Treatment of the alcohol intoxications: ethylene glycol, methanol

and isopropanol
Stuart Abramson and Ajay K. Singh

Intoxications with ethylene glycol, methanol, and isopropanol are Introduction

among the most common ingestions, in the treatment of which a Intoxications with methanol, ethylene glycol, and
nephrologist plays an important role. These three substances isopropanol have substantial morbidity and signi®cant
have the ideal characteristics for intervention by hemodialysis, mortality. Toxicity from these alcohol moieties is
and the three parent compounds and their metabolites are treatable, if instituted early and rapidly, because no
readily dialyzable. Two of the three substances, ethylene glycol other toxins share characteristics of small volume of
and methanol, are metabolized to more toxic substances, so distribution, lack of protein binding, and the rapid
that an early treatment strategy that removes the parent equilibration with the intravascular space, which renders
compound or blocks its metabolism can prevent the these agents dialyzable. In addition to the use of dialysis,
development of many of the adverse events that are often seen however, recent advances have increased the armamen-
in these ingestions. Fomepizole, an inhibitor of alcohol tarium available for effective treatment. The present
dehydrogenase, slows the metabolism of these substances and review addresses these advances and outlines the current
is now approved by the US Food and Drug Administration for strategy for the treatment of ethylene glycol, methanol,
use in ethylene glycol intoxication. The present review and isopropanol intoxication.
addresses recent advances in the diagnosis and treatment of
intoxication with ethylene glycol, methanol and isopropanol. Curr Ethylene glycol
Opin Nephrol Hypertens 9:695±701. # 2000 Lippincott Williams & Wilkins. Ethylene glycol is a sweet-tasting substance that is a
common constituent of antifreeze. Because of its sweet
taste and its ability to intoxicate, it is sometimes used as a
substitute for ethanol. It is also often found as an
Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, accidental ingestion in children, or as a suicidal agent,
Massachusetts, USA accounting for approximately 0.3% of all exposures and
Correspondence to Dr. Stuart Abramson, Assistant Director, Dialysis Services, Renal 3.0% of all deaths due to poisonings. In 1998 alone, 6281
Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, exposures to ethylene glycol and 27 deaths were reported
USA
to the Toxic Exposure Surveillance System (TESS) [1].
Current Opinion in Nephrology and Hypertension 2000, 9:695±701 The estimated minimum lethal dose for adults is
Abbreviations approximately 100 ml, but a number of patients have
CNS central nervous system survived ingestions of over 2000 ml. In a case report by
FDA US Food and Drug Administration Johnson et al. [2 .], one patient who underwent rapid
NAD nicotinamide adenine dinucleotide
NADH nicotinamide adenine dinucleotide, reduced form treatment with ethanol infusion and hemodialysis in the
TESS Toxic Exposure Surveillance System emergency room survived an ingestion of 3000 ml with-
out sequelea. The ethylene glycol level was found to be
# 2000 Lippincott Williams & Wilkins
1889 mg/dl. There have been other similar reports [3,4 .].
1062-4821

Pharmacokinetics
Ethylene glycol reaches a peak serum level 2±4 h after
ingestion. It is water-soluble and has a volume of
distribution that is equal to that of total body water
(0.6 l/kg). It has a molecular weight of 62 g/mol. Fig. 1
shows the metabolism of ethylene glycol to its end
products. Ethylene glycol is oxidized by alcohol
dehydrogenase in the presence of nicotinamide adenine
dinucleotide (NAD) to glycoaldehyde, which is then
rapidly oxidized to glycolate [5 . .]. Ethanol and fomepi-
zole slow the metabolism of ethylene glycol by inhibit-
ing the enzyme alcohol dehydrogenase. Glycolate is the
toxic metabolite and produces the high anion gap
acidosis. Some part of the acidosis stems from the
production of lactate and is due to the reduction of NAD
to nicotinamide adenine dinucleotide, reduced form
695
696 Diagnostics and techniques

Figure 1. Metabolism of ethylene glycol alcohol coingestion. Review of data from TESS suggests
that most deaths occur during this stage [1].
Lactate
Ethylene glycol The ®nal stage occurs 24±72 h after ingestion and is
NAD
Alcohol characterized by ¯ank pain, acute tubular necrosis,
dehydrogenase
hypocalcemia, and renal failure. During this stage, the
Glycolate
NADH production of oxalate leads to calcium oxalate precipita-
Pyruvate
tion in the kidney and other tissues, and hypocalcemia.
The renal toxicity is probably due to a combination of
hydronephrosis from calcium oxalate crystals and a direct
Glyoxylate
toxic effect from the metabolites of ethylene glycol. Most
renal damage is reversible and renal recovery, which may
take a few months, is the norm, even after anuria [8].
Oxalate
There is very little correlation between serum ethylene
glycol and clinical outcome. Indeed, patients may
Urinary excretion present after their serum levels have begun to decrease
and the ethylene glycol has been converted to its toxic
NAD, nicotinamide adenine dinucleotide; NADH, nicotinamide adenine metabolites. There is better correlation between the
dinucleotide, reduced form. arterial pH, serum bicarbonate or glycolate level and the
clinical outcome. A number of studies of patients
treated with fomepizole have shown that those who
present without acidosis or a high glycolate level do
(NADH), which drives the conversion of pyruvate to well [6 . .,9].
lactate (Fig. 1).
Laboratory abnormalities
Without treatment the elimination half-life of ethylene Ethylene glycol intoxication is characterized by a high
glycol is 3±8 h. Ethanol at a concentration of 100 mg/dl anion gap acidosis, osmolar gap, and hypocalcemia. The
will prolong the half-life ®vefold to 15±20 h. A recent anion gap acidosis is due to both the production of
study by Brent et al. [6 . .] examined the use of glycolate and the reduction of NAD to NADH during
femopizole (4-methylpyrazole) as an alcohol dehydro- the oxidation of ethylene glycol to glycolate. A patient
genase inhibitor in ethylene glycol intoxication. Those may have no acidosis soon after ingestion before the
investigators administered femopizole to 19 patients ethylene glycol has been converted to glycolate. The
with ethylene glycol intoxication and plasma levels gap will grow as the ethylene glycol is metabolized.
greater than 20 mg/dl. They found that a 5 mg/kg
loading dose of fomepizole followed by a 10 mg/kg dose Ethylene glycol will also form an osmolar gap because it
every 12 h was suf®cient to inhibit the metabolism of is osmotically active and has a relatively small molecular
ethylene glycol and increase its half-life to 20 h. weight. The osmolar gap is the difference between the
calculated osmolarity and the osmolarity, as measured by
Symptomatology freezing point depression [10]. There are a number of
The clinical course of ethylene glycol intoxication can be different equations that can be used to calculate the
divided into three phases. The ®rst phase occurs less serum osmolarity, each one giving a slightly different
than 1 h after ingestion and is characterized by mental value. An equation that is easy to use for calculating
status depression, similar to that of alcohol intoxication. osmolarity is as follows:
In severe intoxication, coma, seizures, and respiratory
depression can complicate this phase. This stage lasts 2(Na+) + glucose (mg/dl)/18 + BUN(mg/dL)/
about 12 h as the ethylene glycol is oxidized to 2.8 + ethanol(mg/dL)/4.6
glycoaldehyde and glycolate [7 .].
where BUN is blood urea nitrogen. The osmolar gap is
During the second phase, glycolate has a toxic effect on advantageous because it can be found quickly and add
the cardiopulmonary system. In severe intoxications, evidence for an intoxication. An osmolar gap greater than
patients can develop acidosis, heart failure, pulmonary 10 mOsm/kg is suggestive of intoxication with ethylene
edema or adult respiratory distress syndrome [7 .]. The glycol, methanol, isopropanol, ethylene oxide, or acetone
timing of this stage depends on the metabolism of the [11]. In ethylene glycol intoxication, the serum level of
ethylene glycol to glycolate, and usually starts approxi- the toxin can be estimated by multiplying the osmolar
mately 12 h after ingestion, but will be delayed by gap by 6.2.
 Treatment of alcohol intoxications Abramson and Singh 697

The osmolar gap lacks the sensitivity and speci®city to Ethanol has been used as an inhibitor of alcohol
be an ideal screening test for intoxication. Glycolate does dehydrogenase in ethylene glycol intoxication for 50
not contribute to the osmolar gap so that, as the ethylene years, but has not been approved by the US Food and
glycol is metabolized to glycolate, the osmolar gap will in Drug Administration (FDA). The standard loading dose
fact fall. Therefore, patients who present late after an is 0.6 g ethanol/kg, followed by a constant infusion to
ingestion may have a normal osmolar gap. Another factor keep the blood alcohol level between 100 and 200 mg/
that lowers the sensitivity of the osmolar gap is the dl. The average maintenance dose is 100 mg/kg per h,
considerable variation in the normal osmolar gap in the but is signi®cantly higher for alcoholic persons and for
general population. Indeed, patients may have an patients on dialysis. Blood alcohol levels should be
increased gap that is still below 10 mOsm/kg [12 .]. checked every 1±2 h until a steady state has been
Thus, a high osmolar gap is supportive of ethylene reached, and then every 2±4 h. The potential adverse
intoxication, but a normal gap does not rule it out. On effects of ethanol include central nervous system (CNS)
the other hand, the osmolar gap can also be falsely depression, hypoglycemia, respiratory depression, and
elevated. Patients who are critically ill may have an aspiration.
elevated gap because of the presence of endogenous
substances such as amino acids. Patients with hyperlipi- Fomepizole was recently approved by the FDA as an
demia or hyperproteinemia will have spurious hypo- antidote in ethylene glycol intoxication. It has a number
natremia, leading to an elevated gap. There is also an of potential advantages to the use of ethanol. It is easier
accumulation of osmotically active substances in chronic to dose with more predictable kinetics, and therefore
renal failure [7 .]. does not require blood monitoring. Furthermore, it has
fewer side effects and does not cause CNS depression.
The urine may contain two forms of calcium oxalate Finally, some patients treated with fomepizole may not
crystals in ethylene glycol intoxication. The dumbbell- need observation in an intensive care unit if they are
shaped monohydrate forms are more common, but the otherwise stable [9].
octahedral-shaped dihydrate form is more speci®c for
ethylene glycol intoxication. Individuals who ingest a Fomepizole should be given at a loading dose of 15 mg/
large amount of vitamin C or urate-containing foods may kg followed by 10 mg/kg every 12 h for 48 h. After 48 h,
have monohydrate calcium oxalate crystals in their urine. the dose should be increased to 15 mg/kg every 12 h.
The dihydrate form requires higher oxalate concentra- Fomepizole should be continued until the serum
tions for its formation, and therefore is more indicative of ethylene glycol level is 520 mg/dl and the patient is
intoxication with ethylene glycol [5 . .]. asymptomatic with a normal pH. Fomepizole is dialyzed
and therefore needs to be dosed every 4 h during
Treatment dialysis [13].
Supportive treatment includes airway protection, circu-
latory support, correction of metabolic abnormalities Hemodialysis
and control of seizures. Bicarbonate is indicated for Hemodialysis is very effective at clearing ethylene glycol
patients with pH below 7.3. Asymptomatic hypocal- and its metabolites. The clearance rate of ethylene
cemia is generally not treated because of the risk of glycol ranges between 200±250 cm3/min, depending on
increasing the formation of calcium oxalate crystals. the ®lter and blood ¯ow. Glycolate, which is the major
Seizures may be due to hypocalcemia, but should be toxic metabolite, has a half-life of up to 18 h without
treated ®rst with standard anticonvulsants. There is no hemodialysis, but the half-life is reduced by a factor of
role for the use of activated charcoal, cathartics or six with hemodialysis [14]. Patients with acidosis may
gastric lavage in the treatment of ethylene glycol therefore still bene®t from hemodialysis even in the face
intoxication [5 . .]. Alcoholic persons and patients who of a low serum ethylene glycol level.
are likely to be malnourished should be given thiamine
and pyridoxine. The indications for hemodialysis include those patients
who have, or who are likely to develop the major
There are two currently used antidotes that inhibit the sequelae of ethylene glycol ingestion. These include
metabolism of ethylene glycol. The indications for the patients with metabolic acidosis (pH 57.3) or deterior-
use of an antidote have been outlined by the American ating clinical status with respiratory failure or hypoten-
Academy of Clinical Toxicology [5 . .]. These indications sion. Patients with acute renal failure and a metabolic
include a plasma ethylene glycol concentration 420 mg/ derangement that is unresponsive to standard therapy
dl, a recent ingestion of ethylene glycol and an osmolar should be considered for hemodialysis also. In the past,
gap 410 mOsm/kg or a high clinical suspicion, and two of an ethylene glycol level of 50 mg/dl was considered an
the following: pH 57.3, serum bicarbonate 520 mmol/l, indication for hemodialysis. Recent experience suggests
osmolar gap 410 mOsm/kg, or urinary oxalate crystals. that patients with normal renal function and no acidosis
698 Diagnostics and techniques

may be treated with fomepizole without hemodialysis, Figure 2. Metabolism of methanol

even in the setting of an ethylene glycol level greater
than 50 mg/dl [9,15 .]. These patients require close
monitoring for the development of renal insuf®ciency
Methanol Lactate
or acidosis. NAD
Alcohol
dehydrogenase
Dialysis should be continued until the ethylene glycol NADH
level is less than 20 mg/dl, the acidosis has resolved and Pyruvate
Formaldehyde
there are no signs of systemic toxicity, or until the Lactate
ethylene glycol level is undetectable. Prolonged dialysis Aldehyde NAD
may be required for very high ethylene glycol levels and dehydrogenase
severe acidosis. Both fomepizole and ethanol are cleared NADH
during dialysis. The addition of ethanol to the dialysate Pyruvate
has been shown to maintain blood alcohol levels during Formate
dialysis [4 .]. The use of fomepizole during hemodialysis
Folinic acid
is more straightforward and only requires an increase in
the frequency of the doses to every 4 h to maintain CO2 + H2O
adequate levels [6 . .].
NAD, nicotinamide adenine dinucleotide; NADH, nicotinamide adenine
Methanol dinucleotide, reduced form.
Methanol is a highly toxic alcohol that is found in a
variety of commercial products, including antifreeze,
windshield wiper ¯uid, paint thinner, and rubbing
alcohol. There were 2862 exposures to methanol and effect of methanol before it is metabolized is CNS
19 deaths reported to TESS in 1998 [1]. This represents depression. This is of short duration and is followed by a
0.1% of all exposures and 2.0% of all deaths due to latent period. The latent period is caused by the time it
poisoning. The estimated minimum lethal dose for takes for formate to accumulate, and lasts 14±18 h or
adults is approximately 10 ml, but there are reports of longer with ethanol or fomepizole treatment [19].
patients surviving ingestions greater than 400 ml without
sequelea [16 . .]. The latent period is followed by a number of systemic
®ndings as formate accumulates. Metabolic acidosis can
Pharmacokinetics be severe, and a pH below 7.0 has been found to be the
Methanol is rapidly absorbed after ingestion. It has a strongest predictor of mortality. Patients with a pH
volume of distribution of 0.6 l/kg and a molecular weight below 7.0 have 20 times the mortality as compared with
of 32 g/mol. The metabolism of methanol to its end patients with pH greater than 7.0 [16 . .]. CNS effects in
products is displayed in Fig. 2. Methanol is oxidized by this stage can include headache, lethargy, convulsions,
alcohol dehydrogenase in the presence of NAD to delirium, and coma. Patients who present with seizure or
formaldehyde. Formaldehyde is then quickly oxidized to coma have over 10 times the mortality as patients
formate. Formate produces much of the toxic effect as well without these signs [20].
as the high anion gap acidosis. As with ethylene glycol,
some of the acidosis is due to the formation of lactate. Ocular ®ndings can be prominent and may include
Pyruvate is metabolized to lactate because of the reduction photophobia, central scotoma, visual ®eld defects, ®xed
of NAD to NADH during the oxidation of methanol [17 .]. pupils, and dif®culty with light adaptation. Pupillary
As with ethylene glycol metabolism, ethanol and fomepi- dysfunction has also been shown to be a strong predictor
zole will once again slow the oxygenation of methanol by of mortality. Funduscopic signs include hyperemia, disk
inhibiting alcohol dehydrogenase. edema, and possible optic atrophy [21]. The ocular
®ndings are due to the direct cytotoxic effect of formate
The elimination half-life of methanol is 14±18 h without on the retina. Other systemic ®ndings may include
treatment. Ethanol at a concentration of 100 mg/dl will nausea, vomiting, diaphoresis, and abdominal pain. The
prolong the half-life to 40±50 h. Recent use of fomepi- abdominal pain is often due to pancreatitis [22].
zole in methanol intoxication shows that it also prolongs
the half-life by fourfold to sixfold [18]. Laboratory abnormalities
As stated above, the accumulation of formate produces a
Symptomatology high anion gap metabolic acidosis. Some of the anion gap
Most of the clinical effects of methanol intoxication are is from the increased lactate production. A patient that
due to the accumulation of formate. The major clinical presents early after an ingestion or later after a
 Treatment of alcohol intoxications Abramson and Singh 699

coingestion with both methanol and ethanol may have level greater than 50 mg/dl, a history of consuming
little or no acidosis, making the diagnosis of methanol more than 30 ml methanol, severe acidosis or high
intoxication much more dif®cult. These same patients formate levels, seizures or visual, funduscopic or mental
receive most bene®t from alcohol dehydrogenase inhibi- status changes [24]. Clearance constants with high-
tion, because the ingested methanol still needs to be ef®ciency membranes have been as high as 200 cm3/
metabolized to formate to have its toxic effect [17 .]. min for both formate and methanol [25]. Hemodialysis
can hinder the maintenance of adequate ethanol levels,
Methanol also produces an osmolar gap. A serum level of and a number of authors have described the use of
32 mg/dl increases the measured serum osmolarity by ethanol-enriched dialysate solutions [26 .]. Hemodialysis
10 mOsm/kg. A high serum methanol level should should be continued until the serum methanol level is
therefore cause a gap between the calculated serum undetectable, or until the patient is asymptomatic with
osmolarity and the measured osmolarity by freezing a normal serum pH and the serum methanol level is
point depression [10]. However, patients with methanol below 20 mg/dL.
intoxication may have a normal gap (510 mOsm/kg) if
they present late after ingestion and the methanol has Isopropanol
been converted to formate. Formate does not contribute Isopropanol is a colorless liquid with a bitter taste. It is
to the serum osmolarity because it is balanced by used in the manufacture of acetone and glycerin. It is
sodium, which is included in the calculated osmolarity. often used as the solvent in rubbing alcohol. Most
For this reason, the osmolarity gap should be used to rubbing alcohol contains 70% isopropanol.
help support the diagnosis of methanol intoxication, but
lack of a gap is not suf®ciently sensitive to rule out There were 11 216 exposures to isopropanol and three
intoxication [17 .]. deaths reported to TESS in 1998 [1]. This represents
0.6% of all exposures and 0.3% of all deaths due to
Treatment poisoning. It has a much small percentage of deaths per
Supportive treatment for methanol intoxication is similar exposure as compared with either ethylene glycol or
to that for ethylene glycol, and includes airway protec- methanol. The estimated minimum lethal dose for
tion, circulatory support, correction of metabolic abnorm- adults is approximately 100 ml, but patients have
alities, and control of seizures. Bicarbonate is indicated survived ingestions of over 1000 ml.
for patients with pH below 7.3. The use of folate has not
been rigorously studied in humans, but has been shown Pharmacokinetics
to increase the metabolism of formate to carbon dioxide Isopropanol reaches a peak serum level 15±30 min after
and water. It can be given as a 50 mg intravenous dose ingestion. It is water-soluble and has a volume of
every 4 h for ®ve doses, then once a day [18]. distribution that is equal to that of total body water
Symptomatic patients should be given one dose of (0.6 l/kg). It has a molecular weight of 60 g/mol.
1 mg/kg folinic acid intravenously. Isopropanol is oxidized by alcohol dehydrogenase to
acetone. The elimination half-life of isopropanol is 3±
The main objective of treatment of methanol intoxica- 7 h, but is prolonged with ethanol coingestion [27]. The
tion is to limit the accumulation of formate. This is elimination of acetone is much slower and is due to
done with the same inhibitors of alcohol dehydrogen- excretion in the breath and urine [28].
ase as are used in ethylene glycol intoxication. Both
ethanol and fomepizole have been shown to be Symptomatology
effective in the treatment of methanol intoxication Unlike ethylene glycol and methanol, most of the
[15 .,23]. The regimen for each treatment is similar to clinical effects in isopropanol intoxication are due to
that for ethylene glycol intoxication. They should be the parent compound. Acetone causes only mild CNS
used in any patient with a methanol serum level depression [10]. The clinical signs of isopropanol
420 mg/dl, an anion gap acidosis and a recent history intoxication will occur within 1 h of ingestion, and
of methanol ingestion, or in any symptomatic patient include effects on the central nervous, gastrointestinal,
with a recent history of a methanol ingestion. The and cardiovascular systems. The CNS effects include
treatment should be continued until the level is ataxia, confusion, stupor and coma. The gastrointestinal
undetectable, or both symptoms and acidosis resolve effects include nausea, vomiting, abdominal pain, and
and the level is below 20 mg/dl. gastritis. Patients with severe intoxication can present
with hypotension due to cardiac depression and
Hemodialysis vasodilatation [29]. Hypotension is the strongest
Hemodialysis will remove both methanol and formic predictor of mortality [30]. Many patients will have
acid ef®ciently and will help to correct the acidosis. It `fruity' breath from the acetone elimination via
should be considered in any patient with a methanol respiration.
700 Diagnostics and techniques

Laboratory abnormalities 4 Nzerue CM, Harvey P, Volcy J, Berdzenshvili M. Survival after massive ethylene
. glycol poisoning: role of an ethanol enriched, bicarbonate-based dialysate. Int J
A serum level of isopropanol equal to 60 mg/dl will Artif Organs 1999; 22:744±746.
increase the serum osmolarity by 10 mOsm/l. A high This is one of a number of reports of a favorable outcome with early intervention in
ethylene glycol intoxication.
serum level should therefore produce a gap between the
5 Barceloux DG, Krenzelok EP, Olson K, Watson W. American Academy of
calculated serum osmolarity and that measured by .. Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol
freezing point depression [31]. Acidosis is rare after Poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol 1999; 37:537±560.
This is an excellent review of the diagnosis and treatment of ethylene glycol
isopropanol ingestion, because neither the parent intoxication. As a consensus statement from the American Academy of Clinical
compound nor its metabolites are organic acids. There- Toxicology, it presents a concise algorithm for treatment with supporting data. It
also outlines the use of fomepizole as an antidote for ethylene glycol poisoning.
fore, a ®nding of a high serum or urine acetone level
6 Brent J, McMartin K, Phillips S, et al. Fomepizole for the treatment of ethylene
without acidosis is suggestive of recent isopropanol .. glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med
ingestion [27]. Renal failure can occur in the setting of 1999; 340:832±838.
This study examines the use of fomepizole in ethylene glycol poisoning. Nineteen
signi®cant hypotension. Hypoglycemia can result from patients with ethylene glycol intoxication were given fomepizole, with one death
the interference of gluconeogenesis by isopropanol [10]. and nine patients developing renal failure. The dosing strategy used in this study
can be used for patients being treated with fomepizole both with and without
dialysis. This study also helps to elucidate the prognostic indicators in ethylene
Treatment intoxication treated with fomepizole.
Supportive treatment includes circulatory support with 7 Piagnerelli M, Lejeune P, Vanhaeverbeek M. Diagnosis and treatment of an
.
¯uids or vasoconstrictors in patients with hypotension. unusual cause of metabolic acidosis: ethylene glycol poisoning. Acta Clin Belg
1999; 54:351±356.
Inhibition of alcohol dehydrogenase is not indicated A good review of the symptomatology after ethylene glycol intoxication is
because acetone is less toxic than isopropanol. Hemo- presented.

dialysis is indicated for patients with an isopropanol level 8 LaKind JS, McKenna EA, Hubner RB, Tardiff RG. A review of the
comparative mammalian toxicity of ethylene glycol and propylene glycol. Crit
greater than 400 mg/dl and signi®cant CNS depression, Rev Toxicol 1999; 29:331±365.
renal failure or hypotension [30]. Hemodialysis will 9 Borron SW, Megarbane B, Baud FJ. Fomepizole in treatment of uncompli-
remove both isopropanol and acetone effectively [32]. cated ethylene glycol poisoning. Lancet 1999; 354:831.
High-ef®ciency membranes can produce clearance con- 10 Church AS, Witting MD. Laboratory testing in ethanol, methanol, ethylene
glycol, and isopropanol toxicities. J Emerg Med 1997; 15:687±692.
stants greater than 200 cm3/min for both acetone and This paper reviews the many laboratory abnormalities that are found with these
isopropanol. intoxications.
11 Pappas AA, Gadsden Sr RH, Taylor EH. Serum osmolality in acute
intoxication: a prospective clinical study. Am J Clin Pathol 1985; 84:74±79.
Conclusion
12 Darchy B, Abruzzese L, Pitiot O, et al. Delayed admission for ethylene glycol
Early treatment by a nephrologist for intoxications with . poisoning: lack of elevated serum osmol gap. Intensive Care Med 1999;
ethylene glycol, methanol, and isopropanol can have a 25:859±861.
This is a good review of the origin and usefulness of the osmolar gap in ethylene
profound impact on outcome in these poisonings. These glycol intoxication.
compounds are readily dialyzable and antidotes exist to 13 Jobard E, Harry P, Turcant A, et al. 4-Methylpyrazole and hemodialysis in
prevent the metabolism to more toxic compounds. ethylene glycol poisoning. J Toxicol Clin Toxicol 1996; 34:373±377.
Recently, the FDA has approved fomepizole in ethylene 14 Moreau CL, Kerns II W, Tomaszewski CA, et al. Glycolate kinetics and
glycol intoxication, and it appears to be just as effective hemodialysis clearance in ethylene glycol poisoning. META Study Group. J
Toxicol Clin Toxicol 1998; 36:659±666.
in the treatment of methanol ingestion. For all three of
15 Hantson P, Wallemacq P, Brau M, et al. Two cases of acute methanol poisoning
these toxins, the newer hemodialysis ®lters can remove . partially treated by oral 4-methylpyrazole. Intensive Care Med 1999; 25:528±
the parent compound and its metabolites very ef®- 531.
This study reviews the use of fomepizole as an antidote in methanol intoxication.
ciently. These toxins are unique in their characteristics,
16 Meyer RJ, Beard ME, Ardagh MW, Henderson S. Methanol poisoning. N Z Med
which allow for rapid and effective treatment that can . . J 2000; 113:11±13.

signi®cantly reduce the adverse effects after ingestion. This study is a retrospective review of 24 patients who presented with methanol
intoxication. It reviews the diagnosis and treatment and presents some of the
important prognostic indicators.
17 Sullivan M, Chen CL, Madden JF. Absence of metabolic acidosis in toxic
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 Treatment of alcohol intoxications Abramson and Singh 701

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