LETTER TO EDITOR
Year : 2006 | Volume
: 54 | Issue : 1 | Page : 68--69
Intravenous methylprednisolone could salvage vision in methyl alcohol poisoning
Manoj Shukla, Imran Shikoh, Akbar Saleem
2/19, Ramghat Road, Opposite Niranjanpuri, Aligarh - 202002, India
2/19, Ramghat Road, Opposite Niranjanpuri, Aligarh - 202002
|How to cite this article:|
Shukla M, Shikoh I, Saleem A. Intravenous methylprednisolone could salvage vision in methyl alcohol poisoning.Indian J Ophthalmol 2006;54:68-69
|How to cite this URL:|
Shukla M, Shikoh I, Saleem A. Intravenous methylprednisolone could salvage vision in methyl alcohol poisoning. Indian J Ophthalmol [serial online] 2006 [cited 2019 Aug 21 ];54:68-69
Available from: http://www.ijo.in/text.asp?2006/54/1/68/21628
In the Asian subcontinent methyl alcohol poisoning is a fairly common condition, more so in the poor socioeconomic group, and in its worst form often leads to a bilateral loss of vision. Since it is associated with serious systemic problems, administration of ethyl alcohol, peritoneal dialysis and other forms of supportive treatment such as B-complex and folate reduce mortality but leaves the problem of complete blindness. Whilst the mechanism of retrobulbar optic neuropathy due to metabolites of methanol is fairly accepted, the treatment of optic neuropathy has mainly been limited to the empirical use of oral prednisolone with limited success. No definitive treatment of optic neuropathy due to methyl alcohol poisoning has been reported in the literature so far. We report our experience of the use of methylprednisolone in blindness induced by methyl alcohol poisoning in 17 patients in the age group of 22 to 42 years who presented to us with a history of spurious alcohol consumption.
All of them had a sudden onset of blurring of vision after alcohol intake, which progressed to severe loss of vision with a semidilated or dilated pupil in most of them [Table 1]. They presented to us after a time interval varying from 6 to 45 days as majority of them had been receiving medical treatment for systemic ailments at other centers. A thorough clinical examination was carried out in all the patients which included best corrected visual acuity, slit lamp biomicoscopy, and fundus examination by a direct ophthalmoscope and + 90 D lens. Each patient was administered intravenous methylprednisolone 1 gram in 500 ml ringer lactate slowly over 2 hours after ruling out medical contraindications such as diabetes mellitus, hypertension, osteoporosis etc. The same dose of intravenous methyl prednisolone was repeated on the second and third day in similar fashion. Along with this regimen the patients also received following supportive treatment:
1. Oral cyclendelate (400 mg) once daily for 6 weeks.
2. Intramuscular hydroxycobalamine (1.5 ml) once daily for 1 week.
3. Oral pentoxyphylline (400 mg) once daily for 6 weeks.
After 3 initial intravenous methylprednisolone doses, oral prednisolone (40mg) was given for a period of 14 days along with the supportive treatment. Oral steroids were tapered over a period of 4 to 6 weeks. Patients were asked to report for follow-up every week, wherein ophthalmological evaluation as mentioned earlier was carried out for atleast 3 months.
At the 7th day there was significant improvement in visual acuity by one Snellen's line in 10 out of 17 patients [Table 1]. Three patients showed improvement in visual acuity by 2 Snellen's lines. There was no improvement in 3 cases. Interestingly, one case presenting as no perception of light bilaterally, recovered to 6/6 in both eyes. Examination of the fundus at this follow-up revealed a decrease in peripapillary and disc edema, and restoration of a sluggish pupillary reaction in most of the treated eyes. At the 1 month follow-up 5 cases, which had not shown any visual recovery in the 1st week revealed a gain in visual acuity by one or more Snellen's lines. At 3 months all the patients except one showed good visual recovery. One patient who had shown early improvement in visual acuity at the 7th day and one month follow-up showed deterioration in visual acuity from 6/36 to 1/60 in both eyes. In this case the disc pallor had progressively increased to develop into full-blown primary optic atrophy.
The time of starting treatment after alcohol consumption, which varied from 6 to 45 days, had no effect on the final visual outcome [Table 2]. Three patients who reported for treatment after more than 1 month of alcohol consumption also had a good visual recovery. None of the patients developed any systemic complications as a result of this therapy even at the end of 3 months.
Methanol by itself has low toxicity, however, its metabilites causes most of the toxic effect. Accumulation of formic acid in tissues causes systemic metabolic acidosis and ocular toxicity in patients of methanol poisoning. Visual loss is dependent on the initial dose of methanol ingested and on the interval between ingestion and start of therapy, but the latter is more critical for the outcome. Fundus findings in cases of acute methyl alcohol poisoning vary from peripapillary edema, hyperemia of optic disc and venous engorgement, to pallor of optic disc, attenuation and sheathing of vessels depending upon the time of presentation after alcohol consumption.
Early investigators had tried spinal fluid exchange therapy, sweat baths, thyroid extracts, adrenocorticotrophin hormone, gastric lavage and alkali treatment without any significant clinical response. Ethanol and fomepizole have been used as specific antidotes to methanol in cases of toxicity. Both the agents block the conversion of methanol to formic acid, which is the active toxic metabolite. Bicarbonate administration and haemodialysis are used to correct the systemic acidosis caused by accumulation of formic acid. Folinic acid is administered to enhance the metabolism of formic acid already produced in the body. These forms of therapy prevent the formation of toxic metabolites and its subsequent catastrophic complications but do not have any significant value in treating established methanol toxicity. The treatment modalities already mentioned are beneficial in cases of acute toxicity, as the interval between ingestion and start of therapy is more critical to the outcome than the total dose of methanol ingested., Oral and parenteral steroids have been tried empirically by many investigators with varying results. In a reported study using intravenous steroids for 3 days followed by oral steroids for 11 days, the authors have suggested that intravenous steroids are beneficial in the treatment of methanol induced blindness. However, the interval between ingestion and start of therapy was again found to be a critical factor. We have used intravenous methylprednisolone to treat blindness caused by methyl alcohol poisoning. Our observations in the present series of 17 patients confirm that intravenous methylprednisolone has a beneficial role in the management of cases of methyl alcohol poisoning presenting with decreased visual acuity or complete blindness. Supportive therapy in the form of vasodilators and B-complex supplements may have a minor effect, if any, in the ultimate visual outcome. Nearly all eyes irrespective of time of reporting for treatment showed significant visual improvement at 3 months [Table 2].
Along with the subjective visual improvement, the optic disc also showed decrease in disc edema and clearing of disc margin. Thus it may be logical to believe that cases presenting early would develop less manifest primary optic atrophy following treatment. We therefore recommend all patients to be treated by this regimen irrespective of the amount of visual debility and the time of presentation following methyl alcohol poisoning.
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