LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0

Advanced Emergency Nursing Journal

Vol. 31, No. 3, pp. 206–213
Copyright 
c 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins

A P P L I E D

Pharmacology

Toxic Alcohol Ingestions

Focus on Ethylene Glycol and Methanol
Deanna M. McMahon, PharmD ;
Shane Winstead, PharmD ;
Kyle A. Weant, PharmD

Abstract
The ingestion of toxic alcohols, specifically ethylene glycol (EG) and methanol, provides unique
therapeutic challenges for emergency personnel. If untreated, these agents can result in significant
morbidity and mortality. The toxicity of EG and methanol is dependent on endogenous metabolic
processes rather than the actual parent compound ingested. These metabolites lead to the char-
acteristic metabolic acidosis and cellular dysfunction typically seen with toxic alcohol ingestions.
Fortunately, several options exist for the treatment of these ingestions, which, if implemented in
the appropriate time period, can significantly decrease associated morbidity and mortality. The intent
of this review is to discuss relevant management issues associated with EG and methanol intox-
ication in the emergency department. Key words: alcohol, ethanol, ethylene glycol, fomepizole,
methanol

A LTHOUGH relatively uncommon, poi- permanent organ damage can be decreased.

sonings with ethylene glycol (EG) and
methanol can result in significant mor-
bidity and mortality in the emergency pa-
tient population (Abramson & Singh, 2000;
Megarbane, Borron, & Baud, 2005). The
unique characteristics of these toxins provide
potentially adventitious aspects for treatment.
If treated early, the toxicity of these agents
can be minimized and the risk of death and
Author Affiliations: Department of Pharmacy Ser-
vices, University of Kentucky HealthCare, and Depart-
ment of Pharmacy Practice & Science, College of Phar-
macy, University of Kentucky, Lexington.
Corresponding Author: Kyle A. Weant, PharmD, De-
partment of Pharmacy Practice & Science, College of
Pharmacy, University of Kentucky, 800 Rose St, Room
H109A, Lexington, KY 40536 (kawean2@email.uky.
edu).
The intent of this review is to discuss relevant
management issues in the emergency depart-
ment as well as the current therapeutic prin-
ciples for the treatment of EG and methanol
intoxication.
ETHYLENE GLYCOL
Ethylene glycol is a colorless and odorless,
sweet-tasting substance that can be found in
common household solutions, such as an-
tifreeze, detergents, and polishes (Abramson
& Singh, 2000). In the United States in 2007,
EG was the primary substance in 5,731 expo-
sures and resulted in 27 deaths as reported
in the Toxic Exposure Surveillance System
(Bronstein et al., 2008). The primary route

206
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29
July–September 2009 r Vol. 31, No. 3
of exposure is from oral ingestion through
which it is rapidly absorbed and reaches a
peak concentration in 1–4 hr (Barceloux,
Krenzelok, Olson, & Watson, 1999). This may
occur as a result of an attempt to commit
suicide, a substitute for ethanol, or an ac-
cidental ingestion. More than 80% of expo-
sures in 2007 were accidental and 583 were in
children younger than 6 years. Although wide
variations exist regarding the quantity of EG
that represents a lethal dose, it is typically ref-
erenced as 1.4–1.5 ml/kg body weight or ap-
proximately 100 ml in adults (Abramson &
Singh, 2000; Eder et al., 1998). On the basis of
its dependency on metabolic processes how-
ever, it should be noted that any quantity of
consumption can lead to toxicity.
Pathophysiology and Clinical Symptoms
The toxicity of EG is largely related to its
metabolites rather than the parent compound
itself. Hepatic metabolism is responsible for
80% of the absorbed dose, with alcohol and
aldehyde dehydrogenase serving large roles
in this conversion (Barceloux et al., 1999).
The accumulation of large quantities of the
metabolite glycolate is primarily responsible
for the ensuing metabolic acidosis charac-
terized by a wide anion gap. Subsequent
metabolism results in the formation of ox-
alate, which precipitates with calcium to form
calcium oxalate crystals. These crystals can
form in various tissues throughout the body;
however, their formation in the renal tubules
leads to the subsequent renal dysfunction as-
sociated with this toxic ingestion. The clin-
ical course following a toxic EG ingestion
can typically be broken up into three stages
as described in Table 1 (Abramson & Singh,
2000; Barceloux et al., 1999). Because of mul-
tiple interpatient variables and the typical
coingestion of ethanol, this course is often
variable.
Laboratory Monitoring
Both urine and serum can present evidence
of EG toxicity as well as serving to monitor
potential endpoints of therapy. On admission,
Char Count= 0
Toxic Alcohol Ingestions 207
about half of patients will present with two
forms of calcium oxalate crystals (monohy-
drate or dehydrate) in the urine, often in com-
bination with a concomitant hypocalcemia
(Jacobsen, Akesson, & Shefter, 1982). These
crystals may be present after a period of
about 4–8 hr and up to 40 hr (Barceloux
et al., 1999; Flanagan & Libcke, 1964). An
elevated serum EG level can also be useful
in confirming the diagnosis of a toxic EG in-
gestion. Although false positives can exist,
these are exceedingly rare (Eder et al., 1998;
Martinez, Lubbos, Rose, Swartz, & Kayne,
1998). Interestingly, because of the mecha-
nism of this disorder, there are limited cor-
relations between serum EG and patient out-
come. As each patient’s EG level declines, this
is indicative of its conversion to more toxic
metabolites rather than the resolution of in-
toxication. Fortunately, correlations can be
made between arterial pH, serum bicarbon-
ate or glycolate levels, and clinical outcome
(Borron, Megarbane, & Baud, 1999; Brent
et al., 1999). In the first several hours fol-
lowing ingestion, patients will often present
with an elevated serum osmolality due to the
EG parent compound (Barceloux et al., 1999;
Jacobsen, Bredesen, Eide, & Ostborg, 1982).
However, as this compound is metabolized to
glycolate, this elevation will return to normal
and a high anion gap metabolic acidosis will
develop primarily because of the formation
of glycolic acid (Hewlett, McMartin, Lauro,
& Ragan, 1986; Jacobsen, Ovrebo, Ostborg,
& Sejersted, 1984). As metabolism continues,
serum bicarbonate levels will decrease, con-
tributing to the ensuing acidosis. The elim-
ination of any existing EG concentration in
conjunction with the resolution of acid-base
abnormalities and signs of systemic toxicity
are typically considered the endpoints of ther-
apy (Barceloux et al., 1999).
METHANOL
Methanol, also known as wood alcohol, is
a clear, colorless liquid with a slightly alco-
holic odor that is an additive found in several
commercial products, including antifreeze,
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0

208 Advanced Emergency Nursing Journal

Table 1. Typical clinical course following toxic ethylene glycol

Time period
after ingestion Typical symptoms

Stage 1: Neurological 0.5–12 hr Transient inebriation and euphoria

Stage 2: Cardiopulmonary
Stage 3: Renal
Nausea and vomiting
Metabolic acidosis
Central nervous system depression
Nystagmus, ataxia, myoclonic jerks
Coma and seizures
12–24 hr Tachycardia and mild hypertension
Compensatory hyperventilation
Congestive heart failure
Acute respiratory distress syndrome
Most deaths occur during this stage
24–72 hr Acute tubular necrosis, oliguria, flank pain, and
renal failure

Note. From “Treatment of the Alcohol Intoxications: Ethylene Glycol, Methanol and Isopropanol,” by S. Abramson and
A. K. Singh, 2000, Current Opinion Nephrology Hypertension, 9, pp. 695–701. Copyright 2000 by Lippincott Williams
& Wilkins. Adapted with permission of the author; and from “American Academy of Clinical Toxicology Practice Guide-
lines on the Treatment of Ethylene Glycol Poisoning. Ad Hoc Committee,” by D. G. Barceloux, E. P. Krenzelok, K. Olson,
and W. Watson, 1999, Journal of Toxicology: Clinical Toxicology, 37, pp. 537–560. Copyright 1999 by Marcel Dekker,
Inc. Adapted with permission of the author.

windshield cleaner, paint thinner, and rub-
bing alcohol (Abramson & Singh, 2000;
Barceloux, Bond, Krenzelok, Cooper, & Vale,
2002). It is frequently used as a solvent
in multiple products. In 2007, methanol
was the primary substance in 2,059 ex-
posures and resulted in 11 deaths in the
United States, according to the Toxic Expo-
sure Surveillance System (Bronstein et al.,
2008). Similar to EG, the primary route of
exposure is ingestion, with common rea-
sons being intended suicide, substitution
when ethanol is not available, or uninten-
tional exposure. Oral absorption is rapid,
reaching its peak in 30–60 min (Barceloux
et al., 2002). Close to 90% of cases in 2007
were unintentional exposures, and 510 of
these were patients younger than 6 years
(Bronstein et al., 2008). The quantity of
methanol necessary to cause toxicity is de-
pendent on the concentration of the solu-
tion and the metabolic process involved but
has been documented with as little as 15–
500 ml of a 40% solution in adults (Bennett,
Cary, Mitchell, & Cooper, 1953; Jacobsen &
McMartin, 1986).
Pathophysiology and Clinical Symptoms
Analogous to EG, methanol itself has a rela-
tively low toxicity. Largely its metabolism, pre-
dominantly by the liver, is responsible for the
production of toxic metabolites (Barceloux
et al., 2002; Brent, McMartin, Phillips, Aaron,
& Kulig, 2001). Alcohol dehydrogenase and
formaldehyde dehydrogenase are the primary
enzymes in this metabolic process, and it is
this later metabolism that is responsible for
the formation of formic acid, the agent re-
sponsible for the toxicity of methanol inges-
tion. Formic acid can have an impressively
large number of clinical effects that lead to
the significant morbidity and mortality asso-
ciated with this toxicity (Barceloux et al.,
2002). Formic acid can inhibit mitochondrial
oxidative metabolism leading to an increase
in lactate levels (Nicholls, 1976). This ef-
fect, combined with formic acid itself, pro-
duces the high anion gap metabolic acidosis
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0

July–September 2009 r Vol. 31, No. 3 Toxic Alcohol Ingestions 209

seen in acute methanol poisoning (McMartin, Table 2. Clinical features of methanol

Ambre, & Tephly, 1980). Formic acid also toxicity
contributes to the signature ocular toxicity
seen in this clinical scenario causing optic
Organ system Typical symptoms
disc edema and nerve lesions (Martin-Amat,
McMartin, Hayreh, Hayreh, & Tephly, 1978). Central Headache, vertigo,
In addition, an intricate toxic neurological nervous lethargy, and confusion
process can develop, which presents as cere- system Coma and convulsions
bral edema and necrotic damage in the basal Extrapyramidal symptoms
ganglia (Barceloux et al., 2002). The clinical Ocular Blurred vision and
blindness
course of methanol toxicity is less structured
Photophobia and “feeling
than that of EG toxicity. Often there is an ini-
of being in a snow field”
tial period of 12–24 hr during which only mild Fixed and dilated pupils
central nervous system depression symptoms Gastrointestinal Nausea, vomiting, and
are present followed by a latent period dur- abdominal pain
ing which the metabolic conversion to formic Acute pancreatitis
acid occurs (Barceloux et al., 2002). Similar to Elevated hepatic
EG, this process can also be delayed by sev- aminotransferases
eral hours with the coingestion of ethanol. Kidney Myoglobinuria and renal
Following this latent period, the patient typ- failure (rare)
ically develops a profound metabolic acidosis
and visual disturbances. Common symptoms Note. From “American Academy of Clinical Toxicology
are outlined in Table 2. Practice Guidelines on the Treatment of Methanol Poison-
ing,” by D. G. Barceloux, G. R. Bond, E. P. Krenzelok, H.
Cooper, and J. A. Vale, 2002, Journal of Toxicology: Clin-
Laboratory Monitoring ical Toxicology, 40, pp. 415–446. Adapted with permis-
sion of the author.
Serum methanol concentrations provide sev-
eral unique challenges with regards to inter-
pretation. Small concentrations of methanol sis (Jacobsen, Jansen, Wiik-Larsen, Bredesen,
are present in several fruits and vegetables and & Halvorsen, 1982). Early in the course fol-
can accumulate in binge drinking scenarios lowing methanol ingestion, the patient will
(Barceloux et al., 2002). The mean methanol develop an osmolal gap due to the parent
concentration in one study of drivers sus- compound and any coingestion of ethanol
pected of driving under the influence of (Barceloux et al., 2002). However, as this par-
alcohol was 7.3 mg/dl (Jones & Lowinger, ent compound is metabolized, the patient will
1988). As a result, the American Academy begin to develop a metabolic acidosis and a
of Clinical Toxicology recommends the use bicarbonate deficit, which subsequently leads
of a methanol concentration greater than to the creation of an anion gap (McMartin
20 mg/dl to indicate those at risk for toxic- et al., 1980). Treatment is typically recom-
ity in conjunction with the presence of an an- mended to continue until these abnormalities
ion gap metabolic acidosis (Barceloux et al., are corrected and the serum methanol con-
2002). Although this level should be in- centration falls below 20 mg/dl (Barceloux
terpreted within the context of when the et al., 2002).
methanol ingestion occurred, as lower lev-
els may also indicate toxicity (Kostic & Dart, MANAGEMENT
2003).
Treatment Overview
Of more clinical value, and correlated more
closely with clinical symptoms and mortal- According to the American Academy of Clin-
ity, is the ensuing anion gap metabolic acido- ical Toxicology Practice Guidelines on EG
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0
210
and methanol poisonings, available options
for the treatment of toxic ingestions include
an antidote, hemodialysis, and/or supportive
care (Barceloux et al., 1999, 2002). Because of
the rapid absorption of EG and methanol, gut
decontamination is of limited use in this set-
ting. Activated charcoal is not recommended
because EG and methanol are not likely ad-
sorbed by this agent. The antidotes, ethanol or
fomepizole, are indicated for use if the patient
has a documented plasma EG or methanol
concentration greater than 20 mg/dl, a
witnessed ingestion of either substance in
toxic amounts with an osmolal gap greater
than 10 mOsm/L or a history or high suspi-
cion of poisoning in addition to two of the
following criteria: arterial pH less than 7.3,
serum bicarbonate less than 20 mEq/L, os-
molal gap greater than 10 mOsm/L, and uri-
nary oxalate crystals in the case of EG tox-
icity (Barceloux et al., 1999). The cofactors
pyridoxine, thiamine, and magnesium should
be replenished in patients with suspected vi-
tamin deficiencies, such as alcohol-dependent
patients, to promote the conversion of glyoxy-
late, glycolic acid, and glyoxylic acid to non-
toxic metabolites, respectively. In the setting
of EG overdose, hypocalcemia is typically not
corrected unless the patient is symptomatic
because of concerns over the formation of
calcium oxalate crystals. Folinic acid (leucov-
orin) or folic acid given intravenously may
be used as adjunctive agents to increase the
metabolism of formic acid in methanol over-
dose (Barceloux et al., 2002). Typically, folinic
acid given at a dose of 1 mg/kg (maximum
of 50 mg) administered over 30–60 min ev-
ery 4–6 hr is preferred over folic acid (50 mg
every 4–6 hr) because it does not require
metabolic reduction to a bioactive form. How-
ever, it should be noted that currently no hu-
man studies exist supporting the use of these
agents for this purpose.
Ethanol
Although ethanol has been used as an antidote
for EG and methanol poisonings since the
1940s, there are no prospective trials to sup-
port its use and consequentially it is not Food
Advanced Emergency Nursing Journal
and Drug Administration (FDA)–approved for
either indication. Ethanol binds to the en-
zyme alcohol dehydrogenase more efficiently
than does EG or methanol and inhibits the
subsequent formation of toxic metabolites. It
may be administered intravenously, orally, or
via nasogastric tube depending on the clin-
ical status of the patient. An initial loading
dose of 600–700 mg/kg of ethanol (equiva-
lent to 7.6–8.9 ml/kg of 10% ethanol solu-
tion) should be administered over 60 minutes,
assuming that the patient’s baseline ethanol
level is undetectable, followed by a main-
tenance dose based on the patient’s drink-
ing history (Table 3). If the baseline ethanol
level is elevated, a loading dose should ac-
count for the difference between the target
ethanol level and the patient’s current level.
Ethanol levels should be monitored every 1–
2 hr until a steady state concentration be-
tween 100 and 150 mg/dl is achieved, after
which levels should be checked every 2–4
hr. If the infusion rate or dose is changed at
any time, more frequent monitoring (i.e., ev-
ery 1–2 hr) is indicated until therapeutic lev-
els are reestablished. The levels achieved after
oral ethanol are highly patient dependent and
thereby require the same intensity of moni-
toring as the continuous infusion. Because of
the labor-intensive monitoring required, pa-
tients receiving ethanol should be cared for in
a critical care unit. In addition to necessitating
frequent therapeutic drug-level monitoring,
ethanol can cause a number of adverse events,
including hypoglycemia, respiratory depres-
sion, visual impairment, vomiting, slurred
speech, and mental status changes. Infusion
through a central catheter may be necessary
as the intravenous formulation has been asso-
ciated with local phlebitis (Barceloux et al.,
1999, 2002).
Fomepizole
Fomepizole is FDA approved for the treatment
of methanol and EG toxicities. It inhibits al-
cohol dehydrogenase, preventing the forma-
tion of toxic metabolites responsible for the
sequelae associated with methanol or EG in-
gestion. A one-time loading dose of 15 mg/kg
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0

July–September 2009 r Vol. 31, No. 3 Toxic Alcohol Ingestions 211

Table 3. Therapeutic doses of ethanol based on the patient’s drinking history

Volume of 10%
Absolute ethanol Volume of 43% oral intravenous
dose ethanol solution ethanol solution

Loading dose 600–700 mg/kg 1.8–2.1 ml/kg 7.6–8.9 ml/kg

Nondrinker
Maintenance dose 66 mg/kg/hr 0.2 ml/kg/hr 0.83 ml/kg/hr
Maintenance dose during 169 mg/kg/hr 0.5 ml/kg/hr 2.13 ml/kg/hr
hemodialysis
Chronic drinker
Maintenance dose 154 mg/kg/hr 0.46 ml/kg/hr 1.96 ml/kg/hr
Maintenance dose during 257 mg/kg/hr 0.77 ml/kg/hr 3.26 ml/kg/hr
hemodialysis

Note. From “American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Ethylene Glycol Poison-
ing. Ad Hoc Committee,” by D. G. Barceloux, E. P. Krenzelok, K. Olson, and W. Watson, 1999, Journal of Toxicology:
Clinical Toxicology, 37, pp. 537–560. Copyright 1999 by Marcel Dekker, Inc. Adapted with permission of the author;
and from “American Academy of Clinical Toxicology Practice Guidelines on the Treatment of Methanol Poisoning,” by
D. G. Barceloux, G. R. Bond, E. P. Krenzelok, H. Cooper, and J. A. Vale, 2002, Journal of Toxicology: Clinical Toxicology,
40, pp. 415–446. Adapted with permission of the author.

should be administered intravenously over EG or methanol concentrations are less than

30 min, followed by four doses of 10 mg/kg
every 12 hr, and then a subsequent increase
in the maintenance dose to 15 mg/kg ev-
ery 12 hr is warranted because of autoin-
duction of drug metabolism occurring after
48 hr. This regimen should be continued until
20 mg/dl, and the patient is asymptomatic
with a normal pH (Barceloux et al., 1999,
2002). If hemodialysis is used in combina-
tion with fomepizole, dose adjustments are re-
quired because of the removal of this agent
by dialysis. Table 4 includes the appropriate

Table 4. Fomepizole dosing in hemodialysis

Dose at the beginning of hemodialysis

If less than 6 hr since last fomepizole dose Do not administer the next scheduled dose
If 6 hr or more since last fomepizole dose Administer the next scheduled dose
Dose during hemodialysis
Dose every 4 hr
Dose at the completion of hemodialysis
Time between the last dose and the end of Dose administered at the end of hemodialysis
hemodialysis session
Less than 1 hr Do not administer dose at the end of hemodialysis
1–3 hr Administer 50% of the next scheduled dose
Over 3 hr Administer the next scheduled dose
Maintenance dose after hemodialysis
Give the next scheduled dose 12 hr from last
fomepizole dose

Note. From “Antizol [Package insert],” by Jazz Pharmaceuticals, 2006, Palo Alto, CA: Author. Copyright 2008 by Jazz
Pharmaceuticals. Adapted with permission of the author.
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0
212
fomepizole dosing in relation to the timing
of the hemodialysis session (Jazz Pharmaceu-
ticals, 2006). No therapeutic drug monitoring
is required for fomepizole, allowing patients
to be cared for in an acute care setting rather
than an obligatory intensive care unit. The pri-
mary adverse effects of fomepizole reported
in clinical trials included headache, nau-
sea, and dizziness (Brent et al., 1999, 2001;
Megarbane et al., 2001).
Because of the low incidence of methanol
and EG toxicities, comparison studies
between ethanol and fomepizole are chal-
lenging. However, such investigations are
necessary not only to help determine the
superiority of one agent over another but also
to help reconcile the cost and adverse event
profiles of these agents. A recent retrospec-
tive analysis found that 57% of ethanol-treated
patients had at least one side effect compared
with 12% of fomepizole-treated patients
(Lepik et al., 2009). In addition, ethanol is
much more labor intensive with regards to
critical care nursing and laboratory monitor-
ing (Megarbane et al., 2005). Fomepizole,
on the other hand, has the disadvantage
of having a high acquisition cost that has
contributed to this agent being avoided as an
option and leading to delays in its adminis-
tration (Mycyk, DesLauriers, Metz, Wills, &
Mazor, 2006).
Hemodialysis
Hemodialysis rapidly clears EG and methanol
in addition to their toxic metabolites. Tradi-
tionally, a serum EG or methanol concentra-
tion greater than 50 mg/dl has been used as an
indication for dialysis, although there are in-
sufficient data to suggest that any concentra-
tion represents a starting point for renal tox-
icity. Current recommendations suggest that
hemodialysis should be considered in patients
presenting with an EG or methanol inges-
tion who have a significant metabolic acidosis
(pH less than 7.25–7.30), renal failure, elec-
trolyte imbalances refractory to pharmaco-
logical treatments, and/or hemodynamic in-
stability secondary to the toxic alcohol. The
duration of therapy should be determined on
Advanced Emergency Nursing Journal
the basis of the individual patient case but
may be terminated when the metabolic aci-
dosis is corrected and serum concentrations
are less than 20 mg/dl. Another option is
to cease hemodialysis following the correc-
tion of the metabolic acidosis and continue
an antidote until EG or methanol concentra-
tions are less than 20 mg/dl and the patient is
asymptomatic (Barceloux et al., 1999, 2002;
Megarbane et al., 2005).
CONCLUSION
Although they represent a relatively small por-
tion of poisonings overall, EG and methanol
can cause significant toxicities to various or-
gan systems. It is imperative for all healthcare
personnel to become knowledgeable about
the signs and symptoms of ingestion of these
agents, as well as the various monitoring
parameters essential for accurate diagnosis
and treatment. The availability of ethanol and
fomepizole as antidotes has dramatically en-
hanced our ability to treat these overdoses
and subsequently reduce related toxicities.
REFERENCES
Abramson, S., & Singh, A. K. (2000). Treatment of the
alcohol intoxications: Ethylene glycol, methanol and
isopropanol. Current Opinion in Nephrology and Hy-
pertension, 9(6), 695–701.
Barceloux, D. G., Bond, G. R., Krenzelok, E. P., Cooper,
H., & Vale, J. A. (2002). American Academy of Clini-
cal Toxicology practice guidelines on the treatment of
methanol poisoning. Journal of Toxicology: Clinical
Toxicology, 40(4), 415–446.
Barceloux, D. G., Krenzelok, E. P., Olson, K., & Watson,
W. (1999). American Academy of Clinical Toxicology
practice guidelines on the treatment of ethylene glycol
poisoning. Ad hoc committee. Journal of Toxicology:
Clinical Toxicology, 37(5), 537–560.
Bennett, I. L., Jr., Cary, F. H., Mitchell, G. L., Jr., & Cooper,
M. N. (1953). Acute methyl alcohol poisoning: A re-
view based on experiences in an outbreak of 323
cases. Medicine (Baltimore), 32(4), 431–463.
Borron, S. W., Megarbane, B., & Baud, F. J. (1999). Fomepi-
zole in treatment of uncomplicated ethylene glycol
poisoning. Lancet, 354(9181), 831.
Brent, J., McMartin, K., Phillips, S., Aaron, C., & Kulig,
K. (2001). Fomepizole for the treatment of methanol
poisoning. The New England Journal of Medicine,
344(6), 424–429.
LWW/AENJ AENJ-D-09-00009R1 July 28, 2009 19:29 Char Count= 0
July–September 2009 r Vol. 31, No. 3
Brent, J., McMartin, K., Phillips, S., Burkhart, K. K., Dono-
van, J. W., Wells, M., et al. (1999). Fomepizole for the
treatment of ethylene glycol poisoning. Methylpyra-
zole for Toxic Alcohols Study Group. The New Eng-
land Journal of Medicine, 340(11), 832–838.
Bronstein, A. C., Spyker, D. A., Cantilena, L. R., Jr., Green,
J. L., Rumack, B. H., & Heard, S. E. (2008). 2007 Annual
Report of the American Association of Poison Control
Centers’ National Poison Data System (NPDS): 25th
Annual Report. Clinical Toxicology (Philadelphia),
46(10), 927–1057.
Eder, A. F., McGrath, C. M., Dowdy, Y. G., Tomaszewski,
J. E., Rosenberg, F. M., Wilson, R. B., et al. (1998).
Ethylene glycol poisoning: Toxicokinetic and analyt-
ical factors affecting laboratory diagnosis. Clinical
Chemistry, 44(1), 168–177.
Flanagan, P., & Libcke, J. H. (1964). Renal biopsy observa-
tions following recovery from ethylene glycol nephro-
sis. American Journal of Clinical Pathology, 41, 171–
175.
Hewlett, T. P., McMartin, K. E., Lauro, A. J., & Ragan, F. A.,
Jr. (1986). Ethylene glycol poisoning. The value of gly-
colic acid determinations for diagnosis and treatment.
Journal of Toxicology: Clinical Toxicology, 24(5),
389–402.
Jacobsen, D., Akesson, I., & Shefter, E. (1982). Urinary
calcium oxalate monohydrate crystals in ethylene gly-
col poisoning. Scandanavian Journal of Clinical and
Laboratory Investigation, 42(3), 231–234.
Jacobsen, D., Bredesen, J. E., Eide, I., & Ostborg, J. (1982).
Anion and osmolal gaps in the diagnosis of methanol
and ethylene glycol poisoning. Acta Medica Scandi-
navica, 212(1/2), 17–20.
Jacobsen, D., Jansen, H., Wiik-Larsen, E., Bredesen, J. E., &
Halvorsen, S. (1982). Studies on methanol poisoning.
Acta Medica Scandinavica, 212(1/2), 5–10.
Jacobsen, D., & McMartin, K. E. (1986). Methanol and
ethylene glycol poisonings. Mechanism of toxicity,
clinical course, diagnosis and treatment. Medical Tox-
icology, 1(5), 309–334.
Jacobsen, D., Ovrebo, S., Ostborg, J., & Sejersted, O. M.
(1984). Glycolate causes the acidosis in ethylene gly-
col poisoning and is effectively removed by hemodial-
ysis. Acta Medica Scandinavica, 216(4), 409–416.
Toxic Alcohol Ingestions 213
Jazz Pharmaceuticals. (2006). Antizol [Package insert].
Palo Alto, CA: Author.
Jones, A. W., & Lowinger, H. (1988). Relationship be-
tween the concentration of ethanol and methanol in
blood samples from Swedish drinking drivers. Foren-
sic Science International, 37(4), 277–285.
Kostic, M. A., & Dart, R. C. (2003). Rethinking the toxic
methanol level. Journal of Toxicology: Clinical Toxi-
cology, 41(6), 793–800.
Lepik, K., Levy, A., Sobolev, B., Purssell, R., DeWitt, C.,
Erhardt, G., et al. (2009). Adverse drug events as-
sociated with the antidotes for methanol and ethy-
lene glycol poisoning: A comparison of ethanol and
fomepizole. Annals of Emergency Medicine, 53, 439–
450.
Martin-Amat, G., McMartin, K. E., Hayreh, S. S., Hayreh, M.
S., & Tephly, T. R. (1978). Methanol poisoning: Ocular
toxicity produced by formate. Toxicology and Applied
Pharmacology, 45(1), 201–208.
Martinez, C., Lubbos, H., Rose, L. I., Swartz, C., & Kayne,
F. (1998). False-positive ethylene glycol levels in pa-
tients with diabetic ketoacidosis. Endocrine Practice,
4(5), 272–273.
McMartin, K. E., Ambre, J. J., & Tephly, T. R. (1980).
Methanol poisoning in human subjects: Role for
formic acid accumulation in the metabolic acido-
sis. The American Journal of Medicine, 68(3), 414–
418.
Megarbane, B., Borron, S. W., & Baud, F. J. (2005). Cur-
rent recommendations for treatment of severe toxic
alcohol poisonings. Intensive Care Medicine, 31(2),
189–195.
Megarbane, B., Borron, S. W., Trout, H., Hantson, P.,
Jaeger, A., Krencker, E., et al. (2001). Treatment of
acute methanol poisoning with fomepizole. Intensive
Care Medicine, 27(8), 1370–1378.
Mycyk, M. B., DesLauriers, C., Metz, J., Wills, B., & Mazor,
S. S. (2006). Compliance with poison center fomepi-
zole recommendations is suboptimal in cases of toxic
alcohol poisoning. American Journal of Therapeu-
tics, 13(6), 485–489.
Nicholls, P. (1976). The effect of formate on cytochrome
aa3 and on electron transport in the intact respiratory
chain. Biochimica et Biophysica Acta, 430(1), 13–29.