The advantages of local anesthesia include shorter operating time, quicker postoperative recovery, and possibly decreased morbidity and mortality in select cases. However, retrobulbar placement of local anesthetic is not without risk to the eye or the patient's general health. Perforation of the globe, particularly in myopic patients, and damage to the optic nerve may result in permanent visual loss after retrobulbar injection.^1–3 Respiratory arrest and grand mal seizures have also been reported.⁴ Damage to rectus muscles, typically the inferior rectus, may occur after retrobulbar injection causing diplopia.⁵ These complications can be minimized but not eliminated by use of either a subconjunctival or peribulbar technique of anesthetic administration.⁶ Subconjunctival infiltration with lidocaine allows a limbal peritomy and dissection of Tenon's capsule. Additional lidocaine and bupivacaine then can be administered via retrobulbar irrigation with a blunt cannula. This avoids the passage of sharp needles and diminishes the risks of ocular perforation and intravascular or intraneural injection.⁷ The authors use this technique to supplement general anesthesia and diminish postoperative pain and nausea.⁸

A peribulbar approach may be employed for anesthesia during scleral buckling. This technique also reduces the risk of ocular perforation compared with retrobulbar injections. A 1:1 mixture of 2% lidocaine and 0.5% bupivacaine is injected at the junction of the temporal and central thirds of the inferior orbital rim beneath the globe and just medial to the supraorbital notch. No attempt is made to enter the retrobulbar space. A total of 7 to 10 mL of anesthetic is injected, with two-thirds of the mixture delivered inferiorly and one-third given superiorly.⁹

The major disadvantage of local anesthesia is inadequate analgesia.¹⁰ Using a retrobulbar approach, 0.45% bupivacaine and 1.6% lidocaine provides superior anesthesia as compared with lidocaine alone.¹¹ Either retrobulbar or peribulbar anesthesia may be supplemented during the procedure with a sub-Tenon's capsule irrigation or local infiltration of additional anesthetic. This can be administered via a flexible catheter¹² or with a blunt cannula.¹³ Intravenous sedation with propofol or narcotics such as morphine and fentanyl or neuroleptics such as droperidol may also be helpful. These agents may cause respiratory depression and therefore require close monitoring by skilled personnel.¹⁴

Copious irrigation of the conjunctival sac with sterile saline effectively washes away most debris from the conjunctival surface. Despite irrigation, the conjunctiva usually is colonized by a variety of bacteria. Staphylococcus epidermidis can be cultured in 37% to 70% of patients before scleral buckling.¹⁵ More virulent pathogens, such as Staphylococcus aureus or gram-negative bacteria, including Proteus and Pseudomonas, are present in 5% to 9% of routine preoperative cultures. The presence of these pathogens preoperatively increases significantly the incidence of postoperative buckle infections, even with preoperative topical antibiotic treatment for 1 to 2 days.¹⁵ Although some surgeons use preoperative topical antibiotics, such as fluoroquinolones, there is no compelling evidence that infection rates are diminished.

After irrigation, the skin surface is dried with sterile gauze. This is particularly important when disposable adhesive drapes are used. The goal of surgical draping is to isolate and protect the surgical field from contamination. Common sources of contamination are the oral and nasal cavities.¹⁷ When properly applied, adhesive drapes can effectively seal off these areas from the operative field.

SURGICAL ANATOMY OF CONJUNCTIVA, TENON'S CAPSULE, AND EXTRAOCULAR MUSCLES

Conjunctival opening can be performed either at the limbus or 4 to 8 mm posterior to the limbus.^18,19 Because of the considerable manipulation the conjunctiva undergoes during scleral buckling, radial relaxation incisions are necessary to prevent tearing of the conjunctiva. If a lateral canthotomy is performed, the relaxing incision should be made away from the horizontal meridian to prevent symblepharon formation. The authors routinely use a limbal peritomy and believe this approach allows both better exposure of the sclera and better coverage of the buckle with less postoperative irritation than with a posterior peritomy. In patients with filtering blebs or recent limbal wounds, the peritomy can be extended posteriorly to avoid the area of concern.

Conjunctival opening at the limbus can be facilitated by spreading with scissors beneath Tenon's capsule just posterior to the limbus, thereby avoiding the fusion of conjunctiva and Tenon's capsule, which occurs at the limbus. Once the space between Tenon's capsule and the sclera is entered, conjunctiva and Tenon's capsule can be elevated from the sclera easily and then cut flush at the limbus. With a limbal incision, conjunctiva and Tenon's capsule can be retracted together, usually with less bleeding. If only one or two quadrants are to be buckled, a 360° opening of conjunctiva is not necessary. Conjunctiva and Tenon's capsule can be reflected in the required quadrants only and the appropriate muscles isolated, as described later.

Tenon's capsule is a fascial tissue that invests both the globe and extraocular muscles. Anteriorly it fuses with conjunctiva at the limbus, and posteriorly it ends at the optic nerve sheath. Between Tenon's capsule and the sclera is the interfascial space of Tenon, or simply Tenon's space. Entering this space allows complete exposure of the scleral surface. The extraocular muscles pass through Tenon's capsule, entering Tenon's space to insert on the sclera. At the site of penetration by the individual extraocular muscles, Tenon's capsule reflects posteriorly around the muscles for 10 to 12 mm to form the muscle sheaths. The muscle sheaths are connected by the intermuscular membrane, which, in turn, is connected to the orbital wall by complex fascial arrangements. The retinal surgeon is most concerned with the extraocular muscles after they pass through Tenon's capsule (Fig. 1). At this point they do not possess a muscle sheath but, rather, are invested by episcleral tissue that fuses with the muscle. This tissue forms the falciform folds that fan out from the edges of the muscle to the overlying Tenon's capsule (Fig. 2).

After the peritomy, the space between Tenon's capsule and sclera is entered in the quadrants between the rectus muscles with closed, blunt scissors. Opening the scissors lyses the episcleral fascial connections between Tenon's capsule and sclera. The muscle insertion is then engaged with a muscle hook. The muscle hook should be placed on the sclera and slid posteriorly to the muscle insertion in a circumferential direction. It is then brought anteriorly to engage the insertion. When in the proper space, the muscle hook should glide along the sclera and beneath the muscle with ease. Significant resistance to passage usually means the muscle hook is not on the scleral surface and should be repositioned. The muscle is best engaged by staying anterior to the equator. This also avoids endangering the vortex veins. Once the muscle insertion is engaged, the connections to Tenon's capsule can be identified and separated from the muscle. This is done either by stripping the muscle with a cotton-tipped applicator or with sharp dissection using scissors. When the vertical rectus muscles are isolated, care should be taken not to strip too posteriorly to avoid damaging the levator muscle superiorly or the inferior oblique muscle and Lockwood's ligament inferiorly. After isolation of the muscle is complete, a traction suture is placed around the muscle using either a fenestrated muscle hook²⁰ or a reversed needle; 2-0 black silk is an effective traction suture. All four rectus muscles can be isolated in this manner.

The superior rectus muscle requires additional care to avoid the superior oblique muscle tendon, which inserts 3 to 5 mm posterior to the lateral margin of the superior rectus insertion. Passing the muscle hook from the nasal side anterior to the oblique muscle insertion best avoids engaging the superior oblique muscle tendon. A second method is to rotate the eye inferiorly and grasp the superior rectus muscle insertion with a toothed forceps. The muscle hook then can be passed just posterior to the insertion, thereby avoiding the tendon of the superior oblique (Fig. 3). After the suture is placed around the superior rectus muscle, an inspection for evidence of incarceration of the oblique muscle is made by sweeping posteriorly along the lateral and medial margins of the superior rectus muscle. When incarcerated, the oblique muscle tendon appears as a white band that is pulled anteriorly by the suture.

After all rectus muscles are isolated, the surface of the sclera is inspected in each quadrant for evidence of thinning, staphyloma, or anomalous vortex veins, and the location of any abnormalities is noted before scleral depression or marking of retinal breaks. Scleral thinning may appear as a gray-blue area, sometimes associated with obvious ectasia. Less prominent thinning may appear as radial gray lines. Although scleral thinning may occur anywhere, it is most common superotemporally.²¹

Isolation of the four rectus muscles usually allows adequate access to all areas of the sclera necessary to perform scleral buckling. Rarely, however, a muscle must be removed to adequately expose an area. This usually occurs with breaks beneath muscles or in eyes with tight or small orbits. After the muscle has been isolated, it is elevated with a muscle hook, and a double-armed absorbable synthetic 5-0 or 6-0 suture is passed through the body of the muscle parallel to the insertion and just posterior to the hook. A central knot may be placed. The suture is then passed in a single or double loop through the end of the muscle to occlude the anterior ciliary arteries. With both the suture and hook used for traction, the muscle is elevated from the sclera and cut, leaving a small portion of insertion intact on the sclera. The arms of the suture are secured, and the muscle is allowed to retract posteriorly. A 4-0 silk traction suture is placed through the insertion with at least two passes. After completion of scleral buckling, the muscle is repositioned to the insertion with the double-armed suture (Fig. 4).

After isolation of the rectus muscles, the sclera is exposed and accessible for suturing everywhere except beneath the superior oblique muscle and the inferior oblique muscle. Because of its anterosuperior location and wide insertion, the superior oblique muscle more commonly overlies retinal breaks than does the inferior oblique muscle. When this occurs, fibers of either oblique muscle tendon can be cut to expose the underlying sclera. Of course, care should be taken not to entirely disinsert the muscle and also to avoid any underlying vortex veins. Partial resections of the oblique muscle tendons are well tolerated and do not result in motility disorders.

LOCALIZATION

No aspect of scleral buckling is more critical than accurate placement of the buckle on the sclera. This requires precise localization of retinal breaks on the scleral surface. Several instruments for localization and for marking the sclera have been described.^22–24 Other surgeons prefer to use the wooden end of a cotton-tipped applicator or a diathermy probe. When the sharper scleral markers are used for localization, it is important to inspect the sclera thoroughly. Sharp localizers and diathermy probes should be avoided if the sclera is thin. The authors prefer the O'Connor localizer, which places a 1-mm circular mark on the sclera with mild indentation (Fig. 5). ²⁴ This instrument also has a smooth surface 90° to the marking surface to allow for exploratory depression before final positioning of the probe. Once the proper site is located, the probe is rotated 90° and the sclera marked with mild indentation pressure for approximately five seconds. The scleral mark is then enhanced with a sterile pen, cautery, or both.

Regardless of which technique or instrument is used for localization and scleral marking, accurate placement of the marks with respect to the intraocular pathology is crucial. For small flap tears or atrophic holes, a single mark on the posterior edge of the break is sufficient. Larger flap tears and nonradial tears require localization of both the anterior and posterior extent of the break (Fig. 6). This anteroposterior orientation is particularly important when radial elements are employed. In areas with multiple, closely spaced tears, it is not necessary to mark each break. Marking the most posterior extent and the circumferential extent of the breaks is adequate (Fig. 7). This approach is also sufficient for marking a retinal dialysis. The circumferential extent of the dialysis is marked anteriorly at the edges of the dialysis, and then the most posterior extent is marked (Fig. 8).

If the retina is bullously detached, accurate localization of retinal breaks is difficult. Bullously elevated breaks appear to lie more posteriorly than their true location because of parallax (Fig. 9). This can result in unnecessarily large and posterior buckles. Inaccurate localization can be minimized by first marking the break at its least elevated margin, usually anterior, and then marking the more elevated margins. Other clues, such as the presence of pigment epithelial changes underlying the break and the location of the ora serrata in relation to the break, may be helpful. Rarely, it may be necessary to drain subretinal fluid to flatten the retina before localization; however, this softens the eye, usually necessitating a saline solution injection to restore volume. It also makes further drainage difficult, presumably because of choroidal swelling secondary to hypotony.

TREATMENT OF RETINAL BREAKS

The rationale for the treatment of retinal breaks is to create an adhesion between the retinal pigment epithelium (RPE) and the retina. This is accomplished by inducing a thermal injury with one of three energy sources: diathermy, cryotherapy, or laser. The morphologic and cellular response of the retina and pigment epithelium to each of these energies is essentially similar.²⁵ Two weeks after application, all three methods show comparable effects on retinal adhesive force.²⁶ However, there are significant differences in retinal adhesion immediately after application.²⁶ Photocoagulation increases retinal adhesion within 24 hours of application. Cryopexy reduces retinal adhesion for 1 week after application. Also, there are significant differences in the response the sclera and choroid have to these modalities and in their methods of administration.

Diathermy

Diathermy is produced by high-frequency, 13.56 MHz, alternating electrical current that generates heat because of the impedance (resistance) of the tissue through which it is passed. The heat created by the diathermy energy coagulates tissues. The histologic picture seen after diathermy depends on the intensity with which it is applied and on whether the retina is attached or detached. When the retina is attached and low-intensity diathermy applied, pigment epithelial migration into the inner retina occurs.²⁷ If the retina is detached, however, low-intensity diathermy treatment results in pigment epithelial proliferation between Bruch's membrane and the external limiting membrane following retinal reattachment.¹² High-intensity diathermy treatment in areas of detached retina causes rupture of Bruch's membrane, resulting in fibroblastic proliferation between the choroid and retina when the retina is reattached. The highest-intensity diathermy applications actually rupture the sclera, choroid, and Bruch's membrane, resulting in scar tissue formation across the entire ocular wall.²⁷

Although diathermy produces an effective RPE adhesion, it also induces immediate scleral shrinkage and subsequent scleral necrosis.^12,28 This scleral shrinkage results in increased intraocular pressure during diathermy application. The necrosis induced by diathermy weakens the strength of the sclera both immediately after application and over the long term. This weakening complicates reoperation and also may increase the incidence of scleral abscess formation.²⁹ In addition, penetration of diathermy through intact sclera to the retina depends on the scleral thickness. Thus, variations in scleral thickness result in nonuniform and unpredictable transmission of energy to the retina, which can cause choroidal and retinal bleeding and retinal holes.¹²

The problems of diathermy administration associated with scleral necrosis, shrinkage, and thickness can be minimized by applying it through lamellar scleral flaps, which are discussed later. Transscleral and transconjunctival diathermy without scleral flaps may be administered with a modified diathermy electrode, which causes less scleral damage than conventional diathermy.³⁰ However, because of the full-thickness damage that occurs with diathermy, vortex vein ampullae and long posterior ciliary arteries and nerves must be avoided, even with scleral flaps.^12,31 Techniques of diathermy application are discussed in the section on implants.

Cryotherapy

Cryotherapy (cryopexy) produces an effective pigment epithelial–retinal adhesion without the scleral complications that characterize diathermy. This provides cryotherapy with significant advantages: (a) retinal pathologic conditions can be treated without the need for scleral dissection, and (b) retinal breaks can be treated regardless of their location in relation to vortex veins or long posterior ciliary vessels or nerves.

The histologic response following cryotherapy depends on whether the pigment epithelium alone or the pigment epithelium and the overlying detached retina together are frozen.³² The ability to treat detached retina is another significant advantage over both diathermy and photocoagulation. If only the pigment epithelium is frozen without freezing the overlying retina, the pigment epithelial–retinal adhesion that forms once the retina is reattached shows pigment epithelial hyperplasia and loss of retinal outer segments. Therefore the normal microvillous interdigitations seen between retina and pigment epithelium are missing. If both the pigment epithelium and overlying retina are frozen, the adhesion that results after reattachment demonstrates cellular connections between the retina and pigment epithelium consisting of desmosome formation between retinal glia and pigment epithelium or direct contact between retinal glia and Bruch's membrane.

Current cryotherapy instrumentation employs expansion of high-pressure nitrous oxide at the tip of a probe generating temperatures as low as 89°C. The temperature effect is confined to the tip of the probe by an insulating sleeve. A probe 2.0 to 2.5 mm in diameter usually is used for retinal work. Treatment of retinal breaks and pathologic conditions requires accurate placement of the cryoprobe tip. The surgeon must be certain that the indentation visualized with the indirect ophthalmoscope is the tip of the probe and not the shaft. Confusion between the tip and the shaft of the cryo-probe can cause inadvertent posterior freezes.³³ To minimize the possibility of this complication, the surgeon must indent only with the tip of the cryoprobe (Fig. 10). It is also helpful to perform the first freezes at the most anterior aspect of the area requiring treatment to assess both location and intensity of treatment.

The goal of treatment is to surround all retinal breaks with 1 to 2 mm of contiguous treatment. When possible, treatment should include freezing of the overlying retina, because this results in a stronger adhesion than does treatment of the pigment epithelium alone.²⁵ To avoid the damage of refreezing, treatment should not significantly overlap. The treatment end point is retinal whitening without ice crystal formation.³⁴ Slight whitening of the retina because of retinal edema is noted several minutes after freezing, which helps to assess the adequacy of treatment. If retinal treatment is impossible because of bullous retinal elevation, treatment of the pigment epithelium alone may be performed, or treatment can be deferred until after drainage of subretinal fluid.

For flap retinal tears, treatment is performed contiguously around the tear and then extended anteriorly to the ora serrata. Care is taken not to freeze bare RPE in the bed of the retinal break where there is no overlying retinal tissue. Small retinal breaks and atrophic retinal holes can be treated with single freezes centered on the retinal break (Fig. 11).

One potential disadvantage of cryopexy is dispersion of pigment epithelial cells, which can result in subretinal pigmentary changes after reattachment.^35,36 Also, dispersion of viable pigment epithelial cells capable of causing proliferative vitreoretinopathy has been demonstrated following cryopexy.³⁷ The clinical relevance of cryopexy-induced pigment epithelial cell dispersion in the pathogenesis of proliferative vitreoretinopathy following scleral buckling is controversial. Some retrospective analyses suggest that cryopexy is a risk factor for the development of postoperative proliferative vitreoretinopathy (PVR),^38,39 whereas other studies do not show an association between cryopexy and PVR.⁴⁰ Accordingly, it seems prudent to minimize cryotherapy-induced pigment epithelial cell dispersion by not over treating and by avoiding unnecessary scleral depression of treated areas, which enhances dispersion of viable cells.⁴¹ Therefore localization and examination with scleral depression should be performed before cryopexy.

In addition, although cryopexy does not permanently damage the choroid, it does induce choroidal congestion and hyperemia,²⁷ which may complicate drainage of subretinal fluid through treated areas. Finally, cryopexy causes breakdown of the blood–ocular barrier,⁴² and its use has been implicated as a cause of postoperative cystoid macular edema and exudative detachments after scleral buckling.⁴³ Despite these potential problems, cryopexy remains the choice of most retinal surgeons for the intraoperative treatment of retinal breaks during scleral buckling.⁴⁴

Photocoagulation

Photocoagulation is another means for creating pigment epithelial–retinal adhesion. Laser delivery systems coupled to an indirect ophthalmoscope allow retinal surgeons to use photocoagulation during scleral buckling.⁴⁵ Laser photocoagulation can also be applied postoperatively after retinal reattachment.⁴⁶ The pigment epithelium is the primary chromophore for energy uptake with photocoagulation. Therefore the area of retina to be treated must be either attached or placed in juxtaposition to the pigment epithelium by scleral depression. As a result, treatment of bullously elevated retinal breaks or areas with atrophic or attenuated pigment epithelium may be difficult. Intraoperative transpupillary photocoagulation also requires optimal visualization. Miosis, corneal opacification, cataract, and vitreous hemorrhage may preclude transpupillary photocoagulation.

Transscleral diode laser photocoagulation also may be used to treat retinal pathology.⁴⁷ The long wavelength (810–840 nm) of the diode laser penetrates the sclera and is absorbed by the pigment epithelium. Placing the detached retina in juxtaposition to the pigment epithelium with scleral depression allows treatment of retinal pathology. The desired end point is a gray to gray-white burn. Potential complications include rupture of Bruch's membrane and the pigment epithelium, which may result in choroidal bleeding. Mild thermal effects on the sclera may be evidenced by blue-gray discoloration of the sclera. A potential advantage of transscleral diode photocoagulation over other methods is the ability to treat through preexisting scleral buckling components.⁴⁸ A disadvantage of both transscleral and transpupillary photocoagulation is that photocoagulation is more time consuming and requires more individual treatment spots than cryopexy.

Photocoagulation has several desirable features. It can be delivered with great precision, both in terms of location and intensity. Compared with diathermy and cryopexy, it causes less breakdown of the blood–ocular barrier.⁴² The thermal effect of photocoagulation is confined predominantly to the retina and pigment epithelium, with little or no effect on the choroid or sclera.⁴⁹ Finally, photocoagulation induces an adhesive effect between the retina and pigment epithelium within 24 hours.⁵⁰

EXPLANT TECHNIQUES

Scleral buckling, or indentation, was popularized by Ernst Custodis in 1953.⁵¹ He described placement of a polyviol explant that was sutured to the sclera overlying any retinal break. The explant indented the sclera against the retina and closed the retinal break. Although the precise mechanism by which scleral buckling works remains uncertain, it was Custodis' observations that led to current explant scleral buckling. Lincoff and colleagues further refined Custodis' procedure and introduced cryotherapy as a substitute for diathermy.^52,53 Over the ensuing years, explant techniques and materials have continued to evolve.^34,54

Explant techniques allow accurate and relatively easy placement of scleral buckling material to support retinal pathology. The development and refinement of cryotherapy were major steps in the evolution of explant techniques.⁵³ The ability to treat retinal pathologic conditions effectively without the need for scleral dissection has resulted in explant surgery becoming the procedure of choice for most retinal surgeons.

Buckling Materials

Explants are made of solid silicone rubber or silicone sponges and come in a variety of sizes and shapes. Medical-grade silicone rubber, consisting of cross-linked polydimethyl Siloxane is the most common buckling material used. This solid silicone rubber material was originally described by Schepens and colleagues⁵⁵ for use as scleral implants.

Solid silicone rubber is produced in a variety of sizes and shapes. Three basic shapes are available: straight, symmetric tire, and asymmetric tire. All three shapes can be grooved to accommodate placement of an encircling band. Unlike the straight implants, the tire implants have radii of curvature that approximate the shape of the globe (Fig. 12). The asymmetric tires also provide increased buckle height posteriorly. For many detachments, the authors prefer an asymmetric tire, which allows effective buckling of the ora serrata while minimizing anterior displacement of the encircling band because of its posteriorly placed groove (Fig. 13). This advantage is negated if the tire completely encircles the eye. The thinner anterior edge of this element may also minimize the chance of anterior extrusion. Solid silicone meridional implants can be used as explants. These elements can fit beneath either encircling bands or tires. When radial elements beneath circumferential buckles are indicated, the authors prefer solid silicone meridional elements (Fig. 14).

Silicone sponges also are made of silicone rubber but have many small air-filled pockets that give the sponge great compressibility and elasticity. Unlike true sponges, however, their absorption capabilities are minimal.⁵⁶ Sponges are made in varying sizes and shapes, from 3 mm circular sponges to 5 × 7 mm oblong sponges. They may be grooved or have a central tunnel for anchoring of an encircling band.⁵⁷

Biologic materials, including fascia lata, preserved human sclera,⁵⁸ and gelatin,⁵⁹ also have been used for scleral buckles. Currently, these are rarely used and are discussed primarily for historical interest. Of these, gelatin is the most versatile. As it hydrates, gelatin gradually swells, providing increased buckle height a few days after surgery. Over 3 to 6 months, the gelatin, which is predominantly hydrolyzed collagen, is broken down, and the buckling effect is lost. Gelatin can be used as either an implant⁵⁹ or explant.³⁴

The Miragel implant (Mira, Inc., Waltham, MA) is a nonbiologic hydrogel made of a hydrophilic copolymer of methyl acrylate with 2-hydroxy ethyl acrylate cross-linked with ethylene glycodiacrylate. It was used as an explant from 1981 until 1996, when the manufacturer stopped its distribution. Although no longer available, this buckling material must be familiar to ophthalmologists because of its late-onset complications. Although Miragel implants were reported to be tolerated well in both short- and long-term evaluation,^60,61 complications such as extrusion, fragmentation, limitation of ocular motility, and intrusion of the implant have been reported to occur between 7 and 11 years after implantation.^62–65 Consequently, patients who received this buckle material must be monitored closely over the long term. Often the buckle material must be removed. Indications for removal include buckle exposure, infection, motility disturbance, or intrusion. Intrusion of the buckle may be heralded by recurrent vitreous hemorrhage. Removing the hydrogel is difficult because of the friability of the material. The material must be gently “milked” from the sub-Tenon's location with a muscle hook, extracted with a cryoprobe, or carefully aspirated with small-gauge suction. There have been reported cases of scleral rupture and retinal incarceration during removal of the buckle material. Consequently, extreme care should be taken when traction is applied to the rectus muscles or when exploring the subconjunctival and sub-Tenon's space for buckle fragments.^62,63

Scleral Suture Technique

Explants are secured to the sclera with partial-thickness scleral sutures. When bands, tires, or sponges are used, these sutures are placed in a mattress fashion parallel to the long axis of the element being supported. To support solid silicone meridional elements beneath tires or bands, the surgeon places the mattress suture perpendicularly to the long axis of the meridional element (Fig. 15).

Accurate and effective suture placement is critical to the success of explant procedures. After identification and localization of all retinal breaks and other retinal pathology requiring support, the surgeon selects an appropriate explant. For most detachments, the actual element selected is not as important as the accurate localization and proper placement of the element with respect to the retinal breaks. Proper placement of the element requires effective suturing technique. A spatula needle with a 5-0 nonabsorbable suture such as polyester, nylon, or polypropylene is used.

When suturing, the surgeon must firmly fixate the globe. This is best done by grasping a muscle insertion with a toothed forceps. Magnification with loupes or the operating microscope facilitates suture placement. The suture is passed through the sclera at one-half to three-fourths depth over a distance of 3 to 5 mm, usually in a horizontal mattress fashion. A combination of adequate depth and length is necessary for maximum suture strength.⁶⁶ Once the proper scleral depth has been obtained, the suture should be passed at that level. Uneven passage of the needle induces buckling of the sclera, which may lead to perforation. After the needle has been passed through the sclera and the tip brought out, the needle is released from the needle holder and the tip is grasped. It is important to complete passage of the needle along the arc of the needle, avoiding posterior pressure or dragging on the hub of the needle, which may perforate through the remaining underlying sclera (Fig. 16).

Usually sutures are placed a minimum of 2 mm farther apart than the width of scleral contact for a given element (e.g., 9 mm apart for a 7-mm element). To ensure that the most posterior edge of the retinal break is supported, the surgeon places the posterior suture a minimum of 2 to 3 mm posterior to the scleral localization mark. For encircling elements, placement of the mattress suture in the same meridian as the retinal break or breaks provides additional height beneath the breaks (see Fig. 15).

When one is suturing posteriorly, the vortex veins and their tributaries must be avoided. This sometimes requires straddling a vortex, as seen in Figure 17. Thin sclera also presents problems, and sometimes long suture passes are not possible. In this case, several short bites in areas of thicker sclera may be effective. The use of cyanoacrylate adhesive to support suture bites in thin sclera has been described.⁶⁷ Currently, in eyes with very thin sclera, the authors perform primary vitrectomy techniques for retinal detachment repair.

Some surgeons prefer silicone sponges for explants. Sponges provide a rounded buckling contour, the height of which is easily adjusted by varying the distance between the mattress suture bites. The buckle height obtained with segmental sponge explants persists for at least 3 years.⁶⁸ Sponges are easily trimmed and thus are quite adaptable. They are effective for support of radial tears and are particularly useful for posterior radial tears.⁶⁹

Based on the size of the tear, an appropriate sponge is selected. Sutures are placed 2 to 3 mm beyond the circumferential and posterior extent of the tear as determined by localization (Fig. 18). Usually one or two mattress sutures are placed, and the buckling effect is carried anteriorly to the ora serrata. The anterior suture is usually a simple horizontal mattress; the posterior suture may be either a crossed or simple mattress. Often it is difficult to pass a suture from posterior to anterior when one is working posterior to the equator. A crossed mattress alleviates this problem but does not provide as effective posterior support, as does a simple mattress. Thus the buckle may need to be extended farther posteriorly. When necessary, crossed mattress sutures can be converted to simple mattress sutures (Fig. 19).

Segmental versus Encircling Buckles

Placement of explant material can be either segmental or encircling. Segmental buckles usually are reserved for detachments with single or closely spaced retinal breaks less than one clock hour in total extent or with posterior breaks. These breaks can be effectively closed using radial sponges or segmental placement of circumferential solid silicone elements. The primary advantage of segmental buckles is the relative ease of placement; another advantage is minimal change in refractive error induced by segmental buckles. For posterior breaks, segmental elements allow closure of the break while avoiding the side effects of large posterior encircling elements. However, for most large posterior breaks and all macular holes, the authors prefer closure with gas and vitrectomy techniques.

Although segmental buckles effectively close isolated tears, they do not provide retinal support elsewhere. Specifically, other areas of vitreoretinal traction away from the segmental element are not supported, which may result in the formation of new retinal breaks. Because of the limited support offered by segmental buckles, the authors prefer encircling procedures when possible. Encircling procedures are particularly indicated in: (a) cases with multiple breaks in different quadrants, (b) aphakia, (c) pseudophakia, (d) myopia, (e) diffuse vitreoretinal pathologic conditions, such as extensive lattice degeneration or vitreoretinal degenerations, and (f) proliferative vitreoretinopathy of grade B or greater.^34,54,70 Either sponges or solid silicone rubber can be used as encircling elements. Because of their compressibility, encircling sponges tend to result in a variable undulating contour to the buckle unless multiple sutures are placed in each quadrant. The authors prefer solid silicone elements for encircling procedures.

The anteroposterior position of the encircling element depends on the location of the vitreoretinal pathology to be supported. When retinal breaks in detached retina are associated with traction, the buckle should be positioned so that the posterior edge of the break lies on the posterior crest of the buckle. The buckling effect should extend for 30° on either side of the tear and extend anteriorly to the ora serrata (Fig. 20). If the encircling element is supporting pathologic conditions in attached retina, such as a retinal break, lattice degeneration, or prominent vitreoretinal adhesions, the most posterior aspect of the condition needs to be supported by the encircling element. If no specific pathologic factor is to be supported, the encircling element should support the posterior margin of the vitreous base.

The vitreous base eccentrically straddles the ora serrata, extending more posteriorly on the nasal side. The exact location of the vitreous base sometimes can be determined with indirect ophthalmoscopy and, when this is possible, the vitreous base can be marked on the sclera to ensure accurate placement of the encircling element. If the vitreous base cannot be identified ophthalmoscopically, it can be assumed to lie approximately 3 mm posterior to the ora serrata nasally and 2 mm posterior to the ora serrata temporally (Fig. 21).

A solid silicone band 2.5 mm wide often is used to support the vitreous base or vitreoretinal pathologic condition in attached retina. The encircling band is secured to the sclera with either mattress sutures or through scleral tunnels to prevent migration of the band once it is shortened. It is not necessary to place the band around the greatest curvature of the eye. The ends of the band can be secured with a clove hitch nonabsorbable suture,³⁴ or silicone sleeve.⁷¹ The authors prefer the silicone sleeve because it allows easy adjustment of the band throughout the surgery (Fig. 22).

One result of circumferential encircling scleral buckles is fish-mouthing of retinal breaks.^72,73 This is caused by the relative circumferential shortening of the sclera and choroid induced by the buckle in relation to the retina. This relative excess of retinal surface causes the retina to lie in radial folds over the buckle. These folds, in conjunction with vitreous traction, can result in the failure of retinal breaks to settle over the buckle. The breaks may form an elongated oval configuration in the anteroposterior meridian over the buckle, resembling the open mouth of a fish (Fig. 23). Persistent elevation of the retina resulting from the fishmouth phenomenon can result in surgical failure and therefore needs to be addressed.

There are three basic techniques in the management of fishmouth retinal tears. The easiest is to decrease the height of the circumferential buckle. This usually is effective only if buckle height is excessive. Placement of a radial element beneath the circumferential element effectively closes most fishmouth tears.⁶⁹ The radial element increases the surface area of the pigment epithelium and choroid beneath the break, thereby decreasing the disparity between the retinal surface area and the surface area of the bed of the buckle (Fig. 24). ⁷³ Injection of an intravitreal gas bubble, combined with appropriate positioning, also effectively closes fishmouth tears. The gas is injected through the pars plana under direct visualization with the indirect ophthalmoscope. During the injection, care must be taken to avoid formation of multiple small bubbles, which may then pass through the tear into the subretinal space. This can be prevented by injecting into the most superior aspect of the vitreous cavity. With accurate positioning, a bubble of 0.3 mL is adequate to close retinal breaks of up to one clock hour.⁷⁴ The use of expansile gases, such as sulfur hexafluoride or perfluoropropane, can increase the intraocular volume of gas.

For encircling elements, buckle height can be obtained in two ways. For thin encircling elements, such as solid silicone bands, the explant can be shortened in relation to the circumference of the globe. The best method of determining how much to shorten the band is a visual assessment of the buckle height created by the band.^34,75 The band is shortened only the amount necessary to create the desired buckle height. This helps to avoid the complications of excessive buckle height, such as anterior segment necrosis.⁷⁶ The height and breadth of the scleral indentation obtained are a linear function of the amount the encircling element is shortened.⁷⁷ However, this leads to circumferential shortening of the globe in relation to the retina, predisposing to radial folds on the buckle and the fishmouth phenomenon.^59,73 Increased axial elongation of the globe also occurs.^75,77

The second method of obtaining buckle height is by suture placement without shortening of the element in relation to the ocular circumference. This technique is used with wider and thicker explants such as tires and sponges. The farther apart the bites of the mattress suture are placed, the greater the height of the buckle when the sutures are tightened. This effect requires two sutures per quadrant but provides excellent buckle height by shortening the sclera in an anteroposterior direction rather than circumferentially. With this technique, axial length actually decreases.⁷⁷

IMPLANT TECHNIQUES

The current era of scleral buckling using implant techniques for rhegmatogenous retinal detachment began in 1960 with Schepens and colleagues'⁵⁵ description of scleral dissection, intrascleral placement of silicone buckles (implants), and diathermy. Subsequent modifications and refinement of the technique have been described.¹²

Scleral Dissection

After localization of all retinal breaks requiring support, a lamellar scleral undermining or scleral dissection is performed. The extent of dissection depends on the size of the intended buckle. It is recommended that the lamellar scleral dissection extend 3 mm posterior, 2 mm anterior, and 3 to 4 mm circumferentially beyond the retinal breaks.¹² The dissection is begun with an incision parallel to the limbus at the posterior edge of the retinal breaks. The depth of the incision is considered appropriate if a thin gray layer of sclera remains over the choroid. The lamellar dissection is performed using a blunt dissector with traction on the reflected scleral flaps. Care is taken when dissecting posteriorly to the equator to avoid severing the vortex veins. Modifications of the posterior scleral flap often are necessary to avoid the vortex veins. The size of the scleral dissection is designed to accommodate the width plus the height of the desired implant (Fig. 25).

Diathermy

After completion of lamellar scleral dissection, diathermy is applied. The use of diathermy is the primary reason that lamellar scleral dissection is performed. When diathermy is applied to full-thickness sclera, energy transmission is irregular and unpredictable. Diathermy through full-thickness sclera also induces scleral necrosis and shrinkage.^28,53 These problems are minimized by placing diathermy through the surgically thinned sclera.

Diathermy is applied for 3 to 5 seconds using a blunt conical electrode on the dried scleral surface. The intensity is assessed ophthalmoscopically and then adjusted as required. The diathermy burns leave a 1-mm mark on the thinned scleral surface and are spaced about 2 mm apart in staggered rows parallel to limbus. Treatment is started posteriorly and proceeds anteriorly (Fig. 26). If a stronger than usual chorioretinal adhesion is desired, the intensity of burn, not the number of burns, should be increased.¹² However, excessive intensity may result in retinal holes if attached retina or choroidal hemorrhage are being treated. When diathermy is placed, the long posterior ciliary arteries, nerves, and vortex veins should be avoided. Transillumination viewed through the thinned scleral bed is helpful in identifying these structures.⁷⁸

Buckle Implantation

After placement of diathermy, the silicone implant is trimmed to fit beneath the scleral flaps, and nonabsorbable 4-0 mattress sutures are placed in the scleral flaps. The flaps then are closed with temporary suture ties. An encircling band may be placed through the groove of the implant, beneath the scleral flaps and around the globe.

The band is anchored with scleral tunnels or mattress sutures. The ends of the band are joined with a tantalum clip, nonabsorbable suture, or silicone sleeve (Fig. 27). Drainage of subretinal fluid usually is required and is described later.

If 360-degree buckling with a silicone implant is required, Schepens¹² recommends that this be performed as a two-step procedure. He suggests that a scleral lamellar undermining be made for 220 to 270 degrees and that the implant placed with an encircling band. If this fails to reattach the retina, the remaining sclera is undermined and buckled with a second procedure 2 to 6 weeks later. This apparently diminishes the complications associated with 360-degree scleral dissection, such as anterior segment ischemia and choroidal detachment.

Proponents of implant techniques believe that diathermy is the best means of obtaining a chorioretinal adhesion because of the strength of the adhesion obtained.¹² This belief is based on a presumed correlation between the histologic appearance of diathermized eyes and the strength of the chorioretinal adhesion. Whether or not this correlation is valid is unknown. Comparisons of the tensile strength of chorioretinal adhesions produced by diathermy, cryotherapy, and photocoagulation show little difference among the three methods.^26,79 However, the techniques to measure the tensile strength of chorioretinal adhesions are fraught with methodologic difficulties. Implanted buckles may also have the advantage of being less likely to become infected or extrude.

DRAINAGE TECHNIQUES

The rationale for drainage of subretinal fluid is twofold: to diminish intraocular volume so as to allow elevation of the buckle without difficulties with elevated intraocular pressure, and to allow the retina to settle on the elevated buckle by removing fluid from the subretinal space. Effective drainage of subretinal fluid places the retinal breaks in juxtaposition to the buckle, thereby facilitating closure of the breaks. Although many retinal detachments can be managed effectively without drainage as described later, the authors prefer to drain retinal detachments with one or more of the following characteristics:

1. Bullous detachments. Drainage usually is necessary in these cases so that the retinal break can be placed in juxtaposition to the buckle. This is particularly valid if confluent retinopexy around the tear cannot be obtained because of the bullous elevation.¹⁹
   
2. Inferior breaks. Inferior breaks tend to settle less readily on the buckle than do superior breaks, perhaps because of gravity.⁸⁰ Also, inferior breaks are less effectively managed postoperatively with air injections.
   
3. Proliferative vitreoretinopathy. Proliferative vitreoretinopathy may prevent the retina from settling, resulting in persistence of open retinal breaks. The authors drain all cases of grade B or greater that undergo scleral buckling.
   
4. Highly myopic detachments and aphakic or pseudo-phakic detachments. The syneresis of the vitreous that occurs in myopia or following lens extraction may be a factor in the failure of these retinas to settle on the buckle without drainage.
   
5. Chronic detachments. Subretinal fluid in chronic detachments becomes viscous, assuming the biochemical profile of plasma.⁸¹ The high osmolarity of the fluid may slow resorption by the pigment epithelium.^82,83
   
6. Poor RPE function. Detachments in patients with age-related macular degeneration and high myopia are characterized by prolonged resorption of subretinal fluid, presumably because of decreased ability of the RPE to remove fluid from the subretinal space.
   
7. Eyes intolerant of sustained intraocular pressure rises, such as those with known glaucoma.
   

The selection of an external drainage site is affected by several factors. Obviously the location of subretinal fluid is a primary concern. The authors prefer to select the drainage site after placement of scleral sutures and loose placement of the buckle. This ensures that the location or amount of the subretinal fluid has not changed during the placement of sutures. It is not necessary to drain where the fluid is greatest but where there is adequate fluid to safely enter the subretinal space. When possible, it is preferable to drain just above or below the horizontal meridian, either temporally or nasally (Fig. 28). This location avoids the major choroidal vessels and vortex veins. Usually the vortex veins can be identified ophthalmoscopically and thereby avoided. However, sometimes transillumination may also be useful.⁷⁸ The horizontal meridian allows relatively easy access to the sclera, although in patients with large noses or tight orbits the nasal approach sometimes can be difficult. If subretinal fluid in the horizontal meridian is inadequate, drainage must be performed elsewhere. Usually either side of the vertical rectus muscles avoids major choroidal vessels. The authors try to avoid drainage through areas that have received cryotherapy because of the choroidal hyperemia and congestion that cryotherapy induces.²⁷

Drainage can be performed via either a radial sclerotomy and external observation of the drainage site, or external needle drainage and indirect ophthalmoscopic observation of the needle in the subretinal space. External needle drainage is technically more challenging. It is performed either with the scleral buckle left loose as originally described by Charles in 1985⁸⁴ or with it tightened to an appropriate height and the sutures permanently tied.⁸⁵ Using the technique reported by Charles, Burton, and colleagues reported an 84% successful rhegmatogenous retinal detachment repair with one surgery.⁸⁶ However, subretinal hemorrhage occurred in 22% of cases, and the blood extended subfoveally in four cases. Raising the intraocular pressure by tightening the scleral buckle is thought to mitigate intraocular bleeding. The subretinal hemorrhage rate as described by Jaffe and colleagues was 4%.⁸⁵ To perform external needle drainage, the surgeon uses a 0.5-inch 25-, 26-, or 27-gauge needle attached to a tuberculin, 3- or 5-cc syringe with the plunger removed. The authors prefer the larger gauge needles because these do not bend easily when scleral depressing or while angling the needle to enter the eye. The authors also prefer the larger volume syringe to minimize the water pressure within the syringe. A tuberculin syringe holding its maximum of 1 mL of fluid has more pressure and therefore resistance to drainage when held vertically, compared to a 5-cc syringe. Consequently, more subretinal fluid can be drained with a larger volume syringe before equilibrium exists between the water pressure of the syringe and the intraocular pressure.

The bevel of the needle is directed away from the sclera. With the needle shaft tangential to the sclera to prevent premature scleral penetration, scleral depression is performed to confirm the correct location for drainage. When the correct location is found, the syringe is angled away from the eye and the needle is passed through the sclera and choroid into the subretinal space. The surgeon directly observes the needle with indirect ophthalmoscopy as it passes into the subretinal fluid. The detached retina immediately begins to undulate, signifying that subretinal fluid is leaving via the needle. Pressure must be maintained during the drainage, either by the tightened scleral buckle or by an assistant pulling on the rectus muscle bridle sutures or depressing the sclera. Pulling on the rectus muscle or scleral depression may result in movement of the globe if not done carefully. Any movement makes proper needle position difficult. Such movements are eliminated when the scleral buckle is pretightened. As the retina settles and nears the drainage needle, the needle is slow withdrawn until it is removed from the subretinal space. If the retina is inadvertently penetrated, retinopexy should be applied to the site. If the eye is hypotensive after the drainage, it can be reformed with balanced saline, air, or expansile gas.

A scleral cut down and external drainage does not require indirect ophthalmoscopic observation of the needle passing into the subretinal space. Before entrance into the subretinal space is made, a 3- to 4-mm radial sclerotomy is made with a rounded disposable blade. Care must be taken to cut the sclera perpendicular to its surface to avoid shelving of the wound. As the cutdown approaches the suprachoroidal space, magnification with loupes or with the 20-diopter lens is helpful to visualize residual scleral fibers over the choroid. It is important to remove these fibers because during drainage they may swell and prematurely close the drainage site. The anteroposterior location of the drainage site is dependent primarily on the location of the subretinal fluid and the configuration of the detachment.

When possible, the authors prefer to drain in the posterior third of the bed of the buckle. This provides adequate support of the drainage site in the event of complications such as retinal incarceration or choroidal hemorrhage and also provides immediate effective closure of the drainage site when the buckle is pulled up. If, because of the configuration of the detachment or the position of the buckle, it is not possible to drain in the bed of the buckle, a mattress suture is placed through the margins of the sclerotomy to provide closure once drainage ends. Drainage outside the bed of the buckle may allow the buckle to be pulled up as the drainage proceeds. If the drainage site is in the bed of the buckle, the authors do not close the site with a suture because of the danger of erosion of the suture through the sclera by the pressure of the overlying explant. The authors have never seen fibrous ingrowth at the drainage site.

After the suprachoroidal space is entered, diathermy can be used to shrink the margins of sclerotomy to improve choroidal exposure. The choroid then is inspected under magnification for choroidal vessels. If major choroidal vessels are seen, consideration is given to selecting another drainage site if possible. The choroid is diathermized to decrease the chance of bleeding on entry. The diathermy shrinks the choroid and closes choroidal vessels. Under magnification, diathermy can be seen to change the normal smooth, dark blue color of the choroid to a parchment gray color and texture (Fig. 29).

Entry through the choroid and into the subretinal space can be performed by a variety of techniques using needles, diathermy electrodes, or lasers. When a sharp diathermy electrode is used, the diathermy is activated during entry to minimize the chance of hemorrhage. A flat, insulated diathermy electrode may be used to vaporize the choroid to create a choroidotomy without entering the subretinal space.⁸⁷ This technique was reported to have a low complication rate and was successful in achieving drainage in 83% of cases. The remainder required needle drainage.

Photocoagulation using either an external endolaser probe or an indirect ophthalmoscope laser delivery system can also vaporize the choroid to create a choroidotomy. The endolaser probe is placed within 1 to 2 mm of the exposed choroids, taking care to avoid touching the choroid. When using a green wavelength, a power of 0.5 to 1.5 W and a duration of 0.2 to 0.5 second usually is adequate to form a choroidotomy.⁸⁸ When using an infrared diode wavelength, lower power is necessary. A randomized trial demonstrated external argon laser choroidotomy to be as safe and effective as needle choroidotomy.⁸⁹ However, the use of an endolaser probe is expensive. The expense can be eliminated by using a laser indirect ophthalmoscope delivery system.⁹⁰ With this technique the exposed choroid is visualized using the indirect ophthalmoscope and a 20-diopter lens. The magnification of a 20-diopter lens allows excellent visualization of the choroid and subsequent drainage through the choroidotomy. An initial power of 0.3 W and duration of 0.1 to 0.2 seconds is used. The power is increased in 0.1 W increments until drainage is achieved.

All of the preceding techniques are effective and each may have some advantages in select detachments. For example, laser or diathermy choroidotomy may be preferable in shallow detachments, because they do not require entry into the subretinal space. Charles' technique is particularly useful in eyes with a thickened choroid or posteriorly displaced subretinal fluid. However, for most detachments requiring drainage the authors prefer a simple choroidotomy with a 27- to 30-gauge needle. Entry into the subretinal drainage space can be either perpendicular or tangential to the choroid, depending on the amount and location of the subretinal fluid. Usually a single stab incision of the choroid is made; however, when highly viscous subretinal fluid is expected, a large needle or cutting entry may be used, although this larger choroidal incision may increase the chance of choroidal hemorrhage.

After the subretinal space is entered, the needle is quickly removed and the site inspected under magnification. Usually the presence of fluid around the needle signifies entry into the subretinal space (Fig. 30). As the fluid drains, it is important to maintain a relatively normal and constant intraocular pressure to prevent retinal incarceration or hemorrhage. Indentation of globe at the ora serrata in the meridian of the drainage site facilitates elevation of the retina over the site and allows movement of subretinal fluid to the drainage site (Fig. 31). As the fluid drains, the loss of intraocular volume can be compensated for by indentation with cotton-tipped applicators starting 180° away from the drainage site. The site itself is not manipulated so long as good drainage of subretinal fluid proceeds.

As the subretinal fluid drainage slows, pigment particles may be seen in the subretinal fluid, indicating that drainage is nearing completion. When possible, it is helpful if the surgeon or assistant observes the retina over the drainage site ophthalmoscopically. As the fluid drains, the retina will be seen to flutter like a sail in the wind. If visualization of the retina is attempted, care must be taken not to compromise the external drainage site. Despite attempts to maintain constant intraocular pressure as the fluid drains, the eye may soften; this may result in formation of folds in the choroid, which can close the drainage site.

If drainage slows or stops prematurely, the sclerotomy may be manipulated with a fine-toothed forceps by pulling the sclera either tangentially or perpendicularly to the choroid. This often reopens the site and reestablishes flow. When drainage ceases, the site is closed quickly by tightening the buckle suture nearest the drain or by closing the preplaced sclerotomy suture.

Quick inspection with the indirect ophthalmoscope assesses the extent of residual fluid; during this examination, intraocular pressure must be maintained with the traction sutures. If drainage is deemed adequate, the remainder of the buckle sutures are tightened and secured with temporary ties, starting in the location of the primary retinal break. If additional drainage is necessary, the buckle suture or drain suture is released and the drainage site again manipulated to allow further drainage. If no further fluid is obtained but additional drainage is deemed necessary, the original site can be closed with a mattress suture and a second drain site selected; however, this is rarely necessary.

Drainage occasionally may be excessive, particularly in eyes with liquefied vitreous and large retinal breaks. This may result in loss of vitreous volume through the break into the subretinal space and out the drainage site. This event can be anticipated in eyes with large breaks and liquefied vitreous (e.g., in elderly patients with highly myopic eyes). By selecting a drainage site away from the break, one can indent over the break during drainage, thereby closing the break and preventing passage of vitreous contents into the subretinal space (Fig. 32).

When the amount of drainage appears excessive in relation to the amount of subretinal fluid, loss of liquid vitreous should be suspected. If excessive drainage is obtained, volume usually can be restored by tightening the buckle. If this is inadequate or results in too high a buckle, balanced salt solution or sterile air may be carefully injected through the pars plana to restore volume.

The surgical goal of drainage should be kept in mind. Total drainage of subretinal fluid is not necessary and, in some cases, may not be desirable. The goal is for enough drainage to allow the scleral buckle to close the retinal breaks effectively without excessive elevation of intraocular pressure.

A helpful intraoperative sign to determine the adequacy of subretinal fluid drainage is to assess the contour of the retina in relation to the scleral buckle. If after drainage the retina follows the contour of the buckle, drainage is usually adequate even if there are residual subretinal fluid and retinal folds. However, if after drainage and elevation of the buckle the retina does not appear to follow the contour of the buckle or if the buckling effect is not visible beneath the retina, additional drainage usually is necessary (Fig. 33).

After successful subretinal fluid drainage and closure of the drainage site, the buckle is positioned with the preplaced scleral sutures to achieve appropriate support of the retinal pathology. The sutures overlying the retinal break or breaks are pulled up first, followed by the remainder of the sutures. The band, if present, is then adjusted with the silicone sleeve. As the sutures are tightened, they are secured with temporary ties, and the optic nerve is inspected to ascertain arterial perfusion. Once the buckle is positioned and the band adjusted, the fundus is again inspected to determine the status of the retinal breaks in relation to the position and height of the buckle and perfusion of the nerve. The temporary ties allow easy adjustment of the buckle height or position if necessary. This flexibility is a primary advantage of explant techniques.

After the buckle is positioned and the band adjusted, the perfusion of the retina is reassessed. Perfusion can be ensured by inducing pulsations or closure of the central retinal artery by indenting the globe while visualizing the optic nerve with the indirect ophthalmoscope. If pulsations cannot be induced, it must be assumed that the central retinal artery is closed. The maximum duration of central retinal artery closure during retinal detachment surgery that can safely be tolerated is unknown and probably variable among patients.

The authors do not allow the artery to remain closed for more than 5 minutes. If flow is not spontaneously re-established, the pressure is lowered first by loosening the band and then by loosening the sutures away from the retinal tears and drainage site. Usually, with time, the facility of outflow allows the eye to soften enough to reposition the buckle. If blood flow is not re-established, anterior chamber or vitreous taps, as described later, are considered. When the surgeon is satisfied with placement of the buckle and perfusion of the retina, the temporary suture ties are converted to permanent knots.

NONDRAINAGE PROCEDURES

Nondrainage procedures have been shown to reattach the retina with success rates comparable with those of drainage procedures.^69,91–94 The primary advantage of a nondrainage procedure is the avoidance of the possible complications associated with transchoroidal drainage. In eyes with relatively shallow detachments, the eye may soften enough after scleral depression for examination and cryopexy to allow placement of the buckle without intraocular pressure problems. Waiting several minutes between tightening of the scleral sutures also may soften the eye. However, nondrainage techniques often require lowering the intraocular pressure by either medical or surgical means. Intravenous osmotic therapy with 20% mannitol (1–2 g/kg of body weight) can soften the eye but, because of the time lag involved, is most effective if given preoperatively when a nondrainage procedure is anticipated.

Medical attempts to lower pressure usually are effective only for relatively small buckles. For circumferential buckles extending more than one quadrant, intraocular volume must be removed surgically. In phakic eyes, anterior chamber paracentesis can remove up to 0.3 to 0.4 mL of aqueous at one time. Paracentesis is performed under magnification at the limbus with a blade, which is passed in a shelved manner through the cornea, entering the anterior chamber over the iris to protect the lens. The blade then is rotated, thereby opening the wound to allow aqueous to egress. The depth of the anterior chamber is closely monitored to prevent damage to the lens. When enough drainage has been obtained, the blade is turned back to its original entering position. This closes the corneal wound and minimizes the chance of iris incarceration as the blade is removed. The corneal wound is self-sealing (Fig. 34). This technique is effective also in pseudophakic patients with posterior chamber intraocular lenses and intact posterior capsules or capsulotomies sealed by the intraocular lens. Alternatively, a 30-gauge needle can be used to remove aqueous.

In aphakic patients, limbal entry and drainage often results in vitreous incarceration in the corneal wound. This can be avoided by entering through the pars plana with a 27- or 30-gauge needle on a syringe. The needle is then angled anteriorly through the anterior hyaloid into the anterior chamber, from which aqueous fluid is removed (Fig. 35). If the anterior hyaloid is ruptured and the anterior chamber is filled with vitreous, this technique usually is not effective.

When more than 0.4 mL must be removed, the vitreous cavity must be tapped. This is most safely done through the pars plana using a single sclerotomy and a vitreous cutting instrument (Fig. 36). Using a vitreous cutting instrument alleviates the risks of vitreous traction that are inherent to any attempted needle aspiration of liquefied vitreous. The vitrectomy instrument allows removal of a controlled volume, which can be regulated as the buckle is pulled up.

Although the final reattachment rates for nondrainage procedures are excellent, the time for complete resorption of subretinal fluid can be prolonged. Subretinal fluid persists for more than 1 week in approximately 25% of nondrainage cases.^95,96 Several factors have been implicated in the absorption of subretinal fluid after nondrainage procedures. Increased patient age has been correlated by some investigators^19,93 with prolonged absorption of subretinal fluid, but others have not confirmed this association.⁹⁵ Retinal detachments of greater than 2 weeks' duration require more time for subretinal fluid absorption,⁹⁶ but this relationship may not hold for detachments of more than 1 month's duration.⁹⁵ The relationship of the retinal tear to the buckle at the end of surgery correlates with postoperative fluid absorption.^91,95 Retinal detachments with retinal tears that are closed by the buckle at the time of surgery tend to have complete absorption of subretinal fluid within 2 days. If there is a slight amount of fluid between the retina and the buckle, the residual subretinal fluid usually is absorbed within 1 week. When the retinal breaks are significantly elevated from the buckle at the end of surgery, more than one-half of patients require more than 1 week for complete absorption of subretinal fluid, and approximately 25% require up to 3 months. Nondrainage procedures are facilitated by preoperative and postoperative bed rest. The increasing trend toward outpatient scleral buckling surgery makes effective bed rest difficult.

After final adjustments of the buckle have been made, the sutures are tied and the knots rotated to the posterior edge of the buckle. Retrobulbar irrigation of 4 mL of 0.75% bupivacaine significantly decreases postoperative pain after both general or local anesthesia.⁹⁷ Tenon's capsule is then identified in all quadrants. The authors prefer a layered closure, first closing Tenon's capsule to the muscle insertions in all quadrants (Fig. 37). This ensures that the explant and nonabsorbable sutures are covered by the thick Tenon's capsule and also removes tension on the conjunctival closure, thereby minimizing the possibility of the buckle eroding. During conjunctival closure, the relaxation incisions are closed with a running 6-0 plain gut suture while an attempt is made to evert the edges of the incision to diminish the chance of conjunctival inclusion cyst formation. The conjunctiva is secured at the limbus with one or more sutures (Fig. 38).

INTRAOPERATIVE COMPLICATIONS

Corneal Clouding

During scleral buckling procedures, adequate visualization throughout the case is critical to the success of the operation. Corneal clouding is a common intraoperative problem and usually is caused by epithelial edema from increased intraocular pressure, which occurs during scleral depression. The epithelium may also become damaged by desiccation or mechanical trauma during the procedure. Mild amounts of epithelial edema may be resolved with topical glycerin or by rolling the epithelium with a dry cotton-tipped applicator. Extensive epithelial edema usually requires debridement with a rounded blade. The cornea is scraped centripetally starting about 2 to 3 mm from the limbus to preserve the limbal stem cells necessary for postoperative re-epithelialization (Fig. 39). The debrided epithelial cells are removed with a cellulose sponge to prevent dispersion, which may result in epithelial inclusion cysts.

Miosis

A second intraoperative problem obscuring visualization is miosis, which can occur despite adequate preoperative dilation. It may result from hypotony at the time of drainage or from surgical inflammation caused by cryotherapy or paracentesis. If miosis occurs intraoperatively, additional topical dilation with sympathomimetic and parasympatholytic agents is often helpful. If this is unsuccessful, intracameral epinephrine, 0.2 mL of 1:10,000 dilution, may be considered for aphakic or pseudophakic eyes. The safety of epinephrine in phakic eyes has not been established. Photomydriasis with the argon laser may be obtained by treating the iris stroma midway between the pupil and the angle with an endolaser probe directed through the cornea. This dilates the pupil, but the effect is often short-lived and results in considerable postoperative inflammation. Iris hooks passed through the limbus are useful in pseudophakic and aphakic eyes, but may cause cataract in phakic eyes.

Scleral Perforation

Scleral perforation during placement of scleral sutures is a potentially disastrous complication (Fig. 40). Perforation usually is noticed at the time of suture placement and is heralded by the presentation of blood, pigment, subretinal fluid, or a combination thereof through the suture tract. If perforation is recognized, the retina should be inspected immediately with an indirect ophthalmoscope to determine the depth of the perforation. If the suture is in the choroid or subretinal space without evidence of bleeding or continuing subretinal fluid drainage, nothing additional needs to be done, and placement of remaining suture may be performed if necessary.

If subretinal fluid is lost with continuing drainage through the suture tract, drainage is allowed to proceed while an attempt is made to maintain a constant intraocular pressure. When drainage stops, the retina is inspected to determine if drainage has been adequate. If so, any remaining necessary sutures are placed and the buckle positioned.

If the perforation has created a retinal break, this should be supported by extending the buckle to support the break and treating the break with retinopexy. When scleral perforation results in subretinal hemorrhage, immediate pressure over the perforation site should be applied and the eye positioned to prevent gravitation of the blood beneath the fovea. If massive subretinal bleeding occurs, immediate vitrectomy with internal drainage of subretinal fluid and removal of subretinal blood should be considered.⁹⁸ Smaller subretinal hemorrhages can be displaced from the macula by injecting 0.3 to 0.5 cc of air or gas and positioning the patient face-down postoperatively. The bubble will displace the blood from the macula to the peripheral subretinal space.⁹⁹

Drainage Complications

Despite the use of proper techniques, complications occur during drainage of subretinal fluid.¹⁰⁰ A dry tap usually results from failure to perforate the choroid completely. This can be avoided by advancing the needle steadily until fluid is present around the needle. The possibility of subretinal fluid shifting away from the drainage site can be minimized by visualizing the subretinal fluid immediately before drainage. Retinal perforation may occur if the needle strikes the retina because of shallow subretinal fluid or excessive entry of the needle. If the drainage site is in the bed of the buckle, usually no treatment is required, with the possible exception of retinopexy. If the perforation occurs outside the bed of the buckle, a new, unsupported retinal break has been created, and this requires cryotherapy and adjustment of the buckle for adequate support.

Retinal incarceration may occur despite attempts to avoid large fluctuations in intraocular pressure during drainage. Retinal incarceration is identified by the characteristic dimpled appearance of the retina over the drainage site (Fig. 41). Minimal degrees of incarceration rarely result in retinal breaks, but large amounts of incarceration require support. If incarceration occurs outside the bed of the buckle, the buckle should be modified to support the incarceration site.

Choroidal hemorrhage is perhaps the most feared complication of subretinal fluid drainage; it usually occurs at the time of choroidal perforation and is marked by the appearance of dark red blood at the drainage site. If this occurs, the drain site should be closed as quickly as possible with either the buckle or sclerotomy suture and the intraocular pressure elevated above the systolic perfusion pressure. Because choroidal blood flow is not autoregulated, it is dependent on ocular pressure and therefore can be diminished. This may decrease the severity of the choroidal bleeding. Indentation over the drain site may also limit the extent of the hemorrhage. If the drainage site is temporal, the eye should be positioned to place the drainage site as inferiorly as possible to prevent the subretinal blood from gravitating to the fovea. One advantage of nasal drainage sites is that hemorrhage is less likely to reach the fovea. After the drain is closed, the pressure elevated, and the eye positioned, the extent of the hemorrhage is assessed ophthalmoscopically. If a large amount of blood is in the subretinal space and beneath the fovea, a vitrectomy with internal drainage of subretinal blood or gas injection with postoperative face-down positioning should be considered.

Late complications can occur months to years after drainage. Subretinal choroidal neovascularization can occur at the drainage site.^101,102 This can develop into an angiomatous mass that can decrease vision as a result of vitreous hemorrhage. Treatment of the vascular mass with photocoagulation or cryotherapy may induce resolution of the neovascularization.

POSTOPERATIVE COMPLICATIONS

Complications that follow scleral buckling procedures can occur hours to years after surgery.

Glaucoma

A variety of secondary glaucomas may occur after scleral buckling. However, in the first few days after scleral buckling, routine postoperative discomfort and inflammation may obscure the diagnosis of glaucoma unless the intraocular pressure is measured. Applanation tonometry may be difficult postoperatively; a Tono-Pen, Schiötz tonometer, or pneumotonometry may be helpful.

Angle closure after scleral buckling may occur with or without pupillary block. This is manifested by increased intraocular pressure, corneal edema, and shallowing of the peripheral and sometimes central angle. When pupillary block is present, there is accompanying iris bombé. Usually, however, pupillary block is not present. One presumed mechanism of the angle closure in these cases is shallow detachment of the ciliary body, resulting in anterior displacement of the ciliary body occluding the angle.¹⁰³ The detachment of the ciliary body results from serous fluid in the suprachoroidal space, which only occasionally is associated with posterior choroidal detachments.^104,105 This form of angle closure usually occurs 2 to 7 days after surgery but may occur on the first postoperative day. Accurate gonioscopy often is difficult because of corneal clouding, but slit-lamp examination confirms a shallow peripheral angle. High-frequency anterior segment ultrasound can accurately identify supraciliary choroidal effusions, angle closure, or plateau iris configuration.

Initial management consists of medical therapy to control the intraocular pressure and hourly topical corticosteroids to decrease inflammation and minimize formation of synechia. Medical therapy may be attempted for up to 7 days, but the longer the angle remains closed, the greater the chance for the formation of synechia. Corneal indentation with the four-mirror gonioscopy lens sometimes opens the angle by displacing aqueous between the cornea and iris. This is helpful in assessing the presence of synechia.

If medical therapy is unsuccessful in opening the angle, surgery is necessary. When pupillary block is present or cannot be ruled out, iridotomy with either the argon or YAG laser is performed along with the institution of the medical therapy. A patent iridotomy that fails to deepen the angle and lower the pressure confirms that mechanisms other than pupillary block are operative.

Burton and Folk¹⁰⁶ have described a technique of laser iridoplasty that is helpful in alleviating angle closure without pupillary block. Argon laser burns of 200 μm and 0.2-second duration are placed on the iris as close as possible to the angle. This causes the iris to contract and pull away from the angle. Immediate deepening of the angle can be observed by gonioscopy as the treatment proceeds (Fig. 42).

If laser surgery is unsuccessful, the suprachoroidal space is drained.¹⁰⁷ Radial sclerotomies 3 to 4 mm long are centered over the ciliary body in one to four quadrants, depending on the extent of the angle closure. As the suprachoroidal drainage proceeds, balanced salt solution is injected through a self-sealing limbal stab incision to deepen the anterior chamber (Fig. 43). The anterior chamber injection usually deepens the anterior chamber and opens the angle.

If the angle remains closed despite deepening of the anterior chamber and drainage of the suprachoroidal space, it is probably closed by synechia. The synechia can be lysed mechanically with a spatula,¹⁰⁷ but the authors prefer to open the angle by injecting sodium hyaluronate between the cornea and iris through a corneal stab incision with a blunt 25- to 27-gauge cannula (Fig. 44). ¹⁰⁸ The sclerotomies are left open to allow for further drainage and are covered with conjunctiva. Occasionally the angle closes off again as additional suprachoroidal fluid accumulates, and repeat drainage and anterior chamber deepening may be required. If this occurs, excessive height of the buckle should be considered and the possibility of loosening or cutting the encircling band entertained.

Anterior Segment Ischemia

Another cause of postoperative glaucoma is anterior segment ischemia. This should be suspected after encircling procedures with high buckles, particularly if more than one rectus muscle is disinserted. The initial clinical appearance is marked by stromal corneal edema, fibrinous anterior chamber reaction, elevated intraocular pressure and, occasionally, a shallow anterior chamber. Later changes include iris atrophy, anterior and posterior synechiae, cataract, and corneal vascularization. Distinguishing clinically between anterior segment ischemia and postoperative angle closure may be difficult. Mild cases of anterior segment necrosis respond to medical treatment with topical or systemic steroids; however, in severe cases it is necessary to cut the encircling band. Fortunately, with the current trend to use smaller buckles anterior segment ischemia is rarely seen any longer.

The pathogenesis of anterior segment ischemia is unclear. The association with removal of muscles or damage to posterior ciliary arteries suggests that it results from decreased arterial flow to the ciliary body.¹⁰⁹ However, experimental models suggest that the clinical picture of anterior segment ischemia is caused by obstruction by the encircling band of venous drainage from the ciliary body.¹¹⁰ The role of venous obstruction by the encircling band is consistent with the usual beneficial clinical response after cutting the band. Apparently, compromise of either arterial inflow to the ciliary body or venous outflow from the ciliary body can result in anterior segment ischemia.

Patients with sickle cell (SC) hemoglobinopathy are at greater risk for anterior segment ischemia after scleral buckling, even when an encircling band is not placed.¹¹¹ Use of explants and cryotherapy, as opposed to scleral dissection and diathermy, is recommended. Although the incidence of anterior segment ischemia is approximately 3% in the general retinal detachment population, 71% of patients with SC hemoglobinopathy develop this complication after scleral buckling if appropriate preventive measures are not taken.¹¹¹ Preoperative hemoglobin electrophoresis is necessary in all black patients for whom an accurate hemoglobin analysis is not available. Again, the use of smaller buckles and primary vitrectomy has decreased the incidence of anterior segment ischemia in sickle cell patients.

Infection and Extrusion

Scleral buckling materials constitute foreign bodies and are therefore at risk for infection and extrusion. Clinical features of infected buckling materials differ between cases employing diathermy and scleral implants and those using cryotherapy and scleral explants. Infection in the presence of an implant after diathermy manifests as an acute syndrome with pain, proptosis, vitreitis, and scleral abscess, usually occurring in the first 4 to 9 days after surgery.¹¹² The scleral necrosis induced by diathermy is the key factor in this distinct syndrome. The scleral necrosis facilitates scleral abscess formation and enhances intraocular inflammation.

Infections after cryotherapy and scleral explants do not appear immediately. Usually the infection appears 2 weeks to 2 months after surgery, but cases of infection have been reported as soon as a few days and as long as 13 years after scleral buckling surgery.^112–115 Clinical signs include fistula formation, granuloma formation, purulent discharge, and subconjunctival hemorrhage. Progression of the infection may lead to abscess formation with increasing pain, chemosis, and proptosis. A creamy subretinal exudate and retinal whitening may occur overlying the buckle with an exudative retinal detachment. An accompanying vitreitis begins over the buckle. Although this vitreitis is usually a sterile response to bacterial toxins, endophthalmitis may occur.

Staphylococcus is the most common infecting organism.^112–116 Coagulase-positive S. aureus species and gram-negative species appear earlier and with greater virulence. Coagulase-negative staphylococcus organisms, such as S. epidermidis and S. albus, tend to appear later (months) with a chronic granulomatous response and buckle extrusion. Explant extrusion may also occur without evidence of infection. Although chronic subclinical infection may play a role, mechanical factors involving the explant and suture placement may be involved.¹⁷

The incidence of explant infections and extrusion with modern techniques is about 1%.^113,115,116 Preoperative soaking with antibiotics significantly reduces the incidence of both explant infection and extrusion when soft silicone sponges are used.^56,113 Some authors recommend squeezing of sponges in the antibiotic solution or direct antibiotic injections into the sponge to enhance antibiotic penetration.^113,117 The placement of multiple sponges increases the risk of both infection and extrusion.^117,118 Reoperations also have a higher rate of infection and extrusion.^113,116

Effective management of infected scleral buckling material usually requires removal of any soft silicone sponge or large solid silicone elements. Topical and systemic antibiotics may occasionally result in symptomatic improvement but are rarely curative. When an encircling silicone band is present, it may be left in position if all soft silicone sponges and supporting sutures are removed.¹¹³

The resistance of infected scleral buckles to appropriate antimicrobial therapy involves the formation by bacteria of a glycocalix matrix or biofilm on the silicone elements. This biofilm is an extracellular polysaccharide elaborated by bacteria that functions to enhance bacterial adherence and colonization. Within the biofilm, bacteria are protected from the host response by both mechanical and immunologic mechanisms. The biofilm also limits antimicrobial penetration. Biofilm has been demonstrated on infected scleral buckles by electron microscopy. The presence of the biofilm probably explains the necessity of removing infected scleral buckles despite antimicrobial therapy.¹¹⁹

Scleral buckling material extrusion without evidence of infection also usually requires removal of the offending buckle element. However, if removal of the element is deemed undesirable, scleral patch grafts or processed human donor pericardium may be attempted to cover the element and allow conjunctival reepithelialization over the element.^120,121 Occasionally, extruded explants may be well tolerated for extended periods if the patient continues topical antibiotic treatment.¹²² Removal of scleral buckling material carries a risk of re-detachment of 4% to 33%.¹²³ Patients with elements removed for acute infection run a greater risk of re-detachment than do those in whom elements are removed for extrusion.¹²⁴ Factors associated with re-detachment after removal of scleral buckling material include the extent of vitreous traction present in the original detachment and the size of the original detachment. Eyes with buckles in place for longer duration have less chance of re-detachment after removal.¹¹⁶ The presence of proliferative vitreoretinopathy carries a high risk of redetachment.¹²⁴ Because of the risk of re-detachment after removal of scleral buckling material, placement of photocoagulation around retinal breaks or sites of vitreoretinal traction 2 weeks before removal may be worthwhile when possible.

Choroidal Detachments (Choroidal Edema)

Accumulation of serous or serosanguineous fluid in the suprachoroidal space is a relatively common occurrence after scleral buckling and is referred to as choroidal detachment or choroidal edema (Fig. 45). Choroidal detachments occur after both implant diathermy procedures and explant cryotherapy procedures.^57,125–127 The overall incidence of choroidal detachments in two separate series was about 40%.^57,127

The primary pathogenic factor in the development of choroidal detachments is vortex vein obstruction. This has been demonstrated in animal models^110,125,126 and confirmed in clinical studies.^57,127 Using explant and cryotherapy techniques, the incidence of choroidal detachment correlates with the circumferential length and posterior position of the scleral buckle.¹²⁸ If only one quadrant is buckled or only one vortex vein obstructed, the chance of choroidal detachment is minimal. Placement of scleral sutures no further posterior than 14.0 mm from the limbus also lessens the likelihood of choroidal detachment.

Drainage of subretinal fluid is another factor that correlates with choroidal detachment formation.¹²⁶ Choroidal detachments are less likely to develop with nondrainage procedures. Drainage often results in some degree of hypotony, which appears to exacerbate other factors, such as vortex vein compromise, to induce choroidal detachments.¹²⁵ Patient age also correlates with choroidal detachment formation. Packer et al.¹²⁸ found the incidence of choroidal detachment to be 14% in patients 50 years of age or younger, 35% in patients aged 51 to 65 years old, and 53% in patients 66 years and older. The mechanism of patient age in choroidal formation is uncertain but may reflect age-related changes in the integrity of the choroidal vasculature. The extent of retinal detachment also correlates to a limited degree with choroidal detachment formation. If less than 20% of the retina is detached, choroidal detachment is unlikely, but this may simply reflect that smaller detachments are less likely to have encircling posterior buckles and subretinal fluid drainage.

Although the incidence of choroidal detachment is relatively high, the overall effect of choroidal detachments on vision appears minimal. The presence or absence of choroidal detachment has no effect on final visual acuity or anatomic reattachment.¹²⁸ However, this does not mean that choroidal detachment cannot have a detrimental effect in select cases. As previously described, angle-closure glaucoma with visual loss may occur. Severe choroidal detachment may also result in retinal apposition, and choroidal detachment may occur as part of anterior segment ischemia.

Choroidal detachment usually appears 2 to 4 days after surgery. An associated vitreous haze may be present, which presumably is an inflammatory vitreitis. If the extent of the choroidal detachment is mild to moderate, without risk of retinal apposition, and the pressure is acceptable without angle closure, the natural course is benign with resolution over a few weeks. Antiinflammatory medications such as corticosteroids have been used to treat choroidal detachments.^127,128 However, treatment has not been shown to be of visual benefit. Prevention of choroidal detachment by use of routine postoperative systemic corticosteroids (prednisone, equivalent of 80 mg/day) for 2 to 4 weeks has been described in a nonrandomized study.¹²⁷ Although corticosteroid use appeared to diminish the incidence of choroidal detachments, the final visual acuities were not improved.

In patients with massive choroidal detachment and retinal apposition or angle closure and elevated intraocular pressure, surgical intervention is necessary. For angle closure, choroidal drainage and anterior chamber deepening is performed, as previously described (see the section on glaucoma). When massive choroidal detachment with retinal apposition occurs, a hemorrhagic choroidal detachment should be suspected. This is heralded by a sudden increase in the size of the choroidal detachment, often associated with severe pain. Myopic and elderly eyes are predisposed to hemorrhagic choroidal detachment. Ultrasound may distinguish between hemorrhagic, serous, or combined hemorrhagic-serous detachments. Extensive choroidal detachments with retinal apposition, whether hemorrhagic or serous, are best managed with prompt surgical drainage.¹²⁹

In aphakic or pseudophakic eyes, the choroidal detachments are drained with a transscleral cutdown into the suprachoroidal space while infusing air with an air pump through the limbus or anterior pars plana (Fig. 46). In phakic eyes, the anterior chamber is deepened with a balanced saline solution injection through a limbal stab incision before choroidal drainage. As drainage proceeds, additional balanced saline solution is injected either by syringe or infusion bottle into the anterior chamber. If the pupil is widely dilated, fluid should pass from the anterior chamber into the vitreous cavity as the choroidal detachment drains.

Cystoid Macular Edema

Cystoid macular edema is a well-recognized response to ocular surgery. The pathogenesis of cystoid macular edema remains uncertain, but considerable experimental and clinical evidence implicates prostaglandin-mediated inflammation.¹³⁰ Prostaglandins are compounds derived from cell membrane phospholipids, specifically arachidonic acid; they have multiple effects on microvascular physiology. In the eye, prostaglandins and related compounds increase microvascular permeability, resulting in breakdown of the blood–ocular barrier.¹³⁰ It has been hypothesized that prostaglandins or related compounds mediate the increased permeability of perifoveal capillaries that characterize the angiographic appearance of cystoid macular edema.¹³⁰ Prostaglandin production has been demonstrated in both the retina and uvea.¹³¹ In addition, rhegmatogenous subretinal fluid contains both prostacyclin and thromboxane A2 derivatives.¹³² These prostaglandin-related compounds have potent vasoactive properties. The levels of prostacyclin and thromboxane derivatives in subretinal fluid vary greatly among individual patients.

Regardless of which specific compounds are operative, it is clear that cystoid macular edema occurs as a response to ocular inflammation. The surgical trauma of scleral buckling, subretinal fluid drainage, cryotherapy, photocoagulation, or diathermy results in significant ocular inflammation. It is not surprising, therefore, that cystoid macular edema is a relatively common occurrence after scleral buckling. Using cryotherapy and explant techniques, the incidence of angiographic cystoid macular edema 4 to 6 weeks after surgery in phakic eyes was 25% to 28% in three separate studies.^130,133,134 Aphakic eyes have a higher incidence: 40% to 60%. Age greater than 55 years correlates with cystoid macular edema development, but the preoperative status of the macula with regard to attachment and the drainage of subretinal fluid do not seem to affect cystoid macular edema.¹³⁴

The role of cryotherapy in the pathogenesis of cystoid macular edema is controversial. In one study using diathermy and implant techniques, phakic eyes had a 6% incidence of cystoid macular edema 2 months postoperatively.⁴³ It was speculated that diathermy produces less inflammation and that this accounted for the lower incidence. However, in a randomized trial comparing diathermy and implants with cryotherapy and explants, no difference in the incidence of cystoid macular edema was found in phakic, pseudophakic, or aphakic eyes.¹³⁵

The significance of cystoid macular edema on final visual acuity is difficult to assess. Many additional factors, such as preoperative status of the macula, duration of detachment, and formation of macular pucker, confuse the effect of the cystoid macular edema per se in the relatively small series studied to date.¹³⁴ Miyake et al.,¹³⁰ however, demonstrated that eyes with cystoid macular edema after scleral buckling were statistically less likely to obtain vision of 20/40 or better than were eyes that did not develop cystoid macular edema after buckling. The authors find postoperative ocular coherence tomography is useful for the diagnosis of cystoid macular edema.

Prevention of angiographic cystoid macular edema after scleral buckling by use of topical indomethacin has been reported; in a prospective randomized trial of patients undergoing scleral buckling, the incidence of angiographic cystoid macular edema was lowered from 33% in the placebo-treated group to 13% in the indomethacin-treated group.¹³⁰ However, there was no difference in final visual acuity at 12 weeks between the two groups. For the treatment of established cystoid macular edema, a variety of regimens employing combinations of systemic and topical nonsteroidal antiinflammatory agents and topical, subconjunctival, sub-Tenon's, intravitreal, and systemic corticosteroids have been described. The therapeutic rationale for these treatments is to suppress ocular inflammation. Although no treatment for cystoid macular edema after scleral buckling has been proved effective in a randomized clinical trial, treatment with antiinflammatory agents is reasonable.

Macular Pucker

Macular pucker is a major cause of decreased vision after scleral buckling. The cellular constituents of these preretinal membranes are derived from pigment epithelial cells and retinal glia.¹³⁶ The incidence of macular pucker formation after scleral buckling ranges from 3% to 17%. Risk factors identified for the development of macular pucker include preoperative proliferative vitreoretinopathy of grade B or greater, age, total retinal detachment, vitreous hemorrhage, and vitreous loss during drainage.^135,137,138 Myopic patients have a lower risk than emmetropic patients.¹³⁷ The presence of aphakia, uveitis, cataract, or the use of implants as opposed to explants are not factors for the development of macular pucker.¹³⁷

Motility Disturbances

The incidence of heterotropia in the first 6 weeks after scleral buckling surgery is as high as 80%. Fortunately, the vast majority of these deviations are transient, and the incidence of permanent postoperative diplopia is approximately 4%.^139–143 Encircling elements and the placement of large elements, either implants or explants, beneath rectus muscles are correlated with diplopia. The diplopia is probably the result of orbital scarring or of myoscleral adhesions. Traumatic damage to rectus muscles during buckle placement or as a result of periocular anesthetic injections also may be a factor.⁵ Ocular torsion occurs in about half of patients with post scleral buckling diplopia.¹⁴⁴ The effect of muscle removal and subsequent reattachment on postoperative diplopia is controversial. Some authors believe diplopia is more common after muscle mobilization, particularly that of vertical rectus muscles,¹⁴⁰ whereas others believe that no relationship exists between postoperative muscle imbalance and muscle mobilization.^141,145

Initial management of postoperative heterotropia is conservative, because most cases resolve spontaneously. Surgical management can be difficult because buckling elements beneath muscles can hinder muscle recession and adhesions between muscles and buckling elements tend to reform sometimes requiring buckle removal. Because of the anatomic alterations that occur after scleral buckling, standard strabismus surgery principles may not be applicable. For these reasons, prism therapy usually is preferable. If muscle surgery is necessary, an adjustable suture technique should be considered.^5,139

Changes in Refractive Error after Scleral Buckling

The extent and direction of change in refractive error after scleral buckling depend on the surgical technique employed. Encircling procedures induce the greatest change in refractive error. This change is greater for phakic than aphakic eyes because of anterior displacement of the lens resulting in an increased shift.⁷⁵ The amount of direction of refractive error change is related to the height of indentation induced by the encircling band. In a subjective assessment of buckle height after encircling with a 2-mm wide band, Rubin⁷⁵ found that low to moderate buckle height resulted in −1.56 to 2.24 diopters of change in phakic eyes and −0.74 to 1.14 diopters of change in aphakic eyes. However, high encircling buckles of at least 5 mm indentation resulted in a hyperopic shift of 0.35 diopter for phakic eyes and 0.59 diopter for aphakic eyes. This is because low to moderate buckles induced with this band increase axial length, but higher buckles shorten axial length. Using a 2.5-mm encircling band with varying combinations of radial sponges and 7.5-mm hard silicone elements, Smiddy and colleagues,¹⁴³ found an average increase in axial length of 0.99 mm and an average induced myopia of 2.75 diopters.

Segmental buckles, whether implants or explants, have little effect on refractive error.^143,146 However, large radial elements, such as full-thickness sponges that extend anteriorly beyond the ora serrata, may induce an irregular astigmatism. Changes in corneal topography may also occur with segmental circumferential sponges, steepening in the meridians of the buckle. Encircling buckles tend to produce either corneal flattening with focal central steepening or flattening on one side with steepening on the opposite side. These changes may persist for up to 6 months in an irregular and asymmetric configuration.¹⁴⁷

Changes in refractive error after scleral buckling usually stabilize within 2 to 3 months after surgery.^75,146–148 When symptomatic irregular astigmatism is created by an anterior segmental buckle, a hard contact lens may provide some relief. Removal of the element entirely alleviates the astigmatism.¹⁴⁹ Severe symptomatic aniseikonia or anisometropia may be treated with a hard contact lens or, more recently, with keratorefractive surgery.¹⁵⁰

Failure to Reattach

Although most rhegmatogenous retinal detachments can be cured with scleral buckling, a finite number of retinas remain detached after a single scleral buckling procedure. In a retrospective review of 1,088 consecutive cases of retinal detachment undergoing scleral buckling, Rachal and Burton¹⁵¹ reported an initial success rate with one buckling procedure in 76% of patients compared with their final success rate of 89%. In eyes undergoing reoperation, 83% of the retinas eventually were reattached. They analyzed the reasons for failure after one operation and found that most of these were caused by proliferative vitreoretinopathy precluding closure of a known retinal break.

Presumably, proliferative vitreoretinopathy results in traction on the retinal break that is not relieved by the scleral buckle. Because 83% of their failures eventually were reattached with further buckling, they suggested that greater use of the higher and wider buckles, such as those used in the successful reoperations, may decrease failure rates in cases with preoperative signs of proliferative vitreoretinopathy. In addition to proliferative vitreoretinopathy, there are other causes of failure.¹⁵² Unsupported retinal breaks, either new or not recognized at the time of the initial surgery, may occur. Inadequate buckling also results in failure. Usually these problems can be addressed with appropriate revision of the scleral buckle.

The primary cause of permanent surgical failure is severe proliferative vitreoretinopathy, which accounts for more than 90% of all permanent surgical failures. Scleral buckling alone is inadequate to address the pathophysiology of proliferative vitreoretinopathy in advanced stages. Although a limited number of cases with proliferative vitreoretinopathy can be reattached with scleral buckling,⁵⁴ the authors believe that most cases of proliferative vitreoretinopathy of grade C-1 or worse require primary vitrectomy.

Management of Failed Scleral Buckles

Successful management of failed scleral buckles depends on the cause of failure. Missed retinal breaks, new retinal breaks, and inaccurate buckle placement are obvious causes of failure that can be remedied with appropriate revision of the scleral buckle. As discussed earlier, proliferative vitreoretinopathy is the most common cause of failure and usually requires vitrectomy techniques for repair. Occasionally, despite accurate buckle placement and recognition of all retinal breaks, the retina fails to reattach. This usually results from unrelieved traction on the retinal break and may be a harbinger of severe proliferative vitreoretinopathy.

Sometimes bed rest allows the retina to settle on the buckle. Intravitreal injection of a gas bubble with appropriate positioning usually closes the retinal break and allows the retina to settle on the buckle. If wet folds are on the buckle and the break is not bullously elevated, postoperative photocoagulation around the retinal tear can reattach the retina.¹⁵³ This usually is not effective, however, if there is significant traction on the breaks.

Photocoagulation apparently induces choroidal swelling, which seals the breaks. The laser burns provide some immediate adhesive effect and later mature into strong chorioretinal adhesions. In the presence of significant subretinal fluid beneath the break, gas injection and positioning, followed by photocoagulation on the buckle around the break once the retina is reattached, are often effective.

If attempts to reattach the retina with gas injection and photocoagulation are unsuccessful, formal revision of the buckle to relieve the persistent traction may be performed. This is accomplished by placement of radial elements beneath the buckle or by an increase in the height and breadth of the buckle. Generally, formal revision of the buckle is required only in cases with inferior retinal breaks. Superior breaks in the absence of proliferative vitreoretinopathy are nearly always closed with gas and photocoagulation.

Exudative Retinal Detachment

The presence of increasing subretinal fluid postoperatively does not necessarily imply surgical failure. An exudative retinal detachment after scleral buckling may occur after resolution of the rhegmatogenous fluid.^126,154 This fluid usually begins to accumulate 48 to 72 hours after surgery and may or may not be associated with choroidal detachment. Exudative subretinal fluid usually is turbid, in contrast to clear rhegmatogenous fluid, and shifts markedly with changes in position. The key diagnostic feature in distinguishing exudative fluid from recurrent rhegmatogenous fluid is the relationship of the fluid to the retinal breaks. Exudative fluid is not contiguous with the retinal breaks, which usually are flat on the buckle. Exudative fluid may accumulate rapidly over a few days, resulting in total detachment even in cases that were not totally detached before scleral buckling. Photocoagulation may exacerbate exudative fluid accumulation. Exudative fluid spontaneously resolves over 2 weeks to 3 months; in select cases, systemic corticosteroids appear to speed resolution of the fluid.¹⁵⁵

The cause of exudative detachments after scleral buckling is unknown, although vortex vein obstruction by encircling elements and cryopexy-induced inflammation have been implicated. Postoperative hypotony usually is not a factor.

The strongest predictor of both postoperative reattachment and vision is the preoperative status of the macula. Detachments with the macula attached (macula-on) at the time of surgery have a significantly better anatomic and visual result than do detachments in which the macula is detached preoperatively (macula-off). Cumulative data from three series demonstrated successful anatomic reattachment in 376 of 380 cases of macula-on retinal detachment.^163–165 However, despite this high anatomic success rate, decreased visual acuity can occur; usually this is caused by postoperative macular problems such as cystoid macular edema and macular pucker. Approximately 5% to 10% of eyes with macular-on detachments lose two lines or greater from their postoperative vision.

In eyes with successful retinal reattachment of macula-off detachment, approximately 40% to 60% of eyes have final visual acuity of 20/50 or better.^160,163,166 Histologic studies of experimental retinal detachment and of human autopsy eyes suggest that visual recovery is limited by permanent photoreceptor damage, cystoid macular edema, and epiretinal membrane formation.¹³⁶ The extent and duration of preoperative macular elevation correlates with visual outcome. When the macula is bullously elevated, visual recovery is less.^162,166,167 This is probably caused by permanent photoreceptor degeneration, which in experimental retinal detachment increases as the distance between the pigment epithelium and the photoreceptors increases.¹³⁶

There is a strong correlation between the duration of macular detachment and final visual acuity; decreasing visual acuity occurs with increasing duration of detachment. Hassan and colleagues reported that in eyes with a macula-off retinal detachment and preoperative vision of 20/200 or worse, a final vision of 20/40 or better occurred in 71% of eyes with a duration of macular detachment of 10 days or less; 27% of eyes with a duration of macular detachment of 11 days to 6 weeks; and 14% of eyes with a duration of macular detachment greater than 6 weeks.¹⁶⁸ Other studies demonstrate a similar correlation between duration of macular detachment and final visual acuity, suggesting that macula-off retinal detachments should be repaired within 7 to 14 days when possible.¹⁶⁹ Girard and Karpouzas correlated both the duration of macular detachment and visual recovery.¹⁶² They found that macular detachment of more than 7 days' duration significantly decreased the chance of obtaining 20/50 or better postoperative visual acuity. When the macula was detached for 7 days or less, a shallow detachment had a better visual prognosis than a bullous macular detachment. In fact, this study found that shallow macular detachments of less than 7 days' duration had a visual prognosis similar to macula-on detachments, suggesting that macular function can be restored if detachment-related damage is minimal.

These results are consistent with the anatomic changes associated with experimental retinal detachment.¹³⁶ As the duration of detachment increases beyond 2 weeks, cystoid spaces extend throughout the retina. These spaces decrease in size as the retina becomes increasingly atrophic as the detachment persists. Photoreceptor damage is also related to the duration of detachment. Reattachment of the retina does result in some reversal of the histologic changes seen during detachment, but the extent of recovery depends on the duration of detachment. This work in animals is supported by human autopsy studies that demonstrate permanent photoreceptor damage in eyes after retinal reattachment.^170,171 Experimental work suggests that hypoxia is the primary cause of photoreceptor damage.¹⁷²

The advent of ocular coherence tomography (OCT) allows in vivo correlation of the pathologic and experimental studies of retinal detachment. OCT findings in rhegmatogenous retinal detachment demonstrate intraretinal edema and outer retinal separation within 3 days of retinal detachment. These findings are similar to the progression of cystoid spaces from the inner retina to the outer retina, which begins within 3 days of experimental retinal detachment.¹⁷³ OCT findings correlate with visual results. Higher elevation of the retina and intraretinal separation with outer retinal changes as measured by OCT are associated with poor postoperative vision (Fig. 47). Persistent subclinical subretinal fluid has been documented by OCT as a cause of poor postoperative vision (Fig. 48). This fluid may persist for up to a year. Vision improves with resolution of the subretinal fluid. The etiology of this subretinal fluid in the absence of open retinal breaks is unknown, but persistent posterior vitreous traction and hyperosmolar subretinal fluid have been suggested as pathogenic factors. The authors now use OCT routinely in the postoperative evaluation of retinal detachment patients.^174–176

It is apparent that the probability of anatomic success and level of postoperative visual acuity are multifactorial processes. Today, overall reattachment rates of greater than 90% are expected. In select groups of detachment, such as macula-on detachments and detachments with single breaks, anatomic success rates approach 100%.^{37,162,165,168,177}

Although the basic surgical principles of scleral buckling apply to pseudophakic detachments, there are considerations and problems unique to pseudophakic eyes. As techniques for cataract extraction and lens implantation have evolved, retinal detachment surgery also has evolved to address the particular consequences of the pseudophakic state.

Perhaps the greatest problem in the repair of pseudophakic detachments is the difficulty of visualizing the peripheral retina. Retinal breaks cannot be found in 9% to 20% of pseudophakic detachments, and this may be a risk factor for surgical failure.^54,70,163 This can result from: (a) miosis associated with iris-fixated lenses, (b) difficulty seeing through the edge of the intraocular lens, (c) cortical remnants, and (d) capsular opacification, particularly with small capsulorrhexis incisions. Visualization tends to be more difficult in cases with anterior chamber or iris-fixated lenses. In one series, incomplete visualization of the ora serrata occurred in 44% of eyes with iris-fixated lenses and 27% with anterior chamber lenses.¹⁶¹ The location of the intraocular lens presents specific problems during scleral buckling. With anterior chamber lenses, care must be taken when the sclera is depressed anteriorly not to force the intraocular lens into the angle, which may result in bleeding. The mobility of iris-fixated lenses can result in corneal damage from anterior displacement of the iris and intraocular lens. This can occur at the time of subretinal fluid drainage if the eyes become hypotonus. An intravitreal gas bubble may also anteriorly displace the iris–intraocular lens plane. Placement of a gas bubble, suture, or sodium hyaluronate in the anterior chamber before intravitreal injection prevents the anterior displacement of the intraocular lens (Fig. 49). ^179–181 Postoperatively, pupillary block or choroidal detachment may result in anterior displacement of the intraocular lens against the cornea, requiring reformation of the anterior chamber. Iris-fixated and posterior chamber lenses may dislocate into the vitreous cavity. Overall, posterior chamber intraocular lenses pose the fewest difficulties during scleral buckling. However, the recent trend toward small optical zones and capsulorrhexis may compromise visualization. Because of the problems with poor visualization, encircling procedures usually are indicated in pseudophakic cases.^70,162,182

More than half of pseudophakic detachments occur in the first year after surgery, with an additional 10% to 20% occurring after 2 years. In eyes that develop retinal detachment after YAG capsulotomy or secondary intraocular lens implantation, there is a strong tendency (47%–59%) for the detachment to occur within 3 months of the procedure.¹⁸² Pseudophakic detachments typically present with the macula detached. In two large series the macula was detached in 77% and 81% of cases.^162,182,183

Although earlier reports suggested that anterior chamber and iris-fixated lenses had a poorer anatomic and visual prognosis,¹⁶¹ more recent reports show no difference between these lenses and posterior chamber lenses.^70,162,182 Reported reattachment rates in these series range from 85% to 96%. As with phakic detachments, PVR is responsible for the vast majority of surgical failures.

The visual results for pseudophakic detachments depend primarily on the preoperative status of the macula. As expected, macula-on detachments have an excellent prognosis, with 94% to 96% of eyes obtaining 20/50 or better.⁷⁰ Unfortunately, pseudophakic detachments typically present with the macula detached, and overall visual recovery of 20/40 or better occurs in only approximately 50% of eyes.^70,162,182 Some studies suggest anterior chamber lenses have a poorer visual prognosis,^161,182 whereas other studies find no difference.^70,162 The most common causes for decreased vision after successful reattachment include cystoid macular edema, macular pucker, and photoreceptor dysfunction.^162,182

As the refractive state of pseudophakia has become more important to patients and cataract surgeons, retina surgeons need to consider the refractive implications of retinal detachment repair with scleral buckling. The authors avoid large high scleral buckles in pseudophakic patients and prefer primary vitrectomy techniques with a low encircling band when possible. In the refractive surgery era, scleral buckle induced myopia and anisometropia should be minimized when possible and can be treated with refractive surgery techniques.¹⁸⁴

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