Full thickness macular hole with subfoveal pigment epithelial detachment in chronic central serous chorioretinopathy: A therapeutic challenge.

We describe the diagnostic and therapeutic strategies employed in the management of a patient with subfoveal pigment epithelial detachments (PEDs) combined with full-thickness macular hole (FTMH) and discuss the possible pathophysiology of these diseases occurring concurrently. A 38-year-old patient with a history of central serous chorioretinopathy (CSC) presented with FTMH overlying a large subfoveal serous PED. Multimodal imaging confirmed the same and intravitreal anti-vascular endothelial growth factor (VEGF) injections and eplerenone failed to resolve the PED. Spontaneous resolution of the large PED was observed later and pars plana vitrectomy with internal limiting membrane peeling closed the macular hole successfully. However, the PED with fibrinous CSC recurred postoperatively and low fluence photodynamic therapy (PDT) was done to tackle the same. At 10 months' follow-up, the final vision was 6/9, the macular hole remained closed, and the PED had not recurred. Macular hole formation may be the result of choroidal hyperpermeability and leakage in the backdrop of CSC which gives rise to an exudative component causing mechanical stretching and disruption of the overlying sensory retina. Spontaneous uncomplicated resolution of large subfoveal PED in CSCR is rare. This case was managed with a combination of intravitreal anti-VEGF injections, surgery, and PDT. The therapeutic challenge here was the timing of surgery.

Role of oral acetazolamide in refractory glaucomatous deep cup-related maculopathy.

A 39-year-old man, a known case of primary open-angle glaucoma on treatment, presented with defective central vision in the left eye. On examination, his intraocular pressure (IOP) was 26 mmHg in the right eye and 30 mmHg in the left eye with best-corrected visual acuity of 6/12 in each eye. Fundus examination showed glaucomatous optic neuropathy in both eyes and macular thickening in the left eye. Optical coherence tomography of the left eye showed macular detachment with peripapillary retinoschisis and a hyporeflective tract connecting schitic retina and the deep cup in the absence of an optic disc pit. A diagnosis of glaucomatous deep cup maculopathy (DCM) was made in the left eye, which persisted despite well-controlled IOP and peripapillary laser photocoagulation. The addition of oral acetazolamide (250 mg twice daily) to his regimen resulted in prompt resolution of maculopathy. Glaucomatous DCM is relatively rare, and its primary management is adequate IOP control with antiglaucoma medications. Including oral acetazolamide in the antiglaucoma regimen can help in faster resolution of maculopathy due to its additional effect on retinal pigment epithelial pump induction and stabilization of the pressure gradient.

PHOTODYNAMIC THERAPY-INDUCED ACUTE EXUDATIVE MACULOPATHY: Incidence, Clinical Features, and Long-Term Outcomes.

PURPOSE: To describe the incidence, clinical features, and long-term outcomes of photodynamic therapy (PDT)-induced acute exudative maculopathy (PAEM) in patients who underwent PDT for various indications. METHODS: This retrospective observational case series included all cases who developed massive serofibrinous macular exudation within a week after PDT. Medical records of patients with post-PDT exudative events were reviewed for relevant data and imaging abstraction including optical coherence tomography and indocyanine green angiography features and were subjected to analysis. RESULTS: The incidence rate of PAEM was 4.52%, being noted in 8 eyes (out of 177 PDT sessions in 155 eyes) with a mean age of 70.25 ± 6.65 years. Pre-PDT factors commonly associated with PAEM included age ≥65 years (87.5%), clinical diagnosis of polypoidal choroidal vasculopathy (75%), spot size ≥3,500 µm (100%), best-corrected visual acuity of 20/40 or better (87.5%), low-fluence PDT (87.5%), and the first exposure to PDT (75%). Photodynamic therapy-induced acute exudative maculopathy was noted at a mean interval of 2.9 ± 1.7 days (2-7 days) after PDT. Photodynamic therapy-induced acute exudative maculopathy resulted in significant decrease in mean best-corrected visual acuity from logMAR 0.29 ± 0.21 (approximate Snellen equivalent 20/39) to logMAR 0.91 ± 0.37 (approximate Snellen equivalent 20/163) [P = 0.0018], and significant increase in mean central macular thickness from 228.1 ± 71.8 µm to 481.4 ± 154.8 µm (P = 0.0029). Photodynamic therapy-induced acute exudative maculopathy resolved to baseline or even better tomographic status at a mean interval of 4.6 ± 1.2 weeks, resulting in complete visual recovery compared with baseline. During mean follow-up of 77.8 ± 46.4 weeks after PDT, no activity was noted for a mean duration of 26.3 ± 42.5 weeks after resolution. At final visit, mean best-corrected visual acuity and central macular thickness was logMAR 0.49 ± 0.28 (approximate Snellen equivalent 20/62) and 153.6 ± 40.0 µm, respectively, with underlying pathology being stable in 50% of the eyes. CONCLUSION: Photodynamic therapy-induced acute exudative maculopathy is an uncommon complication with self-resolving course and favorable prognosis. Patients undergoing PDT should be warned of the possibility of PAEM. The factors frequently associated with PAEM include elderly age (>65 years), clinical diagnosis of polypoidal choroidal vasculopathy, larger spot size (≥3,500 µm), pre-PDT best-corrected visual acuity of 20/40 or better, low-fluence PDT, and the first exposure to PDT.