Methanol Toxicity Workup

Renal profile

Significant methanol ingestion leads to metabolic acidosis, which is manifested by a low serum bicarbonate level. The anion gap is increased secondary to high lactate and ketone levels. This is probably due to formic acid accumulation.^{[12, 13]}

Serum osmolarity

Methanol ingestion results in an elevated osmolar gap, so in cases of stupor of unknown cause, testing for an osmolar gap should be routine. However, the osmolar gap is a nonspecific finding because it may represent the presence of a low ̶ molecular weight solute, such as ethanol, other alcohols, mannitol, glycine, lipids, or proteins.

The osmolar gap can be calculated using a set formula. To find the osmolar gap, take the measured plasma osmolality and subtract the calculated osmolality. Calculated osmolality requires a serum glucose measurement and is derived as follows:

Calculated osmolality (mOsm/kg) = 2(Na⁺) + (glucose/18) + (blood urea nitrogen [BUN]/2.8)

Serum amylase

Hemorrhagic pancreatitis has been described in as many as two thirds of the patients with methanol poisoning.

Serum methanol

Definitive diagnosis of methanol toxicity requires a confirmed increase in the serum methanol level with gas chromatography. Peak levels are achieved 60-90 minutes after ingestion, but they do not correlate with the level of toxicity and thus are not a good indicator of prognosis.

Electroretinography/visual evoked response

Two cases of methanol toxicity were evaluated using these studies. Characteristic findings correlated well with pathologic results and postulated toxicity. Loss of retinal sensitivity was coupled with scotomata in both patients evaluated. In addition, decreased amplitudes were found on visual evoked-response testing, although latencies were normal.^[14]

Methanol appears to affect the basal ganglia, primarily the putamen. Because of the availability of advanced neuroimaging techniques, the putaminal damage tends to be detected much earlier in current practice than it was in the past.

CT scanning

Computed tomography (CT) scanning may reveal the characteristic changes of bilateral putaminal necrosis with varying degrees of hemorrhage, in addition to involvement of the cerebral white matter. However, the lesions may not be well localized when compared with magnetic resonance imaging (MRI) findings.

Moreover, often the initial CT scan is normal and several days may elapse before lesions become evident.

MRI

A characteristic finding is bilateral putaminal necrosis with or without hemorrhage, probably as a result of the direct toxic effects of methanol metabolites. This finding is certainly not specific for methanol toxicity, because it can be seen with other diseases, such as Wilson disease, Leigh disease, and stroke.^[15]

Other findings that have been described include cerebral and intraventricular hemorrhage, diffuse cerebral edema, cerebellar necrosis, subcortical white matter necrosis, optic nerve necrosis, and even enhancement of necrotic lesions.^[15]

In a series of 4 patients, MRI performed within 2 weeks of methanol intoxication demonstrated changes in the putamen of all 4 patients.^[16] Three of these patients had white matter lesions within the occipital/frontal lobes. Interestingly, in patients who recovered without extrapyramidal symptoms, the lesions regressed within several weeks. The authors recommend MRI as a prognostic tool and as a means of differentiating methanol intoxication from other conditions, such as hypoglycemia and carbon monoxide poisoning.