Introduction: We report a case of type III uveal effusion syndrome (UES) suspected to be related to pachychoroid spectrum disease. Patient concerns: A 42-year-old man became aware of visual field constriction and deterioration of visual acuity in his right eye. Diagnosis: Upon examination, a bullous non-rhegmatogenous retinal detachment was observed in the inferior 2 quadrants of the right eye fundus, and the subretinal fluid moved with postural changes. The axial length in that eye was 22.36 mm, thus indicating no nanophthalmia. Preoperative indocyanine green angiography revealed dilated choroidal vessels in the posterior pole of the right eye and mild leakage in the late phase. Optical coherence tomography examination revealed choroidal thickening in both eyes. Interventions: For treatment, we first performed sclerotomy, and the intraoperative findings showed no thickening of the sclera. Following surgery, reattachment of the retina was not achieved. Outcomes: Thus, we next performed vitrectomy, which led to successful reattachment of the retina. Lessons: In this case, we theorize that pachychoroid spectrum disease might have been involved in the pathogenesis of type III UES.

Purpose: Retinal arterial macroaneurysm (RAM) has been reported in association with branch retinal vein occlusion (BRVO), and usually BRVO precedes RAM. We present a long-term follow-up case report of unilateral multiple RAMs that developed BRVO following ruptured RAM in the same retinal quadrant. Case Presentation: An 80-year-old woman presented with floaters in her right eye in June 2012. Visual acuity (VA) was 20/25 in her right eye with posterior capsular opacity. Her fundus showed the first ruptured RAM at the superotemporal vascular arcade with subinternal limiting membrane and subretinal hemorrhages not involving the macula. These were absorbed gradually with a VA of 20/20. After 2 years, the second RAM at the proximal superotemporal vascular arcade developed and impending BRVO occurred with macular edema at the distal site of the RAM. With the RAM located close to the arteriovenous crossing, her VA was dropped to 20/60. Intravitreal injection of ranibizumab was performed and macular edema was resolved with improved vision of 20/30. Three months later, she realized a sudden vision loss of 2/200. Her posterior pole showed massive pre- and subretinal hemorrhages, and vitrectomy was performed. The source of bleeding was the third RAM’s rupture in a different artery. Her vision improved to 20/30. The unaffected eye showed no RAMs. Conclusion: We experienced a long-term follow-up case of multiple RAMs showing different courses. We should cautiously note that BRVO can occur following RAM at the arteriovenous crossing.

Rationale: Here we report the case of a patient who required closure with an autologous scleral patch graft during reoperation after developing marked scleral thinning in the late stage after pars plana phacoemulsification and aspiration (PPPEA). To the best of our knowledge, this is the first reports of the procedure being used for the treatment of a thinned scleral section post PPPEA. Patient concerns: This study involved a 73-year-old woman who had undergone vitreous surgery combined with PPPEA for retinal detachment in her right eye 8 years earlier and subsequently underwent intraocular lens (IOL) ciliary sulcus suture fixation. Diagnoses: She became aware of visual disturbance in her right eye and slit-lamp examination revealed the dislocation of the IOL. Interventions: To remove the dislocated IOL and resuture the nasal loop back onto the ciliary sulcus of the patient's right eye, a 25-guage trocar was placed on the superior temporal side. Outcomes: Subsequent removal of the trocar from the patient's right eye left an approximately 3-mm-wide oval-shaped gap at the trocar insertion site due to extreme thinning of the sclera in that area; that is, the location where the PPPEA was performed. Since suture fixation failed to stop intraocular fluid leakage, an inferior free half-thickness scleral flap was created to patch the scleral wound. Postsurgery, the leakage in that eye stopped and the intraocular pressure was stable. No complications were observed during the 1-year-postoperative follow-up period. Lessons: Since thermal injuries during PPPEA may lead to postoperative scleral thinning, surgeons should avoid the site of a prior PPPEA when constructing a scleral wound during reoperation.

Introduction: Chorioretinal folds accompanied by central serous chorioretinopathy (CSC) are relatively uncommon. Here, we report CARE-compliant 2 patients with bilateral CSC chorioretinal folds and CSC that was followed-up for 2 years. Patient concerns: Case 1 was a 68-year-old female who complained of central visual field disturbance in her left eye. At the initial visit, her visual acuity (VA) was 20/20 in her right eye and 20/40 in her left. She had a history of systemic hypertension and an optic neuropathy in her left eye 20 years previously. Case 2 was a 63-year-old female with CSC in her right eye. Her VA at her first visit was 20/200 in her right eye and 20/20 in her left. Diagnosis: In case 1, an examination revealed serous retinal detachment (SRD) in the macula and optic disc atrophy in her left eye and both fundi showed chorioretinal folds. Fluorescein angiography showed a fluorescein leakage area in her left eye. In case 2, examination of fundus showed marked SRD in her right macula and both fundi had chorioretinal folds. fluorescein angiography showed a fluorescein leakage area and indocyanine green angiography showed vascular hyperpermeability, but no choroidal neovascularization. Interventions and outcomes: In case 1, the patient rejected the photocoagulation treatment. Her SRD resolved spontaneously and the VA improved to 20/20 in her left eye nine months after the first visit. But the chorioretinal folds in both eyes remain till date. In case 2, photodynamic therapy was planned; however, her SRD disappeared spontaneously. Photocoagulation therapy was performed at the leak point and her VA improved to 20/20, but the bilateral chorioretinal folds remain till date. There has been no recurrence of CSC in both the patients in the 2 year follow-up. Conclusions: The exact mechanism of CSC remains uncertain. Choroidal vascular abnormalities, such as choroidal hyperpermeability and dilated choroidal vessels associated with congested vortex veins, have been previously reported even in the unaffected eye of CSC patients. We theorize that the bilateral chorioretinal folds in CSC patients were possibly induced by the outflow congestion of the vortex vein due to the marked CSC and choroidal dysregulation. As the choroid expanded due to CSC, the overlying Bruch membrane was forced into folds. Further investigation of the pathophysiology of CSC is needed.