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Ophthalmology – Choroidal Neovascularization
Choroidal neovascularization (CNV) refers to the formation of abnormal new blood vessels originating from the choroid that penetrate through defects in Bruch’s membrane into the subretinal space. These vessels often form a fibrovascular complex that is fragile and prone to leakage, leading to accumulation of fluid, lipid exudation, and hemorrhage. Over time, this process can result in the formation of a disciform scar and permanent vision loss. CNV is not a standalone disease but a complication of many underlying disorders affecting the retinal pigment epithelium (RPE)–Bruch’s membrane–choriocapillaris complex.
Epidemiologically, the incidence and prevalence of CNV vary depending on the underlying condition. It is most commonly associated with age-related macular degeneration (AMD), which is the leading cause of irreversible vision loss in individuals over 65 years in developed countries. Advanced AMD affects tens of millions of people worldwide. The likelihood of developing CNV increases significantly with age and is influenced by systemic and genetic factors.
Risk factors depend largely on the underlying disease. In AMD-related CNV, advancing age, smoking, hypertension, hyperlipidemia, obesity, and reduced physical activity play significant roles. A strong family history also increases risk, reflecting a genetic predisposition. Genetic studies, including twin studies and genome-wide analyses, support the multifactorial inheritance pattern of AMD and its complications such as CNV.
The pathophysiology involves disruption of Bruch’s membrane, which allows neovascular tissue from the choriocapillaris to grow into the subretinal space. This process is driven by proangiogenic factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor, and other inflammatory mediators. CNV can be classified based on its location relative to the RPE, including type 1 (sub-RPE), type 2 (subretinal), or mixed forms.
Clinically, patients typically present with sudden onset of decreased central vision, often accompanied by metamorphopsia and paracentral scotomas. On examination, findings may include RPE elevation, subretinal fluid, lipid exudates, hemorrhage, and a gray-green lesion beneath the retina. These features reflect the leakage and instability of the neovascular membrane.
Diagnosis is primarily made using imaging techniques. Fluorescein angiography helps identify leakage patterns and differentiate between classic and occult CNV. Optical coherence tomography (OCT) is essential for detecting structural changes such as subretinal fluid, intraretinal edema, and RPE detachment, and is also useful for monitoring response to treatment.
Management has evolved significantly with the advent of anti-VEGF therapy, which is now the standard of care. Intravitreal injections of agents such as ranibizumab or bevacizumab inhibit neovascular growth and reduce leakage, often stabilizing or improving vision. In selected cases, particularly extrafoveal lesions or non-AMD etiologies, laser photocoagulation or photodynamic therapy may be considered. Surgical options such as vitrectomy are reserved for complications like submacular hemorrhage.
The prognosis depends on the location of the lesion and the extent of damage at presentation. Early detection and treatment significantly improve visual outcomes. However, recurrence is common, requiring ongoing monitoring with tools such as the Amsler grid and serial imaging.
Complications include subretinal fibrosis, persistent or recurrent fluid accumulation, and, in severe cases, massive subretinal hemorrhage that can lead to retinal detachment and profound vision loss.
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