Alcohol Poisoning: Methanol and Ethylene Glycol

Alcohols

Methanol

• Competitively inhibits alcohol dehydrogenase (ADH)
• Formic acid, a toxic metabolite, targets the optic nerve
• Formic acid causes early-stage metabolic acidosis
• By binding to cytochrome oxidase, formic acid disrupts oxidative phosphorylation
• Lactic acidosis is caused by formic acid inhibiting oxidative phosphorylation
• Can be found in windshield washer fluid and counterfeit alcohol
• Signs and symptoms appear 12-24 hours post-ingestion
• Symptoms of poisoning includes CNS depression, metabolic acidosis, and visual disturbances
• Blindness can occur with as little as 30 mL, and fatality at 100 mL after ingestion

Ethylene Glycol

• Colorless, odorless, sweet in taste, and liquid
• Competitively inhibits ADH
• Degraded through the same metabolic pathways as methanol
• Oxidation of ethylene glycol to oxalic acid by hepatocytes results in toxicity
• Aldehyde dehydrogenase converts glycolic acid into oxalic acid
• Oxalic acid binds to calcium, forming calcium oxalate crystals that damage the heart, brain, lungs, and kidneys

Ethylene Glycol Toxicity

First Stage (0.5 - 12 hours)

• More intoxicating than methanol and ethanol, resulting in CNS depression, seizures, and coma
• Patients appear "drunk" without smelling of alcohol
• Calcium oxalate crystals deposit in the brain, leading to CNS toxicity, cerebral edema, and meningismus within 4-12 hours
• Binding of calcium by oxalic acid leads to hypocalcemia, which can cause prolonged QT intervals, arrhythmias, and myocardial depression

Second Stage (12 - 24 Hours)

• Tachypnea occurs as the body attempts to counteract metabolic acidosis caused by toxic metabolites
• Multiorgan failure (CHF, lung injury, myositis) occurs because of widespread crystal deposition
• Most deaths occur in the second stage

Third Stage (24 - 72 Hours)

• Acute renal failure occurs due to crystal deposition, but full recovery is possible within weeks to months

Alcohol Poisoning Treatment

Methanol and Ethylene Glycol Toxicity

• Historically, IV ethanol was used
• Ethanol competes with ADH and binds with a higher affinity than methanol and ethylene glycol
• Fomepizole is the preferred initial therapy since it inhibits ADH, preventing the production of harmful metabolites
• Fomepizole treatment should be followed up with dialysis
• Additional measures include replenishing folic acid for methanol poisoning
• In treating ethylene glycol poisoning, thiamine and pyridoxine must be replenished

Isopropyl Alcohol (Isopropanol)

• Common in alcoholics when alcohol is unavailable
• Present in rubbing alcohol, disinfectants, and hand sanitizers
• Signs and symptoms include extreme intoxication, nausea, vomiting, abdominal pain, acetone odor, and osmolar gap without anion gap acidosis
• Treatment focuses on supportive care

Seafood-Associated Toxins

Scombroid

• Common pseudo-allergenic food poisoning syndrome
• Caused by improper storage of dark-meat fish like tuna, mackerel, ski-jack, and bonito
• When temperatures are >32°F, bacterial proliferation occurs, converting histidine to histamine
• Histidine decarboxylase converts histidine to histamine
• It is frequently misdiagnosed as a fish allergy
• Symptoms begin rapidly, usually from 10 minutes to 1 hour after ingestion, and typically resolve within 6 hours
• You may notice a 'peppery' flavor to the fish
• Symptoms may mimic anaphylaxis, including oral burning sensation, facial flushing, erythema, urticaria, itching, and may progress to bronchospasm, angioedema, and hypotension
• Treatment includes parenteral antihistamines; severe cases involving hypotension, bronchospasm, or airway edema also require epinephrine, solumedrol, and albuterol nebulizer solution

Ciguatera Poisoning

• Most reported seafood illness globally
• Consumption of fish containing accumulated ciguatoxins, produced by microscopic algae called dinoflagellates
• Reef finfish like barracuda, amberjack, moray eel, grouper, snapper, and parrotfish are sources of ciguatoxins
• Ciguatoxins increase sodium ion permeability, causing depolarization of axons
• Because it is heat and acid-stable it cannot be removed by cooking/freezing
• Diagnosis is primarily based on clinical findings and reported fish consumption history
• GI symptoms appear 2-12 hours after consumption and resolve within 1-4 days
• Neurologic symptoms usually appear within 2 days and include the classic presentation of cold allodynia (hot-cold reversal), paresthesia (stocking-glove & perioral), headache, and dizziness
• Subsequent consumption of fish, alcohol, caffeine, and nuts can trigger the recurrence of symptoms
• Some patients develop cardiovascular complications, including heart block, bradycardia, and hypotension
• The treatment is mainly supportive

Tetrodotoxin

• Heat-stable neurotoxin found in the liver and skin of pufferfish (fugu) and certain angelfish
• Bacteria that produce tetrodotoxin are consumed and accumulate in high doses up the food chain
• Voltage-gated Na+ channels in nerve tissue are blocked by the neurotoxin, preventing depolarization
• Patients may complain of perioral numbness within 30 minutes after ingestion
• Symptoms are dose-dependent and include nausea, diarrhea, paresthesia, weakness, dizziness, and loss of reflexes
• Focus on airway management for possible respiratory failure is essential for supportive care treatment