In this case series, we present 2 cases of previously healthy farmers, who presented with symptoms of a cholinergic crisis that developed several hours after ingestion of camel milk. The initial case was treated with supportive medical care without using antidote as no history of direct exposure to pesticides was available.The second case presented with symptoms of cholinergic crisis that developed several hours after the ingestion of camel milk. Clinical features included slurred speech, headache, vomiting, diarrhea, frequent ­micturition, muscle fasciculation, chest discomfort, and atrial fibrillation. The patient developed bradycardia that responded to intravenous atropine. Routine investigations were unremarkable, but acetylcholinesterase and pseudocholinesterase levels were both low. The patient was managed with intravenous fluids, analgesia, atropine, and pralidoxime, which were administered when he developed respiratory symptoms secondary to excessive secretions. The following day, the patient was asymptomatic and discharged. On the medical history, the patient denied any other ingestion including food and drink or potential organophosphate exposure on the day of symptom onset. Application of organophosphate pesticides to the mammary glands of camels has been used for many decades against Sarcoptes scabei cameli, a mite that causes a dermal infestation in camels similar to human scabies infections.

No abstract

This case is of a 76-year-old man with a known history of hypertension, type 2 diabetes mellitus, and ischemic heart disease, who presented to our department with chest pain and palpitations. His electrocardiogram showed a ventricular tachycardia (VT), but fortunately our patient was hemodynamically stable. A trial of adenosine was given to convert the patient’s heart back to sinus rhythm, but was unsuccessful and the rhythm remained as VT. Soon after, the patient suddenly became hemodynamically unstable as his blood pressure acutely declined; thus, the decision to perform a direct current cardioversion was taken. Bearing in mind that the patient was still awake, he was given 10 mg of intravenous etomidate as a pre-procedural sedative. During the time it took to prepare for the procedure, the patient’s rhythm reverted from VT to a regular sinus rhythm, raising his blood pressure back to normal and achieving hemodynamic stablility, negating the need of any electrical or chemical cardioversion. Our patient was then handed over to the cardiology team for an emergency percutaneous coronary intervention procedure and an implantable cardioverter-defibrillator procedure, both of which were successful. Etomidate was used in this case for the purpose of sedation, and as luck would have it, it seems that it had also incidentally reverted the arrhythmia back to normal.