James W. Hung, MD,
Bradford J. Shingleton, MD
Contents
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Open-Angle Glaucomas |
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Closed-Angle Glaucomas |
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Treatment of Glaucoma after Cataract Surgery: General Principles |
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CHAPTER HIGHLIGHTS |
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Advances in instrumentation and cataract surgical techniques have resulted in shorter operating time, smaller incisions, and earlier visual rehabilitation. However, glaucoma following cataract surgery can still be a problem. Elevation in intraocular pressure (IOP) may occur early or late in the postoperative course and can be associated with either an open or closed angle. Many causes exist for IOP elevation after cataract surgery, and it is inappropriate to categorize them all under the terms aphakic or pseudophakic glaucoma.
As cataract surgery has evolved, so have the types of postoperative glaucoma. With the decline in intracapsular cataract surgery and rigid anterior chamber lenses, enzyme glaucoma and the uveitis-glaucoma-hyphema (UGH) syndrome are rarely seen. Planned extracapsular cataract surgery and posterior chamber lens implants brought a rise in pigmentary glaucoma as a result of pigment release from the ciliary sulcus and posterior iris. The widespread use of viscosurgical agents with cataract surgery plays a significant role in early postoperative IOP elevation. Phacoemulsification and clear corneal incisions have lessened glaucoma from wound compression caused by tight suture closure. Clear corneal phacoemulsification also allows cataract surgery to be done in normal and glaucomatous eyes with less risk of postoperative IOP worsening and, indeed, IOP is often reduced after phacoemulsification. The use of topical anesthesia allows glaucoma patients to continue using their antiglaucoma medications without interruption. At the same time, new types of postoperative anterior segment complications, such as capsular block, are being seen.
Surgeons must also realize that glaucoma after cataract surgery does not always result directly from the surgery itself but may occur after postoperative interventions, such as neodymium: yttrium-aluminum-garnet (Nd:YAG) posterior capsulotomy.
This chapter reviews the wide-ranging differential diagnosis of glaucoma after cataract surgery (Table 50-1) and presents the therapeutic options for the ophthalmologist.
Table 50-1 -- Glaucoma after cataract surgery
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Open-angle glaucomas |
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Closed-angle glaucomas |
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UGH, Uveitis-glaucoma-hyphema. |
Open-angle glaucomas
Primary open-angle glaucoma
Primary open-angle glaucoma may first become apparent following cataract surgery secondary to anatomic alterations, the natural evolution of the disease, or both. In the early era of cataract surgery, incomplete wound closure with aqueous leakage and low pressure (hypotony) were relatively common. Today, the incidence of inadvertent aqueous leakage is low because of improved incision architecture, finer suture material and more advanced closure techniques. Particularly in planned extracapsular surgery, tight-closure techniques,[1,][2]suture compression,[3] and edema[4] may mechanically distort the filtration angle and further compromise aqueous outflow, leading to elevated IOP. Scleral tunnel and clear cornea phacoemulsification techniques reduce but do not eliminate this problem.[2] Even if preoperative IOP control is satisfactory, the risk of an acute pressure rise following uncomplicated intracapsular or extracapsular cataract surgery is greater in eyes with pre-existing glaucoma than in healthy eyes.[5,][6]
Besides alterations in angle configuration, early open-angle postoperative IOP increase after cataract surgery may be the result of retained viscosurgical, postoperative inflammation, bleeding, or pigment dispersion.[7]
The long-term effect of cataract surgery on glaucoma control varies depending on the method of cataract extraction. Following intracapsular and extracapsular surgery, several studies have reported IOP reduction for weeks to months.[8,][9] Other groups have found no long-term pressure reduction.[5,][6,][10] With clear corneal phacoemulsification, several authors have shown an associated reduction in IOP in normal and glaucoma suspect eyes.[11–16] Patients with glaucoma were shown to have a reduction in IOP plus a lowering in the number of medications necessary to control postoperative IOP.[11] The need for medications tends to slowly increase with time. However, clear-corneal phacoemulsification should not be performed with the intent of achieving better IOP control, but for the secondary benefit of the IOP likely remaining stable or slightly reduced for up to 5 years.[17]
Cataract surgery in eyes with preexisting filtration blebs may result in IOP elevation and decrease in bleb size, but IOP may still remain acceptable for long-term control.[6,][18,][19]
The presence of a properly positioned posterior-chamber intraocular lens (IOL) implant does not affect IOP. Although closed-loop, anterior chamber IOLs occasionally produce significant IOP elevation, the current semiflexible, one-piece, open-loop style lenses are associated with fewer problems.[20]
An early postoperative rise in IOP may be minimized with topical beta-blockers,[21] topical apraclonidine,[22] systemic carbonic anhydrase inhibitors,[23] topical prostaglandin analogues,[24] and intracameral carbachol.[23] In addition, judicious use and removal of viscosurgical substances are recommended (see Viscosurgical agents). Nonsteroidal anti-inflammatory drugs are ineffective in preventing or decreasing the magnitude of the pressure elevation.[25] Sterile anterior-chamber decompression with the release of aqueous via the paracentesis incision may provide temporary relief of IOP elevation. It is important to check the IOP 30–60min after decompression because recurrence of IOP elevation may occur.[26]
Persistent postoperative IOP elevation resulting from primary open-angle glaucoma mandates standard treatment protocols. Earlier and more aggressive management is indicated in patients with significant pre-existing glaucomatous optic nerve damage.
Blood-induced glaucomas
Hyphema
Blood in the anterior chamber during the early postoperative period typically originates from the scleral cataract incision, an iridectomy, or pupillary sphincter tears.
Patients with postoperative hyphemas may be asymptomatic or have decreased vision. Circulating or layered red blood cells, or both, are seen in the anterior chamber with an open angle. An endocapsular location is an unusual type of postoperative hemorrhage.[27] Pupillary block is uncommon but may develop if bleeding extends into the posterior chamber, occludes an iridectomy, or both. If the anterior hyaloid face is not intact, blood may be seen in the vitreous cavity.
Open-angle glaucoma occurs from trabecular meshwork obstruction by red blood cells, platelets, fibrin, and hemosiderin-filled macrophages. Secondary angle-closure glaucoma results from peripheral anterior synechiae that may develop in the setting of persistent large hyphemas and inflammation.
Any amount of intraocular bleeding may elevate IOP, but larger hyphemas usually cause higher IOPs.[28] Postoperative hyphemas, and glaucoma resulting from them, are generally self-limited and resolve without complications. Management depends on the degree of IOP elevation, the status of the optic nerve, and the presence or absence of sickle cell anemia. A healthy optic nerve can withstand a moderate IOP rise without damage and does not require antiglaucoma therapy. Medical treatment is favored if the IOP is acutely elevated to >40mmHg or persistently elevated to >30mmHg for 2 weeks.[28] In the presence of pre-existing glaucomatous optic-nerve damage or sickle cell disease, earlier and more aggressive management is required.[28] Aqueous suppressants, especially topical beta-blockers and topical or oral carbonic anhydrase inhibitors (avoided in sickle cell patients), are the preferred medical approach. Hyperosmotic agents may be helpful (e.g., oral isosorbide, 2mL/kg, or intravenous mannitol, 20% solution, 2mL/kg over 30min). It is best to avoid using miotics and prostaglandin analogues, which may exacerbate intraocular inflammation, as well as adrenergic agents, which cause vasoconstriction. Additional therapeutic measures include frequent administration of topical corticosteroids (every 1–2h) to decrease inflammation; elevating the head of the bed to minimize posterior blood layering; and, if medically possible, avoiding aspirin, aspirin-containing products, sodium warfarin (Coumadin), and nonsteroidal anti-inflammatory agents. Cycloplegics, systemic steroids, and aminocaproic acid are not commonly used for postsurgical hyphemas.
Despite medical therapy, surgical intervention may be required in situations of uncontrolled IOP, corneal blood staining, or a clot of prolonged duration.[28] Traditional IOP criteria for surgical intervention to avoid optic nerve damage in hyphemas are an IOP of >50mmHg for 5 days or >35mmHg for 7 days. Pre-existing optic nerve damage or sickle cell disease warrants earlier interventions;[27,][29] an IOP of <25mmHg is desirable in these circumstances. Any sign of corneal blood staining warrants surgical intervention.[28] Patients with compromised endothelial cell function may require earlier intervention. Large clots that persist longer than 10 days or total hyphemas lasting more than 5 days are often evacuated to avoid peripheral anterior synechiae and corneal blood staining.
Surgical techniques for hyphema evacuation include anterior-chamber washout, with or without coaxial irrigation–aspiration, automated cutting-aspiration of clot material, or clot expression (Figure 50-1). Simple removal of circulating red blood cells and debris often suffices for IOP control, but visual rehabilitation is hastened by clot removal. If vitreous is admixed with blood in the anterior chamber, automated cutting-aspiration equipment is required for surgical removal.
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Figure 50-1 Surgical techniques for evacuation of postsurgical hyphemas. A, Anterior chamber washout. B, Irrigation and aspiration of blood. C, Coaxial automated cutting and aspiration of clot. D, Clot expression. E, Bimanual irrigation and automated cutting. |
Late hyphemas (swan syndrome)
Anterior segment hemorrhage months to years after cataract surgery may arise from neovascularization at the surgical incision site,[30–35] vascular iris tufts in contact with anterior chamber IOL haptics in the ciliary sulcus, or blood vessels in contact with posterior chamber IOL haptics in the ciliary sulcus (see also Uveitis-glaucoma-hyphema syndrome and neovascular glaucoma). Patients typically have painless, transient blurring of vision. Visual acuity and IOP depend on the amount of bleeding and trabecular meshwork function. Diagnosis of anterior-chamber bleeding sites is made by gonioscopic identification of neovascularization at the previous wound site or in areas of peripheral anterior synechia formation. It is uncommon to see bleeding directly from these vessels, but red blood cell “dusting” on the corneal endothelium may be present.
Treatment is often limited to topical medications as needed to control inflammation and IOP. Many eyes have only a single, isolated incident. Recurrent hemorrhages are best managed by laser goniophotocoagulation to the offending vessel when visible, although success with limbal cryopexy has also been reported.[31,][36] Long-term acuity deficits or intractable glaucoma are uncommon.[31]
Recurrent bleeding that is related to the haptic placement of an anterior-chamber lens typically requires an IOL exchange. Posterior-chamber lenses without haptic notches or bulbs can often be rotated 90° to position the haptics away from vessels. Haptic cutting and IOL exchange may also be required.
Ghost cell glaucoma
Erythrocytes begin degenerating within a few days after a vitreous hemorrhage.[37] After 1–3 weeks, they are tan and khaki colored, less pliable, spherical, devoid of intracellular hemoglobin, and freely mobile.[37] These cells are called “ghost cells.” After cataract surgery, an intact anterior hyaloid face largely prevents movement of cells into the anterior chamber, but any disruption allows easy access (Figure 50-2). Secondary open-angle glaucoma is produced from obstruction of the trabecular meshwork by the ghost cells. IOP may be normal or may rise rapidly to high levels if large numbers of cells are present.[37] Elevated pressure can persist for several months. A fine dusting of ghost cells may be seen on the corneal endothelium, and a layering of cells in the anterior chamber has the appearance of a tan hypopyon (Figure 50-3). The angle is normal or shows a slight khaki discoloration to the trabecular meshwork.
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Figure 50-2 Mechanism of ghost cell glaucoma. A, Clotted blood in the anterior and posterior chamber. B, Erythrocytes degrade to ghost cells. C, Rigid khaki-colored ghost cells enter the anterior chamber from the reservoir in vitreous humor through disrupted posterior capsule and anterior hyaloid face. Obstruction of the trabecular meshwork leads to glaucoma. |
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Figure 50-3 Tan “hypopyon” characteristic of ghost cell glaucoma. |
Standard medications are often ineffective in lowering IOP until the number of ghost cells in the anterior chamber has decreased. If the IOP remains persistently elevated despite maximally tolerated medical therapy, an anterior-chamber washout should be considered. Recurrent IOP elevation is common even with repeated anterior-chamber washouts, and a vitrectomy to remove the reservoir of posterior segment ghost cells may be required.[38]
Uveitis
Glaucoma rarely results from the mild postoperative inflammation that is routinely seen after cataract surgery. More commonly, glaucoma occurs in eyes with pre-existing uveitis or in eyes with a more severe inflammatory response. Uveitic glaucoma can be open angle, closed angle, or a combination of both. Open-angle glaucoma results from inflammation-related alterations in the trabecular meshwork. Changes include swelling of the trabecular matrix, endothelial cell dysfunction, or accumulation of inflammatory cells and debris.[39]Corticosteroid treatment and endogenous prostaglandins may also contribute.[40] Angle-closure glaucoma can occur from peripheral anterior synechiae, posterior synechiae, or rubeosis iridis.
Cataract surgery in patients with heterochromic iridocyclitis may be associated with secondary open-angle glaucoma.[41] In these eyes, gonioscopy typically discloses an open angle with fine, iris blood vessels that differ from the coarse, arborizing vessels associated with neovascular angle closure.[42] On entering the anterior chamber, bleeding may occur from these vessels. A secondary, open-angle glaucoma has also been reported in conjunction with episcleritis in a patient with a transscleral-fixated posterior-chamber implant.[43]
Clinical symptoms of uveitis include pain, photophobia, and decreased vision. Any findings on examination may include miosis, perilimbal injection, keratic precipitates, cells and flare in the anterior chamber, and, occasionally, fibrin.
Postoperative uveitic glaucoma is managed medically by controlling inflammation with frequent corticosteroid use. Cycloplegic and sympathomimetic agents are given to prevent or break posterior synechiae. For severe intraocular inflammation, periocular or systemic anti-inflammatory medication may be needed. Elevated IOP is treated with topical beta-blockers, topical or systemic carbonic anhydrase inhibitors, and hyperosmotic agents. Miotic agents and prostaglandin analogues are avoided. Iridectomies should be created to relieve pupillary block when indicated. Laser trabeculoplasty is largely ineffective. If medical therapy fails, filtration surgery with adjunctive antifibrotic treatment or seton placement is indicated.
Rarely, noninflammatory pigment cells circulating in the anterior chamber after posterior chamber IOL implant surgery may be associated with glaucoma.[44] This typically arises with sulcus-fixated IOLs and resultant haptic erosion of pigment from the ciliary body or posterior iris. Iris transillumination may be seen in the area of iris-haptic contact. On gonioscopy, the trabecular meshwork demonstrates dense pigmentation similar to pigment dispersion syndrome. Standard antiglaucoma therapy is instituted, but rarely IOL rotation, removal, or exchange is required.
Uveitis-glaucoma-hyphema syndrome
Uveitis combined with glaucoma and hyphema results from an IOL implant rubbing against the iris. It was a more frequent problem with early versions of iris-fixated and anterior-chamber IOLs[18,][45–50] but is also reported with posterior chamber implants.[44,][51–53] Causes include imperfections in implant construction, improperly sized lenses, or imperfectly positioned lenses. Initially, patients are treated conservatively with ocular anti-inflammatory and antiglaucoma medications. Patients with persistent glaucoma, recurrent hemorrhage, or endothelial decompensation require the removal of the implant. If the trabecular meshwork has not been irreversibly damaged, the glaucoma will subside.[45,][47,][50]
Lens particle glaucoma
Residual cortical material after cataract extraction can cause significant IOP elevation by either open- or closed-angle mechanism.[54] This glaucoma typically occurs early in the postoperative period, although it can occur years later if a Soemmering's ring cataract suddenly opens. Nd:YAG laser rupture of an epithelial pearl may be the precipitating factor. The patient presents with a red, painful eye. Keratic precipitates, anterior chamber inflammation, and retained lens material are seen.
Lens material causes severe obstruction of trabecular outflow channels,[55] but unlike phacolytic glaucoma, high-molecular-weight proteins are lacking. Obstruction to outflow may also result from macrophages filled with lens material, inflammatory cells, or persistent inflammation. Treatment with topical corticosteroids and antiglaucoma medications, excluding miotic and prostaglandin agents, is usually sufficient until IOP normalizes. Severe inflammation or persistent pressure elevation, or both, may require surgical removal of the residual lens material.
Dislocated nuclear fragments
With the rise in popularity of phacoemulsification as the preferred method for cataract surgery, the incidence of inadvertent posterior capsule tear and loss of nuclear fragments into the vitreous cavity also increased (Figure 50-4).[56–61] Lens dislocation into the vitreous most often occurs during lens emulsification or cortical cleanup.[57,][61–64] It tends to be inversely correlated with the experience of the surgeon performing the phacoemulsification. Other risk factors include inadequate zonular support (pseudoexfoliation, trauma, previous vitrectomy), very hard nuclei, deep-set eyes, poorly dilated pupils, or patient movement during surgery.[57,][61,][62,][65–67]
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Figure 50-4 Dislocated nucleus fragment in vitreous humor. |
Lens fragments in the vitreous are a serious problem. Lens particles left in the eye during cataract surgery seem to induce an inflammatory reaction that is somewhat proportional to the size of the displaced fragment.[58] Patients may develop significant visual loss, chronic uveitis, secondary glaucoma, corneal edema, and retinal detachment.[58,][68–72] One study reported a 52% incidence of glaucoma in eyes with retained lens fragments.[58]
Small pieces of lens cortex or a small chip of nucleus without significant corneal edema or glaucoma may only require medical management with topical corticosteroids.[73] However, larger lens fragments are best managed by consultation with a vitreoretinal surgeon. Removal of large lens fragments in the vitreous by an anterior segment approach is not recommended. Aggressive attempts at lens-fragment removal with lens loops, forceps, anterior vitrectomy, or phacoemulsification handpiece should not be done. These maneuvers typically result in vitreoretinal traction and carry a higher risk of retinal tears, retinal detachment, and potential corneal edema or decompensation. The best approach by the cataract surgeon is to perform a thorough cleanup of the vitreous and cortex using appropriate automated vitrectomy cutting instrumentation. An IOL, either anterior or posterior depending on the available capsular support, may be placed. The presence of an IOL does not interfere with the vitrectomy or removal of lens fragments.[58,][70,][71] The cataract incision should then be tightly closed with sutures. The patient should be referred in a timely fashion to a vitreoretinal surgeon for a three-port pars plana vitectomy-fragmentectomy.[58,][72]
Studies on the timing of vitrectomy for removal of retained lens fragments allow some general conclusions to be drawn. Vitrectomy need not be performed the same day. A reasonable time frame for vitrectomy is within 1–2 weeks. Visual acuity is generally improved with vitrectomy within this time frame.[58,][61,][68–76] There may be a lower chance of elevated IOP in eyes undergoing early vitrectomy.[66,][72,][74,][76] However, a delay in vitrectomy allows time for corneal edema to clear, elevated IOP to be treated, and the patient to be prepared for further surgery.[77,][78] Although retinal detachment is the major source of poor visual outcome, excellent visual results are typically achieved. Elevated IOP is managed with standard antiglaucoma medications. Several studies have shown that removal of lens fragments has a beneficial effect on the secondary glaucoma.[70–72,][76,][79]
See Chapter 44, Intraoperative complications of phacoemulsification surgery, for further discussion of displaced lens fragments after cataract surgery.
Corticosteroids
Intraoperative or postoperative administration of topical, periocular, or systemic corticosteroids may produce secondary open-angle glaucoma.[80–88] Topical corticosteroids, a mainstay of postoperative cataract care, are most commonly implicated. Although a less frequent cause of IOP elevation, administration of periocular repository corticosteroids can result in a significant IOP rise that is often delayed.[80,][85–88] These depot preparations are used in the treatment of cystoid macular edema or uveitis to increase intraocular drug concentrations and reduce the need for frequent instillation of drops.[80,][85–88]
Corticosteroid-induced glaucoma is related to the drug preparation, potency, frequency of administration, and duration of application. With depot preparations, drug release is primarily regulated by the biochemical composition of the corticosteroid. Highly water-soluble compounds diffuse rapidly and are short acting, whereas water-insoluble preparations persist longer.
Individuals with primary open-angle glaucoma,[89] their first-degree relatives,[90] diabetics,[91] and patients with high myopia[92] seem to be at higher risk for steroid-related IOP elevation. In patients without these predisposing factors, the clinician cannot predict which patients will have a pressure rise. Patients of any age may be affected. IOP elevation can occur in the presence of a functioning filter or seton device.[93,][94]
Corticosteroids raise IOP by reducing aqueous outflow[95] through effects on glycosaminoglycan metabolism.[96] The release of enzymes that depolymerize glycosaminoglycans is inhibited, and glycosaminoglycans accumulate within the trabecular meshwork.
Diagnosis requires a high index of suspicion and careful questioning. The predominant clinical finding is IOP elevation. The onset of IOP elevation is variable and can be significantly delayed. It may rise within the first week after the start of corticosteroid treatment or not until months or years later. Patients are usually asymptomatic. Eyes generally are not inflamed despite an increased IOP. Depending on the degree and duration of IOP elevation, optic nerve head cupping and visual field loss may or may not be present.
The first step in the management of corticosteroid glaucoma is to stop topical steroid therapy. Clinically significant IOP elevation is treated with the standard antiglaucoma medications. Careful follow-up and monitoring are required. In most cases, IOP returns to normal within days to weeks, although persistent elevation can occur. If corticosteroid medications must be continued, decreasing the strength and frequency or changing the type of corticosteroid and mode of administration may be useful.[97] If periocular corticosteroids have been given, excision of residual steroid material should be considered if IOP cannot be controlled medically.[84,][85,][87,][88] Biochemical analysis of excised depots has shown that significant amounts of periocular corticosteroids can remain for long periods. Laser trabeculoplasty is generally not helpful. If IOP is medically uncontrolled or progressive optic nerve damage occurs, patients require filtering, non-penetrating deep sclerectomy, or tube shunt surgery.
Viscosurgical agents
Viscosurgical agents were introduced into ophthalmic surgery in the early 1970s[98] and have expanded the options available to ophthalmic surgeons greatly by protecting tissue surfaces from mechanical damage, maintaining anterior chamber depth, and assisting in hemostasis. Since then, many materials with varying physical and biochemical properties have become commercially available. Some of these agents include Healon (1% sodium hyaluronate), Healon GV (1.4% sodium hyaluronate), Healon 5 (2.3% sodium hyaluronate), Viscoat (3% sodium hyaluronate/ 4% chondroitin sulfate), Amvisc (1.6% sodium hyaluronate), Vitrax (3% sodium hyaluronate), and OcuCoat (2% hydroxypropylmethylcellulose). Orcolon, a polyacrylamide polymer, was removed from the market because of severe uveitis and secondary glaucoma[99] resulting from contamination with microspheres that obstructed outflow.
The most common complication from use of viscosurgical agents in cataract surgery is a significant, and potentially dangerous, IOP elevation in the early postoperative period.[100–104]The IOP rise peaks between 4 and 7h postoperatively, and returns to normal within 24–72h.[105–108] Ocular pain and blurred vision are common presenting symptoms. Corneal edema and stagnation of circulating cells in the anterior chamber may be seen on the slit-lamp examination. The angle is open.
Viscosurgical substances leave the eye through the trabecular meshwork as relatively unchanged large molecules. Even in the presence of intraocular inflammation, little degradation of the viscosurgical substance occurs.[109] Studies demonstrate that these molecules elevate IOP by impairing aqueous humor outflow.[109] Eyes with insufficient trabecular meshwork function before surgery are more likely to have a significant elevation of IOP.[110]
IOP changes after viscosurgical use in cataract surgery have been studied by numerous clinicians. Lane et al.[111] compared early postoperative IOP after use of Healon, Viscoat, and OcuCoat. All three agents produced significant IOP elevation at 4h postoperatively. Holzer et al.[108] found a moderate increase in IOP postoperatively for Healon 5, Viscoat, OcuCoat, and Healon GV. The highest mean IOP was at 4h, with the highest to lowest IOP by agent being Healon 5, Viscoat, OcuCoat, and Healon GV. At 24h postoperatively, all groups had a mean IOP of <20mmHg.
To reduce the incidence of postoperative IOP elevation, ophthalmic surgeons evacuate the viscosurgical agent at the completion of the procedure. However, its removal only lessens, not eliminates, the incidence of IOP elevation.[102,][103,][105] Rates of removal vary from agent to agent. Highly viscous agents, such as Healon, Healon GV, and Healon 5, can cause significant IOP increases but require significantly less time to remove from the eye. Conflicting reports exist on the effectiveness of prophylactic treatment with topical beta-adrenergic agents and systemic carbonic anhydrase inhibitors.[112,][113]
In the early postoperative period after cataract surgery, IOP should be monitored closely. A clinically significant IOP rise should be treated with either simple release of aqueous via the paracentesis site[114] or antiglaucoma medications. If IOP elevation persists, surgical evacuation of the viscosurgical agent or filtration/seton surgery may be necessary to prevent visual loss.
See Chapter 6 for a detailed discussion of viscosurgical agents.
Capsular block syndrome (or capsular bag distention syndrome)
Capsular block syndrome occurs in patients who have had cataract removal with implantation of a posterior-chamber IOL in the capsular bag after an anterior continuous curvilinear capsulorrhexis.[115–119] Most cases occur immediately postoperatively, but capsular block has been observed as long as 5 years after surgery.[118]
Clinical features of this syndrome include an unexpected myopic overrefraction, anterior displacement of the optic and iris diaphragm, shallowing of the anterior chamber, increased space between the optic and posterior capsule, adherence of the anterior capsule to the IOL, and occasionally a persistent uveitis. Early postoperatively, the IOP may be normal or elevated. If untreated, eyes with capsular block syndrome develop glaucoma, posterior synechiae, and/or posterior capsule opacification with debris within the capsular bag.
To develop this problem, the anterior capsulorrhexis must be smaller than the IOL optic and a viscosurgical agent used. The condition results from a blockage of the egress of fluid contents within the capsular bag. Lens particulates and viscosurgical material are prevented from passing between the IOL optic and the anterior capsule. It is not exactly clear what mechanism draws fluid into the capsular bag and results in its distention.
Postoperatively, capsular block is relieved by performing an Nd-YAG laser anterior capsulotomy peripheral to the edge of the IOL, if observable directly or by first creating a peripheral iridectomy, or by a posterior capsulotomy if anterior capsule cannot be visualized.[119] Although it is uncommon, persistent IOP elevation is treated with standard antiglaucoma medications.
Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser capsulotomy
Short-term increases in IOP after an Nd:YAG capsulotomy are well documented[120–123] and they can result in significant and vision-threatening IOP elevation in both aphakic and pseudophakic patients.[124,][125] IOP elevation commonly occurs in the first 2h after the procedure, but may occur later. The rise is typically transient, but may persist.[126] The new onset of glaucoma or the worsening of pre-existing glaucoma can occur.[127] Patients with pre-existing glaucoma appear to be more susceptible to a rise in IOP[128] and should be monitored with extra caution and over the long term after the procedure.[129]
Intermediate and long-term changes in IOP following Nd:YAG capsulotomy also occur.[129–132] Long-term IOP problems after Nd:YAG capsulotomy appear to be correlated with the IOP measurement 1h following the procedure. Therefore, any patient who has a short-term rise in IOP should be checked regularly thereafter for the possibility of developing long-term IOP problems.[129]
The IOP elevation is caused by reduced facility of outflow from plugging of the trabecular meshwork with capsular particles, inflammatory cells, and protein, as well as from prostaglandin-mediated effects.[133] The number of laser pulses and total energy delivered do not appear to be contributing factors.[127]
Patients undergoing Nd:YAG capsulotomy require close medical observation to detect and treat postoperative pressure elevation. Although varying results have been reported, prophylactic use of timolol,[134] pilocarpine, topical dorzolamide,[135] acetazolamide,[136,][137] and topical apraclonidine[138] has been shown to be highly effective in preventing acute pressure spikes following laser treatment. Persistent IOP elevation is managed with standard antiglaucoma medications.
See Chapter 51 for an extensive discussion of Nd:YAG laser capsulotomy.
Vitreous in the anterior chamber
Secondary open-angle glaucoma from vitreous in the anterior chamber is uncommon. It may occur (1) after intracapsular surgery with iatrogenic or spontaneous breakage of the anterior hyaloid face, (2) after extracapsular surgery with iatrogenic capsular rupture and incomplete vitrectomy, or (3) after posterior capsulotomy.[139,][140]
Vitreous within the anterior chambers of enucleated eyes results in trabecular meshwork obstruction and secondarily a decrease in aqueous outflow[139] (Figure 50-5). In human eyes, uncertainty exists as to whether vitreous alone, inflammation, or a combination of factors actually causes glaucoma.
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Figure 50-5 Vitreous humor filling the anterior chamber through the posterior capsule opening, leading to obstruction of trabecular meshwork. |
IOP elevation is seen a few weeks or months after surgery. Anterior segment inflammation is often minimal. Pressure elevation is treated with standard antiglaucoma therapy. Hyperosmotic and mydriatic agents may help by retracting vitreous from the angle. The effect of miotic agents is variable. Anterior vitrectomy may be successful for medically uncontrolled glaucoma.[139] However, even total removal of vitreous from the anterior chamber and angle does not ensure resolution of the glaucoma.
Cyclodialysis cleft closure
A cyclodialysis cleft is a separation between the scleral spur and ciliary body that produces a direct communication between the anterior chamber and the suprachoroidal space. Cleft formation may occur as an inadvertent complication of cataract surgery. It is, fortunately, an uncommon problem.
Clefts vary in size, and small ones are especially difficult to see with gonioscopy. The size of the cleft is not related to the degree of hypotony.[141]
Postoperative ocular hypotony is the initial typical clinical presentation. Other clinical features include: reduced visual acuity, anterior chamber shallowing, choroidal effusions, optic nerve edema, and macular edema.
Treatment is directed at partial or complete closure of the cyclodialysis cleft. Conservative medical management involves atropine 1% drops twice daily. Cycloplegia helps to promote contact between the sclera and choroid. Miotics and topical steroids are avoided. If medical therapy fails, cyclodialysis clefts can be closed with argon laser, cryotherapy, or placement of sutures.[141,][142]
IOP may acutely rise to high levels from either spontaneous or therapeutic closure of the cleft.[143,][144] The pressure rise is usually rapid and severe, but generally transient. Management of IOP elevation includes topical beta-adrenergic blockers, topical alpha-2 agonists, topical or systemic carbonic anhydrase inhibitors, and hyperosmotic agents. Miotics should be avoided.
Alpha-chymotrypsin (enzyme) glaucoma
Although rarely seen today, alpha-chymotrypsin glaucoma was very common following enzyme zonulolysis in intracapsular cataract extraction.[145] In 1964, Kirsch[146] first reported glaucoma from the use of alpha-chymotrypsin in human cataract extraction.
This condition results from acute obstruction of the trabecular meshwork outflow channels by zonular fragments. Scanning electron microscopy of animal eyes demonstrates particulate material blocking the trabecular meshwork near Schlemm's canal and within the uveal meshwork; saline-perfused control eyes show no material.[147] Particles vary in size and shape. Transmission electron microscopy identifies them as zonular fragments and not alpha-chymotrypsin or its by-products. Zonular fragments have also been documented in human eyes.[148] Tonography studies document an impaired facility to outflow. Pilocarpine lowers pressure and improves outflow except during peak pressure rise.[145]
The onset of the IOP rise occurs during the first several days after cataract surgery and may last days to weeks.[50] Clinical findings include mild-to-severe elevation in IOP, corneal edema, normal anterior-chamber depth, and an open angle. IOP elevation is dose dependent. Patients with pre-existing glaucoma have a slightly greater or no greater incidence of this glaucoma. Tonography shows no long-term alteration in trabecular meshwork outflow between 2 and 6 months postoperatively in patients who had previously demonstrated a postoperative pressure increase.[149]
The pressure rise may be prevented or minimized by using a 1:10,000 enzyme dilution instead of 1:5000, limiting the volume used, and irrigating the anterior chamber. Prophylactic use of timolol and acetazolamide may also be of benefit.[36,][150] Any postoperative pressure rise should be managed conservatively with antiglaucoma medications until spontaneous resolution occurs, which is usually within 1 week.
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Closed-angle glaucomas
Pre-existing angle closure
Patients with a previous history of angle-closure glaucoma have an increased risk of glaucoma following cataract surgery, especially if significant angle closure is present preoperatively. However, the degree of preoperative synechial closure is not proportional to the potential severity of postoperative glaucoma. Intense postoperative inflammation and/or prolonged flattening of the anterior chamber can result in permanent peripheral anterior synechiae. A shallow or flat anterior chamber following cataract extraction is commonly associated with a wound leak, choroidal detachment, or both. Medical therapy is initiated, but early surgical intervention may be required to prevent, reduce, or avoid synechial closure, as well as other complications.
Pupillary block
A pupillary block represents a blockage of aqueous humor flow from the posterior chamber to the anterior chamber. It develops when the pupillary space and iridectomies are occluded with vitreous,[151–155] gas,[156] blood,[28] inflammatory materials,[40] capsule,[157] lens cortical material, IOL,[158] or silicone oil.[159] This entity is the most common cause of angle-closure glaucoma following cataract surgery with or without IOL implantation and may complicate both intracapsular[160] and extracapsular cataract extraction.[158,][161–163]Anterior-chamber, iris-plane, and posterior-chamber IOL implants have been reported with pupillary block. In addition, pupillary block may occur in the presence of peripheral and sector iridectomies.[158,][161–164]
Aphakic pupillary block glaucoma presents days to weeks following surgery with a shallow or flat anterior chamber, elevated IOP, and occlusion of the pupillary space, iridectomies, or both. Pseudophakic block with an anterior chamber implant presents the same way except that (1) the central anterior chamber is deep (the optic holds the iris under it posteriorly), and the peripheral chamber is shallow or flat with an iris bombé configuration (Figure 50-6) or (2) the chamber is uniformly shallow. Although dependent on the stage of glaucoma development, gonioscopy usually shows the filtration angle to be closed.
|
Figure 50-6 Iris bombé with pupillary block. |
Medical and laser therapies are used to break pupillary block, deepen the anterior chamber, and prevent chronic angle-closure glaucoma. Iris dilation with cycloplegic-mydriatic agents often eliminates pupillary block. Pupillary block from air can be treated with patient positioning and mydriasis. Elevated IOP is treated with topical beta-adrenergic blockers, topical or systemic carbonic anhydrase inhibitors, and hyperosmotic agents, as needed. Prostaglandin analogues are typically not recommended for angle-closure glaucoma. A laser iridectomy is recommended in conjunction with medical therapy to prevent recurrence. The laser iridectomy is often easier to create before pupillary dilation. Gonioscopy should be performed soon after elimination of pupillary block to assess for residual angle closure. If peripheral anterior synechiae persist, argon laser gonioplasty may be helpful to reduce synechiae and should be performed promptly to maximize success.[165] Surgical goniosynechialysis,[166] filtration surgery, or seton placement may be required for cases of extensive synechiae and high IOP (Table 50-2). The role of routine surgical iridectomy with posterior chamber implants is controversial. Because the risk of pupillary block is low, the general tendency with phacoemulsification and self-sealing incisions (corneal or scleral) is to not perform an iridectomy.[162,][167,][168]
Table 50-2 -- Treatment sequence for pupillary block
|
Reverse pupillary block or “sticky pupil” syndrome may be noted intraoperatively. This blockage of communication between the anterior chamber and the posterior chamber is due to a seal of viscosurgical agent between the iris and the IOL. Any chamber deepening results in an exaggerated concave configuration. Blockage is relieved by the removal of the viscosurgical agent.
Malignant glaucoma (posterior aqueous diversion)
The term malignant glaucoma conveys the message of a serious form of glaucoma that responds poorly to conventional glaucoma therapy and may result in serious vision loss. The terms ciliary-block glaucoma and posterior aqueous diversion are also used to describe this condition. Both of these terms better describe the pathophysiology, which is blockage of anterior movement of aqueous humor near the junction of the ciliary processes, lens equator, and anterior vitreous face. Aqueous humor is then diverted posteriorly into and behind the vitreous cavity with resultant forward movement of the vitreous and shallowing of the anterior chamber (Figure 50-7). Impermeability of the anterior hyaloid membrane and vitreous body to the anterior flow of aqueous humor has been found as perfusion pressure is elevated.[169] Impermeability may be increased by hyaloid to ciliary body apposition. The sequence of events in malignant glaucoma is thought to be initiated by the increased pressure behind a posteriorly detached vitreous, by compaction of the vitreous and, further, decreased fluid movement through it.
|
Figure 50-7 Malignant glaucoma with posterior aqueous diversion and shallowing of anterior chamber. |
Malignant glaucoma may occur following cataract surgery with or without associated trabeculectomy.[170,][171] Phakic eyes with a history of angle-closure glaucoma and a degree of closed angle at the time of surgery are at highest risk.[172] Onset may occur intraoperatively or months after surgery.
Clinical characteristics and response to medical therapy, surgery, or both, distinguish malignant glaucoma from choroidal detachment, pupillary block, and suprachoroidal hemorrhage (Table 50-3; see Figure 50-7). In malignant glaucoma, both the central and peripheral anterior chambers are shallow or flat. IOP may be normal or elevated. Choroidal detachment is not seen. Unlike pupillary block glaucoma, clinical findings persist despite having a patent iridectomy. If patency of the iridectomy is questioned, an additional iridectomy should be made to definitively rule out pupillary block. Serous and hemorrhagic choroidal detachments have a characteristic fundus appearance, and a choroidal tap confirms the presence of fluid or blood in the suprachoroidal space.
Table 50-3 -- Distinguishing characteristics of shallow or flat anterior chamber
|
Malignant Glaucoma |
Serous Choroidal Detachment |
Pupillary Block |
Suprachoroidal Hemorrhage |
Wound Leak |
|
|
Onset |
Intraoperatively or any time thereafter |
Within the first postoperative week |
Early or late postoperatively |
Intraoperatively or within the first week |
Within the first postoperative week |
|
Anterior chamber |
Shallow or flat |
Shallow or flat |
Shallow or flat |
Shallow or flat |
Shallow or flat |
|
Intraocular pressure |
Normal or elevated |
Low |
Normal or elevated |
Normal or elevated |
Low |
|
Fundus |
No choroidal detachment |
Smooth, light brown choroidal elevations |
Normal |
Dark brown or red choroidal elevation |
Choroidal detachment may or may not be present |
|
Patent iridectomy present |
Yes |
Yes |
No |
Yes |
Yes |
|
Relief by iridectomy |
No |
No |
Yes |
No |
No |
|
Relief by suprachoroidal fluid drainage and anterior chamber reformation |
No |
Yes |
No |
Yes |
No |
Medical therapy for malignant glaucoma includes mydriatic-cycloplegic agents (1% atropine, 0.25% scopolamine, 10% phenylephrine),[173] topical or systemic carbonic anhydrase inhibitors, hyperosmotic agents, and topical beta-blockers.[174] Mydriatic-cycloplegic agents presumably act by tightening the lens-iris diaphragm and pulling the lens back against the vitreous, thus stopping the cycle of posterior fluid migration. Miotic or prostaglandin therapy is ineffective and may precipitate or aggravate malignant glaucoma. Medical therapy is continued until the IOP is satisfactorily reduced and the anterior chamber deepens. If treatment is successful, all medications, except cycloplegic agents, are gradually discontinued. Indefinite continuation of cycloplegia is essential to prevent relapse. If medical treatment is unsuccessful after a few days, further therapy with laser or surgery is indicated. In cases of aphakia or pseudophakia, the Nd:YAG laser may be used to disrupt the anterior hyaloid face.[165,][171,][175] Surgical intervention involves pars plana aspiration of liquid vitreous and restoration of the anterior chamber depth with or without goniosynechialysis.[176,][177] (See also Chapter 45.)
Neovascular glaucoma
Neovascular glaucoma is a secondary angle-closure glaucoma that results from the growth of new blood vessels on the anterior surface of the iris and across the anterior-chamber angle. These vessels grow rapidly and may lead to complete synechial closure of the angle. Iris neovascularization results from retinal hypoxia, typically seen in diabetes mellitus, central retinal vein occlusion, and carotid occlusive disease.[178] Hypoxia leads to the production of a soluble angiogenic factor that causes the proliferation of new blood vessels.[179]The presence of an intact posterior capsule or anterior hyaloid appears to prevent anterior movement of this factor.[180–182] Disruption of the capsule is associated with an increased incidence of rubeosis. The preoperative presence of proliferative diabetic retinopathy also carries a significantly greater risk of the development of neovascular glaucoma following cataract surgery.[180,][183]
Several stages exist in the development of rubeosis and neovascular glaucoma. Neovascularization typically begins at the pupillary margin and progresses toward the root of the iris. Interestingly, new vessels may first form around peripheral iridectomies.[184] Patients may have few early symptoms. With advanced disease, the eye becomes very painful with poor vision, conjunctival injection, corneal edema, and very high IOPs. Gonioscopy in early cases shows a normal and open angle, but as the condition progresses, abnormal vessels and areas of synechial closure are seen across the angle. Blood vessels that cross the scleral spur and arborize onto the trabecular meshwork are definitely abnormal.[178] Rubeotic glaucoma can progress to total angle closure within days. Distinguishing `between an open and closed angle is important because an open angle signifies an opportunity for achieving vessel regression with panretinal photocoagulation. Panretinal photocoagulation should be performed in rubeotic eyes with retinal ischemic disorders.[184]
Elevated IOP is treated with topical and systemic aqueous suppressants. Because of the presence of inflammation, miotic and prostaglandin agents are avoided. Cycloplegics and topical corticosteroids are used to reduce inflammation. In the early stages of disease, panretinal photocoagulation is performed with the hope of causing vessel regression and preservation of an open angle. It may be possible to avoid glaucoma surgery. Laser goniophotocoagulation appears to be of little value. Intravitreal antiangiogenic drugs such as bevacizumab (Avastin) have shown promise in reducing anterior segment neovascularization. If the IOP is significantly elevated despite medical treatment, and vision is endangered, urgent filtering surgery with antimetabolite supplementation is required. If this surgery is unsuccessful, seton devices or cyclodestructive procedures have shown some success. The rate of phthisis following cyclodestructive procedures may approximate 10%. Eyes with neovascular glaucoma and no vision are not candidates for surgical therapy. Comfort is best achieved with chronic use of cycloplegic agents and topical steroids.
Epithelial and fibrovascular ingrowth
Epithelial and fibrovascular ingrowth results from either epithelial growth or connective tissue growth into the anterior chamber and across the trabecular meshwork. Both conditions were more common with intracapsular cataract extraction and early surgical techniques. The incidence has significantly decreased over the past decade.[185,][186] Associated risk factors include complicated or difficult surgery and poor wound construction or closure with leakage.
The diagnosis of epithelial downgrowth is often delayed. Symptoms may be vague and include tearing, dull pain, redness, photophobia, and blurred vision.[187] Examination may show wound gape, a filtering bleb, and a fistulous tract with positive Seidel testing. Retroillumination of the cornea shows a translucent membrane that is demarcated by a gray line. The leading edge of this line often has a thickened and scalloped appearance (Figure 50-8). Unlike corneal graft rejection, keratic precipitates are not associated with this line. Corneal edema and deep corneal vascularization may be present. Anterior segment cells and flare are seen. Iris involvement is often extensive and can be delineated with the argon laser. Gonioscopy also helps to assess the extent of epithelialization. Membranes may also grow over the pupil, vitreous face, or IOL implants.
|
Figure 50-8 Epithelial downgrowth with retrocorneal membrane. |
The clinical picture for fibrous ingrowth differs slightly, with membranes appearing gray or white and demonstrating more irregular leading edges. Vascularization is more commonly present.
Histopathologic studies and electron microscopy show that nonkeratinized, stratified squamous epithelium grows over the posterior cornea, angle, iris, ciliary body, vitreous, and retina.[188] Epithelium is also usually seen along the surgical wound, which may or may not have incarcerated tissue. A chronic inflammatory cell infiltrate is frequently present within the tissues.
Glaucoma almost invariably occurs with downgrowth[186] and may result from synechial closure of the angle, pupillary block, and inflammation-related changes. Hypotony may also occur, secondary to a fistula and wound leak.
No medical therapy exists to stop progression from either epithelial or fibrovascular ingrowth.[189] Surgery is the mainstay of treatment. Before surgery is performed, the extent of ingrowth on the iris is delineated with the argon laser. White burns indicate the presence of epithelium. Surgical therapy requires removal of the involved iris, vitreous, and implant. Cryotherapy is applied to the cornea, angle, and ciliary body to devitalize remaining epithelium. Salvage of the globe is the prime consideration. Filtration with antifibrotic agents or seton devices may be needed for pressure control.
See Chapter 53 for a detailed discussion of epithelial and fibrous ingrowth.
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Treatment of glaucoma after cataract surgery: general principles
As noted previously, all efforts are made to determine the cause of the IOP elevation that develops after cataract surgery. Therapy is directed toward elimination or treatment of the specific cause (Table 50-4). In general, mainstays of therapy include topical and systemic aqueous suppressants. Miotic and prostaglandin agents may be helpful in open-angle glaucomas when there is no inflammation or chamber shallowing. However, disruption of the blood–aqueous barrier[184] and cystoid macular edema in the early postoperative period have been reported after cataract surgery in patients receiving topical latanoprost.[190–199] Adrenergic agents are generally avoided because of the possibility, albeit small, of cystoid macular edema that may develop after cataract surgery. Apraclonidine and brimonidine are helpful adjuncts for acute therapy of high IOP spikes and are beneficial for short-term IOP treatment from days to weeks. Oral and intravenous osmotic agents are occasionally needed for profound IOP elevations. Eye surgeons should always be alert to the possibility of corticosteroid- or cycloplegic-induced glaucoma that may require cessation of steroid and cycloplegic therapy.
Table 50-4 -- Glaucoma after cataract surgery: treatment sequence
|
Conventional laser treatment for glaucoma after cataract surgery generally involves laser iridectomy for pupillary block and laser trabeculoplasty for open-angle glaucoma. Argon laser trabeculoplasty and selective laser trabeculoplasty may not be as effective in the pseudophakic patient as in the phakic patient, but still may be helpful treatment modalities for many patients. Laser gonioplasty may be able to reduce synechiae in recently closed angles. Laser therapy is also indicated for malignant glaucoma and neovascular glaucoma, as noted earlier.
Surgery for glaucoma is occasionally required in aphakic and pseudophakic patients. Decisions concerning surgical technique and location of surgery depend largely on the status of the conjunctiva, vitreous, and IOL. Most surgeons prefer to operate in areas of conjunctiva that have not been disrupted by previous surgery.[19] At the same time, it is generally preferable to perform surgery superiorly rather than inferiorly to avoid exposing filtration blebs to a greater risk of infection. Filtration surgical techniques may be either partial thickness or full thickness. Vitreous must be removed if it is present in the area of the sclerectomy. The position of the IOL may direct the surgeon's choice of operative location. In eyes without significant limbal scarring, non-penetrating deep sclerectomy procedures, including viscocanalostomy and canaloplasty may be indicated.
If surgery is required for IOP control, a filtration procedure with intraoperative antifibrotics may be preferred. A limbal-based conjunctival flap is preferred to reduce leaks, but a fornix-based conjunctival flap may be used if necessary. Tight scleral flap closure is favored to minimize the risk of suprachoroidal hemorrhage. Selective laser suture lysis or releasable sutures are used postoperatively to facilitate aqueous egress. Supplemental use of 5-fluorouracil is also added postoperatively if necessary.
If standard filtration surgery with mitomycin-C fails, a tube-shunt seton device is often the next option. Deep sclerectomy procedures (viscocanalostomy and others) may be effective, particularly in eyes with minimal limbal scarring from previous procedures. Aphakic and pseudophakic eyes undergoing laser and surgical procedures more commonly require supplemental glaucoma medications for IOP control postoperatively than do phakic eyes. Because of the risk of visual loss and phthisis, cyclodestructive procedures are reserved for patients in which filtration or tube-shunt procedures fail. Transscleral cyclophotocoagulation is our preferred ciliary body destructive procedure of choice. Endocyclophotocoagulation is not associated with as great an IOP reduction as the transcleral route, but produces much less inflammation.
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