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68 I NDIAN J OURNAL OF OPHTHALMOLOGY Vol. 54 No. 1

Intravenous methylprednisolone
could salvage vision in methyl
alcohol poisoning
Dear Editor,
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.1
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.

Table 1: Visual status of patients following intravenous methylprednisolone therapy

S. No. Time interval between Visual acuity at V/A at 1 week V/A at 1 month V/A at 3 months
alcohol consumption and presentation
the start of treatment
(in days)
RE LE RE LE RE LE RE LE

1. 12 CF at 1 foot HM CF at 1 foot CF at 1 foot 6/60 6/36 6/60 6/36

2. 8 No PL No PL CF at 1 foot HM 6/36 6/36 6/36 6/36
3. 14 CF at 1 foot CF at 1 foot 6/60 6/60 6/60 6/60 6/60 6/60
4. 7 6/60 6/60 6/36 6/36 6/60 6/36 6/36 6/36
5. 6 1/60 1/60 6/36 6/36 6/24 6/36 6/24 6/36
6. 27 CF at 1 foot 6/60 6/60 6/36 6/36 6/36 6/36 6/36
7. 8 HM HM HM HM 6/60 6/60 6/60 6/60
8. 45 No PL No PL 6/6 6/6 6/6 6/6 6/6 6/6
9. 19 1/60 3/60 6/60 6/36 6/24 6/24 6/24 6/24
10. 32 PL + 1/60 1/60 6/60 6/60 6/60 6/60 6/60
11. 12 6/60 6/60 6/60 6/36 6/36 6/36 1/60 1/60
12. 11 PL + PL + PL + PL + PL + PL + PL + PL +
13. 6 CF at 2 feet CF at 1 foot 4/60 4/60 6/60 6/60 6/36 6/36
14. 15 1/60 1/60 3/60 3/60 3/60 3/60 6/60 6/60
15. 17 6/60 6/60 6/36 6/36 6/36 6/36 6/36 6/36
16. 12 HM HM 3/60 3/60 6/60 6/60 6/60 6/60
17. 30 3/60 2/60 6/60 6/60 6/36 6/36 6/12 6/18
RE – Right eye
LE – Left eye
CF – Counting fingers
PL – Perception of light
HM – Hand movement perception
V/A – Visual acuity

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January 2006 Letters
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.2 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.3 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.4
Early investigators had tried spinal fluid exchange therapy,
sweat baths, thyroid extracts, adrenocorticotrophin hormone,
gastric lavage and alkali treatment without any significant
clinical response.5 Ethanol and fomepizole have been used as
specific antidotes to methanol in cases of toxicity.6 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.2 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.3,6 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.7
We have used intravenous methylprednisolone to treat
69
Table 2: Final visual outcome at 3 months following
intravenous methylprednisolone treatment
Cases showing visual No. of cases Percentage
improvement 15 88.2%
Cases not showing visual 01 05.9
improvement
Cases showing late 01 05.9
deterioration after early
improvement
Complications of therapy 0 0
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.
Manoj Shukla, MS; Imran Shikoh, DO;
Akbar Saleem, MS
Correspondence to: Prof. M. Shukla, 2/19, Ramghat Road,
Opposite Niranjanpuri, Aligarh - 202002, India
E-mail: <drmanojshukla@doc.com>
References
1. Gilger AP, Potts AM. Studies on the visual toxicity of
methanol. Am J Ophthalmol 1956;39:63–86.
2. Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA;
American Academy of Clinical Toxicology Ad Hoc Committee
on the Treatment Guidelines for Methanol Poisoning. American
Academy of Clinical Toxicology Practice guidelines for the
treatment of methanol poisoning. J I Toxicol Clin Toxicol
2002;40:415–46.
3. Pappas SC, Silverman M. Treatment of methanol poisoning
with ethanol and hemodialysis. Can Med Assoc J 1982;15:1391–
4.
4. Stelmach MZ, O’ day J. Partly reversible visual failure with
methanol toxicity. Aust N Z J Ophthalmol 1992;20:57–64.
5. Roe O. The role of alkaline salts and ethyl alcohol in the
treatment of methanol poisoning. Quart J Stud Alcohol
1950;11:107–12.
6. Sivilotti ML, Burns MJ, Aaron CK, McMartin KE, Brent J.
Reversal of severe methanol induced visual impairment: No
evidence of retinal toxicity due to fomepizole and
hemodialysis. J Toxicol Clin Toxicol 2001;39:627–63.
7. Sodhi PK, Goyal JL, Mehta DK. Methyl alcohol induced optic
neuropathy treated with intravenous high dose steroids. Int J
Clinic Pract 2001;9:599–602.
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