Branch retinal artery occlusion secondary to dengue fever.

Dengue is known to affect the posterior segment of the eye, with a range of hemorrhagic and inflammatory sequelae. A 28-year-old lady convalescing from dengue fever complained of unilateral blurring of inferior visual field. She was evaluated clinically and with fluorescein angiography. Her best-corrected visual acuity was 20/20 bilaterally. Fundus examination revealed a branch retinal artery occlusion in the right eye. Fluorescein angiogram confirmed the clinical diagnosis; and also revealed a late staining and leakage from the affected arterial segment. The patient maintained status quo over a follow-up of six months. We report a major vascular occlusion complicating classic dengue fever even in the absence of severe systemic manifestations.

Dengue, the commonest cause of arboviral disease, is more prevalent now than ever before and its prevalence is expected to increase globally.1 The ophthalmic manifestations include vitritis, retinopathy (hemorrhages, edema, cotton-wool spots, serous detachments), vasculitis and retinal pigment epithelial (RPE) disturbances.2,3 We report a case of branch retinal arterial occlusion secondary to dengue fever.

Case History

A 28-year-old woman was hospitalized for acute-onset high fever, myalgia, arthralgia and ocular pain. Detailed history- taking, hematological and serological investigations established the diagnosis of classic dengue fever (a positive IgM antibody titer); and ruled out mimicking infections like leptospirosis, typhoid, malaria, syphilis, as well as collagen vascular diseases. Seven days later, during the convalescent phase, the patient noticed blurring of the inferior visual field in the right eye. She presented to us two weeks after the ocular symptoms had started. Best corrected visual acuity was 20/20 bilaterally. On slit-lamp examination, anterior segment was unremarkable in both eyes; no anterior vitreous cells or flare was observed. Fundus examination of the right eye showed a patchy area of partially faded retinal whitening in the superotemporal quadrant of the macula, just encroaching into the fovea, with attenuation and sclerosis of the macular division of the superotemporal branch retinal artery [Fig. 1]. The left fundus revealed a single cotton-wool spot towards the edge of the inferotemporal arcade. Midphase fluorescein angiogram of the right eye showed narrowing of the affected arterial segment, blocked background fluorescence in the area of whitening and delayed arteriovenous transit in the affected vessels. Staining and leakage of the occluded artery was observed in the late phase [Fig. 2]. Kinetic central field charting with Bjerrum′s screen showed an inferonasal field defect corresponding to the area of arterial occlusion. The patient was referred for a detailed cardiac and carotid evaluation - including carotid doppler study and echocardiography - which was unremarkable. She was followed up for three months. Her visual acuity remained 20/20 in both eyes, but the inferior field defect persisted in the right eye.

Figure 1

Fundus view of right eye showing supeficial retinal whitening with narrowing of the occluded artery in the superotemporal quadrant of the macula

Figure 2

Late-phase fluorescein angiogram of the right eye shows staining and leakage of the occluded segment of the branch retinal artery

Discussion

Ophthalmic manifestations of dengue fever are rare but diverse, involving ocular structures from vitreous to uvea.2,3 Both viral and host immune factors are probably involved in the pathogenesis. Different clinico-pathologic manifestations may be caused by different pathogenetic mechanisms: such as hepatic injury may relate more to viral factors; whereas vascular hyperpermeability (contributing to most ocular manifestations) may be mediated predominantly by the immune response.4 Ocular involvement in the convalescent phase of the systemic disease also implicates host immune response rather than direct virus infection.3

The late staining and leakage of the occluded artery in our patient points towards the inflammatory nature of occlusion: circulating immune complexes probably got deposited at the right-angled branch of the artery - narrowed by preexisting vasculitis - precipitating the occlusion. Though retinal capillary non-perfusion secondary to dengue fever has been reported to occur in macula as well as midperiphery,2 we are unaware of any previous report of retinal large-vessel occlusion attributed to systemic dengue. There remains a possibility of a coincident arterial occlusion independent of the sequelae of dengue fever; though the angiographic evidence of vascular inflammation points to the contrary. This complication, which potentially entails significant and permanent visual impairment, occurred in spite of a minimal vasculitis (evident only angiographically) and in the absence of severe systemic disease. The ophthalmologists should therefore be aware that major ocular complications may occasionally follow relatively moderate systemic involvement with dengue fever.