0749-5161/02/1805-0360
5
PEDIATRIC EMERGENCY CARE
Copyright © 2002 by Lippincott Williams & Wilkins, Inc.
DOI: 10.1097/01.pec.0000034335.62465.45
Acute methanol ingestion
THOMAS L. SUTTON, MD, ROBIN L. FOSTER, MD, STEVEN R. LINER, MD
Methanol poisoning is an insidious event that can culminate
in severe metabolic disturbances, permanent neurologic dys-
function, blindness, and death. Although numerous adult cases
have been extensively reviewed, there is a paucity of reports
about pediatric ingestions. We present a case of acute methanol
intoxication in a 6-year-old male patient who presented with
headache, nausea, altered mental status, and drowsiness. His
blood methanol level was 350 mg/dL (109.4 mmol/L), despite
the absence of any history or identifiable source of methanol.
Treatment with ethanol, alkalinization, and hemodialysis re-
sulted in full recovery without residua. Unusual facets of this
case are the child’s relatively older age, the extremely high
methanol blood level, and, most remarkably, the complete lack
of visual disturbances on routine ophthalmologic evaluation.
INTRODUCTION
Toxic exposures in children are extremely common. The vast ma-
jority are ingestions involving a readily identified substance, such as
a household chemical, plant, or medication, and do not result in sig-
nificant toxicity (1, 2). Methanol poisonings, however, are potentially
extremely toxic and can have critical effects on the patient, including
severe metabolic disturbances, permanent neurologic dysfunction,
blindness, and death. Therefore, prompt recognition and treatment are
crucial. Yet, aside from two reports involving infants who inadver-
tently received methanol with their formula (3, 4), there is a paucity
of medical literature concerning methanol ingestions in the pediatric
population. We report a case of methanol toxicity in a 6-year-old child
who did not develop any visual disturbances despite having extremely
high blood methanol levels.
CASE
A 6-year-old healthy male child without any prior significant
medical history presented to the pediatric emergency department
(ED) with a chief complaint of “not feeling well” for the previous
three hours, noticeably decreased energy, and difficulty walking.
Previously, he was reportedly normal upon awakening. After eat-
ing breakfast, he took his grandmother’s handbag to her upstairs
bedroom. The pocketbook contained hydrochlorothiazide, insulin,
metformin, trazodone, and ammonium lactate lotion. Other med-
ications in the home included valproic acid, dextroamphetamine,
and oxycodone-acetaminophen. He returned downstairs a short
From the Departments of Emergency Medicine and Pediatrics, Medical
College of Virginia at Virginia Commonwealth University, Richmond,
Virginia.
Address for reprints: Thomas L. Sutton, MD, 2-501st AV BN; 1st AD,
CMR 477; Box 1179, APO AE 09165; e-mail: TnV_Sutton@msn.com
Key Words: Methanol, acidosis, anion gap, formic acid, osmol gap
360
Vol. 18, No.
Printed in U.S.A.
time later and complained of a headache and feeling tired. He was
noted to have difficulty maintaining his balance. He denied inges-
tion of any medications or other substances. The caretakers denied
having any alcohol in the home.
On arrival at the ED 3 hours after the onset of his symptoms, his
vital signs were within the normal limits for his age, and his exam-
ination results were remarkable only for drowsiness, decreased
muscle tone, and an unsteady, wide-based gait. His deep tendon re-
flexes were symmetric but depressed at 1
/4 in both the upper and
lower extremities. His pupils were symmetric at 4 mm and re-
sponded normally to light.
His initial laboratory evaluation included a complete blood count,
electrolytes, blood urea nitrogen, creatinine, and serum glucose; rapid
whole blood glucose was 87 mg/dL. All test results were within the
normal range for the patient’s age, and a urine drug screen was nega-
tive for benzodiazepines, opiates, cocaine, amphetamines, phencycli-
dine, salicylates, and barbiturates. A blood alcohol screen was ob-
tained. In our institution, this screen is performed by headspace gas
chromatography with flame ionization. It includes ethanol, methanol,
isopropanol, and ethylene glycol. Pending the results of the blood al-
cohol screen, the child was given activated charcoal via a nasogastric
tube and 20 cc/kg of intravenous normal saline.
Over the course of 3 hours after his presentation to the ED, the pa-
tient developed increasing somnolence, and he was transferred to the
pediatric intensive care unit. On arrival in the pediatric intensive care
unit, the patient “woke up” and became increasingly active and talk-
ative but continued to complain of a headache, dizziness, and diffi-
culty holding his head up. However, he did not complain of visual
disturbances. An arterial blood gas analysis revealed metabolic aci-
dosis with a pH of 7.21 and a bicarbonate concentration of 16.4
mEq/L. The anion gap was 23 mEq/L, and the osmol gap was 112
mmol/L. (The measured osmolality was 408 mmol/L, and the calcu-
lated value was 296 mmol/L.) By 9 hours after presentation, the al-
cohol screen obtained in the ED came back and showed a methanol
blood level of 350 mg/dL (109.4 mmol/L). The patient was started
on folic acid supplementation and a continuous intravenous ethanol
drip. A few hours later, he was intubated because of worsening men-
tal status. By 15 hours after his presentation, the pH was normalized
with sodium bicarbonate, and hemodialysis was begun. Methanol
was undetectable in the blood after 8 hours of hemodialysis. Twenty-
five hours after his presentation, a detailed ophthalmologic examina-
tion was performed. This included pupillary dilatation with fundu-
scopic visualization. He did not have hyperemic optic disks or any
other notable abnormality. No visual evoked potentials or elec-
troretinograms were performed at this time. The patient was dis-
charged on the third day with no apparent residua from his ingestion.
He failed to return for a follow-up ophthalmology examination.
A home inspection was performed to locate the possible expo-
sure. However, a bottle of deicer fluid in the neighbor’s car was the
only potential exposure source located.
Vol. 18, No. 5 ACUTE METHANOL INGESTION
DISCUSSION
Poisonings are one of the most common medical emergencies in
children. In 1999, the American Association of Poison Centers re-
ported 2.2 million human poison exposures in the United States.
Children under the age of 6 years made up 52.5% of those inci-
dents, but only 7% involved children between the ages of 6 and 12
years (5). In 1999, alcohols and glycols were involved in 95,913
exposures, and 129 of these exposures were fatal (5). Of the com-
mon alcohols (ie, methanol, ethanol, isopropanol) and ethylene
glycol, ethanol is considerably less toxic but accounts for the ma-
jority of deaths. There were 2517 exposures to methanol (602 un-
der age 19) in that year. Eleven deaths were attributed to methanol;
none involved children (5).
Possessing a single carbon atom, methanol is the simplest of the
alcohols. It is a clear, colorless, volatile liquid that is readily solu-
ble in water. The faint, sweet odor is distinct from ethanol. How-
ever, pure methanol and ethanol taste very similar. There are sev-
eral other names for methanol, including methyl hydrate, methyl
alcohol, methylated spirit, wood alcohol, wood spirit, carbinol, and
wood naphtha. Methanol is mostly used in the manufacture and
synthesis of other chemicals. Commercial uses include windshield
washing and deicing fluids, duplicating machine fluids, carburetor
cleaner, solid canned fuels, shellac, paint thinners and removers,
and model airplane fuel. It is also used as a gasoline additive and to
denature alcohol. Finally, methanol has been used in bootleg
whisky and, as such, has been involved in clusters of methanol in-
toxications (6).
Methanol is readily absorbed through the skin, the gastroin-
testinal tract, and the pulmonary viscera (7–10). Absorption
through the gastrointestinal tract is essentially complete, whereas
the inhalation of methanol results in approximately 60% absorp-
tion (11). Once it is absorbed, methanol is redistributed through-
out the total body water. Areas of increased concentration include
the kidneys, liver, gastrointestinal tract, and the cerebrospinal fluid
(12). The highest concentrations are found in the vitreous humor
and the optic nerve (13).
The toxicity related to methanol is a result of its metabolites (ie,
formaldehyde and formic acid) rather than the parent compound. Be-
cause of the prerequisite metabolism to produce the toxic products,
there is a latent period following exposure (6).
A small fraction of methanol is excreted unchanged by the lungs
and kidneys, but the liver is the primary site of metabolism. Alcohol
dehydrogenase oxidizes methanol to formaldehyde. This is the rate-
limiting step in methanol metabolism and is a saturable process (12).
Although formaldehyde is 30 times more toxic than methanol, it does
not contribute to the toxicity of methanol (6, 14). This is due to its very
rapid oxidation to formic acid by aldehyde dehydrogenase. Formic
acid is approximately six times more toxic than methanol and is re-
sponsible for the toxicity seen with methanol exposures (16, 12, 14).
A folate-dependent step completes the final oxidation of methanol to
carbon dioxide and water (15, 16). This is a relatively slow step, and,
thus, there is accumulation of formic acid leading to the clinical toxic-
ity of methanol, including ocular injury and metabolic acidosis (17,
18, 19). In addition, formic acid inhibits the cytochrome P450 chain,
causing a decrease in the oxidized nicotinamide adenine dinu-
cleotide/reduced nicotinamide adenine dinucleotide ratio and forma-
tion of lactic acid (12, 20).
Methanol blood levels peak at approximately 30 to 60 minutes
after ingestion (6). Because the toxicity is due to formate and not
directly to methanol, methanol blood levels may not correlate with
toxicity. Factors to consider include the following: the actual time
361
of ingestion versus the reported time, the coingestion of ethanol,
pre-existing liver disease, the age of the patient, and individual
variability in metabolism (21). Our patient had a level of 350
mg/dL (109 mmol/L), which is the highest level in a child that we
were able to find in the literature, as well as among the highest re-
ported levels in adults (4, 22, 23). Similar to the blood methanol
level, the toxic dose of methanol has considerable variability. The
lowest reported lethal dose was 4 mL of 100% methanol (1.25
mol), but other patients have survived the consumption of 500 to
600 mL of 40% methanol (7.5 mol) (14). Generally accepted lethal
doses range from 30 to 100 mL (1–3 mol) (21).
The clinical symptoms of methanol toxicity are nonspecific. Mis-
diagnoses have included diabetic ketoacidosis, pancreatitis, menin-
gitis, botulism, and congestive heart failure (6). The acute presenta-
tion resembles ethanol inebriation with cognitive slowing, cloudy
sensorium, dizziness, and gastric discomfort (6, 11, 21). As the meth-
anol is metabolized, these symptoms resolve, and the patient enters a
latency period that can extend from 1 hour to as many as 72 hours;
the typical duration is 12 to 24 hours. If ethanol is also ingested, as is
often the case with bootleg whisky, the latency period can be further
extended, because the ethanol competes with alcohol dehydrogenase
(24). A delay in diagnosis can occur in patients presenting during the
latency phase. The outcome may be compromised as formic acid is
allowed to accumulate. Following the latency period, symptoms re-
turn with increased severity along with additional problems. These
include central nervous system dysfunction such as headache, gener-
alized weakness, convulsions, and coma. Gastrointestinal symptoms
include abdominal tenderness, nausea, vomiting, anorexia, and ele-
vation of the pancreatic enzymes, thereby leading to the misdiagno-
sis of pancreatitis. Even with metabolic acidosis, Kussmaul breath-
ing is uncommon (6).
Disturbance of vision is a presenting complaint in the majority of
methanol intoxications and is one of the most specific clinical find-
ings (6, 17–19, 25, 26). In an episode involving multiple cases in
Atlanta, Georgia, visual disturbance was a universal complaint in
all 115 patients with acidosis and in half of the patients without aci-
dosis. Onset was usually within 6 hours of ingestion (6). Formate
affects the retinal Muller cells (27) and possibly the oligoden-
droglia of the optic nerve (28). By inhibiting cytochrome oxidase,
it may affect neuronal and glial cell membrane polarity (19, 29).
Visual complaints include blurred, dimmed, or cloudy vision; cen-
tral and peripheral scotomata; altered color perception; photopho-
bia; visual field defects; and blindness. Mydriatic pupils with a
sluggish light response are commonly observed, even in patients
who do not have visual complaints (6, 11, 17). The lack of ocular
findings on initial presentation is a positive prognostic sign. Per-
manent visual loss has not occurred in any patient with an initial
normal examination (25). The classic examination findings include
optic disc hyperemia and peripapillary edema (19). Optic disc hy-
peremia is one of the earliest funduscopic findings. Onset is be-
tween 18 and 48 hours after ingestion, and it persists up to 3 days.
Peripapillary edema, which spreads radially, has a slower onset and
can persist for 2 weeks. Adults with chronic methanol poisoning
have exhibited abnormalities on electroretinogram (30). However,
case reports and studies involving adults with visual symptoms and
signs vary concerning these findings, particularly in the acute set-
ting (19, 31). Ocular findings can be transient or permanent. Re-
covery, if it does occur, is usually within 1 week (25).
The laboratory evaluation of a patient who is suspected of hav-
ing methanol exposure should include determination of all com-
mon alcohols (ie, ethanol, methanol, isopropanol) and ethylene gly-
col. A low methanol level does not exclude methanol intoxication,
362 PEDIATRIC EMERGENCY CARE
because the level may have been measured prior to achievement of
peak serum levels or after significant metabolism had already oc-
curred. Low levels (30 mg/dL) have also been seen as a result of
natural fermentation after ingestion of wines and fruit spirits (32).
Levels within the toxic range, however, do confirm the diagnosis,
as does the coexistence of metabolic acidosis. Metabolic acidosis
with accompanying anion and osmol gaps is an important asso-
ciated finding. Elevations of amylase, creatinine, and the mean
corpuscular volume and decreases in serum phosphate are com-
mon.
Although the anion gap is neither specific nor sensitive, a level
above 30 mEq/L strongly suggests the presence of organic acidosis
(33). The measured formate level will correspond with the severity
of symptoms and the prognosis (19, 20, 34). Osterloh et al. (22) has
demonstrated a correlation between the formate level and both the
anion gap and the bicarbonate concentration. His studies suggest
that most of the acidosis seen is due to the formate, but some aci-
dosis is a result of lactic acid.
The osmol gap (the difference between the measured osmolality
and the calculated osmolality of the serum) assumes the presence
of an osmotically active substance such as methanol. Osmolality is
the number of moles of solute dissolved in 1 kilogram of solvent,
whereas osmolarity is the number of moles of solute in 1 liter of
solvent. For medical purposes, the two are interchangeable. Both
are colligative properties of a solution—they are dependent only on
the number of dissolved particles and not on the nature of the
solute. Because most toxins are present in relatively small amounts
and have a high molecular weight, they do not exert an osmotic ef-
fect. However, methanol has a low molecular weight (32 D), and
ingestions may involve gram amounts leading to a significant rise
in the serum osmolality (35). Although the osmotic gap is fre-
quently used to assess methanol intoxication, its reliability and ac-
curacy are questionable (35, 36). Current methods in the determi-
nation of serum osmolality appear to be inadequate, and there is
also debate as to what constitutes the normal range (35, 36). A nor-
mal osmol gap does not exclude the presence of an osmotically ac-
tive substance (35).
Prompt recognition and treatment of methanol ingestion is re-
quired to prevent permanent sequelae and death. Because sudden
deterioration can occur in a seemingly stable patient, it is important
not to delay treatment. The establishment of a secure airway is rec-
ommended. Activated charcoal adsorbs 59% of methanol in vitro if
given at a 5:1 ratio (activated charcoal:methanol) (37). However,
because the absorption of methanol from the gastrointestinal tract
is so rapid, it is unlikely that gastric decontamination with charcoal,
or by any other means such as syrup of ipecac or gavage, will be
beneficial (2, 32, 34).
The main goals of treatment involve treating the acidosis, pre-
venting further oxidation of methanol to its toxic metabolites, and
removing methanol and formic acid. Current therapy includes al-
kalinization, the use of ethanol to competitively inhibit the conver-
sion of methanol to formaldehyde by alcohol dehydrogenase, folic
acid supplementation, and hemodialysis. Fomepizole is a new
treatment that also inhibits alcohol dehydrogenase and may be an
alternative to ethanol.
Alkalinization increases the dissociation of formic acid and de-
creases penetration of formic acid into the central nervous system
(6, 32, 38, 39). However, it may or may not alter the clinical course.
The pH should be frequently assessed to maintain a value within
the normal range. Large quantities may be required to achieve this
result.
Alcohol dehydrogenase has a ninefold greater affinity for ethanol
October 2002
compared with methanol (40). A serum concentration of 100 mg/dL
of ethanol has been shown to protect against the toxic sequelae of a
methanol level as high as 282 mg/dL (23). Consequently, the goal of
therapy is to maintain an ethanol level of 100 to 150 mg/dL. Because
the metabolism and elimination of ethanol show individual variation,
levels need to be monitored frequently (32). Ethanol is not without
its problems, including central nervous system depression, hypo-
glycemia, dehydration, and fluctuating serum concentrations (2, 32).
The Food and Drug Administration recently approved fomepizole
(4-methylpyrazole) for ethylene glycol toxicity, and it is replacing
ethanol as the primary treatment. Several case reports have shown its
effectiveness in treating methanol toxicity as well (41–44). Fomepi-
zole is a synthetic competitive inhibitor of alcohol dehydrogenase. In
the presence of methanol, it prevents the production of toxic metabo-
lites. No formal studies have been performed to compare the efficacy
of ethanol versus fomepizole. However, fomepizole has several no-
table benefits. Because it has a longer and more reliable half-life, it is
given every 12 hours and not as a continuous infusion. This also
eliminates the need to monitor drug levels. It is metabolized by the
cytochrome P450 mixed function oxidase system to 4-carboxypyra-
zole, which is then excreted through the kidney (45). Most impor-
tantly, fomepizole does not alter mental status nor does it cause cen-
tral nervous system depression (6, 37, 46). Side effects include
severe headache, nausea, dizziness, and rash (6, 37, 45). The primary
deterrent for its use is the cost (46). Because it induces its own me-
tabolism, the dose is increased during the treatment course. Initially,
a loading dose of 15 mg/kg is given, followed by a dose of 10 mg/kg
every 12 hours for four doses. The dose is then increased to 15 mg/kg
and continued every 12 hours until the methanol level is lower than
20 mg/dL (46). Fomepizole has not yet been studied in the pediatric
population.
Folic acid and its metabolites are reduced in the liver in patients
with methanol poisoning. Humans and monkeys are unique in the
animal world in that the metabolism of formate to carbon dioxide
is a slow process. Although they use the same pathway, rats rapidly
convert formate and are not subject to its toxic effects (16, 34).
Primates who are folate deficient demonstrate methanol toxicity
at lower levels of methanol ingestion (34). Conversely, administra-
tion of folate has been shown to speed the metabolism of formic
acid in primates that have been made folate deficient. The concen-
trations of folate are reduced in a human with methanol toxicity.
Thus, it is recommended that folate be given intravenously at 50 to
75 mg every 24 hours for at least 24 hours (22).
Hemodialysis will remove both the parent compound and the
toxic metabolite (47). Hemodialysis is recommended if the patient
is symptomatic, has methanol levels greater than 25 mg/dL, or has
metabolic acidosis (32).
CONCLUSIONS
This case of methanol ingestion in a 6-year-old child had several
unique aspects. First, the child was older than the usual age for self-
administration of an unknowingly toxic substance. In addition,
there is usually a clear history of exposure and the substance taken
in pediatric intoxications (1). In this case, identification of the toxin
was accomplished only by laboratory investigation. Finally, de-
spite having the highest blood level of methanol reported in the pe-
diatric population, this child had no ocular complaints or demon-
strable ocular findings. Because of the variable presentation of
methanol intoxication and the well-described latency period, we
suggest that the physician maintain a high index of suspicion for
methanol exposure.
Vol. 18, No. 5 ACUTE METHANOL INGESTION
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