Toxic Alcohols: Not Always

November 2010
Volume 12, Number 11
A Clear-Cut Diagnosis Authors

Nilam Patil, DO
Emergency Medicine Physician, Saint Joseph’s Regional Medical
A 45-year-old woman with a history of depression is brought to the hospital Center, Paterson, NJ
by her family 2 to 3 hours after an intentional ingestion of windshield- Melisa W. Lai Becker, MD, FACEP, FAAEM
Emergency Physician and Director, Division of Medical Toxicology,
washer fluid. Her family wants to know if she is going to be okay and when Cambridge Health Alliance, Cambridge, MA; Instructor in Medicine
she can go home. Her initial triage vital signs include a heart rate of 88 (Emergency Medicine), Harvard Medical School, Boston, MA
beats per minute, a respiratory rate of 14 breaths per minute, and pulse Michael Ganetskty, MD, FACEP
oximetry of 100% on room air. Upon examination, she appears lethargic Clinical Director, Division of Medical Toxicology, Department of
Emergency Medicine, Beth Israel Deaconess Medical Center, Boston,
but neurologically intact and is ambulating without difficulty. As you MA; Clinical Instructor, Harvard Medical School, Boston, MA
order a serum osmolality, electrolytes, and serum ethanol, methanol, and Peer Reviewers
ethylene glycol concentrations, you realize that you haven’t taken care of
Beth Y. Ginsburg, MD
a patient with a toxic alcohol ingestion in years. You wonder if you should Attending Physician, Department of Emergency Medicine, Division of
begin treatment right away, whether hemodialysis is indicated, and how to Medical Toxicology, Elmhurst Hospital Center, Elmhurst, NY; Assistant
interpret the labs once they are reported. A call is placed to the local poison Professor, Department of Emergency Medicine, Mount Sinai School of
Medicine, New York, NY
control center.
Stephanie Hernandez, MD
Department of Emergency Medicine, Division of Medical Toxicology,

T he toxic alcohols that clinicians commonly encounter are ethyl-

ene glycol, methanol, and isopropanol. Adults ingest these either
for suicidal intent or to achieve inebriation, since these substances
Mount Sinai Medical Center; Assistant Professor, Mount Sinai School of
Medicine, New York, NY

CME Objectives

are readily available and cheaper than alcohol. Definitive diagnosis Upon completion of this article, you should be able to:
of toxic alcohol poisoning requires measurement of a serum toxic 1. Describe the pathophysiology and possible complications of
methanol, ethylene glycol, and isopropanol ingestion.
alcohol concentration or detection in the serum of toxic alcohol 2. Distinguish key physical examination findings based on the toxic
metabolites. These required assays are not routinely performed in alcohol ingested.
most hospital laboratories, making the diagnostic process a chal- 3. Know when to begin treatment with ADH inhibitors and/or
hemodialysis.
lenge. For this reason, clinicians often rely on osmolar and anion gap
calculations to guide diagnosis and treatment, but published litera- Date of original release: November 1, 2010
Date of most recent review: October 10, 2010
ture describes many pitfalls in relying solely on these values. Prompt Termination date: November 1, 2013
diagnosis and treatment of toxic alcohol ingestions is critical, since Prior to beginning this activity, see “Physician CME Information”
on page 19.

Editor-in-Chief Nicholas Genes, MD, PhD General Hospital, Harvard Medical Corey M. Slovis, MD, FACP, FACEP International Editors
Andy Jagoda, MD, FACEP Instructor, Department of Emergency School, Boston, MA Professor and Chair, Department
Peter Cameron, MD
Professor and Chair, Department of Medicine, Mount Sinai School of of Emergency Medicine, Vanderbilt
Charles V. Pollack, Jr., MA, MD, Chair, Emergency Medicine,
Emergency Medicine, Mount Sinai Medicine, New York, NY University Medical Center; Medical
FACEP Monash University; Alfred Hospital,
School of Medicine; Medical Director, Michael A. Gibbs, MD, FACEP Director, Nashville Fire Department
Chairman, Department of Emergency Melbourne, Australia
Mount Sinai Hospital, New York, NY and International Airport, Nashville,
Chief, Department of Emergency Medicine, Pennsylvania Hospital,
TN Giorgio Carbone, MD
Editorial Board Medicine, Maine Medical Center, University of Pennsylvania Health
Portland, ME System, Philadelphia, PA Jenny Walker, MD, MPH, MSW Chief, Department of Emergency
William J. Brady, MD Medicine Ospedale Gradenigo,
Assistant Professor; Division Chief,
Professor of Emergency Medicine Steven A. Godwin, MD, FACEP Michael S. Radeos, MD, MPH Torino, Italy
Family Medicine, Department of
and Internal Medicine, Vice Chair Associate Professor, Associate Chair Assistant Professor of Emergency
Community and Preventive Medicine, Amin Antoine Kazzi, MD, FAAEM
of Emergency Medicine, University and Chief of Service, Department Medicine, Weill Medical College of
Mount Sinai Medical Center, New Associate Professor and Vice Chair,
of Virginia School of Medicine, of Emergency Medicine, Assistant Cornell University; Department of
York, NY Department of Emergency Medicine,
Charlottesville, VA Dean, Simulation Education, Emergency Medicine, New York
University of Florida COM- Hospital Queens, Flushing, NY Ron M. Walls, MD University of California, Irvine;
Peter DeBlieux, MD American University, Beirut, Lebanon
Jacksonville, Jacksonville, FL Professor and Chair, Department of
Louisiana State University Health Robert L. Rogers, MD, FACEP,
Emergency Medicine, Brigham and Hugo Peralta, MD
Science Center Professor of Clinical Gregory L. Henry, MD, FACEP FAAEM, FACP
Women’s Hospital, Harvard Medical Chair of Emergency Services,
Medicine, LSUHSC Interim Public CEO, Medical Practice Risk Assistant Professor of Emergency
School, Boston, MA Hospital Italiano, Buenos Aires,
Hospital Director of Emergency Assessment, Inc.; Clinical Professor Medicine, The University of
Medicine Services, LSUHSC of Emergency Medicine, University of Maryland School of Medicine, Scott Weingart, MD, FACEP Argentina
Emergency Medicine Director of Michigan, Ann Arbor, MI Baltimore, MD Assistant Professor of Emergency Dhanadol Rojanasarntikul, MD
Faculty and Resident Development Medicine, Mount Sinai School of Attending Physician, Emergency
John M. Howell, MD, FACEP Alfred Sacchetti, MD, FACEP Medicine; Director of Emergency
Wyatt W. Decker, MD Clinical Professor of Emergency Assistant Clinical Professor, Medicine, King Chulalongkorn
Critical Care, Elmhurst Hospital Memorial Hospital, Thai Red Cross,
Professor of Emergency Medicine, Medicine, George Washington Department of Emergency Medicine, Center, New York, NY
Mayo Clinic College of Medicine, University, Washington, DC; Director Thomas Jefferson University, Thailand; Faculty of Medicine,
of Academic Affairs, Best Practices, Philadelphia, PA Senior Research Editor Chulalongkorn University, Thailand
Rochester, MN
Inc, Inova Fairfax Hospital, Falls Joseph D. Toscano, MD Maarten Simons, MD, PhD
Francis M. Fesmire, MD, FACEP Scott Silvers, MD, FACEP
Church, VA Chair, Department of Emergency Emergency Physician, Department Emergency Medicine Residency
Director, Heart-Stroke Center,
Keith A. Marill, MD Medicine, Mayo Clinic, Jacksonville, of Emergency Medicine, San Ramon Director, OLVG Hospital, Amsterdam,
Erlanger Medical Center; Assistant
Assistant Professor, Department of FL Regional Medical Center, San The Netherlands
Professor, UT College of Medicine,
Emergency Medicine, Massachusetts Ramon, CA
Chattanooga, TN

Accreditation: EB Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. Patil, Dr. Becker, Dr. Ganetsky, Dr. Ginsburg,
Dr. Hernandez, Dr. Jagoda, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this
educational presentation. Commercial Support: This issue of Emergency Medicine Practice did not receive any commercial support.
end-organ damage may be devastating, irreversible, ethylene glycol, methanol, isopropyl alcohol, isopropanol,
and potentially fatal. ethanol, fomepizole, 4-methylpyrazole, hemodialysis,
The American Association of Poison Control Cen- AAPCC, osmolar gap, and anion gap. This literature
ters’ (AAPCC) 2008 Annual Report of the National search focused on adults, children, and pregnant
Poisoning Database System (NPDS) cited 6395 expo- patients. Approximately 80 articles were found and
sures to ethylene glycol, 2272 exposures to methanol, served as the foundation of this evidence-based
and 17,220 exposures to isopropanol. Ethylene glycol review article.
exposures were a factor in 22 reported deaths and The literature regarding management of toxic
methanol in 9 deaths. None of the reported fatalities alcohol ingestions is limited in many ways. First
in 2008 resulted from pure isopropanol exposures.1 and foremost, current guidelines set forth by the
Because not all states require that exposures or toxic American Academy of Clinical Toxicology (AACT)
alcohol ingestions be reported to poison control cen- are based on the Methylpyrazole for Toxic Alcohols
ters, these totals probably underestimate the actual (META) trials, which were prospective studies.2,3
number of toxic alcohol poisonings. In the META trial, only 19 patients were recruited
This issue of Emergency Medicine Practice focuses for the ethylene glycol group and only 11 for the
on the diagnostic approach to toxic alcohol poison- methanol group, and neither had a control group.
ing, as well as the pathophysiology, management, In addition, no large prospective studies support
and treatment specific to each of the toxic alcohols. these guidelines regarding the initiation of alcohol
dehydrogenase (ADH) blockade and the end points
Critical Appraisal Of The Literature of treatment. Finally, the AACT guidelines regard-
ing when to begin treatment in the absence of a toxic
A search of PubMed, Ovid MEDLINE®, the National alcohol concentration are based on anecdotal data.4,5
Guideline Clearing House, and Cochrane Database Unfortunately, because of inherent difficulties in
of Systematic Reviews was carried out using the performing randomized, prospective trials involving
following combination of key words: toxic alcohol, poisoned patients, this is a common limitation of all
the literature on toxicology management.

Etiology And Pathophysiology

Table Of Contents
Critical Appraisal Of The Literature....................... 2 Isopropanol is the most commonly abused toxic
Etiology And Pathophysiology................................ 2 alcohol because it is inebriating, readily available,
Differential Diagnosis................................................ 4 and cheap; it is the least toxic in comparison to
Prehospital Treatment................................................ 4 methanol and ethylene glycol. The critical distinc-
Emergency Department Evaluation........................ 4 tion is that, unlike methanol and ethylene glycol,
Diagnostic Studies...................................................... 5 isopropanol does not cause metabolic acidosis. In
Treatment..................................................................... 8 each case, the parent compounds cause intoxication,
Clinical Pathway For Initial Evaluation Of Toxic but serious toxicity is caused by their metabolites. In
Alcohol Poisoning............................................... 10 order to better understand the treatment modalities
Clinical Pathway For Management Of Methanol for each of these agents, the pathophysiology and
And Ethylene Glycol Poisoning........................11 clinical effects of each toxic alcohol will be discussed
Clinical Pathway For Management Of Isopropanol separately.
Poisoning..............................................................11
Special Circumstances............................................. 12 Methanol
Controversies/Cutting Edge.................................. 12 Methanol (methyl alcohol) is commonly found in
Risk Management Pitfalls For Diagnosis And windshield-wiper fluid and de-icing products. In ad-
Management Of Toxic Alcohol Poisoning....... 13 dition, gas line antifreeze, gelled chafing fuel, paint
Disposition................................................................ 14 removers, shoe dyes, and embalming fluid may
Summary................................................................... 14 contain varying amounts of methanol. The inges-
Case Conclusion....................................................... 14 tion of “moonshine” contaminated with methanol,
References.................................................................. 14 resulting in blindness, has been reported to have
CME Questions......................................................... 17 occurred several times in history.6 Methanol toxicity
Evidence-Based Practice Recommendations for is most commonly reported to be from ingestion, but
this issue....................www.ebmedicine.net/pr11 inhalational and dermal exposures have also been
reported.7,8
Available Online At No Charge To Subscribers Methanol’s pharmacokinetics are well-de-
EM Practice Guidelines Update: “Current Guidelines scribed and follow Michaelis–Menten kinetics. (See
For Diagnosis And Treatment Of Venous Throm- Table 1.) At low concentrations (10 mg/dL), metha-
boembolism,” www.ebmedicine.net/VTE nol follows first-order kinetics and has a half-life

Emergency Medicine Practice © 2010 2 EBMedicine.net • November 2010

of 2.5 to 3 hours. At higher concentrations (100-200 mately 80% undergoes hepatic metabolism and 20%
mg/dL), methanol metabolism follows zero-order is excreted unchanged in the urine. Ethylene glycol’s
kinetics and has no half-life. With zero-order me- elimination depends on renal function. When renal
tabolism, the rate at which methanol is eliminated function is normal, it follows first-order metabolism
is 8.5 to 9 mg/dL/h.9-11 When the patient is treated and has a half-life of 8.5 hours.17 In patients treated
with fomepizole, methanol exhibits first-order with fomepizole, it continues to follow first-order
kinetics and has a longer half-life (54 hours) than kinetics but has a half-life of 14 to 17 hours in patients
ethylene glycol.2,12 with normal renal function and 49 hours in those
Methanol is hepatically metabolized by ADH with impaired renal function.17-19 (See discussion of
to formaldehyde and then converted to formic acid fomepizole, page 8.)
by aldehyde dehydrogenase (ALDH). (See Figure Similar to methanol, it is the metabolites of eth-
1, page 4.) Formic acid can be metabolized to water ylene glycol that are responsible for toxicity rather
and carbon dioxide in the presence of folic acid; this than the parent compound itself. Ethylene glycol
minor metabolic pathway is dependent on folate is hepatically oxidized to glycoaldehyde via ADH
stores. Acidosis occurs secondary to formic acid in the presence of oxidized nicotinamide adenine
buildup and lactic acidosis. Formic acid is thought to dinucleotide (NAD+). Once NAD+ is depleted, the
be responsible for the optic and retinal toxicity seen citric acid cycle is inhibited and anaerobic metabo-
in methanol poisoning.13,14 In addition, formic acid lism is favored, causing the formation of lactate from
inhibits cytochrome oxidase c in the mitochondria pyruvate. Glycoaldehyde is converted to glycolic
and shifts cellular metabolism from aerobic to anaer- acid by ALDH. Glyoxylic acid formed from glycolic
obic glycolysis, resulting in a lactic acidosis. Acido- acid is then metabolized to oxalic acid. Oxalic acid
sis contributes to formate crossing the blood–brain combines with serum calcium to form calcium oxa-
barrier and results in the neurologic effects seen in late; these crystals deposit in the renal tubules and
methanol intoxication.15,16 A small percentage (2.5%) cause nephrotoxicity. The presence in the urine of
of nonmetabolized methanol is excreted through the monohydrate calcium oxalate crystals has been used
respiratory system. to rapidly test for ethylene glycol toxicity; however,
these crystals are not reliable indicators since they
Ethylene Glycol are often confused with hippuric acid crystals and
Ethylene glycol, commonly present in radiator anti- do not always show up in the urine of patients with
freeze, is also found in degreasing agents, foam stabi- subsequently proven ethylene glycol ingestion.3,20,21
lizers, and metal cleaners. It was initially synthesized Thiamine and pyridoxine are cofactors for the
in 1859 by Charles-Adolphe Wurtz, a French chemist, production of nontoxic metabolites. In the presence
and was used as an engine coolant as early as World of thiamine, glycolic acid is metabolized to alpha-
War I. It is an odorless, colorless, and sweet-tasting hydroxy-beta-ketoadipate, while pyridoxine allows
liquid. Peak concentrations of ethylene glycol have for the metabolism of glyoxylic acid to glycine.
been reported 1 to 4 hours after ingestion. Approxi-

Table 1.Toxic Alcohol Pharmacokinetics

Toxic Alcohol Volume of Distribution (L/kg) Rate of Elimination

No Treatment Treatment with Ethanol Treatment with Hemodialysis

or Fomepizole (at 225 mL/min)

Methanol 0.6-0.7 • Low serum concentration First-order kinetics: First-order kinetics:

First-order kinetics: Half-life = 54 h Half-life = 2.5 h
Half-life = 2.5-3.0 h
• High serum concentration
Zero-order kinetics:
8.5-9.0 mg/dL/h
Ethylene glycol 0.5-0.8 First-order kinetics: First-order kinetics: First-order kinetics:
Half-life = 8.5 h with normal Half-life = 14-17 h Half-life = 2.5 h
creatinine clearance with normal creatinine
clearance, 49 h with de-
creased renal function

Isopropanol 0.6-0.7 First-order kinetics: NA NA

Half-life = 2.5-3.5 h

Abbreviations: h, hours; NA, not applicable.

November 2010 • EBMedicine.net 3 Emergency Medicine Practice © 2010

Isopropanol Prehospital Treatment
Isopropanol is the most common toxic alcohol expo-
sure in the United States.1 It is commonly found in Prehospital management includes recognition of
rubbing alcohol and other antiseptic products such the life-threatening sequelae that can occur second-
as hand sanitizers. Unlike methanol and ethylene ary to toxic alcohol ingestion, such as respiratory
glycol, its metabolism does not result in an anion distress and hemodynamic instability from severe
gap acidosis and its toxicity is much milder. Similar metabolic acidosis, traumatic injuries from intoxica-
to methanol and ethylene glycol, it is hepatically tion, and hypoglycemia from concomitant ethanol
metabolized by ADH. Its metabolite is acetone, ingestion. The key to efficiently diagnosing any
which is a ketone. Because acetone does not undergo type of toxic ingestion includes careful inspection
metabolism through ALDH, isopropanol is com- of the scene and the questioning of family members
monly known as the toxic alcohol that causes ketosis and any other bystanders, if present, to identify any
without acidosis. Peak serum concentrations of types of agents that the patient may have ingested.
isopropanol occur within 30 to 60 minutes of inges- In addition, emergency medical services (EMS) per-
tion; peak serum acetone levels occur at 4 hours.22,23 sonnel can often provide crucial historical informa-
Several case reports and studies confirm that isopro- tion if they find empty containers at the scene. Due
panol’s half-life is less than that of acetone (2.5-16.2 to associated QT prolongation from hypocalcemia
h vs 7.6-26 h).24,25 related to ethylene glycol ingestion, EMS may be
instructed to administer calcium carbonate to pa-
Differential Diagnosis tients with ventricular dysrhythmias.

Toxic alcohols should be part of the differential Emergency Department Evaluation

diagnosis of any patient with an elevated anion or
osmolar gap, as well as any inebriated patient with Methanol
a nondetectable serum ethanol concentration. (See Methanol toxicity commonly affects the neurologi-
Table 2.) cal, ophthalmological, and gastrointestinal systems.
Of the 3 toxic alcohols, methanol is the least ine-

Figure 1. Toxic Alcohol Metabolism

Ethylene glycol Methanol Isopropanol

ADH* ADH*

Glycoaldehyde Formaldehyde Acetone

ALDH

Glycolic acid Formic acid

Thiamine Folic acid

Glyoxylic acid alpha-hydroxy-beta- CO2 + H20

ketoadipate

Pyridoxine

*ADH is antagonized by ethanol and fomepizole.

Oxalic acid Glycine
Abbreviations: ADH, alcohol dehydrogenase; ALDH, aldehyde dehydrogenase.

Emergency Medicine Practice © 2010 4 EBMedicine.net • November 2010

briating and does not produce the same degree of Isopropanol
intoxication as ingestion of similar concentrations Isopropanol intoxication is primarily associated with
of isopropanol. Within the first 24 hours, central gastrointestinal and neurologic effects. The emer-
nervous system (CNS) depression, euphoria, and gency clinician may initially notice that the patient’s
inebriation occur. This is followed by a latent period breath has a fruity odor due to ketosis. Gastrointesti-
(between 6 and 30 hours) during which methanol is nal signs include abdominal pain, nausea, vomiting,
metabolized to formic acid, which ultimately leads and hematemesis. Although hemorrhagic gastritis
to systemic effects. was initially thought to be due to direct irritation of
Ophthalmologic symptoms can range from the gastric mucosa by isopropanol itself, Dyer et al
blurry vision, decreased visual acuity, and pho- reported a case due to dermal absorption of isopro-
tophobia to blindness or the classic “snowstorm” panol.33 Neurologic manifestations include CNS
vision. Initially, visual fields are not affected and depression (often more profound than that seen in
patients may have a central scotoma (blind spot). ethanol toxicity in relation to comparable serum al-
These symptoms are followed by hyperemia of the cohol concentrations), nystagmus, ataxia, confusion,
optic nerve and edema of the disc margin and retina. and coma. Acute renal failure, rhabdomyolysis, and
If unrecognized and not appropriately treated, these myoglobinuria may occur secondary to prolonged
changes will result in permanent blindness, absent “down time” prior to resuscitation and treatment.
papillary response, and permanent optic nerve
atrophy.4,12,22 During methanol ingestion epidemics,
Diagnostic Studies
it has been reported that 25% to 33% of patients had
permanent visual sequelae.4,27
Serum Chemistry Values And Serum
Severe methanol intoxication can cause parkin-
Osmolality
sonian features, such as a masked facies, tremors,
Because most hospital laboratories cannot rapidly
and muscle rigidity. Other neurologic symptoms
measure serum concentrations of toxic alcohols, the
reported in the literature include transverse myelitis,
emergency clinician must rely on the basic serum
pseudobulbar palsy, cognitive deficits, and basal
chemistry profile and osmolality to implicate toxic
ganglia hemorrhages. Methanol toxicity causes gas-
alcohol ingestion. Serum electrolytes will allow the
trointestinal symptoms such as abdominal pain with
calculation of anion and osmolar gaps. To properly
or without evidence of pancreatitis and/or hepato-
interpret these gaps, the following laboratory tests
toxicity.4,16,27-30
should be ordered at the same time and from the
same blood sample: electrolytes, osmolality, ethanol
Ethylene Glycol
level, and toxic alcohol concentrations. Arterial and
Although several sources discuss the 3 stages of eth-
venous blood gases are also useful for assessing
ylene glycol toxicity, the emergency clinician should
the degree of intoxication and should be measured
realize that not all patients will exhibit them. These
concurrent with other blood studies.
stages are outlined in Table 3.
In severe cases, delayed cranial nerve deficits
may occur 5 to 20 days after ingestion and can
involve cranial nerves II, V, and VII to XII. Bilateral Table 3. Clinical Stages In Ethylene Glycol
facial neuropathy has commonly been reported.5,32 Toxicity5,31
Stage Symptoms

1: Neurological • Initial: intoxication, euphoria

Table 2. Differential Diagnosis For High (0.5-12 hours) • After 4 to 12 hours, if ingestion is se-

Anion And/Or Osmolar Gap vere: CNS depression, seizures,

meningismus, nystagmus, ataxia,
Elevated Anion Gap Elevated Osmolar Gap ocular external muscle paralysis, hyper-
• Methanol, metformin • Acetone reflexia, muscle spasms, hypocalcemia
• Uremia • Ethanol, ethylene 2: Cardiopulmonary • Tachycardia, mild hypertension, hy-
• Diabetic ketoacidosis glycol, methanol (12-24 hours) perventilation (secondary to metabolic
• Alcoholic ketoacidosis • Mannitol acidosis)
• Paraldehyde, phenformin • Osmotic contrast dyes • Acute respiratory distress syndrome,
• Isoniazid, iron • Propylene glycol congestive heart failure, cardiac dys-
• Lactic acidosis (cyanide, hydro- • Isopropanol rhythmia (secondary to hypocalcemia
gen sulfide, sodium azide) and QTc prolongation)
• Ethylene glycol 3. Renal • Oliguria, flank pain, acute renal failure
• Salicylates, theophylline (24-72 hours) • Renal failure (typically reversible)
• Caffeine, seizures • Bone marrow suppression
• Benzyl alcohol, acetaminophen
Abbreviation: CNS, central nervous system.

November 2010 • EBMedicine.net 5 Emergency Medicine Practice © 2010

 Osmolarity indicates the total number of par- lized to formic acid and glycolic acid, respectively,
ticles in solution per liter, while osmolality indicates a metabolic acidosis develops, thus increasing the
the number of particles per kilogram of solvent. Se- anion gap. These toxic intermediate compounds cor-
rum osmolality should be measured by the freezing- relate with the degree of acidosis and with elevation
point depression method rather than by the vapor- of the anion gap.38-40
pressure method, since the latter technique will
underestimate the concentrations of volatile alcohols Anion Gap
(methanol, ethylene glycol, and isopropanol).34,35 The anion gap provides an estimate of unmeasured
The following equations are used to determine the anions and is calculated as follows:
serum osmolality (Osmm) and osmolar gap (Osmg)
by using the calculated serum osmolarity (Osmc)1: Equation 4: Estimating Anion Gap

Equation 1: Determining Serum Osmolarity Calcu- Anion gap = (sodium) – (chloride + bicarbonate)
lated (Osmc)
What is considered to be a normal anion gap
Osmc = [2 x (sodium)] + (BUN/2.8) + (glucose/18) + (ethanol/4.6) will vary among laboratories, but in most cases it is
approximately 8 to 12 mmol/L. Figure 2 shows the
Abbreviations: BUN, blood urea nitrogen; Osmc, calculated serum reciprocal relationship between the osmolar gap and
osmolarity.
the anion gap. Both of these gaps need to be inter-
preted in relation to the time of alcohol ingestion;
Equation 2: Determining Osmolar Gap (Osmg) early after ingestion, the anion gap may be normal,
whereas late after ingestion, the osmolar gap may be
Osmg = Osmm – Osmc
normal.
Abbreviations: Osmc, calculated serum osmolarity; Osmg, osmolar
gap; Osmm, measured serum osmolality. Detection Of Metabolic Acidosis
In methanol and ethylene glycol toxicity, an arte-
The difference between the measured osmolal- rial blood gas value may reveal a metabolic acidosis
ity and calculated osmolarity is the osmolar gap. The with a compensatory respiratory alkalosis. Isopro-
osmolar gap typically ranges between −14 and +10 panol toxicity does not typically cause a metabolic
mOsm. Since the osmolar gap varies from person to acidosis unless it is due to hypoxia or hypotension.
person, its interpretation can often prove challeng- Metabolic acidosis in ethylene glycol or methanol
ing.36,37 There are no robust data on when to suspect intoxication is primarily due to their toxic metabo-
toxic alcohol ingestion on the basis of the osmolar
gap. Hovda et al proposed that an osmolar gap
of greater than 25 mOsm in the setting of acidosis Figure 2. Relationship Between Osmolar
should suggest toxic alcohol ingestion.38 Toxic alcohol And Anion Gaps38
concentrations (Equation 3) can be estimated based
on the osmolar gap as calculated by Equation 2. 80

OG n Anion gap
Equation 3: Estimating Toxic Alcohol Concentration 70
n Osmolal gap
— S-methanol
[Toxic alcohol (in mg/dL)] = Conversion factor* x Osmg 60
Result of analyzes (mmol/L

— S-formate
AG
or mOsm/kgH20)

*See Table 4 for conversion factors 50

40 OG
The conversion factor (see Table 4) is based on the AG
molecular weight of each substance. 30
The parent compound accounts for the osmolar
gap. As methanol and ethylene glycol are metabo- 20
AG OG
10

Table 4. Conversion Factors 0

Early Intermediate Late
Toxic Alcohol Conversion Factor
Abbreviations: AG, anion gap; OG, osmolar gap.
Methanol 3.2
Ethanol 4.6 Reproduced with kind permission from Springer Science+Business
Isopropanol 6.0 Media: Intensive Care Medicine. Anion and osmolal gaps in the diag-
nosis of methanol poisoning: clinical study in 28 patients. Volume 44,
Ethylene glycol 6.2
January 2004, pages 1842-1846, Hovda KE.

Emergency Medicine Practice © 2010 6 EBMedicine.net • November 2010

lites. In addition, lactic acid generated from anaero- hours and are excreted up to 40 hours after inges-
bic metabolism and hypotension (in very ill patients) tion.50 As seen in Figure 3, 2 forms of calcium oxa-
contributes to the acidosis. A falsely elevated lactate late crystals exist: monohydrate crystals, which are
level in ethylene glycol toxicity may occur on some shaped like needles; and dihydrate crystals, which
assays, owing to the similarity in the structures of are shaped like envelopes. Jacobsen et al found that
lactate and glycolic acid.41,42 dihydrate crystals are seen within 5 hours after
ingestion and monohydrate crystals within 7 hours
Other Common Laboratory Abnormalities after ingestion.50 Monohydrate calcium oxalate
Hypocalcemia and renal failure can be seen in stones in the urine were initially thought to be a
patients with ethylene glycol toxicity. Oxalic acid reliable diagnostic test to rapidly help in diagnos-
chelates serum calcium to form calcium oxalate ing ethylene glycol toxicity; however, they are often
crystals that are deposited in the proximal renal confused with hippuric acid crystals and therefore
tubule, resulting in nephrotoxicity.43,44 (See Table 5.) are not reliable.20,21 Crystals may be absent early in
Hypocalcemia can also cause QTc prolongation and the course of the ingestion and do not reliably show
lead to ventricular dysrhythmias. Falsely elevated up in the urine.3
creatinine can be seen in isopropanol intoxication. Using Wood’s light to examine the urine has
Acetone is known to interfere with colorimetric been used as an adjunctive test for detecting eth-
creatinine assay, specifically ones that use the Jaffe ylene glycol. Sodium fluorescein, a component of
alkaline picrate reaction. The clinician should be many brands of antifreeze, is used by mechanics to
aware that blood urea nitrogen (BUN) remains nor- detect coolant leaks. The Wood’s lamp, a source of
mal despite an elevated creatinine.45-47 ultraviolet energy, excites sodium fluorescein and
produces visible urine fluorescence. Many studies
Toxic Alcohol Concentrations have shown that the finding of fluorescence with
The definitive diagnosis for any toxic alcohol Wood’s lamp is neither specific nor sensitive, since
ingestion can be determined by measurement of the confirmation of actual fluorescence may be
the serum concentration for that specific alcohol. operator-dependent and other medications and food
Turnaround and reporting times for results of these products can also cause the urine to fluoresce.51,52
tests are typically prolonged because most hospital
laboratories do not have the dedicated gas chro- Imaging
matography and mass spectrometry equipment Brain imaging may be useful in diagnosing possible
necessary for this test. Since several hours may pass methanol and ethylene glycol exposures. Following
before a serum concentration can be obtained, the methanol exposure, findings on computed tomogra-
potential for increased morbidity and mortality is phy (CT) of the brain — particularly within the first
great if treatment decisions are delayed pending 24 hours — are usually normal. The most common
these results. In addition, because of the high volatil- finding is bilateral putamen necrosis, followed by
ity of these substances, toxic alcohol concentrations necrosis of the caudate nucleus. Basal ganglia hem-
may be falsely low if the collecting tubes are not orrhages are also a common finding. Findings on
airtight.48,49 magnetic resonance imaging (MRI) can include atro-
phy of the optic chiasma, prechiasmatic optic lesions,
Urine Tests
Many sources discuss urinary microscopy and
Wood’s lamp fluorescence as useful diagnostic Figure 3. Calcium Oxalate Crystals
tests for ethylene glycol toxicity. These tests should
be used as adjuncts; decisions to begin treatment
should not be based solely on them. Calcium oxalate
crystals can be detected in the urine within 4 to 8

Table 5. Common Laboratory Abnormalities

Toxic Alcohol Anion Osmolar Other Laboratory
Gap Gap Results
Ethylene glycol + (late) + (early) Hypocalcemia, renal
Left and center images show calcium oxalate crystals in the “needle”
failure, low bicar-
shape; the right image shows the crystals in the “envelope” shape.
bonate
Methanol + (late) + (early) Low bicarbonate Clinical Chemistry by Eder, et al. Copyright 1998 by AMERICAN ASS-
SOCIATION FOR CLINICAL CHEMISTRY, INC. Reproduced with
Isopropanol − + Falsely elevated
permission of AMERICAN ASSOCIATION FOR CLINICAL CHEMIS-
creatinine
TRY INC., in the format Journal via Copyright Clearance Center.

November 2010 • EBMedicine.net 7 Emergency Medicine Practice © 2010

occipital lesions, cerebral edema, and lesions of the Ethanol
subcortical white matter.4,53-56 Because patients with Since the 1940s, ethanol has been used as an antidote
methanol intoxication are at increased risk for basal for ethylene glycol and methanol despite never be-
ganglia hemorrhages, it is common practice to avoid ing approved by the U.S. Food and Drug Adminis-
heparinization of the circuit during hemodialysis. tration (FDA) for this indication.60 Based on in vitro
Ethylene glycol exposures can cause cerebral studies, ethanol’s affinity for ADH is greater than
edema, with compression of the supratentorial that of ethylene glycol (by 67-fold) or of methanol
ventricular system. Abnormalities identified on CT (by 15-fold).48 The intravenous (IV) loading dose
may include reversible hypodensities in the thala- is 0.6 to 0.8 g/kg of body weight in a 10% ethanol
mus, basal ganglia, pons, and temporal lobe that are solution in dextrose in water (D5W) (volume/vol-
consistent with meningoencephalitides.5,57 Although ume), followed by a maintenance dose of 80 to 130
cerebral edema often appears ominous on CT imag- mg/kg/h IV. Higher maintenance doses are used in
ing, it can resolve rapidly upon treatment of the tox- patients with chronic alcoholism or during hemo-
icity. Hemorrhagic necrosis of the putamen, globus dialysis. If IV ethanol is not available, oral ethanol
pallidus, and thalamus have also been seen on MRI can be used. The oral loading dose is 0.8 g/kg in a
but are not very common.29,57,58 20% ethanol solution diluted in orange juice. The
oral maintenance dose is 80 mg/kg/h and should
Treatment be increased to maintain a serum ethanol concentra-
tion of 100 to 150 mg/dL. Chronic alcoholics should
Initial treatment in alcohol toxicity consists of ad- be placed on an oral maintenance dose of 150 mg/
dressing airway, breathing, and circulation issues kg/h, while patients on hemodialysis should be
and stabilizing patients with life-threatening events. placed on a oral maintenance dose of 250 mg/kg/h.
Standard recommendations are to maintain
Gastrointestinal Decontamination serum ethanol concentrations at 100 mg/dL; how-
Methods for gastrointestinal decontamination after ever, several cases suggest that lower serum lev-
an ingestion of toxic alcohols have not been well els are just as effective.61-65 Side effects of ethanol
studied. According to the AACT guidelines, toxic treatment include hypoglycemia, CNS depression,
alcohols are rapidly absorbed, so such decontamina- intoxication, thrombophlebitis, and hypotension.4,5,66
tion is of little value.4,5 Activated charcoal should be Cobaugh et al found that 90% of their patients had
administered if co-ingestions are suspected, provid- at least 1 episode of hypoglycemia (glucose less than
ed that the patient has an intact airway. Anecdotal 80 mg/dL) while receiving IV or oral ethanol.66 In a
evidence supports the use of gastric aspiration if retrospective study, Hantson et al studied 26 patients
large amounts of alcohol have been ingested and the with ethylene glycol and methanol intoxication
patient can be treated very quickly after the inges- who were receiving ethanol infusions. They found
tion.59 For more information on current guidelines that the infusion rate had to be changed an average
on gastrointestinal decontamination, see the August of 12 times, most likely due to the fact that ethanol
2010 issue of EM Practice Guidelines Update, “Current induces its own metabolism.67 Due to these potential
Guidelines For Gastrointestinal Decontamination In side effects, patients receiving an ethanol infusion
The Emergency Department.” are typically admitted to the intensive care unit for
close monitoring.
Antidotes
Fomepizole
Treatment with fomepizole or ethanol will inhibit
When compared with ethanol, fomepizole (4-meth-
the action of ADH and thus stop the conversion
ylpyrazole) has 8000 times the affinity for ADH.17,18
of the parent compounds, methanol and ethylene
The FDA approved fomepizole as treatment for
glycol, to their respective toxic metabolites.2,3 (See
ethylene glycol toxicity in 1997 and for methanol
Figure 1, page 4.) Treatment should begin as soon as
possible, since this antidotal therapy is not helpful
once the parent compound has already been metabo-
lized. According to the AACT guidelines, fomepizole Table 6. Indications To Start Antidotal
should be the first-line therapy.4,5 Ethanol should Therapy For Methanol Or Ethylene Glycol
be administered only if fomepizole is not available. Toxicity4
Either treatment should begin when methanol or • Serum concentration of methanol or ethylene glycol > 20 mg/dL
ethylene glycol concentrations exceed 20 mg/dL and • History or suspicion of methanol or ethylene glycol ingestion and
should be continued until concentrations drop be- 2 of the following:
low this level. Note that ADH inhibitors are not used l
Osmolal gap > 10 mOsm
for isopropanol toxicity (see section on Isopropanol l
Arterial pH < 7.3
Intoxication, page 12). See Table 6 for indications l
Serum bicarbonate < 20 mmol/L
for beginning antidotal therapy. l
Presence of urinary oxalate crystals

Emergency Medicine Practice © 2010 8 EBMedicine.net • November 2010

toxicity in 2000. The evidence in support of fomepi- 8.) Burning at the infusion site is the most common
zole therapy comes from the 2 Methylpyrazole for side effect, so diluting fomepizole in 100 mL of 0.9%
Toxic Alcohols (META) trials that demonstrated its normal saline or D5W with infusion over 30 minutes
efficacy.2,3 Its advantages over ethanol include easier is recommended. Fomepizole is contraindicated in
dosing, more predictable kinetics, and fewer side ef- patients who are allergic to pyrazole derivatives.
fects.11 Its primary and significant disadvantage is its
high cost (about $1,000 per 1.0-g vial). Sodium Bicarbonate
Lepik et al compared the adverse drug events With acidosis, the toxic metabolites penetrate end-
associated with ethanol versus fomepizole therapy organ tissues, and the severity of the acidosis cor-
over a 10-year period.11 This cohort study included relates with overall outcome. Prospective trials have
172 patients, 140 treated primarily with ethanol not explored how to administer sodium bicarbonate;
and 32 with fomepizole. Over half the ethanol- however, according to AACT guidelines, an arte-
treated patients had an adverse drug event due rial pH less than 7.3 should be treated with sodium
to the therapy, in contrast to 12% of those treated bicarbonate administration to keep the pH between
with fomepizole. The predominant adverse effect 7.35 and 7.45.4,5 The authors recommend adding
was CNS toxicity (48% in the ethanol group vs 2% 150 mEq of sodium bicarbonate to 1 L of D5W and
in the fomepizole group). Asymptomatic hypogly- infusing this solution at a rate of 150 to 200 mL/h
cemia (serum glucose 49-68 mg/dL) was found in in adults or 1.5 to 2 times the maintenance dose in
5 of the ethanol-treated patients but in none of the children. When correcting acidosis in the setting of
fomepizole-treated patients. This study reinforced ethylene glycol toxicity, hypocalcemia may be exac-
the well-accepted safety profile of fomepizole com- erbated. In addition, hypokalemia may occur and
pared with ethanol. should be replaced as needed.
The current IV dosing regimen for fomepizole,
based on preclinical studies and recommended by Hemodialysis
the AACT, is outlined in Table 7. After 48 hours, Methanol And Ethylene Glycol Intoxication
fomepizole induces its own metabolism, so the dose Hemodialysis is very efficient in increasing the
must be increased to 15 mg/kg. Its low volume of elimination of both the parent compounds, metha-
distribution (0.6-1.0 L/kg) and low degree of protein nol and ethylene glycol, and their toxic metabolites.
binding makes it amenable to patients receiving AACT guidelines are outlined in Table 9.
hemodialysis; therefore, it should be administered Hemodialysis should be considered when these
every 4 hours during dialysis treatments. (See Table serum toxic alcohol concentrations exceed 50 mg/
dL, regardless of renal functional status or the pres-
ence of acid-base abnormalities. Recent studies and
Table 7. Fomepizole Dosing (Intravenous)4,5 case reports suggest that hemodialysis may not
be needed if treatment with fomepizole is started
Loading Dose • 15 mg/kg early after ethylene glycol ingestion and there is no
Maintenance Dose • 10 mg/kg every 12 h (x 4 doses), evidence of acidemia or alterations in renal func-
then 15 mg/kg every 12 h tion.12,17,68,69 However, this practice will probably
not be efficient for patients with methanol intoxica-
tion, since methanol’s half-life can reach to 54 hours.
Table 8. Fomepizole Dosing In Patients On Methanol is eliminated very slowly when ADH is
Hemodialysis inhibited; therefore, several weeks of treatment with
fomepizole alone may be required if hemodialysis is
At the beginning of hemodialysis never initiated. (See Table 1, page 3). Hemodialysis
• If < 6 hours since last dose, do not administer dose should be continued until acidemia resolves, signs
• If ≥ 6 or more hours since last dose, administer next scheduled of end-organ damage (eg, renal failure with ethylene
dose glycol and visual disturbances with methanol) have
During hemodialysis
• Administer dose every 4 hours
Table 9. Indications For Hemodialysis In
When hemodialysis is completed Methanol And Ethylene Glycol Toxicity4,5
If the time between the last dose and the end of hemodialysis is:
• < 1 hour: do not administer dose at the end of hemodialysis • Metabolic acidosis ( pH < 7.25-7.30)
• 1-3 hours: administer half of next scheduled dose • Vision abnormalities
• > 3 hours: administer next scheduled dose • Renal failure
• Electrolyte abnormalities not responsive to conventional treat-
Maintenance dosing off hemodialysis ment
• Give next scheduled dose 12 hours from the last dose adminis- • Hemodynamic instability refractory to intensive care treatment
tered • Serum concentration > 50 mg/dL

November 2010 • EBMedicine.net 9 Emergency Medicine Practice © 2010

 Clinical Pathway For Initial Evaluation Of Toxic Alcohol Poisoning

Altered mental status or suspicion of toxic alcohol ingestion

1. Check ABCs
2. Provide IV line and oxygen as needed
3. Check fingerstick blood glucose
4. Question EMTs, family, and friends
5. Order toxicology consult or call local poison control center
(1-800-222-1222)

Check serum osmolality, ethanol level, electrolytes, renal function,

ABG, and methanol, isopropanol, and ethylene glycol levels
(Class II)

See Clinical Pathway For Management

High suspicion of isopropanol ingestion? YES
Of Isopropanol Poisoning, page 11

NO

See Clinical Pathway For Management Of Methanol

And Ethylene Glycol Poisoning, page 11

Abbreviations: ABCs, airway, breathing, circulation; ABG, arterial blood gas; EMT, emergency medical technician; IV, intravenous.

Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.
Class I Class II Class III Indeterminate tatives from the resuscitation
• Always acceptable, safe • Safe, acceptable • May be acceptable • Continuing area of research councils of ILCOR: How to De-
• Definitely useful • Probably useful • Possibly useful • No recommendations until velop Evidence-Based Guidelines
• Proven in both efficacy and • Considered optional or alterna- further research for Emergency Cardiac Care:
effectiveness Level of Evidence: tive treatments Quality of Evidence and Classes
• Generally higher levels of Level of Evidence: of Recommendations; also:
Level of Evidence: evidence Level of Evidence: • Evidence not available Anonymous. Guidelines for car-
• One or more large prospective • Non-randomized or retrospec- • Generally lower or intermediate • Higher studies in progress diopulmonary resuscitation and
studies are present (with rare tive studies: historic, cohort, or levels of evidence • Results inconsistent, contradic- emergency cardiac care. Emer-
exceptions) case control studies • Case series, animal studies, tory gency Cardiac Care Committee
• High-quality meta-analyses • Less robust RCTs consensus panels • Results not compelling and Subcommittees, American
• Study results consistently posi- • Results consistently positive • Occasionally positive results Heart Association. Part IX. Ensur-
tive and compelling Significantly modified from: The
Emergency Cardiovascular Care ing effectiveness of community-
Committees of the American wide emergency cardiac care.
Heart Association and represen- JAMA. 1992;268(16):2289-2295.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual
needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright © 2010 EB Practice, LLC d.b.a. EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of
EB Practice, LLC d.b.a. EB Medicine.

Emergency Medicine Practice © 2010 10 EBMedicine.net • November 2010

 Clinical Pathway For Management Of Methanol
And Ethylene Glycol Poisoning

One or more of the following 1. Administer fomepizole 15 mg/

criteria?: kg (Class III)
2. Work up other reasons for
• Anion gap > 12 presentation
No, or toxic alcohol levels
• Osmolar gap > 10 3. Consider isopropanol ingestion
not readily available
• Ethylene glycol > 20 mg/dL if there is ketosis and osmolar
• Methanol > 20 mg/dL gap without other apparent
• Evidence of metabolic acidosis cause (particularly without aci-
• Evidence of renal failure dosis). See Clinical Pathway
For Management Of Isopropa-
YES nol Poisoning.
4. Admit to ICU

Administer fomepizole 15 mg/kg

(Class II)

Ethylene glycol Methanol

1. Administer thiamine 100 mg IV 1. Administer folinic acid (leucov-

AND administer pyridoxine 100 orin) 50 mg IV OR administer
mg IV (Class III) folic acid 50 mg IV (Class III)
2. Order renal consult if 2. Order ophthalmologic consult
• presentation is delayed, 3. Consider renal consult for
• patient is acidemic, or potential hemodialysis if
• there are signs of renal • ingestion is large,
insufficiency • presentation is delayed,
3. Admit to ICU or
• there are visual distur-
bances
4. Admit to ICU

Clinical Pathway For Management Of Isopropanol Poisoning

Isopropanol ingestion

Is patient symptomatic? 1. Administer proton-pump inhibitor (Class III)

NO
2. Clear from a toxicologic standpoint

YES

1. Administer proton-pump inhibitor (Class III)

2. Admit to ICU vs general medical floor if
• persistent CNS depression or
• hemorrhagic gastritis

See Class of Evidence Definitions, page 10.

Abbreviations: CNS, central nervous system; ICU, intensive care unit; IV, intravenous.

November 2010 • EBMedicine.net 11 Emergency Medicine Practice © 2010

improved, and serum methanol and/or ethylene Fomepizole is a Category C drug. Several case
glycol concentrations drop below 20 mg/dL. reports have been published in which pregnant pa-
tients with methanol intoxication have been treated
Cofactors with ethanol or fomepizole.7,79-81 Two case reports
The administration of cofactors will promote the me- that describe chronic methanol inhalation during
tabolism of intermediate metabolites into nontoxic pregnancy found fetal cerebral infarcts, bilateral
metabolites, although substantial clinical evidence of frontal cortical leukomalacia, and intraventricular
their efficacy is not currently available. In ethylene hemorrhage.7,79 One of these cases suggests that
glycol toxicity, pyridoxine and thiamine increase methanol crosses the placenta.79 Ethanol should not
the metabolism of glycine and alpha-hydroxy-beta- be used in the treatment of pregnant patients, since
ketoadipate, respectively. In methanol toxicity, either it is teratogenic and can cause fetal alcohol syn-
folinic acid (leucovorin) or folic acid promotes the drome.
metabolism of formic acid.70,71 (See Table 10.) Very few case reports have been published for
ethylene glycol or isopropanol intoxication in preg-
Isopropanol Intoxication nancy.
Treatment for isopropanol intoxication is typically
supportive. Treatment with ADH inhibitors is not Controversies/Cutting Edge
indicated, since isopropanol’s metabolite — acetone
— is not as toxic as its parent compound.72 Proton- Hemodialysis In Isopropanol Intoxication
pump inhibitors may be helpful, since hemorrhagic Isopropanol ingestions are generally treated sup-
gastritis can occur. Hemodialysis is rarely indicated portively. Clearance of isopropanol during hemodi-
but has been reported when isopropanol levels alysis was significantly increased according to a case
exceed 150 to 400 mg/dL, and it can increase the report of a 61-year-old male who arrived comatose
rate of clearance of both isopropanol and acetone.46 in the ED, was hypotensive (blood pressure 80/60
Hemodialysis should be considered if a patient is mm Hg), and had a serum isopropanol concentra-
hemodynamically unstable or comatose.73,74 tion of 309 mg/dL. Two hours after hemodialysis
was initiated, this patient began responding to
Special Circumstances verbal commands.74 Much of the literature cites this
case in support of dialysis for patients with large iso-
Pediatric Patients propanol ingestions who are comatose or hypoten-
Children who ingest more than a taste of ethylene gly- sive or who have serum concentrations greater than
col or any amount of methanol are referred by poison 400 mg/dL. In addition, isopropanol is amenable
control centers to the ED for evaluation.75 In children to dialysis owing to its low volume of distribution,
18 months to 4.5 years of age, a mouthful is between 5 low protein binding, and low molecular weight.
and 10 mL and could potentially result in concentra- Contrary to this thinking, Trullas et al argue that no
tions that exceed 20 mg/dL of either toxic alcohol.76 sequelae have been reported after these ingestions
No guidelines are currently available from the AACT and therefore dialysis is not in order, even in life-
or the AAPCC for treating children with toxic alco- threatening situations.73
hol ingestion. In addition, the FDA has not officially
approved fomepizole for use in children. Several case Rapid Toxic Alcohol Test Kits
studies and case series report the administration of As mentioned previously, toxic alcohol concentra-
fomepizole to pediatric patients.77,78 Fomepizole is tions are not readily available in the majority of
preferred over ethanol in children, since they are at risk hospitals, so appropriate treatment is often delayed.
for hypoglycemia (secondary to poor glycogen stores), In an informal survey reported by the University
hypothermia, and CNS depression. of Maryland, the turnaround time for obtaining
an isopropanol, methanol, or ethylene glycol level
Pregnancy was 1 hour, not including the transport time.82 In
Limited data are available regarding the treatment a prospective study based on data from the New
of pregnant patients with toxic alcohol ingestion. York City Poison Control Center, the sensitivity and
specificity of a rapid veterinary qualitative ethylene
glycol kit were determined in humans.83 Twenty-
Table 10. Dosing Regimens For Cofactors four samples were tested with this kit, and the
results were compared with those of the traditional
Ethylene glycol Thiamine: 100 mg IV every 6 hours AND gas chromatography method. Sensitivity was 100%,
Pyridoxine: 100 mg IV every 6 hours while the specificity was 88.8%. Of the 24 samples,
Methanol Folinic acid (leucovorin):1-2 mg/kg (up to 50 15 were confirmed (by gas chromatography) for eth-
mg) IV every 4 to 6 hours OR ylene glycol, 5 for methanol, and 4 were negative for
Folic acid: 50 mg IV every 4 to 6 hours both of these alcohols. This kit qualitatively tested

Emergency Medicine Practice © 2010 12 EBMedicine.net • November 2010

 Risk Management Pitfalls For Diagnosis And Management
Of Toxic Alcohol Poisoning

1. “The anion and osmolar gap were normal, so I are usually sent to outside laboratories, and
didn’t begin treatment.” results are often not quickly available. Fomepi-
Treatment with an ADH inhibitor should be zole decreases the metabolism of each of these
initiated as soon as possible if there is significant alcohols to their toxic metabolites and decreases
suspicion of either methanol or ethylene glycol the incidence of nephrotoxicity (ethylene glycol)
ingestion. At some point, both the anion and and ophthalmologic (methanol) toxicity.
osmolar gaps may be within normal limits (see
Figure 2, page 6). TIME = KIDNEY (for ethylene 7. “I thought isopropanol ingestion should be
glycol) and EYES (for methanol). treated with fomepizole, like methanol and
ethylene glycol.”
2. “He always comes in intoxicated, so I didn’t Isopropanol’s metabolite, acetone, does not
even think of a toxic alcohol ingestion.” cause an acidosis. Inhibiting ADH will prolong
Chronic alcoholics are at risk for methanol, isopropanol’s half-life as well as its CNS depres-
ethylene glycol, or isopropanol ingestion, since sive effects.
these substances are readily available. It can be
challenging to identify a toxic alcohol inges- 8. “Gastric lavage should be attempted in every
tion in a chronic alcoholic, especially if routine poisoned patient.”
serum ethanol concentrations are not checked. Gastric lavage is not recommended for toxic
Frequent reevaluation of the intoxicated patient alcohol ingestion unless the patient has ingested
is required to ensure that clinical improvement large amounts and presents immediately after
is occurring. ingestion. To properly perform gastric lavage, a
32-French gauge orogastric tube must be placed,
3. “The patient was not intoxicated, so I didn’t which can often present a challenge. In addition,
think they actually ingested the toxic alcohol.” this procedure has the potential to cause aspira-
Patients vary in their degree of tolerance and tion and esophageal rupture.
may not exhibit inebriation at levels that are
potentially toxic. 9. “My patient’s methanol level was 100 mg/dL
with no signs of acidemia, renal failure, or
4. “The methanol level was 10 mmol/L, so I didn’t visual disturbances. The last time I took care of
begin treatment.” an ethylene glycol–intoxicated patient I used
The clinician should realize that treatment with only fomepizole as treatment; hemodialysis
fomepizole (or ethanol) should begin when didn’t have to be initiated.”
levels of ethylene glycol or methanol are greater Methanol’s long half-life results in a very long
than 20 mg/dL. Laboratories may report these clearance time. Hemodialysis should be initiated
values in different SI units. in large methanol ingestions even in the absence
of acidemia, visual disturbances, or renal failure.
5. “The child’s mother stated that he drank only a
mouthful of windshield-washer fluid.” 10. “I didn’t think the poison control center was
A mouthful in a child is estimated anywhere open so late at night.”
between 5 and 10 mL and can potentially cause Poison control centers in the U.S. are open 24
methanol levels to exceed 20 mg/dL. Failing to hours a day, 7 days a week. By calling 1-800-222-
treat methanol toxicity can cause irreversible 1222, you will be referred to your local poison
blindness. control center. These centers have specialists
trained in overdoses and have access to a toxi-
6. “I was waiting for the ethylene glycol and cologist at all times.
methanol levels to come back before I ordered
fomepizole; then I found out it was a send-out
test.”
Requests for ethylene glycol and methanol levels

November 2010 • EBMedicine.net 13 Emergency Medicine Practice © 2010

positive for an ethylene glycol level as low as 27 Summary
mg/dL. The only discrepancy occurred in 1 sample,
which was found to be a false positive. Toxic alcohol ingestion is a challenging diagnosis in
the ED. Asking the paramedics, family, and friends
Disposition about the presence of containers at the scene is often
the key to determining whether such an inges-
Patients can be cleared from a toxicologic stand- tion has occurred. Diagnostic tests such as osmolar
point if they do not have evidence of end-organ and anion gaps can help support the diagnosis but
damage, are hemodynamically stable, and have should not be used to exclude this diagnosis. Ulti-
a methanol or ethylene glycol concentration less mately, serum concentrations are necessary to guide
than 20 mg/dL. Admission to the ICU is war- treatment. Fomepizole therapy should be initiated
ranted in cases of acidemia or when signs of end- as soon as possible for methanol or ethylene glycol
organ damage are evident. Patients who are not ingestions to inhibit the conversion of these com-
likely to have methanol or ethylene glycol inges- pounds to their toxic metabolites.
tion, have normal anion and osmolar gaps, are
not acidemic, and improve after several hours of Case Conclusion
observation can be cleared even if a toxic alcohol
concentration is not readily available. Alcoholic An IV line was placed, fomepizole was administered in
ketoacidosis is often confused with toxic alcohol a dose of 15mg/kg, and the patient was placed on fall
ingestion. If alcoholic ketoacidosis is suspected precautions. Lab work revealed the following: an anion
and if acidemia and the anion gap are improving gap of 25, an arterial pH of 7.25, an osmolar gap of 30,
with treatment (ie, fluids, dextrose, thiamine), the and a BUN:creatinine ratio of 13:0.6. Her ethanol level
patient can be cleared if the toxic alcohol concen- was nondetectable. After another discussion with the local
tration is not readily available. Admission to ICU poison control center, you realized that most windshield-
should be considered when there are signs of end- washer fluids contain methanol and some may contain
organ damage or acidemia. Finally, transfer to a ethylene glycol. You consulted nephrology regarding the
tertiary care hospital is necessary if fomepizole or need for hemodialysis and she was admitted to the ICU,
hemodialysis is not readily available. at which time results of the methanol and ethylene glycol
tests were still pending. A methanol concentration of 70
mg/dL was found 24 hours after admission, warranting
fomepizole therapy until her methanol level was less than
20 mg/dL. Hemodialysis was initiated upon admission to
the ICU and was discontinued once her acidemia resolved.
Cost-Effective Strategies Three days later, the patient was transferred to psychiatry,
neurologically intact.

1. If an ingestion of methanol or ethylene is References

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administered as soon as possible. Delaying this Evidence-based medicine requires a critical ap-
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2. Treatment for large methanol ingestions should equally robust. The findings of a large, prospective,
include a renal consult for hemodialysis even randomized and blinded trial should carry more
if there is no sign of acidosis. Methanol’s long weight than a case report.
half-life (up to 30 hours) and Michaelis–Menten To help the reader judge the strength of each
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