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 Ocular examination may reveal blurred

vision, decreased visual acuity, retinal edema, optic atrophy,

or hyperemia of the optic disc in methanol poisoning.

Abdominal tenderness or blood on rectal examination

may indicate isopropanol ingestion as it is classically

associated with hemorrhagic gastritis.

DIAGNOSTIC STUDIES

..... Laboratory

A basic metabolic panel is indicated to determine renal

function, acid-base status, and calculate an anion gap (the

normal range is 8-12 mEq/L). Obtain an arterial blood gas

to ascertain the degree of acidosis. A serum ethanol level is

required in all cases of suspected toxic alcohol poisoning,

as this result impacts the osmol gap equation and helps

determine the timing of ADH inhibition.

An osmol gap can be a useful screening test for toxic

alcohol poisoning if calculated early after the ingestion.

Send a serum sample to the laboratory to measure

osmolality. The osmol gap is equal to this value minus the

0

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Time course

calculated osmolality (2*Na + glucose/18 + blood urea

nitrogen/2.8 + ethanol/4.6). Traditionally a normal osmol

gap is < 10 mEq/L, but in actuality will normally range

between -7 to + 14. It is the toxic alcohol parent compound that contributes to the osmol gap, and elevated

gaps occur early after ingestion before the metabolism of

the toxic alcohols into their poisonous byproducts. Later,

as the toxic organic acid metabolites build up and the

parent compound levels decrease, an anion gap metabolic

acidosis becomes the predominant finding, with the

osmol gap becoming less significant (Figure 55- 1).

Ethylene glycol and methanol can result in a simultane ­

ous anion gap metabolic acidosis and elevated osmol gap.

Because isopropanol is not metabolized into an organic

acid, ingestion typically results in an elevated osmol gap

in the absence of an elevated anion gap. Because isopropanol is rapidly converted to acetone, a serum acetone

level can help identify isopropanol poisoning in this

setting.

Calcium oxalate crystals on urine microscopy or urine

fluorescence under ultraviolet light (due to the addition of

fluorescein to most commercial antifreeze) may be clues

for ethylene glycol poisoning, but the absence of either

should not be used to rule out exposure.

Most importantly, serum toxic alcohol levels

(quantitative ethylene glycol, methanol, and isopropanol)

should be ordered STAT in cases of suspected toxic alcohol

poisoning to confirm ingestion and guide management. It

is important to recognize that toxic alcohol tests are rarely

performed in hospital laboratories and must be sent to an

off-site reference lab in most cases, so results may not be

available for several hours.

..... Imaging Studies

Although imaging studies do not help diagnose toxic

alcohol poisoning, methanol exposure has been

reported to cause basal ganglia hemorrhage or infarct.

Computed tomography imaging of the head should

also be considered when the mental status does not cor ­

relate with the presumed exposure or associated trauma

is a concern.

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.A. Figure 55-1 . Relationship of degree of osmolal ity and acidosis

during the course of ethylene g lycol or methanol poisoning. Used

with permission from Mark B. Mycyk, MD.

TOXIC ALCOHOLS

MEDICAL DECISION MAKING

History alone may be sufficient to prompt a work-up for

toxic alcohol poisoning. In the absence of a reported ingestion, an unexplained anion gap acidosis or elevated osmol

gap should prompt further evaluation for a toxic alcohol.

Order STAT serum tests for all toxic alcohols (ethylene

glycol, methanol, and isopropanol). Initiate care based on

the presumptive clinical diagnosis and do not delay ED

treatment awaiting laboratory confirmation, as even in

ideal scenarios these levels will often take several hours to

measure. The initiation of antidotal therapy to inhibit

ADH should be the management priority early after an

ingestion before the onset of acidosis, whereas hemodialysis should be the priority in cases with a delayed presenta ­

tion when severe acidosis is already present (Figure 55 -2).

TREATMENT

Attention to the airway in cases of CNS depression

should take precedence. IV fluids should be administered

to treat hypotension and maintain renal perfusion in all

cases of toxic alcohol poisoning. In cases of isopropanol

ingestion, no additional treatment is necessary. In cases

of ethylene glycol or methanol poisoning, initiate ADH

inhibition until the ethylene glycol or methanol level is

<20 mg/dL and no acidosis is present. ADH may be inhibited with either IV fomepizole (load = 15 mglkg) or an IV

ethanol infusion (to achieve a serum ethanol level between

100-150 mg/dL).

Obtain early nephrology consultation to facilitate

emergent hemodialysis if the ethylene glycol or methanol

level is >50 mg/dL to filter out the parent compound and

any accumulated toxic metabolites. Emergent dialysis is

also indicated in cases of renal failure or severe acidosis

irrespective of the ethylene glycol or methanol level to

remove any remaining toxic metabolites and improve the

systemic acid-base status. In cases of ethylene glycol

poisoning, both thiamine 10 mg IV and pyridoxine

50 mg IV every 6 hours may help convert glyoxylic acid to

nontoxic metabolites. In cases of methanol poisoning,

folic acid 50 mg IV every 4 hours may help convert formic acid to C02 and Hp.