in the subject’s breath.

This is converted to BAC using Physical Appearance

the observations that 1) alveolar air normally contains 193
close to 5.5% (by vol) of CO2 i.e. 190 mg of CO2 in 2100 ■■ Methanol is the simplest of the primary alcohols and is a
ml of alveolar air at 34°C, and 2) the weight of alcohol colourless, highly polar, flammable liquid.
present in 1 ml of blood is equal to that present in 2100 ■■ Pure methanol has a faintly sweet odour at ambient tempera-
ml of alveolar air. Proper breath sampling is essential tures; crude methanol may have a repulsive, pungent odour.
to the correct analysis of breath alcohol. For correct ■■ It has a bitter taste.
sampling the operating procedure is performed so as
to obtain what is described as alveolar air or deep-lung Uses and Sources
breath. This requires the collection of the end portion 1. Antifreeze (10 to 50%)
of a prolonged forced expiration, which is necessary to 2. Carburettor cleaner (20%)
avoid too much mixing with dead space air, i.e. air that is 3. Denatured spirit (5 to 10%): While denatured spirit most
not totally in equilibrium with the BAC. From numerous often is a mixture of ethanol (90 to 95%) with methanol (5
experiments conducted it is now well established that to 10%), occasionally other substances may be used instead
there is an excellent corelation between the breath and of the latter, e.g. acetone, aniline dyes, benzene, cadmium,
blood level, and the ratio is generally 2100 : 1. This is camphor, castor oil, diethyl phthalate, ether, petrol, isopro-
based on Henry’s law which states that when a volatile panol, kerosene, nicotine, pyridine bases, sulfuric acid, or

Chapter 14   Inebriants

chemical (ethanol) is dissolved in a liquid (blood) and terpineol.
is brought to equilibrium with air (alveolar breath), 4. Embalming fluid (20%)
there is a fixed ratio between the concentration of the 5. Leather dyes (30%)
volatile compound (ethanol) in air (alveolar breath) and 6. Paint remover
its concentration in the liquid (blood), and the ratio is 7. Varnish and shellac (5%)
constant at a given temperature, i.e. in this case 34°C 8. Windshield washing fluid (35 to 95%).
which is the temperature at which the breath usually
leaves the mouth. Usual Fatal Dose
4. Ethanol and Medical Practice ■■ About 70 to 100 ml (range: 15 to 250 ml).
a. The medical profession is generally considered to be ■■ Serious toxicity may occur from ingestion of 0.25 ml/kg of
one of the noble professions and it therefore behoves 100% methanol, and fatalities might occur from ingestion
a doctor to conduct himself at all times with decency of 0.5 ml/kg of 100% methanol.
and decorum. Although he can use his discretion with
reference to moderate consumption of alcohol when not Mode of Action
on hospital duty, or when he is not dealing with patients, ■■ Methanol is rapidly absorbed through the skin, respira-
he can be held liable in the following situations: tory tract and gastrointestinal tract. Peak plasma levels are
–– A surgeon performing an operation under the influ- usually reached within 30 to 60 minutes following inges-
ence of alcohol can be prosecuted under S.304-A tion, although a long latent period (roughly 18 to 24 hours)
of the IPC if the patient dies during the course of usually is seen before toxic symptoms develop.
surgery. The fact that he was drunk at the time of ■■ In the liver, methanol is metabolised to formaldehyde
the operation is likely to be considered as strong (by alcohol dehydrogenase) and then to formic acid (by
evidence of rashness. aldehyde dehydrogenase) which is responsible for retinal
–– A doctor may be sued for damages in the event of toxicity as well as metabolic acidosis.
the patient suffering damage or death due to his ■■ There are two pathways for metabolism of formic acid,
negligent conduct. If he was intoxicated at the time oxidation via the catalase-peroxidase system, or metabo-
he administered treatment it would only strengthen lism by the tetrahydrofolic acid-dependant one-carbon
the evidence against him. pool which is catalysed by 10-formyl-tetrahydrofolate
–– Patient management under the influence of alcohol synthetase. Since metabolism is slow, significant levels of
will be considered as infamous conduct (profes- methanol can be found in the body for up to seven days
sional misconduct), and the doctor is liable to be after ingestion.
proceeded against by the State Medical Council.
The drunken doctor runs the risk of his name being Clinical Features
erased from the medical register. 1. Symptoms may be delayed for 12 to 24 hours (Range: 1
to 72 hours). The earliest manifestations include vertigo,
Methanol headache with stiff neck (meningismus), nausea, vomiting,
and abdominal pain.
Synonyms 2. Later there is ocular toxicity characterised by blurred or
Methyl alcohol; Methyl hydroxide; Monohy­droxymethane; dimmed vision (“flashes” or “snowstorm”), and photo-
Colonial spirit; Columbian spirit; Pyroxylic spirit; Wood phobia. Constricted visual fields, spots before the eyes,
alcohol; Wood naphtha; Wood spirit. sharply reduced visual acuity, optic atrophy, blindness, and
 nystagmus have all been described. Ophthalmologic exami- Parkinsonism, toxic encephalopathy, and polyneuropathy.
194 nation usually reveals dilated pupils with sluggish light Permanent ocular abnormalities may include pallor of the
reaction. Fixed dilated pupils suggest severe poisoning. optic disc, attenuation and sheathing of retinal arterioles, a
Fundoscopy (Fig 14.8) reveals hyperaemia of optic disc diminished pupillary light reaction, reduced visual acuity,
followed by retinal oedema. Irreversible sequelae include central scotomata, and defects of optic nerve fibre bundles.
optic atrophy and visual field impairment.
3. Metabolic acidosis (high anion gap) is usually severe. A pH Diagnosis
of less than 7.0 and bicarbonate less than 10 mEq/L are not Obtain CBC, electrolytes, urinalysis, and arterial blood gases
uncommon following significant intoxication. The onset of in symptomatic patients or those with a history of significant
acidosis may be delayed up to 18 to 48 hours, especially if exposure. Measure serum pH and electrolytes.
ethanol has also been ingested. Therefore, the absence of 1. High anion gap acidosis.
acidosis does not rule out a significant methanol ingestion. 2. Elevated osmolal gap.
4. Other features include tachycardia, hypotension, and hypo- 3. Hypophosphataemia.
thermia. Convulsions are a late feature and may be followed 4. Elevated creatine phosphokinase.
by coma. 5. Elevated amylase.
5. Hypomagnesaemia, hypokalaemia, and hypophosphataemia 6. Blood methanol level: more than 50 mg/100 ml indicates
Section 5    Neurotoxic Poisons

have been reported. serious poisoning. A detectable formic acid level may be
6. Occasionally a patient develops transient Fanconi syndrome consistent with methanol poisoning, as methanol is metabo-
(hypouricaemia, hypophosphataemia, glycosuria, and lised to formic acid.
hyperchloraemic metabolic acidosis). 7. CT Scan/MRI—Symmetrical areas of necrosis in the
7. Acute necrotising pancreatitis may result from severe putamen of the brain are a classic finding in cases of acute
methanol poisoning. lethal methanol toxicity. However, these findings are also
8. Cause of death is usually respiratory failure, which may present in other conditions, such as Wilson’s disease and
precede the cessation of heart beat by several minutes. In Leigh’s disease, and are not pathognomonic for methanol
fatal methanol poisoning cases, marked sinus bradycardia poisoning.
may develop with widening of the pulse pressure. Further,
severe hypotension, requiring fluid and vasopressor therapy, Treatment
occurs terminally in severe methanol intoxications. Patients with abnormal vital signs, visual disturbances, pulmo-
9. The most common permanent sequelae following recovery nary oedema, evidence of renal dysfunction, high methanol
from severe poisoning are optic neuropathy, blindness, levels, significant acidosis, or coma should be admitted to an
intensive care unit.
1. Stomach wash with sodium bicarbonate.
2. Ipecac-induced emesis is not recommended because of the
potential for CNS depression.
3. Activated charcoal does not adsorb significant amounts of
methanol. Its use in the face of ingestion may be indicated
to prevent absorption of co-ingested substances.
4. Antidotes (Fig 14.9):
a. Ethanol is the specific antidote since it preferentially
competes for the same enzyme (alcohol dehydrogenase)
and prevents the metabolism of methanol which is then
excreted unchanged in the urine. Ethanol has about 20
times the affinity for alcohol dehydrogenase compared

Fig 14.8: Fundoscopic picture—methanol poisoning

(Pic: Dr. S Senthilkumaran) Fig 14.9: Methanol antidotes–mechanism of action
to methanol. This competitive effect of ethanol gains -- Formate blood concentration is less than 1.2
more time for excretion of unchanged methanol from mg/100 ml. 195
the body, and it also inhibits the formation of methanol -- Methanol-induced acidosis (pH, blood gases),
metabolites that produce severe acidosis. Formic acid clinical findings (CNS), electrolyte abnormali-
is metabolised to carbon dioxide and water via a folate ties (bicarbonate), serum amylase, and osmolal
dependant system. gap have resolved.
–– Mode of administration: –– Patients who concurrently ingested ethanol and
-- 10% ethanol at a dose of 10 ml/kg administered methanol may have a normal acid-base profile
IV over 30 minutes, followed by 1.5 ml/kg/hr, despite a dangerously elevated blood methanol
so as to produce and maintain a blood ethanol level. Consider implementing the ethanol treatment
level of 100 mg/100 ml. Blood ethanol levels regimen in these patients until a methanol level
should be maintained at 100 to 130 mg/100 ml can be determined. Determine blood ethanol level
(21.7 to 28.2 mmol/L). It is safer to maintain before beginning ethanol therapy and modify the
a blood ethanol concentration greater than loading dose accordingly.
130 mg/100 ml than to have it fall below 100 b. In Western countries, a new antidote has been intro-
mg/100 ml. duced viz., 4 methyl pyrazole (4MP), or fomepizole
»» Preparation from absolute ethanol: If single which does not cause CNS depression (unlike ethanol).

Chapter 14   Inebriants

use vials of pyrogen free absolute ethanol Upto 20 mg/kg of 4MP in divided doses have been
are not available, tax-free bulk ethanol can given for 5 days without any demonstrable toxicity. The
be used, but it is not pyrogen free. A 0.22 usual dose is 15 mg/kg, followed 12 hours later by 10
micron filter should be used to minimise mg/kg 12th hourly for 4 doses, and then increased to 15
particulate matter. A 10% (V/V) solution can mg/kg 12th hourly for as long as necessary. Fomepizole
be prepared by any of the following methods: is easier to use clinically, requires less monitoring, does
⌂⌂ Remove 50 ml from 1 litre of 5% ethanol not cause CNS depression or hypoglycaemia, and may
solution and replace with 50 ml of abso- obviate the need for dialysis in some patients.
lute alcohol. c. Sodium bicarbonate IV : 500 to 800 ml of 7.5% solu-
⌂⌂ Replace 100 ml of fluid from one litre tion, slowly.
of dextrose 5% in water with 100 ml of d. Folinic acid IV: 1 to 2 mg/kg, 6th hourly. It hastens the
absolute ethanol. elimination of formic acid. Folinic acid (5-formyltet-
⌂⌂ Add 59 ml of absolute ethanol to one rahydrofolic acid, i.e. 5-FTHF), or leucovorin or
litre of 5% ethanol solution. citrovorum factor is a biologically active form of folic
⌂⌂ Add 112 ml of absolute ethanol to one acid (pteroylglutamic acid) which is an essential water
litre of dextrose 5% in water. soluble vitamin.
⌂⌂ Adding 59 ml of 95% ethanol solution 5. For convulsions: Attempt initial control with a benzodiaz-
to one litre of 5% ethanol solution (if epine (diazepam or lorazepam). If seizures persist or recur
absolute alcohol is not available). administer phenobarbitone.
⌂⌂ 59 ml of 95% ethanol provides 56 ml of 6. Haemodialysis is very effective in removing methanol,
ethanol (0.95 × 59 ml = 56 ml). formaldehyde, and formic acid. While ethanol treatment
⌂⌂ One litre of 5% ethanol solution is also quite effective, it is extremely difficult to main-
provides 50 ml of ethanol (0.05 × 1000 tain therapeutic ethanol levels for long periods of time.
ml = 50 ml). Haemodialysis is strongly recommended in patients with
⌂⌂ 56 + 50 = 106 ml of ethanol divided by acidosis or serum methanol levels of greater than 25 to 50
a total volume of 1059 ml = 10% (V/V). mg/100 ml. Haemoperfusion is not effective. Peritoneal
»» Alternatively, 1 ml/kg of 95% ethanol in dialysis and continuous venovenous haemofiltration are
fruit juice (180 ml) can be given orally over less effective.
30 minutes. For maintenance, administer
0.17 to 0.28 ml/kg/hr as 50% ethanol in Autopsy Features
fruit juice. 1. Cyanosis is very prominent, especially in the upper parts
»» If neither of these is practicable, give 125 of the body.
ml of a distilled alcoholic beverage (gin, 2. Liver and kidneys show toxic damage.
vodka, whisky, or rum) orally, diluted in 3. Lungs may reveal oedema, emphysematous changes, and
glucose solution or juice, and repeat as desquammation of alveolar epithelium.
required cautiously. 4. Eyes show evidence of retinal oedema.
–– Ethanol therapy should be continued until the 5. Viscera must be preserved in saturated solution of sodium
following criteria are met: chloride and not rectified spirit, as in the case of all alcohols.
-- Methanol blood concentration, measured by a In addition to the routine viscera, it is advisable to preserve
reliable technique, is less than 10 mg/100 ml. one cerebral hemisphere.
 Forensic Issues ■■ It can also cause haemolytic anaemia, myopathy, and acute
196 renal failure.
Most of the cases of methanol poisoning are accidental arising ■■ A characteristic odour of acetone is usually perceptible in
out of either an alcoholic (deprived of ethanol for any reason) the breath.
consuming methanol containing products, or because of inten-
tional adulteration of ethanol (especially arrack) resulting in Diagnosis
mass deaths. The latter are referred to quaintly as “liquor trag- ■■ Ketonuria.
edies” and are reported in Indian newspapers at depressingly ■■ Determine serum isopropanol concentration and blood
regular intervals from all parts of the country. glucose. Blood isopropanol concentrations of 128 to 200
mg/100 ml, measured within hours after ingestion, have
Isopropanol been associated with deep coma and death.
■■ The absence of hyperglycaemia or glucosuria when acetone
Synonyms is present helps differentiate between alcohol intoxication
Isopropyl alcohol, 2-propanol, Blue heaven.* or diabetic ketoacidosis versus isopropanol intoxication
■■ Isopropanol is metabolised to acetone. As acetone may
Physical Appearance contribute to CNS depression, its blood level should
Section 5    Neurotoxic Poisons

Colourless, volatile liquid with a faint odour of acetone and a also be routinely obtained and followed. Acetone may be
slightly bitter taste. detectable in the urine by 3 hours after ingestion, and in
the blood by one-half to one hour after isopropanol inges-
Uses tion. A high serum or urinary acetone without metabolic
1. Rubbing alcohol (70%), for massage. acidosis is strongly suggestive of isopropanol intoxication.
2. Disinfectant. ■■ Increased osmolal gap.
3. Antifreeze. ■■ High anion gap metabolic acidosis.
4. Paint remover.
5. Window cleaning solution. Treatment
6. Toiletries (hair tonics, after-shave lotions). ■■ Skin decontamination in the case of dermal exposure.
7. Industrial solvent. ■■ Stomach wash and activated charcoal in the case of inges-
tion. However, many investigators are of the opinion that
Usual Fatal Dose activated charcoal does not adsorb isopropanol efficiently.
■■ About 250 to 300 ml. ■■ Haemodialysis: Useful in patients demonstrating marked
■■ In terms of blood level: > 300 mg%. symptoms (persistent hypotension, coma) unresponsive to
standard therapy.
Toxicokinetics ■■ Supportive measures, including correction of hypotension,
Isopropanol can be absorbed through all routes. In the body it is metabolic acidosis, etc.
rapidly metabolised by alcohol dehydrogenase. Approximately
80% is converted to acetone and the remainder is excreted Forensic Issues
unchanged in the urine. Acetone is excreted in the urine and breath, Isopropanol may be generated spontaneously in a dead body,
and also metabolised to acetate, formate, and carbon dioxide. presumably due to bacterial or other putrefaction processes.
This fact must be borne in mind when subjecting viscera to
Mode of Action chemical analysis.
Isopropanol is two to three times more potent than ethanol as
a CNS depressant. Ethylene Glycol
Clinical Features Synonyms
■■ Lethargy, vertigo, headache, confusion, ataxia, dysarthria, 1,2-Ethanediol; Glycol alcohol.
nystagmus, miosis, abdominal pain, gastritis, haemorrhagic
tracheobronchitis, hypotension, and apnoea. Isopropanol Physical Appearance
is generally believed to produce greater CNS depression Colourless, syrupy, odourless, non-volatile liquid, with a bitter-
than ethanol at comparable blood levels. Deep coma and sweet taste.
areflexia are common following severe intoxication.
■■ Ketonaemia and ketonuria may be present, generally Uses
without metabolic acidosis. 1. Antifreeze: Ethylene glycol lowers the freezing point of
■■ Emesis and haemorrhagic gastritis may occur following water. More than 25% of the ethylene glycol produced is
ingestion. used in antifreeze and coolant mixtures for motor vehicles.

* In hospitals, isopropanol is often coloured blue to distinguish it from other colourless liquids, which has led to the designation “blue heaven” by abusers.