A 66-Year-Old Woman With Central Vision Loss

Ronald C Gentile, MD; Brooke Nesmith, MD

Disclosures

November 02, 2016

Discussion

Choroidal neovascularization (CNV) is a sight-threatening complication of many retinal diseases that causes degeneration of the macula. CNV is the pathologic growth of new abnormal blood vessels that originate from the choroidal circulation. These new blood vessels grow through breaks in the Bruch membrane and enter the sub-RPE and/or subretinal space.[1]

The exact cause of CNV is not known, but it is believed to be the result of an imbalance in the homeostasis of the RPE–Bruch membrane–choriocapillaris complex that results from tissue expression of molecules that favor angiogenesis and the development of new blood vessels.[2] CNV contains blood vessels that grow abnormally and are prone to leak, bleed, and fibrose, which results in damage to the overlying neurosensory retina and photoreceptor layer, and is a cause of significant and permanent vision loss.

One primary stimulus for the development of CNV is believed to be hypoxia, which induces a complex angiogenic process that involves the interplay and interaction of different molecules.[3] The most well-known proangiogenic molecule at this time is vascular endothelial growth factor (VEGF), and anti-VEGF intravitreal injections are the current standard treatment for CNV.[3] Additional molecules have been implicated in the development of CNV, including insulin-like growth factor 1, fibroblast growth factor 2, pigment epithelium-derived factor, and endostatin.[4] Research is currently underway to develop CNV therapies that target these molecules.[4]

Many retinal diseases are complicated by CNV. To determine the underlying etiology of CNV, a good history must be obtained and the patient's complete ocular examination findings, as well as other systemic and physical features, must be considered.

The most common cause of an elderly patient presenting with CNV in the United States is exudative age-related macular degeneration (AMD), or wet AMD. Exudative AMD accounts for only 10% to 20% of all cases of AMD; the other 80% to 90% are nonexudative, or dry, AMD. However, exudative AMD is responsible for more severe vision loss.[5] In this patient, however, dilated fundus examination of both eyes did not reveal any of the hallmark features associated with AMD, such as drusen (yellow subretinal deposits) and RPE irregularities, such as hyperpigmentary or hypopigmentary changes.

Another form of macular degeneration, idiopathic polypoidal choroidal vasculopathy (IPCV), is more common in Asian and African American patients, such as the patient in this case. IPCV is associated with a characteristic choroidal lesion that consists of a network of choroidal vessels ending in an aneurysmal bulge.[6] This characteristic vascular lesion is best seen on indocyanine green angiography. Clinically, these appear as reddish-orange polyp-like lesions. However, the patient in this case did not present with any of these features.

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