Evoked potentials investigation of visual dysfunction after methanol poisoning

Objective: To present results of electrophysiologic investigations of the v isual toxicity observed during the early stage of methanol poisoning. Design: Retrospective, clinical study. Setting: A 7-bed intensive care unit in a university hospital. Patients: Nineteen patients admitted with a diagnosis of acute methanol poi soning. Interventions: Visual evoked potentials were obtained within the first 48 h rs after admission; a clinical follow-up examination was performed in 11 pa tients, and 12 patients were followed up by visual evoked potentials beyond the same delay. Correlations between the occurrence of an optic neuropathy and clinical, biological, and electrophysiological data were studied. Measurements and Main Results: A significant correlation was found between arterial pH and blood formate concentration (r(2) = 0.58, p = .003), betwee n blood formate and bicarbonate concentrations (r(2) = 0.36, p = .02), and between delay from ingestion and blood formate concentration (r(2) = 0.44, p = .017). Clinical outcome was correlated not only with the bicarbonate (p = .007), formate (p = .018), and methanol (p = .03) concentrations and art erial pH (p = .004) but also with a well-defined electrophysiologic pattern during the acute stage. An index of global cortical functioning greater th an or equal to 3 was associated with death, whereas a global cortical funct ioning index less than or equal to 2 was associated with survival (p = .005 8). Moreover, a statistically significant difference in long-term visual im pairment was found between the subgroup with abnormal wave III morphology o r a global cortical functioning index of 1-2 and the subgroup with normal w ave III morphology and a global cortical functioning index <1 (p = .015). Results of the electrophysiologic studies were expressed as retinal dysfunc tion and optic nerve injury. Five patients had normal findings on electroph ysiologic examination. Ten patients had early signs of retinal dysfunction that were fully reversed in the eight patients who were followed, Ten patie nts had persistent electrophysiologic signs of optic neuropathy. Conclusions: Although reversible retinal dysfunction is evident in the earl y stage of human methanol poisoning, its absence does not preclude developm ent of optic neuropathy, The occurrence of optic neuropathy and early elect rophysiologic data are correlated.