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Chapter 136 – Rhegmatogenous Retinal Detachment

Chapter 136 – Rhegmatogenous Retinal Detachment









• A condition in which fluid from the vitreous cavity passes through a full-thickness retinal defect into the subretinal space to cause separation of the neural retina from the underlying retinal pigment epithelium (RPE).



• Seen clinically as an elevation and separation of the neural retina from the underlying RPE.

• One or more retinal breaks (holes, tears, or dialyses).



• Vitreous liquefaction.

• Posterior vitreous detachment.

• Vitreoretinal traction.

• Vitreous cells (pigment and/or hemorrhage).

• Flashes (photopsia) and floaters.

• Scotoma corresponds to the area of retinal elevation.





Rhegmatogenous retinal detachments are an important potential cause of reduced visual acuity, particularly in the subgroup of individuals who are predisposed to the development of retinal tears. Nearly all symptomatic rhegmatogenous retinal detachments progress to total blindness unless they are repaired successfully. Timely recognition of the symptoms and signs of retinal detachment is important to maximize the chances of a favorable surgical outcome and preserve visual acuity.


The essential requirements for a rhegmatogenous retinal detachment include a neural retinal break (rhegma = rent or rupture) and vitreous liquefaction sufficient to allow vitreous fluid to pass through the break into the subretinal space. The usual pathological sequence that results in retinal detachment is vitreous liquefaction followed by a posterior vitreous detachment (PVD), which in turn causes a retinal tear at the site of a significant vitreoretinal adhesion ( Fig. 136-1 ). All ocular conditions that are associated with an increased prevalence of vitreous liquefaction and PVD or with an increased number or extent of vitreoretinal adhesions are associated with a higher incidence of retinal detachment.

Factors That Cause Retinal Detachment

The major factors associated with the development of retinal detachment include retinal breaks, vitreous liquefaction and



Figure 136-1 Classical pathogenesis of rhegmatogenous retinal detachment. The detached vitreous gel has caused a retinal tear by exerting traction upon the retina at the site of a vitreoretinal adhesion. Liquid in the vitreous cavity passes through the break into the subretinal space.

detachment, traction on the retina (vitreoretinal traction), and intraocular fluid currents associated with movement of liquid vitreous and subretinal fluid. The majority of eyes with retinal breaks do not develop retinal detachment because the physiological forces present are sufficient to hold the retina in place. Retinal attachment is usually maintained by[1] :

• An adhesive-like mucopolysaccharide in the subretinal space

• Oncotic pressure differences between the choroid and subretinal space

• Hydrostatic or hydraulic forces related to intraocular pressure

• Metabolic transfer of ions and fluid by the retinal pigment epithelium (RPE)

Retinal detachment occurs when the combination of factors that promote retinal detachment overwhelms the normal attachment forces.


Retinal breaks are traditionally classified as holes, tears, or dialyses. Retinal holes are full-thickness retinal defects that are not associated with persistent vitreoretinal traction in their vicinity. They usually occur as a result of localized atrophic intraretinal abnormalities.

Retinal tears are usually produced by PVD and subsequent vitreoretinal traction at the site of a significant vitreoretinal





Figure 136-2 Retinal detachment. Retinal tears are due to vitreoretinal traction. Persistent traction frequently causes extensive retinal detachment (on left). If the traction results in a break that is not associated with persistent vitreoretinal traction (on right), the tear acts as a retinal hole and detachment is quite unlikely.

adhesion ( Figs. 136-1 and 136-2 ). Vitreous traction usually persists at the edge of a tear, which promotes progression of the retinal detachment.

Dialyses are linear retinal breaks that occur along the ora serrata. Although most are strongly associated with blunt ocular trauma, dialyses can occur spontaneously in certain individuals.


Aging of the human vitreous (synchysis senilis) is characterized by liquefaction of the vitreous gel and the occurrence of progressively enlarging pools of fluid (lacunae) within the gel. These optically empty liquid spaces continue to coalesce as age advances; extensive liquefaction within the vitreous cavity leads to a reduction in both the shock-absorbing capabilities and the stability of the gel. Accelerated vitreous liquefaction is associated with significant myopia, surgical and nonsurgical trauma, intraocular inflammation, and a variety of other congenital, inherited, or acquired ocular disorders.

Posterior vitreous detachment, routinely termed PVD, usually occurs as an acute event after significant liquefaction of the vitreous gel. The precipitating event is probably a break in the posterior cortical vitreous in the region of the macula.[2] This is followed by the immediate passage of intravitreal fluid into the space between the cortical vitreous and retina ( Fig. 136-3 ). Characteristically, this rapid movement of fluid and the associated collapse of the remaining structure of the gel result in extensive separation of the vitreous gel and retina posterior to the vitreous base, especially in the superior quadrants. Partial PVDs usually progress rapidly (within days) to become complete ( Fig. 136-4 ).


Vitreoretinal traction has a number of causes, which range from simple action of gravitational force on the vitreous gel to prominent transvitreal fibrocellular membranes. Gravitational force is important and probably accounts for the high percentage of superior retinal tears (80%). However, rotational eye movements, which exert strong forces on all vitreoretinal adhesions, are probably more important causes of ongoing vitreoretinal traction.[3] When the eye rotates, the inertia of the detached vitreous gel causes it to lag behind the rotation



Figure 136-3 Separation of the posterior cortical vitreous. An acute event, posterior vitreous detachment usually begins with an apparent break in the cortical vitreous that overlies the macula. Fluid from a central lacuna flows through this hole and separates the cortical vitreous from the retina.

of the eye wall and, therefore, the attached retina. The retina at the site of a vitreoretinal adhesion exerts force on the vitreous gel, which causes the adjacent vitreous to rotate. The vitreous gel, because of its inertia, exerts an equal and opposite force on the retina, which can cause a retinal break or separate the neural retina farther from the pigment epithelium if subretinal fluid is already present ( Fig. 136-5 ). When the rotational eye movement





Figure 136-4 Gross pathological appearance of a total posterior vitreous detachment. The cortical vitreous has separated from the retina except at the vitreous base. (Courtesy of W. Richard Green, MD.)

stops, the vitreous gel continues its internal movement and exerts vitreoretinal traction in the opposite direction.

In addition to gravitational and inertial forces, vitreoretinal traction can be caused by contracture of intraocular fibroproliferative tissue associated with trauma, retinal vascular proliferative disorders, and other conditions. This type of traction does not always create a retinal break. Instead, a traction retinal detachment may be produced. There are classical features that often are used to differentiate this type of detachment from the rhegmatogenous variety.[4] Sometimes significant vitreoretinal traction initially causes a localized traction detachment, which later becomes more extensive with the development of a retinal break.


Continuous flow of liquid vitreous through a retinal break into the subretinal space is necessary to maintain a rhegmatogenous retinal detachment because subretinal fluid is absorbed continually from the subretinal space via the RPE. This flow is encouraged by vitreoretinal traction, which tends to elevate the retina from the RPE. Rotary eye movements cause liquid currents in the vitreous to push against the gel adjacent to the retinal break and to dissect beneath the edge of a retinal break into the subretinal space ( Fig. 136-6 ). Subsequent eye movements also have an inertia effect on the subretinal fluid that favors extension of the retinal detachment ( Fig. 136-7 ).

Conditions That Predispose an Eye to Retinal Detachment

Retinal detachments are relatively unusual in the general population—the accepted annual incidence figure is approximately 1:10,000.[5] However, a variety of ocular and systemic disorders are associated with pathological vitreous liquefaction, premature vitreous detachment, and extensive sites of vitreoretinal adhesion. These conditions, therefore, are also associated with increased chances of retinal detachment. Particularly important predisposing entities include high myopia, pseudophakia and aphakia, blunt and penetrating ocular trauma, and cytomegalovirus retinitis associated with acquired immunodeficiency syndrome.



Figure 136-5 Vitreoretinal traction caused by eye movements. When the eye rotates, the inertia of the vitreous gel causes it to lag behind the eye movement, which effectively causes vitreoretinal traction (“drag”) in the opposite direction and the production of a retinal tear.



Figure 136-6 Extension of retinal detachment associated with eye movements. Rotary eye movement causes movement of the vitreous gel, which increases traction upon the retinal break. In addition, liquid currents dissect beneath the edge of the retinal tear and push against the vitreous gel adjacent to the tear. All three factors promote extension of the retinal detachment.





Figure 136-7 Extension of subretinal fluid associated with eye movements. In addition to exacerbating vitreoretinal traction, rotary eye movement has an inertia effect upon subretinal fluid that causes it to dissect further between the retina and pigment epithelium.

Although cataract surgery has been performed on only approximately 3% of the general population, up to 40% of eyes with retinal detachment have had prior cataract surgery.[6] Retinal detachment represents the most significant potential postsurgical complication of cataract surgery, as it occurs in nearly 1% of pseudophakic eyes.[7] Removal of the natural lens is believed to increase the risk of retinal detachment because of its effect on vitreous liquefaction and subsequent premature PVD.[8] The status of the posterior capsule determines the rapidity of vitreous liquefaction. It is clear that opening the posterior capsule, either surgically or with a neodymium:yttrium-aluminum-garnet laser, significantly increases the incidence of retinal detachment.[9]

High myopia (>6.0D myopia) is associated with at least a threefold increased incidence of retinal detachment.[10] Severe ocular trauma is believed to be responsible for 10–15% of retinal detachments, and up to 50% of patients who have a diagnosis of cytomegalovirus retinitis develop a rhegmatogenous retinal detachment within 1 year.[11]

Risk factors for retinal detachment are not mutually exclusive and may be additive. For example, prior cataract extraction and nonsurgical trauma are more likely to be complicated by retinal detachment in myopic eyes. Pathological vitreoretinal changes often occur bilaterally—patients who have a retinal detachment in one eye usually have a substantially increased risk of retinal detachment in the fellow eye, provided that additional acquired risk factors are comparable.


The early symptoms of acute retinal detachment are the same as those of acute PVD—the sudden onset of tiny dark floating objects, frequently associated with photopsia (flashes). Photopsia flashes are usually brief, in the temporal visual field, and are best seen in the dark immediately following eye movement. Loss of visual field does not occur until sufficient fluid has passed through the retinal break(s) to cause a retinal detachment



Figure 136-8 Superotemporal rhegmatogenous retinal detachment. The neural retina is elevated in the area of detachment and the macula remains uninvolved. Visual field defect associated with retinal detachment shows that peripheral vision is lost inferonasally, corresponding to the area of detachment. The visual defect is an inverted image of the retinal detachment.

posterior to the equator. Retinal detachments with a relatively small amount of subretinal fluid (less than two disc diameters from the break) are often not accompanied by visual field loss; these are termed subclinical detachments. Rarely, but especially in young female myopes, asymptomatic retinal detachment can occur. This is most common inferiorly and usually occurs as a result of atrophic holes in lattice degeneration. [12]

The vast majority of retinal breaks are located at the equator or more anteriorly; subretinal fluid initially accumulates in the retinal periphery, where it causes a corresponding loss of peripheral vision in the area that is related inversely to the location of the retinal detachment ( Fig. 136-8 ). The loss of peripheral vision (a “curtain effect”) increases as the detachment enlarges; central visual acuity is lost when subretinal fluid passes beneath the macula. Frequently, patients do not notice any symptoms until the macula becomes involved.

Retinal breaks associated with small amounts of subretinal fluid are difficult to detect; however, the diagnosis becomes more obvious as the retinal detachment increases in size. A stereoscopic vitreoretinal examination typically reveals an elevated sensory





Figure 136-9 Location of the retinal break. Retinal detachments that involve both quadrants on the same side of the vertical meridian are usually caused by a retinal break within 1–1.5 clock hours of the superior margin of the detachment.

retina in the area of detachment, but the critically important identification of all retinal breaks may remain difficult—it is considerably easier to diagnose the retinal detachment than to detect all retinal breaks.

The effects of gravity mean that the topography of a retinal detachment is of major value in the prediction of the most likely locations of retinal breaks. [13] Retinal breaks are usually present superiorly within the area of detachment. Thus, if a retinal detachment involves one upper quadrant or both the superior and inferior quadrants on one side of the vertical meridian, the responsible retinal break is likely to be near the superior edge of the detachment ( Fig. 136-9 ). Retinal detachments that involve the inferior quadrants tend to follow the same rules, but the progression of the detachment is often much slower, and symmetrical spread of subretinal fluid may occur on both sides of the break. Therefore, detachments that involve one or both inferior quadrants may have a break near the superior margin of the detachment or in the meridian that bisects the area of detachment ( Fig. 136-10 ). Nevertheless, because multiple retinal breaks are common, the entire periphery of the detached retina must be meticulously examined.


If the retina can be visualized well, the diagnosis of rhegmatogenous retinal detachment is made on the basis of clinical examination. In eyes with opaque media, the presence of a retinal detachment is usually determined ultrasonographically; the location and identification of the causative retinal breaks are based upon the configuration of the detachment as well as on the patient’s history and associated findings.

The vast majority of retinal detachments are diagnosed easily with a binocular stereoscopic evaluation of the entire retina. Areas of retinal detachment are recognized by elevation of the neural retina from the RPE and loss of pigment epithelial and choroidal detail beneath the elevated retina ( Fig. 136-11 ). Retinal breaks are also discovered by direct visualization. Indentation of the peripheral retina (scleral depression) is employed to visualize the entire anterior retina and to view the



Figure 136-10 Location of the retinal break. Retinal detachments that involve both lower quadrants but extend farther superiorly on one side are usually caused by a retinal break within 1–1.5 clock hours of the superior margin of the retinal detachment or by a break in a meridian that bisects the margins of the retinal detachment.



Figure 136-11 Rhegmatogenous retinal detachment. The inferior temporal portion of the retina is detached and the subretinal fluid makes visualization of the pigment epithelium and choroid relatively difficult.

retinal surface at different angles, which facilitates the identification of full-thickness retinal defects.


Retinal detachments that occur as a result of retinal breaks must be distinguished from several conditions in which retinal blood vessels are clearly separated from the pigment epithelium. These include retinal detachments from other causes and retinoschisis (see Box 136-1 ). Choroidal lesions that elevate the overlying retina and intravitreal pathology that simulates an elevated retina may also be confused with retinal detachment.





Figure 136-12 Traction retinal detachment. The central area of retinal elevation is localized and due to areas of visible vitreoretinal traction associated with proliferative diabetic retinopathy.




Differential Diagnosis of Rhegmatogenous Retinal Detachment



• Proliferative diabetic and other retinopathies

• Following penetrating trauma



• Inflammatory disorders

• Choroidal neoplasms

• Retinal vascular tumors and other disorders



• Age-related

• Congenital sex-linked



• Choroidal detachments

• Choroidal tumors



• Vitreous hemorrhage




The distinction between different types of retinal detachment can be difficult to make in eyes with small or undetectable retinal breaks and features associated with intraocular proliferation or exudation. In some cases, both a rhegmatogenous and a traction or exudative component may be important in the pathogenesis of the detachment. This is particularly common in eyes with proliferative diabetic retinopathy and retinal detachment. Pure traction detachments usually have a concave surface, and the shape, location, and extent of the detachment can be accounted for by the evident vitreous traction (see Fig. 136-12 ). Diabetic retinal detachments with a rhegmatogenous component are usually more extensive and often have a convex contour (see Fig. 136-13 ). Exudative detachments from a variety of causes are characterized by shifting subretinal fluid, which assumes a dependent position beneath the retina. In most cases, the fluid is located inferiorly and its source within or beneath the retina is apparent (see Fig. 136-14 ).


A variety of systemic disorders are associated with rhegmatogenous retinal detachment. In the most important situations, the ocular disorder is either an additional manifestation of a hereditary systemic abnormality (usually an inherited disorder of collagen) or



Figure 136-13 Combined retinal detachment. Vitreoretinal traction associated with proliferative diabetic retinopathy has caused a tiny retinal break; the area of retinal elevation is more extensive and more convex than usually found in a pure traction detachment.



Figure 136-14 Exudative retinal detachment. The small amounts of subretinal fluid (note the retinal striae) are due to leakage from an inflammatory process that involves the choroid and retinal pigment epithelium.

the result of complications of a systemic disease. The most important entity in the former group is Stickler’s syndrome, in which a predisposition to retinal detachment is associated with a variety of facial and skeletal abnormalities. The most important systemic diseases associated with the complication of retinal detachment are diabetes mellitus and acquired immunodeficiency syndrome.


The initial research of Jules Gonin,[14] which culminated in a proven pathogenesis and therapy of retinal detachment, was devoted to the pathological examination of eyes with this disorder. Retinal breaks, liquefaction and collapse of the vitreous gel, and visible vitreoretinal adhesions were all well documented prior to the first surgical cure. Nutrition of the outer retina is lost during retinal detachment, so the first visible pathological retinal changes occur in the outer segments of the photoreceptors.[15] Long-standing retinal detachments are associated with further atrophy of the photoreceptor layer and cystic degeneration within the retina ( Fig. 136-15 ).[16] The vitreous macromolecular changes that result in liquefaction of the gel have not been identified.

Successfully repaired retinal detachments show a variety of histopathological abnormalities. There is a high incidence of epiretinal membrane formation (76%). [17] Cystoid macular







Figure 136-15 Retinal detachment. A, An artifactitious neural retinal detachment shows no fluid in the subneural retinal space, pigment adherent to the tips of the photoreceptors, and good preservation of the normal retinal architecture in all layers. B, A true retinal detachment shows material in the subneural retinal spaces and degeneration of the outer retinal layers. (From Yanoff MS, Fine S, eds: Ocular pathology, ed 5. Philadelphia: 2002; WB Saunders.)

edema (10%) is common as well, along with significant photoreceptor atrophy in about 27% of eyes.


The aim of retinal detachment therapy is to counter the factors and forces that cause retinal detachment and to reestablish the physiological conditions that normally maintain contact between the neural retina and pigment epithelium. The main goal of surgery (i.e., to close each retinal break) usually is sufficient to reattach the retina. Long-term closure of retinal breaks also may require permanent reduction or elimination of vitreoretinal traction, accompanied by maneuvers designed to offset the harmful effects of fluid currents in the vitreous cavity.

At present, most retinal surgeons use scleral buckling techniques and the creation of a chorioretinal adhesion around each break to eliminate and counteract vitreoretinal traction.[18] These procedures are discussed in Chapter 103 . Vitrectomy techniques are performed in selected cases; these are discussed in Chapter 104 . Contemporary options in the management of primary rhegmatogenous retinal detachment are given in Box 136-2 , and one of these (pneumatic retinopexy) has become more popular in the past few years.[19]


Rhegmatogenous retinal detachment was an essentially incurable disorder until approximately 80 years ago. Surgical success



Options for the Management of Primary Retinal Detachment





• Encircling with/without drainage

• Segmental with/without drainage



• Lincoff balloon

• Absorbable buckling materials



• Routine

• With drainage of subretinal fluid or intravitreal liquid






rates have now improved to such a degree that, with one or more surgical procedures, approximately 95% of all retinal detachments can be successfully repaired (i.e., the retina is returned to its normal anatomical position with no residual subretinal fluid). The two most common reasons for failure of retinal detachment surgery are:

• Failure to identify and/or close all retinal breaks

• Proliferative vitreoretinopathy

Unfortunately, visual results after anatomically successful surgery do not necessarily reflect this high rate of success.

Postoperative visual acuity is most dependent upon the extent of damage to the macula caused by the retinal detachment. If the macula becomes detached by subretinal fluid, some degree of permanent damage to vision usually occurs in spite of surgical reattachment. In eyes with no macular detachment present, 85% can be expected to have 20/40 vision or better. Conversely, about 10% of eyes with normal or near-normal vision undergo visual loss after successful repair of a macula-sparing detachment.[20] Of eyes with macular detachment, only 50% have 20/40 vision or better. Of those with preoperative visual acuity worse than 20/200, fewer than 15% achieve 20/50 or better vision.[21] Some investigators believe that eyes treated with pneumatic retinopexy finally gain better vision than comparable eyes treated with scleral buckling, but this point remains highly controversial.

In addition, sometimes responsible for disappointing postoperative vision are complications caused by:

• The pathophysiology of retinal detachment,

• The subsequent reattachment surgery, or

• Progressive ischemic or infectious retinal damage.

The most common of such entities, other than macular damage from the detachment, are cystoid macular edema (5–10%) and epiretinal membrane formation (5%).[22]





1. Wilkinson CP, Rice TA. Michels retinal detachment, Ch 8. Philadelphia: Mosby–Year Book; 1997:471–516.


2. Eisner G. Biomicroscopy of the peripheral fundus: an atlas and textbook. New York: Springer-Verlag; 1993:45.


3. Rosengren B, Osterlin S. Hydrodynamic effects in the vitreous space accompanying eye movements: significance for the pathogenesis of retinal detachment. Ophthalmologica. 1976;173:513–24.


4. Wilkinson CP, Rice TA. Michels retinal detachment, Ch 6. Philadelphia: Mosby–Year Book; 1997:335–90.


5. Haimann NH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol. 1982;100:289–92.


6. Goldberg MF. Clear lens extraction for axial myopia. An appraisal. Ophthalmology. 1987;94:571–82.


7. Javitt JC, Street DA, Tielsch JM, et al. Retinal detachment and endophthalmitis after outpatient cataract surgery. Ophthalmology. 1994;101:100–6.





8. Duker JS. In: Steinert RF, ed. Cataract surgery: technique, complications, and management. Philadelphia: WB Saunders; 1995:434–8.


9. Tielsch JM, Legro MW, Cassard SD, et al. Risk factors for retinal detachment after cataract surgery. A population-based case control study. Ophthalmology. 1996;103:1537–45.


10. Austin KL, Palmer JR, Seddon JM, et al. Case-control study of idiopathic retinal detachment. Int J Epidemiol. 1990;19:1045–50.


11. Wilkinson CP, Rice TA. Michels retinal detachment, Ch 4. Philadelphia: Mosby–Year Book; 1997:175–250.


12. Brod RD, Flynn HW, Lightman DA. Asymptomatic rhegmatogenous retinal detachments. Arch Ophthalmol. 1995;113:1030–32.


13. Lincoff H, Geiser R. Finding the retinal hole. Arch Ophthalmol. 1971;85:565–9.


14. Gonin J. Le décollement de la rétine. Lausanne: Librairie Payot and Co; 1934:13–52.


15. Kroll AJ, Machemer R. Experimental retinal detachment in the owl monkey. III. Electron microscopy of the retina and pigment epithelium. Am J Ophthalmol. 1968;66:410–27.


16. Green WR. Retina. In: Spencer WH, ed. Ophthalmic pathology. An atlas and textbook, Vol 2. Philadelphia: WB Saunders; 1985:905–13.


17. Wilson DJ, Green WR. Histopathologic study of the effect of retinal detachment on 49 eyes obtained post mortem. Am J Ophthalmol. 1987;103:167–79.


18. American Academy of Ophthalmology. The repair of rhegmatogenous retinal detachment. Ophthalmology. 1996;103:1313–24.


19. Wilkinson CP. What is the ‘best’ way to fix a routine retinal detachment? In: Lewis H, Ryan SJ, eds. Medical and surgical retina. St Louis: Mosby; 1994:85–102.


20. Wilkinson CP. Visual results following scleral buckling for retinal detachments sparing the macula. Retina. 1981;1:113–16.


21. Burton TC. Recovery of visual acuity after retinal detachment involving the macula. Trans Am Ophthalmol Soc. 1982;80:475–82.


22. Greven CM, Sanders RJ, Brown GC, et al. Pseudophakic retinal detachments. Anatomic and visual results. Ophthalmology. 1992;99:257–62.

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