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| CASE REPORT |
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| Year : 2019 | Volume
: 8
| Issue : 2 | Page : 122-124 |
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Bilateral optic atrophy in snake envenomation – A case report
Ravala Siddeswari, Sikindar Mohan, Santosh Kante, Tejaswi Ponnam
Department of General Medicine, Siddhartha Medical College/Government General Hospital, Vijayawada, Andhra Pradesh, India
| Date of Submission | 30-Apr-2019 |
| Date of Acceptance | 26-Jun-2019 |
| Date of Web Publication | 30-Jul-2019 |
Correspondence Address:
Dr. Ravala Siddeswari
Department of General Medicine, Siddhartha Medical College/Government General Hospital, Vijayawada, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_57_19
Ocular complications following snake bite are usually rare. Snake bite accounts for 4% of all ophthalmoplegias. Optic neuritis and optic atrophy following snake bite have been reported in very few cases. Various causes of optic neuritis following snake bite have been postulated, including capillary damage and extensive hemorrhage, allergy to ASV and the direct toxic effect of snake venom. Here, one such rare case of optic atrophy following snake bite, admitted at Government General Hospital, vijayawada is discussed.
Keywords: Anti-snake venom, 20 min whole blood clot test, snakebite envenomation, viper bite
How to cite this article:
Siddeswari R, Mohan S, Kante S, Ponnam T. Bilateral optic atrophy in snake envenomation – A case report. J NTR Univ Health Sci 2019;8:122-4 |
| Introduction | |  |
The venomous snakes of the world belong to the families Viperidae, Elapidae, Lamprophiidae, and Colubridae. Most snakebites occur in developing countries with temperate and tropical countries in which the population subsist on agriculture and fishing.
Snake venoms are highly variable and complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and other constituents. Among the deleterious components are hemorrhagins that promote vascular leakage and cause both local and systemic bleeding.
Systemic findings are extremely variable and can include tachycardia or bradycardia, hypotension, generalised weakness, changes in taste, mouth numbness, muscle fasciculations, pulmonary edema, renal dysfunction, and spontaneous hemorrhage (from essentially any anatomic site).[1]
Such hemorrhages in anatomical sites such as cerebrum and retina are reported here in this case.
| Case Report | | |
A 28-year-old male patient presented to the triage in altered sensorium with an alleged history of snakebite. His friends identified the snake to be a “viper.” The patient was brought to the hospital within 3 h of snakebite.
The patient was conscious but irritable moving all four limbs spontaneously. He had hematemesis, hematuria, and bleeding from bite site. Both his conjunctiva appeared congested. Ptosis was evidently seen.
His vitals at the time of admission were pulse rate – 102/min, regular, blood pressure – 90/60 mmHg, SpO2 – 99% at room air, Glucometer Random Blood Sugar (GRBS) 84 mg/dL, and temperature – 98.4°F. His Glassgow coma scale (GCS) was 15 (E4 V5 M6).
His 20 min whole blood clotting time (WBCT) at the time of admission was 60 min.
A plain computed tomographic (CT) scan of the brain was done, which was normal at the time of admission.
His investigations revealed elevated prothrombin time/international normalized ratio and activated partial thromboplastin time. Other hematological investigations revealed an elevated reticulocyte count, elevated indirect, and total bilirubin with raised lactate dehydrogenase levels. His creatinine levels showed elevations within 24 h of admission, alarming of an impending renal failure.
He was started on anti-snake venom (ASV), initially with 20 vials as WBCT is >60 min. WBCT was repeated every 6 h, and 10 vials of ASV were administered each time till WBCT <20 min. A total of 80 vials were administered to reduce WBCT to <20 min.
Three days following his admission, the patient had paucity of movements on left upper and lower limbs. A repeat CT brain was done which showed a large intraparenchymal bleed in the right parieto-occipital region.
Treatment was continued with Fresh Frozen Plasma (FFP), platelet concentrate, antibiotics (as mentioned above), and heparin-free hemodialysis to treat acute onset of renal failure. Neurosurgeon, neurologist, and nephrologist were consulted. Slowly, the patient's general condition improved, was extubated, ptosis corrected, but he complained of blurring of vision for which ophthalmologist's opinion was taken.
14-03-2018: Pupils' normal size reacting to light. c/o headache.
His condition was diagnosed as retinal edema with choroidal sclerosis, due to previous hemorrhages that underwent process -→ clot -> exudation ->>> resorption. He was prescribed prednisolone and timolol eyedrops and was advised for regular follow-up. Fundoscopy findings before discharge [Table 1] and findings after discharge [Table 2].
22-03-2018: Vision both eyes 2/60, fundoscopy showed foveal reflex in both eyes, media clear.
16-04-2018: Vision was 6/60 right eye and 3/60 left eye. Fundus – optic disc mild temporal pallor present. The diagnosis was suspected to be retrobulbar optic neuritis.
Magnetic resonance imaging (MRI) brain: Parenchymal bleed involving cortex of right parietal lobe. Microhemorrhages in cortex and white matter of bilateral cerebral and cerebellar hemispheres [Figure 1].
MRI orbit: No obvious abnormality was detected.
Visual evoked potential studies done in both eyes showed prolonged P-100 latence wave forms on the left side. No recruitable wave forms seen on the right side. Findings were suggestive of bilateral optic nerve neuropathology.
21-04-2018: Retinoscopy showed bilateral optic atrophy [Figure 2].
Intravenous steroids followed by oral steroids treatment were continued. Supportive treatment like methylcobalamine and calcium were given.
14-06-2018:
| Discussion | | |
The first case was described by Davenport and Budden (1953) in which bilateral secondary optic atrophy developed; the patient received antivenine serum on the day of the bite and the changes in eyes first appeared 6 days later.
The vascular changes in the fundi may parallel the vascular changes noted in the kidneys by Casper (1955), and optic neuritis resulting from such severe hemorrhages did not differ from that caused by factors other than snake bite.[2]
Ocular complications following snake bite are usually rare. Snakebite accounts for 4% of all ophthalmoplegias. Optic neuritis and optic atrophy following snake bite have been reported in very few cases. Various causes of optic neuritis following snake bite have been postulated, including capillary damage and extensive hemorrhage, allergy to ASV, and direct toxic effect of snake venom.[3]
Injury to the optic nerve fibers in any part of their course from retina to the lateral geniculate body leads to degeneration of optic nerve and subsequent optic atrophy.[4]
Slow progressive visual failure is usual in optic atrophy depending on the cause, but the onset may be abrupt in vascular occlusion trauma or severe optic neuritis.
The development of optic atrophy is usually slow depending on its cause, but it may take 6 weeks to first appear after optic nerve transection due to trauma.
In most instances, optic atrophy is bilateral, with the disc appearing chalky white in color with clearly distinct margins.
Due to subtle ophthalmoscopic differences, it is realized that the pathological process is the same in both primary and secondary or consecutive optic atrophy, so distinction is no longer made.[5]
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
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Lei C, Badowski NJ, Auerbach PS, Norris RL. Disorders caused by venomous snake bites and marine animal exposures, chapter 474. Kasper DL, Hauser SL, et al., editorsIn: Harrison's Principles of Internal Medicine. 19 th ed. McGraw Hill; 2015. p. 3714-5.  |
| 2. | A. Guttmann-Friedmann. Case notes on blindness after snake bite. Br J Ophthalmol 1956;40:57-9. |
| 3. | Kumar PK, Ahuja S, Kumar PS. Bilateral acute anterior uveitis and optic disc edema following a snake bite. Korean J Ophthalmol 2014;28:186-8. |
| 4. | Sihota R, Tandon R. Diseases of the optic nerve, chapter 22. In: Parson's Diseases of the Eye. 22 nd ed. Elsevier; 2015. p. 362. |
| 5. | Kennard C. Neuro-ophthalmology, chapter 8. In: Donaghy M. The Brain's Diseases of the Nervous System. 11 th ed. USA: Oxford University Press; 2001. p. 247-8. |
[Figure 1], [Figure 2]
[Table 1], [Table 2]
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