One-minute ophthalmology: “To PI or not to PI”

A 56-year-old female patient presented to the outpatient department with complaints of diminution of vision in both eyes for 1 week associated with headache. She had no significant ocular or systemic history. Her best-corrected visual acuity was 6/18 in both eyes on Snellen chart. The anterior segment revealed bilateral shallow occludable angles, confirmed on gonioscopy, with occasional cells in the anterior chamber [Fig. 1]. Intraocular pressure (IOP) was 20 mm Hg bilaterally on applanation tonometry. She underwent fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) [Fig. 1].

Figure 1.

(a and b) Anterior segment images of both eyes showing conjunctival hyperemia with a shallow anterior chamber and a crystalline lens, (c and d) fundus fluorescein angiography showing bilateral pinpoint hyperfluorescence with pooling of dye, suggestive of exudative retinal detachments, and (e and f) optical coherence tomography images showing an altered foveal contour with subretinal fluid, retinal pigment epithelium (RPE) undulation, and thickened choroid

What will be your preferred line of management?

1. Improve sleep habits and topical or oral carbonic anhydrase inhibitors

2. Immediate laser peripheral iridotomy (PI)

3. Intravenous methylprednisolone

4. Extrapulmonary antitubercular therapy (ATT) regimen

Findings and management

FFA showed delayed choroidal perfusion, pinpoint hyperfluorescent spots with pooling in subretinal space, and disk leakage along with choroidal detachments [Fig. 1a and b]. OCT revealed an altered foveal contour with subretinal fluid, retinal pigment epithelium (RPE) undulation and thickened choroid [Fig. 1b and c].

Diagnosis: Vogt–Koyanagi–Harada (VKH) disease—acute uveitic stage

Correct Answer: C. Intravenous methylprednisolone

Discussion

The acute presentation of VKH syndrome is characterized by the presence of bilateral serous retinal detachments, papillitis, and mild-to-moderate vitritis with increased retinal–choroidal–scleral (RCS) thickness.[1] Prodromal symptoms include fever, meningismus (headache, malaise, nausea, and stiffness of the neck and back), audio-vestibular manifestations (sensorineural hearing loss, tinnitus, aural fullness, and vertigo), and hyperesthesia of the scalp or orbital pains. The symptoms precede ocular disease, and they arise from a combination of choroidal and meningeal inflammation.[2] The shallow anterior chamber, in this case, is due to the ciliary effusion, and laser PI is more likely to worsen the inflammation and thus be counterproductive. The convalescent stage follows the acute uveitic stage, a few months later. It is characterized by depigmentation of the integument and choroid.[3] FFA features are characteristic and help differentiate VKH from other conditions, such as multifocal central serous chorioretinopathy (CSCR) and posterior scleritis. Intravenous methylprednisolone at 1 gram for 3 days is the recommended management line, followed by tapering doses of oral steroids at 1 mg/kg body weight.

Early initiation of immunosuppressives has been shown to reduce long-term complications of VKH and provide a good steroid-sparing effect.[3] Our patient was also started on methotrexate at 20 mg weekly dose with folic acid supplementation, under rheumatologist guidance. She is currently clinically stable with a resolution of serous detachments, and on the last follow-up, she showed no signs of inflammation.

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.