Maurice F. Rabb

Retinal arterial macroaneurysms

Retinal arterial macroaneurysms represent a distinct clinical entity. Macroaneurysms are seen in the elderly with a marked female predominance and a strong association with hypertension and arteriosclerotic vascular changes. The classic appearance provides an easy diagnosis; however, variable presentations, such as subretinal hemorrhage, macular exudate, and epiretinal membranes can make the diagnosis difficult. The differential diagnosis of retinal arterial macroaneurysms include retinal telangiectasia, angiomatosis retinae, venous macroaneurysms, background diabetic retinopathy, and cavernous hemangioma. The clinical characteristics of the reported cases are summarized, and our series of 60 patients is presented. The natural history of most macroaneurysms is spontaneous involution without loss of vision. However, visual loss may occur secondary to macular edema, exudate, hemorrhage and neurosensory retinal detachment, and photocoagulation may expedite visual recovery. Photocoagulation treatment may be applied directly to the macroaneurysm, indirectly by surrounding the macroaneurysm, or as a combination of these two methods.

Idiopathic polypoidal choroidal vasculopathy of the macula

OBJECTIVE The authors evaluated the clinical, fluorescein, and indocyanine green (ICG) angiographic characteristics of the macular variant of idiopathic polypoidal choroidal vasculopathy (IPCV). DESIGN Observational case series. PARTICIPANTS The records, photographs, and fluorescein and ICG angiograms of eight eyes of seven patients with IPCV lesions confined to the macula were reviewed. MAIN OUTCOME MEASURES The visual acuity, fundus examination, fluorescein and ICG angiographic characteristics, and clinical course were compared. RESULTS All patients demonstrated polypoidal lesions arising from macular choroidal vessels on ICG angiography. One patient had bilateral lesions. These lesions appeared hyperfluorescent in the early phases of both fluorescein and ICG angiography. Late-phase leakage was seen in cases associated with subretinal fluid or exudate. None of these patients demonstrated polypoidal lesions arising from the peripapillary choroidal circulation or peripapillary choroidal neovascularization. Three eyes with polypoidal lesions that were associated with subretinal fluid and exudates were treated with photocoagulation. Five eyes were not treated. Final visual acuity ranged from 20/20 to hand motions. Severe visual loss was associated with vitreous and subretinal hemorrhage, but this resolved without permanent severe visual loss in several cases. CONCLUSIONS In the macular variant of IPCV, ICG and fluorescein angiography demonstrate characteristic macular polypoidal lesions without evidence of peripapillary lesions. The vascular origin of these polypoidal lesions appears to be the macular choroidal circulation. This is distinguished from classic IPCV, in which lesions appear to arise from the peripapillary choroidal circulation. Visual prognosis appears to be good, with most patients retaining visual acuity of 20/80 or better. If subretinal fluid or exudates reduce visual acuity, photocoagulation should be considered.

Ocular manifestations of sickle hemoglobinopathies.

The ocular manifestations of sickle cell hemoglobinopathies, while often not severe enough to affect vision, may develop in proliferative stages, resulting in arteriolar-venular anastomoses, neovascular proliferations, vitreous hemorrhage and retinal detachment. The authors review the historical, biochemical, and geographic aspects of the disease, and provide detailed descriptions of findings in theconjunctiva, uvea and fundus, with particular emphasis on the retina. Pathogenesis, histopathologic and clinical appearance, and modes of treatment are discussed.

Cone-rod dystrophy. A clinical and histopathologic report.

Clinical, histopathologic, and electron microscopic findings in two postmortem eyes from a 29-year-old black man and the clinical and electrophysiologic findings of his 33-year-old sister, both of whom had bilateral atrophic macular lesions, confirmed the diagnosis of cone-rod dystrophy in these two patients. Light microscopy revealed a loss of photoreceptor cells primarily in the peripheral retina and macula, with relative preservation of both rod and cone cells in the equatorial area. Electron microscopy showed abundant lipofuscin-like granules aggregated in the basal portion of the retinal pigment epithelial cells. In the macular area, many retinal pigment epithelial cells were atrophic. The phagocytic capacity of the retinal pigment epithelium appeared to remain intact. The accumulation of lipofuscin-like granules in the retinal pigment epithelium may be one of the significant pathologic changes of this dystrophy.

Ocular pathology : clinical applications and self-assessment

Introduction. Development Anomalies. Cornea. Lens and Pathology of Intraocular Lenses. Pathology of Refractive Surgery. Glaucoma. Uvea. Fundus. Retinoblastoma, Leukokoria and Phakomatoses. Optic Nerve. Conjunctiva and Eyelids. Questions and Answers. Colour Plates.

Subretinal Neovascularization with Geographic (Serpiginous) Choroiditis

Three patients with geographic choroiditis developed subretinal neovascular membranes associated with subretinal hemorrhage and serous elevation of the retina. Proximity of the membrane to the foveal avascular zone prevented photocoagulation of the neovascular membrane in one patient. Central visual acuity remained 6/60 (20/200) despite systemic corticosteroid therapy. The neovascular membranes in the other two patients were obliterated by argon laser photocoagulation with preservation of central vision. The inflammatory process of geographic choroiditis can disrupt Bruchs membrane, allowing occasional choroidal vascular growth. Concomitant destruction of choroidal vessels may account for rarity of subretinal neovascularization in geographic choroiditis.

Macular and perimacular vascular remodelling sickling haemoglobinopathies.

The posterior pole vasculature of 100 patients with different sickling haemoglobinopathies was studied prospectively over a period of three years. Various abnormalities of the posterior pole vasculature were seen in 29 per cent of the patients. Continuous remodelling of the macular and perimacular vasculature occurred. Visual acuity was variably affected and sometimes remained intact.

Diabetic Retinopathy in Blacks

Diabetic eye disease, particularly diabetic retinopathy, is the leading cause of new cases of legal blindness in people 20–74 yr of age in the United States. The prevalence and rate of diabetes in this age-group are higher in Blacks than in Whites. The rate of blindness from diabetic eye disease is also higher in Blacks than in Whites. Severe macular edema, the most frequent cause of decreased vision in diabetic retinopathy, appears to be more common in Blacks. Risk factors for developing macular edema include poorly controlled hypertension, hyperglycemia, and duration of disease. The higher prevalence of hypertension in Blacks may contribute to the increased severity of diabetic retinopathy. Further evaluation is necessary to determine the influence of race on the severity of diabetic retinopathy.

Spontaneous Regression (Autoinfarction) of Proliferative Sickle Retinopathy

Of 45 patients with proliferative sickle retinopathy in stages III, IV, and V, nine patients (eight with hemoglobin SC disease, one with sickle cell thalassemia) showed spontaneous regression (autoinfarction) of retinal sea fans. One mechanism involved in autoinfarction of neovascular tissue is progressive, centripetal retraction of the anterior vascular arcade of the peripheral retina. In addition, vitreous traction on feeder vessels may result in sluggish blood flow and occlusion of these vessels, or may tear the sea fan completely away from its feeder vessels. In view of the many incidences of vitreous hemorrhages that occur in patients with proliferative retinopathy, however, we recommend treatment of neovascularization rather than prolonged observation.

Myopic Macular Degeneration

Light from the object you are looking at directly is focused onto a tiny area of the retina called the macula at the back of the eye. The macula is about 4mm across and is responsible for detailed central vision and most colour vision. It provides the vision you need to read, recognise faces, drive a car, see colours clearly, and any other activity that requires detailed, fine vision. The rest of the retina gives you side vision (peripheral vision).