Treatment of Ethyl Alcohol (Ethanol) Poisoning

Pathophysiology - Why It Causes Toxicity

• Enhancement of GABA-A receptor activity (inhibitory)
• Inhibition of NMDA receptor activity (excitatory)
• Resulting in dose-dependent CNS/respiratory depression

Ethanol metabolism - Lippincott Illustrated Reviews: Pharmacology

Blood Ethanol Concentration (BEC) and Clinical Signs

Note: Tolerant heavy drinkers show markedly less impairment at the same BECs. Co-ingestion of other CNS depressants (benzodiazepines, barbiturates, antihistamines) significantly worsens toxicity at lower BECs.

Treatment of Acute Ethanol Intoxication

1. Airway and Breathing (First Priority)

• Ensure a patent airway; place in lateral decubitus ("recovery position") to prevent aspiration
• If respiratory depression is mild: careful observation is sufficient
• If respiratory depression is severe: endotracheal intubation for airway protection and ventilatory support
• Intubation and mechanical ventilation are unusual for ethanol intoxication alone

2. Gastric Lavage

• Consider if absorption is not yet complete (early presentation) and airway is protected
• Activated charcoal is generally not useful (ethanol is absorbed rapidly and does not bind well)

3. IV Fluids

• IV fluid resuscitation for hypotension and dehydration
• Correct fluid and electrolyte disturbances

4. Glucose

• Check blood glucose; administer dextrose if hypoglycemia is present (ethanol inhibits gluconeogenesis)

5. Thiamine (Vitamin B1) - Mandatory

• Give thiamine before glucose in any patient with altered mental status or suspected chronic alcohol use disorder
• Prevents and treats Wernicke encephalopathy (confusion, ataxia, oculomotor abnormalities)
• Dose for Wernicke: 500 mg IV three times daily for 3-5 days
• All patients with suspected ethanol use disorder should receive thiamine

6. Folate

• Administer folate (ethanol depletes folate stores)

7. Clinical Monitoring

• Serial neurological and vital sign monitoring until clinical sobriety
• Observe for 4-6 hours in the emergency department as ethanol is metabolized
• Do not discharge until the patient has returned to their neurological baseline

8. Hemodialysis (Rarely Required)

• Ethanol is freely miscible with water and can be removed by hemodialysis
• Reserved for extremely high blood alcohol levels or severe cardiovascular compromise
• Note: May precipitate withdrawal in a patient with alcohol use disorder

Differential Diagnosis - Do Not Miss

• Hypoglycemia (diabetic coma)
• Other drug intoxication (opioids, benzodiazepines, sedatives)
• Cardiovascular accidents (stroke, TIA)
• Head trauma / skull fracture (especially if the patient fell)
• Diabetic ketoacidosis (can produce similar breath odor to alcohol)
• Metabolic encephalopathy

Blood ethanol levels are necessary to confirm intoxication. Do not rely solely on breath odor - similar odors can occur in DKA or other metabolic acidoses. Serum glucose, metabolic panel, and a low threshold for head CT are appropriate.

Managing Alcohol Withdrawal (Special Consideration)

• Benzodiazepines are first-line (symptom-triggered, protocol-based dosing)
  • Lorazepam 1-2 mg IV/IM or diazepam 5-10 mg IV, titrated to symptoms
• Phenobarbital is an alternative in refractory cases
• Use symptom-triggered protocols (e.g., CIWA-Ar scale) - fixed-dose schedules are less effective and may cause under- or over-treatment
• Dexmedetomidine is not recommended - does not target GABA/glutamate systems and does not prevent seizures
• High-dose IV thiamine (as above)

Long-Term / Definitive Treatment of Alcohol Use Disorder

• Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 3518-3520
• Washington Manual of Medical Therapeutics, p. 1097
• Lippincott Illustrated Reviews: Pharmacology, pp. 1566-1571

Ethyl Alcohol Poisoning - As Per Reddy's Forensic Medicine & Toxicology (36th Ed., 2026)

K.S. Narayan Reddy - The Essentials of Forensic Medicine and Toxicology, 36th Edition

Description

Mechanism of Action

1. Higher centers in the cerebrum are depressed first; the primitive hindbrain/respiratory center is inhibited last
2. Cerebral forebrain center inhibition causes mood changes like elation and excitation
3. Direct toxic effect on cardiac, thyroid, and hepatic cells
4. Intracellularly binds with GABA receptor enzyme in brain cells
5. Inhibits NMDA (N-methyl-D-aspartate) enzyme - prolonged abuse causes upregulation of this inhibitory response, leading to tolerance and withdrawal signs

Acute Poisoning - Signs and Stages

Stage 1 - Excitement / Inebriation / Sobriety

• BAC < 50 mg%
• Mild euphoria, easy socialization, high boasting speech

Stage 2 - Euphoria

• BAC 50-100 mg%
• Decreased attention span and cognitive function
• Loss of inhibitions, talkativeness, sociability
• Nausea, dizziness, palpitations, flushed red face
• Subconjunctival suffusion (red eyes), salivation, dilated pupils

Stage 3 - Excitement

• BAC 100-150 mg%
• Incoordination of muscular movements (ataxia)
• Loss of self-control, slurred speech, delirium
• Sleepiness, disorderly behavior, abusive language
• Alcohol gaze nystagmus

Stage 4 - Coma and Death

• Decreased response to painful stimuli, labored breathing
• Pupillary constriction, brisk reflexes (early)
• Later: loss of consciousness, deep sleep (usually lasts 4-6 hours)
• McEwan's Sign: Painful stimulus (slap on temple) causes pupil to dilate then re-contract
• Very rarely enters deep coma - alcohol alone will not kill unless:
  • Asphyxia occurs (aspiration of food bolus - "Café coronary")
  • Comorbidities / concomitant diseases
  • Exposure to cold while under the influence

BAC decreases by approximately 15 mg%/hour; once BAC falls below 100-150 mg%, the person regains consciousness.

Treatment of Acute Ethyl Alcohol Poisoning (Reddy's)

1. Maintain airway - primary priority; prevent aspiration
2. Watch renal functions in deeply comatose patients
3. Flumazenil may be considered for patients with hepatic encephalopathy
4. Vitamin B supplementation - alcoholic addicts have vitamin B (especially thiamine) deficiency

Fatal Dose and Death

• Adults: 5-8 g/kg (6-10 mL/kg) body weight
• Fatal BAC: >500 mg%
• Fatal period: 12-24 hours
• Causes of death:
  1. Depression of respiratory center (BAC usually >500 mg%)
  2. Asphyxia - inhalation of food bolus (café coronary)

Autopsy Findings

1. Suffused red conjunctiva
2. Signs of asphyxia
3. Alcoholic fruity odor from body cavities and stomach
4. Stomach mucosa congestion

Bedside Tests for Alcohol

Chronic Poisoning / Alcoholism

Types (Jellinek's Classification)

Systemic Complications of Chronic Alcoholism

Withdrawal Signs (Timeline)

Medico-Legal Aspects (Drunkenness)

1. Signs of consumption - sweating, mild pupillary dilation, conjunctival suffusion, salivation, alcoholic breath odor, increased pulse volume
2. Signs of influence - slurred speech, unable to walk straight, cannot touch tip of nose with finger, alcohol gaze nystagmus
3. Signs of intoxication - vomiting, constricted pupil, semiconscious/altered sensorium, brisk reflexes or unconscious

Important caveat: These signs may also be seen in epilepsy, viral meningitis, brain tumors, head injury, methyl alcohol poisoning, tranquilizers, sedative-hypnotics, CO poisoning, and other conditions. The examining doctor must rule these out before certifying drunkenness.

Methanol (Methyl Alcohol) Poisoning - As Per Reddy's Forensic Medicine & Toxicology (36th Ed., 2026)

K.S. Narayan Reddy - The Essentials of Forensic Medicine and Toxicology, 36th Edition, pp. 530-531

Description / Properties

• Synonyms: Wood alcohol, wood naphtha, pyroxilic acid, Columbian spirit, monohydroxy methane
• Formula: CH₂OH
• Appearance: Colorless, highly polar, flammable liquid with a faintly sweetish odor and bitter taste

• Carburetor cleaner (20%)
• Antifreeze (10-50%)
• Denatured/methylated spirit (5-10%) - mixed with ethyl alcohol (90-95%)
• Embalming fluid (20%)
• Leather dyes (30%)
• Varnish, shellac, paint remover, windshield cleaner
• Solvent in manufacture of cholesterol, streptomycin, vitamins, hormones
• Nail polish removers, paints (substance abuse among adolescents)

Fatal Dose

• 15-250 mL (average: 70-100 mL)

Mechanism of Action (Metabolism)

1. Well absorbed by inhalation, oral, and parenteral routes; peak blood level reached in 30-60 minutes
2. Alcohol dehydrogenase (ADH) in liver metabolizes methanol → Formaldehyde → Formic acid
3. Formaldehyde and formic acid are highly toxic - they cause metabolic acidosis and neurological symptoms (especially optic nerve and retinal damage)
4. Metabolism of methyl alcohol is slow - unmetabolized methanol can be found in blood for up to 1 week

Key point: The latent period before toxicity (18-24 hours) is because metabolites (formic acid) accumulate slowly. This "silent period" is a classic exam point.

Signs and Symptoms of Poisoning

Diagnosis

1. High anion gap metabolic acidosis
2. Elevated osmolal gap
3. Hypophosphatemia
4. Elevated CPK and amylase
5. Blood methanol level
6. Detectable formic acid in blood
7. CT/MRI: Evidence of basal ganglia (putamen) degeneration
8. Fundoscopy: Retrobulbar edema, hyperemia
9. Optical coherence tomography (OCT)

Treatment (Reddy's)

1. Gastric Decontamination

• Stomach wash (gastric lavage) with sodium bicarbonate

2. Antidote - Ethanol (Specific Antidote)

• Ethanol is the specific antidote - both methanol and ethanol compete for the alcohol dehydrogenase (ADH) enzyme, but ethanol has a higher affinity for ADH than methanol
• This competitively blocks the metabolism of methanol, preventing formation of the toxic formaldehyde and formic acid
• Given as whisky, gin, or vodka at 2.5 mg/kg (i.e., approximately 175 mL)

Reddy also provides a dosing table for ethanol therapy (Table 29.4):

3. Hemodialysis

• Most effective treatment to remove methanol and formaldehyde from the body

4. Folinic Acid

• Supplementation is essential in almost all cases
• Dose: 1-2 mg/kg IV
• Folinic acid accelerates the conversion of formate to CO₂ and water, reducing formic acid accumulation

Postmortem / Autopsy Features

1. Cyanosis is a prominent feature
2. Edema and emphysematous lungs
3. Long-standing cases: Basal ganglia degenerative changes (putamen)
4. Preservation of viscera for chemical analysis in saturated NaCl solution

Medico-Legal Aspects

1. Accidental poisoning is most common - especially via indigenous methylated spirits
2. Intentional adulteration of ethyl alcohol with methyl alcohol causes mass deaths - these are called "Liquor Tragedies" (attract significant media and public attention)
3. Substance abuse - nail polish removers, paints used as solvents, especially among adolescents

Comparison: Ethanol vs. Fomepizole as Antidote

Carbon Monoxide (CO) Poisoning - As Per Reddy's Forensic Medicine & Toxicology (36th Ed., 2026)

K.S. Narayan Reddy - The Essentials of Forensic Medicine and Toxicology, 36th Edition, pp. 534-536

Description / Properties

• Synonyms: Carbonic oxide, Carbon oxide, Exhaust gas, Flue gas
• Pure CO is an odorless, colorless, non-irritating gas, lighter than air
• It gives no warning of its presence - this is why it is so dangerous

Important: Domestic gas (LPG - mixture of propane and butane) does not contain CO. Endogenous CO from haem degradation never reaches toxic levels; normal plasma COHb = 1-5%, up to 7-8% in smokers.

Sources

1. Incomplete combustion of any fuel - wood, charcoal, gas, kerosene
2. Automobile exhaust (most common environmental source)
3. Fires (house fires, enclosed spaces)
4. Paint remover - especially methylene chloride (metabolized to CO in the body)
5. Tobacco smoke - mainstream cigarette smoke contains up to 5% CO by volume
6. Shisha/hookah water pipes - CO poisoning reported after prolonged smoking
7. Ingestion or inhalation of methylene chloride

Fatal Dose

• COHb level >50-60% is potentially lethal
• A CO concentration of 5,000 ppm in air is lethal after 5 minutes of exposure

Toxicokinetics

• Lungs avidly absorb CO
• CO combines with:
  • Hemoglobin: 85% → forms Carboxyhemoglobin (COHb)
  • Myoglobin: 15%
• Elimination occurs exclusively through the lungs

Mode of Action (Mechanism)

1. CO has an affinity for hemoglobin 230-270 times greater than that of oxygen
2. Despite adequate PO₂ in blood, there is reduced arterial oxygen content
3. CO causes a leftward shift of the oxyhemoglobin dissociation curve - impairing offloading of oxygen from Hb to tissues
4. Net result: decreased oxygen carrying capacity + decreased tissue oxygen delivery
5. CO also inactivates mitochondrial cytochrome oxidase - interferes with cellular respiration directly
6. Profound hypotension in severe poisoning due to:
   • Activation of guanyl cyclase → smooth muscle relaxation
   • Displacement of nitric oxide from platelets → vasodilation

Clinical Features

Acute Poisoning

Chronic Poisoning

Differential Diagnosis

Diagnosis

1. COHb Level (Co-oximetry)

• Normal: 0-5% (up to 10% in heavy smokers)
• Done spectrophotometrically using a co-oximeter
• Arterial or venous blood (in lithium heparin tube)

2. Pulse Oximetry

• Unreliable in CO poisoning - standard pulse oximetry cannot distinguish COHb from OxyHb (both absorb at similar wavelengths), so SpO₂ will appear falsely normal

3. Arterial Blood Gas (ABG)

• PO₂ is usually normal (CO doesn't reduce dissolved O₂)
• O₂ saturation (calculated) is decreased
• A gap between measured and calculated HbO₂ indicates need for COHb measurement
• Metabolic acidosis is invariably present

4. ECG

• May reveal myocardial damage: ST depression or elevation

5. Chest X-ray

• May show ground-glass appearance, perihilar haze, peribronchial cuffing, intra-alveolar edema (pulmonary edema)

6. Ancillary Investigations

• Elevated serum creatine kinase (CK) and lactate dehydrogenase (LDH)
• Elevated creatinine
• Hypokalemia and hyperglycemia
• Neuropsychometric testing indicated after moderate-to-severe poisoning

Bedside Tests for COHb

Treatment

Step 1 - Admission Criteria

• Neurologic signs or symptoms
• Chest pain
• Abnormal ECG
• Metabolic acidosis
• COHb level >20%

Step 2 - Remove from Environment + Oxygen (100%)

• Immediate removal from the contaminated environment
• Administer 100% oxygen through a tight-fitting mask or endotracheal tube
• Continue until COHb falls to 15-20%
• Monitor cardiac and respiratory status continuously

Half-life of COHb: ~5 hours on room air → ~40 minutes on 100% normobaric oxygen → ~20 minutes on 100% oxygen at 2.5 ATA (hyperbaric)

Step 3 - Monitor for Cerebral Edema

• Serial neurological examinations
• CAT scans
• Fundoscopic examination

Step 4 - Correct Metabolic Acidosis

• If metabolic acidosis persists despite correction of hypoxia and adequate fluid resuscitation
• Give IV sodium bicarbonate

Step 5 - Control Convulsions

• IV diazepam and phenytoin in the usual manner

Step 6 - Correct Hypotension

• Adequate fluid resuscitation with crystalloids

Step 7 - Antidote: Hyperbaric Oxygen (HBO) (Specific Antidote)

Autopsy Features

1. Cherry red (pink) color of skin - especially in areas of postmortem lividity; in dark-skinned individuals, look at inner lips, nail beds, tongue, palms, soles
2. Cutaneous bullae (skin blisters) - sometimes seen at calves, buttocks, wrists, knees
3. Cherry pink blood and tissues throughout
4. Diluted blood in water held against light appears pink/red (vs. brown in normal blood)
5. Pulmonary edema
6. White matter of brain is firmer than usual; brain retains shape better after removal
7. In delayed deaths: Necrosis and cavitation of basal ganglia - especially globus pallidus and putamen (classic finding)
8. Petechiae and ring-shaped hemorrhages in white matter
9. Focal myocardial necrosis
10. Blood collection: preferably from a peripheral vein; if unavailable, heart blood, body cavities, or bone marrow can be used (preserve with sodium fluoride)

Medico-Legal Importance

1. Next to CO₂, CO is the most abundant atmospheric pollutant - progressively increasing
2. Accidental - most common; especially in ill-ventilated areas with incomplete combustion
3. Suicidal - historically via coal gas ovens in UK; now less common since LPG replaced coal gas (LPG has little/no CO)
4. Homicidal - by confining victim in a closed space with a CO source
5. Tobacco smoke is an important source of CO contamination