This is a case report of a 57-year-old female who presented to our institution with serpiginous choroiditis in both eyes (worse in the left than the right). She had originally been diagnosed 20 years prior, with prior treatment including oral prednisone and subtenon's triamcinolone acetonide injections. She presented with a visual acuity of 20/70 right eye (OD) and hand-motion left eye (OS). Dilated funduscopic examination was remarkable for chorioretinal scars in the posterior pole with an active area of fovea-threatening choroiditis in the right eye. The left eye had extensive chorioretinal scars in the posterior pole contiguous with the optic nerve head and a fibrotic subfoveal scar with subretinal fluid and blood.
Fundus autofluorescence (FAF) depicted hypofluorescent serpentine-like lesions, with a hyperautofluorescent edge in close proximity to the fovea OD (Figure 1). Optical coherence tomography (OCT) revealed temporal outer retinal atrophic changes without fluid OD (Figure 2). On fluorescein angiography, these lesions exhibited early hypofluorescence with late staining at the edges in both eyes. Laboratory testing for tuberculosis, syphilis, sarcoidosis, and toxoplasmosis were negative.
The SC was initially treated with a combination of oral prednisone, azathioprine, and cyclosporine. Despite treatment, the inflammation persisted, and after three months, immunosuppressive therapy was escalated to include a 3-month course of intravenous cyclophosphamide and intravitreal triamcinolone acetonide (IVTA). The patient was unable to tolerate side effects from this regimen and thus was changed to mycophenolate with oral prednisone after another 3 months. She was unable to tolerate this either, and ultimately stopped further treatment nine months after her initial presentation. She also developed a juxtafoveal choroidal neovascular membrane (CNVM) requiring intravitreal bevacizumab (IVB) twice. The SC remained in remission for two years without treatment other than a preventative IVTA and oral steroid burst given at the time of cataract surgery with intraocular lens implantation during this time period. She also required occasional IVB for the CNVM.
After 2 years, she returned with vision complaints from a reactivation of the SC and CNVM. Her visual acuity was still 20/60 in her right eye. At this point, she resumed systemic therapy and initiated a new course of cyclophosphamide and oral prednisone. She also received IVB for her CNVM. However after 3 months, she again stopped further systemic treatment due to intolerable side effects. At that time, visual acuity was reduced to 20/200 in the right eye.
Within 4 months of stopping treatment, she had recurrent inflammation again. To avoid further systemic side effects, a local steroid treatment regimen was initiated with repeated IVTA that was then transitioned to dexamethasone 0.7 mg intravitreal implants (Ozurdex, Allergan) on a pro re nata (PRN) basis. She also received ranibizumab PRN for the CNVM. She repeatedly required dexamethasone implant injections every 2-4 months to treat recurrent inflammation; thus, the regimen was changed to scheduled dexamethasone implant injections every 8 weeks. During the following 3 years, after receiving 4 ranibizumab intravitreal injections and 14 dexamethasone implant injections, her visual acuity was 20/400 and intraocular pressure was stable with anti-ocular hypertensive drops.
In an effort to reduce the treatment burden from frequent injections, an attempt was made to reinitiate mycophenolate, but she was intolerant to therapy within 2 months. Fluocinolone acetonide intravitreal implant was then provided to the right eye. This was placed 6 weeks after the last dexamethasone implant, and since then, no further intravitreal or systemic treatments have been required. The patient has undergone regular monitoring with clinical exams and multimodal imaging, including OCT and FAF. Upon evaluation 15 months after fluocinolone acetonide implant placement, there was no recurrence of inflammation evident (Figures 1 and 2), and repeat assessment at 20 months revealed stability of findings. The visual acuity in the right eye remained stable at 20/300. Her intraocular pressure has been stable without the need for additional therapy. Through this entire course, her left eye has been stable at a visual acuity of hand motion and no additional therapies have been performed.