Dengue-Induced Inflammatory, Ischemic Foveolitis and Outer Maculopathy: A Swept-Source Imaging Evaluation.

PURPOSE

Dengue maculopathy can present with a unique constellation of features resulting in significant central visual morbidity. We aim to describe various findings of dengue-induced inflammatory, ischemic foveolitis, and outer maculopathy (DIII-FOM) and assess the serial changes in vitreous inflammation, retinal structure, and vascularity using swept-source OCT (SS-OCT) and OCT angiography (OCTA).

DESIGN

Retrospective case series.

PARTICIPANTS

A total of 32 eyes (16 patients; 7 male) with dengue fever (positive serology for NS1 antigen) were enrolled in the study.

METHODS

In this study, serial assessments of ocular findings and imaging using fundus photography, SS-OCT, and SS-OCTA were performed. All the patients received 0.5 to 1 mg/kg/day oral prednisolone that was tapered over 4 to 6 weeks.

MAIN OUTCOME MEASURES

Outcome measures included functional change, that is, improvement in best-corrected visual acuity (BCVA), structural changes in the vitreous and retinal layers on SS-OCT, and retinal perfusion on OCTA.

RESULTS

The mean age of the patients was 29.17±10.91 years. Swept-source OCT showed vitreous cells (32 eyes; 100%), disruption of outer retinal layers (foveolitis) (24 eyes; 75%), and conical foveal elevation (22 eyes; 68.75%). After initiation of systemic corticosteroids, all the eyes showed resolution of vitreous cells and improvement in the integrity of retinal layers. Mean BCVA improved from an initial 0.80±0.33 logarithm of the minimum angle of resolution (logMAR) to 0.23±0.36 logMAR. Retinal plexus flow deficit (superficial plexus: 0.10±0.12 mm; deep plexus: 0.29±0.13 mm) persisted in all eyes and correlated well with initial BCVA (P < 0.05).

CONCLUSIONS

The pathophysiology of dengue maculopathy involves both ischemic and inflammatory components. Early institution of corticosteroid therapy may help in resolution of the inflammation-driven vitreoretinal alterations, but ischemia of the deep retinal plexuses may persist and may be the cause of permanent structural and functional changes.