In North America, most retinal detachment surgeries are performed by retinal specialists.Proliferative Vitreoretinopathy and Giant Retinal Tears These patients may benefit from direct referral to a retinal specialist to avoid the delay associated with additional examination by a general ophthalmologist or optometrist. Thus, patients with extramacular detachment require more urgent management, even though they may present with excellent central visual acuity. When the macula detaches, the potential to maintain normal vision is often lost. If the patient exhibits acute visual field loss, whether subjective or demonstrable by confrontation, immediate referral is recommended. If the patient has additional risk factors (e.g., myopia, previous cataract surgery, trauma, retinal detachment in the fellow eye, family history of detachment), suspicion of retinal detachment is heightened. All patients with acute onset of flashes or floaters should be referred to an ophthalmologist ( Table 4). Prompt referral and evaluation of patients who are suspected of having retinal tears are important because treatment of retinal tears is highly effective in preventing retinal detachment, and because progression of retinal detachment into the macula typically results in permanent visual loss. Fixed field defects of variable size occur in patients with retinal vascular occlusion these patients often have hypertension or other atherogenic diseases, lack acute flashes, floaters, or other risk factors for retinal detachment, and may exhibit flame hemorrhage or arteriolar plaques by ophthalmoscopy. Visual loss from a transient ischemic attack may be unilateral, but is episodic, not persistent or progressive as in cases of retinal detachment, and may be accompanied by other neurologic symptoms. Even in patients with severe field loss caused by cerebral disease, the macula is spared and central vision persists. Visual field loss caused by retinal detachment begins suddenly, usually in the periphery, and progresses toward the central visual axis over hours to weeks patients may describe this as a dim “shadow” or “curtain.” Field loss caused by stroke or other central nervous system processes is always bilateral, stable, and homonymous, due to crossing of nasal retinal projections at the optic chiasm. However, in 10 to 15 percent of patients with symptomatic posterior vitreous detachment, a retinal flap tear or hole forms as the vitreous pulls away from the retina, especially in the periphery where the retina is thinner ( Figure 2c). 4 Posterior vitreous detachment is harmless by itself, though bothersome floaters (blood or retinal pigment epithelium cells) may develop and persist. Approximately one in four persons develops a posterior vitreous detachment between 61 and 70 years of age, and nearly two thirds have posterior vitreous detachment after 70 years of age. 3 Eventually, the vitreous partly separates from the retinal surface, which is known as posterior vitreous detachment ( Figure 2b). As persons age, this macromolecular network begins to liquefy and collapse, the vitreous shrinks, and vitreo-retinal traction develops. The vitreous humor is a hydrated gel whose structure is maintained by a collagenous and mucopolysaccharide matrix ( Figure 2a). The key pathogenetic steps of rhegmatogenous retinal detachment are illustrated in Figure 2. The third and most common type is rhegmatogenous retinal detachment.
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