• Written By: J. Fernando Arevalo, MD, FACS

    This retrospective study found that enhanced depth imaging spectral-domain optical coherence tomography (EDI-OCT) revealed a localized increase in choroidal thickness with bulging of the outer retina in patients with non-acute uveitic Vogt-Koyanagi-Harada (VKH) disease. The authors propose that this finding, which is easily and non-invasively identified, may help monitor posterior segment disease activity in patients with VKH disease in the non-acute uveitic stage.

    This study is important because detection of choroidal inflammation in VKH disease is still a challenge. Progression to sunset glow fundus has been observed despite apparent good clinical control of inflammation. Indocyanine green angiography (ICGA) permits choroid inflammation detection but is invasive, time-consuming and costly.

    The authors write that the new EDI-OCT sign described here does not substitute for ICGA signs, but it can complement subclinical posterior segment inflammatory evaluation. They also note that localized choroidal thickening has already been described in patients with ocular toxoplasmosis or choroidal tumors; however, unlike the choroidal bulging observed in this series of patients, an associated retinal or choroidal lesion was invariably observed in these scenarios on clinical exam.

    The authors reviewed sequential clinical and imaging data from all eyes noted to have the choroidal bulging on EDI-OCT performed as part of the follow-up protocol in an ongoing longitudinal VKH disease study being conducted at a uveitis clinic at a university hospital in Sao Paulo.

    Choroidal bulging was observed in four eyes of three patients with VKH disease in the non-acute uveitic stage (median disease duration 55.3  ±  40.3 months, range 10 to 108). In all eyes, the bulging was identified by the presence of anterior chamber cells and/or fundus angiographic (fluorescein and indocyanine green) findings.

    Changes in the thickness of the choroidal bulging accompanied the variation in the clinical and angiographic signs of inflammation; simultaneous observation of EDI-OCT and ICGA showed transient dark dots at the exact location of the choroidal bulging. Actually, ICGA changes anticipated choroidal bulging detection on EDI-OCT in all cases, which sounds logical since bulging probably represents the accumulation of inflammatory elements/fluid associated with the presence of transient granulomas, which usually take some time to build up. Indeed, the choroidal bulging indications occurred faster than the distribution of dark dots on ICGA.

    Diffuse thickening of the choroid has already been described in the early and convalescent/chronic stages of VKH and has been suggested to represent a sign of disease activity. Nevertheless, as previously described, progressive choroidal thinning related to disease duration occurs, and diffuse thickening during disease exacerbation in the non-acute uveitic stage of the disease may be subtle and difficult to detect.