Complications Common to Nonpenetrating Surgeries

Nonpenetrating glaucoma surgery encompasses techniques that involve a deep dissection to the level of Descemet’s membrane, allowing aqueous seepage. The major techniques covered by the term “nonpenetrating surgery” are deep sclerectomy with or without implant and viscocanalostomy. In large meta-analyses comparing nonpenetrating procedures to trabeculectomy, trabeculectomy resulted in lower intraocular pressures (IOP) but a higher risk of postoperative complications. Although nonpenetrating surgery is successful in lowering IOP, the amount of IOP lowering is typically not as low as can be achieved with trabeculectomy. Consequently, patient selection with regard to the target IOP is important in the decision of whether or not to perform a nonpenetrating procedure. The goal of nonpenetrating procedures is to lower IOP with fewer complications than are seen with trabeculectomy. The complications that can occur can be easily understood and predicted by an understanding of the techniques and modifications, as well as knowledge and mechanisms of the adjustments that can be used postoperatively to enhance success. After appropriate anesthetic, the techniques involve a deep dissection in the sclera to the limbus. In the case of deep sclerectomy, after the initial half-thickness flap is fashioned, a second deeper flap is created and excised. This dissection is taken to the level of Descemet’s membrane, allowing controlled flow of aqueous. A fine forceps may be used to strip the outer wall of Schlemm’s canal, further enhancing the flow. The space created by the excision can then be filled with an implant, such as collagen (AquaFlow™ Collagen Glaucoma Drainage Device; STAAR® Surgical Company, Monrovia, California) or hyaluronate (SK Gel®; Corneal Laboratories, Paris, France). For viscocanalostomy, Schlemm’s canal is identified and dilated by using viscoelastic. With deep sclerectomy, intraoperative or postoperative antimetabolites may be used to try to increase success rates by limiting the inflammatory response. Goniopuncture to the Descemet’s window is often required postoperatively (in up to 67% of cases) to enhance flow and lower IOP. The available evidence on complications of nonpenetrating glaucoma surgery is relatively sparse and may be challenging to interpret. Comparative studies between trabeculectomy and nonpenetrating surgery would seem to show fewer complications in the nonpenetrating group.

Tube Shunt Related Complications in Pediatrics

Although medical therapy is usually an excellent therapeutic option in the adult population, in children it is often ineffective or associated with an undesirable risk:benefit ratio. Therefore, surgical intervention is frequently required for adequate control of glaucoma in young patients. The initial surgical approach for management of glaucoma in children includes goniotomy and trabeculotomy, each with a high success rate. When these interventions fail or have a high likelihood of failure (i.e., in patients with Sturge-Weber syndrome, aniridia, anterior chamber dysgenesis, or congenital glaucoma), tube shunt procedures are often required. Tube shunts were first used in the pediatric population by Molteno and colleagues in 1973 and have since grown in popularity and secured an integral role in the treatment of refractory glaucoma in infants and children. Possible complications and causes for failure of tube shunt devices in children are very similar to those in adults; however, issues such as tube migration and retraction must be anticipated in the child’s growing eye. One of the most frustrating, and unfortunately the most common, complications is tube malposition. While tube malposition is not entirely specific to the pediatric population, it occurs far more frequently in children than in adults. (See Chapter 30 for information about tube malposition in adults.) Incidence of tube malposition in pediatric patients ranges from 3% to 35%. In infants and young children, the tube tends to retract from the eye and/or migrate towards the cornea in the anterior chamber. The initial presentation of tube migration is often tube-cornea touch at the proximal end of the tube near the insertion site. In severe cases, tube migration can lead to transcorneal extrusion of the tube. Secondary complications, including corneal decompensation, cataract, iris abnormalities, and endophthalmitis, can result from these initial insults if tube malposition is not identified early and appropriately addressed. The cause of tube migration and retraction is likely multifactorial, but there are 2 basic mechanisms thought to be at fault: 1) somatic growth causing concomitant tube migration and 2) elasticity of the buphthalmic eye, allowing shrinkage as intraocular pressure (IOP) decreases and tube straightening due to “memory.”

Tube Shunt Related Complications of the Orbit

Orbital complications during or after glaucoma filtering or tube shunt surgery are relatively rare but may pose a significant treatment challenge or threat to vision. The incidence of complications is highly variable, and transient events may not be reported as frequently as those that persist. A variety of orbital complications occur following glaucoma surgery. Complications may be categorized as mechanical, infectious, neurogenic, or myogenic. However, each complication may be multimodal and fall into more than one category. Mechanical complications are the most frequent type of orbit complication related to glaucoma surgery and more specifically to tube shunt implantation. Mechanical complications include ptosis, lid retraction, strabismus, and proptosis. Several theories address why ptosis may occur after ocular surgery and why it may be either transient or permanent. The levator muscle may be damaged or dehisced by an eyelid speculum, leading to a lid droop. Bridle sutures, which are often used during glaucoma surgery, have also been implicated as they apply counter traction against the superior rectus muscle. Prolonged eyelid edema and local anesthesia have each been more strongly associated with postoperative ptosis. For more information on ptosis, see Chapter 25. Strabismus after tube shunt implantation is most commonly related to either the device itself or to scarring and fibrosis that develop postoperatively. Transient strabismus may be related to swelling or edema of local tissues and may also follow retrobulbar injection. The strabismus is usually incomitant and does not present with a characteristic pattern of deviation; thus, prisms and other nonsurgical treatments are seldom adequate. Although strabismus following tube shunt surgery is usually transient, persistent diplopia may occur. The type of implant, size, location, and material each play a role. Implants with larger surface areas have a higher incidence of motility disturbance due to mass effect. Tube shunt plates that require placement below the rectus muscles risk direct muscle injury or adhesion scarring to the implant. In addition, a pseudo-Brown’s syndrome may be created by a superonasal implant due to interference with the superior oblique muscle function. The bleb that develops around the tube shunt reservoir can also act as a mass.

Early Hypotony

Ocular hypotony in the early postoperative period following tube shunt surgery is relatively common. The pressure level at which structural compromise of the eye and resultant secondary complications (e.g., shallow/ flat anterior chamber, serous and/or hemorrhagic choroidal detachment, chorioretinal folds, corneal folds) occur varies considerably. Some patients may tolerate extremely low pressures well for extended periods of time. However, an increased amount of secondary complications is often seen with intraocular pressures (IOPs) below 6 mm Hg. For the purpose of the ensuing discussion, we will adopt a definition of hypotony based solely on this pressure criterion without regard to the clinical state of the eye. An understanding of the causes of hypotony is critical to its prevention as well as its treatment. The etiologies of hypotony can be broken down into 2 broad categories: general (Table 34.1) and device-specific (Table 34.2). The device-specific causes can be further categorized into those that occur with valved devices and those that occur with non-valved devices. Aqueous flow around the tube at the scleral insertion site may result in early postoperative hypotony regardless of the type of tube shunt used. A 23-gauge needle generally creates a tight track in an area of normal sclera with little potential for excess flow around the tube. Rarely, however, the scleral entry track can be significantly wider than the external diameter of the tube, resulting in peri-tube flow and a low IOP, which are particularly likely to occur following excessive manipulation of the scleral opening as it is created or during tube insertion. The use of a 22-gauge or wider needle will increase the risk of peri-tube flow. Leak around the tube may also occur when a 23-gauge needle is used to create the fistula through an area of abnormally thin, ectatic sclera. Additionally, when 2 or more scleral openings are made in an effort to optimize tube placement, aqueous flow through an unused scleral entry site may result in overfiltration and early postoperative hypotony if the sclerostomy is not tightly closed. Aqueous hyposecretion secondary to ciliary body dysfunction may also result in transient ocular hypotony in the early postoperative period.

Scleral Perforation

Scleral perforation during tube shunt implantation is a rare complication. In a recent publication of the Tube Versus Trabeculectomy Study, 3 out of 107 patients in the tube shunt group had scleral perforation during placement of a device. Merino-de-Palacios et al reported scleral perforation during tube shunt surgery in 1 of 86 eyes. The type of device used does not seem to be important in the incidence of scleral perforation. In the Tube Versus Trabeculectomy Study, Baerveldt® devices (Abbott Medical Optics, Inc., Santa Ana, California) were used exclusively, and Ahmed™ Glaucoma Valves (New World Medical, Inc., Rancho Cucamonga, California) and Molteno® implants (Molteno Ophthalmic, Ltd., Dunedin, New Zealand) were used in the study by Merino-de-Palacios et al. Serious sequelae, such as endophthalmitis or retinal detachment, have not been reported in recent literature following scleral perforation during tube shunt placement; nonetheless, this complication should be prevented and, if it does occur, managed promptly. Patients who are believed to have an increased risk for scleral perforation are myopic patients (>-6.00 D) and patients with previous extraocular muscle surgery. Patients with previous scleral buckle surgery, autoimmune diseases, scleritis, or any other conditions that cause or perpetuate thinning of the sclera potentially increase the risk. Patients with previous scleral buckling procedures who require tube shunt surgery will benefit from having the device anchored behind the buckle or directly over the buckle. No attempt should be made to dissect under the buckling device, as dissection may lead to the buckle anchoring sutures perforating the eye. The most common site for tube shunt implantation is the superotemporal quadrant, between the superior and lateral rectus muscles. This location offers the benefit of having the implant hidden under the superior eyelid, no oblique muscles in the region, and better intraoperative exposure, allowing the surgeon to place the implant farther from the limbus. The plate of the implant is usually attached to the sclera approximately 8–10 mm posterior to the limbus. This is also the thinnest portion of the sclera. Exposure when implanting the tube shunt is probably the most important factor in avoiding scleral perforation.

Complications Specific To Ex-Press™ Shunts

The EX-PRESS™ Glaucoma Filtration Device (Alcon Laboratories, Inc., Fort Worth, Texas) has been commercially available in the United States since 2002 and was originally developed by Optonol, Inc. (Kansas City, Kansas) for implantation directly under the conjunctiva for an indication of control of intraocular pressure (IOP). It is a nonvalved, stainless steel device almost 3 mm long with an external diameter of approximately 400 microns and a 50 or 200 micron lumen, depending on the model. It has an external disc at one end and a spur-like extension on the other to prevent extrusion. The EX-PRESS™ shunt is one option for controlling IOP available to today’s glaucoma surgeon. The challenges and complications involved with EX-PRESS™ shunts are addressed below, as well as how to manage and prevent such scenarios. The original unguarded technique of implantation under the conjunctiva resulted in numerous complications, including hypotony, extrusion, and, most commonly, erosion of the implant. Typically, there was a period of hypotony followed by failure and erosion of the implant. Endophthalmitis has also been associated with an exposed implant. To avoid complications associated with subconjunctival implantation, Dahan and Carmichael proposed implanting the device under a scleral flap. This technique has greatly reduced erosions, and EX-PRESS™ shunts have been reported to have a lower rate of hypotony than trabeculectomy (15.8% with EX-PRESS™ shunt versus 22.5% in trabeculectomy). Since 2003, the manufacturer has recommended all users only implant the device under a scleral flap. Like all filtration surgery, failure is most commonly from episcleral and subconjunctival fibrosis. As with traditional filtration surgery, intraoperative adjunctive antimetabolites, such as mitomycin-C, may be used to limit the degree of postoperative scarring. However, should failure due to fibrosis occur, there are several options. The first is to add topical medications or perform laser trabeculoplasty. The second is to perform bleb revision or needling with an antifibrotic agent. Finally, as in a failed trabeculectomy, the surgeon may abandon the EX-PRESS™ shunt and perform a second unrelated procedure.

Noncorneal Complications

Most glaucoma specialists advocate the use of 5-fluorouracil (5-FU) and mitomycin-C (MMC) in various concentrations during the intraoperative and postoperative periods to help inhibit postoperative scarring, the primary cause of filtration surgery failure. Although the increased use of antifibrotic agents as adjunctive therapy to guarded filtration surgery has improved the likelihood of operative success, there are many additional complications associated with this class of medications. It is the nature of filtration surgery as it is performed today that successful drainage of aqueous comes with a price. Any adjunct that improves the intraocular pressure (IOP)-lowering success of surgery must be assessed in light of this increased risk. A leaking bleb is one of the most common complications seen after trabeculectomy and may occur at any point postoperatively. This complication has been reported with an incidence ranging between 17% and 42% according to one review. More recent estimates have been somewhat lower, at between 8% and 14.6%. The longer the postoperative follow-up, the greater the cumulative likelihood of bleb leakage. It is imperative that the bleb be checked periodically for leaks, primarily through examination and standard Seidel testing. Use of antifibrotic therapy is associated with increased formation of thin-walled cystic blebs, which are more likely to result in both short-term and long-term complications. The timing of a bleb leak will dictate management. Many early postoperative bleb leaks resolve without intervention but can significantly decrease the likelihood of trabeculectomy success. Early postoperative bleb leaks are often attributed to surgical technique and can generally be avoided by use of appropriate blunt instruments and careful attention to surgical detail. The simple use of nontoothed forceps when handling the conjunctiva can prevent small buttonhole conjunctival tears, which often result in early postoperative bleb leaks. However, even with careful manipulation, friable conjunctival tissue can be prone to small tears. While some have advocated the use of light cautery, or even tissue adhesives to close bleb leaks, the use of such techniques has diminished in the antifibrotic era. Intraoperative suturing of buttonholes is definitive.

Corneal Complications

The desired effects of antifibrotic agents 5-fluorouracil (5-FU) and mitomycin-C (MMC) in glaucoma filtration surgery result from their ability to limit postoperative scarring by inhibiting vascular proliferation and fibroblastic transformation. However, these same mechanisms of action can have deleterious effects on surrounding normal tissues such as the cornea. Knowing how to use these agents is important in preventing antifibrotic-related complications. 5-FU is an inhibitor of DNA synthesis, specifically thymidylate synthetase, and blocks thymidine from being incorporated into DNA. In addition to affecting DNA synthesis, 5-FU also may be incorporated into RNA, interfering with RNA synthesis and therefore protein synthesis. Thus, it is more toxic to actively proliferating cells. In glaucoma filtration surgery, 5-FU is generally administered intraoperatively (50 mg/mL for 5 minutes). 5-FU can also be administered as a subconjunctival injection postoperatively with a dosage of 5.0–7.5 mg in 0.1–0.15 mL solution directly from the 50 mg/mL bottle. A series of injections may be given over several weeks and titrated based on clinical response. In addition to glaucoma filtration surgery, 5-FU has also been used for other ophthalmic applications such as pterygium surgery, lacrimal surgery, and during vitrectomy to prevent proliferative vitreoretinopathy. MMC is an alkylating agent that crosslinks DNA. It requires enzymatic activation via cytochrome p450 prior to exerting its inhibitory effects on DNA synthesis. MMC activity is independent of cell cycle and affects both actively replicating and nonreplicating cells. However, variations in enzymatic activity among individuals may contribute to the differences in efficacy, as well as toxicity of MMC. In glaucoma filtration surgery, MMC is typically administered as a single intraoperative application. It is applied after dissection of the conjunctival flap and prior to the formation of the scleral flap. Most surgeons use a dose of 0.1–0.5 mg/mL with an exposure time of 1–5 minutes depending upon the clinical indication. MMC use has also been well established for refractive surgery to prevent corneal haze after photorefractive keratectomy in patients at high risk of developing corneal haze, pterygium surgery, and corneal intraepithelial neoplasia. For more information on 5-FU and MMC in glaucoma surgery, see Chapter 3.

Ptosis

Ptosis of the upper eyelids is a well-known complication of most forms of ocular surgery. The incidence of ptosis following glaucoma surgery is reported to range from 6 to 12%. The etiology has not been entirely established; however, it is believed to be multifactorial, and several contributing factors have been identified. Identification of the etiology is important since this will often dictate the management. The ptosis may be transient, resolving within days, or persistent. The management of acquired ptosis following glaucoma surgery is critical since surgical over correction can expose a filtering bleb and lead to serious complications, including endophthalmitis. Transient ptosis following surgery is more common than persistent ptosis and may recover within 12 to 72 hours. It may be caused by anesthetic, lid edema, or hematoma formation in the eyelid or muscle. A retrobulbar or peribulbar block with lidocaine may affect the levator muscle. Similarly, direct infiltration of the eyelid will block the distal fibers of the oculomotor nerve. The primary factors postulated to cause ptosis include muscle or nerve damage from local block, a superior rectus bridle suture or corneal traction suture, general anesthesia, eyelid edema, traction applied by the speculum, and levator aponeurosis dehiscence. The lid speculum has been identified as a cause of ptosis regardless of the type of ocular surgery. Superior forces are placed on the upper eyelid while a superior bridle suture or corneal traction suture directs forces downward. These opposing forces may cause a stretching or frank dehiscence of the levator aponeurosis. One study specifically looked at the role of the bridle suture and did not find a significant contribution to ptosis development versus those cases that did not use a bridle suture. Rather, lid edema, neuromuscular block, and the lid speculum itself were identified as causative factors. It has been suggested that prolonged eyelid edema leads to disinsertion of the levator aponeurosis in susceptible populations, such as the elderly. This has not been borne out in other studies; however, some of the same factors that cause prolonged edema may also cause persistent ptosis, specifically inflammation.

Descemet’s Membrane Detachment

Corneal injury resulting from glaucoma surgery has been well described. Causes of injury can range from direct mechanical manipulation to the often more subtle pharmacologically induced injuries that occur with use of antifibrotic medications. Descemet’s membrane detachment (DMD) occurs uncommonly during or after intraocular surgery and has been linked with a variety of procedures ranging from simple clear cornea cataract extraction to deep lamellar keratoplasty. The corneal endothelium, which rests upon Descemet’s membrane, functions as a pump to keep the stroma from becoming swollen. Therefore, DMD results in focal corneal edema and possibly bullous keratopathy. If detachment of Descemet’s membrane extends far enough centrally, visual acuity may become sufficiently compromised to necessitate corneal transplantation surgery (either full-thickness penetrating keratoplasty [PKP] or Descemet’s stripping with automated endothelial keratoplasty [DSAEK]). In glaucoma surgery, DMD often results from the mechanical manipulation that occurs with creation of the cornealtrabecular meshwork opening. Knowing how to accurately diagnose and treat DMD can prevent disastrous consequences and preserve vision. Mackool and Holtz proposed separating DMD into 2 categories, planar and nonplanar, depending on the distance of separation between Descemet’s membrane and the posterior corneal stroma. Planar DMD involves less than 1 mm separation of Descemet’s membrane from the corneal stroma and may be limited to the periphery or extend from the periphery to central regions. Nonplanar DMD involves greater than 1 mm separation of Descemet’s membrane from the corneal stroma and may also be categorized as limited to the periphery or extending to central regions. The significance of this classification was the belief that planar DMD was more likely to spontaneously resolve while nonplanar DMD required surgical intervention. Assia and colleagues also split DMD into 2 categories: DMD with scrolling of tissue and DMD without scrolling of tissue. They believed this classification more accurately described potential for spontaneous resolution in that nonscrolled DMD was more likely to resolve without surgical intervention, even if its location was >1mm from the posterior corneal stroma. While useful as a general guide, these classification systems are not foolproof, and each case of DMD should be viewed independently.