Management of Ethanol and Methanol Poisoning PDF Print E-mail
Written by Dr. Niru Prasad   
THE GUIDELINES FOR MANAGEMENT OF ETHANOL, METHANOL AND ETHYLENE GLYCOL POISONING AT THE EMERGENCY ROOM

By
Niru Prasad, M.D., F.A.A.P.,  F.A.C.E.P.

Department of Emergency Medicine

Henry Ford Hospital

West Bloomfield Center
Department of Ambulatory Pediatrics

St. Joseph Mercy Hospital

Pontiac


Ethanol Overdose
Introduction
Pharmacokinetics
Absorption and Metabolism
Clinical Symptoms Produced by Ethanol Overdose
Diagnosis, Laboratory Analysis and Treatment



Ethanol is the most commonly abused drug in the United States, with approximately 10 percent of 

the adult population qualifying as alcoholics. Approximately 40 percent of the medical hospital 

admissions are related to ethanol abuse and multisystem organ dysfunctions secondary to chronic 

alcohol intake.   The chronic alcohol intake can lead to numerous metabolic complications such as 

hypoglycemia,  ketoacidosis,  electrolyte  disorders,  neurologic disorders, withdrawal  seizures,  

delirium  tremens,  gastritis, hepatitis, pancreatitis, as well as hematologic disorders.  It is very 

important for the emergency physicians to recognize these patients.   The adolescents and young 

adult suicide rates are frequently associated with ethanol abuse and overdose.  It is also important to 

remember that the depressed level of consciousness in alcoholics could also be due to subdural 

hematoma, meningitis, and other central nervous systems lesions.  Alcohol abuse is often associated 

with suicide,homicide, drowning, physical abuse, and motor vehicle accidents.
The forms of alcohols are:
	Ethyl alcohol (ethanol)

	Ethylene glycol

	Isopropyl alcohol (isopropanol)

	Methyl alcohol

	Propylene glycol

	Diethylene glycol
All of these forms of alcohol are low molecular weight, water soluble substances with prominent 

multiorgan toxicity.
Pharmacokinetics of Ethanol
Ethanol is absorbed in an unaltered state from the stomach and small intestine, metabolized by the 

liver and excreted through the kidneys.  It has been recently  postulated that the presence of 

alcoholic dehydrogenase in gastric mucosa degrades some of the absorbed ethanol, and histamine 

H-2 antagonist inhibits alcohol dehydrogenase  hence patients taking acid suppressing drugs are 

more prone to alcohol toxicity with ethanol intake.   Several hepatic enzymes convert ethanol to 

acetaldehyde. These enzymes are cytoplasmic alcohol dehydrogenase,  catalase,  and a microsomal 

ethanol oxidizing system.
	Metabolism of Ethanol 

		Ethanol

                   ¯ 	(alcohol dehydrogenase)
		Acetaldehyde

	     	     ¯     (alcohol dehydrogenase)
		Acetic acid

		   ¯ 	(Kreb's cycle)

		   ¯ 

		Carbon dioxide and water



The alcohol dehydrogenase pathway is the predominant system for alcohol metabolism.   The 

second pathway is the microsomal ethanol oxidizing system located in the endoplasmic reticulum. 

This system may be associated with cytochrome P-450 mixed function oxidase system in the liver.   

The third system involves the catalase located in the prioxisomes.
The rate of metabolism of ethanol is in the rage of 15 to 25 milligrams per deciliter per hour.
	12 mg/dl/hour in nondrinkers

	15 mg/dl/hour in social drinkers

	30 mg/dl/hour in alcoholics
A 150 pound person metabolizes 10 ounces of beer in one hour. Effects Produced by Ethanol Metabolism
1.	Drug Interactions
2.	Carbohydrate Metabolism

A.	Hypoglycemia in the presence of inadequate food intake.

B.	Inhibition of galactose metabolism

C.	Hyperglycemia

D.	Hypomagnesemia.
3.	Protein Metabolism

A.	Increased synthesis of lipoproteins

B.	Decreased synthesis of albumin and other proteins.
4.	Lipid Metabolism

A.	Increase in liver lipids (fatty liver)

B.	Increase in serum triglycerides
5.	Increase in Lactate Production

A.	Lactic acidosis

B.	Decrease  in  uric  acid  secretion  and  resultant Hyperuricemia.
6.	Other Effects

A.	Ketoacidosis

B.	Increased catecholamine release

C.	Interference with citric acid cycle

D.	Decreased serum level of phosphate



The acute organ toxicity directly related to ethanol:

A.   	Central nervous system

	Acute intoxication syndromes Withdrawal syndromes.
B.   	Gastrointestinal system

	Acute gastritis

	Acute pancreatitis

	Acute fatty liver of alcoholism

	Alcoholic hepatitis
C.	The other common manifestations

	Alcoholic cardiomyopathy

	Alcoholic skeletal myopathy

	Hematologic abnormalities

	Endocrine disorders
The early manifestation of intoxication such as altered mood and impaired cognition are seen at an alcohol blood level of 

25 to 50  mg/dl.    Impaired performance  and judgement  are  seen in individuals with alcohol levels of 40 to 60 mg/dl.   

The legal intoxicated blood level of alcohol is 100 mg/dl. When ethanol concentration exceeds 250 mg/dl patient is at High 

risk of coma. A level about 450 to 500 mg/ml may be fatal.  The symptoms of acute ethanol ingestion are further 

complicated by the use of other drugs,  sedatives,  or other toxic alcohols such as isopropyl alcohol.
The Acute Symptoms Related to Ethanol Blood Level

	Symptoms				Concentration

						(mg per 100 ml)

	Mild muscle incoordination		50 -100 mg/ml
	Slow react ion time

	Blurred vision

	Incoordination

	Decreased inhibition			50 mg/100 ml
	Decreased motor skill			100 - 300 mg/ml
	Stupor

	Hypoglycemia

	Hypothermia				300 - 400 mg/ml
	Coma

	Respiratory failure

	Death					>400 mg/ml



The initial management of the overdosed patient is control of airways, intravenous 

fluids, drawing blood for electrolytes and alcohol  level  and drug screening,  gastric  

lavage,  activated charcoal, and close monitoring of vital signs.  If patient presents 

with altered mental status, 2 mg of Naloxone, 25 gm of glucose and 50 to 100 mg of 

thiamine should be given.  A continuous infusion of glucose saline should be 

administered with multivitamins.

Treatment of Ethyl Alcohol Overdose
	Condition     			Treatment
	Altered mental status		Naloxone

					Glucose

					Thiamine
	Hypoventilation			Mechanical

					ventilation
	Ketoacidosis			Glucose

					Normal saline
	Hypotension			Normal saline

					Trendelenburg's

					position;

					Vasopressor
Alcohol Withdrawal Seizures
The withdrawal seizures occur in an estimated 5 to 33 percent of alcoholic and consist of one or 

more generalized tonic clonic convulsion.   Since the withdrawal seizures are self-limited, patients 

generally do not need treatment.  However, patients with a prior history of seizures, Head injuries, 

status epilepticus, need treatment with intravenous Valium, Ativan and Dilantin.  A recommended 

regimen consists of intravenous Valium 2 mg every two minutes, or 1 mg of Ativan I.V., followed 

by Dilantin I.V. 40 mg per minute for a total dose of 15 mg/kg.
Delirium tremens is the most serious and delayed manifestation of ethanol withdrawal that usually 

occurs two to four days after cessation of drinking, and is characterized by severe confusion state 

with delirium, visual and sensory Hallucinations and sign of increased autonomic activities like 

tachycardia, Hyperpyrexia, and diaphoresis. The symptoms usually subside in two to three days and 

may be fatal in 5 to 15 percent of patients.
1.   I.V. Fluids

2.   Valium  5 to 10 mg or Ativan 2 mg frequent I.V. injections until symptoms subside.

3.   Haldol 5 mg I.V. every six hours as needed

4.   Propranolol 0.5 to 1 mg I.V., or 40 to 80 mg po to control tremors.

5.   Atenolol up to 100 mg po per day with Valium shorten the duration of withdrawal syndrome.
Dehydration is due to profound agitation,  decreased oral intake, and diaphoresis, and is corrected 

by I.V. fluid therapy.
Wernicke's encephalopathy is another fatal complication of alcoholism and is characterized by 

cerebellar ataxia,  mental confusion, and oculomotor disturbance. The patient should receive 100 

mg I.V. thiamine.  However, severely malnourished alcoholics might need up to 1000 mg of 

thiamine  I.V.  to reverse  the ophthalmoplegia.    Since thiamine  is a  co-factor  in glucose 

metabolism, the administration of glucose to a thiamine deficient patient may exacerbate this 

deficiency; hence, patient  should receive thiamine before glucose. Since Hypomagnesemia may 

cause thiamine resistance,  intramuscular magnesium 1 to 2 cc of 50 percent solution should be 

given with thiamine.
Drug Interaction
Ethanol is synergistic with narcotics and sedative-hypnotics. Abuse of combinations of drug with 

alcohol may lead to respiratory arrest and coma.
Disuifiram,  a drug used for detoxification,  blocks  the activity  of  the  enzyme  aldehyde  

dehydrogenase, leading  to accumulation of acetaldehyde in the blood.  Within five to ten minutes 

of ethanol ingestion, the patients on Antabuse develop headache, nausea, flushing, tachycardia, and 

hypotension secondary to vomiting and dehydration.    Treatment  is  supportive with intravenous 

fluids and norepinephrine for severe hypotension.
Isopropyl Alcohol
This is the second most commonly ingested alcohol and is present in rubbing alcohol, skin and hair 

products and antifreeze. Children  might  suffer  toxicity  from  inhalation,  and  from transdermal 

absorption during sponging
Pharmacology and Metabolism
The absorption of isopropyl alcohol is rapid, and within 30 minutes of ingestion, 80 percent of the 

alcohol circulates in the blood, leading to CNS depression. The potential lethal dose of isopropyl 

alcohol is 2 to 4 cc/kg.
		Isopropyl Alcohol

			¯ 	

					alcohol dehydrogenase

			¯ 

		     Acetone

					    ¯        ¯ 

		 Lungs  	Kidneys





Clinical Symptoms
These patients present to the emergency room with headache, dizziness, poor coordination, mental 

confusion due to alcohol and acetone.  The abdominal pain, vomiting, hematemesis, are due to 

local gastric irritation.  These patients do not have the breath odor  of  ethanol.    The  obtunded 

patients  might  also  have hypoglycemia, ketosis, myoglobinuria, and rhabdomyolysis.
Laboratory Investigations
These include CBC, electrolytes with BUN, creatinine, serum osmolality, ketones, arterial blood 

gasses, and urinalysis.
Treatment and Disposition
1.	Gastric lavage and emesis if ingestion is within two hours.

2.	Activated charcoal for multi-drug ingestion

3.	I.V.  Fluids  to  correct  high  anion  gap  acidosis  and 

	hypoglycemia

4.	Hemodialysis is indicated for serum isopropyl alcohol level 

	greater  than  400  mg/cc,   refractor  Hypotension  and 

	deteriorating vital signs.
Methanol Ingestion
Methanol is a highly toxic alcohol obtained from distillation of wood. Methanol is present in 

antifreeze and windshield washer fluid, carburetor fluids, glass cleaners, Sterno, paint strippers, 

and gasoline substitutes.  Methanol ingestion can cause serious sequelae due to multiorgan damage, 

including permanent blindness, and death.
Pharmacology and Metabolism
Methanol is rapidly absorbed from the gastrointestinal tract and blood levels peak 30 to 90 minutes 

after absorption. The smallest lethal dose reported is 15 cc of 40 percent methanol. This is 

metabolized by the liver and excreted through the kidneys.



				 Methanol
												¯ 

			       Formaldehyde
												¯ 

			       Formic acid
												¯ 

				 Folate
												¯ 
			       C02 and H20
Clinical Manifestations of Methanol Intoxication
	General

		Mental Confusion

		Metabolic acidosis

		Long latent period, often 12 to 24 hours
	Gastrointestinal

		Nausea

		Vomiting

		Severe abdominal pain

	Neurologic

		Headache

		Dizziness

		Seizures, stupor, coma

	Visual

		Diminished sensation of light

		Photophobia burred vision

		Retinal edema

		Hyperemia of optic disk

Laboratory Investigation
These include:  CBC, electrolytes, calcium, amylase, serum osmolality, ethanol and methanol 

levels, arterial blood gases and urinalysis.    A severe  anion gap metabolic  acidosis  is  the 

significant finding of methanol ingestion.
Osmolal gap = measured serum osmolality - calculated serum 

osmolality
Calculated serum osmolality (mosm/kg) = 2 (na+) + glucose + BUN

						    18	2.8
The normal osmolal gap is less than 10 mosm/1. A High osmolal gap indicates the 

presence of ethanol, ethylene glycol, methanol, isopropyl alcohol, mannitol, or glycerol in 

blood.  Patients with peak methanol level below 20 mg/di are asymptomatic; a level 

greater than 25   to 50 mg/di have serious ingestions needing therapy, and those with levels 

above 150 mg/di often die if not treated early.
These same investigations are suggested for patients with ethylene glycol ingestion and the 

treatment for these two conditions is very similar.
Ethylene Glycol Ingestion
It is a colorless, odorless substance and the ethylene glycol intoxication  is  usually due  to  

suicide  attempt,  accidental ingestion, or due to consumption as ethanol substitute.   The 

sources of ethylene glycol are: antifreeze, brake fluid, coolant, windshield fluids, some 

detergents, lacquers, and polishes.
Pharmacology and Metabolism
			Ethylene glycol

				¯ 		Alcohol dehydrogenase

			 Glycolaidehyde	
				¯ 		Alcohol dehydrogenase

										     ¯  	

			  Glycolic acid		Lactic dehydrogenase

										     ¯ 			Glycolic acid oxidase
				¯ 

Pyridoxine		Glyoxylic acid		Thiamine

	  ¯ 			¯ 			   ¯ 		¯ 

Glycine      ¿ 	  Oxalic acid	Formic acid    aHydroxy-

					       bKetoadipate		


	Stage I				(30 minutes to 12 hours)

					Intoxicated patient with no alcohol odor

					Nausea and vomiting

					Metabolic acidosis

					Crystalluria

					Myoclonus

					Seizure and death
	Stage II			(12 to 24 hours)

					Tachypnea, tachycardia

					Hypertension

					Cyanosis

					Pulmonary edema

					Bronchopneumonia

					Cardiac Enlargement
	Stage III			(36 to 48 hours)

					Crystalluria

					Costovertebral angle tenderness

					Tubular necrosis with oliguria

					Renal failure
Treatment of Methanol and Ethylene Glycol Toxicity
1.   Prevent further absorption by Ipecac or lavage, activated charcoal and cathartics.

2)   Alkalinization by 2  to  3  mg/kg of  intravenous  sodium bicarbonate.

3.   Ethanol therapy

4.   Calcium chloride I.V.  gm for ethylene glycol ingestion.

5.   Thiamine 50 mg to 100 mg for ethylene glycol

6.   pyridoxine 2 to 5 gm I.V. for ethylene glycol

7.   Folic acid 50 to 100 mg I.V. for methanol

8.   Dialysis
Ethyl Alcohol Therapy
Ethyl alcohol therapy is suggested for management of ethylene glycol and methanol ingestion because it completes with alcohol 

dehydrogenase--the enzyme responsible for breakdown of methanol and ethylene glycol.  Ethyl alcohol saturates this enzyme, increases 

the half-life of ethylene glycol from 3 to 17 Hours.   Therefore, the administration of ethanol leads to increased excretion of unchanged 

compound through kidneys, hence prevents the body organ damage due to toxic metabolites.



	Dose		95% Ethanol	40% Ethanol	10% Ethanol

	Loading		1 cc/kg		2.5 cc/kg	100 cc/kg
	Maintenance

	w/o dialysis	0.1 cc/kg/hr	0.3 cc/kg/hr	l cc/kg/Hr
	Maintenance

	with dialysis	0.3 cc/kg/hr	1 cc/kg/hr	3 cc/kg/hr



In summary,  the author has discussed the management of ethanol, isopropyl alcohol, methanol, 

ethylene glycol poisonings with particular emphasis on early diagnosis and proper management of 

these patients.  The Hospitalization, psychiatric, and social service evaluations should be made on 

these overdosed patients with proper emphasis on long-term management and guidance of the 

patient.