Sergey Zakharov1, Daniela Pelclova1, Pavel Diblik2, Pavel Urban1, Pavel Kuthan2, Olga Nurieva1, Katerina Kotikova1, Tomas Navratil3,4, Martin Komarc5, Jaromir Belacek5, Zdenek Seidl6, Manuela Vaneckova6, Jaroslav A Hubacek7, Ondrej Bezdicek8, Jiri Klempir8, Maksim Yurchenko9, Evzen Ruzicka8, Michal Miovsky10, Barbara Janikova10, Knut Erik Hovda11. 1. a Toxicological Information Center, Department of Occupational Medicine , First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 2. b Department of Ophthalmology , First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 3. c Department of Biomimetic Electrochemistry , J. Heyrovský Institute of Physical Chemistry of the AS CR , v.v.i, Prague 8 , Czech Republic. 4. d Institute of Medical Biochemistry and Laboratory Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague , Prague 2, Czech Republic. 5. e Institute of Biophysics and Informatics, First Faculty of Medicine of Charles University in Prague, General University Hospital , Prague 2, Czech Republic. 6. f Department of Radiology , First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 7. g Centre for Experimental Medicine, Institute for Clinical and Experimental medicine , Prague 4 , Czech Republic. 8. h Department of Neurology and Center of Clinical Neuroscience , First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 9. i Institute of Clinical and Experimental Dental Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 10. j Department of Addictology , First Faculty of Medicine, Charles University in Prague and General University Hospital , Prague 2, Czech Republic. 11. k The Norwegian CBRNe Centre of Medicine, Department of Acute Medicine , Oslo University Hospital , Oslo , Norway.
Abstract
CONTEXT: Visual disturbances due to the toxic effect of formic acid in acute methanol poisonings are generally transient. The subjective symptoms of visual toxicity may resolve within few weeks and fundoscopic signs of acute optic neuropathy subside within 1-2 months; therefore, the prevalence of long-term visual sequelae in the population of survivors of poisonings may be underestimated. OBJECTIVE: To study the prevalence and character of long-term visual sequelae of acute methanol poisonings based on the data from the Czech mass methanol outbreak in 2012. PATIENTS AND METHODS: A total of 50 patients with confirmed methanol poisoning were included in this longitudinal cross-sectional study, median age: 48 (range, 23-73) years. The following tests were performed: optical coherence tomography or OCT with evaluation of the retinal nerve fibers layer (RNFL), visual evoked potentials (VEP), magnetic resonance imaging (MRI) of brain, complete ocular examination (visual acuity/field, color vision, contrast sensitivity, and fundus), neurological examinations, and biochemical tests. RESULTS: Of 50 patients, 7/50 (14%) were discharged with diagnosed visual sequelae and 6/50 (12%) were discharged with both visual and central nervous system sequelae of poisoning. On the follow-up examination, 20/50 (40%) of the patients had long-term visual sequelae, with 8% of blindness. A total of 38% of the patients had abnormal (28% borderline) findings on RNFL, and 40% had abnormal (18% borderline) VEP. Among the patients discharged without detected visual sequelae, 8/37 (22%) had abnormal RNFL and VEP. Patients with visual sequelae had brain lesions more often (70% vs. 27%, p < 0.01). MRI identified optic nerve lesions in 2/20 cases with abnormal VEP only. The groups with and without visual sequelae differed in serum methanol, ethanol, HCO3-, formate, pH, anion gap, and base deficit (all p < 0.01). Visual disturbances on admission and coma were more prevalent in the patients with visual sequelae (p < 0.05). Patients with positive serum ethanol on admission were 93% less likely to have optical axonal damage (OR: 0.07 (95% CI: 0.01-0.8); p < 0.05). No association was found between visual sequelae and type of antidote administered, mode of hemodialysis, or folate substitution. Pre-hospital administration of ethanol seemed beneficial: these patients were 90% less likely to have abnormal RNFL findings (OR: 0.10 (95% CI: 0.02-0.52); p < 0.01). CONCLUSIONS: The long-term visual sequelae were clearly underestimated on discharge, suggesting a significantly higher amount of patients with long-term sequelae than earlier reported. Thorough examinations before discharge and during follow-up will likely uncover a higher morbidity also after methanol poisonings in general.
CONTEXT: Visual disturbances due to the toxic effect of formic acid in acute methanol poisonings are generally transient. The subjective symptoms of visual toxicity may resolve within few weeks and fundoscopic signs of acute optic neuropathy subside within 1-2 months; therefore, the prevalence of long-term visual sequelae in the population of survivors of poisonings may be underestimated. OBJECTIVE: To study the prevalence and character of long-term visual sequelae of acute methanol poisonings based on the data from the Czech mass methanol outbreak in 2012. PATIENTS AND METHODS: A total of 50 patients with confirmed methanolpoisoning were included in this longitudinal cross-sectional study, median age: 48 (range, 23-73) years. The following tests were performed: optical coherence tomography or OCT with evaluation of the retinal nerve fibers layer (RNFL), visual evoked potentials (VEP), magnetic resonance imaging (MRI) of brain, complete ocular examination (visual acuity/field, color vision, contrast sensitivity, and fundus), neurological examinations, and biochemical tests. RESULTS: Of 50 patients, 7/50 (14%) were discharged with diagnosed visual sequelae and 6/50 (12%) were discharged with both visual and central nervous system sequelae of poisoning. On the follow-up examination, 20/50 (40%) of the patients had long-term visual sequelae, with 8% of blindness. A total of 38% of the patients had abnormal (28% borderline) findings on RNFL, and 40% had abnormal (18% borderline) VEP. Among the patients discharged without detected visual sequelae, 8/37 (22%) had abnormal RNFL and VEP. Patients with visual sequelae had brain lesions more often (70% vs. 27%, p < 0.01). MRI identified optic nerve lesions in 2/20 cases with abnormal VEP only. The groups with and without visual sequelae differed in serum methanol, ethanol, HCO3-, formate, pH, anion gap, and base deficit (all p < 0.01). Visual disturbances on admission and coma were more prevalent in the patients with visual sequelae (p < 0.05). Patients with positive serum ethanol on admission were 93% less likely to have optical axonal damage (OR: 0.07 (95% CI: 0.01-0.8); p < 0.05). No association was found between visual sequelae and type of antidote administered, mode of hemodialysis, or folate substitution. Pre-hospital administration of ethanol seemed beneficial: these patients were 90% less likely to have abnormal RNFL findings (OR: 0.10 (95% CI: 0.02-0.52); p < 0.01). CONCLUSIONS: The long-term visual sequelae were clearly underestimated on discharge, suggesting a significantly higher amount of patients with long-term sequelae than earlier reported. Thorough examinations before discharge and during follow-up will likely uncover a higher morbidity also after methanol poisonings in general.
Entities:
Keywords:
acute methanol poisoning; health sequelae of poisoning; hospital treatment; long-term visual damage; treatment outcome
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