INTOKSIKASI ALKOHOL

Background
Although any alcohol can be toxic if ingested in large enough quantities, the term toxic alcohol
has traditionally referred to isopropanol, methanol, and ethylene glycol.[1] Prompt recognition and
treatment of patients intoxicated with these substances can reduce the morbidity and mortality
associated with these alcohols.
This article discusses not only the three toxic alcohols but also ethanol. For discussion of the
individual agents, see Methanol Toxicity and Ethylene Glycol Toxicity; for discussion of
pediatric ethanol ingestion, see Ethanol Toxicity. Ethanol withdrawal is a serious and potentially
life-threatening problem, which is discussed in Withdrawal Syndromes.

Pathophysiology

Ethanol
Ethyl alcohol (ethanol; CH3 -CH2 -OH) is a low molecular weight hydrocarbon that is derived
from the fermentation of sugars and cereals. It is widely available both as a beverage and as an
ingredient in food extracts, cough and cold medications, and mouthwashes.
Ethanol is rapidly absorbed across both the gastric mucosa and the small intestines, reaching a
peak concentration 20-60 minutes after ingestion. Once absorbed, it is converted to acetaldehyde.
This conversion involves three discrete enzymes: the microsomal cytochrome P450 isoenzyme
CYP2E1, the cytosol-based enzyme alcohol dehydrogenase (ADH), and the peroxisome catalase
system. Acetaldehyde is then converted to acetate, which is converted to acetyl Co A, and
ultimately carbon dioxide and water.[2]
Genetic polymorphisms coding for alcohol dehydrogenase, the amount of alcohol consumed, and
the rate at which ethanol is consumed all affect the speed of metabolism. Chronic alcoholics and
those with severe liver disease have increased rates of metabolism. However, as a general rule,
ethanol is metabolized at a rate of 20-25 mg/dL in the nonalcoholic but at an increased rate in
chronic alcoholics.
Isopropanol
Isopropyl alcohol (isopropanol; CH3 -CHOH-CH3) is a low molecular weight hydrocarbon. It is
commonly found as both a solvent as well as a disinfectant. [3] It can be found in many
mouthwashes, skin lotions, rubbing alcohol, and hand sanitizers. Because of its widespread
availability, lack of purchasing restrictions, and profound intoxicating properties, it is commonly
used as an ethanol substitute.
Isopropanol is rapidly absorbed across the gastric mucosa and reaches a peak concentration
approximately 30-120 minutes after ingestion. Isopropanol is primarily metabolized via alcohol
dehydrogenase to acetone. A small portion of isopropanol is excreted unchanged in the urine.
The peak concentration of acetone is not present until approximately 4 hours after ingestion. The
acetone produces CNS depressant effects and a fruity odor on the breath.[4]

1
Methanol
Methyl alcohol (methanol; CH3 OH) is widely used as an industrial and marine solvent and paint
remover. It is also used in photocopying fluid, shellacs, and windshield-washing fluids. Although
toxicity primarily occurs from ingestion, it can also occur from prolonged inhalation or skin
absorption.[5, 6, 7] Methanol is rapidly absorbed from the gastric mucosa, and achieves a maximal
concentration 30-90 minutes after ingestion.[8]
Methanol is primarily metabolized in the liver via alcohol dehydrogenase into formaldehyde.
Formaldehyde is subsequently metabolized via aldehyde dehydrogenase into formic acid, which
ultimately is metabolized to folic acid, folinic acid, carbon dioxide, and water. A small portion is
excreted unchanged by the lungs.
Formic acid is responsible for the majority of the toxicity associated with methanol. Without
competition for alcohol dehydrogenase, methanol undergoes zero-order metabolism, and is thus
is excreted at a rate of 8.5 mg/dL/h to 20 mg/dL/h. Once methanol experiences competitive
inhibition, from either ethanol or fomepizole, the metabolism changes to first order. In this later
scenario, the excretion half-life ranges from 22-87 hours.
Ethylene glycol
Ethylene glycol (CH2 OH-CH2 OH) is an odorless, colorless, sweet-tasting liquid, which is used
in many manufacturing processes. Domestically, it is probably most commonly encountered in
antifreeze. It is absorbed somewhat rapidly from the gastrointestinal tract, and peak
concentrations are observed 1-4 hours after ingestion.[7]
Ethylene glycol itself is nontoxic, but it is metabolized into toxic compounds. Ethylene glycol is
oxidized via alcohol dehydrogenase into glycoaldehyde, which then undergoes metabolism via
aldehyde dehydrogenase into glycolic acid.[9] The conversion to glycolic acid is somewhat rapid.
In contrast, the conversion of glycolic acid to glyoxylic acid is slower and is the rate-limiting
step in the metabolism of ethylene glycol.
Glyoxylic acid is subsequently metabolized into several different products, including oxalic acid
(oxalate), glycine, and alpha-hydroxy-beta-ketoadipate. The conversion to glycine requires
pyridoxine as a cofactor, while the conversion to alpha-hydroxy-beta-ketoadipate requires
thiamine as a cofactor. The oxalic acid combines with calcium to form calcium oxalate crystals.
In the presence of normal renal function and no competitive inhibition for alcohol
dehydrogenase, the excretion half-life of ethylene glycol is approximately 3 hours. However, in
the presence of fomepizole or ethanol, alcohol dehydrogenase undergoes competitive inhibition,
and the resulting excretion half-life increases to approximately 17-20 hours.

Epidemiology
Frequency
Alcohol intoxication is common in modern society, largely because of its widespread availability.
More than 8 million Americans are believed to be dependent on alcohol, and up to 15% of the
population is considered at risk. In some studies, more than half of all trauma patients are
intoxicated with ethanol at the time of arrival to the trauma center. In addition, ethanol is a
common coingestant in suicide attempts.

2
Mortality/Morbidity
Acute intoxication with any of the alcohols can result in respiratory depression, aspiration,
hypotension, and cardiovascular collapse.
Ethanol
Although many patients present with ethanol intoxication as their sole issue, many other patients
have ethanol intoxication as part of a larger picture. Thus, the morbidity is often from
coingestants or coexisting injuries and illnesses.
Chronic use results in hepatic and gastrointestinal injuries. Coma, stupor, respiratory depression,
hypothermia, and death can result from high concentrations of acute ethanol intoxication.
Chronic alcoholics, as well as children, are at risk for hypoglycemia.
Isopropanol, methanol, and ethylene glycol
In 2012, 16,458 cases of isopropanol ingestions, 8773 cases of isopropanol toxicity (from
sources including rubbing alcohol, cleaning agents, and hand sanitizers) were reported to US
Poison Control Centers. Of these, 65 patients were classified as experiencing "major" morbidity,
with one patient dying.[10]
In the same year, 1,612 cases of methanol ingestion and 5,869 cases of ethylene glycol ingestion
were reported. Of those intoxicated with methanol, 26 patients were classified as experiencing
"major" disability, and 6 additional patients died. For those patients who were intoxicated with
ethylene glycol, 205 patients were classified as having "major" disability, with an additional 23
patients dying.[10] It is important to recognize that these numbers likely underestimate the true
incidence of exposure, however, because of both a failure to recognize the ingestion as well as a
failure to report the suspected or known ingestion to a poison control center.
The primary toxicity with isopropanol is CNS depression. These CNS manifestations can include
lethargy, ataxia, and coma. In addition, isopropanol is irritating to the GI tract. Therefore,
abdominal pain, hemorrhagic gastritis, and vomiting can be observed. Unlike methanol and
ethylene glycol, isopropanol does not cause a metabolic acidosis.
The toxicity with methanol occurs from both the ensuing metabolic acidosis, as well as the
formate anion (formic acid) itself.[11] Although the eye is the primary site of organ toxicity, in the
later stages of severe methanol toxicity, specific changes can occur in the basal ganglia as well.
Pancreatitis has been reported following methanol ingestion. Hyperventilation will occur as a
compensatory mechanism to counteract the acidosis.
As previously stated, ethylene glycol itself is nontoxic. The majority of the metabolic acidosis
occurs from glycolic acid. One form of morbidity occurs when oxalate combines with calcium to
form calcium oxalate crystals, which accumulate in the proximal renal tubules, thereby inducing
renal failure. Hypocalcemia can ensue, and cause coma, seizures, and dysrhythmias. Autopsy
studies have confirmed that the calcium oxalate crystals are deposited not only in the kidneys but
in many other organs, including the brain, heart, and lungs.
Age
Ethanol intoxication is common in older teenagers through adulthood. The toxic dose for an adult
is 5 mg/dL, whereas the toxic dose in a child is 3 mg/dL. Children are at higher risks of
developing hypoglycemia following a single ingestion than are adults.

3
Most isopropanol ingestions occur in children younger than 6 years. Most methanol and ethylene
glycol ingestions occur in adults older than 19 years.

History
A history of inebriation with associated slurred speech, ataxia, and impaired judgment is
common in the initial stages of intoxication of each of these alcohols. Depending on the dose
ingested, this may be followed by progressive levels of CNS depression, coma, and premorbid
multiorgan failure. The history that can be obtained varies with the timing of presentation. The
onset of the later stages of toxic alcohol intoxication can also be delayed if ethanol is coingested,
prolonging the time it takes to develop metabolic acidosis and other symptoms. The following
focuses on symptoms that may be unique to each alcohol.
Ethanol ingestion
The history itself can often point to a diagnosis of ethanol intoxication. An associated history of
chronic alcoholism alters metabolism, associated comorbidities, and the expected course of
recovery. A detailed discussion of this topic is beyond the scope of this article (see Ethanol
Toxicity).
Attempting to elicit what has changed recently may reveal the immediate reason for presentation.
A history of coingestants may also alter the patient's course.
Isopropanol ingestion
Following an isopropanol ingestion, the patient may not complain of anything specific. Rather,
the patient may simply appear intoxicated, as with ethanol intoxication.
A history of abdominal pain, nausea, and sometimes hematemesis may be obtained.
Methanol ingestion
Following methanol ingestion, a patient is initially inebriated as with the other alcohols. Other
symptoms can be delayed for up to 12-24 hours.
The patient may complain of headache, nausea, or anorexia. Occasionally, the patient may
complain of shortness of breath related to hyperventilation.
Because one of the primary end-organs involved in methanol is the eye, the patient may
complain of difficulty seeing. Specifically, vision is often described as a "snow field," though a
variety of visual complaints may be verbalized.
Ethylene glycol ingestion
Ethylene glycol toxicity occurs in three stages, as follows:
The first stage, called the neurologic phase, can occur in less than 1 hour after ingestion
and lasts up to 12 hours. During this stage, the patient appears inebriated. The patient
may not have any other significant findings during this stage. Occasionally, hypocalcemia
can occur at this point and induce muscle spasms and abnormal reflexes.
The second stage, which occurs between 12 and 24 hours after ingestion, is referred to as
the cardiopulmonary stage. During this stage, the patient frequently develops mild
tachycardia and hypertension. Acute respiratory distress syndrome (ARDS) can also

4
 occur. These findings are believed to result from calcium oxalate crystal deposition in the
lung parenchyma and myocardium. Significant hypocalcemia can occur at this stage, with
QT prolongation and associated arrhythmias. Expect hyperventilation as metabolic
acidosis progresses.
The third stage, also called the renal stage, typically starts after 24 hours. During this
stage, flank pain and acute renal failure can occur. A premorbid patient with ethylene
glycol toxicity typically presents comatose, hyperventilating, and in multiorgan failure.

Physical
See the list below:
Ethanol ingestion
o The symptoms of ethanol intoxication depend on both the serum concentration as
well as the frequency at which an individual ingests ethanol. Thus, a person who
consumes large amounts of ethanol on a daily basis may appear sober at the same
serum ethanol level at which a novice drinker exhibits cerebellar dysfunction.
o As a general rule, levels less than 25 mg/dL are associated with a sense of warmth
and well-being. Euphoria and decreased judgment occur at levels between 25-50
mg/dL. Incoordination, decreased reaction time/reflexes, and ataxia occur at
levels of 50-100 mg/dL. Cerebellar dysfunction (ie, ataxia, slurred speech,
nystagmus) are common at levels of 100-250 mg/dL. Coma can occur at levels of
greater than 250 mg/dL, whereas respiratory depression, loss of protective
reflexes, and death occur at levels greater than 400 mg/dL.
Isopropanol ingestion
o As previously stated, the patient who consumes isopropanol may appear
inebriated, as with ethanol. Isopropanol concentrations of 50-100 mg/dL typically
result in intoxication, which can progress to include symptoms such as dysarthria
and ataxia, while lethargy or coma can be seen with levels exceeding 150 mg/dL.
Cardiovascular depression can occur with levels exceeding 450 mg/dL.
o The presence of acetone may induce a fruity odor on the patient's breath.
Methanol ingestion
o Unlike ethanol or isopropanol, methanol does not cause nearly as much of an
inebriated state. If a patient has coingested ethanol, signs or symptoms specific to
methanol intoxication are delayed.
o The patient may be hyperventilating.
o If vision is impaired, ocular examination may reveal dilated pupils that are
minimally or unreactive to light with hyperemia of the optic disc. Over several
days, the red disc becomes pale, and the patient may become blind. Typically,
subjective complaints precede physical findings in the eye.
Ethylene glycol ingestion

5
 o The physical findings depend on the stage of the presentation. Thus, the patient
may present simply inebriated or progressively more acidotic as renal failure,
cardiovascular dysfunction, and coma develop.
o Examination findings correlate with the symptoms, as previously described.
o In patients who survive severe intoxication, calcium oxalate crystal deposition
may occur in the brain parenchyma and can induce cranial neuropathies. These
findings typically occur as the patient is recovering from the initial intoxication.
The cranial nerves most commonly involved include cranial nerve II, V, VII, VIII,
IX, X, and XII.

Differential Diagnoses
Acute Hypoglycemia
Barbiturate Toxicity
Benzodiazepine Toxicity
Depression and Suicide
Diabetic Ketoacidosis
Emergent Management of Pancreatitis
Emergent Management of Subarachnoid Hemorrhage
Emergent Treatment of Alcoholic Ketoacidosis
Encephalitis
Ethylene Glycol Toxicity
Gamma-Hydroxybutyrate Toxicity
Hyperosmolar Hyperglycemic Nonketotic Coma
Isoniazid Toxicity
Lithium Toxicity
Meningitis
Metabolic Acidosis in Emergency Medicine
Opioid Toxicity
Sedative-Hypnotic Toxicity
Stroke, Hemorrhagic
Toxicity, Heroin
Valproate Toxicity
Laboratory Studies
Following consumption of any type of alcohol, the extent of the workup depends partly on the
history. However, because the patient's sensorium is likely to be altered and a history

6
unobtainable or inaccurate, a thorough physical examination is important to evaluate for occult
injuries; laboratory clues can also become invaluable.
If the possibility of a suicide attempt is raised, an electrocardiogram and basic toxicology screen,
including measurement of salicylate and acetaminophen concentrations, become important.
In addition, if ingestion of a toxic alcohol is suspected, a serum ethanol level and basic
electrolytes, including a serum bicarbonate level are vital, as the latter are needed to calculate an
anion gap. In such a situation, specific serum toxic alcohol levels immensely help guide
management. If these are unavailable, calculation of an osmolar gap can sometimes be helpful,
though its exclusive use is fraught with pitfalls. [12] These issues are best discussed with the local
poison control center. Arterial blood gases and other tests that measure associated organ
dysfunction also become important in cases of poisoning with toxic alcohols.
An important point is that laboratory abnormalities vary dramatically over the course of the
patient's presentation and any laboratory abnormalities must be interpreted with the time frame
of the patient's presentation in mind. Failing to do so is a common and important pitfall. Thus,
early in the course of intoxication with a toxic alcohol, a patient will have neither an anion gap
nor an osmolar gap though their serum toxic alcohol level will be highest shortly after ingestion.
However, as metabolism of the toxic alcohol occurs, the anion and osmolar gaps develop as
metabolites are formed and the toxic alcohol level drops.[13] Other laboratory abnormalities also
develop as end-organ damage occurs. Coingestion of alcohol delays all the laboratory value
changes as well as the signs and symptoms of toxic alcohol-induced injury.
Ethanol
The single most important laboratory test in a patient who appears intoxicated with ethanol is a
serum glucose level. Hypoxia, head injury, seizures, and other metabolic disturbances must be
excluded by either history or physical examination or sought with the appropriate tests. The
routine use of a serum blood alcohol level is controversial, largely because it is unlikely to affect
management in a patient who is awake and alert. Many clinicians consider the patient safe for
discharge once they are clinically (not numerically) no longer intoxicated.
In patients who are chronic alcoholics, anemia, thrombocytopenia, elevation of hepatic
transaminase levels, and a prolongation of the prothrombin time can be observed. These need not
be routinely checked in a patient who presents simply for alcohol intoxication but may be useful
if changes from baseline are suspected.
Isopropanol
Serum levels of isopropanol can be obtained but are somewhat of limited value, as the treatment
is largely supportive. However, they can be useful in confirming the diagnosis.
After correcting for all other variables, including ethanol, the serum isopropanol level can be
estimated by multiplying the remaining osmolar gap by 6.0. Serum ketones will often be
positive, although the patient should not be acidotic. Because ketones will be present in the
serum as early as 30 minutes after ingestion, if there is no coexisting ethanol ingestion, the
absence of ketones effectively rules out isopropanol ingestion.
Depending on the assay used in the laboratory, significant ketosis can cause interference with the
creatinine assay. As such, the serum creatinine level can be falsely elevated.
Methanol

7
Serum methanol levels should be obtained when this diagnosis is suspected. As previously
stated, both the osmolar and anion gap should be obtained. After correcting for all other
variables, including ethanol, the serum methanol level can be estimated by multiplying the
remaining osmolar gap by 3.2.
Ethylene glycol
A serum ethylene glycol level should be obtained when this diagnosis is suspected. The osmolar
gap and anion gap should also be obtained. After correcting for other variables, including
ethanol, the serum ethylene glycol level can be estimated by multiplying the remaining osmolar
gap by 6.2.
A baseline creatinine and BUN level should be obtained in all cases of ethylene glycol
intoxication. These values can then be followed to check for the development of renal failure.
In addition, the urine can be examined for evidence of fluorescence. In antifreeze, fluorescein is
added to the liquid to permit mechanics to identify the source of a fluid leaking from a car.
However, fluorescein is excreted in the urine faster than ethylene glycol. Thus, fluorescence can
be eliminated before the patient even arrives in the emergency department. As such, the presence
of fluorescence of urine under a Wood's lamp is not a sensitive test. In addition, because certain
containers themselves fluoresce, the presence of fluorescence is neither sensitive nor specific.
Despite this, a positive test that differentiates urine fluorescence from that of its container may be
a quick bedside clue pointing toward ethylene glycol intoxication.
Both a serum calcium level and an electrocardiogram should be obtained, since hypocalcemia
may occur as calcium combines with oxalate in the form of calcium oxalate crystals.
Osmolar Gap
Measuring the osmolar gap is important when toxic alcohols ingestion is suspected. The osmolar
gap is determined by subtracting the calculated osmolality from the measured osmolality. The
serum osmolality should be determined by freezing point depression rather than by heat of
vaporization.
The serum osmolality can be calculated by the following formula:
Osm = (2) (Na+) + BUN/2.8 + Glucose/18 + EtOH/4.6 + Isopropanol/6.0 + MeOH/3.2 +
Ethylene glycol/6.2
In the above formula, if, for example, an ingestion of methanol is suspected, the osmolality
should be calculated using the sodium, BUN, and glucose. The ethanol level is also measured
and then factored into the equation. If isopropanol and ethylene glycol are not suspected, they
can be eliminated from the equation. Then, once the osmolar gap is determined, multiply the
osmolar gap by 3.2 to determine the estimated methanol level.
It is important to recognize that neither the presence nor absence of an osmolar gap can be used
to confirm or exclude a toxic alcohol ingestion. With both methanol and ethylene glycol, the
alcohols are metabolized from an alcohol to an aldehyde, and ultimately to an acid. As such,
shortly after an ingestion, the patient may have an osmolar gap without an anion gap. Similarly,
in the later stages of an ingestion, a patient may have an anion gap without an osmolar gap.
Prehospital Care

8
The prehospital care provider has several important interventions available. First, the prehospital
provider should search for any empty containers near the patient. In addition, a blood sugar level
should be obtained on anyone who appears intoxicated. Local protocols and the skill level of the
provider dictate additional prehospital care for patients with altered mental status.
Emergency Department Care
As with all emergency patients, initial treatment should focus on the airway, breathing, and
circulation. Gastric decontamination is rarely necessary for any of the alcohols. An exception to
this may be a patient who presents immediately after ingestion of a toxic alcohol in whom one
might reasonably expect to be able to recover a significant amount of the toxin via aspiration
through a nasogastric tube.

Treatment of ethanol and isopropanol intoxication is largely supportive. [14] Because of the
hemorrhagic gastritis that can follow isopropanol ingestion, H2 blockade or proton-pump
inhibitors may be helpful. Hemodialysis, while effective, is rarely indicated, and should
only be used in the setting of profound hemodynamic compromise.[4]

Once either methanol or ethylene glycol intoxication are suspected, treatment should be
initiated without delay. Fortunately, since both alcohols are metabolized by alcohol
dehydrogenase, the treatment is the same, and differentiating which of the two toxic
alcohols is responsible is not necessary before implementing treatment.[14]
o
The primary antidotal treatment of methanol or ethylene glycol involves blocking
alcohol dehydrogenase. This enzyme can be inhibited by either ethanol or
fomepizole.[15, 16, 17] Toxic alcohol levels are frequently not immediately available.
Thus, ideally, if methanol or ethylene glycol poisoning is suspected, the patient
should receive a loading dose of fomepizole while the levels are being obtained.
Because the next dose of fomepizole is not due for an additional 12 hours, this
strategy allows 12 hours for the blood to be processed at a reference laboratory
before additional treatment is needed. Inhibition of alcohol dehydrogenase with
ethanol may be substituted for treatment with fomepizole (see below), though
recent studies have highlighted the greater safety of fomepizole as a treatment,
when available.[11, 9] In some patients, treatment with fomepizole alone may
represent definitive treatment and can prevent the need for hemodialysis.[18]
o
In addition to blocking alcohol dehydrogenase, significant metabolic acidosis
should be treated with sodium bicarbonate infusions. If methanol is suspected,
folinic acid should be administered at a dose of 1 mg/kg, with a maximal dose of
50 mg. It should be repeated every 4 hours. If folinic acid is not immediately
available, folic acid can be substituted at the same dose. If ethylene glycol
overdose is suspected, the patient should also receive 100 mg of intravenous
thiamine every 6 hours and 50 mg of pyridoxine every 6 hours. The purpose of
the thiamine and pyridoxine is to shunt metabolism of glyoxylic acid away from
oxalate and favor the formation of less toxic metabolites.
o
In methanol overdose, sodium bicarbonate should be administered liberally, with
the goal being to completely reverse the acidosis. Based on experimental studies,
formate appears to be excreted in the kidneys at a much higher rate when the
patient is not acidotic. In addition, when the patient is not acidotic, formic acid

9
 dissociates to formate at lower rates so that less formate crosses the blood-brain
barrier. Thus, in methanol intoxication, correcting the acidosis actually speeds up
elimination of the toxic compound and decreases toxicity.
o
If ethanol is used, the recommended target serum concentration is 100-150
mg/dL. Because ethanol inhibits gluconeogenesis, hypoglycemia is common in
patients on an ethanol infusion.[19] Hypoglycemia is particularly prevalent in
pediatric patients on such drips. Thus, serum glucose levels must be checked
frequently, at least every 2 hours. In addition, because it is difficult to attain a
steady serum concentration of ethanol, the ethanol level also must be checked
frequently, and titrations made.
A 5% or 10% ethanol solution can be made in the pharmacy. If giving
ethanol, a loading dose of 600 mg/kg should be given, followed by a drip
of 66-154 mg/kg/h with chronic alcoholics requiring doses at the higher
end of the scale. Ethanol can be given either intravenously or orally.
In addition to hypoglycemia, additional adverse effects from ethanol
infusion include inebriation, CNS depression, pancreatitis, and local
phlebitis. Because of the phlebitis that occurs with ethanol infusions, some
advocate that ethanol should only be administered via a central venous
line.

Ethanol infusions are not only labor intensive, but once the costs of the frequent blood
glucose and serum ethanol levels are accounted for, ethanol antidotal therapy is
frequently more expensive than fomepizole. Thus, because of the lower overall cost and
the ease of administration and safety considerations, fomepizole has become the preferred
antidote for methanol or ethylene glycol poisoning.[20]

Fomepizole should be administered as a loading dose of 15 mg/kg. Subsequent doses
should be at 10 mg/kg every 12 hours for 4 doses. Because fomepizole actually induces
its own metabolism after 48 hours of treatment, if additional doses are needed, the dose
should be increased to 15 mg/kg. Fomepizole needs to be re-dosed during hemodialysis.
The package insert or local poison center can help with the re-dosing strategy.
Fomepizole should be continued until the serum ethylene glycol or methanol
concentrations are less than 20 mg/dL.

Hemodialysis is frequently required in patients with significant methanol or ethylene
glycol ingestions.[14, 18] Indications for hemodialysis include (1) arterial pH < 7.10, (2) a
decline of >0.05 in the arterial pH despite bicarbonate infusion, (3) pH < 7.3 despite
bicarbonate therapy, (4) rise in serum creatinine level by 90 mmol/L, and (5) initial
plasma methanol or ethylene glycol concentration 50 mg/dL.
Consultations
See the list below:
For patients with ethanol intoxication who appear to have issues with dependence or
abuse, one can consider referral to an alcohol detoxification facility. Consult a
toxicologist for all known or suspected cases of isopropanol, methanol, or ethylene glycol
ingestion. If a toxicologist is not immediately available at the medical center where the
patient is located, the regional poison control center can be contacted at (800) 222-1222.
10
 Consult a nephrologist for any known or suspected cases of methanol or ethylene glycol
intoxication to assist in the decision making for hemodialysis
Medication Summary
Fomepizole (eg, 4-methylpyrizole, 4-MP, Antizol) has greater affinity for alcohol dehydrogenase
than ethanol or methanol and has a considerably better safety profile than ethanol. Fomepizole
has been approved by the US Food and Drug Administration (FDA) for ethylene glycol
poisoning, but it is also useful for managing methanol poisoning.
Pharmacologic antidotes
Class Summary
These agents prevent formation of toxic metabolites in methanol ingestions (not useful with
isopropanol or ethanol ingestions). Therapy generally is maintained until methanol levels are less
than 20 mg/dL.
Fomepizole (4-MP, Antizol)
DOC for ethylene glycol and methanol poisoning because of ease of administration and better
safety profile than ethanol. Inhibitor of alcohol dehydrogenase. In contrast to ethanol, 4-MP
levels do not require monitoring during therapy.
Begin fomepizole treatment immediately upon suspicion of methanol/ethylene glycol ingestion
based on the patient's history or anion gap metabolic acidosis, increased osmolar gap, oxalate
crystals in the urine, or a documented serum methanol/ethylene glycol level. Adjust dosing
during hemodialysis; see package insert.
Ethanol
Has 10-20 times greater affinity for enzyme alcohol dehydrogenase than methanol does, blocking
production of toxic metabolites.
Believed to inhibit ADH when serum levels exceed 0.05 g/dL (50 mg/dL). Titration to serum
levels between 0.10 g/dL (100 mg/dL) and 0.15 g/dL (150 mg/dL) typically used.
Measure patient's initial blood level. May be administered PO/IV.
Folic acid (Folvite)
Adjunctive agent in methanol ingestion. Member of vitamin B-complex that may enhance
elimination of toxic metabolite formic acid produced when methanol is metabolized. Useful in
methanol and possibly ethylene glycol toxicity. Leucovorin (folinic acid) is active form of folate
and may be substituted for folic acid.
Folic acid should be administered for several days to enhance folate-dependent metabolism of
formic acid to carbon dioxide and water.

Further Inpatient Care

See the list below:
Patients with significant ingestions of toxic alcohols require hospital admission in a
closely monitored setting such as the intensive care unit.

11
 Patients who are chronic alcoholics may be at risk of alcohol withdrawal if admitted to
the hospital.
Transfer
See the list below:
Patients with ethanol intoxication can be observed until they are no longer clinically
intoxicated and then discharged.
Patients with isopropanol ingestion may require observation in the hospital.
Patients with known or suspected methanol or ethylene glycol intoxication should be
monitored closely, probably in an intensive care unit.
Complications
See the list below:

Ethanol ingestion complications:
o Hypoglycemia is common.[19] The etiology is multifactorial but largely related to
decreased glycogen stores and malnutrition in children and chronic alcoholics, as
well as ethanols inhibition of glycogenolysis.
o Patients with acute intoxication may exhibit "holiday heart," in which
dysrhythmias, especially atrial fibrillation, occur following a heavy drinking
episode. Ethanol lowers the threshold for developing atrial fibrillation.
o Cirrhosis, esophageal varices, and erosive gastritis are common in patients who
use ethanol on a frequent basis.

Ingestion of isopropanol is associated with hemorrhagic gastritis.

Ingestion of methanol is associated with blindness, acidosis, coma, cardiovascular
collapse, and death.

Ingestion of ethylene glycol is associated with renal failure, acidosis, coma,
cardiovascular collapse, and death.[15]

KEPUSTAKAAN

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2. Hornfeldt CS. A report of acute ethanol poisoning in a child: mouthwash versus cologne,
perfume and after-shave. J Toxicol Clin Toxicol. 1992. 30(1):115-21.
3. Martz W. A lethal ingestion of a household cleaner containing pine oil and isopropanol. J
Anal Toxicol. 2010 Jan-Feb. 34(1):49-52.
4. Slaughter RJ, Mason RW, Beasley DM, Vale JA, Schep LJ. Isopropanol poisoning. Clin
Toxicol (Phila). 2014 Jun. 52(5):470-8.

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5. ATSDR. Methanol toxicity. Agency for Toxic Substances and Disease Registry. Am Fam
Physician. 1993 Jan. 47(1):163-71.
6. Aufderheide TP, White SM, Brady WJ, et al. Inhalational and percutaneous methanol
toxicity in two firefighters. Ann Emerg Med. 1993 Dec. 22(12):1916-8.
7. Coulter CV, Farquhar SE, McSherry CM, Isbister GK, Duffull SB. Methanol and
ethylene glycol acute poisonings - predictors of mortality. Clin Toxicol (Phila). 2011 Dec.
49(10):900-6.
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