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BRIEF REPORT
Year : 1999  |  Volume : 47  |  Issue : 3  |  Page : 191-192

Cortical blindness : An unusual sequela of snake bite


University College of Medical Sciences, Delhi, India

Correspondence Address:
U Dhaliwal
University College of Medical Sciences, Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 10858776

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How to cite this article:
Dhaliwal U. Cortical blindness : An unusual sequela of snake bite. Indian J Ophthalmol 1999;47:191-2

How to cite this URL:
Dhaliwal U. Cortical blindness : An unusual sequela of snake bite. Indian J Ophthalmol [serial online] 1999 [cited 2019 Sep 23];47:191-2. Available from: http://www.ijo.in/text.asp?1999/47/3/191/14917

Several ophthalmic effects may follow snake bite; this report describes an instance of cortical blindness that resulted from snake bite.

Snake venoms are complex heterogenous poisons with multiple effects. The ophthalmic effects of envenomation are varied and some of those described are: ptosis, muscle palsies, haemorrhages into the conjunctiva, anterior chamber, vitreous or retina, lid oedema, conjunctival chemosis, retinal and optic nerve oedema, pupillary changes, optic neuritis, optic atrophy, cataract, and venom ophthalmia.[1],[2] Cortical blindness resulting after snake bite is rare and was reported in 1993 from South Africa.[1] An analysis of 1040 cases of snake bite treated at a referral hospital in India[2] revealed 58 cases with ophthalmic manifestations; however, no case of cortical blindness was seen. We describe a case where the patient developed cortical blindness as a sequel to cobra bite.

A 6-year-old boy was brought to this hospital unconscious and with laboured respiration 3 hours after he sustained a cobra bite, witnessed by the father. The bite was painful and the child reported drowsiness soon after. He was rushed to a local healer who tried traditional remedies like burning incense, beating away the spirit with a broomstick and mumbling incantations. By this time the child became unconscious. In these 2 hours no drug had been administered. He was then taken to a local hospital but since antivenin was not available, he was transferred to this tertiary-care institution. En route, he had cardiac arrrest for which cardiac massage was done by the accompanying paramedical worker.

On arrival at the intensive care unit he was unconscious and responded feebly only to deep pain. Respiration was laboured and shallow and mild cyanosis had set in. The blood pressure was normal and pulse rate was 110/min. There was evidence of gastric bleeding on naso-gastric intubation, but no bleeding was noted from any other site. Fang marks were found on the ring finger of the right hand, with swelling but no blistering. The pupils were dilated, reacting to light, and the ocular fundus showed mild disc oedema in both eyes.

Laboratory investigations revealed leukocytosis with mild neutrophilia, normal electrolytes, and normal renal, hepatic, and coagulation profiles. Endotracheal intubation with assisted ventilation was initiated and polyvalent antivenin infusion started immediately after a negative reaction to skin testing. Neostigmine, antibiotics and other supportive treatments were given. Although the consciousness level began improving by the next day, neurological defects persisted. At 8 days post-bite, the child was conscious but disoriented, and had quadriparesis with grossly normal sensations, increased muscle tone, hypertonic deep tendon reflexes, and extensor plantars. He was aphasic and had left upper motor neuron facial nerve palsy. Perception of light was absent in both eyes in spite of normal pupils and ophthalmoscopically normal fundus oculi.

Though magnetic resonance imaging was advised soon after the patient presented, the family was unable to bear the expenses. Computerised tomographic scan of the brain, with a fee waiver, was possible at a semi-charitable institution at one month post-bite. It showed infarctions in the region of the basal ganglia on both sides and lucent areas in the right frontal, temporal, parietal and both occipital lobes, suggestive of old multi-focal ischemia Figure. The ventricular system was mildly dilated. By 4 months the child was responding to commands, had regained partial use of the right upper limb only and had no cranial nerve palsy. By 6 months he was speaking but his cortical blindness has persisted for over the 3 years of follow up.

[TAB:2]Discussion[/TAB:2]

The incidence of snake bite is probably underestimated. A large number of victims die unreported, particularly in rural areas, where folklore and witch-doctors hold sway. Morbidity and mortality are also related to the nonavailability of or delay in administration of antivenin. Antivenin is the only specific treatment for envenoming and often causes marked symptomatic improvement. Cobra venom is predominantly neurotoxic, resulting in flaccid paralysis, including respiratory paralysis.[3] Neurotoxicity may appear as early as 3 minutes after the bite[3] but may be delayed for 19 hours.[4] Mild envenoming may cause no neurotoxic effects or only mild ones like ptosis or external ophthalmoplegia. Severe envenoming, however, results in death or disability. Most deaths after cobra bite are due to respiratory failure. If the patient has been well oxygenated, the neurotoxic effects may reverse completely in response to antivenin or anticholinesterase4 or they may wear off spontaneously in a week.[3]

Cobra venom can cause blindness by damaging the retinal cells, causing bilateral optic neuritis or it can cause cortical blindness.[1] Damage to the retina or optic nerve is due to the direct effect of the venom; or hypersensitivity reaction to antivenin; or extensive haemorrhage and capillary damage.[3],[5] It causes derangement of the pupillary light reflex and ophthalmoscopically visible abnormalities. Cortical effects after neurotoxic snake bite are less well studied. Direct damage to the central nervous system by venin has not been described. An experimental study in 1985[6] suggested that cobra venom decreased cerebral blood supply thereby decreasing the supply of blood-borne substances, including venom, to the brain. The effect on the brain is more likely related to respiratory paralysis and cardiac arrest that occurs after neurotoxic envenomation. The child described here had cardiac arrest and prolonged resiratory paralysis following snake bite. This resulted in widespread cerebral hypoxia as documented in the CT scan. Early respiratory support followed by antivenin treatment could have substantially reduced hypoxic brain damage. Paucity of literature on cortical blindness following neurotoxic snake bite may be a reflection of the high mortality of those patients in whom respiratory paralysis is prolonged or severe.

This case highlights the need for evaluation of victims of neurotoxic snake bite for early signs of respiratory depression and prompt respiratory assistance even if antivenin is not available. The catastrophic consequences of persistent neurological deflicits, including blindness, may thus be minimised in victims who survive.

 
  References Top

1.
Berger RR, Brook S. Cobra bite: Ophthalmic manifestaions. Harefuah 1993;125:265-66 [In Hebrew].  Back to cited text no. 1
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2.
Eapen KE, Anthrayose CV, Mani EJ, Joseph E. Indirect ocular trauma-ocular manifestations of snake bite. Proceedings of the All India Ophthalmological Conference 1996;67-68.  Back to cited text no. 2
    
3.
Sanford JP. Snake bites. In: Bennet JC Plum F, editors, Cecil's Textbook of Medicine, 20th ed. Philadelphia, USA:W B Saunders Company; 1996. p 1951-53.  Back to cited text no. 3
[PUBMED]    
4.
Mitrakul C, Dhamkrong-At A, Futrakul P, Thisyakorn C, Vongsrisart K, Varavithya C, et al. Clinical features of neurotoxic snake bite and response to antivenom in 47 children. Am J Trop Med Hyg 1984;33:1258-66.  Back to cited text no. 4
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5.
Menon V, Tandon R, Sharma T, Gupta A. Optic neuritis following snake bite. Indian J Ophthalmol 1997;45:236-37.  Back to cited text no. 5
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6.
DiMattio J, Weinstein S, Streitman J. In vivo effects of snake venoms on passive and facilitated glucose transport across blood-ocular and blood-CSF barriers of the rat. Toxicon 1985;23:63-71.  Back to cited text no. 6
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