The syndemic of COVID-19 and methanol poisoning in Mashhad, Iran

The Case Files

Hospital records of thirty patients with methanol poisoning were studied. Neurologic manifestations at presentation including coma, seizures and decreased visual acuity were seen in nineteen patients. The mean blood pH at presentation was significantly lower in the patients with these neurologic signs and symptoms than in the eleven patients without them (p less than 0.05). Methanol levels at presentation tended to be higher in patients with neurologic manifestations at presentation and these patients tended to present later after methanol ingestion than those patients without neurologic manifestations. Fifteen patients with methanol poisoning developed serious neurologic sequelae or died. The mean blood pH was significantly lower in this patient group than in those who survived without neurologic sequelae (p less than 0.05). Methanol levels at presentation were not different in the patients who developed neurologic sequelae or died as compared to those who did not. The time from ingestion of methanol to presentation at the hospital was however significantly longer in those patients who developed neurologic sequelae or died (p less than 0.05). Initiation of treatment within eight hours of ingestion of methanol was associated with a better clinical outcome.

Toxic alcohol poisoning is regularly encountered in emergency departments and intensive care units (ICUs). Most patients present with an altered level of consciousness, but the subsequent course and spectrum of neurologic complications and outcomes is highly variable. We performed a population-based, multicenter retrospective cohort study of critically ill patients with toxic alcohol poisoning admitted to ICUs in Alberta, Canada, between 2007 and 2019 to describe neurologic sequelae, including seizures, coma, neuroimaging abnormalities, persistent cognitive or visual impairment, and mortality. Multivariate analysis was performed to identify predictors of poor outcome. We identified 104 patients, including 55 (53%) with methanol ingestion, 36 (35%) with ethylene glycol ingestion, and 13 (13%) with isopropanol ingestion. In patients who underwent neuroimaging, abnormalities were detected in 9 of 24 (38%) with methanol toxicity, 5 of 20 (25%) with ethylene glycol toxicity, and 0 of 10 with isopropanol toxicity (p = 0.07). Basal ganglia were commonly involved with both methanol and ethylene glycol poisoning, but prominent subcortical involvement and restricted diffusion were observed only with methanol poisoning. The composite of death, persistent cognitive impairment, or visual loss occurred in 13 (24%) patients with methanol poisoning, compared with one (3%) with ethylene glycol poisoning and none with isopropanol poisoning (p = 0.006). Among patients with methanol toxicity, greater elevation of the anion gap and lower Glasgow Coma Scale score were independent predictors of poor outcome. No patient with an anion gap ≥ 28 at presentation had a favorable recovery. Progression to death by neurologic criteria occurred in 3 of 55 (5%) patients with methanol poisoning and in none with other toxic alcohols. Methanol overdose is the most common form of toxic alcohol poisoning to result in ICU admission. Poor neurologic outcomes may occur especially with methanol poisoning, with more than one in five patients dying or having persistent cognitive or visual impairment. A wide anion gap independently predicts poor outcome, emphasizing the importance of expeditious recognition and treatment.

Methanol poisoning in Klang Valley, Malaysia: Autopsy case series

Methanol is a highly toxic alcohol

Methanol Ingestion

Methanol poisoning is a challenging issue due to its inducing acute multiple organ failures, and especially due to a lack of preparedness, available antidotes, and management protocols. The current study presents six cases of methanol poisoning that attended the emergency department of King Abdul Aziz Specialist Hospital, Taif, Saudi Arabia, between March and November 2022. All of the patients suffered from severe metabolic acidosis and visual impairment following the ingestion of homemade alcoholic beverages and colonia. Three patients were comatose, suffered from post-cardiac pulmonary arrest, and, finally, died, while the other three were non-comatose and discharged from the ICU after improvement. Management was based on clinical symptoms and other laboratory findings due to a shortage of methanol level measurement resources. The antidote, fomepizole, was not given to all of the cases due to its deficiency, and ethanol was given only to one patient due to difficulties in administering it without monitoring its concentration. Methanol poisoning and its outbreak provide insights into the dangers of hazardous homemade alcohol and other pharmaceutical preparations that might be adulterated with methanol, particularly to the shortage of suitable diagnostic testing and antidotes in addition to poor resources for management of intoxicated patients in some regions of Saudi Arabia.

History and Physical Exam and Simple Math Go a Long Way in Developing a Diagnostic Differential: A Case of Methanol Poisoning

Treatment thresholds for methanol poisoning are based on case reports and published opinion. Most guidelines recommend treatment for a methanol level > or = 20 mg/dL in a nonacidotic patient. No supportive data have been offered nor has the time of the exposure been addressed. For instance, no distinction has been drawn between a methanol level drawn 1 hr vs. 24 hr from ingestion. We analyzed all published cases of methanol poisoning to determine the applicability of the 20 mg/dL threshold in a nonacidotic patient, specifically those arriving early for care (within 6 hr) with a peak or near-peak blood methanol concentration. Using predefined search criteria, a systematic review of the world literature was performed using MEDLINE and EMBASE. In addition, each article's references were hand searched for pre-1966 articles, as were fatality abstracts from all U.S. poison centers. Human cases were included if they reported a known time of a single methanol exposure, acid-base data, blood methanol, and blood ethanol (if not acidotic). Dating to 1879, 372 articles in 18 languages were abstracted using a standard format; 329 articles (2433 patients) involved methanol poisoning, and 70 articles (173 patients) met inclusion criteria. Only 22 of these patients presented for care within 6hr of ingestion with an early methanol level. All but 1 patient was treated with an inhibitor of alcohol dehydrogenase (ADH). A clear acidosis developed only with a methanol level > or = 126 mg/dL. The patient that did not receive an ADH inhibitor was an infant with an elevated early methanol level (46 mg/dL) that was given folate alone and never became acidotic. Intra and inter-rater reliability were 0.95. Nearly all reports of methanol poisoning involve acidotic patients far removed from ingestion. The small amount of data regarding patients arriving early show that 126 mg/dL is the lowest early blood methanol level ever clearly associated with acidosis. Contrary to conventional teaching, there are case reports of acidosis after only a few hours of ingestion. The data are insufficient to apply 20 mg/dL as a treatment threshold in a nonacidotic patient arriving early for care. Prospective studies are necessary to determine if such patients may be managed without antidotal therapy or dialysis.

Introduction: Methanol intoxication is a well-recognized toxicological emergency. While most cases of significant methanol poisoning occur via ingestion, there are reports in the literature of poisoning resulting from the inhalational route. We report a series of methanol intoxications secondary to inhalational abuse of a methanol containing lacquer thinner presenting to an inner city Emergency Department. Methods: A laboratory database was searched for methanol levels > 5 mmol/L. (16mg/dL). from January 1, 2010 to December 31, 2015. A chart review was completed to determine mode of poisoning, clinical presentation, treatment, and disposition. Results: We found 35 patients who made a total of 83 emergency department (ED) visits with a methanol level > 5mmol/L. (16mg/dL). The methanol levels ranged from 5.3-39.6 mmol/L. (16.96 -126.72 mg/dL) . 73% of poisonings were secondary to inhalation of a methanol-containing lacquer thinner. The median age of these patients was 43 years, and 49% were male. The majority of patients (96%) resided in the core area. The most frequent chief complaints were substance abuse/intoxication, gastrointestinal complaints, and chest pain. 18% of patients described visual symptoms. Treatments were fomepizole only (59%), fomepizole plus hemodialysis (26%), and hemodialysis alone (2%). 49% of patients were discharged from the ED, while 28% and 23% were admitted to an intensive care unit (ICU) and an internal medicine ward respectively. There were no cases of blindness. We describe a cohort of patients who developed methanol poisoning from inhalation of a methanol containing lacquer thinner that required treatment with fomepizole and hemodialysis. While almost 1/3 of these patients were admitted to ICU, 49% were discharged from the emergency department after a course of fomepizole. The etiology of this outbreak was found to be a change in the formulation of the lacquer thinner, substituting a higher concentration of methanol for toluene. The manufacturer and a number of local retail outlets were contacted. This resulted in the product being taken off the shelves by the retail outlets, and eventually, a change in the product formulation by the manufacturer, with a resultant decrease in the methanol content. After these actions, we have not seen any additional presentations of inhalational methanol intoxication. Conclusion: We report the largest case series to date of patients who presented with methanol intoxication, requiring fomepizole and/or hemodialysis, secondary to inhalation of a methanol containing lacquer thinner. Physician advocacy regarding the etiology of this outbreak resulted in collaboration with retail outlets and subsequent action by the manufacturer. This ended the outbreak.

Methanol poisonings pose a major risk especially where illegal alcohol is consumed. The source of the methanol in the drinks are debated. We aimed to evaluate whether home distillation of alcohol made from rice was capable of producing toxic amounts of methanol. Twenty households with homemade alcohol production in Phu Tho province in Vietnam were included in this pilot study. We followed the whole production process and an alcohol sample from each household was analysed for methanol content. 17 (85%) of the samples contained detectable levels of methanol. The median concentration was 9 mg/L (range 2-37 mg/L). To develop clinical symptoms of methanol poisoning from the sample with the highest concentration would require drinking more than 424 L. Homemade alcohol from rice did not contain sufficient amount of methanol to cause toxicity in our study. This supports the theory of methanol being added to ethanol post production for economical purposes as the main source of mass poisonings.

Unwell after drinking homemade alcohol – A case of ethylene glycol poisoning

Acute methanol intoxication is not an unusual poisoning. It can have serious neurological sequelae. We emphasize how neuroimaging can help in distinguishing methanol poisoning from other causes of acute unconsciousness in alcoholic patients such as hypoglycemic brain damage and carbon monoxide poisoning or head injury, which are frequently observed in alcoholic patients and are also responsible for altered sensorium. The most important findings in MR brain imaging in methanol poisoning have been bilateral putaminal hemorrhagic necrosis. Other less common findings are subcortical and deep white matter lesions, cerebral and cerebellar cortical lesions, and midbrain lesions, cerebral and intraventricular hemorrhage, and even enhancement of necrotic lesions, we found almost the entire spectrum of MRI findings in this patient with methanol poisoning. Neurological sequelae can entail the course and prognosis in methanol poisoning. The patient died because of ventilator-associated pneumonia that developed in the course of prolonged hospitalization.

Methanol intoxication is rare in developed countries. Early identification and elimination of the methanol metabolites are vital to an optimal prognosis. A characteristic brain imaging finding is bilateral basal ganglia necrosis and subcortical white matter changes. Here, we report a rare neuroradiological feature called the lentiform fork sign in a patient with methanol intoxication who survived the acute poisoning stage. We report a 31-year-old woman who presented to the emergency department with acute-onset incoherent speech, consciousness disturbance, and a high-anion-gap metabolic acidosis caused by methanol intoxication. She was treated with antidote administration of fomepizole and enhanced methanol elimination through hemodialysis. Neurological sequelae of cognitive decline and parkinsonism developed, with preserved vision. Brain MRI showed bilateral putaminal necrosis and subcortical white matter changes. The apparent diffusion coefficient map showed low signal intensities in the putamen and globus pallidus bilaterally, with brightly hyperintense rims surrounding both putamina that resembled a fork, indicating a lentiform fork sign. She then had sequelae of cognitive decline and delayed parkinsonism feature, which are compatible with the brain lesions on neuroimage studies. Methanol poisoning is an uncommon life-threatening event, and neurological sequelae result from the accumulation of formic acid, a methanol metabolite that inhibits cytochrome c oxidase in mitochondria, leading to neuronal injury. Methanol intoxication should be considered in patients with imaging findings of bilateral basal ganglia necrosis with lentiform fork sign and a metabolic acidosis of unknown origin.

Oral methanol intoxication is common, but dermal intoxication is rare. We report a previously healthy 19-month-old female infant admitted to the emergency department (ED) with vomiting and tonic-clonic seizure. On physical examination, she was comatose and presented signs of decompensated shock with Kussmaul breathing. Her left thigh was edematous, with purple coloration. Methanol intoxication was suspected due to high anion gap metabolic acidosis (pH, 6.89; HCO3, <3 meq/L) and exposure to spirit-soaked bandages (%96 methanol) for 24 hours and 3 days. The patient's serum methanol level was 20.4 mg/dL. She was treated with fomepizole and continuous venovenous hemodialysis (CVVHD) in the pediatric intensive care unit, and methanol levels decreased to 0 mg/dL after 12 hours. During follow-up, massive edema and subarachnoid hemorrhage in the occipital lobe were detected by computed tomography of the brain. The patient died after 7 days.Although methanol intoxication occurs predominantly in adults, it must be considered in children with high-anion gap metabolic acidosis. This case report demonstrates that fatal transdermal methanol intoxication can occur in children, and it is the second report in the English literature of transdermal methanol intoxication in an infant.