|Year : 2021 | Volume
| Issue : 2 | Page : 326-328
Venom induced macular infarction
Janani Sreenivasan1, PS Rajesh1, Muna Bhende1, S Ambika2
1 Shri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, Chennai, Tamil Nadu, India
2 Department of Neurophthalmology, Medical Research Foundation, Chennai, Tamil Nadu, India
|Date of Submission||07-Jul-2020|
|Date of Acceptance||28-Nov-2020|
|Date of Web Publication||01-Apr-2021|
Dr. Muna Bhende
Shri Bhagwan Mahavir Vitreoretinal Services, Medical Research Foundation, Sankara Nethralaya, 18, College Road, Chennai, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Venomous snake bites, a serious health issue in Asian countries, may be associated with multiorgan involvement, although ocular manifestations are relatively uncommon. Herein, we report a case of snakebite induced macular infarction. A seventeen-year-old girl presented with a history of viper snake bite in the right ankle, followed by a sudden painless drop in vision in the left eye, 20 days back with BCVA of 20/600. Left eye fundus examination revealed temporal pallor of the optic disc with retinal whitening in the macular area, and sclerosed macular branch arteriole, consistent with macular infarction. She was managed conservatively.
Keywords: Hemotoxicity, macular infarction, snake venom, transient central retinal artery occlusion
|How to cite this article:|
Sreenivasan J, Rajesh P S, Bhende M, Ambika S. Venom induced macular infarction. Indian J Ophthalmol Case Rep 2021;1:326-8
Snakebite is an important health hazard with significant morbidity and mortality and is more prevalent in tropical countries. Although ocular involvement after a snake bite is not uncommon, vision-threatening complications are rare, including acute angle-closure glaucoma, vitreous and retinal hemorrhage, central retinal artery occlusion (CRAO), macular infarction, exudative retinal detachment, optic neuritis, globe necrosis, endophthalmitis, and blindness caused by cortical infarction.,,,,,, We report a case of macular infarction, due to snake bite.
| Case Report|| |
A 17-year-old girl sustained a viper bite on the lateral side of the right ankle, followed by loss of consciousness for 8 hours. She developed cellulitis of the right lower limb and was treated at a nearby hospital with Anti-Snake Venom, intravenous fluid and antibiotics. She noticed a painless loss of vision in the left eye (OS) as soon as she regained consciousness. She was diagnosed elsewhere as OS optic neuritis, venom-induced and treated with Intravenous Methyl Prednisolone 1 gram (3 days) followed by oral steroids for one week. The patient reported minor visual improvement after the same. Blood tests including complete blood count, basic coagulation tests and renal function tests were unremarkable. She presented 20 days after the snake bite with BCVA of 20/20 in the right eye (OD) and 20/200 in OS. OD examination [Figure 1]a was unremarkable. Intraocular pressure was normal in both eyes. In OS, there was relative afferent pupillary defect and fundus examination [Figure 1]b showed clear media, temporal pallor of optic disc with retinal whitening in macular area, sclerosed macular branch arteriole, with splinter hemorrhage superior to the fovea and cherry red spot. The investigations showed normal study of OD [Figure 1]c and [Figure 2]a. Optical coherence tomography of OS [Figure 1]d showed hyperreflectivity of the inner retinal layers, secondary to intracellular edema, suggesting arteriolar occlusion. FFA of OS [Figure 2]b, [Figure 2]c, [Figure 2]d showed complete arterial filling except for macular arterioles at 22 seconds and the best comparative image (right and left eye) available is at 1 min 27 seconds, wherein right eye shows complete filling of all arteries but left eye showed irregular calibre of arterioles supplying the macular area with reduced filling of dye at the terminal ends with A-V transit time of 5 seconds. Electrodiagnostic tests of OD was normal [Figure 3] and [Figure 4]a. In OS, full-field ERG [Figure 3] was normal whereas Flash Visually Evoked Potentials [VEP] [Figure 4]b showed normal P2 latency with reduced amplitudes. Systemic examination was unremarkable. At this point, it was felt that the role of vasodilators and other systemic medications was questionable, and she was advised to have periodic follow-ups.
|Figure 1: (a-d) Colour fundus photo of right eye (a) is normal and of the left eye (b) shows mild disc pallor with retinal whitening in the macular area, sclerosed macular branch retinal arteriole (red arrow), superficial hemorrhages superior to fovea and cherry red spot. Spectral domain Optical Coherence tomography of right eye (c) is normal and of the left eye (d) shows hyperreflectivity in the inner retinal layers suggesting intracellular edema secondary to arterial occlusion|
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|Figure 2: (a-d): Fundus fluorescein angiogram of the right eye (a) appear normal whereas of the left eye (b- early phase, c-late phase, d- enlarged view) show irregular calibre of arterioles supplying the macular area with reduced filling of dye at the terminal ends (red arrows)|
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|Figure 3: Full field Electroretinogram of right eye (upper) and left eye (lower) is within normal limits|
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|Figure 4: (a and b): Flash Visually Evoked Potentials of right eye (a) shows normal P2 latency with normal amplitude and of the left eye (b) shows normal P2 latency with reduced amplitude|
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| Discussion|| |
India, being a tropical country is a habitat for a large variety of snakes. Venomous snake bites result in multisystem derangements., Ocular involvement albeit rare can be due to chemical injury to the eye from spitting of highly irritant snake venom, direct injury leading to penetrating injuries with bite marks, conjunctival and corneal lacerations., Anterior segment findings include Subconjunctival hemorrhages, hyphema, keratomalacia, bilateral angle-closure glaucoma, and uveitis. The posterior segment manifestations reported are CRAO, macular infarcts, and retinal and vitreous hemorrhages.,,,,, Snake venom is a complex heterogeneous substance that predominantly affects the synapse (neurotoxic) or coagulation pathway (hemotoxic). Bilateral ptosis and ophthalmoplegia are common ocular manifestations of neurotoxic snake bites. Hemotoxic venom has procoagulant enzymes that initiate coagulation cascade and enzymes causing fibrinolysis and thrombocytopenia that result in disseminated intravascular coagulation (DIC), compounded by hyperviscosity and hypoperfusion leading to vascular occlusion. Hemorrhagins (complement-mediated toxic components of viperine venom) cause vasospasm, endothelial damage, and increased vascular permeability.,,
Snakebite induced macular infarct could be due to occlusion of macular end-arterioles or secondary to transient CRAO.,,,, Since patient presented 20 days later, classical clinical and angiographic features of CRAO may not be evident and ERG did not show a negative waveform or subnormal b wave. In transient CRAO, the visual outcome depends on the duration; retina suffers no detectable damage with CRAO for up to 97 minutes; between 105 and 240 minutes, partial retinal recovery seen on VEP and at 240 minutes, almost total optic nerve atrophy occurs with massive irreversible retinal damage.,, Thus, a transient CRAO lasting longer than 105 minutes can cause reduction in VEP amplitudes,, as seen in this patient. When the circulation in central retinal artery is restored, retinal capillaries in the macular region do not refill due to marked ischemic swelling of retinal ganglion cell layer that leads to compression and occlusion of capillaries, leading to macular infarction., The cause of unilateral affection is unclear but may be due to anatomical variation in blood vessels. The low-grade DIC process could be due to cellulitis, if associated with septicemia but it is unlikely here as cellulitis was localized to the lower limb, as per history and hospital records.
The cause of vision loss in the patient could be due to macular infarct secondary to transient CRAO or isolated macular infarct with toxic optic neuropathy. In delayed presentations of snakebite, identification of exact cause of visual loss becomes difficult due to absence of classical findings, as exemplified in our case. Jalali et al. suggested that electrophysiological tests in such cases can help to reach a definite diagnosis. Both scenarios can have RAPD and subnormal VEP amplitudes. While transient CRAO is reported with snake bite more often than optic neuropathy, absence of subnormal b wave in the ERG makes it debatable. In either case, the visual prognosis is poor despite medical treatment. The limitations of the study include lack of follow-up and OCTA documentation.
| Conclusion|| |
This case highlights the importance of ophthalmic examination of all snakebite cases, which can help in the diagnosis of vision-threatening ocular complications and assessment of visual prognosis, with management being largely supportive.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Naik AS, Ranjan R, Manayath GJ. Transient central retinal artery occlusion following viperine snake bite. Can J Ophthalmol 2017;52:e205-8.
Praveen Kumar KV, Praveen Kumar S, Kasturi N, Ahuja S. Ocular manifestations of venomous snake bite over a one-year period in a tertiary care hospital. Korean J Ophthalmol 2015;29:256-62.
Chu ER, Weinstein SA, White J, Warrell DA. Venom ophthalmia caused by venoms of spitting elapid and other snakes: Report of ten cases with review of epidemiology, clinical features, pathophysiology and management. Toxicon 2010;56:259-72.
Singh J, Singh P, Singh R, Vig VK. Macular infarction following viperine snake bite. Arch Ophthalmol 2007;125:1430-1.
Hayreh SS. Acute retinal arterial occlusive disorders. Prog Retin Eye Res 2011;30:359-94.
Jalali S, Padhi TR, Bansal R, Sahoo K, Basu S, Mathai A. Visual loss with inner retinal dysfunction, after snake bite: Two case reports. Doc Ophthalmol 2013;127:155-63.
Patel R, Gopalakrishnan M, Haris EM. Central retinal artery occlusion following viperine snake bite. Ophthalmol Retina 2018;2:172-3.
Hayreh SS. Transient central retinal artery occlusion following viperine snake bite. Arch Ophthalmol 2008;126:870-1; author reply 871.
Varma DD, Cugati S, Lee AW, Chen CS. A review of central retinal artery occlusion: Clinical presentation and management. Eye (Lond) 2013;27:688-97.
Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723-36.
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