Multifocal Central Serous Chorioretinopathy Associated with Steroids in a Patient with Myasthenia Gravis
A 40-year-old white male was referred to our clinic due to a 15-day history of bilaterally blurred vision and metamorphopsia. He had a history of myasthenia gravis for which he had been treated with oral prednisolone and azathioprine during the last 2 years. His best-corrected visual acuity (BCVA) was 8/10 in the right eye (OD) and 9/10 in the left eye (OS).\nFundoscopy revealed a few small, yellow-whitish circumscribed macular elevations and one larger, irregularly shaped parafoveal elevation in OD (fig. ). Similar small macular lesions were also noted in OS. Fluorescein angiography showed multiple areas of early hyperfluorescence and late leakage in OD (fig. ). Similar but less pronounced angi-ography findings were seen in OS (fig. ). Optical coherence tomography (OCT) revealed RPE detachment, elevation of the neurosensory retina and highly reflective subretinal fluid mostly in OD (fig. ).\nThe diagnosis of multifocal CSCR was made. As the patient's myasthenia could not be optimally controlled at the time, the treating neurologist advised against prednisolone discontinuation. Unfortunately, we noticed further deterioration of the BCVA and subfoveal expansion of the subretinal fluid in OD, so it was decided to administer an intravitreal injection of ranibizumab in this eye. One month later, his BCVA had deteriorated to 3/10 in OD and 7/10 in OS. Fundoscopy revealed that the area below the fovea in OD was enlarged with the deposition of material presumed to be fibrin in the subretinal space. OCT demon-strated further elevation of the neurosensory retina and a more irregular subretinal accumulation of highly reflective material (fig. ). Indocyanine green angiography excluded neovascularization and polyp-like vascular abnormalities. Low-fluence photodynamic therapy (PDT) was performed. We administered verteporfin i.v. at a dose of 6 mg/m2 over 10 min, waited for 5 min and then directed the diode laser at the larger lesion of leakage in OD, using a wavelength of 689 nm and laser energy of 25 mJ/cm2. After the first application, the laser spot was directed at the second and the third lesion of leakage in OD (fig. ). As the patient's myasthenic symptoms improved, it became possible for the attending neurologist to reduce the dose of prednisolone, increase the dose of azathioprine and add neostigmine. One month later, and while undergoing prednisolone tapering, his BCVA in OD had improved to 6/10 with no subretinal fluid, while the area with the fibrin deposition had nearly disappeared (fig. ). The BCVA in OS improved to 10/10 over the next couple of months. To date, 1 year after treatment, the patient's BCVA remains stable at 6/10 in OD and 10/10 in OS with no signs of active disease. The patient's myasthenia is currently well controlled with azathioprine and neostigmine.