Chapter 27
Rhegmatogenous Retinal Detachment
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A rhegmatogenous retinal detachment (RRD) occurs when fluid from the vitreous cavity passes through a break in the neurosensory retina into the potential space between the retinal pigment epithelium (RPE) and the neurosensory retina. Throughout this chapter, the terms neurosensory retina and retina are used interchangeably. Although retinal breaks are present in 5% to 10% of the general public, most never lead to an RRD.1–7 In the general population, the estimated incidence of RRD is 1 in 10,000.8 After an RRD in one eye, the risk of RRD is estimated to be approximately 10% in the fellow eye.9–12

Various characteristics of a retinal break and the remaining ocular structures determine whether a retinal break will remain asymptomatic or cause an RRD. This chapter discusses the pathogenesis of RRD and the predisposing factors. The prophylactic management of retinal tears and the treatment of RRD are introduced as well.

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Many retinal breaks that lead to RRDs are precipitated by posterior vitreous detachments (PVDs). As one ages, biochemical changes in the matrix of the vitreous gel cause progressive liquefaction (syneresis) of the central vitreous.13–15 Throughout the vitreous cavity, liquefied cavities develop and ultimately coalesce. In many patients, the posterior cortical vitreous develops breaks that allow liquefied vitreous to pass into the potential space between the posterior hyaloid face and the retina. Once this occurs, a partial PVD can progress to a complete PVD rapidly.13 At the vitreous base, the cortical vitreous adheres strongly to the retinal surface. Vitreous traction at the posterior aspect of the vitreous base predisposes to retinal breaks at this location (Fig. 1).16

Fig. 1. Vitreous traction at the posterior aspect of the vitreous base predisposes to retinal breaks at this location. Both flap tears (horseshoe tears) and operculated tears may occur. (Courtesy of Hilel Lewis, MD, Cleveland, OH, and Allan Kreiger, MD, Los Angeles, CA.)

When patients experience an acute PVD, they often note the onset of floaters. These floaters are often shadows cast by remnants of glial tissue adherent to the posterior hyaloid face.17 Up to half of patients who experience an acute PVD note the onset of photopsias (flashes of light) in addition to the floaters.18–20


The incidence of retinal tears after a symptomatic PVD is approximately 15%.18,20–25 Up to 20% of patients note the presence of a large number of small floaters, which usually correspond to a vitreous hemorrhage. Such hemorrhages frequently result from a torn blood vessel on the surface of the retina or optic nerve.20,22,24,26 When a PVD is accompanied by any vitreous hemorrhage, the incidence of retinal tears is approximately 70%. By comparison, only 2% to 4% of eyes have tears when a PVD is not accompanied by vitreous hemorrhage.18,20–25 The presence of pigment clumps in the anterior vitreous or anterior chamber (“tobacco dust”) alerts the clinician to a high likelihood of a retinal tear. This finding indicates the presence of RPE cells that have passed through a retinal break.

When a patient has potential symptoms of a PVD, a complete ocular examination is essential, including indirect ophthalmoscopy with scleral depression or fundus biomicroscopy with a three-mirror contact lens. When a vitreous hemorrhage obscures the peripheral retina, B-scan ultrasonography can be used to rule out an RRD and to evaluate a variety of other pathologic conditions. Although a skilled ultrasonographer can identify some (usually larger) retinal tears, a negative study does not rule out a retinal tear. Careful follow-up is suggested for such patients until the vitreous hemorrhage has cleared enough to allow a complete retinal examination. If an RRD or tear is present in the setting of dense vitreous hemorrhage, pars plana vitrectomy is generally indicated to obtain a view of the retina and to allow treatment of the underlying pathology.

Some authors have estimated that only 1 in 70 eyes with retinal breaks goes on to develop an RRD.6,7 There are several mechanisms in place that normally keep the retina attached. The physical interdigitation of the apical portions of the RPE cells with the photoreceptors of the neurosensory retina is one such mechanism.27 Actin contained in the cell sheaths of the RPE cells is believed to play an active role in this process.28 A second active mechanism is the removal of subretinal fluid by the RPE. A variety of ion channels and cotransporters are involved in this process.29

Several passive mechanisms also contribute to keeping the retina attached. First, the interphotoreceptor matrix between the RPE and the neurosensory retina acts as a biologic glue that secures the two surfaces.30 Further resistance to the development of an RRD is provided by the high oncotic pressure in the protein-rich choroid that promotes the absorption of fluid from the inner ocular structures.28 Because the retina offers hydraulic resistance to the diffusion of fluid from the vitreous to the choroid, the relative pressure of the vitreous helps to hold the retina in place.31–33 Finally, in eyes with little vitreous liquefaction, the formed cortical vitreous impedes the flow of fluid into the subretinal space in the event of a retinal break.34


When a retinal break occurs, several factors can catalyze detachment of the retina. Retinal breaks associated with vitreous traction are referred to as tears, and they tend to cause RRDs.9,35,36 In particular, flap tears are associated with a higher risk of RRD than other retinal breaks because the breaks are held open, facilitating the flow of fluid from the vitreous cavity into the subretinal space (Fig. 2). Also, liquefied vitreous can pass through retinal breaks more easily than more formed vitreous, especially if the flow of the vitreous is turbulent.37 In the case of an operculated retinal tear, the traction on the surrounding retina is relieved, and the risk of subsequent RRD is minimized (Fig. 3). A retinal dialysis is a tear at the junction of the neurosensory retina and the nonpigmented epithelial layer of the pars plana. Although not strictly a retinal tear, a retinal dialysis allows liquefied vitreous to enter the subretinal space, causing an RRD. Retinal dialyses frequently result from blunt trauma to the globe, and they are most likely to occur inferotemporally or superonasally (Fig. 4).38–40

Fig. 2. A. Flap (horseshoe tear) with a rolled posterior edge. Bridging vessels can be seen. B. A flap tear associated with a small rhegmatogenous retinal detachment. (A courtesy of William E. Benson, MD, Philadelphia, PA.)

Fig. 3. Operculated break with a cuff of subretinal fluid.

Fig. 4. A. Traumatic retinal dialysis resulting from blunt trauma. B. Retinal detachment in the same eye.


Retinal holes arise from atrophy of the retina, or tangentially oriented forces that create a dehiscence in the retina. Atrophic retinal holes are prone to occur in areas of lattice degeneration and in the walls of retinoschisis cavities. Atrophic holes are far less prone to cause RRD than are retinal tears.6,9,41,42

Macular holes likely result primarily from tangential and to a lesser extent anteroposterior traction from the overlying cortical vitreous.43,44 It is unusual for a macular hole to lead to an RRD, except in highly myopic globes.45,46

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Lattice degeneration of the retina is characterized by focal thinning of the inner retinal layers associated with liquefaction of the overlying vitreous and strong vitreous attachments to the margins (Fig. 5). Hyalinized blood vessels in areas of lattice often take on the characteristic lattice appearance for which this condition is named. Areas of lattice are frequently elliptical and oriented parallel to the ora. These patches are often multiple, and they occur most often in the superior and the inferior retinal periphery.47 Some variants of lattice are oriented perpendicular to the ora, often straddling the peripheral retinal vessels—a configuration referred to as radial or meridional lattice.

Fig. 5. A. Lattice degeneration with pigmentation. Hyalinized blood vessels are seen in the lattice. B. Photomicrograph of lattice degeneration demonstrating focal thinning of the inner retinal layers and associated liquefaction of the overlying vitreous with vitreous attachments to the margins. (Courtesy of William Tasman, MD, Philadelphia, PA.)

One third of all RRDs are associated with lattice, although lattice is estimated to occur in only 6% to 10% of the general population.4,23,48–51 This condition is bilateral in one third of those affected, and it is more prevalent in myopic versus hyperopic eyes.4,23,48–51 Two forms of retinal breaks are associated with lattice: atrophic holes in the lattice, and flap tears at the posterior border or at the ends of the patch.

Atrophic holes occur in about one third of the patients with lattice and are frequently present in young patients. RRD is a rare complication of atrophic holes in lattice; when it occurs, it tends to progress slowly.4,51,52 Due to their relatively benign nature, treatment is rarely warranted for these atrophic holes. Horseshoe tears associated with lattice, in contrast, have a more ominous prognosis. The retinal flap is generally adherent to the detached cortical vitreous face, and this holds the tear open. These flap tears, especially when they are symptomatic, can cause rapidly progressive RRD.9,36,42,51,53


Although present in only 10% or less of the general population, significant myopia is associated with 42% of all RRDs.23,50 This higher incidence of RRD among myopic eyes has been attributed to a variety of causes. The incidence of PVD is higher for any given age group in people with myopia compared with those with emmetropia and hyperopia.14,54 Further, the incidence of lattice degeneration is increased in myopes.4 Finally, the peripheral retina is more vulnerable to developing retinal tears in myopic eyes.28 When symptomatic retinal tears are present in patients with moderate to high myopia, prophylactic treatment should be undertaken.


Cataract extraction is an independent risk factor for RRD. The incidence of RRD after intracapsular cataract extraction is greater than after extracapsular cataract surgery. After uncomplicated surgery, the risk of RRD is estimated to be 2% to 5% with intracapsular surgery and approximately 1% with extracapsular. In contrast, the incidence of RRD is 0.01% to 0.05% in the general phakic population.8,55–58

Vitreous loss during cataract surgery increases the risk of RRD 4.5-fold to approximately 5%.56,59 Likewise, YAG capsulotomy increases the risk of RRD 3.9-fold.60–62 Other risk factors that increase the risk of RRD with cataract extraction include myopia, young age, white race, prior RRD surgery, and RRD in the fellow eye.18,56,57,63,64

The causative retinal break is most frequently located superotemporally in phakic, pseudophakic, and aphakic RRDs. Nonetheless, both superonasal breaks and breaks that go undetected at the time of intervention are more common after cataract extraction.65–68 The tendency for breaks to be smaller and more anterior, combined with the postsurgical changes in the anterior segment, combine to make tears difficult to localize. Overall, the rate of missed breaks after cataract surgery ranges from 5% to 16% versus 2% to 5% in phakic patients.50,68,69 Although careful localization of breaks is always a critical step in RRD repair, particular attention must be paid in patients who have had cataract extraction.

The risk of RRD in the fellow eye is 26% to 41% for patients who are aphakic.64,70 In patients who have had congenital cataracts removed from both eyes, the risk of developing an RRD in the fellow eye after RRD approaches 70%; thus, these patients must have meticulous follow-up.71


Three quarters of traumatic RRDs occur in males, largely because they are more likely than females to engage in contact sports or fighting.72,73 The leading cause of RRD in children and adolescents is blunt trauma.72–74 Blunt trauma generally compresses the contents of the eye in an anteroposterior direction, causing a compensatory expansion of the globe in an equatorial plane. Despite the elastic nature of the vitreous, rapid compression of the eye due to trauma can transmit severe traction to the vitreous base, causing many types of pathology. Linear or horseshoe tears at the posterior vitreous base, tears in the nonpigmented epithelium of the pars plana at the anterior vitreous base, and retinal dialyses are the most common forms of tears that follow such trauma.75–77

The most common locations for retinal breaks due to trauma are inferotemporal and superonasal.76,78 Most traumatic retinal breaks are believed to occur at the time of impact.75,79 As a result of the formed nature of the vitreous in young patients, the progression of RRD after trauma tends to be relatively slow.

Blunt trauma can also cause focal areas of retinal necrosis directly corresponding to the site of impact and traumatic macular holes, which have been attributed to contrecoup damage.28

Penetrating and perforating injuries frequently cause RRD. In these cases, the prognosis depends on the extent of the injury.76,80–82 The management of these injuries is beyond the scope of this chapter.


A variety of conditions in which fibrovascular proliferation occurs have a higher risk of RRD. In proliferative diabetic retinopathy, neovascularization and fibroglial tissues proliferate in response to retinal ischemia. As the vitreous contracts with PVD, these abnormal proliferations can place traction on the retinal surface, causing either a simple tractional retinal detachment or a combined tractional and rhegmatogenous retinal detachment (Fig. 6). Fibrovascular proliferation occurring in retinopathy of prematurity, in proliferative sickle cell retinopathy, and in the aftermath of retinal vein occlusions can cause RRD through a related mechanism.

Fig. 6. Tractional retinal detachment in a patient with proliferative diabetic retinopathy.


Infections that cause full-thickness retinal necrosis can lead to RRD. Cytomegalovirus retinitis, acute retinal necrosis syndrome, postoperative bacterial endophthalmitis, and other retinal infections may cause retinal holes to form that may ultimately lead to RRD.83


HEREDITARY HYALOIDEORETINOPATHIES. This group of conditions is typified by accelerated vitreous syneresis that leads to a classic “optically empty” vitreous in which fibrous bands and membranes are often present. Common features of these hyaloideoretinopathies include myopia, cataract, optic atrophy, RPE and choroidal atrophy, lattice degeneration, retinoschisis, and glaucoma.61,70,84

The first group of hyaloideoretinopathies characterized by these ocular findings includes Wagner's disease, erosive vitreoretinopathy, and Jansen's disease. Of these, erosive vitreoretinopathy and Jansen's disease both predispose to RRD.

Stickler's syndrome is a rare inherited hyaloideoretinopathy associated with several systemic findings. The systemic associations include midfacial flattening, cleft palate, Pierre Robin malformation, and a variety of skeletal abnormalities. The presence of Stickler's syndrome signifies a strong risk of RRD (Fig. 7).

Fig. 7. Photograph of a fibrous band in the “optically empty” vitreous of a patient with Stickler's syndrome.

CONGENITAL (JUVENILE) RETINOSCHISIS. The presence of a characteristic spokelike pattern of foveal change alerts the examiner to this condition. In the peripheral retina, schisis tends to develop between the nerve fiber layer and the balance of the retina (Fig. 8). Holes commonly develop in the inner wall of these schisis cavities but are generally inconsequential. In contrast, holes in the outer wall of these cavities are rare but can lead to RRDs.28,85

Fig. 8. A. Characteristic spokelike pattern of foveal change in X-linked juvenile retinoschisis. B. Peripheral retinoschisis with a vessel bordered by inner-wall holes on either side. (Courtesy of William Tasman, MD, Philadelphia, PA.)

EHLERS-DANLOS SYNDROME. This autosomal dominant condition is characterized by abnormal collagen throughout the body. These patients are predisposed to both myopia and RRD.

GOLDMANN-FAVRE SYNDROME. This is an autosomal recessive condition in which cataract, peripheral and macular retinoschisis, radial lattice degeneration, accelerated vitreous syneresis, and retinitis pigmentosa-like peripheral retina changes are evident. These patients are prone to RRDs, which often prove difficult to repair.

MARFAN SYNDROME. As with Ehlers-Danlos, there is an increased risk of myopia and lattice degeneration, leading to a high incidence of RRDs. When ectopia lentis is present, cataract removal is often associated with vitreous loss, which places these patients at an even higher risk for RRD.

OTHER ABNORMALITIES. Patients with the so-called morning glory syndrome are predisposed to RRD because liquefied vitreous may pass through defects in the anomalous disc into the subretinal space. Likewise, tears present in choroidal colobomas may also cause RRD.86

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A recently detached retina loses its transparency and assumes a gray, translucent appearance. Eye movements typically cause the detached retina to undulate in a characteristic manner. Fine, irregular corrugations are usually present and are the result of intraretinal edema.87,88 The fine details of the choroidal vasculature are somewhat obscured by the overlying detached retina (Fig. 9). Within days of an RRD, outer retinal degeneration starts to occur.89,90 The magnitude of the photoreceptor damage that occurs is related to the height and the duration of the RRD.88 At this early stage, the circulation of the inner retina is not affected; thus, the inner retina remains well preserved. If the retina is reattached within a week, most of the cellular changes are reversible.91 RPE cells underlying the RRD can be released into the subretinal fluid and may pass through the retinal break into the vitreous cavity. These cells may be appreciated in the anterior vitreous, where they are known as tobacco dust.87,88,92

Fig. 9. Recent rhegmatogenous retinal detachment showing loss of the normal retinal transparency and irregular corrugations.

In 1971, Lincoff and Gieser93 reported four guidelines for locating retinal breaks causing RRDs. The propagation of an RRD is determined by the location of the causative break, anatomic barriers (i.e., the optic nerve, the ora serrata, and existing chorioretinal adhesions), and the effect that gravity has on the subretinal fluid in the upright position (Fig. 10):

Fig. 10. The configuration of a retinal detachment can help to localize the causative retinal break. A. A superior retinal detachment that crosses the 12-o'clock meridian. In total detachments or superior detachments that cross the midline, the primary hole is usually within 1 clock hour of the 12-o'clock meridian. If the detachment extends more inferiorly on either the nasal or temporal side, the causative break is usually on the same side of the 12-o'clock meridian. B. A superotemporal retinal detachment. The break lies near the superior edge of the detached retina. In superior nasal or temporal detachments, the hole lies within 1.5 clock hours of the highest border 98% of the time. C. An inferior retinal detachment. The break lies nasal to the optic nerve and the subretinal fluid extends higher nasally. In inferior detachments, the higher side indicates to which side of the disc an inferior hole lies 95% of the time. When an inferior detachment is bullous (not shown), the primary hole often lies above the horizontal meridian.93

  1. In superior nasal or temporal detachments, the hole lies within 1.5 clock hours of the highest border 98% of the time.
  2. In total detachment or superior detachments that cross the midline, the primary hole is at the 12-o'clock position or in a triangle, the apex of which is at the ora serrata and the sides of which intersect the equator 1 hour to either side of the 12-o'clock position. This occurs 93% of the time.
  3. In inferior detachments, the higher side indicates to which side of the disc an inferior hole lies 95% of the time.
  4. When an inferior detachment is bullous, the primary hole lies above the horizontal meridian.93


Progressive atrophy of all retinal layers occurs if the retina remains detached.88 A chronically detached retina takes on a smooth contour and becomes semitransparent. In some cases, cystic spaces develop in the detached retina. Atrophy and depigmentation of the underlying RPE also develop in these eyes.28 When an RRD remains static for 3 months or more, RPE metaplasia may occur at the border of the detachment. Ophthalmoscopically, this corresponds to either a pigmented or depigmented demarcation line. Most RRDs that are surrounded by a demarcation line eventually progress; nonetheless, surgical repair of these eyes has an excellent prognosis (Fig. 11).94

Fig. 11. A chronic retinal detachment with a pigmented demarcation line. Note the stippled retinal pigment epithelial changes in the area of the chronic detachment.

In very long-standing RRDs, extensive capillary nonperfusion can result, leading to peripheral retinal neovascularization.95 Moreover, intraocular pressure can rise if the trabecular meshwork becomes impeded by pigment clumps or the outer segments of photoreceptors.96,97


After RRD, proliferative vitreoretinopathy occurs in approximately 10% of cases, of which one quarter require additional surgical intervention.98,99 The severity can vary greatly.100 In its mildest form, the only findings are vitreous haze and pigment clumps (grade A). Moderate proliferative vitreoretinopathy (grade B) is manifested by early cellular proliferation, which may occur on either or both sides of the retina.101,102 The involved retina may become stiffened, and its surface may take on a wrinkled appearance. Also, the retinal vessels may become tortuous and the edge of the retinal break may become rolled. Finally, with severe proliferative vitreoretinopathy (grade C), full-thickness retinal folds (“star folds”) may occur (Fig. 12).

Fig. 12. Proliferative vitreoretinopathy with a star fold.

In moderate to severe disease, the proliferative membranes are composed mostly of dedifferentiated RPE cells; nonetheless, glial cells, fibrocytes, myofibroblasts, and macrophages may also be present.103–105 Proliferative vitreoretinopathy is most likely to occur in the inferior retina, and it is postulated that RPE cells settle out of the vitreous onto the inferior retinal surface in a gravity-dependent fashion, where they eventually cause proliferative vitreoretinopathy.106

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It is important to be able to distinguish an RRD from an exudative or a tractional retinal detachment. Likewise, an area of retinoschisis must also be differentiated from an RRD. Although the management of each of these conditions is discussed in detail elsewhere, a brief description of each condition is provided below.


A variety of inflammatory, neoplastic, and other conditions can cause a breakdown of the normal blood-retina barrier, allowing fluid to collect in the subretinal space. The surface of the detached retina is generally smooth, and the location of the detachment may shift as the patient adjusts the position of the head (Fig. 13).

Fig. 13. Peripheral detail of a bullous retinal detachment.


Vitreous membranes resulting from proliferative vitreoretinopathy, various proliferative retinopathies, or trauma may pull the retina away from the RPE. In purely tractional detachments, the retinal surface has a convex, taut configuration. No full-thickness retinal breaks would be expected to be present (see Fig. 6).


Retinoschisis occurs when the retina is split into two layers or walls by a mucopolysaccharide-rich viscous fluid. Significant senile retinoschisis, usually a split in the outer plexiform layer of the retina, is most often a bilateral process. Its smooth, dome-shaped appearance helps to differentiate it from an RRD. In contrast to the RPE atrophy seen with long-standing RRD, the underlying RPE is typically normal and devoid of demarcation lines.107,108 Unlike with RRD, tobacco dust, vitreous hemorrhage, or flap tears are not expected to be present (Fig. 14).

Fig. 14. Senile degenerative retinoschisis with outer-wall holes. (Courtesy of William E. Benson, MD.)

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Laser photocoagulation, administered with either a slit-lamp or indirect ophthalmoscopic delivery system, is an effective modality for the treatment of retinal breaks to prevent RRD. The goal of laser treatment is to seal the retina to the RPE and choroid around the break. This is accomplished by surrounding the break with two or three rows of nearly confluent laser burns. If a break occurs in a patch of lattice, the entire patch of lattice and the break should be surrounded with laser burns. A firm chorioretinal scar forms in 7 to 10 days (Fig. 15).

Fig. 15. A. A fairly posterior retinal flap tear. B. The same tear after laser photocoagulation. C. Another horseshoe tear adjacent to a patch of pigmented lattice. Both the tear and the adjacent lattice are surrounded by laser photocoagulation burns. (Courtesy of William E. Benson, MD, and William Tasman, MD, Philadelphia, PA.)

Transscleral cryotherapy, applied transconjunctivally under ophthalmoscopic visualization, is another effective means of creating a chorioretinal adhesion around a retinal break. The break is surrounded by contiguous cryotherapy applications to the surrounding attached retina. As with laser photocoagulation, if the break occurs in an area of lattice, the cryotherapy spots should surround the entire patch of lattice. A firm chorioretinal adhesion is not established for 7 or more days after treatment (Fig. 16).

Fig. 16. A flap tear recently treated with cryotherapy. (Courtesy of William E. Benson, MD, Philadelphia, PA.)


If a flap tear is symptomatic (i.e., caused by a PVD and accompanied by complaints of flashes or floaters), the probability of RRD is very high (25% to 90%).9,28,36,42 Treatment of these symptomatic flap tears with laser photocoagulation or cryotherapy dramatically reduces the risk of RRD.109–113

When no symptoms of flashes or floaters accompany a flap tear, the risk of RRD is low enough that observation is appropriate in most eyes.6,41,42,114 The presence of subretinal fluid, lack of subretinal pigment, and superior location would favor treatment of a flap tear without definite symptoms.


If an operculated tear is noted in a location where no tear was seen on previous examination or if it is symptomatic (i.e., accompanied by flashes or floaters), there is a moderate risk of RRD.9,36 If an operculated tear is superiorly located, large, or associated with vitreous hemorrhage, treatment should be administered. Likewise, if vitreoretinal traction is noted at the edges of the operculated tear, the break should be treated.

If no symptoms of flashes or floaters are present, round breaks with or without operculae are unlikely to lead to RRD6,41,42,114 and may simply be observed.


Although it has been established that lattice degeneration is a risk factor for RRD, only a few eyes with lattice go on to develop RRD. Even when atrophic holes are present in areas of lattice, RRD is unusual.115 Careful observation is all that is needed in these cases.


When symptomatic round breaks occur in pseudophakic or aphakic eyes, the risk of RRD is 1% to 5%.55,56,58 Treatment is warranted in these situations. Nonetheless, asymptomatic tears and round holes can generally be observed safely in these patients unless the break is large, posteriorly located, or collecting subretinal fluid.28,42,116


As stated above, after RRD in one phakic eye, the risk of a detachment in the fellow (phakic) eye is estimated to be approximately 10%.9–12 Treatment of vitreoretinal abnormalities (especially retinal tears) has been shown to reduce the risk of RRD.12,110,113 Folk and associates117 demonstrated that prophylactic treatment of lattice degeneration in fellow phakic eyes reduced the risk of RRD from 5.1% to 1.8%. In this setting, prophylactic therapy should be considered.

Pseudophakic and aphakic fellow eyes have an even higher incidence of RRD than phakic fellow eyes.64,70 Treatment of all retinal breaks is clearly indicated, and treatment of lattice degeneration and vitreoretinal tufts is reasonable.64,118

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Left untreated, an RRD will usually progress. The rate of progression depends on the viscosity and turbulence of the vitreous, the location of the break, and the presence of vitreous traction at the site of the break. Retinal detachments due to superior breaks propagate more quickly than inferior breaks due to the effect of gravity.

Surgery to reattach the retina is warranted to prevent further visual field loss and to recover as much visual function as possible from the detached retina. Timely intervention is important because the sooner the retina is reattached, the better the recovery of function.119 If an RRD is threatening to detach the macula, surgery should be performed as soon as possible.120 Even if the macula has detached, prompt surgical repair within 2 to 3 days frequently recovers reasonable central vision.

The various techniques of RRD repair are discussed in detail elsewhere in this volume, but an overview of the basic techniques is provided.


The rationale of scleral buckling surgery is to indent areas of the sclera, choroid, and RPE that underlie a retinal break so that the RPE tamponades the causative retinal break. By closing the retinal break, the flow of liquefied vitreous into the subretinal space is prevented, allowing the retina to reattach. This buckling effect is accomplished by suturing a piece of inert material to the sclera in the area corresponding to the retinal break. Transscleral cryotherapy is typically performed to create a focal chorioretinal scar, which helps to seal the tear in the area of the break(s). Drainage of the subretinal fluid or intraocular gases may be used to facilitate retinal reattachment, but these measures are not always necessary (Fig. 17).

Fig. 17. Scleral buckle procedure. The external buckling element indents the sclera, choroid, and retinal pigment epithelium. This tamponades the retinal break.


Pneumatic retinopexy is an effective alternative to the scleral buckling technique for selected uncomplicated primary detachments.121,122 This procedure involves treatment of the retinal break (retinopexy) with cryotherapy or laser photocoagulation and intraocular injection of an inert gas, which acts as a pneumatic tamponade. Transscleral cryotherapy may be applied to the retinal break before the injection of the gas. In contrast, laser photocoagulation is applied after the gas bubble has been injected and the retina surrounding the break is reattached. Laser photocoagulation or transscleral cryotherapy should be applied to retinal breaks present in attached retina before injection of the intraocular gas.

Careful patient selection allows a success rate comparable to that of scleral buckling surgery.123–125 This technique is useful when the causative retinal break or small cluster of breaks is located in the superior 8 clock hours of the peripheral retina. This technique has gained considerable popularity as an alternative to scleral buckling since it was introduced in the late 1980s (Fig. 18).126

Fig. 18. Pneumatic retinopexy. The inert gas bubble internally tamponades the retinal break, allowing the subretinal fluid to resorb.


Another technique for RRD repair is the temporary use of an inflatable balloon to indent the sclera, choroid, and RPE. The principles of this procedure are analogous to those of scleral buckling. All of the retinal breaks are localized and treated with cryotherapy. Alternatively, laser photocoagulation may be applied instead of cryotherapy; however, as is the case in pneumatic retinopexy, this must be applied in the postoperative period once the retina is reattached.

Rather than permanently attaching an inert buckle to the eye, an inflatable balloon is placed in the area of the causative retinal break(s) through a small conjunctival and Tenon's incision and then inflated. After several days, the balloon is deflated and removed.127 This technique avoids some of the long-term complications of scleral buckles such as infection, extrusion, refractive change, and motility disturbances. Nonetheless, the procedure is useful only for detachments with a single break or a closely spaced cluster of breaks, and the single-operation success rate is somewhat lower than for scleral buckling techniques.127–129 This technique tends to be cumbersome for the patient and is not widely used at this time.


Another useful approach to RRD repair is a primary pars plana vitrectomy. This technique involves internal drainage of the subretinal fluid, a gas-fluid exchange, and laser photocoagulation or cryotherapy of the reattached retina.130,131 Because the vitreous is removed, vitreous traction on retinal breaks is eliminated during surgery. In cases with significant vitreous hemorrhage, this technique allows visualization and treatment of the retinal breaks, which would not be approachable with other techniques. Nonetheless, this technique is generally reserved for more complicated detachments.


If a patient is unwilling or physically unable to tolerate a surgical intervention, laser photocoagulation of the attached retina surrounding an RRD may be used to wall off the detachment. Nonetheless, this technique applies to a limited number of patients. Recently, this method has gained popularity in the setting of limited retinal detachments from quiescent cytomegalovirus retinitis.132,133

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2. Okun E: Gross and microscopic pathology of autopsy eyes. Part III. Retinal breaks without detachment. Am J Ophthalmol 51:369, 1961

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6. Byer NE: Prognosis of asymptomatic retinal breaks. Arch Ophthalmol 92:208, 1974

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