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   Table of Contents      
CASE REPORT
Year : 2018  |  Volume : 66  |  Issue : 3  |  Page : 466-468

Bilateral central retinal artery occlusion as presenting manifestation of human immunodeficiency virus infection


1 Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India
3 Department of Histopathology, Post Graduate Institute of Medical Education and Research, Chandigarh, India

Date of Submission06-Oct-2017
Date of Acceptance21-Nov-2017
Date of Web Publication26-Feb-2018

Correspondence Address:
Dr. Reema Bansal
Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_906_17

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  Abstract 


A 30-year-old male with bilateral acute visual loss presented with retinal edema in the posterior pole and peripapillary region with extensive retinal hemorrhages. Fluorescein angiography revealed delayed arterial filling in the right eye and absent arterial filling in the left eye, suggesting bilateral central retinal artery occlusion. Systemic evaluation revealed a history of chronic low-grade fever and generalized lymphadenopathy. HIV (ELISA) was positive, and other systemic comorbidities were ruled out. Cervical lymph node biopsy stained positive for acid-fast bacilli, with large areas of necrosis, palisaded by epithelioid cell granulomas, macrophages, and multinucleated giant cells, suggesting lymph node tuberculosis. Despite antiretroviral and antitubercular therapy, he developed optic atrophy at 4 weeks.

Keywords: Central retinal artery occlusion, HIV, tuberculosis


How to cite this article:
Bansal R, Jain S, Gupta V, Sharma A, Bal A, Jain S. Bilateral central retinal artery occlusion as presenting manifestation of human immunodeficiency virus infection. Indian J Ophthalmol 2018;66:466-8

How to cite this URL:
Bansal R, Jain S, Gupta V, Sharma A, Bal A, Jain S. Bilateral central retinal artery occlusion as presenting manifestation of human immunodeficiency virus infection. Indian J Ophthalmol [serial online] 2018 [cited 2024 Mar 28];66:466-8. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2018/66/3/466/226127



The spectrum of HIV retinopathy frequently includes microvascular occlusions and rarely involves large retinal vessels, affecting veins more commonly than arteries.[1] The largest series on retinal vascular occlusions in HIV reported a single case of central retinal artery occlusion (CRAO) among 2484 patients studied retrospectively.[2] Few isolated case reports have described CRAO in diagnosed cases of HIV infection.[3],[4]

The risk profile for retinal artery occlusion includes a number of cardiovascular factors. While certain systemic and ocular factors predispose to central retinal vein occlusion (CRVO), the risk profile of a combined CRAO and CRVO differs and involves a number of systemic comorbidities in the form of various cardiovascular risk factors.[5] We report a case where bilateral CRAO was the presenting manifestation of HIV infection.


  Case Report Top


A 30-year-old male presented with bilateral, painless loss of vision (left followed by right eye) for 3 weeks. The visual acuity was counting fingers at 1 m in both eyes with normal intraocular pressures. The anterior segment was unremarkable in both eyes. Fundus examination revealed retinal edema of the posterior pole and peripapillary region with scattered hemorrhages in all quadrants of both eyes [Figure 1]a and [Figure 1]b. Fluorescein angiography (FA) revealed delayed arterial filling with cilioretinal artery sparing in the right eye and absence of arterial filling in the left eye, suggestive of bilateral CRAO [Figure 1]c and [Figure 1]d. A secondary CRVO was considered due to the presence of extensive retinal hemorrhages. A prompt hematology, cardiology, and rheumatology consultation was sought. Systemic evaluation revealed a history of low-grade fever (since 4 months) and generalized lymphadenopathy. Hemogram, chest X-ray, blood culture, coagulation profile, serum electrolytes, renal/liver function tests, ultrasound abdomen, carotid Doppler, and two-dimensional echocardiography were normal. Antinuclear antibody, antineutrophil cytoplasmic antibody, Treponema pallidum hemagglutination assay, antiphospholipid antibody, serum homocysteine, hepatitis B surface antigen, anti-hepatitis C virus, and cytomegalovirus (CMV) IgM antibody were nonreactive. C-reactive protein (20 mg/ml) and erythrocyte sedimentation rate (40 mm/1st h) were elevated. HIV was positive by ELISA. Histopathological examination of cervical lymph node biopsy showed large areas of necrosis, peripherally palisaded by well-formed epithelioid cell granulomas, macrophages, and multinucleated giant cells. Stain for acid-fast bacilli was positive, suggestive of lymph node tuberculosis (TB). The CD4+ T-lymphocyte count was 450 cells/μL. The patient was started on antiretroviral therapy, along with antitubercular therapy. Visual acuity at 4 weeks of follow-up was hand movements in both eyes, with optic disc pallor and resolving hemorrhages.
Figure 1: Wide-field fundus photographs of the right eye (a) and the left eye (b) showing retinal edema of the posterior pole and peripapillary region, scattered retinal hemorrhages in all quadrants and retinal arteries narrowing. Fluorescein angiography in the right eye (c) revealed delayed arterial filling with small island of macular perfusion and absent retinal perfusion in the left eye (d)

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  Discussion Top


A combined CRAO and CRVO involves a number of systemic comorbidities in the form of various cardiovascular risk factors such as arterial hypertension, diabetes mellitus, hypercholesterolemia, coagulation disturbances, chronic smoking, hyperuricemia, and systemic vasculitis.[5] Although not completely understood, the retinal vascular abnormalities in HIV infection have been attributed to focal retinal ischemia, elevated fibrinogen, erythrocyte aggregation, reduced perifoveal blood flow, degeneration in the blood vessels, deposition of circulating immune complexes, presence of HIV within retinal endothelial cells, and a higher resistive index in the central retinal artery.[6],[7],[8] These factors precipitate the development of thrombi in HIV-infected patients. Further, an increased risk of atherosclerosis in HIV has been linked to genetic predisposition, virus-induced vasculitis and as a complication of highly active antiretroviral therapy. When compared with HIV-negative individuals of the same age, the retinal macrovascular occlusions in HIV-positive patients are more common and potentially blinding.[2] While CRVO is most common of these, it has not been reported with simultaneous CRAO in HIV-infected patients. Biswas et al. have reported CRVO due to herpes zoster as the initial presentation in an acquired immunodeficiency syndrome (AIDS) patient.[9] A combined hemi-CRVO with branch retinal artery occlusion in HIV was reported by Dunn et al.[2] A simultaneous CRAO with CRVO may occur secondary to infections, inflammations, or trauma. Our patient had a combined bilateral CRAO and CRVO with sparing of cilioretinal artery in the right eye. It is difficult to say if the closed loop circulation or compressive arteriopathy arising from CRVO led to CRAO in our patient. The presence of cilioretinal artery sparing (which is derived from choroidal circulation) in the right eye of our patient may indicate CRAO as the primary event, accompanied by hemodynamic alterations producing hemorrhagic retinopathy manifesting as CRVO. Furthermore, the absence of optic disc edema and venous tortuosity indicate less likelihood of CRVO as the initiating event. A stasis of axoplasmic flow, as known in HIV retinopathy, may have been widespread enough to cause CRVO-like retinopathy in the presence of CRAO. In our patient, fundus FA in both eyes was suggestive of CRAO. In the presence of widespread retinal hemorrhages in all quadrants, we believe that CRVO probably occurred as a secondary phenomenon rather than a simultaneous CRVO as it is difficult to comment upon the latter due to the absence of venous tortuosity. Development of immune complexes by the opportunistic infection agent was postulated in the pathogenesis of a simultaneous branch retinal artery and vein occlusion in a patient with AIDS and CMV retinitis.[10]

None of the systemic (hypertension, extraocular thrombotic disease, sickle cell trait, cardiovascular disease, hemophilia) or ocular (background HIV retinopathy, hypertensive retinopathy, diabetic retinopathy, myopic degeneration, optic nerve drusen) associations of retinal macrovasculopathy in HIV patients, as described by the previous reports, was present in our patient.[2],[3],[4] It is difficult to say whether generalized lymphadenopathy (tubercular) in our patient was directly linked to the combined CRAO and CRVO. A combined vasculopathy has also been attributed to optic nerve inflammation.[11] Wen et al. from China reported a case of combined CRVO with CRAO in HIV suggesting it as a part of systemic vascular disease in AIDS.[12] No association of retinal vascular occlusion with antiphospholipid syndrome was found in our HIV-infected patient, consistent with literature review.[2]

Occlusive retinal vasculitis is a well-known feature of ocular TB, with or without an underlying systemic TB infection, usually involving the veins. Arterial occlusion is extremely rare, with extraocular (pulmonary or miliary) TB and CRAO (or CRVO) existing in the same patient, besides other rare inflammatory (syphilis, periarteritis nodosa, and temporal arteritis) associations with CRAO. Since no perivascular sheathing/infiltrates were seen in our patient, we believe that the presence of tuberculous lymphadenopathy is probably coincidental and not associated with retinal vascular occlusions.

As thrombophilia (heritable or acquired) is a major risk factor for retinal vascular occlusions, these patients are at an increased risk of developing deep vein thrombosis, pulmonary embolism, or large-vein thrombosis at other sites.[13] CRAO in HIV-infected patients differs from that in non-HIV individuals in occurring at a much younger age and not being associated with carotid vascular disease.[2]


  Conclusion Top


Visual loss is generally poor, consistent with the natural course. As CRAO requires prompt evaluation for systemic diseases, HIV screening should be included in the baseline workup of young adults presenting with such an ophthalmic emergency.

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 Top

1.
Handwerger BA, Urban AW, Gottlieb JL. Retinopathy as the initial presentation of human immunodeficiency virus 2 infection. Arch Ophthalmol 2000;118:1695-6.  Back to cited text no. 1
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2.
Dunn JP, Yamashita A, Kempen JH, Jabs DA. Retinal vascular occlusion in patients infected with human immunodeficiency virus. Retina 2005;25:759-66.  Back to cited text no. 2
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3.
Lenci LT, Chin EK, Almeida DR. Central retinal artery occlusion in a young HIV-infected patient on highly active antiretroviral therapy. Retin Cases Brief Rep 2017;11:160-2.  Back to cited text no. 3
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Erdol H, Turk A, Caylan R. An unusual cause of central retinal artery occlusion: Acquired immunodeficiency syndrome. Eur J Ophthalmol 2007;17:671-3.  Back to cited text no. 4
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Schmidt D. Comorbidities in combined retinal artery and vein occlusions. Eur J Med Res 2013;18:27.  Back to cited text no. 5
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Engstrom RE Jr., Holland GN, Hardy WD, Meiselman HJ. Hemorheologic abnormalities in patients with human immunodeficiency virus infection and ophthalmic microvasculopathy. Am J Ophthalmol 1990;109:153-61.  Back to cited text no. 6
    
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Yung CW, Harris A, Massicotte S, Chioran G, Krombach G, Danis R, et al. Retinal blood flow indices in patients infected with human immunodeficiency virus. Br J Ophthalmol 1996;80:723-7.  Back to cited text no. 7
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Dejaco-Ruhswurm I, Kiss B, Rainer G, Krepler K, Wedrich A, Dallinger S, et al. Ocular blood flow in patients infected with human immunodeficiency virus. Am J Ophthalmol 2001;132:720-6.  Back to cited text no. 8
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Biswas J, Deka S, Padmaja S, Madhavan HN, Kumarasamy N, Solomon S, et al. Central retinal vein occlusion due to herpes zoster as the initial presenting sign in a patient with acquired immunodeficiency syndrome (AIDS). Ocul Immunol Inflamm 2001;9:125-30.  Back to cited text no. 9
    
10.
Conway MD, Tong P, Olk RJ. Branch retinal artery occlusion (BRAO) combined with branch retinal vein occlusion (BRVO) and optic disc neovascularization associated with HIV and CMV retinitis. Int Ophthalmol 1995;19:249-52.  Back to cited text no. 10
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11.
Duker JS, Cohen MS, Brown GC, Sergott RC, McNamara JA. Combined branch retinal artery and central retinal vein obstruction. Retina 1990;10:105-12.  Back to cited text no. 11
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12.
Wen F, Chen X, Li H, Liao R, Wu D. Bilateral central retinal vein occlusions combined with artery occlusions in a patient with acquired immune deficiency syndrome. Yan Ke Xue Bao 2002;18:27-9.  Back to cited text no. 12
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Schockman S, Glueck CJ, Hutchins RK, Patel J, Shah P, Wang P, et al. Diagnostic ramifications of ocular vascular occlusion as a first thrombotic event associated with factor V Leiden and prothrombin gene heterozygosity. Clin Ophthalmol 2015;9:591-600.  Back to cited text no. 13
    


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