Retinal Toxicity Induced by Systemic Drugs

Abstract

The retina is the light-sensitive tissue that lines the inside of the eye. The optical elements within the eye focus an image onto the retina of the eye, initiating a series of chemical and electrical events within the retina. Nerve fibers within the retina send electrical signals to the brain, which then interprets these signals as visual images. The retina is relatively protected from systemic drug administration because of the blood-retinal barrier, a highly selective mechanism adapted to providing a regulated homeostatic environment for this highly specialized tissue. However, a number of drugs have been associated with retinal toxicity. The toxicity of systemic drugs has different mechanisms. This toxicity can be grouped into: 1. Pigmentary retinopathies:. • Chloroquine, hydroxychloroquine: Retinal effects include retinal parafoveal granularity of the retinal pigment epithelium (RPE) with loss of the foveal light reflex and bilateral paracentral visual field change, best seen with red test (early in disease); bull's-eye appearance of the macula (late in the disease); vascular attenuation and peripheral fine granular pigmentary changes. • Thioridazine: Thioridazine toxicity has been described as a progressive chorioretinopathy', but this designation can be misleading. During the first year after thioridazine exposure retinal pigmentation evolves from a granular to a patchy or nummular appearance. However, visual function and the electroretinogram typically improve during this period. Some cases may show chorioretinal atrophy and functional loss many years later, but there is little evidence for ongoing drug-related progression. Late atrophy may represent degeneration of cells that were injured subclinically at the time of initial drug exposure. Although thioridazine toxicity produces an evolving pigmentary disturbance, functional changes must be monitored independently of fundus appearance.