MP-TSCPC is effective at lowering IOP and decreasing the need for ocular antihypertensive medications. Eyes with limited visual potential or at high risk for incisional glaucoma surgery can successfully be treated with MP-TSCPC as a reasonable and effective alternative to traditional CPC. These results present short-term data and both longer follow-up and further studies are necessary.

Aqueous suppression initiated in the early postoperative period while IOPs were still in the low-teens and was able to reduce the incidence of IOP spike associated with the HP without an increased complication rate.

PurposeTo report the outcomes of patients who underwent goniotomy with the Kahook Dual Blade (KDB) either as a standalone procedure or in combination with cataract extraction.Patients and methodsThis retrospective chart review included 111 eyes of 90 patients who underwent KDB goniotomy from January to November 2016 at Glaucoma Associates of Texas. KDB goniotomy was combined with cataract surgery in 100 eyes. The main outcome measures were postoperative intraocular pressure (IOP) and number of IOP lowering medications.ResultsPreoperatively, mean IOP was 17.1 ± 4.7 mmHg (range 8–34 mmHg) and mean number of IOP lowering medications was 2.4 ± 1.3 (range 0–6). Postoperatively, mean IOP was 14.9 mmHg, 13.9 mmHg, 14.1 mmHg, 14.4 mmHg, and 14.7 mmHg at 1, 3, 6, 9, and 12 months follow-up, respectively (all p <0.004). Mean numbers of IOP lowering medications were 0.8, 1.0, 1.0, 1.0, and 1.6 at 1, 3, 6, 9, and 12 months follow-up, respectively (all p <0.001). The cumulative reoperation rates for uncontrolled IOP after KDB were 0%, 1.0%, 2.1%, and 4.6% at 3, 6, 9, and 12 months, respectively. Eyes with a preoperative IOP >21 mmHg were significantly more likely to undergo reoperation (p = 0.038, log-rank test). There were no serious complications at any time point in the follow-up period.ConclusionThe Kahook Dual Blade results in a reduction in IOP and use of glaucoma medications after one year of follow-up. Further prospective studies are needed to fully characterize safety and efficacy.

Purpose of review Intraocular pressure (IOP) elevation and glaucoma progression following corneal transplantation, specifically, penetrating keratoplasty, Descemet’s stripping endothelial keratoplasty, and Boston keratoprosthesis, are well described causes of ocular morbidity. Depending on the procedure performed, the incidence of glaucoma is highly variable. Several etiologic factors have been identified, the most common being synechial angle closure and corticosteroid-induced IOP elevation. The purpose of this review is to describe the various treatment strategies for glaucoma following corneal transplantation. Recent findings Medications and laser treatments are usually first-line therapies for postoperative IOP elevation. Surgical intervention, including filtering surgery and glaucoma drainage devices, may be necessary to control IOP and prevent progressive glaucomatous damage. Summary Glaucoma is a common complication of corneal transplantation, and the degree of aggressiveness is often related to the indication for corneal surgery. Although postoperative IOP elevation may be controlled with medical therapy alone, refractory cases may require glaucoma surgery. In all cases, early detection and intervention are necessary to optimize patient outcomes.

The ISNT rule alone has a high sensitivity but relatively low specificity. Application of the IS rule in eyes with increased CDR yields a much higher specificity for differentiating normal from more advanced glaucomatous eyes. A combination of different features of the optic disc (increase of CDR and ISNT or IS rule) improves the specificity of optic disc evaluation for glaucoma.

Purpose of review The surgical management of retinal disorders, including scleral buckling procedures, pars plana vitrectomy, and intravitreal injections of gas or silicone oil, can lead to short-term elevations in intraocular pressure (IOP) and ultimately long-term glaucomatous damage if not treated in a timely manner. Glaucoma in these cases is commonly refractory to conventional therapies. This review highlights the treatment strategies for glaucoma in eyes that have previously undergone vitreoretinal surgery. Recent findings Although medical therapy is often used initially to control a temporary rise in IOP, laser and surgical therapy may be required to treat sustained IOP elevation and subsequent glaucomatous damage in eyes that have undergone intraocular surgery for retinal disorders. Glaucoma drainage devices are an important treatment modality, particularly when there is high risk of failure with filtering surgery. Summary Previous vitreoretinal surgery is a known risk factor for the development of glaucoma. Treatment is usually initiated with medical therapy, however, surgical intervention is frequently required to control IOP and prevent progressive glaucomatous damage in patients with refractory glaucoma.

Although there is a currently a revolution in angle-based procedures, subconjunctival filtration surgery with mitomycin C (MMC) wound modification remains a vital skill for glaucoma surgeons. MMC is a potent antifibrotic agent that has been an invaluable adjunct for successful glaucoma filtration surgery for over 20 years, but it must be used judiciously to avoid serious complications, including hypotony, corneal decompensation, bleb avascularity, bleb leaks, blebitis, and endophthalmitis. The purpose of this report is to describe the historical lessons learned from MMC use, along with updated methods of MMC delivery during primary trabeculectomy, bleb needling at the slit lamp, bleb revisions in the operating room, and newer and less invasive ab-interno filtering procedures. Information for the review was gathered using an extensive search on PubMed, a review of all available peer-reviewed literature, and the authors’ personal clinical judgment and experience.

Feedback inhibition by horizontal cells regulates rod and cone photoreceptor calcium channels that control their release of the neurotransmitter glutamate. This inhibition contributes to synaptic gain control and the formation of the center-surround antagonistic receptive fields passed on to all downstream neurons, which is important for contrast sensitivity and color opponency in vision. In contrast to the plasmalemmal GABA transporter found in non-mammalian horizontal cells, there is evidence that the mechanism by which mammalian horizontal cells inhibit photoreceptors involves the vesicular release of the inhibitory neurotransmitter GABA. Historically, inconsistent findings of GABA and its biosynthetic enzyme, L-glutamate decarboxylase (GAD) in horizontal cells, and the apparent lack of surround response block by GABAergic agents diminished support for GABA's role in feedback inhibition. However, the immunolocalization of the vesicular GABA transporter (VGAT) in the dendritic and axonal endings of horizontal cells that innervate photoreceptor terminals suggested GABA was released via vesicular exocytosis. To test the idea that GABA is released from vesicles, we localized GABA and GAD, multiple SNARE complex proteins, synaptic vesicle proteins, and Cav channels that mediate exocytosis to horizontal cell dendritic tips and axonal terminals. To address the perceived relative paucity of synaptic vesicles in horizontal cell endings, we used conical electron tomography on mouse and guinea pig retinas that revealed small, clear-core vesicles, along with a few clathrin-coated vesicles and endosomes in horizontal cell processes within photoreceptor terminals. Some small-diameter vesicles were adjacent to the plasma membrane and plasma membrane specializations. To assess vesicular release, a functional assay involving incubation of retinal slices in luminal VGAT-C antibodies demonstrated vesicles fused with the membrane in a depolarization- and calcium-dependent manner, and these labeled vesicles can fuse multiple times. Finally, targeted elimination of VGAT in horizontal cells resulted in a loss of tonic, autaptic GABA currents, and of inhibitory feedback modulation of the cone photoreceptor Cai, consistent with the elimination of GABA release from horizontal cell endings. These results in mammalian retina identify the central role of vesicular release of GABA from horizontal cells in the feedback inhibition of photoreceptors.