Alcohol poisoning is a significant medical concern, particularly involving ethanol and methanol. While ethanol toxicity is frequently encountered due to recreational consumption, methanol poisoning is less common but far more dangerous. Methanol ingestion can cause severe metabolic acidosis and irreversible blindness. Understanding the mechanisms, clinical features, and management of both forms of alcohol poisoning is essential in clinical toxicology.
Ethanol Poisoning
Ethanol is rapidly absorbed from the stomach and small intestine, reaching peak blood concentrations within 30 to 90 minutes. It is primarily metabolized in the liver by alcohol dehydrogenase. Toxicity occurs when consumption exceeds metabolic capacity, leading to central nervous system depression and impaired vital functions.
Mechanism of Toxicity
- Enhancement of GABA-mediated inhibition
- Inhibition of NMDA receptors
- Accumulation of toxic metabolites such as acetaldehyde
Clinical Features
- CNS depression: impaired judgment, confusion, ataxia, stupor
- Respiratory depression at higher levels
- Hypoglycemia, especially in children
- Nausea, vomiting, gastritis
- Hypotension, tachycardia
- Hypothermia
Investigations
- Blood ethanol concentration
- Blood glucose levels
- Electrolytes and arterial blood gases
- Serum osmolality and osmolar gap
Management
- Airway and breathing support
- Monitor vitals and consciousness level
- Correct hypoglycemia with IV dextrose
- Treat hypothermia with warming measures
- IV fluids for dehydration
Most ethanol toxicity cases resolve with supportive care, but severe intoxication may require airway protection and close monitoring.
Methanol Poisoning
Methanol is an industrial solvent found in antifreeze, paint removers, and illicit alcohol. It is extremely dangerous because its metabolites—formaldehyde and formic acid—are highly toxic to the optic nerve and central nervous system.
Mechanism of Toxicity
Methanol itself is minimally toxic, but its metabolites cause severe acidosis and cellular injury.
- Formaldehyde formation causes CNS depression
- Formic acid accumulation leads to metabolic acidosis
- Direct optic nerve toxicity results in blindness
Clinical Features
Symptoms typically develop after a latent period of 12 to 24 hours.
Initial Symptoms
- Dizziness, headache
- Nausea and vomiting
- Mild CNS depression
Progressive Symptoms
- Deep, rapid breathing (Kussmaul respiration)
- Severe metabolic acidosis
- Visual disturbances: “snowfield vision,” blurred vision, photophobia
- Blindness due to optic nerve damage
- Seizures and coma in severe poisoning
Investigations
- Arterial blood gases showing high anion gap metabolic acidosis
- Elevated osmolar gap
- Serum methanol levels (if available)
- Fundoscopy for optic disc edema
Management of Methanol Poisoning
Methanol poisoning is a medical emergency that requires aggressive and often specialized treatment. The goals of management are to prevent methanol metabolism, correct acidosis, and remove toxic metabolites.
1. Inhibit Methanol Metabolism
- Fomepizole – first-line antidote; inhibits alcohol dehydrogenase
- Ethanol infusion – alternative when fomepizole is unavailable
2. Correct Acidosis
- IV sodium bicarbonate to correct metabolic acidosis
- Monitor pH and electrolytes frequently
3. Enhance Elimination
- Hemodialysis for severe poisoning, metabolic acidosis, visual symptoms, or high methanol levels
4. Supportive Care
- Maintain airway and ventilation
- Treat seizures with benzodiazepines
- Provide IV fluids for hydration
- Correct electrolyte abnormalities
Key Differences Between Ethanol and Methanol Toxicity
- Ethanol: mainly CNS and respiratory depression
- Methanol: severe metabolic acidosis and visual damage
- Methanol requires antidotes and dialysis; ethanol usually does not
Detailed Notes:
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PATH: PHARMD/ PHARMD NOTES/ PHARMD FOURTH YEAR NOTES/ CLINICAL TOXICOLOGY/ ALCOHOL – ETHANOL, METHANOL.