Dear Editor,
We read with great interest the interesting case report titled 'A case of optic nerve atrophy with severe disc cupping after methanol poisoning' presented by Yong Woon Shin and Ki Bang Uhm published in the last issue of Korean Journal of Ophthalmology [1]. In the description of the case, the authors mentioned that the patient had metabolic acidosis and mildly elevated methanol levels at presentation; however, only conservative therapy was performed. It seems that the patient was in the acute phase of methanol toxicity at presentation and antidotal therapy (fomepizole or ethanol in association with hypertonic sodium bicarbonate, folic or folinic acid, and even hemodialysis) should have been initiated.
Was the patient managed in the ophthalmology department or was he transferred to a clinical toxicology unit for treatment? Were corticosteroids or other treatment modalities initiated for the treatment of his visual disturbance? We would like to ask the authors if the conservative therapy consisted of these modalities or not. And if these treatments were not performed for the patient, what was the reason? According to our experience [2], these treatment modalities could have improved the ophthalmologic signs and symptoms of the patient and even prevented the progression of ophthalmologic sequelae. In such cases, it is acceptable and even necessary to focus on the toxicological management of the methanol-poisoned patient rather than just focusing on the ophthalmologic signs. Furthermore, the authors did not mention anything about the visual condition of the patient during the 4-year period before re-examination of his ophthalmologic status except by history taking. According to our experience [2], patients who present with blindness may experience recovery of vision anytime between a few days until 1 month after hospital discharge which may persist for 1 to 9 months. After this period, they may re-experience reduced vision which may progress to total blindness.
References
1. Shin YW, Uhm KB. A case of optic nerve atrophy with severe disc cupping after methanol poisoning. Korean J Ophthalmol. 2011; 25:146–150. PMID: 21461231.
2. Sanaei-Zadeh H, Zamani N, Shadnia S. Outcomes of visual disturbances after methanol poisoning. Clin Toxicol (Phila). 2011; 49:102–107. PMID: 21370946.
3. Dethlefs R, Naraqi S. Ocular manifestations and complications of acute methyl alcohol intoxication. Med J Aust. 1978; 2:483–485. PMID: 739940.
4. Ingemansson SO. Clinical observations on ten cases of methanol poisoning with particular reference to ocular manifestations. Acta Ophthalmol (Copenh). 1984; 62:15–24. PMID: 6720270.
5. Onder F, Ilker S, Kansu T, et al. Acute blindness and putaminal necrosis in methanol intoxication. Int Ophthalmol. 1998-1999; 22:81–84. PMID: 10472766.
6. Paasma R, Hovda KE, Jacobsen D. Methanol poisoning and long term sequelae: a six years follow-up after a large methanol outbreak. BMC Clin Pharmacol. 2009; 9:5. PMID: 19327138.
Dear Editor,
We appreciate the comments of Drs. Sanaei-Zadeh and Zamani regarding our manuscript. They indicated that we did not provide sufficient medical history for the patient compared with the ophthalmologic findings. The purpose of the case study was to describe an unusual optic disc finding after methanol poisoning rather than to describe the toxicological management, and therefore we summarized the patient's medical history only briefly. The previous medical record provided by the patient was not sufficient to explain his general medical conditions and treatments except for ophthalmologic data. We are sorry that we did not describe what kinds of treatment were performed during the acute stage of the disease. According to the history we obtained, the patient consistently stated that he had experienced no changes of visual symptoms after the initial insult. After re-examination in our hospital, the patient was lost to follow up again and further follow-up ophthalmic evaluation was impossible. We thank Drs. Sanaei-Zadeh and Zamani for their interest in our case.