Intraocular Lens Exchange for Anterior Chamber Intraocular Lens,induced Corneal Endothelial Damage

Arthur F. Coli, MD, Francis W. Price, Jr., MD, William E. Whitson, MD

Background: Anterior chamber and iris-plane intraocular lenses (IOls) have been implicated in causing corneal endothelial damage and progression to pseudophakic bullous keratopathy.

Methods: The authors performed IOl exchanges on 1 02 eyes with signs of early corneal decompensation or progressive endothelial cell loss associated with these an­terior chamber or iris-plane IOls. Replacement IOls were posterior chamber lenses sutured to the iris (87 eyes), sutured to the sclera (3 eyes), or placed in the Ciliary sulcus (12 eyes).

Results: Seventy-two eyes (71 %) had the same or improved vision after a mean follow-up period of 18.6 months (range, 6 to 60 months). Only 24 eyes (23.5%) pro­gressed to corneal decompensation. Of the eyes that decompensated, 75% had pre­operative endothelial cell counts of 500 cells/mm2 or less (P < 0.0001), and 83% had preoperative signs of early corneal decompensation (P < 0.001). Biomicroscopic signs of early corneal decompensation seen preoperatively in 50 eyes resolved in 17 eyes (34%) and remained unchanged in 12 eyes (24%) at the last postoperative follow-up visit.

Conclusion: Removal of anterior chamber and iris-plane intraocular lenses in eyes showing signs of endothelial damage may prevent progreSSion to pseudophakic bullous keratopathy if performed before a critical degree of endothelial cell loss or dysfunction has developed. Ophthalmology 1993;100:384-393

Numerous clinical and histopathologic studies have doc­umented a higher ocular complication rate for anterior chamber and iris-plane intraocular lenses (IOLs) com­pared with posterior chamber IOLs.l-4 The anterior chamber IOLs, especially rigid and closed-loop types, are associated with a higher rate of corneal edema, uveitis,

glaucoma, and macular edema.5-7 Pseudophakic bullous keratopathy, most commonly associated with anterior chamber IOLs, is the most common indication for pen­etrating keratoplasty in this country.8,9 Studies of pene­trating keratoplasty performed for pseudophakic bullous keratopathy have shown higher donor endothelial cell loss with retained iris-plane and anterior chamber IOLs when compared with retained posterior chamber IOLs lO and a higher rate of graft failure with retained anterior chamber IOLs.lI,12

Originally received: September 13, 1991. Revision accepted: October 16, 1992.

From Corneal Consultants of Indiana, Indianapolis.

Presented as a poster at the American Academy of Ophthalmology An­nual Meeting, Anaheim, October 1991.

Supported by the Cornea Research Foundation of America, Indianapolis, Indiana.

The authors have no proprietary interest in the development or marketing of any devices or materials mentioned.

Reprint requests to Francis W. Price, Jr. , MD, 9002 N Meridian St, Suite 100, Indianapolis, IN 46260.

384

Several series have documented successful fixation of posterior chamber IOLs in the absence of capsular support in patients not undergoing simultaneous penetrating ker­atoplasty.I3-25 Techniques for IOL fixation vary widely, but basically involve either fixation to the sclera, fixation to the iris, or some combination ofthe two. Capsule and sulcus-fixated posterior chamber IOLs have lower reported rates of cystoid macular edema, pupillary-block, glau-

Coli et al . Anterior Chamber IOL-Induced Corneal Endothelial Damage

coma, uveitis, and corneal edema.8,9,26,27 They also may provide a mechanical barrier against endophthalmodo­nesis, anterior movement of the vitreous, which may be associated with the development of cystoid macular edema, retinal detachment, and corneal endothelial cell 10ss.28

We retrospectively reviewed a series of patients with preoperative signs of corneal endothelial damage or pro­gressive endothelial cell loss who underwent anterior chamber or iris-plane IOL removal with secondary pos­terior chamber IOL implantation. Intraocular lens ex­change may help prevent progression to pseudophakic bullous keratopathy and the need for penetrating kera­toplasty if performed before a critical degree of endothelial cell damage has developed.

Materials and Methods

We reviewed the charts of all eyes undergoing IOL ex­change without penetrating keratoplasty between De­cember 1986 and December 1990 in the practice of Cor­neal Consultants of Indiana. In this 4-year period, 125 eyes underwent IOL exchange for corneal endothelial damage believed to be secondary to anterior chamber or iris-plane IOLs. Twenty-three ofthose eyes were excluded because of follow-up less than 6 months. Evidence of en­dothelial damage included clinical signs of corneal stromal and epithelial edema coupled with a low endothelial cell count (ECC) (39), improper positioning or dislocation of the IOL threatening the corneal endothelium (11), sig­nificant progressive decrease in ECC over time (10), or a low ECC «900 cells/mm2) in the presence of a rigid or closed-loop anterior chamber IOL where it was believed the IOL was causing progressive damage to the eye (42). In this latter group, the average preoperative ECC was 564 cells/mm2 and associated preoperative diagnoses were cystoid macular edema (71 %), chronic uveitis (26%), and glaucoma (12%).

All ECCs were performed with a Keeler Model CSP-580 wide-field specular microscope (Keeler Instruments, Inc, Broomall, PA). Central, nasal, inferior, temporal, and superior fields were photographed at a magnification of 40X. Kodak TMAX 400 black and white film was used. The prints were then examined under magnification through an overlying grid calibrated for 40X magnification with a size equivalent of 0.0 1 mm2 per box. Cell density per mm2 was determined by counting at least 100 cells, dividing by the number of squares used and then multi­plying by 100. The mean ECC was then calculated for each patient. Preoperative ECCs were obtained in all pa­tients except 3. All ECCs were performed within 2 months of surgery, except for two, which were performed 7 months preoperatively. Ten patients had serial preoperative ECCs. An attempt was made to obtain serial ECCs at approxi­mately 6 and 12 months after IOL exchange, but this was not possible in several cases because of difficulties with patient follow-up.

All surgeries were performed by FWP or WEW. Local or general anesthesia was used, depending on patient co-

operation. A 7- to 9-mm incision was fashioned I-mm posterior to the limbus with a sapphire blade set at 0.30-to 0.35-mm depth. A beveled incision was carried forward to form a three-step wound. All lenses were removed carefully under a generous cushion of sodium hyaluronate to protect the corneal endothelium and in a controlled fashion to avoid damage to the angle structures. In most cases, the haptics were cut free from the optic using haptic cutters. The haptics were then slid from their synechial tunnels. Methods of Stable flex anterior chamber IOL re­moval have been reported.29,30

Vitrectomies were performed in all cases except two. In one case, two vitrectomies were performed with pre­vious surgeries, and in the other case, vitrectomy was not necessary because the vitreous was back far enough to allow placement of the IOL in the ciliary sulcus with cap­sular support. Most earlier cases were performed with an­terior vitrectomies (18), but all later cases were performed with pars plana vitrectomies (72). Anterior vitrectomies were performed with a mechanical vitrector alone, while pars plana vitrectomies were performed with the aid of a fiberoptic light source as well as an infusion fundus contact lens. All sclerotomies were placed 3.5-mm posterior to the limbus. The goal of all pars plana vitrectomies was to remove all vitreous lying within the pupil as well as pos­terior to the iris as far peripherally as could be visualized. The central vitreous also was removed, but no attempt was made to remove vitreous directly overlying the retina.

All secondary IOLs were posterior chamber IOLs. An attempt was made to place the IOL in the ciliary sulcus when there was adequate capsular support. If capsular support was inadequate or absent, iris-suturing was the preferred means of fixating the IOL. Scleral-fixation was used only if iris support was inadequate.

The iris-sutured IOL technique is an adaptation of a technique previously reported for use with penetrating keratoplasty. 3 I The posterior chamber IOL used is a 6-mm optic, 4-hole modified J-loop lens with 0 0 angled haptics. A special 9-0 polypropylene suture on a 4-mm straight taper needle (Ethicon 0-9904) is passed through the mid-peripheral iris at the 3- and 9-0'clock positions using a Sutherland microforceps (Grieshaber #612.91) (Figs 1 A and B). One free end of each suture is then passed through the two positioning holes along the same axis as the haptics of the IOL. A loose loop-tie is then placed in each of the sutures (Fig lC), and the IOL is then inserted through the limbal incision and then posterior to the iris, taking care not to entangle the sutures in the haptics. The implant is positioned so that the haptics are at the 3- and 9-0'clock positions, and the sutures are pulled snugly so that the optic rests just posterior to the iris. Several ad­ditionalloop throws are placed, and the suture is trimmed at the knot. The knot is then allowed to retract under the iris (Fig 10). No specific attempt is made to ensure place­ment of the haptics in the ciliary sulcus.

The technique of scleral fixation is an adaptation of a previously reported technique.23 In these cases, a 7-mm optic IOL with broad C-loop polypropylene haptics is used. There is a 15 0 angulation to the haptics and no

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Ophthalmology Volume 100, Number 3, March 1993

Figure 1. Iris-sutured intraocular lens (IOL) technique. A, 4-mm straight needle held with microforceps and passed through midperipheral iris. B. needle regrasped and passed again so that both ends of the suture exit through the pupil. C. sutures passed through the iris on both sides, one free end passed through a positioning hole of the IOL and a loose loop-tie placed. D. IOL positioned posterior to the iris. Haptics ideally positioned in ciliary sulcus, although pathological study of postmortem specimens demonstrated that haptics are usually not in sulcus and that iris sutures are the primary means of support.

posItIoning holes. The tips of the Prolene haptics are beaded using a hot cautery. The free end of a 10-0 poly­propylene suture attached to a CIF-4 needle (Ethicon) is tied to the apex of the haptic. The needles are then passed posterior to the iris at the 6- and 12-0'clock positions, through the ciliary sulcus, and then out through the sclera approximately l-mm posterior to the limbus. The lens is inserted posterior to the iris and the slack on the sutures pulled up. Each of the sutures is then tied to itself after taking a small bite of adjacent sclera with the needle. Fix­ation of the inferior suture is completed under a partial thickness, triangular scleral flap fashioned before opening the eye. Fixation of the superior suture is performed so that the knot is buried within the superior limbal wound.

The lens used for placement ofIOLs in the ciliary sulcus is a 7-mm optic posterior chamber IOL with broad C­loops. In these cases, careful inspection of the residual capsule is performed by retracting the iris 3600

• If ade­quate capsular material is present, the IOL is carefully placed in the ciliary sulcus. Fixation stability of the IOL

386

is tested by moving the implant in all directions to ensure that centration remains.

Lysis of peripheral anteri(lr and posterior synechiae was performed in 3 cases. Iridoplasty was performed using 10-0 polypropylene on a taper needle in 5 cases to help achieve a more normal configuration of the pupil or to enhance iris-fixation of the IOL. A Molteno implant also was concurrently placed in I eye because of poorly con­trolled glaucoma preoperatively.

All patients were seen within the first 2 to 3 postop­erative days and began receiving topical steroids and antibiotics. Topical steroids were continued for several weeks to months, depending on the degree of inflam­mation or presence of cystoid macular edema. Patients were seen as required for routine postoperative care. Sev­eral eyes received retrobulbar or subtenons injections of 40 mg methylprednisolone acetate suspension for treat­ment of persistent or recurrent cystoid macular edema postoperatively. Best-corrected visual acuity was deter­mined by refraction.

Coli et al . Anterior Chamber IOL-Induced Corneal Endothelial Damage

Table 1. Concurrent Preoperative Diagnoses

Decompen-Overall sating Group

(N = 102) (N = 24)

No. (%) No. (%)

Cystoid macular edema 47 (46) 6 (25) Chronic uveitis 22 (22) 11 (46)·

Glaucoma 13 (13) 5 (21) Dislocated IOL 10 (10) 3 (13)

Macular degeneration 5 (5) 3 (13)

Prior penetrating keratoplasty 2 (2) 0 Prior retinal detachment 2 (2) (4)

IOL = intraocular lens.

• Significance (P = 0.002) was found using the chi-square test for the correlation of preoperative chronic uveitis with corneal decompensation.

Results

One hundred two eyes underwent IOL exchange for an­terior chamber IOL or iris-plane IOL-induced corneal en­dothelial damage. Concurrent preoperative diagnoses are listed in Table 1. The mean patient age was 71 years. There were 59 females, 43 males, 68 right eyes, and 34 left eyes. Eighty-seven eyes had IOLs sutured posterior to the iris, 3 were sutured to the sclera, and 12 were placed in the ciliary sulcus with adequate capsular support. The

number and types of IOLs removed are listed in Table 2. There were no intraoperative complications.

Postoperative complications are listed in Table 3. There were no cases ofIOL dislocation or suture breakage. Cor­neal decompensation occurred in 24 patients (23.5%). Method ofvitrectomy or means of secondary IOL-fixation did not correlate with corneal decompensation. However, as expected, a lower preoperative ECC did correlate with progression to corneal decompensation (Table 4). Seventy­five percent ofthose who decompensated had preoperative ECCs of 500 cells/mm2 or less (P < 0.0001) (Fig 2). No eyes decompensated that had ECCs greater than 1000 cells/mm2 preoperatively. The average overall preopera­tive ECC was 634 ceUs/mm2. However, the average pre­operative ECC of those patients who decompensated was 481 cells/mm2 versus 684 ceUs/mm2 for those who did not decompensate. As seen in Table 1, a history of chronic uveitis preoperatively also correlated with corneal de­compensation postoperatively (P = 0.002).

Biomicroscopic evidence of early corneal decompen­sation was present in 50 eyes preoperatively. Seventeen of the 50 eyes (34%) showed clearing of these signs post­operatively, 12 eyes (24%) showed no change, and 1 eye (2%) showed some increase in edema, but no progression to bullous keratopathy or worsening of their preoperative visual acuity. Twenty of these 50 eyes (40%) progressed to complete corneal decompensation postoperatively (P < 0.001). Persistent peripheral postoperative corneal edema developed in five patients where there was no sign of corneal edema preoperatively.

Of the 24 eyes that developed corneal decompensation postoperatively, 7 eyes (29%) showed no signs of clearing

Table 2. Intraocular Lenses Removed

Non-Decompensating Decompensating Type Group (no.) Group (no.) Total

Stableflex 37 5 42 Leiske 7 1 8 Iris-supported 6 6 Hessburg 4 3 7 Dubroff 5 1 6 Azar 91Z 3 4 7 Choyce 5 2 7 Kelman Multiflex 2 3 Omnifit 1 3M McGann 3 1 4 Pannu 3 1 4 Novaflex Tennant 2 2 Spanflex 1 3M CW4742 1 Oleo L-3 Intermedics 018 1

Total 78 24 102

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Ophthalmology Volume 100, Number 3, March 1993

Table 3. Postoperative Complications (N = 102)

Complication

Corneal decompensation Persistent/worsening uveitis Worsening glaucoma Retinal detachment Late postoperative hyphema (after starting

coumadin 1.5 yrs postoperatively) Wound separation/filtering cyst

No.

24 3 3 2

(%)

(23.5)

(2.9) (2.9) (2.0)

(1.0) (1.0)

their edema after IOL exchange. The remaining 17 eyes that went on to decompensation cleared their central cor­neas several weeks after surgery but then eventually de­compensated at an average of 10.8 months postoperatively (range, 5 to 33 months). Seventeen of these 24 eyes (71 %) later underwent successful penetrating keratoplasty. Best­corrected visual acuity noted at the last follow-up visit was found to be the same or improved in 7 of the 17 grafted eyes (41%) compared with before IOL exchange. Reasons for worse visual acuity included irregular astig­matism (4), macular degeneration (4), hyphema (1), and graft scarring (1). The remaining 7 eyes that were not grafted have declined or are awaiting penetrating kera­toplasty.

Overall mean follow-up to the last office visit for both groups was 18.6 months (range, 6 to 60 months). Seventy-

five of 102 patients (74%) had follow-up of greater than 12 months postoperatively. Mean follow-up for the non­decompensating eyes was 17.4 months (range, 6 to 60 months). Mean follow-up for the decompensating eyes to the last office visit was 22.3 months (range, 6 to 43 months). However, the longer follow-up of the decom­pensating eyes is misleading because the majority of these eyes later underwent penetrating keratoplasty and thereby required longer follow-up. Furthermore, the follow-up of the nondecompensating eyes is skewed by the fact that they were sent back to their referring ophthalmologist and lost to follow-up sooner than those with a more compli­cated postoperative course. Therefore, to allow for better comparison with the nondecompensating eyes, follow-up of the decompensating eyes was counted from the time of surgery to the time they had reached the end point of total corneal decompensation. For those who never cleared their cornea after IOL exchange, 3 months was arbitrarily chosen as the follow-up time. Mean follow-up for the decompensated group as determined above was 8.7 months (range, 3 to 33 months) (Table 4).

Visual acuity results are presented in Table 5. The mean postoperative visual acuity on the last follow-up visit was 20/60. Seventy-two of 102 eyes (71%) had the same or improved visual acuity on their last postoperative visit; 50 eyes (49%) had 20/40 or better visual acuity. In eyes with preoperative cystoid macular edema, visual acuity improved in 30 eyes (64%), remained unchanged in 6 eyes (13%), and worsened in 11 eyes (23%). In the non­decompensated group, 16 of78 eyes (21 %) had a decrease

Table 4. Preoperative Endothelial Cell Counts

Non-Decompensating Decompensating

Preoperative Group Group

% Decompensated Endothelial Me~n Mean by Preoperative % Decompensated Cell Count Follow-up Follow-up Endothelial Cell Overall (cells/mm2

) No. (mas) No. (mas)" Total Count (N = 102)

:::;400 9 16.2 8 10.5 17 47 8 401-500 16 13.4 10 7.8 26 38 10 501-600 12 16.2 2 3.0 14 14 2 601-700 12 18.8 1 14.0 13 8 1 701-800 8 15.9 1 3.0 9 11 1 801-1,000 11 17.5 2 12.0 13 15 2

1,001-1,500 4 19.0 0 4 1,501-2,000 2 30.0 0 2

>2,000 1t 24.0 0 1 Not done 3t 24.3 0 3

Total 78 17.4 24 8.7 102 24

• Follow-up to time of complete corneal decompensation. Follow-up of 3 months was chosen for those patients whose corneas never cleared post­operatively.

t Anterior chamber intraocular lens loose/intermittent touch.

t Three not performed because of significant intraocular lens touch or vault; one not performed already showing signs of corneal decompensation.

388

Coli et al . Anterior Chamber IOL-Induced Corneal Endothelial Damage

50

45 "0

~ 40

UI c: 35 C1> Co E 30 0 0 25 C1> 0 C 20 C1>

~ 15 C1> a.

10

5

0

Percent Corneal Decompensation versus

Preoperative Endothelial Cell Count .(8)

················ .. '(10)

\, ( ). ",.""",. .. MM '" ,m., (:~'... .. ....... (2)

........... .. .......... . ........... (1)

(1)

~400 401· 501· 601· 701· 801· 1001· 1501· >2000 500 600 700 800 1000 1500 2000

Preoperative Endothelial Cell Count (cells / mm2)

Figure 2. Risk of postoperative corneal decompensation significantly higher (P < 0.0001) in patients with preoperative endothelial cell counts of 500 cells/mm2 or less.

in visual acuity from their preoperative level. Reasons accounting for decreased visual acuity in this group are: unknown (5), cystoid macular edema (3), macular degen­eration (5), retinal detachment (2), and posterior vitreous detachment with vitreous hemorrhage occurring 7 months postoperatively (1).

Serial preoperative ECCs were performed on 10 eyes and showed a mean decrease in cell density of 28% over a range of 9 to 15 months (mean, 11.8 months). Forty­five eyes had both preoperative and postoperative ECCs performed, with postoperative ECCs performed in a pe­riod from 4 to 15 months after surgery (mean, 9.9 months). In this group, the mean preoperative ECC was 695 cells/mm2 with a mean cell loss of 9.4% over this early postoperative period.

Discussion

Intraocular lens exchange may help prevent progression to pseudophakic bullous keratopathy in eyes showing signs

of progressive corneal endothelial damage secondary to anterior chamber or iris-plane IOLs. Preventing the need for penetrating keratoplasty is very significant in the el­derly population undergoing these surgeries considering the increased morbidity and prolonged time to recovery after penetrating keratoplasty. Numerous studies have documented the increased complications associated with anterior chamber IOLs, and especially their propensity to cause damage to the corneal endothelium.2-7 Many series recommend exchange of anterior chamber IOLs for pos­terior chamber IOLs at the time of penetrating kerato­plasty for pseudophakic bullous keratopathy in order to prevent further damage to the corneal graft. 10-12.18,31-33 However, newer Kelman-style open-loop anterior cham­ber IOLs may not be associated with corneal endothelial damage like the older closed-loop and rigid anterior chamber IOLs. This was shown by recent series that im­planted the newer anterior chamber IOLs at the time of IOL exchange and keratoplasty for pseudophakic bullous keratopathy.34-36

Several series of sutured posterior chamber IOLs have included isolated cases of IOL exchange for decreasing endothelial cell count or corneal damage secondary to anterior chamber IOLs,23,24 but the optimal timing for such exchange is not known and the utilization of these techniques is becoming more widespread. We have re­ported our experience with exchanging implants so that a baseline can be established in determining the optimal time for surgical intervention. Because of the retrospective nature of our study and the lack of a control group, this question can still not be definitely answered. Many eyes that underwent successful IOL exchange may have re­tained good visual acuity and clear central corneas even without IOL exchange over the same or longer follow-up. However, many eyes showed signs of reduced ongoing endothelial damage following IOL exchange. Seventeen of 50 eyes (34%) showed complete resolution of preop­erative corneal edema following IOL exchange. Postop­erative ECCs stabilized in several patients who had pro­gressive decline in serial ECCs before IOL exchange. Fur­thermore, in patients with concurrent preoperative cystoid

Table 5. Visual Acuity Results

Preoperative Cystoid Macular All Patients Edema

Preoperative Postoperative Preoperative Postoperative

Visual Acuity No. (%) No. (%) No. (%) No. (%)

~20/40 40 (39) 50 (49) 10 (21) 21 (45) 20/50-20/70 24 (24) 23 (23) 14 (30) 10 (21) 20/80-20/100 15 (15) 12 (12) 10 (21) 6 (13)

20/200-20/400 17 (17) 12 (12) 10 (21) 6 (13)

Counting fingers 6 (6) 1 (1) 3 (6) 3 (6)

Hand motions 0 4 (4) 0 (2)

Total 102 102 47 47

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Ophthalmology Volume 100, Number 3, March 1993

macular edema, visual acuity improved in 30 of 47 (64%) eyes. Chronic preoperative uveitis resolved in 19 of 22 (86%) eyes after IOL exchange.

The likelihood of progression to corneal decompen­sation after an IOL exchange was high in eyes with pre­operative cell counts less than 500 cells/mm2 (18 of 43 eyes, 42%), and in eyes with preoperative signs of early corneal decompensation (20 of 50 eyes, 40%). Patients in this category should be counseled on the high risk of re­quiring a penetrating keratoplasty after IOL exchange as well as the option of avoiding IOL exchange unless pseu­dophakic bullous keratopathy develops-at which time IOL exchange could be done concurrently with penetrat­ing keratoplasty. However, more than 50% of eyes in this high-risk category (preoperative ECC .::;; 500 cells/mm2) did not decompensate after an average follow-up of 14.8 months, and, therefore, IOL exchange may have delayed or prevented the need for penetrating keratoplasty. Intra­ocular lens exchange on eyes with higher preoperative ECCs entails significantly less risk of corneal decompen­sation. Physicians may be more secure in the option of IOL exchange for eyes which, based on clinical judgment and experience, may be at a high risk for progressing to pseudophakic bullous keratopathy.

Studies using quantitative morphometric analysis of the corneal endothelium have shown that measurements of polymegathism (coefficient of variation of cell area) and pleomorphism (percent hexagonal cells) are more sensitive indicators of endothelial damage and function than changes in cell density alone. 37-45 Preoperative pleo­morphism has been found to correlate with postoperative corneal edema38 and pleomorphism and polymegathism after surgery may be a sign of continuing stress or damage to the endothelium.39-41 Therefore, examining the pre­operative ECC alone in these eyes may not necessarily be predictive of progression to pseudophakic bullous kera-

Figure 3. Iris-sutured intraocular lens (IOL) after IOL exchange. Dimpling of iris at sites of suture fixation (arrows). A Hessburg anterior chamber IOL was causing inferior peripheral corneal edema (open arrows) and elongation of pupil as shown. The inferior corneal edema has remained stable several months postoperatively. The preoperative endothelial cell count was 1075 cells/mm2

•

390

Figure 4. Hessberg anterior chamber intraocular lens inducing peripheral corneal edema (arrowheads) overlying haptic (arrow). There was no corneal edema 2.5 years ago when patient was first seen. Endothelial cell count has declined from 929 to 346 cells/mm2 over 2.5 years.

topathy. However, the majority of these eyes showed a high degree of pleomorphism and polymegathism on sub­jective analysis of preoperative endothelial photographs. Increased pleomorphism would be expected with the in­crease in cell size46 with such low ECCs (90% with ECC .::;; 1000 cells/mm2).

Endothelial damage with anterior chamber IOLs may be related to eye rubbing,47,48 endothelial touch from dis­location or significant vaulting of the IOL,3.6,47-49 or breakdown in the blood-aqueous barrier leading to chronic inflammation that is directly toxic to the corneal endothelium.3,50 Figures 3 and 4 show corneal edema lo­calized over an anterior chamber IOL haptic suggestive of intermittent touch. Also, our finding that a history of chronic uveitis preoperatively correlated with corneal de­compensation after IOL exchange (P = 0.002) is sup­portive of the theory that chronic inflammation is directly toxic to the corneal endothelium.

In this series, the complication rate is low except for the high rate of corneal decompensation in those eyes with preoperative ECCs less than 500 cells/mm2 or signs of early corneal decompensation. Seventy-one percent of the eyes that decompensated did so at a mean of 10.8 months postoperatively and the remaining 29% showed no signs of clearing their corneal edema after surgery. The average follow-up of the nondecompensating group was the same or greater than the decompensating group when broken into separate groupings of preoperative ECC (Ta­ble 4).

Three eyes in this current study had persistent or wors­ening uveitis postoperatively. However, this may be just the tendency of those particular eyes to have uveitis rather than being induced by the sutured IOL itself. We agree

Coli et al . Anterior Chamber IOL-Induced Corneal Endothelial Damage

with Stark et al20 that iris-sutured posterior chamber IOLs do not increase the risk of cystoid macular edema or uve­itis. We have, as have they, experienced that cystoid mac­ular edema and uveitis occurring preoperatively with an­terior chamber or iris-plane IOLs will sometimes clear after IOL exchange.

Most series of suture-fixated posterior chamber IOLs without penetrating keratoplasty involve scleral fixa­tion. 13.16,17,19-21,23-25 However, we prefer iris-fixation, given the risk of bleeding and the potential for ciliary body damage from making a blind pass of a needle posterior to the iris in an attempt to place it through the ciliary sulcus. Price and Whitson51 have reported on 1 patient who developed a suprachoroidal hemorrhage several days after placement of a scleral-fixated IOL. Endoph­thalmitis52-53 and episcleritis54 have also been reported to be associated with the externalized polypropylene knots, which sometimes occur after scleral fixation.

Our technique of suture-fixating a posterior chamber IOL to the posterior aspect of the iris has been modified from the technique used to suture-fixate IOLs during penetrating keratoplasty.31 We also use this technique

Figure 5. Pupillary dilation with iris-sutured intraocular lens. A, undilated with dimpling of iris at sites of suture fixation (arrows). B, adequate pupillary dilation with some limitation along the 3- and 9-0' clock axis

because of the sutures.

when placing secondary posterior chamber IOLs in cases of aphakia, after removal of dislocated anterior and pos­terior IOLs, and for eyes undergoing IOL exchange for cystoid macular edema or uveitis-glaucoma-hyphema syndrome associated with anterior chamber IOLs. Al­though technically difficult, this procedure has been greatly facilitated by the use of fine intraocular forceps and a newly designed 4-mm needle attached to a 9-0 polypro­pylene suture. A histopathologic study of eyes obtained post mortem with iris-sutured posterior chamber IOLs showed the IOLs to be well-tolerated. 55 In most instances, the primary means of support was the sutures themselves, as most of the haptic loops were not situated in the ciliary sulcus, but rather were suspended behind the iris and cil­iary body. However, the presence of the haptics may be useful in providing stability and minimizing optical tilt. None of our patients is noted to have pseudophakodo­nesis. Adequate pupillary dilation to allow fundus ex­amination is still possible despite the iris sutures (Figs SA and B). We have not experienced any cases of lens dis­location or suture breakage in this series.

We perform mechanical vitrectomies on all patients at the time of IOL exchange if their posterior capsules are not intact. Also, vitrectomy may playa role in the reso­lution of persistent cystoid macular edema. 56 Visual acuity improved in 64% of patients with preoperative cystoid macular edema. We performed anterior vitrectomies in the earlier patients but later switched to pars plana vi­trectomies because we are better able to remove vitreous strands from behind and around the pupil, and also be­cause we feel it is less damaging to the corneal endothe­lium. Also, vitrectomy ensures safe manipulation of the secondary posterior chamber IOL within the vitreous cavity.25 We have also found that our retinal detachment rate is very low (2.0%).

References

I. Stark WJ, Worthen DM, Holladay JT, et aI. The FDA report on intraocular lenses. Ophthalmology 1983;90:311-17.

2. Apple DJ, Mamalis N, Loftfield K, et al. Complications of intraocular lenses. A historical and histopathological review. Surv Ophthalmol 1984;29: I-54.

3. Apple DJ, Brems RN, Park RB, et al. Anterior chamber lenses. Part I: Complications and pathology and a review of designs. J Cataract Refract Surg 1987;13:157-74.

4. Apple DJ, Hansen SO, Richards SC, et al. Anterior chamber lenses. Part II: A laboratory study. J Cataract Refract Surg 1987;13:175-89.

5. Smith PW, Wong SK, Stark WJ, et al. Complications of semiflexible, closed-loop anterior chamber intraocular lenses. Arch Ophthalmol 1987;105:52-7.

6. Reidy JJ, Apple DJ, Googe JM, et al. An analysis of sem­iflexible, closed-loop anterior chamber intraocular lenses. J Am Intraocul Implant Soc 1985;11:344-52.

7. Apple DJ, Olson RJ. Closed-loop anterior chamber lenses [letter]. Arch Ophthalmol 1987; 105: 19-20.

8. Robin JB, Gindi JJ, Koh K, et al. An update of the indi­cations for penetrating keratoplasty: 1979 through 1983. Arch Ophthalmol 1986; 104:87-9.

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