Faculty Bibliography

Choroidal neovascularization (CNV) is typically characterized as an invasion of blood vessels, but it is important to recognize concurrent inflammatory and mesenchymal cell infiltration. A two component model of CNV can be thought to be composed of a vascular component and an extravascular component. Macular damage is possible through either. Given the redundancy and complex interaction among biologic systems involved in the production of CNV, it is likely that a monotherapeutic approach will not be fully effective. The vascular component of CNV arises through the orchestrated interaction of a number of growth factors such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), which maintains pericyte viability. The vascular component of CNV can be selectively targeted with anti-VEGF and anti-PDGF drugs or nonselectively with such modalities as ionizing radiation. The extravascular component can be targeted selectively by inhibiting specific cytokines such as tumor necrosis factor alpha or nonselectively with antiinflammatory drugs such as corticosteroids

PURPOSE: To report the clinical characteristics of a newly defined entity, age-related choroidal atrophy. DESIGN: Retrospective, observational case series. METHODS: The choroidal thickness was measured in images obtained by positioning a spectral-domain optical coherence tomography device close enough to the eye to acquire an inverted image. Seven sections each comprised of 100 averaged scans were obtained within a 5 x 15-degree or larger rectangle to encompass the macula and temporal juxtapapillary retina. The choroidal thickness of patients less than 125 mum in thickness were included, whereas eyes with myopia of 6 diopters or more, a history of uveitis, trauma, ionizing radiation, photodynamic therapy, intravitreal corticosteroid injection, or tapetoretinal dystrophy were excluded. The patients were evaluated for visual acuity, macular appearance, and the presence of glaucoma. RESULTS: There were 28 eligible eyes of 17 patients with a mean age 80.6 years (standard deviation, +/- 7.3 years). All eyes had a tessellated fundus appearance. The mean subfoveal choroidal thickness was 69.8 mum and became even more attenuated nasally. Of the 18 eyes that had no evidence of late age-related macular degeneration (AMD), the mean visual acuity was 20/40, there were pigmentary changes in the macula that arose in part from the choroid potentially mimicking early AMD, and a rarefaction of the choroidal vessels under the macula. Concurrent late AMD was found in the 10 remaining eyes. Glaucoma was present in 6 patients (35.3%), all of whom had peripapillary atrophy. The choroid was seen to become nearly obliterated before the demarcation of the beta-zone of peripapillary atrophy. CONCLUSIONS: Age-related choroidal atrophy affects older individuals in whom posterior pole abnormalities develop that may mimic and also be associated with findings typical for AMD. Patients with age-related choroidal atrophy may be at higher risk for glaucoma

PURPOSE: To measure macular choroidal thickness in normal eyes at different points using enhanced depth imaging (EDI) optical coherence tomography (OCT) and to evaluate the association of choroidal thickness and age. DESIGN: Retrospective, observational case series. METHODS: EDI OCT images were obtained in patients without significant retinal or choroidal pathologic features. The images were obtained by positioning a spectral-domain OCT device close enough to the eye to acquire an inverted image. Seven sections were obtained within a 5 x 30-degree area centered at the fovea, with 100 scans averaged for each section. The choroid was measured from the outer border of the retinal pigment epithelium to the inner scleral border at 500-mum intervals of a horizontal section from 3 mm temporal to the fovea to 3 mm nasal to the fovea. Statistical analysis was performed to evaluate variations of choroidal thickness at each location and to correlate choroidal thickness and patient age. RESULTS: The mean age of the 30 patients (54 eyes) was 50.4 years (range, 19 to 85 years), and 14 patients (46.7%) were female. The choroid was thickest underneath the fovea (mean, 287 mum; standard deviation, +/- 76 mum). Choroidal thickness decreased rapidly in the nasal direction and averaged 145 mum (+/- 57 mum) at 3 mm nasal to the fovea. Increasing age was correlated significantly with decreasing choroidal thickness at all points measured. Regression analysis suggested that the subfoveal choroidal thickness decreased by 15.6 mum for each decade of life. CONCLUSIONS: Choroidal thickness seems to vary topographically within the posterior pole. The thickness of the choroid showed a negative correlation with age. The decrease in the thickness of the choroid may play a role in the pathophysiologic features of various age-related ocular conditions

PURPOSE: To describe the internal structure of pigment epithelial detachments (PEDs) seen in eyes with age-related macular degeneration (AMD) as imaged with enhanced depth imaging (EDI) spectral-domain optical coherence tomography (OCT). DESIGN: Retrospective observational case series. METHODS: The images were obtained by positioning a spectral-domain OCT device close enough to the eye to obtain an inverted image and 7 sections, each comprised of 100 averaged scans, were obtained within a 5 degrees x 15 degrees or larger rectangle to encompass the PED and accompanying neovascularization if present. The resultant images were reinverted and compared with fluorescein and indocyanine green angiographic findings. RESULTS: The full extent of the choroid was visualized under the PED in each of the 22 consecutive eyes imaged with EDI OCT. The entire PED cavity filled with hyperreflective tissue in 11 eyes. In the remaining 11 regions, what appeared to be serous fluid and collections of reflective material were found within the PED. The reflective material was seen to be contiguous with subretinal pigment epithelial neovascularization, had angiographic suggestive of fibrovascular proliferation, and was seen to course up along the back surface of the retinal pigment epithelium (RPE). Intravitreal ranibizumab injection caused PED flattening with apparent contracture of the accumulated material within the PED. CONCLUSIONS: PEDs in the context of AMD show material suggestive of choroidal neovascularization, frequently on the back surface of the RPE. These findings can help explain the pathogenesis of PEDs, retinal vascular anastomosis with choroidal neovascularization, and RPE tears

Occult macular dystrophy is a rare macular disorder in which patients have bilaterally decreased visual acuity without any significant ophthalmoscopic findings. Using spectral domain optical coherence tomography, the authors found a defect in the junction between the inner and outer segments of the foveal photoreceptors in a patient with occult macular dystrophy

PURPOSE: To evaluate intravitreal injection of ranibizumab as a potential treatment for decreased visual acuity (VA) secondary to central retinal vein occlusion (CRVO). DESIGN: Prospective, interventional case series. METHODS: Patients with CRVO prospectively recruited from a practice were administered intravitreal ranibizumab 0.5 mg (Lucentis; Genentech Inc, South San Francisco, California, USA) at baseline and monthly for two additional doses. The patients were given additional ranibizumab if they had macular edema as determined by optical coherence tomography or any new intraretinal hemorrhage. Patients were evaluated for number of required injections, side effects, changes in VA, and macular thickness. RESULTS: There were 20 eyes of 20 patients who at baseline had a mean age of 72.1 years, a mean VA of 45.8 Early Treatment of Diabetic Retinopathy letters, and a mean central macular thickness of 574.6 microm. Of the 20 eyes, five previously had received intravitreal triamcinolone and 11 had received intravitreal bevacizumab (Avastin; Genentech Inc). At 12 months of follow-up, the mean VA improved to 64.3 letters and the central macular thickness decreased to 186 microm (both different than baseline values; P < .001) using a mean of 8.5 injections. The change in macular thickness was not correlated with the change in VA. In one patient with a history of transient ischemic attack, an ischemic stroke developed but no sequela resulted. In another patient, vitreomacular traction developed, but the patient had improved acuity as compared with baseline. There were no infections, retinal tears, or detachments. CONCLUSIONS: Intravitreal ranibizumab used over a period of one year improved mean VA, with low rates of adverse events, in patients with CRVO

OBJECTIVE: To describe cases of acute zonal occult outer retinopathy (AZOOR) in patients previously diagnosed as having multiple evanescent white dot syndrome (MEWDS). METHODS: In a retrospective case series, we studied fundus photographs, fundus autofluorescence images, optical coherence tomographic scans, fluorescein and indocyanine green angiograms, visual fields, and results of electroretinography. RESULTS: Three patients diagnosed as having MEWDS developed clinical, angiographic, autofluorescence, visual field, and/or electrophysiologic evidence of AZOOR. Spectral domain optical coherence tomographic findings disclosed attenuation of the photoreceptor inner segment-outer segment junction in areas of AZOOR involvement. In 1 patient, hyperautofluorescence on fundus autofluorescence images during the MEWDS episode coincided with the area of involvement of AZOOR. CONCLUSIONS: Development of AZOOR may occur in patients with MEWDS, suggesting that the conditions may share a common genetic susceptibility and/or pathogenetic factor. Although the typical visual prognosis after MEWDS is excellent, subsequent diagnosis of AZOOR may portend a worse outcome

PURPOSE: To describe a patient with birdshot retinochoroidopathy (BRC) with bilateral choroidal neovascularization (CNV) who was treated with intravitreal injection of bevacizumab and antiinflammatory medications. METHOD: Interventional case report. PATIENT: A 35-year-old woman with bilateral CNV associated with BRC. RESULTS: The patient was treated with intravitreal injection of triamcinolone, photodynamic therapy, and intravitreal injection of bevacizumab in one eye, while the fellow eye was treated with intravitreal injection of triamcinolone. Immunosuppressive therapy was performed in the course of the treatment. Not only did the neovascularization respond, but the birdshot lesions vanished as well. DISCUSSION: BRC can have secondary CNV that, as in the current case, responds favorably to treatment. We serendipitously observed regression of the choroidal inflammatory lesions with intravitreal injection of triamcinolone.

PURPOSE: To report an association between polypoidal choroidal vasculopathy (PCV) and choroidal nevus in two patients. METHODS: Two patients with subretinal exudation associated with a choroidal nevus had a complete ophthalmologic examination, slit-lamp biomicroscopy, color fundus photography, fluorescein angiography (FA), and indocyanine green angiography (ICG). RESULTS: In the two eyes of the two patients with choroidal nevus, choroidal neovascularization with PCV-like characteristics was detected by ICG angiography. CONCLUSIONS: PCV-like vascular changes can be associated with choroidal nevus, and ICG can help delineate the nature of the neovascularization in patients with choroidal nevus.