Intentional use of topical latanoprost with resulting macular edema to help in the closure of a failed, chronic, macular hole.

Purpose: To report a case where the induction of macular edema with topical latanoprost coupled with in-office gas injection effectively sealed a persistent, chronic, macular hole. Observations: A 70-year-old, pseudophakic, patient presented with a stage three, chronic, macular hole (MH) and vision reduced to 20/200. The symptoms had been present for 18 months. Patient had surgery with pars plana vitrectomy (PPV), complete internal limiting membrane (ILM) peel to the arcades, 30% SF6 gas, and excellent face down positioning for five days. Two weeks after surgery the macular hole failed to close, and the edges of the hole were blunted with very little retinal edema and vision reduced to 20/400. The patient did not want to go back to the operating room. After informed consent, the patient was started on topical latanoprost 0.005% on the operative eye twice a day for six weeks. After latanoprost induction of cystoid macular edema (CME), the patient had 0.7 cc of pure C3F8 injected into the vitreous cavity in the office and was instructed to be face down for five days. Two weeks later the macular hole was closed with vision of 20/80. Last corrected vision eight months later was 20/50. Conclusions and Importance: The findings in this case suggest that induction of CME facilitated the closure of a chronic, persistent, macular hole with a simple gas injection in the office and face down positioning for five days.

Long-Term Favorable Visual Outcomes in Patients with Large Submacular Hemorrhage.

Submacular hemorrhage (SMH) has been reported to be toxic to the retina based on animal studies. However, observational studies of patients with neovascular-related SMH and those treated with intravitreal anti-vascular growth factor (anti-VEGF) therapy have shown many favorable visual acuity outcomes. We report two cases of neovascular-related SMH with ten or more years of follow-up. The first case was an 83-year old female with a history of nonexudative age-related macular degeneration in both eyes presenting with sudden decrease in vision (20/400) in her right eye due to a large SMH, treated with anti-VEGF therapy. Over the next following months, there was resolution of the hemorrhage and return of good visual acuity. At 10-year follow-up, visual acuity was 20/30 in the right eye. The second case was a 49-year old female with a history of presumed ocular histoplasmosis syndrome (POHS), presenting with sudden vision loss (20/400) in her right eye due to large, thick SMH. With observation and intermittent anti-VEGF therapy, there was resolution of the hemorrhage. At 30-year follow-up, visual acuity was 20/20 in the right eye.

Nutritionally variant streptococci causing endophthalmitis associated with intravitreal anti-vascular endothelial growth factor injection.

PURPOSE: To describe the clinical course and microbial properties of the first two reported cases of nutritionally variant Streptococci (Granulicatella adiacens and Abiotrophia defectiva) endophthalmitis following intravitreal anti-vascular endothelial growth factor injection (IVI). OBSERVATIONS: A 74 year-old female developed Granulicatella adiacens endophthalmitis following IVI. The patient underwent a pars plana vitrectomy and visual acuity recovered to 20/30 in six weeks. Similarly, an 88 year-old male developed Abiotrophia defectiva endophthalmitis after IVI. After a pars plana vitrectomy, the visual acuity recovered to 20/60 at five weeks. CONCLUSIONS AND IMPORTANCE: Endophthalmitis due to Streptococcus species has traditionally resulted in uniformly poor visual outcomes. However, nutritionally variant Streptococci, now reclassified as Granulicatella and Abiotrophia species, appear to have a less aggressive clinical course and better visual acuity outcomes. To the authors' knowledge, these are the first reports of nutritionally variant Streptococci following IVI related endophthalmitis.

SDF-1 is both necessary and sufficient to promote proliferative retinopathy.

Diabetic retinopathy is the leading cause of blindness in working-age adults. It is caused by oxygen starvation in the retina inducing aberrant formation of blood vessels that destroy retinal architecture. In humans, vitreal stromal cell-derived factor-1 (SDF-1) concentration increases as proliferative diabetic retinopathy progresses. Treatment of patients with triamcinolone decreases SDF-1 levels in the vitreous, with marked disease improvement. SDF-1 induces human retinal endothelial cells to increase expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenitors, and reduce tight cellular junctions by reducing occludin expression. Both changes would serve to recruit hematopoietic and endothelial progenitor cells along an SDF-1 gradient. We have shown, using a murine model of proliferative adult retinopathy, that the majority of new vessels formed in response to oxygen starvation originate from hematopoietic stem cell-derived endothelial progenitor cells. We now show that the levels of SDF-1 found in patients with proliferative retinopathy induce retinopathy in our murine model. Intravitreal injection of blocking antibodies to SDF-1 prevented retinal neovascularization in our murine model, even in the presence of exogenous VEGF. Together, these data demonstrate that SDF-1 plays a major role in proliferative retinopathy and may be an ideal target for the prevention of proliferative retinopathy.

Vitreous levels of vascular endothelial growth factor and stromal-derived factor 1 in patients with diabetic retinopathy and cystoid macular edema before and after intraocular injection of triamcinolone.

BACKGROUND: Diffuse macular edema (DME) and/or aberrant neovascularization (NV) can cause vision loss in diabetic retinopathy (DR) and may be modulated by growth factors and chemokines. The chemokine stromal-derived factor 1 (SDF-1) is a potent stimulator of vascular endothelial growth factor (VEGF) expression, the main effector of NV, and the key inducer of vascular permeability associated with DME. Circulating endothelial cell precursors migrating in response to SDF-1 participate in NV. OBJECTIVE: To investigate the relationship between SDF-1 and (VEGF) in vitreous of patients with varying degrees of DR and DME before and after intraocular injection of triamcinolone acetonide, used to treat refractory DME. METHODS: In this prospective study, 36 patients were included and observed for 6 months. Vitreous VEGF and SDF-1 levels were measured by enzyme-linked immunosorbent assay in samples obtained immediately before and 1 month after injection of triamcinolone. RESULTS: Both VEGF and SDF-1 were significantly higher (P<.01) in patients with proliferative DR than in patients with nonproliferative DR. Levels of SDF-1 were markedly increased in patients with DME compared with those without DME. Vascular endothelial growth factor correlated with SDF-1 levels and disease severity (r(2) = 0.88). CONCLUSIONS: Triamcinolone administration resulted in dramatic reductions of VEGF and SDF-1 to nearly undetectable levels, eliminated DME, and caused regression of active NV. Our results support a role for SDF-1 and VEGF in the pathogenesis of the adverse visual consequences of DR and suggest that the elimination of DME with regression and/or initiation of fibrosis of NV after triamcinolone injection may be due to the suppression of VEGF and SDF-1.

Management of posteriorly dislocated posterior chamber intraocular lenses by vitrectomy and pars plana removal.

PURPOSE: To report a large series of eyes in which there was a posterior dislocation of a posterior chamber intraocular lens (PCIOL). During vitrectomy, the dislocated intraocular lens (IOL) was removed through an enlarged pars plana sclerotomy. An anterior chamber IOL (ACIOL) was implanted primarily or secondarily. METHODS: We conducted a retrospective chart review of 59 eyes of 58 patients with posterior dislocation of a PCIOL. RESULTS: Fifty-four eyes (92%) had improved visual acuity after surgery. Sixty-six percent (39 of 59) of eyes achieved at least 20/40 vision; 25% (15 of 59) of eyes achieved a visual acuity of 20/50 to 20/200; and 8% (5 of 59) of eyes achieved less than 20/200 vision. In 32 (54%) eyes, PCIOL removal was combined with primary implantation of an ACIOL. In 27 (46%) eyes, the PCIOL was removed and the referring ophthalmologist placed a secondary ACIOL. Intraoperative complications consisted of limited suprachoroidal hemorrhage in 2 (3%) eyes. Postoperative complications consisted of retinal detachment in 5 (8%) eyes, cystoid macular edema in 13 (22%) eyes, and vitreous hemorrhage in 3 (5%) eyes. CONCLUSION: Posterior dislocation of a PCIOL may be managed safely by removal of the dislocated PCIOL through the pars plana.

Diode laser photocoagulation to the ridge and avascular retina in threshold retinopathy of prematurity.

PURPOSE: To report results applying diode laser photocoagulation to both the peripheral avascular retina and the ridge in stage 3+ threshold retinopathy of prematurity. METHODS: The authors performed a retrospective review of 82 consecutive eyes in 43 preterm infants with threshold disease who had both the peripheral avascular retina and the ridge treated with diode laser photocoagulation. With a minimum follow-up of 3 months, these eyes were evaluated for intraoperative and postoperative complications and long-term anatomic results. RESULTS: A favorable anatomic outcome occurred in 79 eyes (96%). There were no intraoperative complications. Postoperative intraocular hemorrhage occurred in eight eyes (10%) and resolved without sequelae. Supplemental laser was required in only two eyes (2%). CONCLUSIONS: Diode laser photocoagulation to the ridge and peripheral avascular retina in threshold retinopathy of prematurity is associated with a favorable anatomic outcome. The risk of postoperative intraocular hemorrhage and the need for supplemental laser photocoagulation is low.