Roger F. Steinert, MD
Contents
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Pathophysiology |
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Differential Diagnosis of Postoperative Corneal Edema |
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Treatment of Postoperative Corneal Edema |
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CHAPTER HIGHLIGHTS |
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Corneal endothelial decompensation after cataract extraction is a well-known, although rare complication of all types of cataract surgery. The overall incidence is less than 1%. This chapter reviews the differential diagnosis and treatment of corneal edema after cataract surgery. Chapter 21 addresses combined penetrating keratoplasty and cataract surgery in patients with preoperatively compromised corneas.
Pathophysiology
The final common pathway for corneal stromal edema occurring after cataract surgery is inadequate endothelial pump function used to keep the corneal stroma and epithelium in their relatively dehydrated and clear state.[1] Elevated intraocular pressure can overwhelm the corneal endothelial pump. Reduction in intraocular pressure (IOP) will reverse the edema in such cases. In a marginally compensated endothelium, lowering of IOP with antiglaucomatous medications from a high-normal to a low-normal reading can make a critical difference in corneal clarity.
The corneal endothelium acts to dehydrate the cornea both actively through an adenosine triphosphate-driven bicarbonate ion pump[2–4] and passively through the integrity of the cellular membrane barrier.[5,][6] The adult human corneal endothelium has little ability to replicate in order to replace damaged cells.[7–10] Endothelial cells do migrate, enlarge, and undergo fibroblastic metaplasia in an effort to cover denuded areas of Descemet's membrane and reestablish the intercellular junctions.[10–12] An adaptive increase in the number of pump sites per cell may occur in diseased corneas.[1] Therefore, some cases of corneal edema will improve over several weeks to months. Inflammation may also transiently reduce endothelial pump function.[13] Elimination of the inflammation may be accompanied by restoration of corneal clarity.
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Differential diagnosis of postoperative corneal edema
Table 49-1 lists the principal causes of postoperative corneal edema after cataract surgery.
Table 49-1 -- Principal causes of corneal edema after cataract surgery
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Detachment of Descemet's membrane |
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Postoperative glaucoma |
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Inflammation |
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Brown-McLean syndrome |
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IOL: Intraocular lens |
Surgical trauma is often the culprit in unexpected postoperative corneal endothelial decompensation. Direct local injury to the endothelium with an instrument or a portion of the intraocular lens (IOL) implant will result in a discrete patch of edema. Over time, the migration of adjacent endothelial cells can restore corneal clarity if the area of injury is not overly large. Diffuse edema may result from difficulty in delivering the nucleus in extracapsular cataract extraction or prolonged ultrasound in phacoemulsification, particularly if all or part of the nucleus is fragmented in the anterior chamber. A high volume of balanced salt solution (BSS) infusion alone is generally well tolerated by the corneal endothelium, but prolonged infusion studies have demonstrated increased endothelial injury with regular BSS compared to the enhanced BSS formula use.[14–18]
Toxicity from a variety of chemical contaminants may result in diffuse endothelial decompensation. It is frequently, but not always, accompanied by other evidence of intraocular toxicity, most notably a fixed and dilated pupil and elevated IOP.[19,][20] This syndrome is often called toxic anterior segment syndrome (TASS) (see Chapter 48). In more extreme cases, toxicity will result in an excessive inflammatory reaction, ciliary body shutdown and hypotony, or acute retinal inflammation or retinal necrosis (or both).
When toxicity is suspected, all intraocular solutions and medications are suspect and should be reviewed. More commonly, toxicity results from agents not intended for use inside the eye or agents used in excessive concentration. Examples include detergents used in cleaning reusable instruments, incorrect concentrations of additives, use of preserved instead of nonpreserved additives in infusions, or confusing an intended intraocular medication with some other substance that is toxic. Antibiotics particularly can be suspect. Errors in dilution medications may occur. External antibiotics may also inadvertently enter the anterior chamber, particularly through an unsutured wound. A subconjunctival bolus superiorly overlying a superior corneal scleral tunnel may be expressed into the anterior chamber through lid pressure, for example. Aminoglycoside antibiotics, in particular, have profound retinal toxicity at all but the extremely low concentrations.
Detachment of the Descemet's membrane is usually recognized intraoperatively. If not, slit-lamp examination postoperatively is diagnostic.[12,][21–24] A glassy membrane similar to the lens capsule will be seen separated from the posterior stroma. If extensive, the exact configuration of the detached membrane can be difficult to interpret. Localized detachments are often in close proximity to their proper anatomic location. If the Descemet's membrane can be brought back into proper anatomic apposition with the posterior stroma, and the endothelium itself has not been irreversibly damaged, the endothelial pump function will itself reattach the Descemet's membrane because of the relative vacuum created by the endothelial pump. This is best accomplished surgically by introduction of an air bubble through a paracentesis wound inferiorly. This can be performed intraoperatively or postoperatively in the operating room or at the slit-lamp microscope in favorable cases. Only when the Descemet's membrane is held away from the stroma by traction is a suture needed. A full-thickness through-and-through 10–0 nylon suture can forcefully reappose an area of intractable detachment (Figure 49-1). Instrumentation of the membrane itself should be avoided if possible because of the local injury to the endothelium that will occur. Use of viscoelastic agents should be avoided in an effort to reappose the Descemet's membrane. If the viscoelastic agent enters between the posterior corneal stroma and the Descemet's membrane, it will prevent reattachment of the membrane and may remain as a barrier indefinitely. Finally, although reattachment of the Descemet's membrane and restoration of corneal clarity is urgent, it is not a true emergency. The endothelium is bathed in aqueous, even in the detached form. The endothelium will remain viable while an orderly reintervention is planned. Abnormal endothelial proliferation will occur with prolonged detachment or improper adhesion.[12,][25,][26]
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Figure 49-1 A, Detached Descemet's membrane is seen as a glassy membrane in the anterior chamber behind an area of corneal edema. The detachment may be extensive with curling of the Descemet's membrane in on itself well away from the area of edema, or it may be a shallow detachment only seen with a thin slit beam. Often a small amount of blood is trapped at the edge of the inferior detachment (arrows). B, Most Descemet's membrane detachments can be reapposed by placing a large air bubble in the anterior chamber through an inferior paracentesis. C, Particularly where extensive detachment or traction on the membrane exists that cannot be fully relieved, a through-and-through 10–0 nylon suture is needed to forcefully reappose the Descemet's membrane and prevent aqueous access into the space between the posterior corneal stroma and the separated membrane (arrow). After several weeks, the suture may be removed in most cases. |
Unsuspected low preoperative endothelial cell density
A small portion of the population has a low endothelial cell density not heralded by the presence of corneal guttae.[27,][28] To detect these patients preoperatively, some cataract surgeons perform routine preoperative specular microscopy with endothelial cell counts. Other surgeons argue against this routine testing in view of its expense and the fact that a low cell count should not alter the surgical technique; in all cases, the surgeon presumably employs the best available technique to minimize endothelial cell injury. Careful inspection with a broad oblique beam at high magnification under the slit-lamp biomicroscope can, in fact, disclose the endothelial cell pattern. With practice, the surgeon can make a good estimate of the endothelial cell density and pattern. Formal specular microscopy with endothelial cell photography can then be reserved for cases of probable abnormality rather than used as a screening tool.
An occasional patient will experience unexpected corneal edema after apparently atraumatic surgery. In the absence of preoperative specular microscopy, the status of the endothelium in the fellow eye should be examined. A case of naturally low cell density will almost always be bilateral. Examination of the fellow eye will, therefore, help in the differential diagnosis of unexpected postoperative corneal edema.
IOL syndromes are a leading cause of corneal decompensation many years after the surgery. A loose anterior-chamber IOL or a large or loose pupillary-supported iris plane IOL will directly traumatize the corneal endothelium, cause a progressive attrition of endothelial cells, and ultimately lead to clinically evident corneal edema. The edema will characteristically begin in a localized zone over the area of trauma but will progress as the remaining endothelial cells migrate into the area of damage.
Corneal edema beginning many years after IOL implantation may be due to excessive loss of endothelium at the time of surgery, followed by ongoing normal or accelerated attrition of the remaining endothelium. So-called, closed-loop anterior-chamber IOLs are no longer marketed (Azar 91Z from IOLAB, Leiske Surgidev Style 10, Stableflex from Optical Radiation Corporation, Hesburg from IntraOptics) and have a much higher rate of late corneal decompensation than any other anterior-chamber lenses, especially the Kelman three-foot (Omnifit) and four-foot (Multiflex) styles.[29–31] Many surgeons suspect that all anterior-chamber lenses have a higher rate of long-term complications than do posterior-chamber lenses, whereas other surgeons believe that this perception arises because anterior-chamber lenses are typically employed in complicated cases in which posterior capsule support has been compromised. Adequate data to prove or disprove these viewpoints may never be available.
Late-onset corneal edema associated with anterior-chamber lenses is often preceded by or accompanied by cystoid macular edema, a phenomenon that has been termed the cornea-retina syndrome. A generally accepted explanation for this syndrome is that the anterior-chamber IOL causes chronic subclinical inflammation. Prostaglandins are the inflammatory mediators most often suspected as being capable of causing both cystoid macular edema and corneal endothelial cell loss.
The anterior-chamber IOLs in these cases of cornea-retina syndrome are typically not loose. In fact, gonioscopy reveals peripheral iris synechiae around the closed-loop haptics (Figure 49-2). Special techniques are required to explant these closed-loop anterior-chamber IOLs, as detailed in Figures 49-3 and 49-4 (see also Chapter 46). Simple traction on incarcerated haptic will cause iridodialysis and severe bleeding.
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Figure 49-2 Gonioscopic examination of a Stableflex anterior chamber lens shows typical peripheral anterior synechia formation around the distal haptic loop (arrow). |
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Figure 49-3 Technique for explantation of a Surgidev Style 10 (Leiske) anterior chamber intraocular lens (IOL). A, Through an inferotemporal paracentesis, a haptic cutting instrument (Rapazzo haptic cutter, Storz Instruments) is introduced to cut one arm of the inferior haptic. Through the superior wound, with the anterior chamber maintained by viscoelastic solution, both arms of the superior haptic are cut. B, Using two IOL manipulating hooks, the IOL is then rotated gently. The inferior haptic uncurls and is drawn through the inferior peripheral anterior synechia without tearing the synechia, which would result in bleeding and an iridodialysis. C, The rotated IOL is then delivered through the superior wound, taking care not to snag the iris or the wound on the transected haptic. D, The remaining superior haptic is then grasped with a forceps and rotated out of the superior peripheral anterior synechia. |
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Figure 49-4 Technique for explantation of a Stableflex-style anterior chamber intraocular lens (IOL). A, Through an inferotemporal paracentesis, a haptic cutter transects the lateral arm of the haptic. B, Sinskey-style hook engages the “toe” of the haptic by direct visualization if possible or by carefully passing it within the two haptic struts. With gentle traction on the “toe,” the haptic unfolds and is drawn through the inferior peripheral anterior synechia, avoiding bleeding or iridodialysis. C, Freed from the peripheral anterior synechia, the haptic is now loose within the anterior chamber. The same maneuver is now performed on the remaining haptics that are entrapped in peripheral anterior synechia. This should be determined by preoperative gonioscopic inspection and confirmed directly at surgery. Not all four haptics are necessarily engaged in peripheral anterior synechia. Sometimes the “toes” cross, as illustrated in the superior haptics (6 o'clock position in the figure). The IOL hook must engage only the desired haptic and avoid engaging the wrong haptic or both haptics simultaneously. After freeing all of the haptics, the IOL is delivered through the wound. D, In occasional cases of extreme inflammatory reaction, the peripheral anterior synechia entirely covers the “toe” of the haptic or both arms of the haptic. In this case, it is best to simply transect the two arms of the haptic as distal as possible and leave the remaining haptic in the angle. The acute angle of the “toe” does not allow a haptic to “uncurl” out of the synechia with traction on the “heel” or upper “leg” of the haptic. |
A loose IOL causing corneal edema can be differentiated from the cornea-retina syndrome in two ways. Clinical examination with gonioscopy usually is diagnostic. Specular microscopy also is often diagnostic when the corneal edema is localized to a peripheral area. If the localized edema is due to trauma from a loose IOL, the endothelial cell density increases with increasing distance from the area of edema. In contrast, in the cornea-retina syndrome, the corneal endothelial density will be very low and borderline to maintain compensation throughout the remaining clear cornea.
If the cornea decompensates centrally and penetrating keratoplasty is performed, most surgeons will exchange a closed-loop anterior-chamber IOL for either an open-loop anterior-chamber IOL or a suture-fixated posterior-chamber IOL.[32–38] The best type of replacement IOL remains undetermined in regard to both short-term complications and long-term graft survival and recovery of vision.
Management of a patient with late-onset cystoid macular edema or localized corneal edema in the presence of an anterior-chamber IOL is problematic. In most cases of late-onset cystoid macular edema and essentially all cases of localized corneal edema, the endothelium will be severely depleted even when the cornea remains clinically clear. Nevertheless, the longer cystoid macular edema persists, the more likely that it will cause irreversible macular damage even if acute leakage resolves. The author's approach to new late-onset cystoid macular edema is an intense course of topical steroids and nonsteroidal anti-inflammatory agents (e.g., dexamethasone, 0.1%, or prednisolone acetate, 1%, combined with ketorolac, 0.5% [Acular], or diclofenac, 0.1% [Voltaren], both four times daily). If the cystoid macular edema does not improve over 1 month, or resolves but then recurs, exchange of the closed-loop anterior-chamber IOL is strongly indicated. Improvement may occur with a replacement Kelman-style anterior chamber IOL, but the author favors moving to another fixation site, either peripheral iris suture fixation or trans-scleral suture fixation of a posterior-chamber IOL, for the best long-term results. The surgeon must perform atraumatic surgery if the fragile cornea is to remain compensated. Explantation must use the techniques outlined in Figures 49-3 and 49-4. Secondary IOL implantation is reviewed in Chapter 41. Cystoid macular edema is covered in detail in Chapter 54, and management of intraocular inflammation is discussed in Chapter 57.
Table 49-2 outlines the decision-making steps for managing complications of closed-loop anterior-chamber IOLs.
Table 49-2 -- Treatment of corneal edema
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IOL: Intraocular lens; DSEK: Descemet-stripping endothelial keratoplasty; DSAEK: Descemet-stripping automated endothelial keratoplasty; DLEK: deep lamellar endothelial keratoplasty; DMEK: Descemet membrane endothelial keratoplasty |
Peripheral corneal edema
Perhaps the rarest and most benign form of corneal edema is the syndrome described by Brown and McLean.[39,][40] In the classic syndrome, an aphakic patient experiences peripheral corneal stromal and epithelial edema that spares the superior cornea. Pigment deposits are present on the underlying endothelium. A central zone of 5–7mm remains clear and compact indefinitely despite the peripheral edema. The peripheral iris may show transillumination, but the trabecular meshwork is not necessarily hyperpigmented. If the patient is bilaterally aphakic, the syndrome is usually present in both eyes. There is no clinical inflammation, and the cause is unknown. Although the classic presentation is following intracapsular cataract extraction, it may occur after extracapsular cataract extraction.[41] Moreover, although the syndrome is said to occur only 6 years or more postoperatively, the author has seen the syndrome appear 3 months after sulcus suturing of a posterior chamber lens in a 40-year-old patient with prior extracapsular extraction of a traumatic cataract (Figure 49-5).
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Figure 49-5 A, Slit-lamp photomicrograph of a patient with Brown-McLean syndrome of peripheral corneal edema (arrow). B, High magnification reveals classic pigment deposits on the endothelium underlying the area of edema (arrow). |
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Treatment of postoperative corneal edema
Hypertonic solutions
Hypertonic solutions, typically 5% sodium chloride ophthalmic preparations, can improve the visual function of a patient with mild, predominantly microcystic epithelial edema. This will be particularly beneficial to the patient on awakening in the morning, when edema is maximal because of lack of evaporation during the night when the eyelids are closed. Use of a 5% sodium chloride ointment at bedtime will also help reduce the accumulation of edema while the eyelids are closed during sleep. However, the use of hypertonic solutions is only palliative. It does not improve or restore endothelial pump function or the integrity of the cell barrier.
Anti-inflammatory therapy
Reduction of intraocular inflammation may be of benefit in some cases of postoperative edema. Inflammation can cause transient dysfunction of the endothelial pump. Moreover, inflammation may cause some degree of endothelial cell death. By extrapolation, pharmacologic treatment of inflammation with topical steroids and perhaps nonsteroidal anti-inflammatory drugs may help to maximize the surviving endothelium, thus improving the chances that corneal clarity will ultimately return postoperatively. This supposition has not been rigorously proved, but most clinicians will treat patients with strong topical steroids, such as prednisolone acetate (1%) or dexamethasone (0.1%) as often as every 1–2h in cases of acute postoperative corneal edema. Steroid therapy may be of no benefit in non-inflammation-related corneal edema, however. Topical dexamethasone did not differ from placebo in the rate of occurrence of corneal edema in a controlled study of patients with Fuchs’ dystrophy.[42]
Corneal transplantation
Restoration of vision in an eye with irreversible corneal edema requires either a posterior lamellar endothelial transplant (Descemet-stripping endothelial keratoplasty (DSEK), Descemet-stripping automated endothelial keratoplasty (DSAEK), deep lamellar endothelial keratoplasty (DLEK), and Descemet membrane endothelial keratoplasty (DMEK)) or full-thickness penetrating keratoplasty. A final decision about proceeding with keratoplasty should usually be deferred 2–3 months postoperatively in case of acute decompensation after cataract surgery. In some cases of marginal corneal endothelial function, clarity is regained within this time frame. If there is active ongoing inflammation, the decision to proceed with keratoplasty should be deferred while intense anti-inflammatory therapy continues, to enhance the probability of transplant survival and restoration of the patient's own corneal clarity. In occasional cases of severe striae with both stromal and epithelial edema, the situation may be so clearly irreversible that it is in the patient's best interest to proceed with penetrating keratoplasty earlier than 3 months after the original cataract extraction.
The treatment options for corneal edema are listed in Table 49-2.
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References
[1]. Waring G.O., Bourne W.M., Edelhauser H.F., et al: The corneal endothelium: normal and pathologic structure and function. Ophthalmology 1982; 89:531.
[2]. Maurice D.M., Riley M.V.: The cornea. In: Graymore C.N., ed. Biochemistry of the eye, New York: Academic Press; 1970.
[3]. Kaye G.I., Tice L.W.: Studies on the cornea. V. Electron microscopic localization of adenosine trisphosphatase activity in the rabbit cornea in relation to transport. Invest Ophthalmol 1966; 5:22.
[4]. Barfort P., Maurice D.: Electrical potential and fluid transport across the corneal endothelium. Exp Eye Res 1974; 19:11.
[5]. Maurice D.M.: Cornea and sclera. In: Davson H., ed. The eye, 3rd ed.. New York: Academic Press; 1984.
[6]. Kreutziger G.O.: Lateral membrane morphology and gap junction structure in rabbit corneal endothelium. Exp Eye Res 1976; 23:285.
[7]. Flaxel J.T., Swan K.C.: Limbal wound healing after cataract extraction: a histological study. Arch Ophthalmol 1969; 81:653-659.
[8]. Kloucek F.: The corneal endothelium. Acta Univ Carol [Med] (Praha) 1967; 123:321-373.
[9]. Van Horn D.L., Edelhauser H.F., Aaberg T.M., et al: In vivo effects of air and sulfur hexafluoride gas on rabbit corneal endothelium. Invest Ophthalmol 1972; 11:1036-1038.
[10]. Capella J.A.: Regeneration of endothelium in diseased and injured corneas. Am J Ophthalmol 1972; 74:810-817.
[11]. Iwamoto T., DeVoe A.G.: Electron microscopic studies on Fuchs’ combined dystrophy. I. Posterior portion of the cornea. Invest Ophthalmol 1971; 10:9-28.
[12]. Waring G.O., Laibson P.R., Rodriques M.: Clinical and pathologic alterations of Descemet's membrane: with emphasis on endothelial metaplasia. Surv Ophthalmol 1973–1974; 18:325-368.
[13]. Dohlman C.H., Hyndiuk R.A.: Subclinical and manifest corneal edema after cataract extraction. Transactions of the New Orleans Academy of Ophthalmology, Symposium on the Cornea, St Louis: Mosby; 1972:214.
[14]. Edelhauser H.F., Van Horn D.L., Hyndiuk R.A., et al: Intraocular irrigating solutions: their effect on corneal endothelium. Arch Ophthalmol 1975; 93:657-658.
[15]. Dikstein S., Maurice D.M.: The metabolic bases to the fluid pump in the cornea. J Physiol 1972; 221:29-41.
[16]. Dikstein S.: Efficiency and survival of the corneal endothelial pump. Exp Eye Res 1973; 15:639-644.
[17]. Anderson E.I., Fischbarg J., Spector A.: Fluid transport, ATP level, and ATPase activities in isolated rabbit endothelium. Biochem Biophys Acta 1973; 307:557-562.
[18]. Anderson E.I., Fischbarg J., Spector A.: Disulfide stimulation of fluid transport and effect on ATP level in rabbit endothelium. Exp Eye Res 1974; 19:1-10.
[19]. Breebaart A.C., Nuyts R.M.M.A., Pels E., et al: Toxic endothelial cell destruction of the cornea after routine extracapsular cataract surgery. Arch Ophthalmol 1990; 108:1121-1125.
[20]. Nuyts R.M.M.A., Edelhauser H.F., Pels E.I.I., et al: Toxic effects of detergents on the corneal endothelium. Arch Ophthalmol 1990; 108:1158-1162.
[21]. Samuels B.: Detachment of Descemet's membrane. Trans Am Ophthalmol Soc 1928; 26:427-437.
[22]. Scheie H.G.: Stripping of Descemet's membrane in cataract extraction. Trans Am Ophthalmol Soc 1964; 62:140-152.
[23]. Sparks G.M.: Descemetopexy: surgical reattachment of stripped Descemet's membrane. Arch Ophthalmol 1967; 78:31-34.
[24]. Zeiter H.J., Zeiter J.T.: Descemet's membrane separation during five hundred forty-four intraocular lens implantations. J Am Intraocul Implant Soc 1983; 9:36-39.
[25]. Donaldson D.D., Smith T.R.: Descemet's membrane tubes. Trans Am Ophthalmol Soc 1966; 64:89-109.
[26]. Kroll A.J.: Proliferation of Descemet's membrane. Arch Ophthalmol 1969; 82:339-343.
[27]. Kayes J., Holmberg A.: The fine structure of the cornea in Fuchs’ endothelial dystrophy. Invest Ophthalmol 1964; 3:47-67.
[28]. Stocker F.W.: The endothelium of the cornea and its clinical implications, 2nd ed.. Springfield, Ill, Charles C. Thomas, 1971.
[29]. Solomon K.D., Apple D.J., Mamalis N., et al: Complications of intraocular lenses with special reference to an analysis of 2500 explanted intraocular lenses (IOLs). Eur J Implant Refract Surg 1991; 3:195.
[30]. Lim E.S., Apple D.J., Tsai J.C., et al: An analysis of flexible anterior chamber lenses with special reference to the normalized rate of lens explantation. Ophthalmology 1991; 98:243.
[31]. Price Jr F.W.: Factors contributing to corneal decompensation with the Stableflex lens. J Cataract Refract Surg 1988; 14:53-57.
[32]. Kozarsky M., Stopak S., Waring G.O., et al: Results of penetrating keratoplasty for pseudophakic corneal edema with retention of intraocular lens. Ophthalmology 1984; 91:1141.
[33]. Speaker M.G., Lugo M., Laibson P.R., et al: Penetrating keratoplasty for pseudophakic bullous keratopathy. Ophthalmology 1988; 95:1260.
[34]. Kornmehl E.W., Steinert R.F., Odrich M.G., et al: Penetrating keratoplasty for pseudophakic bullous keratopathy edema associated with closed-loop anterior chamber intraocular lenses. Ophthalmology 1990; 97:407-414.
[35]. Schein O.D., Kenyon K.R., Steinert R.F., et al: A randomized trial of intraocular lens fixation techniques with penetrating keratoplasty. Ophthalmology 1993; 100:1437-1443.
[36]. Price Jr F.W., Whitson W.E.: Visual results of suture-fixated posterior chamber lenses during penetrating keratoplasty. Ophthalmology 1989; 96:1234-1240.
[37]. Soong H.K., Meyer R.F., Sugar A.: Posterior chamber IOL implantation during keratoplasty for aphakic or pseudophakic corneal edema. Cornea 1987; 6:306-312.
[38]. Soong H.K., Musch D.C., Kowal V., et al: Implantation of posterior chamber intraocular lenses in the absence of lens capsule during penetrating keratoplasty. Arch Ophthalmol 1989; 107:660-665.
[39]. Brown S.I., McLean J.M.: Peripheral corneal edema after cataract extraction: a new clinical entity. Trans Am Acad Ophthalmol Otolaryngol 1969; 73:465-470.
[40]. Brown S.I.: Peripheral corneal edema after cataract extraction. Am J Ophthalmol 1970; 70:326-329.
[41]. Flaxel J.T., Swan K.C.: Limbal wound healing after cataract extraction: a histological study. Am J Ophthalmol 1969; 81:653-659.
[42]. Wilson S.E., Bourne W.M., Brubaker R.F.: Effect of dexamethasone on corneal endothelial Fuchs’ dystrophy. Invest Ophthalmol Vis Sci 1988; 29:357.