History and exam

Key diagnostic factors

common

loss or deterioration of central vision

Sudden and significant; it is often the leading symptom on presentation.

For eyes with nonrhegmatogenous RD, visual loss may be sudden or more gradual; in case of an exudative RD, the central vision may remain very good for a long time despite the presence of submacular fluid. For eyes with a hemorrhagic RD, a sharply circumscribed central scotoma presents acutely.

flashes of light

Preceding symptoms such as flashes of light may be elicited on questioning. The flashes are typically seen in the temporal visual field, and they are easiest to notice in a dark environment.

The stimulated retina evokes the sensation of discrete points of light, called phosphenes, in response to a stimulus from light or a tractional/mechanical force.[39]

uncommon

loss of peripheral visual field

If noticed before the central visual acuity deteriorates, it is usually described by the patient as a dark veil, cloud, or curtain that suddenly blocks his or her view.

For eyes with tractional RD, visual loss is a very gradual process.

Other diagnostic factors

common

floaters

Indicate vitreous opacity due to aging. However, certain presentations may suggest retinal pathology.

The sudden onset of a large central floater suggests the presence of posterior vitreous detachment (PVD) and an operculum.[39]

Numerous small floaters are suggestive of retinal hemorrhage.[39]

Risk factors

strong

posterior vitreous detachment

Presumed posterior vitreous detachment (PVD) with no sensation of flashes (asymptomatic PVD) has a low risk of rhegmatogenous RD: <1% per year over long-term follow-up.[13][14]

However, the risk increases dramatically if symptoms occur.

increasing age

The risk of rhegmatogenous RD increases with age due to structural changes of the vitreous gel.[15][16]

Vitreous syneresis increases in both incidence and severity with age, even in the absence of another contributing risk factor. Syneresis and/or vitreoschisis in the presence of vitreoretinal adhesion is prone to transmit traction forces onto the retina as the gel moves, thus promoting retinal breaks.

myopia

Increases the risk of nontraumatic rhegmatogenous RD in proportion to the increase in axial length.[16][17]​​​ ​High myopia (exceeding -8 D) may accelerate the breakdown of the normal vitreous gel structure and weaken the retina by stretching the eye wall.​[14][18]​​ Myopia is expected to increase in importance as a risk factor among children and adults due to the global epidemic of progressive myopia.[19]​​

previous cataract surgery

RD typically occurs approximately 1.5 to 2.3 years after cataract surgery due to postsurgical anatomic and biochemical alterations in the vitreous.[16][20]​​

​Lens removal allows the vitreous body to move forward freely in the increased space, accompanied by syneresis which is also accelerated.[21] The risk also increases dramatically after complications, such as vitreous loss, due to the extra traction exerted on the vitreous base during vitreous prolapse or its trimming. Nd:YAG capsulectomy also appears to increase risk, probably by accelerating the degeneration of vitreous gel structure.[22]

trauma

Contusions and various open globe ocular injuries that alter the structure of either the vitreous or the retina increase the risk of rhegmatogenous RD.​[17][19]​​[23]

Depending on the type of trauma, rhegmatogenous RD may occur due to traction within days to weeks of an open globe injury or months to years of a contusion.

previous ophthalmic surgery

Surgical interventions such as scleral buckling, heavy cryopexy, or laser retinopexy are rare risk factors for exudative RD.[3][4]​ Risk may also increase with keratorefractive surgery, though this only appears to exist among patients with high myopia (including patients with phakic intraocular lenses).[17]

intraocular tumor

Coexistent tumors such as choroidal melanoma or retinoblastoma are recognized risk factors for exudative RD.[2]

vitreous hemorrhage

Risk depends on the cause of the bleeding.[24]

Vitreous hemorrhage and rhegmatogenous RD may have a weak (e.g., diabetes) or strong (e.g., trauma) association, or even a reverse relationship (i.e., the vitreous hemorrhage may result from a retinal vessel tearing when the rhegmatogenous RD forms).

affected fellow eye

Fellow eyes have a 10% increased risk of developing rhegmatogenous RD, especially in cases with peripheral retinal lesions.[25][26]

diabetes mellitus

A common cause of tractional RD, and the second major cause of vision loss in patients with diabetes (after diabetic retinopathy).

retinopathy of prematurity

Severe retinopathy of prematurity increases the risk of RD. This increased risk persists throughout life.[27]

weak

ocular inflammation/infection

Rhegmatogenous RD may result from retinal necrosis after herpes zoster or herpes simplex infection or from a secondary scarring process (e.g., Toxocara infection).[28][29]

Congenitally transmitted or acquired ocular toxoplasmosis (Toxoplasmosis gondii) is the most common cause of posterior uveitis in children, causing RD in 6% and retinal breaks in another 5%.[19]

Exudative RD may be due to an inflammatory processes in the vitreous, retina, uvea, or posterior sclera (e.g., Vogt-Koyanagi-Harada syndrome).[2]​ Other causes include vascular anomalies (e.g., Coats disease) and central serous chorioretinopathy. The subretinal fluid is usually more viscous than in other types of RD.

peripheral retinal degeneration

Peripheral areas of the retina become thinner, making them weaker and more prone to developing tears or holes.[14]​ The risk of rhegmatogenous RD depends on the type of degeneration.

Oral bay, meridional fold, lattice, or white (without pressure) forms are weak risk factors.[13][30][31][32][33]

Retinoschisis and cystic tuft degeneration represent strong risk factors.[34][35]

anatomic abnormality

Eyes with certain pathologies (e.g., optic nerve pit) can accumulate subretinal fluid, with patients only reporting symptoms when the fluid passes under the macula.

age-related macular degeneration

Rarely, the neovascular complex results in massive bleeding, which can break through into the vitreous.

phosphodiesterase-5 inhibitor use in men

Case reports and small epidemiologic studies indicate potential risk of ocular adverse events, including serious RD, when using phosphodiesterase-5 inhibitors (e.g., sildenafil, tadalafil, vardenafil). One large cohort study has reported a significant incidence rate ratio of 2.58 (3.8 cases per 10,000 person-years).[36]

genetic and vascular causes in childhood

Various genetic and vascular conditions that arise during childhood can increase the risk of RD.[19]​ These include familial exudative vitreoretinopathy, Norrie disease, incontinentia pigmenti, persistent fetal vasculature, x-linked retinoschisis, Stickler syndrome, Marfan syndrome, and nontraumatic inferotemporal retinal dialysis.

childhood tumors

Various tumors that arise during childhood can increase the risk of RD.[19]​ Retinoblastoma is associated with increased risk when patients undergo globe-conserving treatment (50% exudative, 50% rhegmatogenous). Less common causes include choroidal hemangioma, medulloepithelioma, and choroidal osteoma.

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