ALCOHOLS

ETHANOL AND METHANOL

 INEBRIANTS
• Inebriants are substances that induce Intoxication or Inebriation.
• These substances typically have Psychoactive effects and can impair
one's physical and mental faculties.
• Common inebriants include:
1. Alcohols
2. Barbiturates
3. Benzodiazepines
4. Chloral hydrate
 ALCOHOLS
• Alcohols are compounds with one or more hydroxyl (-OH) groups attached to a
carbon atom.
• They are derived from hydrocarbons and are classified based on the number of
hydroxyl groups they have.
• Monohydroxy Alcohols:
• Have one hydroxyl group.
• Examples: Ethanol (alcoholic drinks), Methanol (solvent), and Isopropanol (rubbing alcohol).
• Commonly used in both recreational and industrial settings.
• Dihydroxy Alcohols (Glycols):
• Have two hydroxyl groups.
• Examples: Ethylene glycol (antifreeze) and Propylene glycol (used in food and cosmetics).
• Used in industrial processes and chemical synthesis.
• Trihydroxy Alcohols:
• These are actually polyols or sugars, not typical alcohols.
• Example: Glycerol (glycerin), used in cosmetics and food.
• Not typically used for intoxication but serve important industrial and
biological roles.
ETHANOL (ETHYL ALCOHOL / GRAIN
ALCOHOL)
Physical Appearance:
• Clear, colorless liquid.
• Faint fruity odor.
• Sweetish burning taste.
• Water and lipid-soluble.
Sources of Ethanol:
1.Synthetic Production:
• Mostly made from ethylene by direct hydration.
2.Fermentation:
• Produced by fermenting sugar, cellulose, or starch. Used to make
beverage alcohol. This is the process carried out by yeast, where glucose
(a sugar) is converted into ethanol and carbon dioxide in the absence of
oxygen (anaerobic conditions).
• C₆H₁₂O₆ (glucose) → 2 C₂H₅OH (ethanol) + 2 CO₂ (carbon dioxide)
3.Enzymatic Hydrolysis of Cellulose.
4.Methanol Reaction:
• Produced by reacting methanol with synthesis gas at 185°C and pressure.
5.Azeotropic Distillation:
Used to create anhydrous ethanol.
6.Beverage Production:
Produced by fermenting sugar (from cereal, fruit, or vegetable) with yeast.
• Beer is brewed from malted cereal
• Whisky is made by adding yeast to malted mash.
7.Distillation is used for strong alcoholic beverages.

Ethanol Content in Alcoholic Beverages

Uses of Ethanol
Usual Fatal Dose of Ethanol
 Toxicokinetics
Toxicity Routes:
• Ethanol is toxic via
 Oral,
 Inhalation,
 Subcutaneous,
 Intravenous,
 Intra-arterial,
 Intraperitoneal, And
 Dermal Routes.
Absorption:
• 20% -stomach
• 80% -small intestine.
• Maximum blood alcohol concentration(BAC): 30-90 min after
consumption.
• Absorption can be delayed by food, undiluted ethanol, and congeners
in alcohol.
Gender Differences:
• Women have higher blood alcohol levels than men after consuming
the same amount due to lower gastric alcohol dehydrogenase activity.
• Women may experience liver damage at lower alcohol levels
compared to men.
 Excretion of Alcohol
1. Absorption of Alcohol into the Bloodstream
• Oral ingestion
• Absorption in the stomach
• Absorption in the small intestine
The majority of alcohol is absorbed into the bloodstream through the
walls of the small intestine.
The alcohol then circulates throughout the body via the bloodstream.
2. Transport through the Bloodstream
• Once alcohol is absorbed, it enters the bloodstream and is
transported throughout the body, including the brain, where it exerts
its effects (e.g., intoxication or impairment).
3. Metabolism in the Liver
• Alcohol Dehydrogenase (ADH) Enzyme: Most of the alcohol is
metabolized by the liver, primarily by the enzyme alcohol
dehydrogenase (ADH).
First step of metabolism
• ADH breaks down ethanol (alcohol) into acetaldehyde, a toxic compound that
can cause damage to cells.
• Acetaldehyde is further broken down by the enzyme acetaldehyde
dehydrogenase (ALDH) into acetic acid (also known as acetate), which is less
toxic
• Acetic acid is converted into carbon dioxide (CO₂) and water (H₂O).
• These by products are either exhaled through the lungs or eliminated
through the urine.
Acetic acid → Carbon dioxide (CO₂) and Water (H₂O)
4.Excretion of Alcohol and Metabolites
• While most of the alcohol is metabolized in the liver, a small
percentage (5-10%) is not metabolized and is excreted unchanged
from the body. This process involves:
• Through the Lungs: The lungs excrete a significant portion of the
unmetabolized alcohol.
• Breath Alcohol: Unmetabolized ethanol is exhaled through the lungs. This is
why breath alcohol tests (like the Breathalyzer) can detect the amount of
alcohol in the bloodstream.
• Through the Kidneys: A small amount of alcohol is excreted
in the urine.
• Through the Sweat Glands: A very small amount of alcohol is
also excreted through the skin in sweat, which may
contribute to the smell of alcohol on a person's body.
5.Final Excretion
• Exhalation of CO₂ and Water: The final products of alcohol
metabolism, carbon dioxide (CO₂) and water (H₂O), are
exhaled through the lungs. CO₂ is removed from the
bloodstream by the lungs and released into the atmosphere
with each breath.
• Urinary Excretion: Water and any remaining metabolites are
excreted through the urine.
 Lung Excretion and Henry’s Law
• According to Henry's Law, the concentration of ethanol in the alveolar
air is directly proportional to its concentration in the blood.
[ETHANOL (BLOOD)]=KH​PETHANOL
⋅ (ALVEOLAR AIR)​
• The ethanol in your blood is constantly in equilibrium with ethanol in
your alveolar air
• The ratio of ethanol in the blood to ethanol in the breath is typically
around 2,100:1 under normal conditions.
• This means that for every 2,100 molecules of ethanol in the blood,
there will be one molecule of ethanol in the breath.
• This ratio is used by breathalyzer devices to estimate blood alcohol
content (BAC) based on a breath sample.
 ETHANOL MODE OF ACTION
Old Theory:
• Initially, it was believed that ethanol (alcohol) primarily affects the brain by
disrupting the cell membranes. This theory suggested that alcohol would fluidize
or distort the cell membranes of neurons, making it harder for the brain cells to
function normally
Current Ideas:
• One current theory suggests ethanol enhances GABAergic function, interacting
with GABA-A receptors and chloride ion channels. GABA is an inhibitory
neurotransmitter, so this interaction could explain CNS depression.
• NMDA(N-methyl-D-aspartate) Receptors: A more convincing theory is that
ethanol blocks certain brain receptors (NMDA), which are involved in memory
and learning.
 PHARMACOLOGICAL EFFECTS OF ETHANOL
A. Central Nervous System (CNS)
• CNS Depression: Alcohol slows down brain activity, affecting coordination
and judgment.
• Stimulating Effects: Such as increased sociability, confidence, and a sense
of euphoria. This is typically due to alcohol's impact on neurotransmitter
systems, particularly Dopamine and GABA.
• Impaired Cognitive Function: Alcohol can mess with memory,
concentration, and thinking.
• Mood Swings: Alcohol can cause sudden changes in mood, like going from
happy to sad quickly.
• Severe Intoxication: Drinking too much can lead to confusion, stupor, or
even coma.
• Chronic Use and Sleep Issues: Long-term alcohol use messes up sleep,
causing disturbed or poor-quality sleep.
 B.CARDIOVASCULAR SYSTEM:
• Increased Heart Rate: Alcohol can raise the heart rate (tachycardia) in
moderate amounts.
• Vasodilation: It causes blood vessels to widen, leading to warm,
flushed skin.
• No Improvement in Coronary Blood Flow: Alcohol doesn't improve
blood flow to the heart and can even constrict blood vessels in some
cases.
• Worsens Angina: Ethanol-induced vasoconstriction can make chest
pain (angina) worse.
• Reduced Risk of Heart Disease: Moderate, regular alcohol use may
lower the risk of coronary heart disease.
 C.GASTROINTESTINAL TRACT:
• Stimulates Secretion: In normal amounts, alcohol increases stomach
acid and saliva production.
• High Concentrations Inhibit Secretion: Drinking large amounts of
alcohol (over 40%) can reduce stomach secretion and harm the
stomach lining.
• Erosive Gastritis: High alcohol levels can cause irritation and damage
to the stomach, leading to gastritis.
• Chronic Effects: With regular excessive drinking, the damage becomes
more severe and chronic. Over time, alcohol can cause:
Chronic Gastritis
Pancreatitis
Cirrhosis
 D.GENITO-URINARY SYSTEM:
• Increased Urination: Alcohol inhibits the hormone ADH, which leads to
more frequent urination.
• Not an Aphrodisiac: While alcohol may lower inhibitions and make
people feel more sexual, it actually reduces sexual responsiveness in
both men and women.
• Chronic Effects on Men: Long-term heavy drinking can cause issues like
Impotence,
Sterility,
Testicular shrinkage and
Breast enlargement (Gynaecomastia)
• Chronic Effects on Women: In women, long-term alcohol use increases
the risk of breast cancer.
 Clinical Features of Acute Ethanol Intoxication (Poisoning)

1.Progression of Intoxication Symptoms

2.Rare Reactions
3.Distinct Odor
4.Pupil Response
5.Temperature and Blood Pressure Issues
6.Respiratory Changes
7.Visual and Eye Movements
8.Metabolic Disturbances
9.Medico-Legal Aspects
10.Pathological Intoxication
11.Mimicking Other Conditions
1.Progressive Symptoms of Intoxication:
• Initial Stages:
• Alcohol first causes excitement and lowered inhibitions.
• Followed by slurred speech, lack of coordination, and an unsteady walk.
• Drowsiness and stupor may occur, and eventually, it can lead to a coma.
2.Rare Reactions:
• Allergic Reactions:
• Rarely, alcohol can cause allergic reactions like hives, nasal congestion, and
headaches.
• In severe cases, these reactions can be life-threatening.
• Cardiac Dysrhythmias:
• Binge drinking can sometimes cause irregular heart rhythms, like atrial
fibrillation.
3.Distinct Odor:
• Breath Odor: The breath of an intoxicated person often smells due to
compounds in alcoholic drinks (like wine, beer, or whisky), not the
ethanol itself.
• Persistence of Odor: Even after a person sobers up, the odor can linger
for a while.
4.Pupil Response:
• Dilated Pupils (Mydriasis): Especially in the initial stages of intoxication.
• Pupil Constriction in Severe Stages: In very severe intoxication (stupor
or coma), the pupils may constrict.
• Pupils Dilate Before Death: Just before death, the pupils may dilate
again.
• McEwan Sign: This sign, based on pupil dilation, is not reliable for
diagnosing alcoholic coma.
 MACEWE N’S SIGN
• Aka. Crack pot sign
• EIicited by percussion of skull
• Amplified sound can be
heard from Steth from other
end
• Indicative of separated
sutures due to raised intra
cranial tension
5.Temperature and Blood Pressure Issues:
• Hypothermia: Alcohol dilates blood vessels near the skin, causing
heat to escape
• Low Blood Pressure and Fast Heart Rate
• Chest Pain: In people with variant angina (a type of chest pain caused
by coronary artery spasm), alcohol can trigger a spasm in the
coronary arteries or cause a decrease in blood flow to the heart,
leading to chest pain.
6.Respiratory Changes:
• Slow Breathing: Alcohol can slow down breathing early on.
• Rapid Breathing: In severe cases, alcohol can cause fast breathing,
especially in metabolic acidosis.
7.Visual and Eye Movements:
• Double Vision and Eye Movement Problems
• Spontaneous Eye Movement
• Vision Problems: Long-term drinking can cause nerve damage,
leading to vision loss, but it can improve with B vitamin treatment.
8.Metabolic Disturbances:
• Acidosis: Alcohol can cause too much acid in the blood (lactic or
ketoacidosis) due to metabolism issues.
• Low Blood Sugar (Hypoglycemia): Alcohol can lower blood sugar,
causing seizures or coma, especially in children.
 Diagnosis of Ethanol
Intoxication
1.Bedside Test
• Mix 1 ml of the unknown solution, 1 ml of acetic acid, and 1 drop of H₂SO₄.
Heat for 1 minute. A fruity odor indicates ethanol.
Ethanol + Acetic Acid → Ethyl Acetate (fruity odor) + Water
2.Blood Alcohol Level (BAC):
• Measurement: BAC is usually measured using immunoassay or gas
chromatography, but results may take several hours.
3.Serum Electrolytes and Glucose:
• Check for:
• Hypoglycaemia
• Hypokalaemia
• Metabolic Acidosis
4.Other Lab Tests:
• Check for:
• BUN (Blood Urea Nitrogen), Creatinine
• Liver Enzymes
• CPK (Creatine Phosphokinase)
5.Osmolality:
• Serum Osmolality Formula:
• Blood ethanol levels can be estimated using the formula:
• BAL (Blood Alcohol Level) in g/L = Osmolal gap / 27.
6.Urinary Ethanol:
• Urinary ethanol can be tested, but may be falsely high in diabetics.
 CHRONIC POISONING (ALCOHOLISM,
ETHANOLISM)
1.Alcoholism Overview:
Alcoholism is when someone drinks a large
amount of alcohol over a long period of time.
• It’s characterized by:
• Strong craving for alcohol.
• Blackouts during intoxication.
• Withdrawal symptoms when stopping alcohol
 Diagnosis
• Blood Alcohol: Usually low because the body has metabolized most of
the alcohol, especially in withdrawal or chronic use.
• Blood Glucose: Slightly high due to stress hormones like cortisol,
especially in conditions like alcoholic ketoacidosis.
• Ketone Testing: Only detects acetone and acetoacetate, missing beta-
hydroxybutyrate, the main ketone in alcoholic ketoacidosis.
• Metabolic Acidosis: Occurs because the body breaks down fat for
energy, producing acidic ketones and causing a high anion gap.
• Serum Ketones: Very high in alcoholic ketoacidosis due to increased
ketone production.
• Electrolytes: Low potassium and chloride (hypokalemia and
hypochloremia) are common, caused by dehydration, vomiting, or
diarrhea, and worsened by acidosis.
General Treatment for Alcohol Withdrawal:
• Rehydrate: Give normal saline with dextrose to restore fluids.
• Potassium: Add potassium if needed.
• Thiamine: Give 50-100 mg to prevent brain damage (Wernicke-
Korsakoff syndrome).
Delirium Tremens (DTs) (3-5 days after alcohol stops):
• Symptoms: Confusion, hallucinations, shaking, fever, fast heart rate,
sweating, and high blood pressure.
Treatment for DTs:
• Environment: Keep the person in a calm, well-lit place.
• Agitation: Give Diazepam (starting with 10 mg IV, then 5 mg every 5
minutes until controlled).
• Thiamine: Continue giving thiamine.
• Fluids: Correct dehydration and electrolyte imbalances.
Wernicke-Korsakoff Syndrome:
• Wernicke's Encephalopathy (early): Drowsiness, confusion, memory
problems, and coordination issues from thiamine deficiency.
• Korsakoff’s Psychosis (chronic): Long-term memory problems and
making up false memories.
Treatment:
• Thiamine: Give 50-100 mg IV daily for 5-7 days to treat Wernicke's.
• Fluids: Make sure the person is well-hydrated and balanced
 TREATMENT FOR ACUTE ETHANOL POISONING:

• Airway Protection & Ventilation: Ensure the airway is clear and provide
breathing support if needed.
• Activated Charcoal: Not effective for alcohol poisoning.
• Stomach Wash: To remove alcohol from the stomach.
• Thiamine (100 mg IV): Prevents Wernicke’s encephalopathy.
• Dextrose:
• If blood glucose is low (<60 mg/100ml), give 25g IV for adults or 0.5-1g/kg for
children.
• Thiamine should be given before glucose to prevent brain damage.
• Intravenous Fluids: Replenish fluids lost due to alcohol.
• Medications:
• Flumazenil (3 mg IV) may help reverse alcohol's respiratory depression.
• Hemodialysis: Used in severe cases to remove alcohol quickly, especially if liver
function is impaired.
 TREATMENT FOR CHRONIC ETHANOL
Treatment of Withdrawal:
POISONING
• Carbamazepine: Effective for alcohol withdrawal, including delirium tremens.
• Chlormethiazole: Used for withdrawal but has abuse potential.
• Clonidine & Gamma-Hydroxybutyric Acid: Help manage withdrawal symptoms.
• Tiapride: For psychological distress, especially during abstinence.
Aversion Therapy (De-addiction):
• Disulfiram:
• Prevents alcohol breakdown, causing unpleasant symptoms when alcohol is consumed (e.g.,
nausea, headache).
• Dose: 250 mg/day; taken orally, and alcohol should be avoided during treatment.
• Side Effects: Can include headache, nausea, and liver issues, so regular monitoring is needed.
Supportive Psychotherapy:
• Group Therapy: Support through group sessions, sharing experiences, and mutual
help.
METHAN
OL
 SYNONYMS
• Methyl hydroxide
• Mono hydroxyl methane
• Colonial spirit
• Columbian spirit
• Pyroxylic spirit
• Wood alcohol
• Wood naphtha
• Wood spirit
 PHYSICAL APPEARANCE &
CHARACTERISTICS
• Appearance: Methanol is a colorless liquid.
• Polarity: It is highly polar, meaning it has a strong ability to dissolve in
water and other polar solvents.
• Flammability: Methanol is highly flammable, meaning it can easily
catch fire when exposed to heat or flame.
• Odour:
Pure methanol - faintly sweet odour
Crude methanol - repulsive, pungent odour
• Taste: Methanol has a bitter taste.
 USES OF METHANOL
• Antifreeze: Methanol stops liquids from freezing in cold
weather because it has a low freezing point.
• Carburettor Cleaner: It dissolves grease and dirt, helping to
clean the carburettor.
• Denatured Spirit: Methanol makes alcohol undrinkable,
making it safe for cleaning and industrial use.
• Embalming Fluid: Methanol helps preserve bodies by
preventing decay.
• Leather Dyes: It helps dissolve and spread the
dye evenly on leather.
• Paint Remover: Methanol breaks down paint,
making it easier to remove.
• Varnish and Shellac: It helps dissolve these
materials so they can spread evenly and dry
properly.
• Windshield Washing Fluid: Methanol helps
remove ice and dirt from windshields in cold
weather.
 FATAL DOSE
• Fatal Dose of Methanol: Drinking 70 to 100 ml of
pure methanol can be deadly.
• Toxic Dose: Drinking 0.25 ml of methanol per kg
of body weight can cause serious harm.
• Deadly Dose for an Average Person:
A person weighing 70 kg (about 154 lbs) could
die from drinking around 35 ml of pure methanol.
 MODE OF ACTION
• Absorption: Methanol is quickly absorbed through the skin, lungs, and
stomach. It reaches high levels in the blood in 30 to 60 minutes.
• Delayed Symptoms: Symptoms of poisoning usually appear 18 to 24
hours after ingestion.
• Metabolism in the Liver:
• Methanol is converted to formaldehyde. CH₃OH (methanol) → CH₂O
Formaldehyde is then converted to formic acid. CH₂O → HCOOH
• Toxic Effects: Formic acid causes eye damage (retinal toxicity) and acid
buildup in the blood (metabolic acidosis).
• Slow Breakdown: Formic acid is broken down slowly, so methanol can
remain in the body for up to 7 days.
 CLINICAL FEATURES

• Initial Symptoms (12 to 24 hours after ingestion):

• Vertigo (dizziness)
• Headache with stiff neck
• Nausea and vomiting
• Abdominal pain
• Ocular Toxicity (Eye Symptoms):
• Blurred vision or dimmed vision (“flashes” or “snowstorm”)
• Sensitivity to light (photophobia)
• Constricted visual fields, spots before eyes, reduced vision, optic atrophy,
blindness
• Dilated pupils with slow reaction to light
• Severe poisoning can cause fixed dilated pupils
• Retinal swelling and optic disc hyperaemia (redness) in eye exam
• Permanent damage: optic atrophy, vision loss, and visual field problems
• Metabolic Acidosis occurs when there's a significant accumulation of acid in the blood,
leading to a high anion gap.
• In severe cases, bicarbonate levels can fall below 10 mEq/L.
• It may take 18-48 hours for acidosis to develop, especially if ethanol is involved.
• HCOOH (formic acid) → Cellular damage via inhibition of cytochrome c oxidase → Tissue
hypoxia, acidosis
Symptoms:
Rapid heart rate (tachycardia)
• The body attempts to buffer the excess acid, often causing an increase in cardiac output to
help maintain perfusion.
Low blood pressure (hypotension)
• Formic acid decreases the contractility of the heart, reducing the heart's ability to pump
blood effectively
Low body temperature (hypothermia)
• Methanol poisoning can directly affect thermoregulation in the hypothalamus, impairing the
body’s ability to generate and maintain heat.
Seizures and coma in severe cases
Electrolyte Imbalance:
Low magnesium (hypomagnesemia)
• Magnesium is a crucial intracellular ion, and acidosis can promote magnesium
movement from the extracellular fluid into cells, leading to lower magnesium
levels in the blood (hypomagnesemia).
Low potassium (hypokalemia)
• In response to acidosis, the kidneys increase excretion of hydrogen ions (H⁺)
to help restore normal blood pH. To maintain electrical neutrality, potassium
ions (K⁺) are often excreted along with hydrogen ions, leading to potassium
wasting in the urine
Low phosphate (hypophosphatemia)
• Similar to magnesium and potassium, phosphate is excreted by the kidneys. In
the context of severe metabolic acidosis, the kidneys may increase the
excretion of phosphate, contributing to low blood levels of phosphate
Fanconi Syndrome:
Fanconi syndrome is a renal disorder characterized by dysfunction of the proximal
tubules in the kidneys, which leads to impaired reabsorption of several substances. It
results in the loss of electrolytes, sugars, amino acids, and phosphate into the urine.
Key features
• Low phosphate in the urine due to impaired renal reabsorption.
• Low uric acid levels in the urine (due to impaired renal handling).
• Low sugar (glucose) in the urine, caused by dysfunction in glucose reabsorption in
the renal tubules
Pancreatitis:
• Severe methanol poisoning can cause inflammation of the pancreas.
• The body may respond to the metabolic stress caused by methanol poisoning by
increasing fat breakdown (lipolysis). This can increase free fatty acids in the
bloodstream, which can contribute to pancreatic injury and inflammation, a
hallmark of pancreatitis.
Cause of Death:
• Respiratory failure (breathing stops before the heart).
• Slow heart rate, low blood pressure, and requires intensive treatment.
Permanent Effects After Recovery:
Vision issues: optic neuropathy, blindness.
• Optic neuropathy is a hallmark of methanol poisoning due to the toxicity of
formic acid on the optic nerve. The optic nerve is very sensitive to formic acid,
and prolonged exposure can lead to ischemic damage (damage due to lack of
blood flow) and degeneration of the nerve fibers.
Nervous system issues: Parkinsonism, brain damage, nerve damage.
• Brain damage can result from cerebral hypoxia (reduced oxygen supply to the
brain) caused by metabolic acidosis and mitochondrial dysfunction. This can lead
to cognitive impairments, severe neurological deficits, and permanent brain
damage.
Eye problems: pale optic disc (paleness of the optic nerve), thin retinal arteries,
poor pupillary light reaction.
 DIAGNOSIS
1.Blood Tests:
• Complete Blood Count (CBC): Helps assess general health
and detect signs of infection, anemia, or other issues.
• Electrolytes: To check for imbalances (like low magnesium,
potassium, and phosphate) that may occur with poisoning.
• Urinalysis: To assess kidney function, detect abnormal
substances in urine, and monitor for Fanconi syndrome or
other kidney damage.
• Arterial Blood Gases (ABG): To measure pH levels and check
for metabolic acidosis (a high anion gap, indicating methanol
poisoning).
2.Key Diagnostic Findings:
High Anion Gap Acidosis:
• Methanol metabolism produces formic acid, which causes metabolic acidosis, reflected as a
high anion gap (difference between positively and negatively charged ions in the blood).
Elevated Osmolal Gap:
• An elevated osmolal gap suggests the presence of an unmeasured substance (like methanol)
in the blood, indicating poisoning.
Hypophosphataemia (Low Phosphate):
• Methanol poisoning can cause kidney damage and disrupt phosphate balance in the body,
leading to low phosphate levels.
Elevated Creatine Phosphokinase (CPK):
• Elevated CPK levels can indicate muscle injury, which may occur due to metabolic
disturbances or poisoning.
Elevated Amylase:
• This can indicate pancreatitis (inflammation of the pancreas), a potential
complication of severe methanol poisoning.
What is the Osmolal Gap?
• The osmolal gap is the difference between the measured osmolality of
blood and the calculated osmolality.
• Measured osmolality: The actual concentration of particles (e.g., salts,
glucose, urea) in the blood, measured in a lab.
• Calculated osmolality: A value estimated using a formula based on the
concentrations of common substances in the blood, such as sodium,
glucose, and blood urea nitrogen (BUN).
• Osmolal Gap=Measured Osmolality−Calculated Osmolality

• In methanol poisoning, methanol and its metabolites (formaldehyde and

formic acid) accumulate in the body, contributing to an increase in the
measured osmolality.
Methanol and Formic Acid Levels:
• Methanol level > 50 mg/100 ml in blood shows serious poisoning.
• Formic acid in blood confirms methanol poisoning because methanol turns
into formic acid in the body.
Imaging (CT/MRI):
• The putamen (a part of the brain) can show symmetrical areas of cell death
(necrosis) in cases of severe methanol poisoning.
 TREATMENT
1.General Management:
• Severe Cases (e.g., abnormal vital signs, visual problems, coma, high
methanol levels) should be admitted to the Intensive Care Unit (ICU).
Specific Treatments:
• Stomach wash with sodium bicarbonate to help neutralize the acid.
• Ipecac-induced vomiting is not recommended due to possible CNS
depression (brain effects).
• Activated charcoal doesn’t absorb methanol but can be used to
prevent absorption of other substances if taken together with
methanol.
 2.ANTIDOTE : ETHANOL
Competes for the Same Enzyme:
Ethanol competes with methanol for the alcohol dehydrogenase enzyme.
Prevents Toxic Breakdown:
This stops methanol from being broken down into formaldehyde and formic
acid, which are toxic.
Stronger Affinity:
Ethanol binds to the enzyme 20 times stronger than methanol, so it slows
down methanol’s breakdown.
Excretes Methanol Safely:
Because the breakdown is slowed, the body can excrete methanol
unchanged through urine.
Prevents Acidosis:
By blocking formic acid production, ethanol helps avoid severe acidosis (too
much acid in the body).
Initial Dose:
• 10% ethanol solution: 10 ml/kg of the patient’s body weight
should be given IV (intravenously) over 30 minutes.
Maintenance Dose:
• After the initial dose, the patient should receive 1.5 ml/kg/hr of
10% ethanol to maintain blood ethanol levels of 100-130 mg/100
ml.
If IV Ethanol is Unavailable:
• Use bulk ethanol or 95% ethanol mixed with fruit juice.
• You can also use alcoholic beverages (like vodka, gin, rum, or
whisky) mixed with juice or glucose solution, giving 125 ml of the
beverage, and repeat as needed.
When to Stop Ethanol Therapy:
• Methanol blood concentration is below 10 mg/100 ml.
• Formate (formic acid) level is below 1.2 mg/100 ml.
• Acidosis and other symptoms (like CNS effects, electrolyte
imbalances) have resolved.
NOTE:
• If the patient drank ethanol with methanol, it could affect their body's
balance.
• They might still have high methanol levels.
• Ethanol treatment should start right away until the methanol levels are
checked.
In short: Start ethanol treatment even if ethanol was already drunk, until
methanol levels are confirmed.
 OTHER ANTIDOTES
4-Methyl Pyrazole (Fomepizole):
• New antidote used in place of ethanol in Western countries.
• Does not cause CNS depression (unlike ethanol).
• Dosing:
• 15 mg/kg initially, then 10 mg/kg every 12 hours for 4 doses, then back to 15
mg/kg every 12 hours.
• Up to 20 mg/kg can be used safely for 5 days.
• Advantages: Easier to use, requires less monitoring, does not cause
CNS depression or hypoglycemia, and may reduce the need for
dialysis.
Sodium Bicarbonate IV:
• Administer 500-800 ml of 7.5% sodium bicarbonate solution slowly to help
correct acidosis (low blood pH).
Folinic Acid (Leucovorin):
• Administer 1-2 mg/kg every 6 hours via IV.
• Helps speed up the elimination of formic acid, the toxic by-product of
methanol.
For Seizures:
• Start with benzodiazepines (like diazepam or lorazepam) to control seizures.
• If seizures continue, give phenobarbital.
Dialysis:
• Hemodialysis is very effective in removing methanol, formaldehyde, and
formic acid from the body.
Dialysis is recommended for:
• Severe acidosis or methanol levels above 25-50 mg/100 ml.
• Other methods like hemoperfusion, peritoneal dialysis, and continuous
venovenous hemofiltration are less effective.
TREATMENT SUMMARY
1. Fomepizole: Main antidote, easier to use than ethanol.
2. Sodium Bicarbonate: Helps correct blood acidity.
3. Folinic Acid: Helps remove toxins faster.
4. Seizure Control: Use benzodiazepines first, then phenobarbital if
needed.
5. Dialysis: For severe cases with high methanol levels or acidosis.