Chapter 24
Complications of Glaucoma Surgery
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Suprachoroidal hemorrhage is a serious complication that can be seen during or after any intraocular surgery. If it occurs intraoperatively and cannot be controlled (i.e., expulsive hemorrhage), it can lead to loss of vision. The incidence of this complication in the general population after cataract extraction is approximately 0.2%.1–3 The incidence of suprachoroidal hemorrhage in glaucoma patients undergoing various types of intraocular surgery has been reported to be 0.73%.4–6 Ocular risk factors for suprachoroidal hemorrhage include glaucoma, aphakia, pseudophakia, previous vitrectomy, vitrectomy at the time of glaucoma surgery, myopia, and postoperative hypotony. Systemic risk factors are arteriosclerosis, high blood pressure, tachycardia, and bleeding disorders. The source of the hemorrhage usually is one of the posterior ciliary arteries, particularly the point of entrance of the short posterior ciliary vessels into the suprachoroidal space. There seems to be a vascular necrosis and subsequent rupture of the vascular wall.7

Intraoperative suprachoroidal hemorrhage can be associated with sudden collapse of the anterior chamber. The patient may complain of sudden pain breaking through the local anesthesia. If the process is gradual, a dark mass can be observed through the pupil to evolve slowly, but if the process is abrupt the hemorrhage is more expulsive.

Postoperative suprachoroidal hemorrhage usually occurs within the first week after glaucoma surgery and usually is associated with postoperative hypotony4–6 (Fig. 1). The development of a suprachoroidal hemorrhage typically is acute and associated with the sudden onset of severe pain. Examination of the anterior segment frequently reveals a shallow anterior chamber and a normal or high intraocular pressure (IOP). On fundus examination, a detached and dark choroid is noted. The choroidal elevations have a dark, reddish brown color. Some patients present with bleeding into the vitreous cavity and, uncommonly, retinal detachment. Ultrasonography can be used to diagnose suprachoroidal hemorrhage when fundus examination is not possible.

Fig. 1. Slit-lamp photograph. A. Massive suprachoroidal hemorrhage after Molteno tube shunt implantation. The tube with an intraluminal suture in place can be seen. B. Slit-beam illumination reveals a flat anterior chamber.

Intraoperatively, once a suprachoroidal hemorrhage has been identified, prompt and secure closure of the incision is the first goal of the treatment, with gentle repositioning of prolapsed uvea. The surgeon's finger can be used to tamponade the incision site temporarily while sutures are placed. Meanwhile, intravenous acetazolamide (500 mg) and mannitol 20% (1 to 1.5 g/kg) are administered. Once the eye has been closed, the anterior chamber can be reformed through the incision or a paracentesis tract. After this point, a conservative approach probably is appropriate. Some authors advise immediate drainage of the hemorrhage through posterior sclerostomies (usually not possible because it rapidly clots), sometimes combined with a vitrectomy in aphakic patients, especially if the hemorrhage is large. Prognosis for recovery of vision is good as long as the eye can be closed without loss of uvea.

Treatment of postoperative suprachoroidal hemorrhage is directed toward control of the IOP and relief of pain. Most of these eyes do well with this conservative management, and surgical drainage usually is not necessary.8 The indications for drainage include intolerable pain, a persistent flat anterior chamber, and massive “kissing” choroidal detachments (see later). A waiting period of about 7 days after a suprachoroidal hemorrhage is advised for the fibrinolytic response to liquefy the clot and allow for more effective evacuation of the suprachoroidal space. Drainage through a sclerotomy into the suprachoroidal space reveals liquefied blood, which usually is red or black. Occasionally, the fluid drained is a mixture of clear, straw-colored fluid and reddish to black liquefied blood. Bleeding into the vitreous cavity at the time of the hemorrhage and retinal detachment worsen the visual prognosis.


Several steps can be taken in high-risk eyes. Before surgery, correction of bleeding problems and discontinuation of inhibitors of platelet aggregation (i.e., acetylsalicylic acid) is recommended. Preoperative intravenous mannitol at the time of surgery should be used. Prophylactic sclerostomies can be helpful. Use of viscoelastic and tight suturing of the scleral flap to prevent hypotony are recommended. The patient is urged to restrict activities (bending, weight lifting) and to avoid Valsalvapositive conditions (constipation, vigorous coughing, sneezing, or nose-blowing) during the early postoperative period.


Hyphema is a common postoperative occurrence in glaucomatous eyes after filtration surgery, surgical peripheral iridectomy, and trabeculotomy. Bleeding commonly arises from the ciliary body or cut ends of the Schlemm's canal, although it also might arise from the corneoscleral incision or iris.

In general, hyphema presents at surgery or within the first 2 or 3 days after surgery. Intraoperatively, if a bleeding spot does not stop spontaneously, it must be identified and coagulated. During filtration surgery, bleeding is decreased by performing the internal sclerostomy as far anteriorly as possible.

In most cases, no treatment is necessary and the blood is absorbed within a brief period of time. Cycloplegics, corticosteroids, restriction of activity, and elevation of head of the bed 30° to 45° (to prevent blood from obstructing a superior sclerostomy) are recommended. Increased IOP can occur, particularly if the filtering site is obstructed by a blood clot, and it should be treated if necessary with aqueous suppressants. Injection of tissue-plasminogen activator may be considered (see later). Surgical evacuation is considered depending on the level of IOP, size of hyphema, severity of optic nerve damage, likelihood of corneal blood staining, and presence of sickle trait or sickle cell anemia (infarction of the optic nerve can occur at relatively low IOP, and carbonic anhydrase inhibitors are contraindicated). Liquid blood can be easily removed with irrigation. If a clot has formed, it can be removed by expression with viscoelastic or with a vitrectomy instrument set at low vacuum.


Hypotony (i.e., IOP less than 6 mmHg) after glaucoma surgery can result from excessive aqueous outflow (related to excessive filtration [see later], wound leak, or cyclodialysis cleft) or to reduced aqueous production (related to ciliochoroidal detachment, inflammation, inadvertent use of aqueous suppressants, or extensive cyclodestruction).9 These conditions can coexist. For example, low IOP from overfiltration can induce ciliochoroidal detachment and secondary decreased aqueous production. Possible complications include flat anterior chamber, gradual failure of the bleb, visual loss, cataract, corneal edema, Descemet's membrane folds, choroidal hemorrhage, macular and optic disc edema, and chorioretinal folds (predominantly in young myopic patients). According to Spaeth (Table 1),10 the severity of flat anterior chamber can be classified as grade I when there is peripheral-iris apposition, grade II with pupillary border-corneal apposition, or grade III with lens-corneal touch (see Chapter 15). The central anterior chamber depth also can be described relative to the corneal thickness. Choroidal effusion occurs when fluid collects in the suprachoroidal space (Fig. 2), resulting in forward movement of the lens iris diaphragm with anterior chamber shallowing. On fundus examination, moundlike elevations of the choroid, more commonly in the periphery, are visible.


TABLE 1. Classification of Flat Anterior Chamber

  Grade I, peripheral iris-corneal apposition
  Grade II, pupillary border-corneal apposition
  Grade III, lens-corneal apposition

(Spaeth GL: Glaucoma surgery. In Tasman W, Jaeger EA [eds]: Duane's Clinical Ophthalmology, vol 5, pp 1–53. Philadelphia, JB Lippincott, 1992)


Fig. 2. Composite of ultrasound biomicroscopic examination. A peripheral choroidal effusion (large arrow) is seen as an acoustically hollow area in the suprachoroidal space. The anterior chamber is moderately shallow (small arrow, intraocular lens).

Hypotony Maculopathy

Some patients with intraocular hypotony develop loss of central vision secondary to marked irregular folding of the choroid and retina. Initially, these folds are broad and not sharply delineated. They tend to radiate outward in a branching fashion temporally from the optic disc and concentrically or irregularly nasally to the disc. There may be swelling of the peripapillary choroid simulating papilledema (Fig. 3). The retina often shows a series of stellate folds around the center of the fovea. The retinal vessels are tortuous and sometimes engorged. The primary cause of visual loss is the marked folding of the central retina. Early detection of this condition is important because correction of the cause usually results in visual improvement. In cases of prolonged hypotony, permanent pigmented lines, caused by changes in the retinal pigment epithelium, occur in the macular area and nasally. A postoperative bleb leak and a cyclodialysis cleft were formerly the most common causes of hypotony maculopathy. The incidence of hypotony maculopathy after glaucoma surgery has increased with the use of antifibrotic agents, specifically mitomycin C. A direct toxic of mitomycin cannot be ruled out. The maculopathy is most likely to occur in young myopic patients, who may have a sclera more susceptible to swelling and contraction.11–14

Fig. 3. Fundus photograph. Hypotony maculopathy with choroidal folds, retinal striae, and marked swelling of the peripapillary choroid simulating papilledema.

Phthisis can occur in some complicated cases with severe chronic hypotony. The sclera shrinks and thickens, and the pull of the extraocular muscles deforms and squares the eyeball. There may be retinal gliosis and formation of a cyclitic membrane in the end stage. Ultimately, impairment of intraocular fluid dynamics results in corneal edema, cataract, and calcification of the corneal epithelium, pigment epithelium, and inner choroid.

The initial management of early postoperative hypotony with a formed anterior chamber is conservative. Topical steroids and cycloplegics are used. Restrictions in activity (bending, weight lifting) and avoidance of Valsalva-positive conditions are recommended, especially in patients at risk for suprachoroidal hemorrhage (see earlier). If there is hyposecretion related to intraocular inflammation, ciliochoroidal detachment, or both, the initial treatment consists of intense corticosteroid therapy and long-acting cycloplegics, which stabilize the blood-aqueous barrier. Intervention is indicated in patients with hypotony associated with other complications and in persistent, low IOP with loss of visual acuity and hypotony maculopathy. After filtration surgery, prompt management is indicated, also when there is loss of bleb height. Treatment should be aimed at correcting the specific cause of hypotony. When there is lens-corneal touch (flat anterior chamber, grade III) immediate surgical intervention is necessary to prevent endothelial damage and cataract formation (see Chapter 15). Reformation of the anterior chamber with air, balanced salt solution, or, preferably, a viscoelastic can be done at the slit lamp or under the operating microscope through the paracentesis made intraoperatively. Viscoelastic material is best for maintaining, at least temporarily, the anterior chamber depth. When there are large and appositional choroidal effusions, drainage of the fluid also is necessary (Fig. 4). The technique is described in detail in Chapter 15.

Fig. 4. B-scan ultrasound showing hyperreflective dome-shaped echoes corresponding to the detached choroid-retina, with acoustically hollow content corresponding to the fluid accumulated in the suprachoroidal space.

When hypotony results from overfiltration of a filtering bleb, several options are available. A large bandage contact lens,15 symblepharon ring,16 and Simmons' shell17 can be helpful. Bandage contact lenses should have a diameter of at least 16 to 17 mm to cover the filtering bleb. They are not efficient in severe and chronic cases. The Simmons' shell is a 22-mm, dome-shaped rigid shell of transparent polymethylmethacrylate. A raised platform on the concave inner surface of the shell is positioned over the sclerostomy site. The curvature is designed to selectively indent the perilimbal area when pressure dressing is applied. The Simmons' shell usually is effective; however, it may be uncomfortable. Tonometry is not possible to monitor the IOP. Decentration of the shell is frequent unless sutured to the conjunctiva. It requires close (daily) monitoring, and corneal complications (epithelial defects and abrasions) are common. It is particularly difficult for monocular patients. Several chemical and thermal treatments have been used to induce an inflammatory reaction in the filtering bleb, which modify the morphologic features of the filtering blebs and increase the IOP. These procedures include topical application of 0.25% to 1% silver nitrate or 50% trichloracetic acid to the bleb surface,18 cryotherapy,19 diathermy and cauterization,20 argon laser,21 and, recently, the neodymium:yttriumaluminum-garnet (Nd:YAG) thermal laser.22 More than one treatment session might be needed to achieve the desired goal. Possible complications include postoperative discomfort, bleb leak, transient increase in IOP, and corneal edema. Cryotherapy is best done under retrobulbar or peribulbar anesthesia. The probe is applied initially to the lateral borders of the bleb. Before starting the freeze, firm pressure is applied with the cryoprobe to bring the bleb surface tissues into apposition with the underlying sclera. Several applications (two to five) using a temperature of -50° to -80°C and a duration of application of 10 to 30 seconds are used. Nd:YAG thermal laser treatment of overfiltering and leaking blebs has been described more recently. It is best done under regional anesthesia. For this procedure, the continuous-wave mode is required. Energy levels range between 3.0 and 4.0 J, with the laser offset between 0.9 and 1.2 mm and the aiming beam focused in the conjunctival epithelium. The goal is to induce whitening and wrinkling of the conjunctival epithelium. A grid pattern of 30 to 40 spots of laser is placed over the entire bleb. Postoperatively, oral aqueous suppressants and a compressive or “torpedo” (i.e., cotton plug placed directly over the bleb surface) patch are used during the first 48 hours. Injection of autologous blood into the bleb can reduce overfiltration and resolve bleb leaks.23–26 Inflammatory cells and serum proteins from the injected blood may accelerate the inflammatory and healing process, which decreases filtration (Fig. 5). Possible complications include hyphema, endophthalmitis, increase in IOP requiring surgical intervention, bleb failure, corneal blood staining, and corneal graft rejection.27–30 Finally, surgical revision may be needed.31–35 Resuturing the scleral flap and scleral patch grafting (when resuturing is not possible) have been successfully used in patients with hypotony maculopathy associated with overfiltering the filtering bleb. Alternatively, two sets of stitches in the scleral flap, with one set tied tightly, can raise the IOP, stretch the sclera, and flatten chorioretinal folds. Sliding conjunctival flaps or free conjunctival grafts also can be helpful (see later).

Fig. 5. Slit-lamp photograph. Appearance of a filtration bleb after autologous blood injection, which was used to reverse chronic hypotony.


Three conditions should be considered in patients with postoperative flat anterior chamber and elevated or normal IOP: suprachoroidal hemorrhage (see earlier), aqueous misdirection, and pupillary block.

Aqueous Misdirection

Aqueous misdirection, or malignant glaucoma or ciliary block glaucoma, is characterized by a shallowing or flattening of the anterior chamber without pupillary block (i.e., in presence of a patent iridectomy) or choroidal disease (such as suprachoroidal hemorrhage), commonly with an accompanying rise in IOP.36–38 It occurs in 2% to 4% of patients operated on for angle-closure glaucoma but can occur after any type of incisional surgery. The chance of developing malignant glaucoma is greatest in phakic hyperopic (small) eyes with angle-closure glaucoma.

In this condition, aqueous is diverted posteriorly toward the vitreous cavity, increasing the vitreous volume and shallowing the anterior chamber.36 Decompression and shallowing of the anterior chamber appears to be a predisposing factor by inducing forward movement of the peripheral anterior hyaloid. Small choroidal effusions and shallow anterior chamber sometimes occur before the episode of aqueous misdirection. The anterior hyaloid could be placed into direct apposition with portions of the secreting ciliary processes. Thus, aqueous humor might move directly into the vitreous cavity. In hyperopic eyes (with a crowded middle segment), the peripheral anterior hyaloid in its normal position probably is close to the posterior ciliary body. In such eyes, cataract and filtration surgery should be considered as high risk for aqueous misdirection. In aqueous misdirection, a relative resistance to the anterior movement of aqueous humor in the anterior vitreous face or the anterior hyaloid membrane probably occurs. The increased resistance can be related either to abnormal permeability or to available hyaloid surface area for fluid transfer. In normal circumstances, the anterior hyaloid and vitreous offer insignificant resistance to forward fluid flow. In some cases, pupillary block occurs first and is followed by aqueous misdirection. Perhaps a sudden onset of pupillary block forces aqueous humor into the vitreous and expands the vitreous volume, displacing forward the peripheral hyaloid into direct apposition with the ciliary body.39

Aqueous misdirection usually occurs in the early postoperative period after filtration or cataract surgery. The anterior chamber is shallow, and the IOP is high (Fig. 6). However, with a functioning filtration bleb, the IOP may not be high. The peripheral iridectomy is patent, and a dilated examination and B-scan ultrasound confirm the absence of choroidal effusion of hemorrhage. If the adequacy of the surgical iridectomy is in doubt and pupillary block is possible, a laser iridotomy should be performed.

Fig. 6. Slit-lamp photographs. A. Aqueous misdirection. The anterior chamber is shallow. Two patent peripheral iridotomies are barely seen at the 10- and 1-o'clock positions. Intraocular pressure was 42 mmHg. B. Same eye 4 weeks after pars plana tube insertion of aqueous shunt with vitrectomy. The anterior chamber is deep. The temporal iridectomy is enlarged. Intraocular pressure was 12 mmHg. (Azuara-Blanco A, Katz LJ, Gandham SB, Spaeth GL: Pars plana tube insertion of aqueous shunt with vitrectomy in malignant glaucoma. Arch Ophthalmol 116:808, 1998)

Medical treatment and laser and vitreous surgery all have been useful options to treat aqueous misdirection. This condition is initially managed with mydriatic-cycloplegic drops,40 aqueous suppressants, and hyperosmotics. Topical 1% atropine or 1% cyclopentolate four times daily and 2.5% phenylephrine four times daily are used. These agents hopefully result in a posterior movement of the lens-iris diaphragm. In cases of aphakic aqueous misdirection, mydriatic-cycloplegic drops are of little benefit. However, it is reasonable to use them for their effect on relaxation of the ciliary body muscle. Systemic carbonic anhydrase inhibitors and topical beta-adrenergic blocking agents in full doses are important. Osmotics (isosorbide, glycerin, or intravenous mannitol) also can be helpful to decrease the fluid content of the vitreous cavity and can be given every 12 hours. If it is well tolerated and there are no contraindications, the medical treatment is tried for 2 to 4 days. If the condition is relieved (i.e., the anterior chamber has deepened), the hyperosmostic agents are discontinued first, and the aqueous suppressants are reduced or stopped over several days. Phenylephrine drops can be stopped, but the cycloplegic drops should be continued for months to years or, in some cases, indefinitely to prevent the recurrence of this condition. Medical treatment relieves about 50% of cases of aqueous misdirection. If medical therapy is unsuccessful and the ocular media are clear, a Nd:YAG laser capsulotomy and hyaloidotomy is used to disrupt the anterior vitreous face, especially in pseudophakic and aphakic patients.41 The usual beginning laser energy is between 2 and 4 mJ. The focus is placed posterior to the anterior hyaloid. After a successful Nd:YAG hyaloidotomy, a slight deepening usually is seen, which increases over the next hours. In pseudophakic eyes, a peripheral hyaloidotomy is more efficient than a central hyaloidotomy because the lens capsule and intraocular lens can prevent communication between the vitreous cavity and the anterior chamber. In phakic eyes, Nd:YAG hyaloidotomy can be tried through the peripheral iridectomy, focusing behind the zonules but in front of the ciliary body. However, a clear view and sharp focusing may not be possible, and there is a risk of lens or zonular injury. Pars plana vitrectomy should be considered when other therapies fail.42–44 A standard three-port pars plana vitrectomy, removing the anterior vitreous and part of the anterior hyaloid, is done. In phakic patients, the lens sometimes can be spared, but the probability of recurrence is higher. Pars plana tube shunt insertion with vitrectomy has been recommended to treat patients with aqueous misdirection, especially in patients with angle-closure glaucoma. The implantation of the tube shunt through pars plana can help to prevent recurrence of this condition and can help in long-term control of IOP.44

PREVENTION. In high-risk eyes undergoing cataract or filtration surgery, the decompression and shallowing of the anterior chamber should be minimized. In filtration procedures, the use of viscoelastic and a large peripheral iridectomy can be helpful. Postoperative overfiltration should be avoided with a thick scleral flap sutured tighter and with more sutures than usual. Postoperatively, judicious suture lysis or cutting/pulling releasable sutures and slow tapering of cycloplegics are recommended. A postoperative shallow anterior chamber caused by overfiltration should be vigorously treated.

Pupillary Block

Pupillary block can be caused by adhesions between the iris and lens, pseudophakos, or vitreous. The inability of aqueous humor to pass from the posterior to the anterior chamber results in the forward movement of the peripheral iris and closure of the drainage angle. Pupillary block typically occurs as a flat or shallow anterior chamber with normal or elevated pressure. It may be difficult to distinguish from malignant glaucoma.

Although a peripheral iridectomy is intended at the time of filtration surgery, in a few patients only the stroma of the iris is removed and the posterior pigment epithelium is left intact. In these patients, blockage may develop. In other patients, the iris may become incarcerated in the wound or the iridectomy may be obstructed by intraocular tissue such as Descemet's membrane, anterior hyaloid surface, vitreous (in aphakic eyes), or ciliary processes.

Therapy with cycloplegic-mydriatics may resolve pupillary block, but a Nd:YAG peripheral iridotomy should be done. The anterior chamber readily deepens after iridotomy is performed, although in the presence of localized compartments of blockage, multiple iridotomies are necessary. This deepening usually is associated with the sudden escape of aqueous humor through the iridectomy and confirms the diagnosis of pupillary block. If laser iridotomy cannot be completed, a surgical iridectomy should be done.


Unexplained loss of central visual field (i.e., “wipeout”) after glaucoma surgery is rare. Older patients with advanced visual field defects affecting the central field with split fixation are at increased risk. Early, undiagnosed postoperative IOP spikes and severe postoperative hypotony have been suspected as causes for wipeout.45,46

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Intraoperative Complications of Filtration Procedures

Conjunctival buttonholes and tears can lead to failure of bleb formation and flat anterior chamber. The usual cause for conjunctival buttonholes is penetration of the tissue by the tip of a sharp instrument (needle, scissors, blade) or the teeth of a forceps. Buttonholes and tears are more likely to occur in patients with extensive conjunctival scarring. To diagnose a buttonhole intraoperatively, the conjunctiva should be carefully examined at the end of the procedure by filling the anterior chamber and raising the filtering bleb. If recognized, the buttonhole should be closed at the time of surgery. If it is located in the center of the conjunctival flap, a “purse string” closure is attempted, either internally on the undersurface of the conjunctiva or externally if the flap already has been reapproximated. A 10-0 or 11-0 nylon on a tapered (“vascular”) needle should be used. When the conjunctival buttonhole or tear occurs at the limbus, it can be sutured directly to the cornea, which should be de-epithelialized. A mattress suture or, if large, a running suture with 10-0 nylon can be used. When the buttonhole or tear occurs near the incised edge of a limbal-based conjunctival flap, the sutures used to close the conjunctival incision can be placed anterior to the tear to close it.

SCLERAL FLAP DISINSERTION. A thin scleral flap can be torn or amputated from its base during the surgical procedure. If a sclerostomy has not been performed, a new scleral flap should be dissected in a different area. If a sclerostomy has been done already, reapproximation of the scleral flap can be attempted with 10-0 or 11-0 nylon sutures. If unsuccessful, additional tissue usually is necessary to cover the sclerostomy. This can be obtained by transferring a piece of Tenon's capsule or a flap of partial-thickness sclera from the area adjacent to the defect. Alternatively, donor sclera, fascia lata, or pericardium can be used.

VITREOUS LOSS. Vitreous loss during glaucoma surgery is an uncommon complication, especially in phakic eyes. Conditions that may predispose to vitreous loss include high myopia, previous intraocular surgery, trauma, aphakia, and a subluxated lens. Loss of vitreous can be associated with several complications such as corneal edema, epithelial downgrowth, uveitis, retinal detachment, cystoid macular edema, and endophthalmitis. The vitreous can mechanically plug the sclerostomy and lead to filtration failure. Vitreous should be removed from the surgical site and anterior chamber with a vitrectomy instrument, avoiding damage to the lens in phakic eyes. In the aphakic eye with vitreous filling the anterior chamber, an anterior vitrectomy can be planned as part of the primary procedure. In phakic or pseudophakic eyes with vitreous in the anterior chamber, pars plana vitrectomy may be considered to adequately remove the vitreous from the posterior segment and to avoid lens or intraocular lens subluxation and lens injury.

Postoperative Complications of Filtration Procedures

BLEB LEAK. Bleb leaks can occur early in the postoperative period or months to years after filtration surgery. An inadvertent buttonhole in the conjunctiva during a filtering procedure or a wound leak through the conjunctival incision can be responsible for an early leaking bleb. Spontaneous late bleb leaks are more frequent in avascular, thin blebs, which occur more frequently when antimetabolites are used in the filtering procedure and after full-thickness procedures. The incidence of early and late bleb leaks probably is higher in trabeculectomies supplemented with antimetabolites than nonsupplemented surgeries.47,48 Leakage of the filtering bleb can be associated with hypotony, shallow or flat anterior chamber, and choroidal detachment and may increase the chances for bleb infection and subsequent endophthalmitis. Early leaking can flatten the bleb and lead to subconjunctival-episcleral fibrosis, which would jeopardize a satisfactory long-term filtration.

Bleb leaks are detected with the Seidel test (Table 2). The tear film is stained with fluorescein. For this purpose, a fluorescein strip is applied to the inferior tarsal conjunctiva or, gently, directly to the bleb. Without applying pressure, the eye is examined under cobalt blue illumination. If there is a leak, unstained aqueous humor is seen flowing into the tear film (Fig. 7). If there is no spontaneous leakage, pressure may be gently applied to the globe or to the bleb while the suspicious area is examined.


TABLE 2. Seidel's Test

  1. Cobalt blue illumination
  2. Fluorescein stain; fluorescein strips to gently “paint” the bleb
  3. Aqueous humor flowing into the tear film is seen
  4. In absence of spontaneous leakage, pressure may be carefully applied to the globe or to the bleb


Fig. 7. Slit-lamp photograph of a positive Seidel's test result.

The need and urgency of the management of bleb leaks depend on several factors. Some patients, particularly monocular individuals with leaking blebs that have had previous episodes of bleb-related infections, ocular hypotony, shallow or flat anterior chamber, loss of bleb elevation, or reduced vision always should be treated. However, if there are no complications, such as in patients with late leaks with formed blebs, normal IOP, good central vision, and without previous episodes of bleb-related infection, the leak may not require therapy. Observation sometimes is possible to allow spontaneous closure of the leak. Pharmacologic medical treatment with agents that decrease aqueous secretion (topical beta blockers, carbonic anhydrase inhibitors, or both) and discontinuation of topical steroids, with or without patching, may help the spontaneous closure of these defects by reducing flow of aqueous through the fistula. Prophylactic broad-spectrum antibiotic coverage, alternating different antibiotics, is recommended by some. Patient education regarding symptoms of bleb-related ocular infection is crucial for prompt diagnosis and management.

Therapeutic modalities to treat leaking blebs include pressure patching, bandage contact lens,15 Simmons' shell,17 injection of autologous blood,23–30 cryopexy,19 thermal Nd:YAG laser (see earlier),22 cyanoacrylate glue,49–51 fibrin tissue glue,52–53 and surgical revision.54 A large-diameter (17 to 20 mm) soft therapeutic contact lens can be helpful. The contact lens should be kept in place, if possible, for 1 week to allow reepithelization. Broad-spectrum topical antibiotics should be administered to protect against infection, and close observation is mandatory. Fibrin tissue glue is a mixture of fibrinogen and thrombin that induces the formation of a clot, which can seal bleb leaks.52–57 It is a nonirritating procedure that requires no patching. Tisseel (Immuno AG Industries, Vienna, Austria) is a commercialized fibrin glue—not approved by the Food and Drug Administration—that has the disadvantage of being prepared from pooled plasma and thus may have the potential risk of transmitting blood-borne pathogens.57 Autologous fibrin tissue glue is prepared from the patient's blood, therefore eliminating the risk for disease transmission.53 Cyanoacrylate glue (Histo-acryl, B. Brown Melsungen, Germany) adheres to tissues and can effectively close an early bleb leak seen shortly after surgery.49–51 However, the use of cyanoacrylate glue is not recommended in thin, avascular blebs with leaks developed months to years after surgery. The glue must be applied to a dry conjunctival surface, and only a small amount of glue should be used. The use of a bandage contact lens can prevent the adhesive from being dislodged. When other simpler methods have failed and the bleb leak is persistent, surgical intervention is necessary.58–63 It is important to attempt to save the established initial filtration site. Because of the friable nature of the conjunctiva in long-established filtering blebs, it often is impossible to close the defect directly with sutures and, therefore, healthy conjunctival tissue is needed. First, the ischemic and thin-walled bleb tissue is denuded of conjunctival epithelium by blade debridement or cautery to allow long-term adherence of the grafted conjunctiva. Fresh conjunctiva adjacent to the bleb then is mobilized to cover the previous filtration site by rotational, sliding, or free conjunctival grafts. Separate dissection of conjunctiva and Tenon's capsule sometimes aids in closure because although conjunctiva often can be stretched further than Tenon's capsule, the closure of the latter provides more support. The conjunctiva is sutured over the previously abraded peripheral cornea, providing a watertight seal. Amniotic membrane can be used as an alternative substrate (unpublished data, 1998, Budenz et al). With these methods, bleb function usually can be preserved. The use of a donor scleral flap is likely to compromise the function of the filtering bleb. The latter option is most efficient to treat cases of inadvertent bleb after cataract surgery.

EARLY AND LATE FAILURE OF FILTERING BLEB. Failed blebs are those associated with inadequate IOP control and impending or established obstruction of aqueous outflow. The cause of failure of filtering operations can be divided into intraocular, scleral, and extraocular factors. The extraocular changes account for most failures of external filtering operations.64

Early failure of filtering blebs is characterized by a high IOP, deep anterior chamber, and low and hyperemic bleb.54 Failing blebs should be recognized promptly because if obstruction is not relieved, permanent adhesions between conjunctiva and episclera can lead to closure of the fistula. A tight scleral flap and episcleral fibrosis are the most common causes of early bleb failure. Internal obstruction of the fistula by blood clot, vitreous, iris, or incompletely excised Descemet's membrane also is possible.

To reduce postoperative subconjunctival fibrosis and preserve bleb function, postoperative topical steroids are routinely used65 (see Chapter 15). The use of antifibrotic agents in filtering procedures is associated with a higher success rate but also with a higher complication rate (wound leak and hypotony from overfiltration, hypotony maculopathy, and ocular infection). Therefore, an individualized consideration of the risk-benefit ratio is recommended. 5-Fluorouracil (5-FU) usually is administered in 5-mg aliquots during the first 2 weeks after surgery. The dose is adjusted according to the tolerance of the corneal epithelium of each eye. Intraoperative application of 5-FU also has been described (see Chapter 15). Complications associated with the use of postoperative 5-FU include corneal and conjunctival epithelial toxicity, corneal ulcers, conjunctival wound leaks, subconjunctival hemorrhage, or inadvertent intraocular spread of 5-FU. The frequency of complications is reduced with lower titrated dosages of 15 to 50 mg administered in 3 to 10 injections according to individual response.47,66–68 Mitomycin C is approximately 100 times more potent than 5-FU.69 Postoperative complications associated with overfiltration, hypotony maculopathy, bleb leak, and bleb-related ocular infections are more likely to occur when mitomycin C is used.11,13,14,70–73

Digital ocular compression and focal compression can be used to temporarily improve the function of a nonfunctioning filtering bleb. Digital ocular compression can be applied to the inferior sclera or cornea through the inferior eyelid or to the sclera posterior to the scleral flap through the superior eyelid. Focal compression (Carlo Traverso maneuver) is applied with a moistened cotton tip at the edge of the scleral flap (see Chapter 15 for a detailed description).74,75 Because of potential complications, digital ocular compression is suitable for patients who are physically capable of performing it and had a beneficial response to the initial massage by the physician. In the early postoperative period, laser suture lysis can enhance the filtration.76–81 Gonioscopy performed before the laser can confirm an open sclerostomy with no tissue or clot occluding its entrance. Specially designed lenses such as Hoskins, Ritch, or Mandelkorn lens; the central button edge of the Zeis and Sussman lenses; the Goldmann lens; glass rods; or glass pipettes can be used (Fig. 8). The laser parameters recommended are summarized in Table 3. After the suture is cut, if the bleb and IOP are unchanged, ocular massage or focal pressure can be applied. Usually, only one suture is cut at a time to avoid the possible complications of overfiltration. A hole in the conjunctiva may occur because of trauma from the contact lens or the thermal burn of the laser. If there is subconjunctival hemorrhage, suture lysis can be difficult. In these cases, krypton red or a diode laser should be used because their wavelengths are least absorbed by blood. Some sutures have more influence in restricting the aqueous runoff than others. These “key” sutures should be identified during surgery, and greater caution should be advised when cutting them. The timing of suture release is critical. Suture lysis is effective within the first 2 weeks after surgery without antimetabolites; later, fibrosis of the scleral flap may negate any beneficial effect of this procedure. If antimetabolites have been used at the time of surgery, suture lysis can be effective months after surgery.82,83 Releasable sutures are as effective as laser suture lysis. The use of releasable sutures allows the surgeon to tightly close the scleral flap, knowing that the flow can be increased postoperatively. The externalized sutures are easily removed and are effective in cases of hemorrhagic conjunctiva or thickened Tenon's tissue (which would make suture lysis difficult). The disadvantages of releasable sutures include the need for additional intraoperative manipulation and postoperative discomfort from the externalized suture, corneal epithelial defects, and, possibly, increased risk of ocular infection. Several techniques have been described by Wilson84 (mattress-type suture with an externalized knot on the cornea), Shin85 (removable knot passed through the conjunctival bleb), Cohen and Osher86 (loop-knot suture externalized through the cornea), Hsu and Yarng87 (an externalized hemibow tie in the center of the filtering bleb), Maberley and associates88 (a two-arm “U” suture that leaves no exposed suture end until one arm of the suture is removed), and Johnstone and coworkers89 (releasable “tamponade suture”). In patients with incarceration of iris or vitreous occluding the sclerostomy, Nd:YAG Laser internal revision can be tried.90,91 When the cause of filtration failure is a blood clot or fibrinous clot occluding the sclerostomy, tissue plasminogen activator can be helpful.92–95 Recombinant tissue plasminogen activator is a serine protease with clot-specific fibrinolytic activity. It can be injected into the anterior chamber or subconjunctivally, and the dosage is 7 to 10 μg in 0.1 ml. It works rapidly, so that within 3 hours the effect usually is apparent. Hyphema is the most frequent complication28,92 (Fig. 9).

Fig. 8. Slit-lamp photograph. A Hoskins lens is used to improve the view of the trabeculectomy flap sutures.


TABLE 3. Argon Suture Lysis

  1. Pretreatment with topical phenylephrine 2.5% (optional)
  2. Argon laser parameters:

      Spot size: 50 μm
      Exposure time: 0.05–0.1 second
      Power: 500–700 mW (from 200 to 1000 mW)

  3. Topical anesthesia (proparacaine 0.5%)
  4. Contact lens (Hoskins, Ritch, or other)
  5. Focus the beam posterior to the conjunctiva
  6. If intraocular pressure still elevated and bleb unchanged: gentle ocular massage or focal pressure


Fig. 9. Slit-lamp photograph. Severe intraocular bleeding and subconjunctival hemorrhage after intracameral injection of tissue plasminogen activator.

A late failure of filtering bleb can occur after months to years of adequate function, with subconjunctival-episcleral fibrosis the most common cause.64 Several factors accelerate fibrosis, such as a black race, childhood, postoperative subconjunctival hemorrhage, the presence of reactive sutures, and inflammation.54 Less commonly, internal closure of the sclerostomy can occur. A classic example is late closure of the internal sclerostomy by a membrane in patients with iridocorneal endothelial syndrome. “Warning signs” of failing filtration are increased bleb vascularization, bleb inflammation, and bleb thickening. The IOP typically is high.

In patients with subconjunctival-episcleral fibrosis, an external revision can be tried. A 27- or 30-gauge needle is used to cut the edge of the scleral cap and restore aqueous outflow. Entry into the anterior chamber beneath the flap may be important but should be undertaken with extreme caution in phakic eyes. The technique can be repeated as needed.58,96–98 The outcome may be more favorable if there was a previously well-established filtration bleb before the fistula became occluded. Subconjunctival injections of 5-FU for 2 weeks after revision increase the probability of success.99,100 Mitomycin C also has been used in conjunction with needling of blebs.101 Ab externo holmium:YAG laser sclerostomy can be used to restore the bleb function.102–104 Its advantages compared with filtering procedures include a small conjunctival incision, access to areas difficult to operate, technical simplicity, and shorter operative time. The conjunctiva must be mobile in the proposed sclerostomy site. The probe should be directed to the area where the previous sclerostomy and iridectomy were performed. Subconjunctival 5-FU injections are recommended after laser sclerostomy revision.54 Early postoperative hypotony is the rule if the sclerostomy is open, similarly to other full-thickness procedures. Nd:YAG laser external revision also has been described to externally revise failed filtering blebs.105,106 Finally, a repeat glaucoma surgery with another filtration site can be used.

When there is internal obstruction of the sclerostomy, a Nd:YAG internal revision is best. Transcorneal surgical revision with a curved needle or a goniotomy blade rarely is needed.54

ENCAPSULATED BLEBS. Encapsulated blebs are localized, elevated, and tense filtering blebs with vascular engorgement of the overlying conjunctiva and a thick connective tissue54 (Fig. 10). This type of bleb commonly appears within 2 to 4 weeks after surgery.107–113 Encapsulation of the filtering bleb is associated with a rise of IOP after an initial period of pressure control after glaucoma surgery. They can interfere with upper lid movement and tear film distribution, leading to corneal complications such us dellen and astigmatism. Often, it is seen through the eyelid simulating a lid mass. The frequency of bleb encapsulation after trabeculectomies without antimetabolites ranges from 8.3% to 28%.107–111 In trabeculectomies with postoperative 5-FU, the incidence frequently has been reported to be higher.112 The frequency of encapsulated blebs after guarded filtering procedures with mitomycin C is lower.113 Predisposing factors may include male gender and the use of gloves with powder, as well as prior treatment with sympathomimetics, argon laser trabeculoplasty, and surgery involving the conjunctiva.107 The causes of encapsulation are not clearly identified, but inflammatory mediators probably are involved in their development. The long-term prognosis for IOP control in eyes that develop encapsulated bleb is relatively good.

Fig. 10. Slit-lamp photograph. Encapsulated filtering bleb.

Initial management of encapsulated blebs include antiglaucoma medications in cases of elevated IOP, topical steroids, and digital massage.98,110,111 Deciding between conservative management (medical) or a surgical revision usually is dependent on the severity of glaucomatous damage, the level of IOP, and the response to medical management. When surgical revision is needed, the simplest technique is to cut the fibrotic wall with a 27-gauge needle or a Ziegler knife. This procedure can be done at the slit lamp and, if effective, restores aqueous outflow to a larger subconjunctival area. Alternatively, the fibrous tissue can be excised after reopening the conjunctival incision from the previous filtering operation is reopened.114,115 Subconjunctival injections of 5-FU for 2 weeks after bleb revision increases the chances of success.54,99

SYMPTOMATIC BLEBS. Filtering blebs usually are asymptomatic. Some patients have discomfort, which is most common with nasal,116 large blebs extending onto the cornea54 (Fig. 11). Tear film abnormalities with dellen formation and superficial punctate keratopathy may occur.117 Corneal astigmatism, visual field defect, and monocular diplopia have been described in cases in which large filtering blebs had migrated onto the cornea.118

Fig. 11. Slit-lamp photograph. Large avascular thin-walled filtering bleb with corneal extension.

Artificial tears and ocular lubricants can be helpful, especially in patients with abnormal tear film. Several chemical and thermal methods have been used to shrink blebs (see earlier). A temporary medial tarsorrhaphy can alleviate symptoms of a nasal bleb and shift it superiorly. Large blebs that extend onto the cornea can be freed by blunt dissection. The corneal extension can be excised with a cut parallel to the limbus, usually with excellent results. Partial surgical excision and conjunctival flap reinforcement usually are helpful, although bleb failure is a possibility.54,58,119

CATARACT FORMATION AFTER FILTRATION SURGERY. Cataract formation and progression of preexisting cataract can occur after filtration procedures. The reported incidence varies from 2% to 53%.120–123 Lens opacification is the main cause of early visual loss after filtration surgery. Intraoperative lenticular trauma is possible and can be recognized shortly after surgery. Postoperative flat anterior chamber with lens-corneal touch rapidly precipitates cataract formation. Other probable risk factors include age, presence of exfoliation, use of air to reform the anterior chamber, profound hypotony, use of miotics and topical steroids, and inflammation.120–124

Cataract extraction can be associated with an impairment of the function of the filtering bleb. Phacoemulsification of the lens with a corneal incision induces less conjunctival inflammation than large scleral incisions and may be theoretically the best method to preserve the function of the bleb. Postoperative subconjunctival injections of 5-FU can be considered. If the control of IOP is borderline, a combined cataract extraction and filtration procedure may be the best choice.

BLEB-RELATED OCULAR INFECTION. Ocular infections related to filtration procedures can occur months to years after the initial surgery.54,125–137 The incidence of bleb-related ocular infections after filtration procedures not supplemented with antifibrotic agents ranges from 0.2% to 1.5% after midterm and long-term follow-up.126,127 Inferior filtering blebs128–130 and the use of antifibrotic agents during filtration surgery increase the probability of bleb-related ocular infection.47,73,129–131 Thin bleb wall, frequently seen after full-thickness procedures and trabeculectomies with antimetabolites, and bleb leaks probably are associated with a higher risk of infection. Bleb-related ocular infections can affect three compartments: the subconjunctival space, the anterior segment, and the vitreous cavity. Usually, the spread of infection proceeds in that order. Because the fluid within the bleb is continuous with the anterior chamber, the bleb may be considered an exteriorized portion of the anterior chamber. Therefore, an infection of the bleb affecting the subconjunctival space (“blebitis”) has a real potential to rapidly spread posteriorly. The bacteria that cause bleb-related endophthalmitis certainly arise from the ocular flora. The most commonly involved organisms include Streptococcus species, Hemophilus influenzae, and Staphylococcus species.132–135

Patients with bleb-related ocular infection usually present with ocular pain, blurred vision, tearing, redness, and discharge. Examination often reveals conjunctival and ciliary injection (most intense around the bleb edge), purulent discharge, and variable intensity of periorbital chemosis, corneal edema, and anterior chamber reaction, including keratic precipitates and, in some cases, hypopyon. The bleb typically has a milky white appearance with loss of clarity; a pseudohypopyon within the bleb can be observed. A positive Seidel's test result is common, and some patients may have a substantial leak, hypotony, and even flat anterior chamber. Alternatively, an increased IOP is possible because of internal closure of sclerostomy site with purulence and debris. Vitreous reaction is not evident in early cases of blebitis, but untreated, the infection spreads to the posterior segment.54

Bleb-related ocular infections have been classified into three different stages.54 In grade I, there is only bleb involvement (Fig. 12). Erythema around the bleb and milky white appearance of the bleb with loss of clarity is observed. In grade II, the infection has extended into the anterior chamber, and cells and flare are noted. Hypopyon may be seen (Fig. 13). In grade III, the vitreous is involved. If the media is not clear (i.e., dense cataract), B-mode ultrasonography can be helpful to detect involvement of the retrolental area.

Fig. 12. Slit-lamp photograph. Bleb-related ocular infection, grade I (without involvement of the anterior chamber). There is an intense erythema around the filtering bleb.

Fig. 13. Slit-lamp photograph. Bleb-related ocular infection, grade II (with anterior chamber involvement). A small hypopyon is seen.

The general principles that guide the management of ocular infections apply to this condition.54,136 Identifying It the organism responsible is important. A conjunctival sample is routinely collected, stained, and cultured. However, the value of conjunctival culture in the etiologic diagnosis of bleb-related endophthalmitis has little value. A vitreous sample should be obtained in grade III. Antibiotic sensitivities should be determined on positive cultures. In grade I (blebitis without anterior chamber reaction), frequent topical application of a commercially available broad-spectrum antibiotic can be used with close supervision. Steroids can be considered to reduce the intense inflammation and preserve bleb integrity when the infection appears to be controlled. In grade II (the anterior segment but not the posterior segment is involved), treatment with fortified topical antibiotics around the clock is advisable. Topical fortified cefazolin or vancomycin (25 mg/ml) associated with fortified tobramycin (14 mg/ml) or amikacin (50 mg/ml) are likely to be effective against most gram-positive and gram-negative microorganisms. Additional systemic antibiotics such as ofloxacin (400 mg orally twice daily) can be used. In grade III (bleb-related endophthalmitis), intravitreal antibiotics are required, administered either through a pars plana injection at the time of sampling or associated with a vitrectomy. We are currently using 1 mg of vancomycin (10 mg/ml) and 400 μg of amikacin (5 mg/ml). Oral ofloxacin (400 mg orally twice daily) and fortified topical eye drops of the same antibiotics that were injected into the vitreous cavity should be used.54

After resolution of the infection, the function of the filtration bleb may be impaired, especially in eyes that have not received antifibrosis agents.136 Other possible complications include corneal edema, cataract, vitreoretinal traction, and retinal toxicity from the bacteria's toxins or the antibiotics. The visual outcome usually is good in cases with anterior segment involvement and poor when the vitreous is involved, especially with virulent bacteria such as streptococci, coagulase-positive staphylococci, and gram-negative organisms.

Prevention of bleb-related ocular infection is important.54 Some ophthalmologists use long-term topical antibiotics after filtration procedures,137 although the efficacy of this regimen has been questioned. It seems reasonable to use long-term antibiotics in some cases of leaking blebs, inferior blebs, or recurrent bleb-related infections. Conjunctivitis and blepharitis should be treated promptly, and soft contact lens wear should be avoided. Patient education about early symptoms of infection currently is the most important approach to minimize the chances of severe visual loss.


Surgical peripheral iridectomy is necessary in uncooperative patients and those with poor visualization (i.e., angle-closure glaucoma with a hazy cornea), which impedes a laser iridotomy (see Chapter 15). After this procedure, bleeding usually is minimal. Flat or shallow anterior chamber without elevation of IOP usually results from wound leak. It should be reformed promptly because of the risk of aqueous misdirection, which is most likely to occur in patients with angle-closure glaucoma (see earlier).


Implantation of aqueous tube shunts is associated with a significant risk of postoperative complications.137–146 Early postoperative complications include hypotony, flat anterior chamber, choroidal effusions, suprachoroidal hemorrhage (see Fig. 1), aqueous misdirection, hyphema, and increased IOP. The use of intraoperative mitomycin C does not influence the success and complication rate of tube shunt implantation.144–146 Hypotony, the most common complication, usually results from excessive outflow of aqueous humor and may result in flat anterior chamber and choroidal detachment. In cases of flat anterior chamber and choroidal effusions, surgical intervention may be needed (see earlier). Recurrent flat anterior chamber requires temporary tube ligation. Restrictive or valved implants may be less commonly complicated with hypotony than unregulated devices.

High IOP can be related to occlusion of the tube by a fibrin or blood clot, iris, or vitreous. The fibrin or blood may resolve spontaneously; however, an intracameral injection of tissue plasminogen activator helps to dissolve the clot within few hours (see earlier). When the iris tissue occludes the lumen of the tube, a Nd:YAG laser iridotomy or an argon laser iridoplasty may reestablish the patency of the tube. Vitreous incarceration can be treated successfully with Nd:YAG laser, but an anterior vitrectomy may be necessary. Recurrence and closure of the tube is common after successful treatment with the Nd:YAG laser.147 The tube can retract from the anterior chamber. If the tube is too short (i.e., not seen in the anterior chamber), the plate should be moved anteriorly. In nonrestrictive devices, high IOP can be related to a tight ligature, internal occlusion, or both. In these cases, aqueous suppressants are used to control the IOP within an acceptable range for the first 3 to 4 weeks. At this time, profound hypotony is least likely to occur, and the device used to increase the outflow resistance can be safely removed.

Late postoperative complications of aqueous shunting procedures include increased IOP, hypotony, implant migration, conjunctival erosion, corneal edema or decompensation, cataract, diplopia, and endophthalmitis. Late failure with increased IOP can be caused by blockage of the anterior chamber tube opening (see earlier) and excessive fibrosis around the plate. Surgical bleb revision (excision or needling of the fibrous wall) with antifibrosis agents can be helpful. A failed procedure also can be managed by implantation of additional episcleral devices. Corneal decompensation may result from direct contact between the tube and the cornea. When there is tube-cornea touch, repositioning of the tube should be considered, especially in cases where there is risk of endothelial failure (i.e., patients with focal corneal edema, or after penetrating keratoplasty). Diplopia results from mechanical restriction of the extraocular muscles.141 If diplopia is persistent, the shunt may need to be removed or relocated.


The use of cyclodestructive procedures in its various forms usually has been restricted to eyes with recalcitrant and end-stage glaucoma because of their limited predictability. Some eyes require multiple treatments to achieve pressure lowering, whereas others become hypotonous or phthisical after a single session. The cyclodestructive procedures that are currently used are cyclocryotherapy,148,149 noncontact Nd:YAG laser cyclophotocoagulation (CPC),150,151 contact Nd:YAG laser CPC,152,153 contact diode CPC,154,155 and endophotocoagulation.156,157 The latter techniques have the potential for more controlled destruction of the ciliary body processes and a lower incidence of complications compared with cyclocryoablation. For example, the 810-nm semiconductor diode laser has the theoretical advantages of good penetration and selective absorption by the pigmented tissues of the ciliary body. Endophotocoagulation offers the possibility of selectively treating the ciliary body epithelium with relative sparing of surrounding tissues.

Possible complications of cyclocryotherapy include severe pain, elevation of IOP, hyphema (common in eyes with neovascular glaucoma), visual loss (wipeout fixation in patients with advanced optic nerve damage), choroidal detachment, retinal detachment, chronic hypotony, cystoid macular edema, anterior segment necrosis, vitreous hemorrhage, aqueous misdirection, cataract, lens subluxation, and phthisis.148–158 Pain often occurs during the first 2 days after cyclocryotherapy, and strong analgesics (narcotics) should be used routinely. Laser cyclodestructive procedures usually do not require strong analgesia. A major concern is the possibility of phthisis bulbi (0% to 7%) after cyclodestructive procedures. It is more common in neovascular glaucoma and in patients who underwent cyclocryotherapy in four quadrants. It is the least common after diode laser CPC. The possibility of sympathetic ophthalmia after cyclodestructive procedures also is of great concern. It has been reported after noncontact and contact Nd:YAG laser CPC.159–162


Cyclodialysis is not a popular procedure because it is unpredictable. However, some clinicians still use it, especially in aphakic and pseudophakic glaucomas. After the procedure, miotics are used to maintain an open cleft (Fig. 14). Cycloplegics should be avoided. Cyclodialysis lowers the IOP by increasing uveoscleral outflow and, secondarily, by decreasing aqueous humor formation.

Fig. 14. Composite of ultrasound biomicroscopic examination. A cyclodialysis cleft is seen.

Common complications of cyclodialysis are intraoperative bleeding and hyphema, which may decrease the chances of long-term success. Postoperative hypotony is associated with accumulation of fluid between the ciliary body and sclera. If the accumulation of fluid extends posteriorly, it may reach the macula and impair visual acuity. The degree of hypotony is not related to the length of the cleft in the angle that is observed gonioscopically. If visual function is compromised, cryotherapy can be used to partially close the cleft. Cryotherapy may be ineffective or it may induce complete closure of the cleft and elevation of IOP. Surgical closure of the cleft may be necessary. Spontaneous closure of the cleft may occur months after a successful surgery, producing an acute rise of IOP and pain resembling an attack of acute angle-closure glaucoma. In some cases, intensive miotic treatment associated with phenylephrine can reopen the cleft.

Other possible complications include corneal opacity, injury to Descemet's membrane, iridocyclitis, corectopia, lens subluxation, cataract, loss of vitreous, vitreous hemorrhage, retinal detachment and myopic refractive shift.


Trabeculotomy and goniotomy are the first surgical options to treat infants with glaucoma.163–166 Trabeculotomy is preferred when the cornea is so clouded than the angle cannot be properly visualized. Ultrasound biomicroscopy can be used to evaluate the anterior chamber angle before and after surgery in infants with glaucoma and corneal opacity.167 Trabeculotomy also can be a useful option to treat some adult glaucomatous patients.168–169

Severe complications after trabeculotomy and goniotomy are rare. Moderate bleeding into the anterior chamber is common. Blood clots usually resorb within a few days. Intraoperative complications during trabeculotomy can be related to difficulty identifying Schlemm's canal, which is more difficult to locate in infants. The initial goal is to open the outer wall of Schlemm's canal without perforating the inner wall into the anterior chamber. If penetration into the anterior chamber occurs, the iris may prolapse. In this case, an iridectomy may be necessary. If the subciliary space is wrongly probed, forward rotation into the anterior chamber is not possible unless considerable force is exerted, causing cyclodialysis and iridodialysis. If the tip of the trabeculotomy probe is held toward the cornea during rotation, a Descemet's membrane tear can occur, but they usually are small and do not cause corneal edema.

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