on sodium ion channels and muscarinic receptors, leading to cardiac disorders (hypotension and different rhythm disorders including bradycardia, bradydysrhythmias, atrial fibrillation, nodal rhythm, atrioventricular block, and complete atrioventricular block) and respiratory depression. Patients may also exhibit any one symptom out of or combination of dizziness, blurred vision, diplopia, nausea, vomiting, vertigo, headache, sweating/excessive perspiration, extremity paresthesia, impaired consciousness, convulsion, hypersalivation, ataxia, inability to stand, and general weakness. Mad honey intoxication is diagnosed with honey intake history before the appearance of the signs and symptoms (clinical presentation), and the treatment is symptomatic. Prompt treatment includes intravenous infusions of atropine sulfate and fluids (saline infusions or simultaneous infusion of saline with atropine sulfate) if the patient presents bradycardia and severe hypotension. In case of a complete atrioventricular block, a temporary pacemaker is employed. Except for a single case from Lanping County (Southwest China), the prognosis for mad honey intoxication is very good, and no fatalities have been reported in modern medical literature excluding a few in the 1800s. Although fatalities are very rare, mad honey ingestion may still lead to arrhythmias, which can be life-threatening and hard to recognize. This article provides a brief introduction to honey, mad honey and its uses, the effects of mad honey intoxication/poisoning, and its diagnosis, prognosis, and treatment.

Honey has been used as a folk medicine since 2100 BC; however, mad honey is different from normal natural or commercially available honey as it is contaminated with grayanotoxins, which leads to intoxication/poisoning upon consumption.     

Bench to bedside review: Extracorporeal carbon dioxide removal,past present and future

Acute respiratory distress syndrome (ARDS) has a substantial mortality rate and annually affects more than 140,000 people in the USA alone. Standard management includes lung protective ventilation but this impairs carbon dioxide clearance and may lead to right heart dysfunction or increased intracranial pressure. Extracorporeal carbon dioxide removal has the potential to optimize lung protective ventilation by uncoupling oxygenation and carbon dioxide clearance. The aim of this article is to review the carbon dioxide removal strategies that are likely to be widely available in the near future. Relevant published literature was identified using PubMed and Medline searches. Queries were performed by using the search terms ECCOR, AVCO2R, VVCO2R, respiratory dialysis, and by combining carbon dioxide removal and ARDS. The only search limitation imposed was English language. Additional articles were identified from reference lists in the studies that were reviewed. Several novel strategies to achieve carbon dioxide removal were identified, some of which are already commercially available whereas others are in advanced stages of development.     

Hypotension, bradycardia and syncope caused by honey poisoning

Honey intoxication, a kind of food poisoning, can be seen in the Black Sea region of Turkey and in various other parts of the world as well. In this study, 66 patients were hospitalized with a variety of symptoms including nausea, vomiting, salivation, dizziness, weakness, hypotension, bradycardia and syncope several hours after the ingestion of small amounts of honey. All patients had hypotension, and majority had bradycardia. These features resolved completely in 24 h with i.v. fluids and atropine, and none died. In conclusion, honey poisoning should be taken into consideration in the differential diagnosis of acute myocardial infarction and in the patients with vomiting, hypotension and bradycardia.     

Spinal cord stimulation: principles of past, present and future practice: a review

Electric energy have been in use for the treatment of various ailments, including pain, since the time of Pharaohs. The theoretical basis of electrotherapy of pain was provided by the Gate Control Theory of Melzak and Wall. In 1965, Shealey et al. first introduced electrical stimulation of spinal cord for treating pain. At present spinal cord stimulation (SCS) is a well established form of treatment for failed back surgery syndrome, complex regional pain syndrome and refractory pain due to ischemia. The indications for SCS is growing and the technology involved in this is rapidly advancing, however, high level of scientific evidence is still lacking to support this form of therapy due to difficulties in blinding and comparing with control groups. Future developments in SCS could include, combined SCS-drug delivery system, bio feedback and closed loop systems.