PERSISTENT LOCULATED SUBRETINAL FLUID AFTER RHEGMATOGENOUS RETINAL DETACHMENT SURGERY.

PURPOSE: To identify factors associated with persistent subretinal fluid (SRF) after small-gauge pars plana vitrectomy for primary rhegmatogenous retinal detachment. METHODS: This retrospective study included patients from 2 tertiary centers who underwent pars plana vitrectomy for repair of rhegmatogenous retinal detachment between 2013 and 2016. Preoperative and intraoperative parameters were examined for association with development of SRF. RESULTS: Overall, 153 eyes of 153 patients, mean age of 55.2 ± 17.9 years were included. Persistent SRF occurred in 15.0% (n = 23) and was associated with high myopia (65.22 vs. 26.15%, P < 0.001), macula-involving retinal detachment (91.30 vs. 66.15%, P = 0.02), phakic lens status (86.96 vs. 66.15%, P = 0.04), and younger age (47.8 ± 18.7 vs. 56.5 ± 17.5, P = 0.04) while drainage retinotomy was protective (13.04 vs. 34.11%, P = 0.04). In multivariate analysis, high myopia (P = 0.009) and macula-involving retinal detachment (P = 0.004) were associated with SRF, while drainage retinotomy was protective (P = 0.03). Persistent SRF was associated with outer retinal band irregularity (30.4 vs. 9.3%, P = 0.005). There were no significant differences in terms of change in best-corrected visual acuity from presentation (P = 0.70), or final best-corrected visual acuity (P = 0.54). CONCLUSION: Eyes with preoperative high myopia and macular involvement, and those in which a drainage retinotomy was not performed, were more likely to develop persistent SRF.

INCIDENCE AND RISK FACTORS FOR HYPOTONY AFTER 25-GAUGE PARS PLANA VITRECTOMY WITH NONEXPANSILE ENDOTAMPONADE.

PURPOSE: The purpose of this study was to assess the incidence and risk factors for early postoperative hypotony after 25-gauge pars plana vitrectomy with nonexpansile endotamponade. METHODS: A retrospective study of consecutive patients who underwent 25-G pars plana vitrectomy. Hypotony was defined as an intraocular pressure of 5 mmHg or less after surgery and ocular hypertension as an intraocular pressure greater than 21 mmHg. RESULTS: Overall, 307 eyes of 307 patients with a mean age of 61.7 ± 14.3 of which 56.7% were males were included. Hypotony was identified in 5.2% of cases (n = 16) at Day 1 and 0.7% (n = 2) at Week 1 with no hypotony-related complications. The hypotony group had a higher number of previous vitreoretinal surgeries (1.5 ± 1.1 vs. 0.4 ± 0.7, P < 0.001) and a higher prevalence of preoperative ocular hypertension (22.2% vs. 4.8%, P = 0.02), pseudophakia (77.8% vs. 48.4%, P = 0.01), silicone oil removal (61.1% vs. 8.3%, P < 0.001), and external diathermy performed (55.6% vs. 20.1%, P = 0.001). In stepwise multivariate analysis, significant parameters were silicone oil removal (R = 16.34%, odds ratio 13.45, P < 0.001), pseudophakia (R = 5.69%, odds ratio 3.65, P = 0.03), and younger age (R = 2.68%, odds ratio 0.96, P = 0.04). CONCLUSION: Silicone oil removal is a significant risk factor for early postoperative hypotony after 25-G pars plana vitrectomy.

BLOC-1 Brings Together the Actin and Microtubule Cytoskeletons to Generate Recycling Endosomes.

Recycling endosomes consist of a tubular network that emerges from vacuolar sorting endosomes and diverts cargoes toward the cell surface, the Golgi, or lysosome-related organelles. How recycling tubules are formed remains unknown. We show that recycling endosome biogenesis requires the protein complex BLOC-1. Mutations in BLOC-1 subunits underlie an inherited disorder characterized by albinism, the Hermansky-Pudlak Syndrome, and are associated with schizophrenia risk. We show here that BLOC-1 coordinates the kinesin KIF13A-dependent pulling of endosomal tubules along microtubules to the Annexin A2/actin-dependent stabilization and detachment of recycling tubules. These components cooperate to extend, stabilize and form tubular endosomal carriers that function in cargo recycling and in the biogenesis of pigment granules in melanocytic cells. By shaping recycling endosomal tubules, our data reveal that dysfunction of the BLOC-1-KIF13A-Annexin A2 molecular network underlies the pathophysiology of neurological and pigmentary disorders.