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   Table of Contents      
ARTICLES
Year : 1979  |  Volume : 27  |  Issue : 4  |  Page : 103-104

Clinical study of acute toxic amblyopia cases


M.G.M. Medical College, Indore, India

Correspondence Address:
P C Mittal
Department of Ophthalmology, M.G.M. Medical College, Indore (M.P.).
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Mittal P C, Nahata M C, Bhatia S, Ali A. Clinical study of acute toxic amblyopia cases. Indian J Ophthalmol 1979;27:103-4

How to cite this URL:
Mittal P C, Nahata M C, Bhatia S, Ali A. Clinical study of acute toxic amblyopia cases. Indian J Ophthalmol [serial online] 1979 [cited 2019 Oct 22];27:103-4. Available from: http://www.ijo.in/text.asp?1979/27/4/103/32590

Table 1

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Table 1

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In October 1976 mass methanol poisoning took place in Indore. The medical treatment was already given in the form of intra-venous fluids, soda bicarb, systemic steroids and ethanol to combat against generalised acidosis. The following ocular treatment was given along with the above medical line of treatment.

Retrobulbar injection of dexamethasone 1/2 c.c. daily for 7 to 10 days. Injection vitamin B 1 100 mgm. plus B 6 50 mgm. plus B 12 1000 mcg. daily. Vitamin C 500 mgm twice a day. Tablet Duvadilan one tablet four times a day for seven days.


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Within 12 hours 224 persons were admitted out of which 112 (50%) persons died. 76 (64.2%) persons out of 112 survived were having visual complaint. These included blurred vision, defective vision or loss of vision.

In 51 (67%) cases visual loss was transient, vision being restored within 48 hours. In 25 (33%) cases blurred vision persisted and these were followed in greater detail. Out of 25 cases, 10 (40%) cases were having marked diminution of vision and 5 (20%) cases noticed loss of vision, while 10 (40%) cases were complaining of blurring vision only.

The visual acuity was recorded in these 25 cases with in 24 to 36 hours of admission. There was no PL in 8 (16%) eyes (This includes one eye of perforated corneal ulcer), 10 (20%) eyes were having PL, PR only (this includes 2 eyes with mature cataract). Visual acuity below 3/60 was in 12 (24%) eyes, 12 (24%) eyes were having vision between 3/60 to 5/60. 6/60 to 6/18 visual acuity was recorded in 3 (6%) eyes and 5 (10%) eyes were having 6/12 to 6/6 visual acuity. The progress in vision has been summarised in [Table - 1].

Pupils were dilated and fixed in 23 (46%) eyes while sluggish reaction was present in 22 (44%) eyes, brisk in 4 (8%) eyes. Central scotoma was present in 8 (16%) eyes and peri­pheral constriction was detected in 12 (24%) eyes. The field recording was not possible in 30 (60%) eyes because of poor vision.

The fundus changes immediately on admis­sion were characterised by hyperaemia with vary­ing degree of blurring of the disc margin (pro­nounced: 23 (46/) nasal 19 (38%), slight: 5 (10%) macular oedema and venous congestion. Primary optic atrophy set in 6 (12%) eyes and was associated with macular degeneration and arteriolar attenuation. 15 (30%) eyes showed temporal optic atrophy with slight attenuation of blood vessels, while 10 (20°x) eyes showed only slight pallor of the disc with normal blood vessels. 16 eyes (32%) had normal fundus. In no case glaucoma type optic atrophy was noted.

It was noted that significant improvement in visual acuity occurred in a large number of cases by the end of first week. It was interest­ing to note that three cases which had loss of perception of light on first examination had regained perception and projection of rays or finger counting by the end of first week. Many of the cases which had visual acuity better than 3/60 at the end of first week continued to improve gradually. In a few cases visual improvement was noticed even after 3 months. However, one case with visual acuity below 3/60 lost vision. No significant changes in visual status were noticed after three months.

It is possible that the papillo-macular fibres along with ganglion cells are affected being more delicate and sensitive to the toxins. This may be the reason why macular oedema occured in acute stages and temporal atrophy later on.



 
 
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