Article Date: 3/1/2009

Posterior-segment Considerations in Glaucoma Patients Undergoing Cataract Surgery
PEER REVIEWED

Posterior-segment Considerations in Glaucoma Patients Undergoing Cataract Surgery

KIMBERLY DAVIS, MD, FACS · HUNTER STOLLDORF, MD · ANNE L. COLEMAN, MD, PhD

Glaucoma is a significant and growing public health issue in the United States. It is estimated that 1.86% of the US population over the age of 40 is afflicted with primary open-angle glaucoma (POAG), and by 2020 that number will likely increase by 50%.1 Ophthalmologists in the future will be performing cataract extractions on an increasing number of glaucoma patients. Challenges during cataract surgery in these subpopulations range from intraoperative difficulties managing the relatively dynamic anterior chambers of patients with functioning blebs to postoperative IOP elevations and dislocated lenses. Here, we discuss the impact of pre-existing glaucomatous conditions on cataract surgery with attention to posterior complications occurring after cataract surgery in the patient with glaucoma.

PRE-EXISTING GLAUCOMATOUS CONDITIONS

In the glaucomatous population with surgically amenable cataracts, it is helpful to categorize patients into the following populations:

1. Chronic glaucoma
(a) Open angle
(b) Narrow angle

2. History of glaucoma surgery with functioning blebs or drainage tubes

3. Secondary glaucoma
(a) Steroid-responsive glaucoma
(b) Pseudoexfoliative glaucoma

Kimberly Davis, MD, FACS, is the head of glaucoma services and the director of the associate residency program at the US Naval Medical Center in San Diego. Hunter Stolldorf, MD, is an ophthalmology resident at the Naval Medical Center. Anne L. Coleman, MD, PhD, is professor of ophthalmology at the Jules Stein Eye Institute of the David Geffen School of Medicine at UCLA, as well as professor of epidemiology at the UCLA School of Public Health. She holds the Frances and Ray Stark Endowed Chair at UCLA and is director of the Jules Stein Eye Institute Mobile Eye Clinic. The authors report no financial interests in any products mentioned in this article. The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, or the US Government. Dr. Stolldorf can be reached via e-mail at hunter.stolldorf@med.navy.mil.

PATIENTS WITH CHRONIC OPEN-ANGLE GLAUCOMA

The primary consideration when performing cataract extraction on a patient with medically controlled glaucoma is postoperative IOP.

Measurement of IOP shortly after surgery is a poor gauge of what the IOP will be 24 hours postoperatively (Figure 1).2,3 Glaucomatous eyes are also more likely to have exaggerated IOP elevations postoperatively.4,5 Many surgeons recommend a single postop alpha-2 agonist or timolol maleate dose to blunt postoperative IOP spikes.6

Figure 1. Intraocular pressure in normal, pseudoexfoliation syndrome (XFS) and glaucomatous eyes with no prophylactic hypotensive treatment after cataract surgery.

REPRINTED FROM OPHTHALMOLOGY, 115(1), LEVKOVITCH-VERBIN H, HABOT-WILNER Z, BURLA N, ET AL., INTRAOCULAR PRESSURE ELEVATION WITHIN THE FIRST 24 HOURS AFTER CATARACT SURGERY IN PATIENTS WITH GLAUCOMA OR EXFOLIATION SYNDROME, PP. 104-108, COPYRIGHT 2008, WITH PERMISSION FROM ELSEVIER.

Cystoid macular edema (CME), among the most common causes of decreased vision after cataract surgery, is not a complication unique to glaucoma patients. However, the literature is replete with papers implicating prostaglandin analogs (PGAs) as an important factor contributing to CME. Latanoprost was approved by the FDA as the first PGA in 1996 for the treatment of glaucoma and ocular hypertension, and by the end of the decade there were several papers suggesting a relationship between CME and latanoprost.7-12 Moroi et al. published a case series correlating latanoprost usage to CME and CME's resolution after cessation of latanoprost.9 This relationship also exists postoperatively. Yeh et al. identified a 3% rate of postoperative, clinically significant CME within 1 month of uncomplicated phacoemulsification in patients with no known preoperative risk factors for CME other than the use of PGAs for IOP reduction (Figure 2). However, this rate is likely higher for eyes with additional risk factors for developing CME.10,13 With discontinuation of latanoprost and treatment with topical NSAIDs, all of Yeh's study patients had complete resolution of CME and return of visual acuity to normal within 1 month. Interestingly, patients chronically using latanoprost who were instructed to discontinue latanoprost 1 week prior to surgery avoided developing CME. The risk for postoperative CME is highest 30 to 90 days after phacoemulsification, but a small percentage of cases may occur after the initial 3 months.10,14

Figure 2. Postoperative CME in glaucoma patient.

IMAGE APPEARS COURTESY OF THE U.S. NAVAL MEDICAL CENTER, SAN DIEGO.

The 2002 Binkhorst Lecture identified the preservative in latanoprost, benzalkonium chloride (BAK), as the most important etiologic factor contributing to CME.15 BAK is the preservative in approximately 70% of commercially produced eyedrops including Xalatan, Travatan, Azopt, Lumigan, Cosopt, Trusopt, and timolol maleate.16 This preservative is hypothesized to exacerbate the proinflammatory effect of topical antiglaucoma medications. Discontinuation of any nonessential drops containing this preservative should be considered during the treatment of CME.15

PATIENTS WITH NARROW ANGLE AND ANGLE CLOSURE GLAUCOMA

Cataract extraction in patients with narrow angles widens the anterior chamber angle in closed-angle glaucoma patients with subsequent lowering of IOP by 2 to 6 mm Hg.17,18 A similar effect occurs in non-glaucomatous eyes and eyes with POAG. Cataract extraction in a patient with recent peripheral anterior synechia may halt further angle closure.

Hyperopic eyes with crowded anterior segments are predisposed to angle closure glaucoma, challenging cataract surgery, and postoperative complications, such as suprachoroidal hemorrhages. Both long and short axial lengths predispose to suprachoroidal hemorrhage, as do the systemic conditions of hypertension and diabetes.19 The magnitude and rate of IOP decrease are directly correlated to risk of suprachoroidal hemorrhage.20 In general, the drainage of choroidal detachments and hemorrhage is controversial. Prophylactic posterior sclerotomies are occasionally performed in high-risk patients and should be considered for those patients with a prior history of such complications (Figure 3).21 Should a suprachoroidal hemorrhage occur, the prognosis for long-term health of the eye is relatively unchanged without a concurrent retinal detachment or associated loss of choroidal or retinal tissue.22

Figure 3. Posterior sclerotomy creation.

Misdirection of aqueous humor into the vitreous, also known as malignant glaucoma, may occur following any incisional or laser procedure.23-25 The diagnosis is made when a patent peripheral iridotomy or iridectomy exists simultaneously with a symmetrically shallow anterior chamber and an absence of a suprachoroidal effusion or hemorrhage. In contrast, patients with acute angle closure will have an anterior chamber narrower peripherally than centrally. Patients suspected to have malignant glaucoma are first treated with glaucoma pressure–lowering medications and cylcoplegia, but half of patients require further intervention.24

Surgical options with reported efficacy include Nd:YAG capsulotomy, laser ablation of ciliary processes, Nd:YAG laser peripheral iridectomy with hyaloidotomy and cyclophotocoagulation, and pars plana vitrectomy.23,25 The primary goal of the procedure is to re-establish the appropriate flow of aqueous humor. For eyes that are not successfully managed with medications, surgery is required for disruption of the anterior hyaloid face to allow sequestered aqueous from the posterior segment to travel forward into the anterior chamber. Eyes with malignant glaucoma have undergone a biochemical and conductivity change to the vitreous resulting in a compressed and condensed anterior hyaloid face with a relative impermeability to aqueous. Disruption of this interface is crucial to control of IOP.26

CATARACT SURGERY AFTER TRABECULECTOMY

Cataract progression is accelerated following incisional glaucoma surgery, and cataract extraction occurs in approximately half of patients within the first 5 years following glaucoma surgery.27 Unfortunately, phacoemulsification has a significant impact on IOP control in patients with pre-existing functioning blebs. The higher the preoperative IOP, the higher the likelihood for difficult postoperative IOP control. Most postoperative pressure elevations occurring in the early postoperative period are transient and amenable to control with topical pressure-lowering medications. Despite medical IOP control during the postoperative period, 20% to 25% of patients with a history of incisional glaucoma surgery requiring no medical supplementation preoperatively will require supplements permanently after cataract extraction.28 Although this appears to draw a definitive connection between cataract extraction and postoperative elevation of IOP in this population, there is an expected rise over time in IOP in trabeculectomy patients who do not undergo cataract extraction.17 The true mechanism for induction of elevated IOP and flattening of filtering blebs after cataract extraction is not known, but it is believed to be initiated by the general inflammatory response induced by surgery. Subconjunctival scarring causes bleb flattening and resultant dysfunction, but there is not always a direct correlation between bleb appearance and function or IOP control.28 Bleb revision or primary trabeculectomy during cataract surgery are options in those eyes with higher precataract extraction IOP. Filtering blebs that have not fully matured are more likely to fail after cataract extraction than blebs that have matured, and this in turn affects postop IOP control. Failure is due to the susceptibility of the healing bleb to the aforementioned inflammation. An interval between trabeculectomy and cataract extraction of less than 6 months is associated with the need for glaucoma reoperation.28

A functioning bleb acts as a conduit for irrigating fluid during cataract surgery and can cause dramatic anterior chamber fluctuation. Eyelid speculum placement and instrument manipulation may traumatize an existing bleb, resulting in postoperative bleb leaks and hypotony. A cause of a CME-like maculopathy is ocular hypotony. Hypotony occurs from overfiltration secondary to a wound or bleb leak, a large diffuse bleb, or from undersecretion of aqueous, which may be secondary to mitomycin-C toxicity of the ciliary body epithelium. If hypotony occurs, attention to the cause and alteration of glaucoma medication regimen is warranted. Small bleb leaks may be managed with large diameter bandage contact lenses (such as the 20-24 mm diameter Kontur soft contact lens manufactured by Kontact Lens Company, Inc., Richmond, CA), antibiotic eyedrops, and aqueous suppressants. Large leaks may necessitate urgent closure. Cycloplegics provide an internal splint, thus stabilizing the eye. IOL-cornea touch, IOL subluxation, or corneal compromise requires anterior chamber reformation with a cohesive viscoelastic agent. This can be performed at the slit lamp or under the operating microscope. An untreated leak poses a setup for blebitis or endophthalmitis.

The Endophthalmitis Vitrectomy Study, completed in 1995, revolutionized the treatment of cataract surgery–related endophthalmitis. In this study, endophthalmitis was attributed to cataract extraction if it occurred within 6 weeks. The results shifted the preferred practice patterns away from pars plana vitrectomy with intravitreal antibiotics toward "tap and inject," depending on the presenting visual acuity. It is difficult to directly extrapolate these results to glaucoma patients with pre-existing blebs undergoing cataract extraction, as blebs may result in endophthalmitis years after being constructed. In addition, the causative organisms tend to be different. Bleb-associated endophthalmitis (BAE) treatment is controversial and has not been studied prospectively because of its low occurrence rate. Current retrospective studies suggest that "tap and inject" may be less suited for trabeculectomy patients found to have endophthalmitis. In a retrospective study including patients before and after the 1995 shift in preferred practice patterns, Busbee et al. found that patients with blebs receiving "prompt vitrectomy had statistically better visual outcomes, less likelihood of severe visual decline, and a lower incidence of no light perception vision than those treated with tap and inject."29 This finding directly contradicts another retrospective study by Song et al. that purports worse visual outcomes from vitrectomy in BAE.30

CATARACT SURGERY FOLLOWING DRAINAGE-DEVICE PLACEMENT

Phacoemulsification appears to have less of an impact on postoperative IOP control in the population of patients with implanted drainage devices, but the immediate postop period remains susceptible to pressure spikes. It is likely that the device reservoir limits the extent of surgery-mediated, inflammatory-induced conjunctival fibrosis seen in trabeculectomy patients. Drainage device patients typically require no additional pressure-lowering drops and occasionally require less medication up to 1 year postoperatively.31

An additional postoperative complication that can occur during phacoemulsification is obstruction of the drainage device with lens material or vitreous (Figure 4). Some surgeons routinely place a suture or other plug into the tube ostomy to protect against lens material and viscoelastic during phacoemulsification.32 Other surgeons avoid the open tube and perform cataract surgery as if it were not present.33 Another concern in this group is late corneal decompensation, which can have the appearance of pseudophakic bullous keratopathy, except for the segmental nature. Touch between the cornea and tube — either at rest, with eye rubbing, or with blinking — leads to progressive endothelial cell loss and decreased ability to clear the stroma. Bhattacharyya et al. reported 27% of their patients developing irreversible corneal edema, Gujral et al. encountered a rate of 9%, and Erie et al. had no patients with corneal edema.31,33,34 Ensuring no corneal-tube touch greatly increases the chances of avoiding this complication.

Figure 4. Drainage device tube blocked by vitreous following complicated cataract surgery.

The incidence of endophthalmitis after placement of drainage devices is low. Approximately 0.4% of patients will get endophthalmitis within the first year after placement of a drainage device, and the rate after initial trabeculectomy is about 4 times less frequent (ie, 0.1%).35 The rates for endophthalmitis in glaucoma drainage device patients undergoing sutureless, clear corneal cataract surgery are not known, and the incidence of endophthalmitis in this group is confounded by the varying rates of endophthalmitis found throughout the literature today.36

STEROID-RESPONSIVE GLAUCOMA

Approximately 5% to 6% of the general population will develop a marked elevation of their IOP after 4 to 6 weeks of chronic administration of topical steroids, and there is a direct relationship between their frequency, potency, and duration of use.37,38 Patients with POAG and their first-degree relatives are at an increased risk. Patients with a history of significantly elevated IOP may respond within 2 weeks of restarting topical steroids.39 Placement of depot steroids or a steroid implant around the eye, such as is used in the treatment of chronic uveitis, acts to continuously release steroids, bringing the added risk of difficult or intractable IOP control. An intraocular steroid implant, Retisert (fluocinolone acetonide intravitreal implant, 0.59 mg), provides such an example of steroid-induced glaucoma.

This steroid delivery system is highly effective in uveitis management, but it causes dramatic IOP elevations in many patients. According to its manufacturer, Bausch & Lomb, 51% of patients require IOP-lowering drops within 34 weeks of the implant's insertion.40 The use of steroids in the postop period after cataract extraction is unavoidable. For patients with secondary glaucoma from chronic uveitis, the steroids may have played a role in accelerating cataract formation. When steroids cannot be stopped or their discontinuation does not result in a decrease in IOP, medical therapy with topical beta-blockers, alpha-agonists, or carbonic anhydrase inhibitors is necessary. Prostaglandin use should be avoided because of their relative propensity to contribute to inflammation in susceptible patients.

PSEUDOEXFOLIATION GLAUCOMA

Cataract extraction in a patient with pseudoexfoliation glaucoma carries with it unique anterior- and posterior-segment concerns. Pseudoexfoliation occurs in approximately 4% to 6% of patients older than 60 years of age and as much as 8% to 35% of the population over age 70.41

The characteristic deposition of fibrillar material has been found throughout the body, and its fundamental pathogenesis is likely a basement membrane disorder.42 The deposition of extracellular fibrillar material can trigger aqueous outflow difficulties with resultant IOP elevations in 34% of patients.43 Additional complications of cataract extraction in this population are related to its characteristic zonular weakness. Kuchle et al. correlated shallow anterior chamber depths of <2.5 mm in patients with pseudoexfoliation to a 13.4% rate of intraoperative complications. They tied anterior chamber depth to zonular stability with a distended or broken fiber allowing anterior-posterior lens excursion.44 Risk of zonular dehiscence with or without attendant vitreous loss can be 5 to 10 times that of a normal eye.42,45

A dislocated cataractous lens may be removed intact through an extracapsular incision (Figures 5 and 6).46 If the lens has dislocated to the posterior segment, pars plana vitrectomy and lensectomy are required. Retained nuclear lens fragments in the vitreous after cataract extraction require removal because of the significant potential for these fragments to cause inflammation, IOP elevations, and vitreoretinal traction. Complications such as retinal detachment, CME, and secondary glaucoma result in a reduced final visual outcome. The factors that tend to influence how quickly the patient requires pars plana vitrectomy are size of the lens fragment, level of inflammation, and IOP.47


Figure 5. Clinical photograph of a patient with an inferiorly decentered 1-piece polymethyl methacrylate posterior chamber intraocular lens within the capsular bag with complete loss of superior zonular support.

Figure 6. Gross photograph of a one-piece polymethyl methacrylate posterior chamber intraocular lens completely surrounded by an intact capsular bag with a small amount of iris pigment on the anterior surface.

FIGURES 5 AND 6 ARE REPRINTED FROM OPHTHALMOLOGY, 108(10), JEHAN FS, MAMALIS N, CRANDALL AS, INTRAOCULAR PRESSURE ELEVATION WITHIN THE FIRST 24 HOURS AFTER CATARACT SURGERY IN PATIENTS WITH GLAUCOMA OR EXFOLIATION SYNDROME, PP. 1721-1731, COPYRIGHT 2001, WITH PERMISSION FROM ELSEVIER.

Reducing the time between cataract extraction and pars plana vitrectomy should be considered more urgently in a patient with pre-existing glaucoma. Studies report that the sooner an inflammation-inducing agent, in this case retained lens fragments, is removed from the vitreous, the greater the likelihood of avoiding additional complications such as CME, retinal detachment, vitreous traction, and elevated IOP. Chen et al. found a significant difference in the rate of complications between patients who had pars plana vitrectomy 1 day and 1 week after cataract extraction. Their results indicate that waiting up to a week to perform pars plana vitrectomy results in universal IOP elevations and decreases the chance of achieving the best visual potential by 50%.48 A few other studies support the notion that an increasing interval between cataract extraction and pars plana vitrectomy is associated with poorer visual outcomes,49,50 but a time delay may be required if corneal edema limits the posterior view and the preponderance of studies finds no significant difference in waiting several weeks in patients without glaucoma.51-56

Vitreous loss during phacoemulsification is associated with a slight increase in the difficulty of controlling IOP over the long term. This is caused by several factors. Vitreous has an inflammatory effect in the anterior chamber. This inflammatory effect further compromises a poorly functioning trabecular meshwork. Mechanical blockage of the trabecular meshwork in this process can occur via 2 mechanisms: direct angle blockage or through the formation of peripheral anterior synechiae. Experimental evidence in cadaver eyes shows that mechanical blockage with vitreous likely causes less of an IOP elevation over the long term than the inflammatory component caused by vitreous in the anterior chamber.43

Pseudoexfoliation is the most common cause of late lens dislocation, but any condition predisposing to zonular weakness may lead to this complication (eg, uveitis, direct zonular trauma, vitrectomy, high myopia, or connective tissue disorders).57 The incidence of artificial lens dislocation after an uncomplicated phacoemulsification ranges from 0.2% to 3.0%, and this complication can occur at any time.57 Dislocation is caused either by lens problems (eg, haptic dysfunction or asymmetric lens placement) or capsular problems (eg, zonular dehiscence, capsular tear, or blunt ocular trauma). In patients with pseudoexfoliation, Jehan et al. found a mean time from uncomplicated cataract extraction to dislocation of approximately 7 years.58 Between 4% and 6% of percent of patients over the age of 60 and 8% to 35% of those over 70 experience spontaneous late IOL dislocation.41 In cases of obvious lens instability, options include capsular tension ring, anterior chamber lens, or IOL fixation to the sclera or iris.58 Capsular tension rings help provide zonular apparatus stability, but they cannot prevent late dislocation.59 Visual outcomes following surgical management of IOL dislocations are limited by pre-existing pathology and additional postoperative complications.

CONCLUSION

Cataract surgery in the patient with glaucoma carries additional risks, many of which involve the posterior-segment surgeon. Eyes with glaucoma may have other comorbidities, such as pseudoexfoliation, uveitis, or shallow anterior chambers. Preoperative planning, careful anterior-segment surgery, IOP control, and prompt problem recognition can provide this patient population with the best possible outcome. RP

REFERENCES

  1. Friedman DS, Wolfs RC, O'Colmain BJ, et al. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004;122:532-538.
  2. Levkovitch-Verbin H, Habot-Wilner Z, Burla N, et al. Intraocular pressure elevation within the first 24 hours after cataract surgery in patients with glaucoma or exfoliation syndrome. Ophthalmology. 2008;115:104-108.
  3. Ahmed II, Kranemann C, Chipman M, Malam F. Revisiting early postoperative follow-up after phacoemulsification. J Cataract Refract Surg. 2002;28:100-108.
  4. Borazan M, Karalezli A, Akman A, Akova YA. Effect of antiglaucoma agents on postoperative intraocular pressure after cataract surgery with Viscoat. J Cataract Refract Surg. 2007;33:1941-1945.
  5. Shingleton BJ, Rosenberg RB, Teixeira R, O'Donoghue MW. Evaluation of intraocular pressure in the immediate postoperative period after phachoemulsification. J Cataract Refract Surg. 2007;33:1953-1957.
  6. Fry LL. Comparison of the postoperative intraocular pressure with Betagan, Betoptic, Timoptic, Iopidine, Diamox, Pilopine gel, and Miostat. J Cataract Refract Surg. 1992;18:14-19.
  7. Row JA, Hattenhauer MG, Herman DC. Adverse side effects associated with latanoprost. Am J Ophthomol. 1997;124:683-685.
  8. Warwar RE, Bullock JD, Ballal D. Cystoid macular edema and anterior uveitis associated with latanoprost use. Experience and incidence in a retrospective review of 94 patients. Ophthalmology. 1998;105:263-268.
  9. Moroi SE, Gottfredsdottir MS, Schteingart MT, et al. Cystoid macular edema associated with latanoprost therapy in a case series of patients with glaucoma and ocular hypertension. Ophthalmology. 1999;106:1024-1029.
  10. Yeh PC, Ramanathan S. Latanoprost and clinically significant cystoid macular edema after uneventful phacoemulsification with intraocular lens implantation. J Cataract Refract Surg. 2002;28:1814-1818.
  11. Avakian A, Renier SA, Butler PJ. Adverse effects of latanoprost on patients with medically resistant glaucoma. Arch Ophthalmol. 1998;116:678-680.
  12. Heier JS, Steinert RF, Frederick AR Jr. Cystoid macular edema associated with latanoprost use. Arch Ophthalmol. 1998;116:680-682.
  13. Wand M, Gaudio AR, Shields MB. Latanoprost and cystoid macular edema in high-risk aphakic or pseudophakic eyes. J Cataract Refract Surg. 2001;27:1397-1401.
  14. Henderson BA, Kim JY, Ament CS, Ferrufino-Ponce ZK, Grabowska A, Cremers SL. Clinical pseudophakic cystoid macular edema; risk factors for development and duration after treatment. J Cataract Refract Surg. 2007;33:1550-1558.
  15. Miyake K, Ibaraki N, Goto Y, et al. ESCRS Binkhorst Lecture 2002: Pseudophakic preservative maculopathy. J Cataract Refract Surg. 2003;29:1800-1810.
  16. Winfield AJ, Richards RME. Pharmaceutical Practice. New York, NY: Churchill Livingstone; 2004.
  17. Klink J, Schmitz B, Lieb WE, et al. Filtering bleb function after clear cornea phacoemulsification: a prospective study. Br J Ophthalmol. 2005;89:597-601.
  18. Hayashi K, Hayashi H, Nakao F, Hayashi F. Changes in anterior chamber angle width and depth after intraocular lens implantation in eyes with glaucoma. Ophthalmology. 2000;107:698-703.
  19. Sekine Y, Takei K, Nakano H, et al. Survey of risk factors for explusive choroidal hemorrhage: case reports. Ophthalmologica. 1996;210:344-347.
  20. Eriksson A, Koranyi G, Seregard S, Philipson B. Risk of acute suprachoroidal hemorrhage with phacoemulsification. J Cataract Refract Surg. 1998;24:793-800.
  21. Wu W, Dawson D, Sugar A, et al. Cataract surgery in patients with nanophthalmos: Results and complications. J Cataract Refract Surg. 2004;30:584-590.
  22. Spaeth GL, Baez KA. Long-term prognosis of eyes having had operative suprachoroidal expulsive hemorrhage. Ger J Ophthalmol. 1994;3:159-163.
  23. Muqit MMK, Menage MJ. Malignant glaucoma after phacoemulsification: treatment with diode laser cyclophotocoagulation. J Cataract Refract Surg. 2007;33:130-132.
  24. Lois N, Wong D, Groenewald C. NNew surgical approach in the management of pseudophakic malignant glaucoma. Ophthalmology. 2001;108:780-783.
  25. Sharma A, Sii F, Shah P, Kirkby GR. Vitrectomy-phacoemulsification-vitrectomy for the management of aqueous misdirection syndromes in phakic eyes. Ophthalmology. 2006;113:1968-1973.
  26. Epstein DL, Hashimoto JM, Anderson PJ, Grant WM. Experimental perfusions through the anterior and vitreous chambers with possible relationships to malignant glaucoma. Am J Ophthalmol. 1979;88:1078-1086.
  27. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol. 1998;126:487-497.
  28. Rebolleda G, Muñoz-Negrete FJ. Phacoemulsification in eyes with functioning filtering blebs: a prospective study. Ophthalmology. 2002;109:2248-2255.
  29. Busbee BG, Recchia FM, Kaiser R, Nagra P, Rosenblatt B, Pearlman RB. Bleb-associated endophthalmitis: clinical characteristics and visual outcomes. Ophthalmology. 2004:111:1495-1503.
  30. Song A, Scott IU, Flynn HW Jr, Budenz DL. Delayed-onset bleb-associated endophthalmitis. Ophthalmology. 2002;109:985-991.
  31. Erie JC, Baratz KH, Mahr MA, Johnson DH. Phacoemulsificaiton in patients with Baerveldt tube shunts. J Cataract Refract Surg. 2006;32:1489-1491.
  32. Fechter HP. Improvised 3-0 polypropylene plug for the glaucoma drainage tube during phacoemulsification. Ophthalmic Surg Lasers Imaging. 2008;39:86-87.
  33. Gujral S, Nouri-Mahdavi K, Caprioli J. Outcomes of small-incision cataract surgery in eyes with preexisting Ahmed Glaucoma Valves. Am J Ophthalmol. 2005;140:911-913.
  34. Bhattacharyya CA, WuDunn D, Lakhani V, et al. Cataract surgery after tube shunts. J Glaucoma. 2000;9:453-457.
  35. Lalwani GA, Flynn HW, Scott IU, et al. Acute-onset endophthalmitis after clear corneal cataract surgery (1996-2005). Clinical features, causative organisms, and visual acuity outcomes. Ophthalmology. 2008;115:473-476.
  36. Nichamin LD, Chang DF, Johnson SH, et al; American Society of Cataract and Refractive Surgery Cataract Clinical Committee. What is the association between clear corneal cataract incisions and postoperative endophthalmitis? J Cataract Refract Surg. 2006;32:1556-1559.
  37. Armaly MF. Statistical attributes of the steroid hypertensive response in the clinically normal eye. I. The demonstration of three levels of response. Invest Ophthalmol. 1965;4:187.
  38. Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol. 1965;4:198.
  39. Zimmerman TJ, Kooner KS. Clinical Pathways in Glaucoma. New York, NY: Thieme; 2001.
  40. Jaffe GJ, Martin D, Callanan D, et al; Fluocinolone Acetonide Uveitis Study Group. Fluocinolone acetonide implant (Retisert) for noninfectious posterior uveitis: thirty-four-week results of a multicenter randomized clinical study. Ophthalmology. 2006;113:1020-107.
  41. Eagle RCJ, Spencer WH. Lens. In: Spencer WH, ed. Ophthalmic Pathology: An Atlas and Textbook, 4th ed. Philadelphia, PA: WB Saunders; 1996:394.
  42. Ritch R, Schlotzer-Schredhardt U. Exfoliation syndrome. Surv Ophthalmol. 2001;45:265-315.
  43. Damji KF, Konstas AG, Liebmann JM, et al. Intraocular pressure following phacoemulsification in patients with and without exfoliation syndrome: a 2 year prospective study. Br J Ophthalmol. 2006;90:1014-1018.
  44. Küchle M, Viestenz A, Martus P, Hündel A, Jünemann A, Naumann GO. Anterior chamber depth and complications during cataract surgery in eyes with pseudoexfoliation syndrome. Am J Ophthalmol. 2000;129:281-285.
  45. Scorolli L, Scorolli L, Campos EC, Bassein L, Meduri RA. Pseudoexfoliation syndrome: a cohort study on intraoperative complications in cataract surgery. Ophthalmologica. 1998;212:278-280.
  46. Drolsum L, Haaskjold E, Sandvig K. Phacoemulsification in eyes with pseudoexfoliation. J Cataract Refract Surg. 1998;24:787-792.
  47. Scott IU, Flynn HW Jr, Smiddy WE, et al. Clinical features and outcomes of pars plana vitrectomy in patients with retained lens fragments. Ophthalmology. 2003;110:1567-1572.
  48. Chen CL, Wang TY, Cheng JH, Tai MC, Lu DW, Chen JT. Immediate pars plana vitrectomy improves outcome in retained intravitreal lens fragments after phacoemulsification. Ophthalmologica. 2008;222:277-283.
  49. Al-Khaier A, Wong D, Lois N, et al. Determinants of visual outcome after pars plana vitrectomy for posteriorly dislocated lens fragments in phacoemulsification. J Cataract Refract Surg. 2001;27:1199-1206.
  50. Yeo LMW, Charteris DG, Bunce C, et al. Retained intravitreal lens fragments after phacoemulsification: a clinicopathological correlation. Br J Ophthalmol. 1999;83:1135-1138.
  51. Gilliland GD, Hutton WL, Fuller DG. Retained intravitreal lens fragments after cataract surgery. Ophthalmology. 1992;99:1263-1269.
  52. Blodi BA, Flynn HW Jr, Blodi CF, Folk JC, Daily MJ. Retained nuclei after cataract surgery. Ophthalmology. 1992;99:41-44.
  53. Scott IU, Flynn HW Jr, Smiddy WE, et al. Clinical features and outcomes of pars plana vitrectomy in patients with retained lens fragments. Ophthalmology. 2003;110:1567-1572.
  54. Borne MJ, Tasman W, Regillo C, et al. Outcomes of vitrectomy for retained lens fragments. Ophthalmology. 1996:103:971-976.
  55. Hansson LJ, Larsson J. Vitrectomy for retained lens fragments in the vitreous after phacoemulsification. J Cataract Refract Surg. 2002;27:1199-1206.
  56. Kapusta MA, Chen JC, Lam WC. Outcomes of dropped nucleus during phacoemulsification. Ophthalmology. 1996;103:1184-1187.
  57. Gimbel HV, Condon GP, Kohnen T, Olson RJ, Halkiadakis I. Late in-the-bag intraocular lens dislocation: Incidence, prevention, and management. J Cataract Refract Surg. 2005;31:2193-2204.
  58. Jehan FS, Mamalis N, Crandall AS. Spontaneous late dislocation of intraocular lens within the capsular bag in pseudoexfoliation patients. Ophthalmology. 2001;108:1727-1731.
  59. Tsilou E, Rubin BI, Abraham FA, Kaiser-Kupfer M. Bilateral late posterior chamber intraocular lens dislocation with the capsular bag in patient with gyrate atrophy. J Cataract Refract Surg. 2004;30:1593-1594.


Retinal Physician, Issue: March 2009