Retinal Detachment: Imaging of Surgical Treatments and. complications

EDUCATION EXHIBIT 983 RadioGraphics Retinal Detachment: Imaging of Surgical Treatments and Complications1 ONLINE-ONLY CME See www.rsna .org/educati...
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EDUCATION EXHIBIT

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Retinal Detachment: Imaging of Surgical Treatments and Complications1 ONLINE-ONLY CME See www.rsna .org/education /rg_cme.html.

LEARNING OBJECTIVES After reading this article and taking the test, the reader will be able to: 䡲 Discuss the rationales behind the types of surgical intervention for treatment of retinal detachment. 䡲 Describe the different kinds of buckling elements used in surgical treatment of retinal detachment. 䡲 Identify the normal postoperative appearances of the surgical interventions and the pathologic complications.

John I. Lane, MD ● Robert E. Watson, Jr, MD, PhD ● Robert J. Witte, MD ● Colin A. McCannel, MD Rhegmatogenous retinal detachment occurs in 5%–7% of the population with a peak prevalence between 40 and 80 years of age. The objects of treatment are to create a chorioretinal scar at the site of the retinal tear and to mechanically appose the detached sensory retina to the underlying retinal pigment epithelium. This apposition is achieved by means of scleral buckling or intraocular tamponade. In scleral buckling, the eye wall is indented under the retinal tear with a silicone buckling element. In intraocular tamponade, the eye is filled with a bubble of air, gas, or silicone oil. In patients treated with these techniques, neuroimaging commonly demonstrates incidental orbital findings. Familiarity with these techniques is essential if the radiologist is to differentiate normal postoperative findings from ocular disease. Furthermore, the ability to recognize the appearance of uncomplicated ocular surgery is a prerequisite for aiding the surgeon in diagnosis of postoperative complications. ©

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Index terms: Eye, CT, 224.1211 ● Eye, diseases, 224.892 ● Eye, MR, 224.1214 ● Retina, 2245.892 RadioGraphics 2003; 23:983–994 ● Published online 10.1148/rg.234025163 1From

the Departments of Radiology (J.I.L., R.E.W., R.J.W.) and Ophthalmology (C.A.M.), Mayo Clinic, 200 First St SW, Rochester, MN 55902. Presented as an education exhibit at the 2001 RSNA scientific assembly. Received November 18, 2002; revision requested December 17 and received January 21, 2003; accepted January 23. Address correspondence to J.I.L. (e-mail: [email protected]).

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Figure 1. Untreated rhegmatogenous retinal detachment. (a) Ophthalmoscopic photograph shows retinal detachment and associated subretinal fluid. Note the leading edge of the detachment (arrows). (b) Highermagnification photograph shows a large retinal tear. Note the free edges of the tear (arrows), which are elevated by the accumulation of subretinal fluid. (c) Axial computed tomographic (CT) scan shows hemorrhagic subretinal fluid in another patient with retinal detachment (arrow). Note that the detachment spares the optic disk.

Introduction Retinal detachment is defined as separation of the sensory retina from the underlying pigment epithelium in association with accumulation of subretinal fluid. Retinal detachments can be grouped into three main categories: rhegmatogenous, serous or exudative, and tractional. The most common type is rhegmatogenous (from the Greek word rhegma, a “rent” or “rupture”), which is defined as retinal detachment resulting from a break or tear of the sensory retina. Serous retinal detachments occur without the presence of retinal breaks and result from fluid exudation from ocular tumors such as choroidal melanoma, hemangioma, or metastatic disease or from other conditions. Treatments of serous detachments are aimed at the underlying cause of exudation and may include radiation, photodynamic therapy, or photocoagulation. Tractional retinal detachments, frequently seen in patients with diabetic retinopathy, occur when pathologic vitreoretinal adhesions mechanically pull the retina away from the pigment epithelium. Since serous retinal detachment and tractional retinal detachment are different both pathophysiologically and in their

treatment approaches, this discussion will be limited to treatment of rhegmatogenous retinal detachments. Rhegmatogenous retinal detachments are secondary to retinal breaks or tears that allow vitreous fluid to leak into the subretinal space, causing the sensory layer of the retina to separate from the underlying retinal pigment epithelium. Traction forces occurring at points where the vitreous normally attaches to the underlying retina act to detach the sensory retina at the site of the tear. If the tear is not repaired, progressive accumulation of subretinal fluid results in detachment of the entire retina, leading to blindness. A number of the surgical techniques used to repair retinal detachments have characteristic imaging appearances. It is important for radiologists to differentiate expected postoperative findings from ocular disease or surgical complications. In this article, surgical methods for treatment of retinal detachment, their imaging appearances, and their associated complications are reviewed.



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Figure 2. Natural history of untreated retinal detachment. (a) Drawing shows a retinal tear (straight arrow) with accumulation of subretinal fluid (curved arrow) beneath the detached sensory retina. (b) Drawing shows the globe affected by long-term detachment and proliferative vitreoretinopathy. Note the extensive retraction of the sensory retina from the underlying retinal pigment epithelium as a result of contraction of scar tissue. (c) Drawing shows phthisis bulbi. Note the shrunken globe with associated scleral thickening.

Background Rhegmatogenous retinal detachment occurs most commonly between 40 and 80 years of age, with a frequency of 9 –24 per 100,000 population per year (1,2). Retinal detachment is usually associated with a posterior vitreous detachment, a common aging phenomenon involving condensation of collagen fibrils and liquefaction of the vitreous gel. This leads to weakening of the normal vitreoretinal adhesions, allowing the vitreous to spontaneously separate from the retinal surface. There are three main risk factors recognized for development of rhegmatogenous retinal detachments: myopia (nearsightedness), a family history, and retinal detachment in the fellow eye. Other risk factors include the presence of peripheral retinal degenerations such as lattice degeneration, a history of trauma to the eye, and diseases that lead to retinal atrophy such as cytomegalovirus retinitis.

Untreated rhegmatogenous retinal detachment results in loss of visual acuity in all patients, with 9% able only to detect hand motion, 36% able only to perceive light, and the remaining 55% totally blind with no light perception (3). Rhegmatogenous retinal detachments are diagnosed with direct ophthalmoscopic observation (Fig 1a, 1b). Imaging plays no role in diagnosis of untreated retinal detachment, since management can be determined exclusively on clinical grounds. Retinal detachment may be incidentally noticed at head and orbit imaging, particularly if the subretinal fluid is hemorrhagic (Fig 1c). Although the detached retina may be recognized relatively easily at ophthalmoscopy, identifying the location of the retinal breaks or tears can be very difficult. If the detachment is left untreated, vision loss will often proceed to blindness and the eye may undergo progressive degeneration (Fig 2).

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Prompt surgical treatment is essential to prevent potentially devastating complications such as proliferative vitreoretinopathy, hypotony, and phthisis bulbi (atrophic shrinkage of the eye). The most common complication is proliferative vitreoretinopathy, which is defined as membranous scar tissue growth on the retina (Fig 2b). Membrane contracture exerts traction on the retina, resulting in worsening retinal folds and retinal distortion. Proliferative vitreoretinopathy makes subsequent surgical repair more difficult, as the traction exerted by the scar tissue prevents closure of retinal breaks. Once an eye develops proliferative vitreoretinopathy, retinal detachment usually recurs after subsequent surgical interventions. In addition, proliferative vitreoretinopathy can exert traction on the ciliary body, resulting in decreased aqueous humor production and ocular hypotony. Another cause of hypotony in the setting of retinal detachment is increased uveoscleral outflow of intraocular fluid from the subretinal space. Prolonged hypotony is usually followed by shrinkage of the eye with scleral thickening and eventually by metaplasia of the retinal pigment epithelium, leading to intraocular ossification. The end result of this process is a hypotonic, shrunken, and ossified globe, which is referred to as phthisis bulbi (from the Greek word phthien, “to decay”) (Figs 2c, 3). Prior to 1929, retinal detachment resulted uniformly in permanent blindness. In a lecture presented to the Ophthalmological Society of Eastern France that year, Jules Gonin proved his hypothesis that retinal detachment was caused by retinal breaks (4). He proposed that retinal reattachment could be achieved by closing the breaks with thermocautery. Decades of surgical innovation followed, and now retinal detachment is a treatable condition with an excellent prognosis in most cases. Imaging features of these postoperative findings have previously been reported in the radiology literature (5–10). In most cases, these observations are made while evaluating patients for conditions unrelated to their eye procedures. Being familiar with the various surgical techniques can be useful in recognizing normal postsurgical changes.



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Figure 3. Phthisis bulbi. Axial CT scan shows a shrunken left globe with a thickened, calcified sclera.

Surgical Treatments The two primary objectives of surgical treatment for acute retinal detachment are to mechanically appose the sensory retina and retinal pigment layer (“closing the break”) and to prevent the retinal tear from reopening. Reapposing the retina to the underlying retinal pigment epithelium closes the retinal breaks and prevents further fluid migration into the subretinal space. Retinopexy then creates an adhesion of the retina to the pigment epithelium that prevents the retinal break from reopening. Closure of the break and reapposition of the retina are achieved with scleral buckling or the help of intraocular tamponade agents. Surgical techniques used include scleral buckling surgery and vitrectomy surgery (11,12). One or both techniques can be used in combination with retinopexy to prevent the retinal breaks from reopening after reapposition. Most retinopexy procedures require adequate surgical exposure of the sclera overlying the detachment, so it is performed prior to application of a scleral buckle. As part of the surgery, the subretinal fluid can be drained through a small incision in the eye wall or left to be absorbed by the retinal pigment epithelium. In either case, it is highly desirable that the retina appose the eye wall in the areas of the retinal breaks at the conclusion of the surgery so that no further fluid movement can occur from the vitreous cavity to the subretinal space.

Retinopexy Retinopexy is performed by using heating (diathermy), freezing (cryotherapy), or a laser (photocoagulation) to produce a chorioretinal scar around the retinal tear. Diathermy involves applying a



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Figure 4. Surgical treatment of retinal detachment. (a) Intraoperative photograph obtained before placement of a scleral buckle shows use of a direct ophthalmoscope to position a cryoprobe (arrow) directly over a retinal tear, thus producing chorioretinal adhesions. (b) Intraoperative photograph obtained after application of a circumferential silicone band (arrow). Sutures around the extraocular muscles are used to control the position of the eye during the procedure.

to produce focal sites of freezing injury and subsequent adhesions, results in less scleral injury and is the technique of choice (Fig 4a). Small superior retinal detachments can sometimes be treated without the considerable softtissue trauma and costs associated with scleral buckle procedures. Injection of a gas bubble into the vitreous cavity (“pneumatic retinopexy”) can be used to reappose these small detachments (13). The gas bubble is used to cover the retinal break(s), which requires the patient to maintain a prescribed head position during waking hours for 5 days. Once complete reapposition is achieved, laser photocoagulation of the break(s) can be used to prevent recurrent detachment without a surgical exposure. Figure 5. Scleral buckling. Drawing shows a silicone sponge (straight arrow) and a silicone band (arrowhead). The circumferential silicone band compresses the underlying silicone sponge (which is in contact with the sclera), thus producing apposition of the underlying retinal pigment epithelium and the sensory layer of the retina (curved arrow).

radiofrequency probe to the scleral surface, which heats the tissues and produces small focal burns, leading to focal scar adhesions. Although retinopexy was first performed with this modality, diathermy has generally fallen out of favor. Cryotherapy, which entails use of a supercooled probe

Scleral Buckling In scleral buckling surgery, the eye wall is indented under the retinal break to facilitate reattachment of the retinal layers (Figs 4b, 5). Retinopexy prevents the layers from separating again once the retina is reattached. Scleral buckling elements usually consist of silicone materials, either solid silicone rubber or silicone sponge. Any procedure that results in indentation of the eye wall is referred to as scleral buckling. Scleral buckles are typically applied to the eye in one of several configurations or in combination: radial elements

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Figure 6. Large retinal detachment extending from 6 to 10 o’clock in the right eye treated with an encircling silicone rubber band. Axial (a) and coronal (b) CT scans show a high-attenuation scleral band that encircles the right globe (arrows). Note the physiologic calcification at the anteromedial aspect of the left globe (arrowhead in a), which represents calcified scleral plaque at the attachment of the medial rectus muscle.

Figure 7. Large retinal detachment extending from 7 to 10 o’clock in the left eye treated with a circumferential silicone sponge and an encircling silicone rubber band. Axial CT scan shows a circumferential silicone sponge that is isoattenuating to air (arrows) deep to an encircling high-attenuation silicone band (arrowheads).

(oriented parallel to the rectus muscles) and segmental or total encirclements (oriented perpendicular to the rectus muscles). Segmental encirclements span less than 360°, whereas complete encirclements indent the eye circumferentially over 360° like a belt applied too tightly. In all cases, sutures anchored in the sclera are used to secure the buckling elements and to augment the indentation. Scleral buckling elements are left in place as permanent “prostheses” and are removed only if complications occur due to their presence, such as infection, erosion, or exposure.

Figure 8. Small retinal detachment extending from 3:00 to 3:30 in the left eye treated with a radial silicone sponge sutured to the sclera. Axial CT scan shows a radial silicone sponge that is isoattenuating to air (arrow). Note the absence of a high-attenuation silicone band, which was not used in this case.

Buckling elements composed of solid silicone rubber are uniformly hyperattenuating at CT (Fig 6). They appear as an encircling band that surrounds the entire circumference of the globe. Porous silicone sponges appear as segmental or circumferential air-attenuation elements that often extend beneath a high-attenuation encircling band (Fig 7). Sponges applied radially or circumferentially without a hard silicone band will be seen as a small, focal air collection (Fig 8) or ring of air (Fig 9) adjacent to the sclera. Hard silicone rubber and silicone sponge are hypointense on T1- and T2-weighted magnetic resonance (MR) images and are often difficult to appreciate di-



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Figure 9. Large retinal tear in the right eye treated with an encircling silicone sponge and intraocular gas tamponade with C3F8. Axial (a) and coronal (b) CT scans show a circumferential low-attenuation silicone sponge (arrows) and intravitreal gas.

Figure 10. Large retinal detachment in the left eye treated with an encircling silicone rubber band. Axial T1-weighted MR image obtained with fat saturation shows contour deformities of the medial and lateral surfaces of the left globe (arrow) secondary to an encircling silicone band.

rectly with MR imaging. The presence of a scleral buckle is most often detected by means of the resulting deformity of the globe (Fig 10). Most commercially available buckling elements are not radiopaque and therefore present no plain radiographic manifestations, with one exception. Decades ago, the free ends of encircling elements were secured with small metallic clips, which have been replaced by small silicone sleeves. These clips were composed of tantalum (Fig 11), a nonferrous metal, which happens to be MR compatible.

Figure 11. Tantalum clip used to secure the free edges of a silicone band. (a) Anteroposterior radiograph shows a metallic clip at the inferolateral aspect of the left orbit (arrow). (b) Drawing shows the surgical technique.

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Figure 12. Drawing shows use of intraocular air tamponade in conjunction with a scleral buckle for treatment of retinal detachment.

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Figure 13. Large retinal detachment in the left eye treated with an encircling silicone sponge and intraocular air tamponade. Axial CT scan shows the air attenuation of an encircling silicone sponge (arrows) as well as intravitreal air.

Vitrectomy Vitrectomy surgery is retinal attachment surgery approached from the inside of the eye. Three tiny (1-mm) incisions are made in the area of the eye that overlies the darkly pigmented posterior zone of the ciliary body (the pars plana), permitting entry into the posterior vitreous without damaging the optic retina. One of the holes is used to suture in a cannula, through which continuous infusion of a balanced salt solution maintains intraocular pressure during surgery. The other incisions are used to enter the eye with surgical instruments such as a vitrectomy instrument, fiberoptic light pipe, endolaser probe, microforceps, and microscissors. Initially, the vitrectomy instrument is used to remove the vitreous gel from the eye. Scar tissue is peeled off of the retina. Then, the subretinal fluid is drained internally through the existing retinal break or a hole in the retina created for this purpose, which is called a drainage retinotomy. With an endolaser probe, laser retinopexy is then performed around the retinal breaks. At the conclusion of the surgery, the eye is filled with a gas, air, or silicone oil bubble as a tamponade agent.

Tamponade The mechanism of action of tamponade agents is twofold. They close the retinal break(s), and the buoyancy force helps appose the retina to the eye wall while the retinopexy matures or heals. The former is considered by far the more important

Figure 14. Large retinal detachment in the right eye treated with a scleral buckle and intraocular air tamponade. Axial T1-weighted MR image shows intravitreal gas as complete loss of signal with an air-fluid level and a hypointense encircling silicone band (arrows).

mechanism of action. The high surface tension of the bubbles allows them to act as a seal over the retinal break, preventing fluid from moving through the break into the subretinal space. The existing subretinal fluid is absorbed, leading to retinal reattachment. Intraocular gas tamponade agents include air (Fig 12) and mixtures of air and long-acting gases (sulfur hexafluoride [SF6] and perfluoropropane [C3F8]). The main difference in these agents is their duration of action. An air bubble will resorb in 3–5 days after injection, a mixture of SF6 in 10 –14 days, and a mixture of C3F8 in 6 – 8 weeks. Gases may be injected in their pure form, after which they will expand into larger bubbles, driven



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Figure 15. Drawing shows treatment of chronic retinal detachment and proliferative vitreoretinopathy with vitrectomy, scleral banding (arrows), and intraocular silicone oil tamponade.

by the difference in the partial pressure of nitrogen in the gas bubble versus in the body (14). Intraocular gas tamponade results in air attenuation and fluid levels within the nondependent portion of the vitreous cavity (Fig 13). There are no attenuation differences between air and the longer-acting gases at CT. The presence of air within the globe following retinal reattachment should not be misinterpreted as evidence of a postoperative complication such as intraocular infection. Air-fluid levels within the vitreous cavity are more easily appreciated than scleral bands at MR imaging (Fig 14). Silicone oil (polydimethylsiloxane) is different chemically from silicone rubber and has a lower specific gravity than vitreous fluid. This natural buoyancy, together with surface tension differences, makes it a useful agent for intraocular tamponade (Fig 15). Silicone oil provides several distinct advantages over air tamponade. Head positioning is less critical with silicone oil, making it a preferred agent for treatment of children with retinal detachment. Unlike the gas-filled eye, which temporarily leaves the patient with no useful vision, silicone oil is transparent (it does not mix with intraocular fluids or blood) and permits the patient to see after proper refraction. It is left in for at least 8 weeks, after which it is usually removed, although it can be left permanently at the discretion of the surgeon. The retina surgeon may

Figure 16. Chronic retinal detachment with proliferative vitreoretinopathy in the left eye treated with intraocular silicone oil tamponade and an encircling silicone sponge. Axial CT scan shows high-attenuation silicone oil in the anterior aspect of the posterior chamber and the air attenuation of an encircling sponge (arrows).

choose to leave the silicone oil indefinitely if there is evidence of residual traction on the retina or recurrent detachment is noted in a patient with acceptable vision. Oil may also be left in cases of ocular hypotony to prevent development of phthisis bulbi. Overall, the rate of reattachment, visual acuity, and ocular pressure tend to be better in those patients in whom the silicone oil is removed (15). Silicone oil is hyperattenuating to normal vitreous fluid at CT (6,9) (Fig 16). Silicone oil is somewhat variable in its appearance at MR imaging, but in general it is hyperintense to normal vitreous on T1-weighted images and variably hyperintense to hypointense on T2-weighted images. This variability in signal intensity has been ascribed to the differential viscosity of commercially available oils and to variations in imaging parameters (6). At 1.5 T, silicone oil resonates at 290 Hz lower than water, compared with 220 Hz for fat. Since the radiofrequency fat saturation pulse saturates a band of frequencies 75 Hz to either side of the fat resonance, this technique will cause some degree of silicone suppression. The presence of chemical shift artifact and the effects of fat saturation can be used to differentiate silicone oil from vitreous hemorrhage (Fig 17).

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Figure 17. Large chronic retinal detachment and proliferative vitreoretinopathy in the left eye treated with vitrectomy, scleral banding, and intraocular silicone oil tamponade. (a) Axial T1-weighted MR image shows high-signalintensity silicone oil in the vitreous cavity of the left globe and contour deformity from an encircling scleral band. (b) Axial T1-weighted MR image obtained with fat saturation shows a decrease in the signal intensity of the silicone oil. (c) Axial T2-weighted MR image shows chemical shift artifact at the interface between the silicone oil and vitreous fluid (arrow). (d) Axial T2-weighted MR image obtained with fat saturation shows low signal intensity of the silicone oil.

Surgical Complications Complications and side effects arising from scleral buckling procedures are usually diagnosed clinically and include refractive changes, infection, intrusion or extrusion of the buckling elements, strabismus, glaucoma, macular edema, reduced corneal sensitivity, choroidal detachment, and persistent ocular pain (16 –22). Choroidal detachment, in which fluid accumulates in the suprachoroidal space separating the underlying choroid from the sclera, is the most common complication, occurring in 23%– 44% of cases (16). It is usually self-limited, manifesting in the first 24 – 48 hours and spontaneously resolving in approximately 2 weeks. Scleral erosions are usually a long-term complication and are more common with hard silicone rubber elements. Adding

pliable silicone sponges beneath the encircling band minimizes the risk of producing scleral erosions. Unfortunately, the presence of dead space within these sponges also predisposes to infection. Infection usually manifests within 2– 8 months of the procedure and requires removal of the buckle element. The rate of recurrent detachment following buckle removal is as high as 45%, with the highest risk seen in those cases in which this complication arises less than 6 months after surgery (16). Hydrogel buckling elements were introduced in the early 1980s as a potentially superior product to silicone rubber due to its comparatively greater softness and lack of dead space (23). Hydrogel is a hydrophilic polymer (copoly[methyl acrylate-2-hydroxyethyl acrylate]) cross-linked with ethylene diacrylate. It was expected to minimize the likelihood of producing scleral erosions and reduce the risk of infection. However, hydrogel has since been found to be relatively unstable



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Figure 18. Complication of scleral buckling with hydrogel. (a) Intraoperative photograph shows an extruded, swollen hydrogel band encircling the right eye (arrows). (b) Photograph of the surgical specimen shows that the hydrolyzed buckle material has fragmented and expanded. (Reprinted, with permission, from reference 10.)

in vivo. These buckling elements are prone to hydrolysis and fragmentation, which manifest 8 –10 years after the procedure as ocular pain, ophthalmoplegia, and proptosis (17,24) (Fig 18). Hydrogel products were pulled off the market in 1995. Clinical imaging of buckle complications is rarely necessary because most of these problems are readily identified at clinical examination. However, complications resulting from hydrogel buckling elements are not commonly recognized due to their late presentation. These patients often are no longer being followed up by the retina surgeon, and the clinical presentation can prompt an imaging work-up for evaluation of an orbital mass (10). The primary imaging feature of this complication is a circumferential mass sur-

Figure 19. Complication of scleral buckling with hydrogel. Contrast material– enhanced axial (a) and coronal (b) CT scans show a circumferential soft-tissue mass surrounding the globe with a focal dystrophic calcification (arrow) and a peripherally enhancing rim. (Reprinted, with permission, from reference 10.)

rounding and distorting the globe. CT demonstrates characteristic dystrophic calcification and decreased attenuation of the swollen hydrogel buckle (Fig 19). With injection of intravenous contrast material, both CT and MR imaging demonstrate an enhancing capsule surrounding the mass (Figs 19b, 20b). At MR imaging, the signal intensity characteristics of the encircling band are consistent with the swelling and expansion of the buckle material observed intraoperatively. There is a marked increase in volume and in signal intensity on T2-weighted images (Fig 20a), reflecting the increased hydration.

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Figure 20. Complication of scleral buckling with hydrogel. (a) Axial T2-weighted MR image shows a markedly expanded buckle element, which is hyperintense with a low-signal-intensity rim (arrow). (b) Axial contrast-enhanced T1-weighted MR image shows that the buckle element is expanded and has rim enhancement (arrow). (Reprinted, with permission, from reference 10.)

Conclusions Once a devastating occurrence resulting in complete blindness, today retinal detachment is a treatable condition with an excellent prognosis. An understanding of current surgical techniques for retinal detachment will provide the radiologist with the ability to differentiate the normal postoperative appearance of the eye from postsurgical complications.

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10. Lane JI, Randall JG, Campeau NG, Overland PK, McCannel CA, Matsko TA. Imaging of hydrogel episcleral buckle fragmentation as a late complication after retinal reattachment surgery. AJNR Am J Neuroradiol 2001; 22:1199 –1202. 11. Michels RG. Scleral buckling methods for rhegmatogenous retinal detachment. Retina 1986; 6:1– 49. 12. Handa JT. The role of vitrectomy in rhegmatogenous retinal detachment. Semin Ophthalmol 1995; 10:9–16. 13. Hilton GF, Grizzard WS. Pneumatic retinopexy: a two-step outpatient operation without conjunctival incision. Ophthalmology 1986; 93:626 – 641. 14. Tiedeman JS. The role of intraocular gases and air in scleral buckling surgery. Semin Ophthalmol 1995; 10:74 –78. 15. Yamamoto S, Takeuchi S. Silicone oil and fluorosilicone. Semin Ophthalmol 2000; 15:15–24. 16. Ambati J, Arroyo JG. Postoperative complications of scleral buckling surgery. Int Ophthalmol Clin 2000; 40:175–185. 17. Roldan-Pallares M, del Castillo Sanz JL, Awad-El Susi S, Refojo MF. Long-term complications of silicone and hydrogel explants in retinal reattachment surgery. Arch Ophthalmol 1999; 117:197–201. 18. Brockhurst RJ, Ward RC, Lou P, Ormerod D, Albert D. Dystrophic calcification of silicone scleral buckling implant materials. Am J Ophthalmol 1993; 115:524 – 529. 19. Winward KE, Johnson MW, Kronish JW. Transpalpebral extrusion of a silicone sponge exoplant. Br J Ophthalmol 1991; 75:499 –500. 20. Delaney WV, Torrisi PF, Hampton GR, Hay PB, Hart K. Complications of scleral buckling procedures. Arch Ophthalmol 1987; 105:702–703. 21. Lindsey PS, Perce LH, Welch RB. Removal of scleral buckling elements: causes and complications. Arch Ophthalmol 1983; 101:570 –573. 22. Yoshizumi MO, Friberg T. Erosion of implants in retinal detachment surgery. Ann Ophthalmol 1983; 15:430 – 434. 23. Ho PC, Chan IM, Refojo MF, Tolentino FI. The MAI hydrophilic implant for scleral buckling: a review. Ophthalmic Surg 1984; 15:511–515. 24. Hwang KI, Lim JI. Hydrogel exoplant fragmentation 10 years after scleral buckling surgery. Arch Ophthalmol 1997; 115:1205–1206.

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