Michael T. Trese

A new approach to stage 3 macular holes.

PURPOSEnThe purpose of this article is to demonstrate the feasibility of a surgical approach that might be possible in an office setting for idiopathic stage 3 macular holes. The posterior hyaloid of the vitreous and perihole tissue is enzymatically manipulated to create an atraumatic posterior vitreous separation and may stimulate cell proliferation to close macular holes.nnnDESIGNnProspective noncomparative interventional case series.nnnPARTICIPANTSnNine eyes of eight patients with idiopathic stage 3 macular holes were treated.nnnMETHODSnThe patients were treated with an injection of 0.4 IU of autologous plasmin enzyme into the midvitreous cavity and lavage of the vitreous cavity with an infusion light pipe and vitreous cutter followed by filling 70% to 80% of the vitreous cavity with 14% C3F8 and head-down positioning.nnnMAIN OUTCOME MEASURESnPosterior vitreous detachment, macular hole closure, and vision improvement.nnnRESULTSnEight of nine eyes showed a spontaneous posterior vitreous detachment. One eye required minimal suction of less than 50 mmHg to elevate the posterior hyaloid off the retinal surface. Eyes were followed for a minimum of 6 months. All holes closed, and there was an average visual acuity improvement of four lines. The average surgical time for this procedure was 20 minutes.nnnCONCLUSIONSnAutologous plasmin enzyme-assisted vitreous surgery techniques can reduce operative time, expense, and patient inconvenience while maintaining excellent surgical results, which may allow office-based vitreous surgery for idiopathic stage 3 macular holes.

Vitrectomy for Retained Lens Fragments after Phacoemulsification

PURPOSEnPosterior lens fragments after phacoemulsification can be a serious complication of cataract surgery. This study is designed to evaluate the clinical features of eyes after pars plana vitrectomy has been performed to remove posteriorly dislocated lens fragments after phacoemulsification.nnnMETHODSnThe authors performed a retrospective chart review of 126 consecutive eyes of 126 patients with dislocated lens fragments after phacoemulsification, managed with pars plana vitrectomy at Associated Retinal Consultants of Michigan. These eyes were operated on from January 1986 through January 1996.nnnRESULTSnThe relation of the intervals between cataract surgery and vitrectomy to various postoperative clinical parameters was studied. Clinical features at presentation included elevated intraocular pressure (IOP over 25 mmHg) in 52.4% of the eyes, uveitis in 69.6%, and corneal edema in 50.8%. Initial visual acuity was 20/400 or worse in 73.8% of the eyes. The mean preoperative visual acuity was 20/278 (median, 20/400), whereas the mean final visual acuity was 20/40 (median, 20/50) after a mean follow-up of 18.9 months. Retinal detachments were found in 20 eyes: 7 before vitrectomy and 13 during or after it. After surgery, 44% of eyes achieved a final visual acuity of 20/40 or better and 90% were 20/400 or better. The distribution of best-corrected final visual acuities among the eyes showed statistically significant differences based on the type of intraocular lens (IOL) used, with posterior chamber IOL greater than anterior chamber IOL, and anterior chamber IOL greater than aphakia. Reasons for a poor visual outcome included persistent corneal edema (four eyes), retinal detachment (two eyes), central retinal vein occlusion (two eyes), age-related macular degeneration (two eyes) glaucoma (one year), and endophthalmitis (one eye).nnnCONCLUSIONSnThere were no statistically significant differences between early (< 7 days) and delayed (8 days or more) vitrectomy when increased IOP, corneal edema, choroidal effusions, cystoid macular edema, and visual acuity were analyzed. The use of vitrectomy to remove posteriorly dislocated lens fragments has been shown to be an effective treatment method that significantly reduces the inflammatory response and hastens visual recovery.

Autologous plasmin enzyme in the surgical management of diabetic retinopathy.

PURPOSEnThis is a pilot study to assess the use of autologous plasmin enzyme (APE) as an adjunct to vitreous surgery in eyes with advanced diabetic retinopathy.nnnDESIGNnProspective noncomparative interventional case series.nnnPARTICIPANTSnSeven patients with advanced diabetic retinopathy selected at random from our practice population.nnnMETHODSnSeven eyes were treated with APE as an adjunct to standard vitreous surgery. Six eyes had macular tractional retinal detachments, and one eye had refractory macular edema. Three fellow eyes had standard vitreous surgery performed for macular tractional retinal detachments without APE. All 10 eyes had macular edema and background diabetic retinopathy.nnnMAIN OUTCOME MEASURESnThe main outcome measures included induction of a posterior vitreous detachment, retinal reattachment, improvement in visual acuity, and resolution of macular edema.nnnRESULTSnAll seven APE-treated eyes achieved spontaneous or easy removal of the posterior hyaloid including one eye that had vitreoschisis over areas of detached retina. All eyes treated with APE had resolution of intraretinal edema. Retinas of all eyes treated with APE were reattached. The three fellow eyes were treated by vitreous surgery without APE. Two of the three fellow eyes had reattached retinas, but none had resolution of intraretinal edema without further focal photocoagulation treatment. Mean visual acuity improvement was 0.7 logarithm of the minimum angle of resolution (LogMAR) units in APE-treated eyes and 0.1 LogMAR units in eyes without APE. The average follow-up period was 14 months.nnnCONCLUSIONSnThis pilot study suggests that APE may be beneficial in the surgical management of diabetic retinopathy.

Surgical results of persistent hyperplastic primary vitreous

PURPOSEnTo evaluate the surgical success of patients with persistent hyperplastic primary vitreous (PHPV) and to identify preoperative indicators of visual outcome.nnnDESIGNnNoncomparative case series.nnnMETHODSnThe diagnosis of PHPV was made in 35 eyes of 27 patients from 1982 to 1994. In each case, anterior and/or posterior PHPV findings, preoperative testing, surgical procedures, and visual outcomes were documented. Twenty-nine of 35 eyes were managed surgically. Follow-up ranged from 2 months to 12 years.nnnRESULTSnOf the 35 eyes, 2 (5.7%) had strictly anterior PHPV, 8 (22.9%) had strictly posterior PHPV, and 25 (71.4%) had components of both anterior and posterior disease. Initial lensectomy and vitrectomy was performed in 24 eyes (68.6%). Surgery was withheld in four eyes secondary to severity of disease with an unrecordable visual-evoked potential (VEP). Reoperation rate was 32.3% for membrane reproliferation, glaucoma, vitreous hemorrhage, retinal detachment, or strabismus. Best-corrected final visual acuity ranged from 20/60 to no light perception. Six eyes (17%) maintained Snellen visual acuity despite posterior PHPV with some degree of retinal dysplasia.nnnCONCLUSIONSnSurgical treatment of PHPV can result in functional visual outcome despite posterior segment involvement. The degree of ocular malformation, however, will ultimately limit the amount of visual improvement. Preoperative testing, including VEP, may aid in determining surgical candidates.

X-linked recessive familial exudative vitreoretinopathy.

Familial exudative vitreoretinopathy is an inherited disorder characterized by retinal traction, peripheral vitreous opacities, and subretinal and intraretinal exudates. We observed a family in which four boys (the children of three sisters) were affected with this disorder and an X-linked recessive inheritance was apparent. The differential diagnosis includes retinopathy of prematurity, primary hyperplastic primary vitreous, Coats disease, peripheral uveitis, retinoblastoma, and Norries disease, but this differentiation can usually be made on the basis of clinical findings alone. Knowledge of X-linked recessive transmission is important for correct diagnosis and for genetic counseling.

Pharmacologic vitreodynamics: what is it? Why is it important?

Significant advancements have been made in the field of pharmacologic vitreodynamics. Recent studies have demonstrated encouraging results with several enzymatic agents. Both plasmin and microplasmin are able to induce vitreous liquefaction and a posterior vitreous detachment with a single intravitreal injection. If used as a surgical adjunct, these enzymes have the potential to facilitate more complete removal of the vitreous gel, decrease surgical time and reduce intraoperative complications. Patients with vitreoretinal abnormalities may benefit from the prophylactic use of the enzymes. In select cases, enzymatic vitreolysis may even replace surgical intervention. Pharmacologic manipulation of the vitreous may alter the flux of molecules that enter and leave the vitreous cavity, with potential implications for the management of multiple vitreoretinopathies. This review will provide a summary of recent findings and future directions in the field of pharmacologic vitreodynamics.

Norrin treatment improves ganglion cell survival in an oxygen-induced retinopathy model of retinal ischemia

ABSTRACT Treatment of a mouse model of oxygen‐induced retinopathy (OIR) with recombinant human Norrin (Norrie Disease Protein, gene: NDP) accelerates regrowth of the microvasculature into central ischemic regions of the neural retina, which are generated after treatment with 75% oxygen. While this reduces the average duration and severity of ischemia overall, we do not know if this accelerated recovery of the microvasculature results in any significant survival of retinal ganglion cells (RGCs). The purpose of this study was to investigate ganglion cell survival with and without the intravitreal injection of Norrin in the murine model of oxygen induced retinopathy (OIR), using two strains of mice: C57BL/6J and Thy1‐YFP mice. Intravitreal injections of Norrin or vehicle were done after five days of exposure to 75% oxygen from ages P7 to P12. The C57BL/J mice were followed by Spectral‐Domain Optical Coherence Tomography (SD‐OCT), and the average nerve fiber layer (NFL) and inner‐plexiform layer (IPL) thicknesses were measured at twenty‐four locations per retina at P42. Additionally, some C57BL/J retinas were flat mounted and immunostained for the RGC marker, Brn3a, to compare the population density of surviving retinal ganglion cells. Using homozygous Thy1‐YFP mice, single intrinsically fluorescent RGCs were imaged in live animals with a Micron‐III imaging system at ages P21, 28 and P42. The relative percentage of YFP‐fluorescent RGCs with dendritic arbors were compared. At age P42, the NFL was thicker in Norrin‐injected OIR eyes, 14.4 &mgr;m, compared to Vehicle‐injected OIR eyes, 13.3 &mgr;m (p = 0.01). In the superior retina, the average thickness of the IPL was greater in Norrin‐injected OIR eyes, 37.7 &mgr;m, compared to Vehicle‐injected OIR eyes, 34.6 &mgr;m (p = 0.04). Retinas from Norrin injected OIR mice had significantly more surviving RGCs (p = 0.03) than vehicle‐injected mice. Based upon NFL thickness and counts of RGCs, we conclude that Norrin treatment, early in the ischemic phase, increased the relative population density of surviving RGCs in the central retinas of OIR mice. HighlightsNorrin treatment accelerates recovery of the mouse OIR model from ischemic insult.SD‐OCT can compare NFL/GCL (nerve fiber layer/ganglion cell layer) thickness in vivo.Norrin treatment counters thinning of the NFL/GCL in the mouse OIR model.Norrin treatment increases the surviving population density of RGCs in OIR retinas.

Lack of association of the Norrie disease gene with retinoschisis phenotype.

PURPOSEnIt has been reported recently that mice carrying a disrupted Norrie disease gene produced alterations in the murine eye that are similar to congenital retinoschisis. Therefore, it was of interest to determine whether mutations in the Norrie disease gene can account for the disease in families with retinoschisis that do not carry mutations in the retinoschisis gene.nnnMETHODSnThe patient set comprised 5 cases of retinoschisis (1 familial and 4 sporadic), all unrelated to each other. Fundus examination of affected individuals showed foveal and peripheral schisis, and the visual acuity range was 20/40-20/60. Peripheral blood specimens were collected from affected and unaffected family members. DNA was extracted and amplified by polymerase chain reaction amplification of exons of the Norrie disease gene. The amplified products were sequenced by the dideoxy chain termination method.nnnRESULTSnThe data revealed no disease-specific sequence alterations in the Norrie disease gene.nnnCONCLUSIONnAlthough we cannot completely exclude the possibility of the Norrie disease gene as a candidate gene, the above results suggest that the structural and functional changes in the Norrie disease gene are not associated with clinically typical retinoschisis families that do not contain mutations in the coding regions and splice sites of the retinoschisis gene.

Vitreous and Retinopathy of Prematurity: Vitreous Surgery and Visual Results

Retinopathy of prematurity (ROP) is a unique retinal vascular disease because it appears during the development of the normal retinal vasculature and vitreous. It has been suggested that the avascular peripheral retina produces a vasoproliferative factor, which then affects tissue posterior to the retinal ridge (at the juncture of avascular and vascularized retina). This vasoproliferative factor then stimulates neovascularization only in that location. We were curious as to why neovascularization is seen only in the area posterior to the ridge and is not seen at the optic nerve head or in areas anterior yet adjacent to the ridge. We have examined enucleated human eyes at autopsy, as well as animal eyes derived from the Ashton kitten model of ROP, and found that the vitreous is intimately attached to the neurosensory retina posterior to the retinal ridge. Anterior to the retinal ridge, this attachment does not seem to be as strong, as seen by either morphologic or immunohistochemical techniques.

Ocular coherence tomography image data of the retinal laminar structure in a mouse model of oxygen-induced retinopathy

The data presented in this article are related to the research paper entitled “Norrin treatment improves ganglion cell survival in an oxygen-induced model of retinal ischemia” (Dailey et al., 2017) [1] This article describes treatment with the human Norrin protein, an atypical Wnt-protein, to improve the survival of retinal ganglion cells in a murine model of Oxygen-Induced Retinopathy (OIR). That study utilized Optical coherence tomography (OCT) to visualize retinal layers at high resolution in vivo, and to quantify changes to nerve fiber layer thickness. Organization of the laminar structure of other retinal layers in this model in vivo, were not known because of uncertainties regarding potential artifacts during the processing of tissue for traditional histology. The OCT image data provided here shows researchers the retinal laminar structural features that exist in vivo in this popular mouse OIR model. Traditional H&E stained retinal tissue sections are also provided here for comparison.