The Kallakurichi Hooch Tragedy: A Detailed Analysis of Methanol Toxicity
Methanol, a simple alcohol, is a colourless, odourless liquid with a wide range of industrial applications. However, its ingestion can lead to severe toxicity, as tragically demonstrated in the Kallakurichi, Tamil Nadu, incident. The Kallakurichi hooch tragedy of June 2024 was a stark reminder of the perils of illicit liquor consumption. Originating in Karunapuram village, the incident saw a devastating toll of over 60 lives, with numerous others hospitalised due to severe methanol poisoning.
This article delves into the pathophysiology, clinical manifestations, diagnostic workup, and management of methanol poisoning.
Understanding the pathophysiology
Methanol, known as the parent alcohol, is relatively nontoxic initially but primarily affects the central nervous system, causing sedation. Toxicity occurs when methanol is metabolised in vivo and oxidised by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase.
Methanol is primarily metabolised in the liver by ADH to formaldehyde, which is then further oxidised to formic acid by aldehyde dehydrogenase. Formic acid is the main toxic metabolite, inhibiting mitochondrial cytochrome c oxidase, leading to anaerobic glycolysis, lactic acidosis, and direct optic nerve damage, which can result in blindness.
At plasma levels above 20 mg/dL (approximately 6 mmol/L of methanol), metabolites can cause specific end-organ damage. Methanol is also osmotically active, contributing to an increased osmolar gap. The lethal dose ranges from 30-50 ml (0.5 ml/kg), and blindness can occur with as little as 10 ml.
Kinetics of methanol
Methanol is rapidly and completely absorbed after oral ingestion, with peak serum alcohol concentrations occurring within 1-2 hours. Its metabolism occurs in two steps via alcohol dehydrogenase (ADH) and aldehyde dehydrogenase, leading to the production of toxic species. Methanol elimination follows zero-order kinetics in the absence of treatment, at an estimated rate of 8.5 mg/dL (2.7 mmol/L) per hour. If hepatic oxidation is blocked by an ADH antagonist, such as ethanol or fomepizole, toxicity can be decreased. The elimination of formate is partially dependent upon tetrahydrofolate and may accelerate with folic acid administration.
Clinical features
Early symptoms (within hours): Nausea, vomiting, abdominal pain, headache, dizziness, blurred vision.
Late symptoms (hours to days):
● Neurological: Altered mental status, seizures, coma.
● Ocular: Blurred vision, scotomas, blindness (due to optic nerve damage).
● Cardiovascular: Hypotension, tachycardia.
● Respiratory: Tachypnoea, dyspnoea, respiratory failure.
● Metabolic: Severe anion gap metabolic acidosis, lactic acidosis.
Laboratory findings
● Methanol level: Confirmatory test for methanol poisoning.
● Anion gap metabolic acidosis: Reflects the accumulation of formic acid.
● Osmolar gap: Increased due to the presence of methanol.
● Lactate level: Elevated due to anaerobic glycolysis.
● Electrolyte abnormalities: Hyponatremia, hypokalaemia.
● Liver function tests: May show elevation due to hepatic injury.
● Complete blood count: May reveal haemolytic anaemia or thrombocytopenia.
● Arterial blood gas: Demonstrates severe metabolic acidosis with respiratory compensation.
Methanol Toxicity resulting bilateral hyperaemia and oedema of the optic disc, manifesting 6–24 h after methanol intoxication
Diagnostic approach
Diagnosing methanol poisoning requires a high index of suspicion, especially in patients who exhibit unexplained metabolic acidosis, anion gap acidosis, a high osmolar gap, or visual disturbances. The diagnosis is confirmed by measuring methanol levels. Further laboratory tests are needed to assess the severity of the poisoning and guide appropriate management strategies.
Treatment strategies for methanol poisoning
Treatment for methanol poisoning encompasses general supportive measures and specific therapies.
General supportive measures
Initial management includes airway management, oxygen therapy, fluid resuscitation, and electrolyte correction to stabilise the patient and address any immediate concerns.
Specific therapies
Ethanol or fomepizole: Ethanol or fomepizole are used as competitive inhibitors of alcohol dehydrogenase to prevent methanol metabolism. Ethanol is administered as a 10% solution at a dose of 10 ml/kg intravenously over 30 minutes, followed by 1.5 ml/kg/hour in a 100 mg/100 ml solution. Alternatively, 125 ml of a distilled alcoholic beverage can be given orally.
Fomepizole is administered as a loading dose of 15 mg/kg intravenously, followed by 10 mg/kg every 12 hours, with adjustments for hemodialysis or after more than two days of therapy. For patients undergoing hemodialysis, the frequency of fomepizole dosing should be increased to every four hours, and an additional dose should be administered at the beginning of hemodialysis if six or more hours have elapsed since the prior dose.
Hemodialysis: This is effective in removing methanol and formic acid from the blood, especially in severe cases. Indications for hemodialysis include high anion gap metabolic acidosis, evidence of end-organ damage (e.g., visual changes, renal failure), and unexplained metabolic acidosis in suspected toxic ingestion.
Bicarbonate: Sodium bicarbonate is used to correct metabolic acidosis. For patients with a pH below 7.3, an initial dose of 1 to 2 meq/kg via intravenous bolus is suggested. Bicarbonate is available as 8.4% (50 ml = 50 meq) and 7.2% (50 ml = 44.6 meq). Calculate the bicarbonate deficit as (24 - Pts HCO3) × 0.5 × weight meqs deficits. Administer half the calculated dose slowly via IV, followed by infusion over 2-3 hours.
Thiamine: May be beneficial for neurological symptoms.
Ocular Management: Early consultation with an ophthalmologist is crucial for managing any visual damage.
Indications for antidote therapy with fomepizole or ethanol
1. Documented serum concentration: When serum levels of methanol or ethylene glycol are greater than 20 mg/dL (6.2 mmol/L for methanol; 3.2 mmol/L for ethylene glycol).
2. Recent toxic ingestion: When there is a documented history of ingesting toxic amounts of methanol or ethylene glycol and the serum osmol gap exceeds 10.
3. Strong clinical suspicion: When there is a strong suspicion of poisoning and at least two of the following are observed:
● Arterial pH less than 7.3
● Serum bicarbonate less than 20 meq/L (mmol/L)
● Osmol gap greater than 10
● Presence of urinary oxalate crystals
Management of methanol toxicity disaster
The occurrence of more than three cases of methanol poisoning within a 24-hour period in one area indicates a methanol poisoning epidemic. Such an outbreak should be promptly communicated to public health authorities and the police administration. A public announcement system should be utilised to alert the local community about the situation.
Individuals who have consumed alcohol from the same source should be advised to report to a medical centre, even if they are asymptomatic. Upon suspicion of a methanol poisoning epidemic, all neighbouring medical institutes should be alerted to ensure they have sufficient stock of sodium bicarbonate and that hemodialysis facilities are kept ready.
In triage, patients should be prioritised based on the ABCDE approach: Airway, Breathing, Circulation, Disability, and Exposure. A rapid assessment should identify potential methanol poisoning cases using clinical features and basic laboratory tests. Decontamination procedures, such as removing contaminated clothing and irrigating exposed skin, should be implemented promptly.
Mass casualty management should implement disaster response plans, including patient triage, resource allocation, and communication strategies.
Preventive measures for methanol poisoning To prevent methanol poisoning, it is crucial to raise public awareness about the dangers of methanol. Enforcing strict regulations on methanol production and distribution can help control its availability and misuse. Additionally, ensuring proper labelling of methanol-containing products is essential to inform consumers.
Methanol poisoning is a medical emergency with potentially devastating consequences. Early recognition, prompt treatment, and supportive care are crucial for improving patient outcomes. The Kallakurichi tragedy highlights the importance of public health preparedness and prevention strategies.
Dr. Sreekrishnan T. P
MD, MRCEM, FCCM
Consultant in Emergency Medicine and Critical Care
Amrita Hospitals, Kochi