feature Edited by Randall J. Olson, M.D.

Pathological and scanning electron microscopic evaluation of the 91Z intraocular lens

Nick Mamalis, M.D. Steven E. Brady, M.D. David J. Apple, M.D. Robert G. Notz, M.D.

Randall J. Olson, M.D. Salt Lake City, Utah

ABSTRACT We analyzed 18 explanted 91Z anterior chamber lenses by light and

scanning electron microscopy. Intermittent touch of the lens loops to the posterior corneal surface and the anterior chamber angle may have occurred. Erosion of the polypropylene loops into the anterior chamber angle recess and into the iris tissue was also observed. Fibrous tissue, uveal tissue, and inflammatory debris were noted on the loops, forming dense synechias at the points of contact with the angle recess. In some lenses the edges of the optics were sharp. Other significant manufacturing defects were rarely seen, and there was no evidence of degradation of polypropylene loops. The problems regarding surgical removal of this lens are discussed.

Key Words: anterior vaulting, closed loop, flexible loop, intermittent touch, polypropylene loop, scanning electron microscopy, synechia, UGH syndr,ome, 91Z anterior chamber intraocular lens

New anterior chamber intraocular lenses (IOLs) are designed to alleviate many complications associated with older anterior chamber lenses. 1,2 Those fre­quently occurring problems included inflammation, corneal decompensation because of contact between the IOL and the corneal endothelium, and degradation of the nylon haptics of flexible-looped lenses.

Widespread use of rigid-support anterior chamber 10 Ls began after Choyce's serial modifications of Strampelli's original design, culminating in the Mark VIII in 1963. 3 In addition, several flexible­support anterior chamber IOLs remain in use today. Preliminary results with many of these lenses have been encouraging.

From the Departments of Ophthalmology and Pathology, University of Utah School of Medicine, Salt Lake City, Utah.

This study was supported in part by an award from the American Intra-Ocular Implant Society.

Presented in part at the Hogan-Theobald Society Meeting, Park City, Utah, February 29, 1984.

Reprint requests to David J. Apple, M.D., Department of Ophthalmology, 50 North Medical Drive, Salt Lake City, Utah 84132.

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In 1981 the 91Z flexible-support anterior chamber IOL was introduced in an attempt to provide an opti­mal design that would permit three-point fixation, provide compression, allow manipulation of the lens in a closed anterior chamber, minimize potential for iris incarceration, and decrease the incidence of post­operative tenderness. The clinical and core study of this lens was voluntarily terminated by the manufac­turer in August 1983 because of a higher than expected complication rate.

This study analyzes 18 explanted 91Z lenses with several aims: (1) to provide data that might assist in the design and manufacture offuture lenses; (2) to assist the ophthalmologist in identifying problems that may arise

Table 1. Summary of case reports.

Case Date of Duration Number Implantation In Situ

1 7/82 13 months

2 4/82 2 months

3 8/82 4 months

4 11/82 7 months

5 1/83 4 months

6 7/82 6 months

7 4/83 2 months

8 6/82 7 months

9 5/82 11 months

10 9/82 11 months

11 12/82 10 months

12 12/82 10 months

13 6/83 4 months

14 5/82 19 months

15 10/82 12 months

16 9/82 15 months

17 10/82 15 months

18 11/82 14 months

during the follow-up of patients with this lens; and (3) to emphasize that surgical removal of this lens can be difficult and requires careful surgical technique.

OCULAR PATHOLOGY Case 1

The pertinent clinical features of Case 1 are listed in Table 1. The eye was enucleated because of a pneumo­coccal corneal ulcer with hypopyon and absolute glau­coma. This case provided a unique opportunity to study the tissue effects of this lens in a human eye.

External examination of the globe showed opacifica­tion and wrinkling of the cornea with a central focus of white discoloration (Figure 1). Multiple sections of the

Clinical History

Early corneal decompensation and edema, 1/83 Pneumococcal corneal ulcer, hypopyon, 6/83 Enucleation for intractable glaucoma, 8/83

Toxic lens syndrome, IOL removed, 6/82

UGH syndrome, IOL removed, 12/83

UGH syndrome, IOL removed, 6/83

UGH syndrome, 3/83 IOL removed with iridodialysis and vitreous loss, 4/83

CME,8/82 Chronic inflammation, 10/82 Corneal edema, pupillary membrane, glaucoma, 12/82 Loop deeply embedded in angle recess, IOL removed, 1/83

UGH syndrome, loop deeply embedded in angle recess, IOL removed, 6/83

UGH syndrome, IOL removed, 1/83

Pseudophakic bullous keratopathy, IOL removed, 4/83

Hyphema, iris atrophy, 2/83 Recurrent hyphema, loop deeply embedded in angle recess, 7/83 IOL removed, 8/83

Persistent hyphema and uveitis, IOL removal attempt unsuccessful due to adhesions in angle, 9/83

IOL removed by cutting loop, vitrectomy, 9/83

Glaucoma, uveitis, hemorrhage, 3/83 IOL removed, 9/83

Recurrent hyphema and vitreous hemorrhage, IOL removed, 10/83

Hyphema, glaucoma, pain, IOL removed, 12/83

Triple procedure, 10/82 Graft failure, 8/83 Penetrating keratoplasty, IOL removed, 10/83

UGH syndrome, recurrent vitreous hemorrhage, IOL removed, 12/83

Glaucoma, 2/83 UGH syndrome, iris chafing, vitreous hemorrhage, 12/83 IOL removed, 1/84

CME, glaucoma, and uveitis, 5/83 Vitrectomy, IOL removed, 1/84

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Fig. 1. (Mamalis) Case 1: Gross photograph of the enucleated globe showing corneal opacification and a focus of central white discoloration corresponding to an area of acute keratitis.

globe showed forward displacement of the implant to­ward the internal corneal surface and anterior bowing of the iris just posterior to the loops, almost obliterating the anterior chamber. Removing the implant during gross examination of the globe was difficult because of loop adherence to the tissues of the angle recess. These synechias were severed, and a cyclodialysis was cre­ated at the time of lens removal.

There was marked edema of the basal cell layer of the corneal epithelium and bullous separation of the epi­thelium from the underlying Bowman's layer (Fig­ure 2). The superficial stroma was infiltrated with acute

Fig. 2. (Mamalis) Case 1: Photomicrograph of the cornea showing intracellular edema of the basal layers of the corneal epi­thelium and bullous separation of the epithelium from the underlying Bowman's layer. (B) Bowman's layer (hematoxylin and eosin, x 2(0).

and chronic inflammatory cells, corresponding to the site of white discoloration seen in Figure 1. The corneal ulcer that had been noted clinically (Table 1) had re­epithelialized. There were numerous guttata on Descemet's membrane, and the corneal endothelium was totally absent. The round loop had eroded deeply into the ciliary body and was situated adjacent to por­tions of the ciliary muscle (Figure 3). There was fibrosis and a mild chronic inflammatory infiltrate around the site of insertion (Figure 3). Prior to removal, these tissues had adhered to the trabecular meshwork, form­ing a peripheral anterior synechia, which was severed upon removing the lens.

Fig. 3. (Mamalis) Case 1: Photomicrograph of the junction of the iris root (I) and ciliary body (CB) showing the site of erosion of the rounded polypropylene loop into the angle recess. The loop (L) is now completely surrounded by a fibrous capsule, and giant cells are seen in many sections adjacent to the loop. There is a chronic inflammatory reaction in the iris, and the loop has eroded to a position near the ciliary muscle (arrows). (R) Original site of angle recess (hematoxylin and eosin, x 1(0).

Two other indentations on the iris were noted. They were caused by contact with various portions of the "two-point" closed loop. A deep triangular indentation was located opposite the area of deep erosion (Figure 4). The other indentation was located more centrally to­wards the pupil (Figure 4). It was completely sur­rounded by a fibrous capsule (Figure 5) and was also connected to a fibrovascular membrane (Figure 4, ar­rows) that, by serial sectioning, was shown to encase the lens optic. There was atrophy of the iris stroma at the sites where the loops had compressed this tissue (Figure 4). Rubeosis iridis was present. The iris and ciliary body showed a moderate degree of chronic in­flammation with infiltration oflymphocytes and plasma

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Fig. 4. (Mamalis) Case 1: Low-power photomicrograph showing two indentations of the iris, which appeared in addition to that seen in the angle recess in Figure 3. A triangular depression of the iris is present on the left, and there is extensive necrosis and dispersion of iris pigment at this site. This probably represents an erosion site caused by the periphery of the lens optic. Also present is a second iris defect on the right, a site of erosion of the portion of the "two-point" polypropylene loop (L). This defect is in communication with a membrane (arrows) which, in serial sections, was noted to extend completely around the optic (hematoxylin and eosin, x 20).

Fig. 5. (Mamalis) Case 1: Deeper section of the iris lesion seen on the right in Figure 4 showing complete enclosure of the loop (L) by a delicate membrane. The defect at the left of the loop was caused by postmortem lens removal (hematoxylin and eosin, x 80).

cells. Pigmented macrophages and chronic inflamma­tory cells were identified in the trabecular mesh~ork (Figure 6).

Cystoid macular edema (CME) was present, and the retina and optic nerve showed moderate gliosis and atrophy.

SCANNING ELECTRON MICROSCOPY Salient scanning electron microscopic features of the

lens in Case 1 and selected illustrations of the lenses of the 17 other cases (Table 1) are presented. Figure 7 is a prescanning photograph of one of the removed lenses (Case 2). The findings of this lens exemplify some changes seen in most of the lenses we studied. These include the presence of large amounts of uveal and

Fig. 6. (Mamalis) Case 1: Photomicrograph of the trabecular meshwork in an area away from a direct insertion of the polypropylene loop showing infiltration of chronic in­flammatory cells and pigment-laden cells (hematoxylin and eosin, x 150).

fig. 7. (Mamalis) Case 2: Gross photograph of a removed 91Z lens. Note deeply pigmented debris, particularly on the loop on the right (large arrow) and to a lesser extent along almost the entire length of the loop on the left (small arrow). Debris is also em bedded atthe junction of the four loops with the optic. A mild amount of debris is present on the optic itself.

fibrous tissue on the apical portions of the loops (Fig­ure 7, arrows). These tissues had adhered to the lens loops during removal, a finding that correlates with the difficult explantation of some of these lenses. The optic of this lens, and most of the other lenses we studied, showed varying degrees of debris deposition on the sur­face. In almost all cases there was an extensive buildup of fibro-inflammatory debris at the four sites of loop insertion into the optic (Figure 7; see also Figure 10).

Figures 8A to 8e show scanning electron micro­scopic correlates of Figure 7, namely, an extensive

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buildup of debris on the apices of the loops of three lenses (Cases 2, 7, and 8). This material represented a combination of uveal tissue that was detached from the angle recess, fibrous tissue, and inflammatory debris that encircled the loops (Figures 3 and 4). Because of this firm attachment and erosion into the angle recess, many of the IOLs' haptics had to be cut to remove the IOL (Figure 9). This photograph shows how the poly­propylene loops appear to "swell" at the margins of the cut. This is a common occurrence after surgical shear­ing of these loops.

Fig. BA. (Mamalis) Case 2: Scanning electron micrograph of the loop seen on the right in Figure 7. Note the buildup of uveal and fibrous tissue at this site, a site where the lens had eroded into the angle recess and where the uveal tissue was pulled away at the time of removal (x SO) .

Fig. BB. (Mamalis) Case 7: The rounded polypropylene loop of a 91Z lens shows extreme buildup of a large amount of uveal and fibrous tissue remaining on the loop, which was tom from the angle recess during removal (x 20) .

Fig. BC. (Mamalis) Case B: Another scanning electron micro­graph showing buildup of uveal tissue and fibrous tissue on the polypropylene loop, again at the site of removal from the angle recess (x 100).

Fig. 9. (Mamalis) Case 5: Removed 91Z lens showing a site where the surgeon attempted to cut the loop. Note how the polypropylene appears to "swell" at the margin, a com­mon occurrence following cutting or shearing of the loop. No obvious evidence of degradation of the polypropylene is noted (x 125).

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Fig. 10. (Mamalis) Scanning electron micrographs showing a buildup of debris at the site ofloop insertion into the lens optic; this was seen in the majority of removed lenses. Left: Case 1, x 200. Center: Case 7, x ISO. Right: Case 4, x 200.

Deposition oflarge amounts of inflammatory debris and fibrous tissue was not confined to the portions of the loops adjacent to the angle recess but was also common at the junctions of the loops and the lens optics. This deposition was evident in the majority of explanted lenses (Figures 10A-lOC, Cases 1, 4, and 7).

As noted in Figure 7, variable amounts of cells, fibrin, and inflammatory debris were seen on the sur­faces of the lens optics (Figure ll). This finding is consistent with the fact that most of the IOLs were removed due to inflammation or the UGH syndrome.

Examination of the edges of the lens optics of most of these IOLs showed that the borders were often sharp

Fig. 11. (Mamalis) Case 7: This micrograph shows the typical appearance of debris on the lens optic seen in uveitis or the UGH syndrome. The velvety material is composed of inflammatory debris and fibrin (x500).

(Figures 12A and 12B). The optic of one lens displayed breakage at the site of loop insertion (Figure 12B).

Examination of the polypropylene loops of all 18 lenses showed no evidence of cracking or any visible degradation to the loops themselves (Figure 13). Most of the IOLs were within the eyes for a relatively short period.

Fig. 12A. (Mamalis) Case 6: Scanning electron micrograph show­ing the junction of optic and polypropylene loop. Note debris at the site of insertion of the loop. Also note the sharpness of the lathe-cut optic edges (arrows) (x 1(0).

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Fig. 12B. (Mamalis) Case 5; Scanning electron micrograph with similar orientation as seen in Figure 12A. Note the sharp edges of the optic (arrows). There is also a cracklike defect or splitting of the upper surface of the optic, a finding which could be an artifact caused by removal, or more likely represents a manufacturing defect (x200).

Fig. 13. (Mamalis) Case 4; Polypropylene loop showing deposi­tion offibroinflammatory debris on the loop. Much of the debris has been artifactiously separated showing the sur­face of the loop itself, indicating no evidence of swelling, cracking, fissuring, or other evidence of degradation of the loop (x200).

DISCUSSION

The 91Z anterior chamber IOL has a polymethyl­methacrylate (PMMA) optic and closed polypropylene loops. Its design combined the current concepts of flexible loops, three-point fixation, and a planoconvex optic configuration. The flexible, closed-loop system was an attempt to diminish several of the disadvantages allegedly associated with rigid, fixed-length anterior chamber lenses. 4,5

The 91Z lens was introduced in January 1981 and became very popular because it was flexible and easy to insert. Basically all patients did well in the early postoperative period after IOL implantation, but later postoperative complications, e.g., inflammation or UGH syndrome, began to appear.

The clinical studies on the 91Z lens were ultimately terminated in August 1983 for several reasons: (1) the clinical results achieved with the lens had "not been consistent from surgeon to surgeon," and (2) data from the core study indicated that there was a slightly higher incidence of CME, glaucoma, postoperative inflam­mation, and micro-hyphema when compared with premarket-approved anterior chamber lenses.

Our pathologic findings are as follows:

Microsections of the enucleated globe (Case 1) dem­onstrated a forward displacement (or vaulting) of the implant toward the corneal endothelium. However, in this instance, perforation of the cornea and anterior chamber collapse may have exaggerated the picture. Drews6 has described an intermittent touch syndrome that may cause corneal endothelial damage and may also indirectly result in CME. The problem of anterior vaulting caused by the closed-loop configuration of this lens has recently received additional attention (IOL & Ocular Surgery News, October 1, 1983).

Various methods for mechanical testing oflens vault­ing have been reported. 7 Duffin and Olson8 studied the vaulting characteristics of anterior chamber IOLs and found a correlation between lens design and lens vault. Lenses with rectangular-shaped or closed loops usually vaulted the most per unit ofloop compression. Because of its flexibility, the 91Z lens showed the greatest vault per gram of force on the lens loop. Lenses with an open-loop configuration, on the other hand, could be compressed without vaulting. '

In Case 1, we observed erosion of the loops into the anterior chamber angle recess with formation of pe­ripheral anterior synechias and fibrosis around the loop apices. These same findings were noted at surgical removal by most of the clinicians who submitted these lenses. This was confirmed by scanning electron mi­croscopy (SEM) of the explanted lenses; large deposits of fibrous tissue, uveal tissue, and inflammatory debris were located at the exact site where the loops were torn away at removal.

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Tuberville and coauthors9 postulated a sequence of events that might explain this propensity for exuberant fibrosis around the loops, particularly polypropylene loops (reviewed by Apple and coauthorslO). This se­quence includes activation of complement by poly­propylene, which in turn leads to chemotaxis ofleuko­cytes and may subsequently induce inflammation and fibrosis. However, Mondino and Raoll have stated that IOLs, including those with polypropylene loops, do not have a substantial effect on complement levels. This is an area that warrants further study.

Histopathologic examination of the enucleated eye (Case 1) disclosed that various portions of the loop touched and eroded into iris tissue posterior to the lens. Such an erosion could lead to breakdown of the blood-aqueous barrier, a response that leads to anterior segment inflammation. It is impossible to determine to what extent the iris erosion was related to the flat anterior chamber and the infectious process.

Kelman4 emphasized that an intermittent grating of intraocular tissues may create an inflammatory re­sponse. The problem has also recently been addressed by Wiley and coauthors.12 They speculated that late postoperative hemorrhage after 91Z lens implantation was due to chronic pressure or microfrictional forces of the fine, flexible polypropylene loops on the angle structures. The breakdown of the blood-aqueous bar­rier with subsequent release of prostaglandins is also thought to be responsible for the pathogenesis of aphakic or pseudophakic CME.13-15 This mechanism may explain the increased incidence of CME seen in the 91Z lens.

The edges of the optics Were often sharp. Contact between these edges and the iris could therefore lead to tissue erosion. The UGH syndrome has been at­tributed in the past to manufacturing irregularities such as warped anterior chamber footplates of injection-molded lenses16 and imperfect finishing and polishing ofIOL edges,l7

Other manufacturing problems were rarely seen, although occasional defects (Figure 12B) did occur. This lamellar splitting of the optic was possibly a result of faulty insertion of the loop into the optic.

A highly consistent finding was severe buildup of cellular and fibrous debris at the junction of loops and optics. It appears that these junctional sites are prone to excessive accumulation of debris.

No surface alterations of the lens or degradation of the polypropylene loops were found. The latter was a considerable problem in the nylon flexible-loop lenses. 18 However, all of the lenses analyzed by SEM in this study had been implanted for relatively short periods (mean value 9.2 months). Both Drewsl9,20 and ApplelO,21 have shown that any surface change of polypropylene, if it indeed occurs, is probably a long­term phenomenon, requiring a minimum of one and

one-half to two years to appear. Using slitlamp exami­nation, Lieppman22 has noted various changes such as precipitation, .scaling, cracking, and generalized de­composition of polypropylene loops in 91Z lenses. , These changes had become apparent six to 12 months after implantation. This occurred in eight patients who had not worn ultraviolet radiation (UVR) blocking glasses. He apparently did not see this in patients who wore UVR-filtered spectacles. The significance of these findings requires further study.

The use of polypropylene as a loop haptic material for the anterior chamber remains controversial (IOL & Ocular Surgery News, April 1, 1983, pp 10-11, 20; June 15, 1983, pp 3, 11, 16-17; September 15, 1983, pp 3, 26-27). This subject has recently been reviewed by Apple and coauthors.lO

Surgical removal of the 91Z lens may be difficult and can cause tissue damage such as tearing of the iris or iridocyclodialysis as well as anterior segment or vitre­ous hemorrhages. We also experienced this problem while removing the lens during gross examination of Case 1. Figures 7, 8A-8C confirm the clinically ob­served finding that extensive synechia formation and adherence of the loops to uveal tissue are common occurrences with this lens. Therefore, extreme care is required in removing the lens. Beehler23 has reported that removal can best be effected by cutting the loops and threading them through the synechias. Hagan24

reports a technique using the Nd:YAG laser to cut synechias prior to explantation of the pseudophakos. Surgeons contemplating the removal of any anterior chamber lens with looped material should perform careful preoperative gonioscopy and be prepared for synechias around the loops.

REFERENCES

L Strampelli B: Anterior chamber lenses; present techniques. Arch Ophthalmol 66:12-17, 1961

2. Rosen ES: The development and characterization of the intraocular lens. In: Rosen ES, Haining WM, Arnott EJ, eds, Intraocular Lens Implantation . St Louis, CV Mosby Co, 1984, p 50

3. Choyce DP: Anterior chamber implants-past, present and future. The Vlth Binkhorst Medal Lecture . Am Intra-Ocular Implant Soc J 8:42-50, 1982

4. Kelman CD: Anterior chamber lens designs concepts. In: Rosen ES, Haining WM, Arnott EJ, eds, Intraocular Lens Implantation. St Louis, CV Mosby Co, 1984

5. Tennant JL: Anterior chamber lenses. In: Rosen ES, Haining WM, Arnott EJ, eds, Intraocular Lens Implantation . St Louis, CV Mosby Co, 1984, p 279

6. Drews RC: Intermittent touch syndrome. Arch Ophthalmol 100:1440-1441, 1982

7. Isaacson WB, Christie B: Mechanical testing of intraocular lenses. Am Intra-Ocular Implant Soc J 7:344-347, 1981

8. Duffin RM , Olson RJ: Vaulting characteristics of flexible loop anterior chamber intraocular lenses. Arch Ophthalmol 101:1429-1433, 1983

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9. Tuberville AW, Galin MA, Perez HD, Banda D, et al: Com­plement activation by nylon- and polypropylene-looped pros­thetic intraocular lenses. Invest Ophthalmol Vis Sci 22:727-733, 1982

10. Apple DJ, MamalisN, Brady SE, Loftfield K, et al: Biocom­patability of implant materials: A review and scanning electron microscopic study. Am Intra-Ocular Implant Soc J 10:53-66, 1984

11. Mondino BJ, Rao H: Haemolytic complement and IOLs. Acta Ophthalmol 61:76-84, 1983

12. Wiley RG, Neville RG, Martin WG: Late postoperative hem­orrhage following intracapsular cataract extraction with the IOLAB 91Z anterior chamber lens . Am Intra-Ocular Implant Soc J 9:466-469, 1983

13. Obstbaum SA, Galin MA: Cystoid macular oedema and ocular inflammation: The comeo-retinal inflammatory syndrome. Trans Ophthalmol Soc UK 99:187-191, 1979

14. Uram M, Yannuzzi LA: Posterior segment complications of cataract extraction and intraocular lens implantation. In: Rosen ES, Haining W, Amott EJ, eds, Intraocular Lens Implanta­tion. St Louis, CV Mosby Co, 1984

15. Yannuzzi LA, Landau AN, Turtz AI: Incidence of aphakic cystoid macular edema with the use of topical indomethacin.

Ophthalmology 88:947-954, 1981 16. Ellingson F'T: Complications with the Choyce Mark VIII ante­

rior chamber lens implant (tiveitis-glaucoma-hyphema). Am Intra-Ocular Implant Soc J 3:199-201, 1977

17. Keates RH, Ehrlich DR: "Lenses of chance"; Complications of anterior chamber implants. Ophthalmology 85:408-414, 1978

18. Drews RC, Smith ME, Okun N: Scanning electron microscopy of intraocular lenses. Ophthalmology 85:415-424, 1978

19. Drews RC: Polypropylene in the human eye. Am Intra-Ocular Implant Soc J 9:137-142, 1983

20. Drews RC: Quality control and changing indications for lens implantation. Ophthalmology 90:301-310, 1983

21. Apple DJ, Craythom JM, Olson RJ, Little LE, et al: Anterior segment complications and neovascular glaucoma following implantation of a posterior chamber intraocular lens. In press, Ophthalmology, 1984

22. Lieppmann ME: Letter to the Editor: Loop precipitation in the 91Z lens. Am Intra-Ocular Implant Soc J 9:459, 1983

23. Beehler ME: Letter to the Editor: UGH syndrome with the 91Z lens. Am Intra-Ocular Implant Soc J 9:459, 1983

24. Hagan JC: Complications while removing the IOLAB 91Z lens for the UGH + syndrome. Am Intra-Ocular Implant Soc J 10:209-213, 1984

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