Rate of intraoperative complications during cataract surgery following intravitreal injections.

PurposeTo investigate the effect of prior intravitreal injections on intraoperative and postoperative complication rates associated with cataract surgery.MethodsA retrospective cohort analysis reviewed 10 105 cataract surgery procedures performed by experienced surgeons at the Duke Eye Center from 1 January 2005 to 10 December 2012. A group of 197 eyes with prior intravitreal injections was compared with an equal number of matched control eyes without prior injection using the Fisher's exact test of difference in proportions and the Wilcoxon rank-sum test of difference in means. Outcomes analyzed included baseline demographic information, preoperative clinical characteristics, prevalence of intraoperative complications, and postoperative intraocular pressure, glaucoma surgery, and glaucoma medication requirement through 1 year following cataract surgery.ResultsAn increased rate of intraoperative complications was identified during cataract surgery in eyes with prior intravitreal injections compared with control eyes (3 vs 0%, P=0.030). Injection eyes required more glaucoma medications at 1 year, but no difference was identified if steroid injections were excluded. No difference in postoperative IOP or glaucoma surgery was identified. No cases of endophthalmitis were reported.ConclusionsA history of intravitreal injections may be a risk factor for cataract surgery-related intraoperative complications. We hypothesize this may be due to unidentified iatrogenic lens trauma during intravitreal injections. Particular attention to the posterior capsule during preoperative assessment and intraoperatively is recommended in eyes undergoing cataract surgery with a prior history of intravitreal injections.

Phosphodiesterase 3A expression is modulated by nitric oxide in rat pulmonary artery smooth muscle cells.

Phosphodiesterases (PDEs) limit vasodilation in response to a variety of signaling cascades by metabolizing the cyclic nucleotides cAMP and cGMP. The objective of this study was to test the hypothesis that NO regulates expression of PDE3A, a cGMP-inhibited PDE. Incubation of rat pulmonary artery smooth muscle cells (rPaSMCs) with the NO-donor compound S-nitroso-glutathione (GSNO) increased PDE3A gene expression in a dose- and time-dependent manner. NO-donors increased PDE3A protein levels. Total and milrinone inhibitable cAMP PDE activity were increased 2.8 ± 0.1- and 2.0 ± 0.1-fold respectively in extracts of rPaSMCs exposed to GSNO. The effects of GSNO on PDE3A gene expression were mimicked by the soluble guanylate cyclase (sGC) activators YC-1 and BAY 41-2272 and blocked by the sGC inhibitor ODQ. Incubation of rPaSMC with interleukin-1ß and tumor necrosis factor-α induced PDE3A gene expression, an effect which was inhibited by L-NIL, an antagonist of NO synthase 2, or ODQ. Actinomycin D, an inhibitor of RNA polymerase, blocked the GSNO-induced increase of PDE3A mRNA levels, whereas cycloheximide, an inhibitor of protein translation, did not. These observations suggest that NO modulates PDE3A gene expression via mechanisms dependent upon cGMP synthesis and gene transcription. Prolonged exposure to NO may alter the sensitivity of vascular smooth muscle to cGMP- or cAMP-dependent vasodilators, as well as PDE isoform-selective inhibitors.