Toxicology symposia Review Article

Toxic alcohols
Meera Ekka, Praveen Aggarwal
Abstract
Ethanol ingestion with alcoholic intoxication is one of the commonest emergencies followed by alcohol
withdrawal syndrome in chronic alcoholics presenting to the emergency department with medical conditions.
Isolated toxic alcohol (other than ethanol) ingestion cases may report to the emergency department when
inadvertently methanol or ethylene glycol is ingested. In areas with prohibition occasionally outbreaks of toxic
alcohol ingestion are observed. As an emergency physician, it is important to identify toxic alcohol ingestion as
timely treatment will prevent morbidity and mortality.

Keywords: Alcohol ingestion, ethylene glycol, methanol, toxic alcohol

Introduction as ethanol greatly increases the risk of trauma,

especially trauma due to motor vehicle collisions or
The term toxic alcohol has generally referred to violent crimes.[2]
isopropanol, methanol, and ethylene glycol (EG).[1]
However, any alcohol can be toxic if ingested in large Toxicokinetics
quantities. Early recognition and treatment of patients Ethanol is rapidly absorbed across both the gastric
intoxicated with these substances in the emergency mucosa and the small intestines, reaching a peak
department (ED) can reduce the morbidity and concentration 20-60 min after ingestion. Once
mortality associated with these alcohols. absorbed, it is converted to acetaldehyde by the enzyme
alcohol dehydrogenase (ADH). Acetaldehyde is then
Ethyl Alcohol (Ethanol) converted to acetate, which is converted to acetyl CoA,
and ultimately carbon dioxide and water.[3]
Ethanol is a low molecular weight hydrocarbon.
Genetic polymorphisms coding for ADH, the amount
It is widely available both as a beverage and as
of alcohol consumed, and the frequency at which
an ingredient in food extracts, cough and cold
ethanol is consumed all affect the speed of metabolism.
medications, and mouthwashes. Ethanol intoxication
Chronic alcoholics and those with severe liver disease
is common in modern society, largely because of its
have increased rates of metabolism. However, drinkers
widespread availability. It is a common co-ingestant who do not chronically abuse the ethanol eliminate
in suicide attempts. The morbidity is often from it at a rate of 15 mg/dL/h, whereas chronic abusers
co-ingestants or coexisting injuries and illnesses eliminate it around 20-25 mg/dL.
Access this article online
Quick Response Code: Clinical features
Website:
[Link] Acute alcohol intoxication is defined as the pathological
state produced by the ingestion of alcohol. Binge
drinking, which is generally defined as consuming 5
DOI:
10.4103/0971-9903.151733 alcoholic drinks on a single occasion, generally results
in acute intoxication.[4] The character of symptoms

Department of Emergency Medicine, All India Institute of Medical Sciences, New Delhi, India

Address for correspondence:

Dr. Praveen Aggarwal, Department of Emergency Medicine, All India Institute of Medical Sciences, New Delhi, India.
E-mail: peekay_124@[Link]

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Ekka and Aggarwal: Toxic alcohols 39

associated with intoxication varies with severity and primarily supportive. Hypoglycemia and respiratory
symptoms depend on both the serum concentration depression are two important issues to address
as well as the pattern of drinking. Levels <25 mg/dL promptly. Hypoglycemia should be promptly
are associated with a sense of warmth and well-being. detected by rapid bedside glucose determination in
Euphoria and decreased judgment occur at levels all intoxicated patients and should receive dextrose
between 25 and 50 mg/dL. At levels of 50-100mg/dL, infusion. Patients presenting with coma should
incoordination, decreased reaction time/reflexes, and receive at least 100 mg of parenteral thiamine
ataxia occur. Cerebellar dysfunction (i.e., ataxia, slurred to prevent or treat Wernickes encephalopathy,
speech, nystagmus) are common at levels of 100-250 mg/ along with dextrose. Intravenous (IV) crystalloids
dL. Coma can occur at levels of >250 mg/dL, whereas and vasopressures are used to treat hypotension,
respiratory depression, loss of protective reflexes, and if present. Patient with altered sensorium can be
death occurs at levels >400 mg/dL. Hypotension and agitated, violent, and uncooperative. Chemical
tachycardia may occur as a result of ethanol-induced sedation like benzodiazepines may be needed to
peripheral vasodilation, or secondary to volume loss. prevent the patient from harming themselves or
[5]
Acute alcohol intoxication can also induce multiple others. However, caution must be taken as these
metabolic derangements, including hypoglycemia, drugs can worsen the respiratory depression caused
lactic acidosis, hypokalemia, hypomagnesemia, by alcohol. Metadoxine, is a new, specific drug
hypocalcemia, and hypophosphatemia.[6] Children are useful in the treatment of acute alcohol intoxication,
at higher risks of developing hypoglycemia following which accelerate ethanol excretion.[6]
a single ingestion than are adults.
Complications
Laboratory investigations Hypoglycemia is common. Holiday heart syndrome
The single most important laboratory test in a patient may occur in patients with acute intoxication, in which
who appears intoxicated with ethanol is a blood dysrrhythmias, especially atrial fibrillation, occur.
glucose level by bedside finger prick test. Serum Other complications in heavy intoxications include
ethanol concentration and basic electrolytes, blood acute pancreatitis, severe myocardial depression,
gas analysis is also required though measurement of Hypotension, lactic acidosis, pulmonary edema,
serum ethanol concentrations is controversial and is cardiovascular collapse, and sudden death.
not readily available in many centers. Anion gap (AG)
and osmolal gap (OG) should be calculated to rule Isopropanol
poisoning with other toxic alcohols. Urine drug testing Isopropanol is a clear, colorless liquid with a fruity
should be done to rule out other coingestants. odor and a mild bitter taste. Most commonly found
domestically as rubbing alcohol, isopropanol is
Diagnosis also found in numerous household and commercial
Alcohol intoxication as a cause of altered mental status products including cleaners, disinfectants, antifreezes,
is a diagnosis of exclusion and should be considered cosmetics, solvents, inks, and pharmaceuticals. The
only after ruling out more serious conditions such as majority of isopropanol exposures are suicidal, but,
head trauma, hypoxia, hypoglycemia, hypothermia, unintentional in children <6 years of age can occur.
hepatic encephalopathy, and other metabolic and Although isopropanol poisoning appears to be a
physiologic derangements. However, intoxication can reasonably common occurrence, deaths are rare,
be diagnosed more typically by history of ethanol intake, but can result from injury due to inebriant effects,
clinical presentation and by using the measurement of untreated airway compromise due to coma, or rarely,
serum ethanol concentrations. However, routine use of cardiovascular depression and shock following massive
a serum blood alcohol level is controversial, largely ingestion. Supportive care can avert most morbidity
because it is unlikely to affect management in a patient and mortality.
who is awake and alert.
Toxicokinetics
Management in the emergency department Isopropanol is rapidly and completely absorbed
Initial treatment should be focused on the airway, following ingestion with peak plasma concentrations
breathing, and circulation. Gastric decontamination occurring within 30 min. Significant absorption
is rarely necessary for any of the alcohols. The can occur following inhalation or dermal exposure,
treatment for isolated acute ethanol intoxication is especially in infant.[7] Isopropanol is metabolized by

March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
40 Ekka and Aggarwal: Toxic alcohols

ADH to acetone. The elimination of isopropanol is and OG, blood urea nitrogen, and creatinine, serum and
predominantly renal though some pulmonary excretion urine ketones and Arterial or venous blood gas analysis
of isopropanol and acetone occur. In the absence should be done.
of ethanol or fomepizole, the elimination half-life
of isopropanol is between 2.5 and 8.0 h, whereas Diagnosis
elimination of acetone is slower with a half-life Poisoning can be diagnosed using the measurement
following the isopropanol ingestion of between 7.7 and of isopropanol serum concentrations though these
27 h.[8] Both isopropyl alcohol and acetone are rapidly may not be readily available and also of limited value.
cleared by hemodialysis, with clearance rates in excess Diagnosis is, therefore, more typically made on the
of 200 mL/min.[9] basis of the patients history and clinical presentation.
An osmol gap, ketonemia, and/or ketonuria without
Mechanisms of toxicity metabolic acidosis, along with a fruity or sweet odor on
Isopropanol is a central nervous system (CNS) inebriant the breath and CNS depression support the diagnosis.
and depressant; brain stem depression is thought to be Ketone usually present in the serum as early as 30min
the predominant mechanism. In addition, it is irritating after ingestion. If there is no coexisting ethanol
to the GI tract causing hemorrhagic gastritis. Acetone ingestion, the absence of ketones effectively rules
itself is a mild CNS depressant and may exacerbate out the isopropanol ingestion.[11] However, starvation,
the CNS depression caused by isopropyl alcohol. The alcoholic and diabetic forms of ketoacidosis presenting
most common metabolic effects are an increased OG, with depressed mental status and ketosis should be
ketonemia and ketonuria without any AG metabolic ruled out in these patients.[10]
acidosis unlike the toxic alcohols (methanol and EG).
The absence of a high AG metabolic acidosis 4-6 h Management
postingestion is useful to distinguish isopropyl alcohol Supportive care is the mainstay of management with
from methanol or EG intoxication in most cases. The primary emphasis on assessment and stabilization of
lethal dose is 250 mL in humans estimated from various the airway, breathing, and circulation.
sources.
Decontamination
Clinical features There is no role for gastrointestinal (GI) decontamination
Clinical manifestations include varying degrees in most cases of isolated isopropyl alcohol intoxication.
of CNS depression, ranging from inebriation with Activated charcoal may be useful for coingestants.
disinhibition, sedation, stupor and coma.[10] These
effects, due primarily to the parent alcohol, develop Antidote
shortly after exposure, and peak within the 1st h after The primary metabolite acetone is less toxic than
ingestion, however, its metabolite acetone, causes less isopropyl alcohol. Hence, there is no indication for
sedation. Steady improvement in the patients level of ADH inhibition with fomepizole or ethanol following
consciousness is the expected clinical course in mild to isopropyl alcohol exposure.[12] Because of the
moderate poisoning. Severe poisoning due to massive hemorrhagic gastritis that can follow the isopropanol
ingestion present as coma, respiratory depression, ingestion, H2 blockade or proton-pump inhibitors may
hematemesis, pulmonary edema, hemorrhagic be helpful.
tracheobronchitis, shock, and circulatory collapse.
Isopropanol concentrations of 50-100 mg/dL typically Hemodialysis
result in intoxication, which can progress to dysarthria Rare patients with massive intentional ingestions
and ataxia. Lethargy and coma can be seen with levels may be hemodynamically unstable despite IV fluids
above 150 mg/dL. Cardiovascular collapse can occur and vasopressors. These patients with hemodynamic
with levels exceeding 450 mg/dL.[11] instability despite aggressive fluid resuscitation may
require hemodialysis.[9]
Laboratory studies
The following tests and calculations should also be Complications
performed in patients suspected of ingesting isopropyl Severe isopropanol poisoning results in coma,
alcohol: Serum isopropyl alcohol and acetone levels respiratory depression, hematemesis due to
(or serum osmolality if direct serum drug levels are hemorrhagic gastritis, pulmonary edema hemorrhagic
unavailable). Basic electrolytes, with calculation of AG tracheobronchitis, shock, and circulatory collapse.[10]

Journal of Mahatma Gandhi Institute of Medical Sciences March 2015 | Vol 20 | Issue 1
Ekka and Aggarwal: Toxic alcohols 41

Methyl Alcohol stage toxic metabolites are formed.[1] The main systems
involved in methanol toxicity are the neurologic,
Methyl alcohol is widely used as a solvent in many gastroenterologic, and ophthalmologic systems. Eye
household products, such as antifreeze, cleaning involvement is seen approximately in (50%) of patients
solutions, dyes and paint remover. It is also used in and is associated with high methanol intake manifesting
photocopying fluid, shellacs, and windshield-washing at 6 h or more postingestion may be delayed up to 24h.
fluids. Consumption of illegally produced or homemade Eye symptoms include blurred vision, photophobia,
alcoholic beverages containing relatively high levels of visual hallucination (often described as a snow field),
methanol poses risk and had caused several outbreaks partial to complete visual loss which are reversible in
in the past.[13] Poisoning may occur through accidental many patients in the early stage.[14] Ocular examination
ingestion, attempted inebriation or suicide attempt. may reveal dilated pupils minimally or unreactive to light
It can also occur from prolonged inhalation or skin with hyperemia of the optic disc, nystagmus, papilledema,
absorption. Methyl alcohol poisoning is associated retinal edema and hemorrhages; but, over several days,
with significant morbidity and mortality. the red disc becomes pale, and the patient become blind.
Permanent visual sequelae have been described in severe
Toxicokinetics intoxication.[15] Regarding CNS symptoms, patient often
Methanol is rapidly absorbed from the gastric mucosa, alert on presentation. However, altered sensorium,
and achieves a maximal concentration 30-90 min after confusion, severe headache, lethargy and ataxia are
ingestion. Methanol is primarily metabolized in the not uncommon. In severe cases, coma and seizures
liver via ADH into formaldehyde. Formaldehyde is may occur. Parkinson-like extrapyramidal (magnetic
subsequently metabolized via aldehyde dehydrogenase resonance imaging and/or computed tomography of
into formic acid, which ultimately is metabolized the brain may reveal basal ganglia infarct) symptoms
to folic acid, folinic acid, carbon dioxide, and water. have also been reported.[16] Gastroenterological
A small portion is excreted unchanged by the lungs. manifestations include nausea, vomiting, flank pain,
Methanol undergoes zero-order metabolism, and is abdominal pain, GI hemorrhage, diarrhea, liver function
excreted at a rate of 8.5 mg/dL/h to 20 mg/dL/h in the abnormalities, and pancreatiti.[17] Patient may also
absence of competitive inhibition. In the presence of complain of breathlessness related to hyperventilation
competitive inhibitors like ethanol or fomepizole, the as a consequence of severe metabolic acidosis.
metabolism changes to first order. In this later scenario,
the excretion half-life ranges from 22 to 87 h. Ethylene Glycol
Mechanism of toxicity Ethylene glycol is a colorless, odorless, sweet tasting
Formic acid, the major toxic metabolite of methanol liquid, which is used in many manufacturing processes
is responsible for the majority of the toxicity. This and is a common component of antifreeze and de-icing
toxic metabolite is primarily responsible for the solutions around the house. Its a low molecular weight
retinal and optic nerve damage as well as metabolic toxic alcohol that can result in serious morbidity and
acidosis may be caused by disruption of mitochondrial mortality.
electron transport. Specific changes can occur in the
basal ganglia in the later stages. There are reports of Toxicokinetics
pancreatitis with this poisoning. The lethal dose of pure Ethylene glycol itself is nontoxic; but, its metabolic
methanol is estimated to be 1-2 mL/kg bodyweight.[1] byproducts are toxic. EG is oxidized via ADH into
However, there are reports of permanent blindness and glycoaldehyde. Glycoaldehyde subsequently undergoes
deaths with 0.1 mL/kg bodyweight.[1] metabolism via aldehyde dehydrogenase into glycolic
acid.[18] The glycolic acid is converted to glyoxylic
Clinical features acid. This is slower process and the rate-limiting step in
Onset of symptoms ranges from 40 min to 72 h with an the metabolism of EG. Glyoxylic acid is subsequently
average of 24 h depending on the co-ingestion of ethanol metabolized into oxalic acid. The excretion half-life of
as ethanol ingestion delayed the manifestation. Unlike EG is approximately 3h in patients with normal renal
ethanol or isopropanol, it does not cause as much of an function in absence of ethanol or fomepizole. However,
inebriated state.[11] Early stage are mild and transient, in the presence of these two antidotes, ADH undergoes
manifesting as mild euphoria or inebriation, followed competitive inhibition, and the resulting excretion half-
by a latent phase lasting from 6 to 30 h and during this life increases to approximately 17-20 h.[11]

March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
42 Ekka and Aggarwal: Toxic alcohols

Mechanism of toxicity progress, the OG decreases, and AG increases due to

The main toxicity of EG is related to the production accumulation of toxic metabolites. In the last stage,
of oxalic acid and glycolic acid. The toxicity occurs only AG remains high and OG normalized.[14] If the
from both the ensuing metabolic acidosis as well as the AG is unexplained and other possible causes have been
oxalate itself. The oxalic acid combines with calcium excluded, methanol poisoning should be suspected
to form insoluble calcium oxalate crystals, occasionally and considered for empiric treatment of toxic alcohol
leading to hypocalcemia. Hypocalcemia can cause poisoning.[25] In EG poisoning, needle shaped and
coma, seizure and dysrhythmias. These calcium oxalate envelop shaped oxalate crystal may be present in
crystals deposit in various organs causing acute renal urine.[20]
failure and myocardial, neurological and pulmonary
dysfunction.[19,20] Lethal dose vary depending on the Treatment of methanol and ethylene glycol
individual susceptibility to the adverse effects of EG. poisoning
In human, it is reported to be 1.5 mL/kg body weight.[20] Methanol or EG poisoning is a lethal condition needs
immediate resuscitation in the ED. Moderate poisoning
Clinical features required management in ward. However, severe and
Acute EG toxicity can occur through three distinct life threatening poisoning required intensive care in
stages.[11] The first stage (neurologic phase: CNS the Intensive Care Unit (ICU). Prompt consultation
depression), can occur within 30 min up to 12 h. with a poison control center is strongly recommended.
During this stage, the patient appears inebriated, mild Treatment is divided into four categories. It includes
confusion or stupor may be present. The patient may gastric decontamination, general supportive care, use
not have any other significant findings during this of antidotes, and hemodialysis.
stage. Occasionally, hypocalcemia can occur at this
point and induce muscle spasms and abnormal reflexes. Gastric decontamination
As the intoxication progresses, neurological symptoms Gastric decontamination: gastric lavage or activated
can become more profound. EG may cause severe charcoal is not recommended as absorption rate is very
neurological deficits, and even mimic a clinical state rapid.
of brain death.[21] The second stage (cardiopulmonary
stage), occurs between 12 and 24 h after ingestion. General supportive care
During this stage, the patient commonly develops mild It includes IV fluids, mechanical ventilation, sodium
tachycardia and hypertension. Acute respiratory distress bicarbonate therapy, calcium gluconate (in EG)
syndrome can also occur. Significant hypocalcemia and vasopressor indicated in severe poisoning. The
can occur leading to hyperreflexia and arrhythmias.[22] administration of sodium bicarbonate is recommended
Metabolic acidosis arises and patient compensate by in case of severe acidosis (pH 7.3) liberally.[22] Severe
hyperventilation at this stage. The third stage (renal hypocalcemia, due to formation of oxalate crystal,
stage), typically starts after 24-72 h. During this stage, causing symptoms such as muscle spasms or seizures
acute renal failure and flank pain manifest. In severe required calcium gluconate therapy.[22]
intoxication, renal failure appears early and progress to
anuria and in severe cases multiorgan failure and death Therapy with antidotes
can occur.[23] Antidotes are most effective when given in the early
phase of the intoxication, before significant levels
Laboratory studies in ethylene glycol of toxic metabolites are formed. Antidotes therapy
andmethanol poisoning increases the half-life of EG and methanol and prevent
Serum methanol concentration should be obtained, formation of toxic metabolites. Currently, only two
usually determined by gas chromatography, but this antidotes are approved and used to block ADH-
technique is not widely available on 24 h basis in the mediated metabolism of EG and methanol: Ethanol, a
ED. The measurement of OG and AG can be useful in competitive ADH substrate, and fomepizole, an ADH
the diagnosis. In the early phase of intoxication, serum inhibitor.
osmolality can be increased due to increase in methanol
level. An unexplained, large OG is presumptive Criteria for initiating antidotes therapy in EG and
evidence of recent methanol exposure.[24] The higher methanol poisoning include:[22-24] (1) Documented
OG, especially if 20 mOsm/L, is specific for the plasma concentration 20 mg/dL, or (2) documented
presence of alcohol.[25] As the metabolism of methanol recent history of ingesting toxic amounts of EG/

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Ekka and Aggarwal: Toxic alcohols 43

menthol and OG 10 mOsm/L, or (3) suspected EG/ removing both the parent compound and its toxic
methanol ingestion and at least 3 (for EG) or 2 (for metabolites, to correct metabolic acidosis, and
methanol) of the following criteria: A. Arterial pH electrolyte disturbances, thus reducing the duration
<7.3, B. Serum bicarbonate <20 mmol/l, C. OG >10 of hospitalization and antidotal treatment.[22] Current
mOsm/L and d. oxalate crystalluria (for EG only). indications for HD based on clinical experience only
includes:
Fomepizole: Dosing scheme[22,23] 1. Arterial pH <7.3,
For patients not on hemodialysis 2. A decline of arterial pH >0.05 despite bicarbonate
Loading dose 15 mg/kg, followed by 10 mg/kg therapy,
12hourly for 4 doses. After 48 h, dose should be 3. pH <7.3 despite bicarbonate therapy,
increased to 15 mg/kg every 12 hourly. All doses are 4. Initial plasma EG or Methanol concentration
administered intravenously over 30 min.[22,23] 50mg/dL,
5. Renal failure,
For patient undergoing hemodialysis: Two proposed 6. Electrolyte imbalances unresponsive to
protocols[22,23] conventional therapy,
1. A reduction in time interval between fomepizole 7. Deterioration of vital signs despite intensive
doses: Loading dose 15 mg/kg followed by supportive care, and
10mg/kg every 6 hourly for 4 doses and then 8. Visual disturbances (in methanol poisoning).[11,22,23]
4hourly.[22,23]
2. A continuous IV infusion of 1-1.5 mg/kg/h Adjunctive (co-factor) therapies
following the initial loading dose of 15 mg/kg.[22,23] In methanol poisoning, folinic acid or folic acid (if
folinic acid is not available) should be administered at
Adverse effect of fomepizole a dose of 1 mg/kg, with a maximum does of 50 mg
Fomepizole is generally well tolerated. However, every 4 hourly. Folinic acid augment the conversion
injection site irritation, dizziness, tachycardia, of formic acid to carbon dioxide and water by the
headache, transaminitis, agitation and seizure are tetrahydrofolate synthetase, an enzyme dependent
reported.[22,23] on folinic acid. In EG poisoning, Thiamine 100 mg
intravenously every 6 hourly and pyridoxine 50 mg
Ethanol every 6 hourly should be given to shunt metabolism
It is indicated for patients with a known fomepizole of glyoxilic acid away from oxalate and favor the
allergy, or during nonavailability of fomepizole. IV formation of less toxic metabolites.[23,26]
administration is preferred.
Preferred antidote: Ethanol versus fomepizole
Dosing scheme Fomepizole has higher potency to inhibit ADH
Target ethanol concentration is 100-150 mg/dL with longer duration of action, administration is
(1-1.5%). easy, dosing schedule is simple, may obviate the
need for hemodialysis in specific cases, and most
Loading dose important there is no need for fomepizole blood
7.5-12.5 mL ethanol 10% solution in glucose/kg concentration and blood glucose monitoring as
intravenously (0.6-1.0 g/kg) or 2.5 mL/kg orally 40% required in ethanol. Therefore, has low overall
ethanol solution. cost and better safety consideration. These
are the reasons to prefer for fomepizole as an
Maintenance dose (intravenously) antidote instead of ethanol according to clinician
1.4 mL ethanol 10% solution in glucose/kg/h. During preference.[14] However, in one systemic review on
hemodialysis (an additional dose of 1.9 mL ethanol use of ethanol or fomepizole, the conclusion was
10% solution in glucose/kg/h should be administered inconclusive.[27]
intravenously). In adult, 3.3 mL ethanol 10% solution
in glucose/kg/h. Ethanol therapy is labor intensive, require intensive
ICU monitoring. The overall cost of therapy is
Hemodialysis higher than fomepizole when the cost of frequent
It is considered the key element for the treatment in glucose monitoring and measurement of blood
severe EG and methanol poisoning and aimed at ethanol concentrations are accounted. Again

March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences
44 Ekka and Aggarwal: Toxic alcohols

in chronic alcoholics and during hemodialysis, 7. Leeper SC, Almatari AL, Ingram JD, Ferslew KE. Topical
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Source of Support: Nil, Conflict of Interest: No conflict of interest.
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March 2015 | Vol 20 | Issue 1 Journal of Mahatma Gandhi Institute of Medical Sciences