CE U P D A T E -

T O X I C O L O G Y II
Robert H. Williams, PhD, DABCC, FACB, MT(ASCP)
Timothy Erickson, MD, FACEP, FACMT

Evaluating Toxic Alcohol

Poisoning in the Emergency
Setting

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ABSTRACT Ingestion of a toxic alcohol often occurs when
an alcoholic patient cannot obtain ethanol and thus, seeks
an ethanol substitute. Methanol produces visual
disturbances, while ethylene glycol produces pulmonary and
renal disturbances. Ingestion of isopropanol results in
acetone production that can lead to central nervous system
depression. Unlike methanol and ethylene glycol poisoning,
however, isopropanol poisoning generally does not produce
major disturbances in acid-base balance. Most clinical
laboratories do not perform toxic alcohol analyses. Thus, the
clinician relies on interpretation of other clinical laboratory
data to ascertain the presence or absence of a toxic alcohol.
No heart murmur was evident. His abdomen was
soft and nontender, and hypoactive bowel sounds
were noted. Stools were negative for occult blood.
No cyanosis or edema were present in the extremi-
ties. The skin was moist, anicteric, and acyanotic.
Chest radiograph revealed no pulmonary edema.
The urinalysis indicated the presence of glucose
(4+), protein ( + ), oxalate crystals, WBC (3-5),
and RBC (4-6) but no ketones. Results of labora-
tory tests are shown in Table 1.
The patient was given 50% dextrose in water
(D50W), thiamine hydrochloride, and naloxone by
intravenous administration. He did not respond to
treatment and therefore was orally intubated.

This is the second article in a four-part series on clinical toxicology. On completion

Toxic Alcohols
of this series, the reader will be able to correlate clinical findings from the poisoned
Methanol, ethylene glycol, and isopropanol are
patient with data provided by the clinical laboratory that leads to a diagnosis;
differentiate the medical necessity between an acute vs chronic therapeutic
commonly referred to as the toxic alcohols
overdose; and describe the therapeutic interventions used by clinicians for patient (although many laboratory professionals and
management. physicians are not aware that ethylene glycol is
classified as an alcohol). Methanol, also known as
From the Department
Case Presentation "wood alcohol," is found in windshield washer
of Pathology, Division
of Clinical Pathology A 19-year-old man was brought to the emergency fluid and many industrial solvents; ethylene glycol
(Dr Williams), and the department by paramedics after his parents (1,2-ethanediol) is a constituent of antifreeze; and
Department of found him unresponsive at home. According to isopropanol (isopropyl alcohol or 2-propanol),
Emergency Medicine, friends, the patient had consumed several alco- often referred to as rubbing alcohol, is widely
Division of
holic beverages earlier that day following a period used as an antiseptic. Because the toxic alcohols
Toxicology (Dr
Erickson), University of depression. Later that evening, friends picked are found in ordinary automotive and household
of Illinois at Chicago him up to attend a party. After drinking several products, they are easily accessible regardless of
Medical Center, beers and wine at the party, he took a cab home whether ingestion is intentional (eg, when an
Chicago, III.
because he began to feel lethargic and nauseated alcoholic substitutes a toxic alcohol for ethanol)
Reprint requests to and complained of "spots before his eyes." or accidental (eg, when a child ingests the poi-
Dr Williams, On physical examination in the emergency son). Methanol and ethylene glycol produce a
University of Illinois
department, the patient responded only to deep, metabolic acidosis with an increased osmolal
at Chicago Medical
Center, Department painful stimuli. His pulse was 110 beats/min; blood gap.1'2 Isopropanol, which rapidly metabolizes to
of Pathology, Division pressure, 150/70 mm Hg; respiratory rate, 24 acetone, also produces an increased osmolal gap,
of Clinical Pathology breaths/min; and temperature, 35.2°C (95.4°F). His however, it normally does not produce a meta-
(M/C 750), 840 S pupils were dilated, and lateral nystagmus (invol- bolic acidosis unless concomitant hypotension
Wood St, 201GCSB,
untary horizontal movement of the eyes) was causes lactic acidosis. 2 Often the level of iso-
Chicago, IL 60612; or
noted initially. His lungs were clear to auscultation. propanol in a patient is lower than expected or
e-mail:
rwilliam@uic.edu undetectable because of this rapid conversion.
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2 LABORATORY MEDICINE VOLU ME 29, NUMBER 2 FEBRUARY 1998
 TABLE 1. LABORATORY TESTS FOR PATIENT SUSPECTED OF TOXIC ALCOHOL POISONING
Test Patient Result Reference Range
Amylase 700 U/L 25-125 U/L
Anion gap 35 3-11
Arterial blood gas
pH 7.10 7.35-7.45
Po2 231 mm Hg 80-90 mm Hg
Pco2 15 mm Hg 35-45 mm Hg
Calcium 7.0 mg/dL (1.75 mmol/L) 8.6-10.4 mg/dL (2.14-2.60 mmol/L)
Complete blood count
RBC count 5.1 M/uL{5.1 x 1012/L) 4.7-6.1 M/pL (4.7-6.1 x 1012/L)

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WBC count 29 K/pL (29 x 109/L) 4.8-10.8 K/pL (4.8-10.8 x 109/L)
Hemoglobin 15g/dL(150g/L) 14-18 g/dL (140-180 g/L)
Hematocrit 45% (0.45) 42%-52% (0.42-0.52)
Platelet count 120K/pL(120 x 109/L) 150-400 K/pL (150-400 x 109/L)
Electrolytes
Bicarbonate 5 mEq/L (5 mmol/L) 22-28 mEq/L (22-28 mmol/L)
Chloride 105 mEq/L (105 mmol/L) 99-109 mEq/L (99-109 mmol/L)
Sodium 145 mEq/L (145 mmol/L) 136-145 mEq/L (136-145 mmol/L)
Potassium 2.7mEq/L (2.7 mmol/L) 3.5-5.0 mEq/L (3.5-5.0 mmol/L)
Glucose 80 mg/dL (4.4 mmol/L) 70-105 mg/dL (3.9-5.8 mmol/L)
Lactic acid 3.0 mEq/L (3.0 mmol/L) 0.5-2.2 mEq/L (0.5-2.2 mmol/L)
Osmolality 370 mOsm/kg (370 mmol/kg) 279-300 mOsm/kg (279-300 mmol/kg)
Osmolal gap 59 mOsm/kg (59 mmol/kg) <10 mOsm/kg (<10 mmol/kg)
Renal function
Blood urea nitrogen 21 mg/dL (7.5 mmol/L) 10-20 mg/dL (3.6-7.2 mmol/L)
Creatinine 1.0 mg/dL (90 pmol/L) 0.6-1.2 mg/dL (50-110 pmol/L)
Toxicology
Ethanol 50 mg/dL (11 mmol/L) BDL*
Isopropanol/acetone BDL/BDL BDL
Methanol/ethylene glycol 200/70mg/dL (62/11 mmol/L) BDL
Urine screen Negative for drugs of abuse Not detected
*BDL indicates below detectable limits.
Historically, the anion gap is calculated using the following expression:
TABLE 2. COMMON CAUSES OF
Sodium — (chloride + bicarbonate) =12 ± 4 METABOLIC ACIDOSIS AND
INCREASED ANION GAP
The traditional reference interval of 12 ± 4 (or a range of 8-16) is based
on older methodology for determining sodium (flame emission) and chlo- Alcoholic ketoacidosis
ride and bicarbonate (colorimetry). Using ion-selective electrode technol- Aminoglycosides (uremic agents)
ogy, the range for anion gap has decreased to 3 to 11, 3,4 Although in this ASA (acetylsalicylic acid/salicylates)
case the anion gap would be increased regardless of methodology, physi- Carbon monoxide
cians need to be aware of this change, especially in light of the lower refer-
Cyanide
ence interval with the newer methods. Common causes of metabolic
Diabetic ketoacidosis
acidosis resulting in an increased anion gap are listed in Table 2.5,6
The osmolal gap is determined by subtracting the calculated osmolality Ethylene glycol
( O S M ^ ) from the measured osmolality (OSMmeas). The OSM meas should Generalized seizures (toxic)
be determined using a "freezing-point depression" osmometer. A vapor Iron
pressure osmometer cannot be used to estimate alcohol concentrations be- IsonJazid (INH)
cause alcohols contribute significantly to the vapor pressure above the solu- Lactic acidosis
tion.7,8 The increased vapor pressure resulting from alcohol will offset the
Methanol
decreased vapor pressure resulting from other serum solutes, that is, elec-
trolytes, glucose, and blood urea nitrogen (BUN). Thus, the alcohol present Paraldehyde, phenformin
Toluene
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 Methanol
NAD
Alcohol I 7~ *N^
Dehydrogenase | 1
when vapor pressure 1. Visual disturbances usually occurring 12 to 24
Pyruvate
osmometry is used will hours after ingestion
Formaldehyde
Aldehydi cause a spuriously low 2. GI disturbances, often leading to GI bleeding
Dehydrogenase
measurement for serum and pancreatitis
\ pH Dependent
Formic Acid (increased pH) ' Formate osmolality.7,8 3. Metabolic acidosis, which often is delayed.6,14'16
(toxic)
u CO+HO
2 2
(toxic) In toxicology, the
OSMcalc often is deter-
mined by using the
Eye symptoms can include "blurring of vi-
sion," blindness, photophobia (abnormal visual
intolerance to light), constricted visual fields,
Fig 1. Metabolic concentration of the patient's serum sodium "spots before the eyes," and "snowfield" vision.
pathway for (Na), glucose (GLU), BUN, and ethanol On examination, the pupils appear dilated and
methanol. Possibly
toxic pathways are in
(ETOH) in conventional units (Na, mmol/L; may be fixed with hyperemia of the optic disc.

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magenta, others, mg/dL) using this expression1'9: The eye exam often is normal if the patient is
detoxification 0SM seen early in the clinical course, however. Patients
pathways in green,
calc = 2 N a + GLU/20 + BUN/3 + ETOH/5
often complain of GI disturbances, including
and nontoxic
products of
The reference interval is typically less than 10. In nausea, vomiting, and epigastric pain.
detoxification in emergency toxicology it is important to include the Management of methanol poisoning includes
blue. NAD+ indicates ethanol concentration in the expression to account prevention of absorption and gastric decontami-
the oxidized form of for any increase in osmolality caused by ingestion nation. Activated charcoal can prevent absorption
nicotinamide
of common alcoholic beverages.10'11 Conditions to a limited extent. This approach is usually inef-
adenine
often encountered in the emergency setting that fective, however, because methanol is absorbed
dinucleotide; NADH,
the reduced form;
can cause an increased osmolal gap are: within 30 minutes of ingestion. Gastric lavage also
and H+, hydogen ion. is contraindicated for the same reason. Two com-
• Diuretics (mannitol)
mon and practical therapeutic regimens used to
• Ethanol
manage the patient poisoned with methanol in-
• Ethylene glycol
clude administration of ethanol and administra-
• Isopropanol
tion of folic acid. Both these approaches are based
• Methanol
on key reactions noted in methanol's metabolic
6 17
Although an increased osmolal gap is commonly pathway (Fig l). ' Because ADH has a greater
found in cases of toxic alcohol poisoning, the ab- affinity for ethanol than methanol, it will prefer-
sence of an osmolal gap does not rule out toxic entially bind to ethanol as a substrate. Maintain-
alcohol ingestion.1,5'9'10'12'13 ing an adequate level of ethanol in the patient's
blood (100-150 mg/dL) therefore can effectively
Methanol prevent ADH from metabolizing methanol to its
Methanol is rapidly absorbed after it is ingested toxic metabolites. High levels of ethanol can pro-
orally. Serum levels peak within 30 to 90 duce hypoglycemia, however, especially in chil-
18
minutes.2 Methanol is metabolized primarily by dren. The addition of folate accelerates the
alcohol dehydrogenase (ADH), the same enzyme conversion of formic acid to carbon dioxide and
that metabolizes ethanol. The affinity of ADH is water. In severe cases, bicarbonate administration
approximately 10 times greater for ethanol than along with hemodialysis is often necessary.
for methanol, 2 which is the primary reason
ethanol can be used as a therapeutic regimen in Ethylene Glycol
cases of methanol poisoning. Although methanol Ethylene glycol also is rapidly absorbed from the
causes an increased osmolal gap, it in itself is of GI tract. Initial signs of intoxication can occur as
limited toxicity. The metabolites formaldehyde early as 30 minutes after ingestion. Lethal doses
and formic acid (formate), however, are extremely of the alcohol are estimated to be 1.4 mL/kg,
toxic to the central nervous system (CNS) and which is approximately 100 mL in a 70-kg adult.6
gastrointestinal (GI) tract and cause profound Like methanol, ethylene glycol is metabolized by
metabolic acidosis and associated eye symp- ADH; its metabolism leads to the formation of
toms. 2 ' 14 ' 15 High formate levels have been shown several metabolites, including glycolaldehyde,
to correlate with poor patient outcome. glycolate, hippurate, and oxalate (Fig 2), which
The onset of symptoms after ingestion of are directly toxic to the kidney, heart, lungs, and
2 15,19,20
methanol varies greatly (1-72 hours). Patients CNS. ' Ethylene glycol poisoning occurs in
often do not present with severe toxic manifesta- the following three stages:
tions early in the clinical course. Late in their
clinical course, however, they often present with
the following "triad" of symptoms:
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 Fig 2. Metabolic
Ethylene Glycol
pathway for ethylene
Alcohol
Dehydrogenase glycol. Possibly toxic
1. Stage 1 occurs 30 minutes to 12 hours after ' ^NADH + H t x V pathways are in
ingestion and is characterized by metabolic Glycolaldehyde magenta,
Aldehyde detoxification
effects and CNS depression. Symptoms include Dehydrogenase pathways in green,
slurred speech, ataxia, anion gap-metabolic aci- and nontoxic
Glycolic Acid Glyoxylic Acid
dosis, proteinuria, hematuria, and calcium products of
(toxic) (toxic) V detoxification in
oxalate crystals. Thiamine
2. Stage 2 occurs 12 to 36 hours after ingestion
and is characterized by cardiopulmonary effects. a-hydroxy-
/r
xy-
^
Pyridoxine

V
Oxalic Acid

(toxic)
blue. NAD+ indicates
the oxidized form of
nicotinamide
Symptoms include rapid respiration, cyanosis, p-ketoadipate Glycine adenine
pulmonary edema, and cardiomegaly. dinucleotide; NADH,
3. Stage 3 occurs 2 to 3 days after ingestion and is the reduced form;

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26
characterized by renal insufficiency. Symptoms toxic alcohol poisoning. Intravenous adminis- and H*, hydogen ion.
include proteinuria, oliguria, and anuria. tration of ethanol no longer would be required,
and unlike ethanol, 4-MP causes no CNS depres-
Glycolate is the primary metabolite responsi- sion or hypoglycemia.28'29
ble for the severe metabolic acidosis21; accumula-
tion of calcium oxalate crystals (sometimes Isopropanol
hippuric crystals) produces kidney damage lead- Of the three toxic alcohols, isopropanol is the
ing to renal failure.2,6 Calcium oxalate crystals are most potent CNS depressant.2'30,31 It is rapidly
found in the urine as monohydrates (prismlike or absorbed via the GI tract with peak levels (acute
needlelike) or dihydrates (tent- or envelope- intoxication) occurring within 30 minutes of
shaped) (Figs 3 and 4); the dihydrate form is ingestion. It is metabolized rapidly by ADH;
more commonly seen in ethylene glycol poison- however, unlike the other toxic alcohols, iso-
ing. Calcium oxalate crystals are present only in propanol is converted to acetone, another CNS
one third of the cases, however.22 depressant.2'30'31
Visual disturbances, common in methanol Elimination of acetone
poisoning, are rarely encountered in ethylene via the lungs imparts a
glycol poisoning. 23 Late in the clinical course, "fruity" odor to a
pulmonary edema and kidney failure often oc- patient's breath in the
cur, however.23 The transformation of ethylene same manner as in dia-
glycol into oxalate causes an increase in the ratio betic ketoacidosis
of the reduced form of nicotinamide adenine (Table 3).
dinucleotide to the oxidized form, which favors Because it is ab-
the conversion of pyruvate to lactate (increase in sorbed rapidly, iso-
E
lactic acid), which exacerbates the acidosis.6 propanol is twice as o
u
Management of patients with ethylene glycol intoxicating as ethanol Fig 3. Urine calcium oxalate crystals
toxicity is similar to those with methanol poison- —an isopropanol level (monohydrate) (x400). From Terlinsky AS,
ing.6'16'24'25 Because the affinity of ADH is approx- of 100 mg/dL is compa- Grochowski J, Geoly KL, et al. Identification of
imately 100 times greater for ethanol than for rable to an ethanol level atypical calcium oxalate crystalluria following
ethylene glycol ingestion. Am J Clin Path.
ethylene glycol, ethanol also is used as a therapeu- of200mg/dL.2'30'31CNS 1981;76:223-226. Used with permission.
I
tic regimen. Charcoal administration is usually in- manifestations include
effective because GI absorption of ethylene glycol dizziness, headache, mi-
is so rapid. Hemodialysis can be used to effectively otic (pinpoint) pupils,
remove ethylene glycol (similarly to its use in stupor, and coma. Be-
I
methanol poisoning) and its toxic metabolites.26,27 cause isopropanol is a
Although treatment for methanol and ethyl- GI irritant, acute ab-
ene glycol poisoning currently includes continu- dominal pain and he-
ous intravenous infusion of ethanol, matemesis can occur.
hemodialysis, or a combination of the two, a new Acidosis, visual distur-
antidote, 4-methylpyrazole (4-MP), was recently bances, and renal failure,
approved by the Food and Drug Administration which present in other
for ethylene glycol poisoning; approval still is types of toxic alcohol Fig 4. Urine calcium oxalate crystals (dihydrate)
pending for methanol. This compound selectively poisoning, are typically (x400). From Terlinsky AS, Grochowski J, Geoly
inhibits ADH and thus prevents the formation of absent in isopropanol KL, et al. Identification of atypical calcium oxalate
crystalluria following ethylene glycol ingestion.
toxic metabolites in patients being treated for Am J Clin Path. 1981;76:223-226. Used with
permission.
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 TABLE 3. COMMON LABORATORY FINDINGS WITH
ISOPROPANOL INGESTION COMPARED WITH DIABETIC
KETOACIDOSIS American Academy of Clinical Toxicology states
that, to be clinically useful, toxic alcohol levels
Laboratory Finding Isopropanol Diabetic Ketoacidosis must be available within 2 hours. 32 In addition,
Acetonemia + + acetone (like isopropanol) is a CNS depressant,
Acetonuria + + and thus its levels should be determined along
with those of the toxic alcohols. Because
Acidemia - + methanol, isopropanol, and acetone are volatile
Anion gap - substances, they can be determined simultane-
Glucosuria - + ously without a pretreatment step using a gas
chromatograph (GC). Ethylene glycol, however,
Hyperglycemia
is not a volatile substance and therefore often re-

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Osmolal gap + + quires a derivatization step and/or a different
+ indicates present; - , not present. method before GC analysis. Because ethylene
glycol is not a volatile alcohol, it will not be mea-
poisoning.6,30'31 Children younger than 6 years are sured in institutions that define its toxic alcohol
more prone to exposure to isopropanol than to ex- panels as a "volatile screen."
posure to ethanol because isopropanol is more Because most clinical laboratories do not per-
readily available in children's homes. form toxic alcohol screens, the emergency room
Treatment primarily consists of supportive physician generally relies on other clinical signs
care, airway management, administration of in- and common laboratory tests to make the diag-
travenous fluids, and control of GI bleeding.2,16 nosis (Table 4). Test requests usually are sent to a
Hemodialysis rarely is used unless the patient is reference laboratory. Because turnaround times
comatose, has refractory hypotension, or has iso- are often greater than 2 hours owing to increased
propanol levels greater than 400 to 500 transportation times, results from the reference
mg/dL.2,16 laboratory often are used to confirm the presence
or absence of a toxic alcohol for the patient's
Laboratory Assessment chart. If it is suspected that the patient ingested a
A patient suspected of ingesting a toxic alcohol re- toxic alcohol, the clinician will require quantita-
quires immediate medical intervention. The tive data on the specific alcohol in order to ad-
minister appropriate
TABLE 4. LABORATORY TESTS USED TO ASSESS TOXIC ALCOHOLS therapy. For example,
many nephrologists will
Test Reason for Test not perform dialysis on
1. Blood urea nitrogen and creatinine Assess renal function, calculate the osmolality a patient unless the lab-
and osmolal gap oratory provides a
2. CBC Assess the presence of a macrocytic anemia quantitative level for a
(high mean corpuscular volume, low toxic alcohol.
hemoglobin, low hematocrit) and/or a toxic During hemodialy-
metabolic process (elevated WBC count) sis, ethanol levels must
be checked every 2
3. Electrolytes and calcium Assess electrolyte disturbances, calculate the
hours and adjusted to
anion and osmolal gaps, detect hypocalcemia
maintain levels be-
4. Ethanol and toxic alcohol Confirm presence of ethanol or a specific tween 100 to 150
or volatile screen toxic alcohol, monitor ethanol as a mg/dL, along with stat
therapeutic regimen after toxic alcohol blood gases and elec-
ingestion trolytes, until the pa-
5. Glucose Assess presence of hypoglycemia, calculate tient's acid-base status
the osmolality and osmolal gap normalizes. 6 , 1 6 Com-
mon laboratory find-
6. Lactic acid and hypoxia Determine other causes of metabolic acidosis
ings observed with
7. Osmolality (measured) Calculate the osmolal gap ethanol and toxic alco-
8. pH and blood gases Assess ventilatory status and confirm the hol ingestion are com-
presence of metabolic acidosis pared in Table 5.33
9. Urinalysis Detect the presence of ketones (ketoacidosis)
and oxalate crystals (ethylene glycol)
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 TABLE 5. COMPARISON OF ETHANOL AND TOXIC ALCOHOLS USING COMMON
LABORATORY TESTS*
Case History
Follow-Up Metabolic
Acidosis Urine
The patient's ophthal-
With Anion Osmolal Serum Urine Oxalate
mologic disturbances Alcohol Gap Gap Acetone Ketones Crystals
along with the metabolic
acidosis with increased Ethanol -/+ + -/+ -/+ -
anion gap and osmolal Ethylene glycol + + - - +*
gap and the presence of
urinary calcium oxalate
Isopropanol - + + +
crystals (which proba- Methanol + + — — -
bly caused the hypo- *+ indicates present, - , not present.

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calcemia) suggest a poi- bindings depend on presence of alcoholic ketoacidosis or moderate lactic ac idosis.
soning with methanol *Oxalate crystals only occur in one third of cases.
and ethylene glycol.
4. Winter SD, Pearson JR, Gabow PA, et al. The fall of the
The increased white blood count is found com- serum anion gap. Arch Intern Med. 1990;150:311-313.
monly with ingestion of toxic substances. The 5. Gennari FJ. Serum osmolarity: uses and limitations. N
glucosuria is caused by the excess elimination of Engl] Med. 1984;310:102-105.
6. Goldfrank LR, Flomenbaum NE, Howland MA.
glucose resulting from the intravenous infusion Methanol, ethylene glycol and isopropanol. In: Goldfrank LR,
ofD50W. Flomenbaum NE, Lewin NA, et al, eds. Goldfrank's Toxicologic
The patient was immediately given intra- Emergencies. 5th ed. Norwalk, Conn: Appleton & Lange;
1994;827-846.
venous ethanol at a concentration of 5% to 10% 7. Kaplan L. Measurement of colligative properties. In:
by volume. (If administration had been oral, the Kaplan LA, Pesce AJ, eds. Clinical Chemistry—Theory,
concentration would have been higher, that is, Analysis, Correlation. 3rd ed. St Louis, Mo: Mosby-Year Book.
1996:270-276.
20% to 30% by volume.) Hemodialysis, indicated 8. Frier EF. Osmometry. In: Burtis CA, Ashwood ER, eds.
for the patient's visual disturbances, was institut- Tietz Textbook of Clinical Chemistry. 2nd ed. Philadelphia, Pa:
ed after a nephrology consultation. The patient WB Saunders;1994:184-190.
9. Hoffman RS, Smilkstein MI, Howland MA, et al. Osmolal
received sodium bicarbonate to normalize the pH gaps revisited: normal values and limitations. Clin Toxicol.
levels. The toxic alcohol results were methanol, 1993;31:81-93. Test Your
200 mg/dL; ethylene glycol, 70 mg/dL; and iso- 10. Pappas AA, Gadsden RH, Taylor EH. Serum osmolality Knowledge
in acute intoxication: a prospective clinical study. Am J Clin Look for the CE
propanol/acetone, below detectable limits. The Pathol. 1985;84:74-79. Update exam on c
patient recovered with only slight impairment of 11. Traverse WE, Horowitz GL. Experience with osmolality, Toxicology (802) in 0
vision. A psychiatry consultation also was osmolal gap and specific enzymatic ethanol assay. Clin Chem. the April issue of IB
0
1991;37:1003. Laboratory Medicine. 'E
provided for follow-up. 12. Palmisano I, Gruver C, Adams ND. Absence of anion z
Participants will earn £
gap metabolic acidosis in severe methanol poisoning: a case
4 CIVILE credit hours. £
Conclusion report and review of the literature. Am J Kidney Dis. o
1987;9:441^44. u
Although poisoning with one of the toxic alcohols 13. Walker I A, Schwartzband A, Krauss EA, et al. The miss-
is uncommon, rapid diagnosis and laboratory ing gap: a pitfall in the diagnosis of alcohol intoxication by

assessment are essential. Unlike isopropanol
intoxication, which normally requires supportive
therapy, methanol and ethylene glycol intoxica-
tion often necessitate the proper implementation
of ethanol therapy and hemodialysis. Because eth-
ylene glycol, methanol, and isopropanol levels
may not be readily accessible in most hospital set-
tings, the use of other laboratory results (anion
gap and osmolal gap) may be required to make
the diagnosis and begin therapy.©
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Learn what you need t o survive—and thrive—
Toxicol. 1991;29:231-240.
25. Porter GA. The treatment of ethylene glycol poisoning simplified. N
Engl J Med. 1988;319:109-110.
26. Baud FJ, Bismuth C, Gamier R, et al. 4-Methylpyrazole may be an
alternative to ethanol therapy for ethylene glycol intoxication in man. /

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in our rapidly changing profession at
ASCP Workshops for Laboratory Professionals.
Toxicol Clin Toxicol. 1986-87;24: 463^183.
27. Baud FJ, Galliot M, Astier A, et al. Treatment of ethylene glycol poison-
ing with intravenous 4-methylpyrazole. N Engl J Med. 1988;319:97-100.
28. Jacobsen D, Sebastian S, Barron SK, et al. Effects of 4-methylpyrazole,
methanol/ethylene glycol antidote, in healthy humans. / Emerg Med.

San Francisco, California 1990;8:455-461.

29. Jacobsen D, Sebastian CS, Blomstrand R, et al. 4-Methylpyrazole: a
controlled study of safety in healthy human subjects after single, ascending
Park Plaza Hotel (in Burlingame) doses. Alcohol Clin Exp Res. 1988;12:516-522.
March 2-6,1998 30. Lacouture PG, Wason S, Abrams A, et al. Acute isopropyl alcohol intox-
ication. Am J Med. 1983;75:680-686.

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31. Rich J, Scheife RT, Katz N, et al. Isopropyl alcohol intoxication. Arch
Neurol. 1990;47:322-324.
32. American Academy of Clinical Toxicology. Facility assessment guide-
lines for regional toxicology treatment centers. / Toxicol Clin Toxicol.
1993;31:211-217.

Chicago, Illinois 33. Williams RH. Clinical laboratory assessment of ethanol and the toxic
alcohols. In: Leikin JB, Paloucek FP, eds. Lexi-Comp's Poisoning & Toxicology
Handbook. 3rd ed. Hudson, Ohio: Lexi-Comp; 1998:894-905.
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