Alcohol and Methanol Toxicology, with the Widmark Formula

1. Ethyl Alcohol (Ethanol) Toxicology

Absorption and distribution: Ethanol is absorbed rapidly from the stomach (20%) and small intestine (80%), reaching peak blood levels in 30-90 minutes depending on food content. It distributes into total body water, which is why body weight and sex (fat vs. lean mass) determine blood concentration for a given dose.

Blood alcohol level and clinical effect - Table 50.1 (Parikh's Textbook of Forensic Medicine and Toxicology):

BAC (%)	BAC (mg%)	Effect
< 0.03	< 30	Not noticeable
0.03-0.05	30-50	Selective impairment (reaction time, complex skills)
0.05-0.10	50-100	Slight impairment (flushed face, dilated pupils, euphoria)
0.10-0.15	100-150	Under the influence (test errors, staggering on turns)
0.15-0.20	150-200	Drunk (clouded intellect, incoordination)
0.20-0.30	200-300	Very drunk (confusion, marked incoordination, vomiting, amnesia)
0.30-0.35	300-350	Stupor to coma
> 0.35	> 350	Coma to death

Fatal dose/level: A blood level of 0.35% (350 mg%) and above is generally sufficient to cause death, though recovery has been recorded even above 780 mg% in some cases depending on tolerance. Death is usually from respiratory depression, and the fatal period is typically 12-24 hours (occasionally delayed 5-6 days).

Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology, p. 655

2. The Widmark Formula

Devised by the Swedish physician Erik M.P. Widmark, this formula estimates blood/body alcohol content (or back-calculates it to an earlier time) based on body weight, sex, and measured concentration.

For blood alcohol content (BAC):

a = p x r x c

Where:

a = weight of alcohol consumed/present in the body (grams)
p = body weight (kg)
r = Widmark distribution constant - 0.6 for males, 0.5 for females (reflects the proportion of body weight that is water, since ethanol distributes into total body water and women have relatively more fat/less water)
c = concentration of alcohol in blood (mg/kg, i.e., blood alcohol level)

For urine alcohol content:

a = (3/4) x p x r x q

Where q = urine alcohol concentration (mg/kg), and the 3/4 factor corrects for the higher water content of urine relative to blood (urine alcohol runs roughly 1.3:1 to 1.35:1 relative to blood at equilibrium).

Practical/medicolegal use of the formula:

Estimating the total quantity of alcohol a person must have consumed to reach a given BAC.
Back (retrograde) extrapolation - estimating what the BAC "must have been" at an earlier time point (e.g., at the time of a road traffic accident) using the average elimination rate of alcohol (roughly 15-20 mg%/hour), working backward from the time of blood draw.
Cross-checking blood vs. urine alcohol results when only urine is available, and determining whether the person was in the absorptive, peak, or elimination phase (by comparing two urine samples taken 25-30 minutes apart).
P C Dikshit's Textbook of Forensic Medicine and Toxicology
Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology

3. Methyl Alcohol (Methanol) Toxicology

Source/exposure: Methanol (wood alcohol, wood spirit, carbinol) is added to rectified spirit as a denaturant (5% methanol = "methylated spirit") to make it non-drinkable industrially. Most human poisoning is from cheap illicit/spurious liquor adulterated (accidentally or deliberately, for economic gain) with methanol.

Mechanism of toxicity: Methanol itself is not the main toxic agent - it is metabolized by alcohol dehydrogenase to formaldehyde, then to formic acid, which accumulates because it is cleared slowly. This causes a severe metabolic (anion-gap) acidosis, and formic acid is specifically toxic to the retina/optic nerve. Since methanol is excreted slowly, it behaves as a cumulative poison, and symptom severity correlates with the degree of acidosis.

Clinical features:

Often delayed onset (up to 24-48 hrs, longer if ethanol was co-ingested since ethanol competitively blocks methanol metabolism)
Headache, dizziness, nausea, vomiting, abdominal pain
Muscular weakness, depressed cardiac action, dyspnoea, cyanosis
Ocular toxicity is the hallmark: blurred/dimmed vision, photophobia, and in severe cases optic atrophy causing permanent blindness
Convulsions as a terminal event; death from respiratory failure
Autopsy finding considered diagnostic: intestinal contraction (small and/or large bowel resembling a "thick pipe of very narrow lumen")

Fatal dose: Roughly 60-240 mL in adults (as little as 15 mL can cause blindness); in children, 1 mL/kg of denatured alcohol has produced serious toxicity. Fatal period is usually 24-36 hours, occasionally delayed 3-4 days.

Treatment:

Gastric lavage with 5% sodium bicarbonate solution to limit absorption; whole bowel irrigation if available
Correct acidosis - oral sodium bicarbonate 2 g every 2 hours, or IV 50 g sodium bicarbonate in 1 L 5% dextrose with 10-15 units insulin, aiming for plasma bicarbonate ~20 mEq/L; IV molar sodium lactate is also useful
Ethanol as a competitive antagonist - oral 50% ethanol 0.75-1 mL/kg body weight for 3-4 days; it competes for alcohol dehydrogenase and slows formation of toxic metabolites
4-methylpyrazole (fomepizole) - a specific alcohol dehydrogenase inhibitor, blocks formaldehyde/formic acid formation; preferred antidote when available, with few side effects
Folinic acid to accelerate formic acid metabolism
Haemodialysis indicated for: any ocular findings, metabolic acidosis, renal failure, or blood methanol level over 50 mg%
Protect eyes from strong light; supportive/symptomatic care otherwise

Postmortem findings: Marked cyanosis, fluid dark blood, cerebral and pulmonary oedema, inflamed GI mucosa, hepatic necrobiosis, renal tubular degeneration.

Parikh's Textbook of Medical Jurisprudence, Forensic Medicine and Toxicology, pp. 663-665

A quick check of recent systematic reviews/meta-analyses (PubMed, last 2 years) found nothing that contradicts this standard forensic toxicology teaching - the main recent literature (e.g., PMID 40955913, a 2025 systematic review) focuses on adjunctive erythropoietin for methanol-induced optic neuropathy, an experimental/investigational addition rather than a change to the core fomepizole/ethanol-bicarbonate-dialysis protocol above.

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