Retinal detachment is a sight threatening condition with an incidence of approximately 1 in 10000. (1,2) Before the 1920’s, this was a permanently blinding condition. In subsequent years, Jules Gonin, MD, pioneered the first repair of retinal detachments in Lausanne, Switzerland. (3) In 1945 after the development of the binocular indirect ophthalmoscope by Charles Schepens, MD, techniques for retinal detachment repair improved. In the last 50 years techniques in scleral buckling, pneumatic retinopexy and vitrectomy have made the repair of retinal detachments more manageable with better visual outcomes.
Lattice degeneration, peripheral retinal breaks, pathologic myopia, previous intraocular surgery, trauma, previous retinal detachment, and family history are all risk factors for retinal detachment. Lattice degeneration is considered the most important peripheral retinal degeneration process that predisposes to a rhegmatogenous retinal detachment. (4) Other peripheral lesions predisposing to retinal detachment include Ora bays, meridional folds and complexes, and cystic retinal tufts.
Normally, the retinal pigment epithelium is able to maintain adhesion with the overlying neurosensory retina through a variety of mechanisms. These mechanisms include active transport of subretinal fluid and interdigitation of outer segments and the retinal pigment epithelium microvilli. With retinal detachment, these mechanisms are overwhelmed leading to separation of the neurosensory (inner layers) retina from the retinal pigment epithelial layer.
Retinal detachment occurs when subretinal fluid accumulates between the neurosensory retina and the retinal pigment epithelium. This process can occur in three ways. One mechanism involves a break in the retina allowing vitreous to directly enter the subretinal space. This is known as a rhegmatogenous retinal detachment. A second mechanism involves proliferative membranes on the surface of the retina or vitreous. These membranes can pull on the neurosensory retina causing a physical separation between the neurosensory retina and retinal pigment epithelium. This is called a traction retinal detachment. The third mechanism for retinal detachment is due to accumulation of subretinal fluid due to inflammatory mediators or exudation of fluid from a mass lesion. This mechanism is known as a serous or exudative retinal detachment.
Rhegmatogenous retinal detachments are often due to retinal tears associated with posterior vitreous detachment or trauma. Tractional retinal detachments can be seen in proliferative retinopathy due to diabetic disease, sickle cell and other disease processes leading to neovascularization of the retina. Tractional retinal detachments can also be due to proliferative vitreoretinopathy after trauma or surgery. Serous detachments are caused by a number of inflammatory, or exudative retinal disease processes such as Sarcoidosis or choroidal neoplasms.
Patients with known risk factors for retinal detachment should have dilated fundus examination with scleral depression. Protective eyewear is recommended for individuals with high myopia that participate in contact sports. Patients undergoing cataract surgery should be counseled about the importance of reporting symptoms of retinal tears and detachments.
Patients who present with symptoms of new onset photopsias, floaters or visual field loss should be suspected of having a retinal tear or detachment until proven otherwise. Important information in the history includes onset of symptoms, duration of decreased visual acuity, metamorphopsia, any prior trauma, prior surgery, intraocular inflammation, hemorrhage, glaucoma and a complete past medical history and review of systems.
Visual acuity, pupillary examination, visual field testing and intraocular pressure measurement are important parts of the predilated ophthalmic examination to evaluate patients with symptoms of retinal detachment. Additional examination to include color vision and ocular motility should be tailored according to the history provided.
Slit lamp examination of the anterior segment should be completed prior to dilation. Examination of the vitreous for pigment cells followed by a thorough fundus examination to include indirect ophthalmoscopy with scleral depression should be completed. A detailed drawing describing the detachment with location of retinal pathology should be documented.
If there is no view to the posterior pole such as in hemorrhage or media opacity, ultrasound should be used to evaluate the retinal status.
Rhegmatogenous retinal detachment has a characteristic appearance differentiating it from a tractional or serous detachment. A rhegmatogenous retinal detachment has a corrugated appearance and undulates with eye movements. Tractional detachments have smooth concave surfaces with minimal shifting with eye movements. Serous detachments show a smooth retinal surface and shifting fluid depending on patient positioning.
Laboratory testing is only indicated in traction or exudative detachments. If a cause for the traction retinal detachment cannot be determined by history, further laboratory analysis may be required to determine if diabetes, sickle cell, carotid disease or another systemic or ocular process is the source for proliferative retinopathy.
Since exudative detachments may be due to a systemic or ocular inflammatory process, laboratory investigation may be indicated.
Fluorescein angiography may be indicated to further clarify exudative processes such as macular degeneration, central serous chorioretinopathy, and Vogt-Koyanagi-Harada syndrome or other uveitic processes. Ultrasound is a useful imaging modality to evaluate choroidal masses or posterior scleritis.
The differential diagnosis of retinal detachment includes retinoschisis or choroidal mass. Retinoschsis can be distinguished from retinal detachment by appearance on ultrasound, uptake of photocoagulation and absolute versus relative scotoma in the former. Choroidal masses can be distinguished from retinal detachment by observing the characteristics of the A-scan when imaging with ultrasound.
Once a retinal detachment has been identified, one must determine what type of detachment is present. For serous detachments, management is nonsurgical. Any inflammatory disease or underlying mass should be identified and treated if possible.
Surgical management is indicated in rhegmatogenous and tractional detachments. For rhegmatogenous detachments, all retinal breaks should be identified, treated and closed. Techniques for repair include pneumatic retinopexy, scleral buckle or vitrectomy. Pneumatic retinopexy involves the injection of an intraocular gas bubble along with retinopexy using cryotherapy or laser. An important part in the successful repair of retinal detachment with pneumatic retinopexy involves head positioning so that the gas bubble tamponades the retinal tear. Pneumatic retinopexy is typically only used with retinal detachments due to retinal tears in the superior eight clock hours and involving a single break less than one clock hour. Scleral buckles are silicone bands placed around the globe under the extraocular rectus muscles to relieve any traction and support retinal tears. Pars plana vitrectomy with 20 gauge, 23 gauge and 25 gauge instruments involves removal of the vitreous and flattening of the retina through a direct intraocular process. In tractional detachments, traction needs to be relieved with vitrectomy or scleral buckling.
Proliferative retinopathy (PVR) is the most common cause of repair failure and occurs in about 8–10% of patients undergoing primary retinal detachment repair.(5,6) Risk factors for PVR include giant retinal tears, retinal detachments involving more than 2 quadrants, previous retinal detachment repair, cryopexy, vitreous hemorrhage or choroidal detachment. PVR requires surgical intervention to release the traction caused by membranes and has a poor visual prognosis. (7)
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