Methanol intoxication

Clinical History

A 48 year old man was admitted to the emergency room after one day suffering from severe nausea, vomiting and dyspnea. His family found him at his home address confused, pale, diaphoretic and with blurred vision. When admitted, his pupils became arreactive and mydriatic.

Imaging Findings

Two hours later the patient became unconscious (Glasgow Coma Scale: 3), dyspnoeic, diaphoretic, blind and with altered sensorium. Biochemistry revealed severe metabolic acidosis, hyperglycemia and presence of ketone bodies. An unenhanced brain CT was immediately performed, with no findings.

However, symptoms remained and even worsened, so a new cranial tomography was done twelve hours later. This new image procedure showed severe generalized bilateral putaminal low attenuation and frontoparietal subcortical white matter ill-defined hypodense areas most consistent with hemorrhagic necrosis due to methanol intoxication.

Patient died hours later. His serum levels of methanol were 0,4 g/L. Normal values: 0 g/L. Pathology showed necrosis due to hemorrhage in both putamina.

Discussion

Methanol is a clear, colourless volatile liquid [6]. It is found in multiple commercial products such as gasoline antifreeze, paint remover and photocopying fluid [7].

Methanol poisoning may appear after accidental, criminal or suicidal ingestion. It has also been described as a potential adulterant of wine or other alcoholic beverages, due to its similar odor to ethanol [8].

A typical latent period (12-24 hours) has been described for this entity [3, 6, 8, 10], in which this substance is metabolized into formaldehyde and formic acid, which are more toxic than methanol. Furthermore, the optic nerve demyelination is believed to be due to the myelinoclastic effect of formic acid.

Methanol intoxication has typical findings on CT and MRI, which are helpful for diagnosis. Nevertheless, it is important to take into consideration that hypodense basal ganglia on CT are typical findings, but not specific of methanol poisoning and can be seen in other metabolic diseases, which include -but are not limited to- Wilson's disease [4, 5], carbon monoxide poisoning, hypoxic-ischemic insult, Leigh's disease [2], Kearns-Sayre syndrome [6], Creutzfeldt-Jakob encephalopathy or Hallervorden-Spatz disease [13] .

Putaminal necrosis, with or without hemorrhage, and subcortical white matter lesion are the most frequent reported findings in this entity[3]. Cerebral an intraventricular hemorrhage, cerebellar necrosis, diffuse cerebral edema, bilateral subcortical white matter necrosis or edema and optic nerve necrosis have been described in methanol intoxication, as well.

On MRI, nonenhancing subcortical white matter and putaminal hiperintensities are seen in T2WI. On T2-weighted gradient echo (GE) images, a pronounced signal loss might be noticed in both putamina due to hemosiderin deposits. T1WI usually shows generalized low intensity of both putamina.

This particular poisoning damages specially basal ganglia because these gray-matter structures are more vulnerable to metabolic acidosis than the rest of the brain [1]. It has also been suggested that direct toxic effects of methanol metabolites might be responsible for the subcortical and white matter lesions [6, 7], whereas Hsu et al. proposed that putamen is particularly at risk because of its high metabolic demand and also because it lies in the boundary zones of vascular perfusion [11]. However, for some authors the distribution of the lesions seems to be counterevidence of a vascular cause [7]. Other authors found MRI changes consistent with infarcts and actually proposed the hypothesis that the selective neurotoxicity of methanol is due to anoxia, as a result of the inhibition of cytochrome oxidase by formic acid [14]. Therefore, definite pathophysiology of this entity remains unclear.

Treatment options for this poisoning consist in vital support, gastric lavage, correction of acidosis with sodium bicarbonate or folic acid; sometimes ethanol is useful as antidote at the beginning of symptoms, as its affinity for alcohol dehydrogenase enzyme is 10-20 times greater than that for methanol.

The presence of hemorrhagic necrosis in the putamen has been suggested to indicate poor prognosis [12]. Subcortical white matter and optic nerve findings on neuroimaging may indicate poor prognosis as well. Hence, the severity of abnormalities on CT and MRI can be of prognostic value [6].

Differential Diagnosis List

Final Diagnosis

Fatal Methanol intoxication

URL:	https://www.eurorad.org/case/8620
DOI:	10.1594/EURORAD/CASE.8620
ISSN:	1563-4086