What's new in Emergencies, Trauma and Shock? Studying the clinical and biochemical correlates in methanol poisoning

One of the first reported outbreak of Methanol poisoning searched in the Medical Literature Analysis and Retrieval System Online (MEDLINE) database dates back to 1953 reported by Bennet et al. in Kentucky, USA.[1] Several other reported outbreaks have been cited worldwide in the literatures.

The methanol metabolites formaldehyde and formic acid are of toxicologic importance and cause the dominant central nervous and ocular symptoms.[2] Medical management of acute methanol poisoning has changed over time and we now have better understanding of clinical features of methanol poisoning. A physician's awareness of the early symptoms, toxicology, and treatment of this condition and of settings in which poisoning often occurs can avert a disastrous outcome.[3] The study of various clinical and laboratory parameters of methanol poisoning among 178 patients affected by hooch tragedy in Ahmedabad, Gujarat (India) was a single center study highlighting the important epidemiological, clinical and prognostic features from the large methanol outbreak in India. The liquor illegally was made and distributed to public because it was cheap.

Methanol has neurotoxic actions on the human retina due to its metabolite, formic acid, which is a mitochondrial toxin. Visual loss is usually symmetric and most often affects the central visual field, although peripheral visual loss may occur as well. Fixed, dilated pupils and optic atrophy, with or without excavation, are the most common findings in persons with methanol-induced vision loss.[4] Gastrointestinal and visual symptoms predominated in the majority of patient presented to the hospital. GI symptoms predominated compared to visual symptom. As reported in this article patients may experience permanent neurologic deficit or death. Methanol, base deficit and anion gap were measured in forensic laboratory and methyl alcohol levels were found to be four times higher than the allowable dose. Severe acidosis, base deficit and higher methanol levels were associated with higher mortality. It can be concluded that arterial pH or serum standard bicarbonate levels can be used as surrogate indicators of the severity of methanol poisoning.[5] They can be used to guide physicians in the method of detoxification. Management of intoxicated patients has many aspects in a wide spectrum, beginning with decontamination processes and basic supportive care. The most logical therapeutic approach is probably the specific antidotes, when available and/or applicable. On the other hand, many chemicals and drugs, can be removed from the body by means of hemodialysis or hemoperfusion while treating vital sign abnormalities and electrolyte and acid-base disturbances of the patient.

As evident from this outbreak, methanol poisoning still has a high mortality today. Rapid diagnosis and treatment is critical in management of large outbreak. Delayed in hospitalization and diagnosis contributes to increase mortality. The degree of metabolic acidosis from formic acid predicts the outcome. Fomepizole and ethanol are frequently used as an antidote. Fomepizole is expensive and may not be readily available in large outbreaks. Co ingestion of methanol and ethanol may result in delayed onset of symptoms. In addition, the degree of metabolic acidosis is less severe with combined ingestion.

Large scale outbreak of methanol poisoning may be economically driven because it is cheap and intoxicating. Public educations about methanol poisoning and legislative control on production are important in preventing large outbreak due to methanol poisoning.