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| CASE REPORT |
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| Year : 2023 | Volume
: 3
| Issue : 2 | Page : 449-451 |
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Desvenlafaxine vasospasm-related retinal arterial occlusion
Anupriya Chaubey, Sandeep Saxena, Priyanka Sharma
Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh, India
| Date of Submission | 01-Jan-2023 |
| Date of Acceptance | 25-Jan-2023 |
| Date of Web Publication | 28-Apr-2023 |
Correspondence Address:
Sandeep Saxena
Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/IJO.IJO_8_23
A 51-year-old lady presented with a sudden, painless blurring of vision in the left eye. She was on oral antidepressant desvenlafaxine, a serotonin-norepinephrine reuptake inhibitor, for the past 3 years. Her visual acuity was 6/6 OU. Fundus examination of the left eye revealed opacification of the retina as a result of retinal arterial occlusion. Nasal as well as temporal retinal quadrants were involved. Inferior half of the macula was also affected. Fundus fluorescein angiography of the left eye was unremarkable while spectral domain optical coherence tomography of the macula showed microcystic changes. After excluding embolic and nonembolic causes, we hereby report a case of retinal arterial occlusion resulting from desvenlafaxine-associated transient retinal arterial vasospasm, for the first time.
Keywords: Desvenlafaxine, retinal artery occlusion, vasospasm
How to cite this article:
Chaubey A, Saxena S, Sharma P. Desvenlafaxine vasospasm-related retinal arterial occlusion. Indian J Ophthalmol Case Rep 2023;3:449-51 |
Among the clinical presentations of retinal artery occlusion, central retinal artery (CRA) obstruction is present in 57% of cases, branch retinal obstruction in 38%, and cilioretinal artery obstruction in 5%.[1] Hemi-central retinal arterial occlusion is an extremely rare clinical entity and only a few cases have been described so far.[2],[3]
Desvenlafaxine, an antidepressant is a serotonin- norepinephrine reuptake inhibitor (SNRI) that acts by modulating the levels of serotonin and noradrenaline. It has a greater impact on norepinephrine reuptake than serotonin, which attributes to its vasospastic effects. We hereby report a case of retinal arterial occlusion resulting from desvenlafaxine-associated transient vasospasm, to our knowledge, for the first time.[4]
| Case Report | |  |
A 51-year-old lady presented in the retina clinic of our tertiary care center with complaint of sudden, painless blurring of vision in her left eye for 6 days. She has been on oral medication, desvenlafaxine 50 mg once a day for depression for the past 3 years. She was nonhypertensive and nondiabetic. Her systemic examination was unremarkable. On ocular examination, best-corrected visual acuity was 6/6 OU. Anterior segment examination was within normal limits in both the eyes. Fundus examination of the right eye was normal. The left eye revealed opacification of the retina in the nasal as well as temporal quadrants. Inferior half of the macula was also affected [Figure 1]. After psychiatrist consultation, desvenlafaxine was stopped. | Figure 1: Fundus photography of the left eye depicting opacification of retina in the nasal, superior, and inferior retina. Macula is involved inferiorly
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Fundus fluorescein angiography (FFA) (Carl Zeiss VISUCAM 524, Jena, Germany) of both the eyes was unremarkable. No delayed perfusion, no focal emboli, or cattle tracking was observed [Figure 2]. Spectral-domain optical coherence tomography (SD-OCT) (Carl Zeiss, Jena, Germany) of the macula depicted central subfoveal thickness of 217 μm (OD) and 226 μm (OS). Microcystic changes were observed in the retinal inner layers [Figure 3]. Visual field assessment on Humphrey field analyzer (Carl Zeiss 750i, Dublin, CA, USA) of the right eye was within normal limits, whereas the left eye revealed superior altitudinal field defect extending inferiorly on central 24-2 threshold test, SITA-Fast strategy [Figure 4]. Carotid Doppler ultrasonography and two-dimensional (2D) echocardiography were unremarkable. Complete blood counts, coagulation profile, lipid profile, C-reactive protein, and serum homocysteine levels were within normal limits. | Figure 2: Fluorescein angiography of the left eye showing normal perfusion. No emboli or cattle tracking is observed
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 | Figure 3: Spectral-domain optical coherence tomography (SD-OCT) of the macula of the left eye depicting central subfoveal thickness of 226 μm. Microcystic changes are observed in the retinal inner layers
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 | Figure 4: Pattern deviation numeric map of the left eye shows marked depression of the visual field in the superior quadrant (−29 to −23 dB). The inferior quadrant shows depression extending peripherally (−27 to −9 dB) (Left figure). Pattern deviation probability map shows corresponding depression of the visual field, marked in black. (Right figure)
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Patient was advised xanthinol nicotinate (500 mg) sustained release tablet once daily after meal to improve ocular blood flow.
A 6-month follow-up revealed no deterioration in visual acuity in the left eye. The opacification of the retina resolved with improvement in visual field defect.
| Discussion | | |
Central retinal artery originates as a separate stem from the first part of the ophthalmic artery and usually divides into two branches at the disc, each of which further bifurcates into temporal and nasal divisions. There are some known anatomical variations of branching patterns.[5]
Central retinal artery loses the elastic lamina and has a prominent muscularis as it bifurcates at the optic disc. Moreover, the unusually developed muscularis may allow greater constriction of the vessels in response to chemical and pressure changes.[6] These histological changes coupled with the prelamina cribrosa branching of the central retinal artery may make these hemi-trunks more vulnerable to vascular occlusion, especially in subjects with systemic comorbid conditions.
The retinal opacification seen in the posterior pole along the distribution of obstructed vessels is apparently due to impairment of axoplasmic flow in the nerve fiber layer as it advances in the hypoxic retina. In our case, the patient's visual acuity was not hampered as the fovea was spared.
Desvenlafaxine due to its dual serotonin and norepinephrine reuptake inhibition is known to have deleterious effects on cardiovascular system and cause dose-dependent increases in blood pressure.[7] Costagliola et al. described multiple transient vasospasms in the optic nerve leading to ischemic optic neuropathies with long-term usage of selective serotonin reuptake inhibitors.[8] Perry et al.[4] reported that desvenlafaxine has more effect on reuptake of norepinephrine than on reuptake of serotonin. SSRIs modulate peripheral serotonin levels including that in platelets. Moreover, serotonin has been implicated as a powerful activator in platelet aggregation. Lochhead concluded that in atherosclerotic individuals, the susceptibility to this disorder becomes higher due to serotonin-enhancing platelet aggregation on the atheroma of ocular arteries.[9]
Retinal arterial occlusion does not have a propensity for simultaneous bilateral occurrence. In the present case, acute transient vasospasm of the retinal artery caused retinal artery occlusion, which was evident by opacification of the retina in the involved territory. Since the vasospasm was transient so the FFA revealed no abnormalities.
| Conclusion | | |
Patients on oral desvenlafaxine, having transient blurring of vision mandate a vigilant systemic and fundus examination.
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 | | |
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| 2. | Karjalainen K. Occlusion of the central retinal artery and retinal branch arterioles. A clinical, tonographic and fluorescein angiographic study of 175 patients. Acta Ophthalmol Suppl 1971;109:1-95. |
| 3. | Rishi P, Rishi E, Sharma T, Mahajan S. Hemi-central retinal artery occlusion in young adults. Indian J Ophthalmol 2010;58:425-32. [ PUBMED] [Full text] |
| 4. | Perry R, Cassagnol M. Desvenlafaxine: A new serotonin- norepinephrine reuptake inhibitor for the treatment of adults with major depressive disorder. Clin Ther 2009;31:1374-404. |
| 5. | Duke-Elder S. Blood vessels and nerves of the eye. In: Wyber K, editor. The Anatomy of the Visual System. System of Ophthalmology. 1 st ed, vol 2. London: Henry Kimpton; 1969. p. 339-86. |
| 6. | Park SS, Sigelmann J. Anatomy and cell biology of the retina. In: Tasman W, Jaeger EA, editors. Duane's Foundations of Clinical Ophthalmology. 15 th ed, vol 1. Hagerstown MD: Lippincott Williams and Wilkins; 2004. p. 50. |
| 7. | Munoli N, Praharaj K, Bhandary P, Selvaraj AG. Desvenlafaxine- induced worsening of hypertension. J Neuropsychiatry Clin Neurosci 2013;25:E29-30. |
| 8. | Costagliola C, Parmeggiani F, Semeraro F, Sebastiani A. Selective serotonin reuptake inhibitors: A review of its effects on intraocular pressure. Curr Neuropharmacol 2008;6:293-310. |
| 9. | Lochhead J. SSRI-associated optic neuropathy. Eye 2015;29:1233-5. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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