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 Table of Contents  
Year : 2022  |  Volume : 2  |  Issue : 1  |  Page : 177-178

A rare presentation of vasculotoxic and neurotoxic ophthalmic manifestations of snakebite

Department of Medicine, KAP Viswanatham Medical College, Tamil Nadu, India

Date of Submission19-Mar-2021
Date of Acceptance16-Aug-2021
Date of Web Publication07-Jan-2022

Correspondence Address:
Dr. Shafeeqa G Khader
2/D, Ocean Pearl, Rajiv Avenue, Injambakkam, Chennai, Tamil Nadu 600115
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_630_21

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Every year, a substantial number of snakebite cases are reported worldwide, more so from tropical countries. Although the fatality rate is quite low, it is nonetheless considered a medical emergency in view of the possible hematological, neurological, cardiac, and renal complications. The snake venom injected into the body contains a multitude of compounds that are responsible for their multisystem involvement. However, ocular complications following a snakebite are seldom reported in the literature. Our case report deals with the occurrence of transient central retinal artery occlusion and toxic neuritis soon after a snakebite.

Keywords: Central retinal artery occlusion, snakebite, snake venom, toxic neuritis, toxin-mediated vasopasm

How to cite this article:
Khader SG, Sivagnanam H. A rare presentation of vasculotoxic and neurotoxic ophthalmic manifestations of snakebite. Indian J Ophthalmol Case Rep 2022;2:177-8

How to cite this URL:
Khader SG, Sivagnanam H. A rare presentation of vasculotoxic and neurotoxic ophthalmic manifestations of snakebite. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jan 16];2:177-8. Available from: https://www.ijoreports.in/text.asp?2022/2/1/177/334964

Envenomation from snakebites is an important public health problem in many tropical countries. Of the 3000 or so snake species that exist in the world, about 600 are venomous.[1] Although ocular complications following venom exposure are infrequently reported, they might need urgent medical attention. Therefore, it is essential for clinicians to know about their incidence, pathophysiology, workup, and management. Our case deals with how an 18-year old developed sudden monocular loss of vision following a snakebite.

  Case Report Top

An 18-year-old female presented to the outpatient department with an alleged history of snakebite on her left lower limb about an hour earlier. Her chief complaints were pain over the bite site along with giddiness. She had no bleeding manifestations, ptosis, or breathing difficulty. On examination, the patient was drowsy although responding to oral commands, was able to move all four limbs, and her bilateral plantar response remained flexor. The cardiovascular and respiratory systems examination revealed no abnormality. Her single breath count was 20, and the coagulation parameters were within normal limits. The patient was started on intravenous neostigmine 1.5 mg stat preceded by 0.6 mg of atropine to counteract the possible neurotoxicity and intravenous antibiotics for supportive care. Subsequently, 10 vials of anti-snake venom were administered. Around 9 hours later, the patient developed sudden painless loss of vision in the left eye. On assessment, her best-corrected visual acuity in the left eye was only perception of light, in contrast to 6/6 in the right eye. Following this, the swinging light test was performed which demonstrated a relative afferent pupillary defect on the left side. Toxic neuritis was suspected and fundus examination was performed, which showed normal right eye [Figure 1]a and a cherry-red spot in the left eye [Figure 1]b, which suggested central retinal artery occlusion (CRAO). Furthermore, fundus fluorescein angiography was performed which showed significant filling defect in the retinal artery on the left side and dye leakage and hyperfluoroscence of the disc. Optical coherence tomography was also done, which showed increased macular thickness suggesting macular edema along with hyperreflectivity of the inner retina in the affected eye, thus confirming the suspicion of acute CRAO.
Figure 1: (a) Fundus photo of the normal right eye (b) Fundus photo of the left eye shows cherry-red spot at the macula

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Although visual evoked response could not be done in view of peripapillary leak and relative afferent pupillary defect, toxic neuritis could not be ruled out and she was immediately started on methylprednisolone 1 g I.V. in three doses over three days which was then switched to oral prednisolone 1 mg/kg and was weaned off eventually. Over the next 10 days, her visual acuity improved to 6/60 with the earliest vision improvement noted on the sixth day and stabilized at 6/18 around one month later.

  Discussion Top

Snakebite is a common occurrence in rural areas of developing countries. India records the highest annual number of envenomings (81,000) and deaths (nearly 11,000).[1] Ocular manifestations of snakebite can occur due to venom spray, termed as venom ophthalmia, or venom injection.

Snake venoms are classified into neurotoxins (fasciculins, dendrotoxins, and alpha neurotoxins) and cytotoxins (phospholipases, cardiotoxins, and hemotoxins).[2] Neurotoxic envenomation can cause ptosis and external ophthalmoplegia more commonly and optic neuritis rarely, whereas vasculotoxic bite can cause lid edema, chemosis, subconjunctival hemorrhage, hyphema, retinal or vitreous hemorrhage, CRAO, and macular and cortical infarction.[3]

The possible pathogenic mechanism for vascular occlusion could be any one or a combination of vasculotoxic venom-induced vasospasm, toxic vasculitis, DIC-mediated fibrin microthrombi formation, and hyperviscosity-related hypercoagulable condition.[4] Venom-induced consumption coagulopathy is the commonest and is a venom-induced activation of the clotting pathway by procoagulant toxins, resulting in clotting factor consumption and coagulopathy. The procoagulant toxin differs between snakes and can activate prothrombin, factor X, and factor V or consume fibrinogen. The most useful investigation is a prothrombin time/international normalized ratio.[5] Toxic vasculitis, on the other hand, caused by certain viperine species may result in thrombosis or indicate direct action of the venom on vascular endothelial cells. Hemorrhagins—complement-mediated toxic components of Viperidae snake venom—may provoke severe vascular spasm, endothelial damage, and increased vascular permeability, all of which might contribute to vascular occlusion.[6]

Bhalla et al.[7] reported a case of CRAO after snakebite, in which coagulation abnormalities were noted initially but improved with time and were absent at the time of visual loss. The authors suggested that the CRAO could be the result of the direct action of the venom toxins on the retinal artery and not the result of venom-mediated coagulopathy. Similarly, our case exhibited no abnormality in her coagulation parameters, which has led us to the assumption that the transient CRAO could be as a result of hemorrhagin-mediated vasospasm.

With relative afferent pupillary defect and a drastic response to steroids, we suspect our patient could have had a toxic neuritis component as well. Toxic neuritis following a snakebite could be due to the snake venom itself[8] or an allergic reaction to the snake antivenom.[9] Although the cause in our case could not be ascertained, the mainstay of treatment which includes steroids resulted in a marginal improvement in the patient's vision.

  Conclusion Top

In conclusion, a combination of transient CRAO along with superimposed toxic neuritis in the same patient following snakebite has not been reported so far. Thus, periodic dilated fundus examination must be encouraged in all cases of snakebite, which can help in the early treatment of vision-threatening ocular complications.

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There are no conflicts of interest.

  References Top

Kasturiratne A, Wickremasinghe AR, de Silva N, Gunawardena NK, Pathmeswaran A, Premaratna R, et al. The global burden of snakebite: A literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med 2008;5:e218.  Back to cited text no. 1
Omparkash T, Channabasappa S, Balasubramanyam A, Nayak V. Ocular manifestations following Snakebite. Delhi Journal of Ophthalmology 2016;26:188-9.  Back to cited text no. 2
Singh J, Singh P, Singh R, Vig VK. Macular infarction following Viperine snake bite. Arch Ophthalmol 2007;125:1430-1.  Back to cited text no. 3
Tungpakorn N. Unusual visual loss after snakebite. J Venom Anim Toxins Incl Trop Dis 2010;16:519-23.  Back to cited text no. 4
Berling I, Isbister GK. Hematologic effects and complications of snake envenoming. Transfus Med Rev 2015;29:82-9.  Back to cited text no. 5
Bashir R, Jinkins J. Cerebral infarction in a young female following snake bite. Stroke 1985;16:328-30.  Back to cited text no. 6
Bhalla A, Jain A, Banait S, Jajoo UN, Kalantri P. Central retinal artery occlusion: An unusual complication of snakebite. J Venom Anim Toxins Incl Trop Dis 2004;10:311-4.  Back to cited text no. 7
Rao KV. Optic neuritis and ophthalmoplegia caused by snake bite. Indian J Ophthalmol 1981;29:243-5.  Back to cited text no. 8
[PUBMED]  [Full text]  
Mathur SP. Allergy to antivenine serum. Br J Ophthalmol 1959;43:50-1.  Back to cited text no. 9


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