A Narrative Review of Aconite Poisoning and Management.

Aconite poisoning refers to toxicity resulting from plants belonging to the Aconitum genus, which comprises over 350 different species of perennial flowering plants that grow in temperate mountainous areas of the northern hemisphere (North America, Europe, Asia). These plants contain a group of toxins known as aconite alkaloids, which encompass numerous closely related toxic compounds. Conventional teaching from toxicology textbooks has broadly classified these alkaloids based on their mechanism of action, often simplifying them as substances that prevent sodium channel inactivation. However, this is an oversimplified and sometimes inaccurate description, as some aconite alkaloids can act as sodium channel blockers. Aconite alkaloids have a long history of use as poisonous substances and have been historically employed for hunting, assassinations, traditional medicine, and self-inflicted harm. Toxicity can occur due to the consumption of traditional medicines derived from aconitum plants or the ingestion of aconite plants and their derivatives. The clinical manifestations of aconite poisoning may encompass gastrointestinal symptoms, sensory alterations, seizures, and life-threatening dysrhythmias that may not respond to standard treatments. Treatment is primarily supportive however evaluation and management of these patients should be personalized and carried out in collaboration with a toxicologist.

Severe chronic Carboxyhemoglobinemia and polycythemia due to smoking hookah.

Acute carbon monoxide (CO) poisoning due to smoking hookah has been reported and may present similarly to other causes of acute carbon monoxide poisoning with nausea, headache, and loss of consciousness [1]. In the acute poisoned patient, immediate removal from the carbon monoxide source is paramount in addition to administration of oxygen and possible hyperbaric oxygen therapy (HBO) in certain situations. However, cases of chronic CO poisoning, treatment options, and long-term adverse health effects are far less reported but may include atherosclerosis and vague neurologic symptoms [2]. We present a case of a patient who chronically smoked hookah creating a condition of chronic carboxyhemoglobinemia which was discovered during work up for unexplained polycythemia. While being seen in the hematology clinic, he was found to have a blood carboxyhemoglobin of level 33.6% despite being asymptomatic. This is the highest recorded hookah-related carboxyhemoglobin concentration in the medical literature; and the significant chronic carboxyhemoglobinemia explained his polycythemia. This case illustrates that a social history is crucial when assessing the patient with severe carboxyhemoglobinemia as HBO is not indicated in chronic CO poisoning in an asymptomatic patient.