LETTERS 85 setting of 1750-3000 mW for 2 s per shot was performed 2 months after the second PPV. At the 1-year follow up, the patient was free of glaucoma medications with IOP at a low level (range 8-12 mm Hg), and the retina was flat, with BCVA at hand movement. The visual outcome was a result of advanced glaucomatous optic neuropathy (vertical cup/disc ratio of 0.9 with pale neuroretinal rim) and severe diabetic exudative maculopathy. The patient did not return for further follow up. CommentTo our best knowledge, this is the first report of delayed and repeated massive suprachoroidal hemorrhage occurring 3 and 5 days after PPV. Reported ocular risk factors for developing intraoperative suprachoroidal hemorrhage include elevated preoperative IOP, history of glaucoma, axial length greater than 25 mm, pseudophakia, scleral buckling, cryotherapy, external drainage of subretinal fluid, rhegmatogenous retinal detachment, and intraoperative Valsalva maneuvers. 3,4 Reported systemic risk factors include hypertension, atherosclerosis, diabetes, advanced age, and intraoperative tachycardia. 4 Our patient, apart from diabetes and hypertension, had none of these risk factors. There was no hypotony before the suprachoroidal hemorrhage. As the prone position was kept for only 3 days, it cannot explain the hemorrhage on the fifth day. Ciliochoroidal effusion has been reported after PRP. 5 We speculate that PRP might have triggered the suprachoroidal hemorrhage. Further studies are needed to elucidate whether delayed suprachoroidal hemorrhage can be precipitated by factors unrelated to intraoperative suprachoroidal hemorrhage.
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