Ординатура / Офтальмология / Английские материалы / Phakic Intraocular Lenses_Hardten, Lindstrom, Davis_2004

Figure 4-1. Specular microscopy image of a cornea with normal endothelial cell density and relatively small amounts of polymegathism or polymorphism.

Figure 4-3. Specular microscopy image of a cornea with areas of corneal guttata in which endothelial cells are missing, and the density in other areas is very low with significantly increased size of the endothelial cells. This patient has a remote history of corneal transplant rejection. This patient would have a higher risk of endothelial decompensation with intraocular surgery.

Figure 4-2. Specular microscopy image of a cornea with areas of corneal guttata in which endothelial cells are missing, yet the density in other areas is relatively normal. This eye has a slightly higher amount of polymorphism and polymegathism. This patient would have only a slightly higher risk of endothelial decompensation with intraocular surgery.

Figure 4-4. Specular microscopy image of a cornea with a wide variety of shapes and significant polymorphism and polymegathism. This patient would not have a higher risk of endothelial decompensation with intraocular surgery.

Finally, the study did not report a significant change in endothelial cell density in contact lens wearers compared to the controls.

A similar study conducted by Lee et al3 also studied the effects of soft contact lens use as measured in different durations (years of use) on the corneal endothelium. This study correlated with the previously mentioned study in which the authors found that increasing years of soft contact lens use decreased the percentage of hexagonal cells. The authors also found that contact lens wearers had a greater coefficient of variation when compared to noncontact lens wearers. In contrast to the previous study, Lee

et al found that cell density decreased among the contact lens wearers.3

Similar findings with rigid gas permeable (RGP) or polymethylmethacrylate (PMMA) contact lens wear are published. Endothelial polymegathism, pleomorphism, and decreased cell density are induced with PMMA wear.4 Polymegathism and pleomorphism are induced with high oxygen permeability (Dk) gas permeable contact lens wear.5 It does not appear that RGP wear has an effect on endothelial cell density.

Endothelium Over a Lifetime

When determining if the endothelial cell measurement is healthy enough to be able to proceed with a phakic IOL or determining if the patient is developing problems or loss or change of cells postoperatively, it is important to understand the normal human corneal endothelium and the aging process of this endothelium over a lifetime. Mustonen et al conducted a study to measure central corneal cell population looking at 58 eyes of 45 patients.6 All patients had normal corneas without history of trauma, disease, or contact lens use. The mean age was 45 years with a standard deviation of 17. The range was 20 to 84. The corneas were measured in vivo with a scanning slit confocal microscope. The average density of endothelial cells was found to be 3055 + 386 cells/mm2, with a range from 1809 to 3668. As expected, the authors found that endothelial cell density decreases with age, with the largest drop occurring after 80 years of age. There was no correlation between gender or right or left eyes.6

A much larger study conducted by Abib and Barreto retrospectively looked at 784 corneal specular microscopic examinations. All subjects had healthy corneas and no history of contact lens use. The patients were grouped according to age in 10-year intervals from 0 to 100 years. The actual age of patients included in the study was 6 to 97 years old. The study found that the endothelial cell density decreased over time following a linear model. As the cell density decreased, the standard deviation increased. The probability of a cell density less than 2000 cells/mm2 increased starting in the seventh decade and moving on.7

Endothelial Cell Measurement

Preoperative endothelial cell analysis is especially important in those patients with previously documented or suspected abnormalities of the endothelial cells. Either slitscanning corneal microscopy or specular microscopy may analyze endothelial cells. Generally, noncontact specular microscopy is the standard method for determining cell density, polymegathism, and pleomorphism. There are two models of noncontact specular microscopes available: the Konan (Konan Medical Corp, Fairlawn, NJ) and the Topcon (Topcon, Paramus, NJ).8 There are different computer analysis systems to be used with the microscopes. Important emphasis needs to be placed on the reliability and reproducibility of the results obtained from these systems. There can be a wide variability in the outcome variable depending upon how specific computer software is used (ie, automated, semiautomated, or manual).9 In addition to the wide variety of outcome dependent on software, intertechnician variability is very possible. Benetz et al conducted a study to compare different image-analysis systems. The authors concluded that the Konan SP8000

system has the potential to be reliable and useful for a large-scale clinical trial, especially when the dot method for cell density is utilized.8

ANTERIOR CHAMBER

INTRAOCULAR LENS EFFECT

ON CORNEAL ENDOTHELIUM

There have been several reports that have documented progressive endothelial cell loss/compromise with the implant of an anterior chamber IOL in a phakic eye. It needs to be determined if the surgical procedure itself is inducing the change, if the patient had compromised endothelium to begin with, or if it is the placement of the lens in the anterior chamber that is causing the change.10-12

A study conducted by Perez-Santonja et al11 compared the loss of central endothelial cell count measured by specular microscopy after implantation of the Worst-Fechner (now the Artisan) iris-claw lens (Ophtec BV, Groningen, Netherlands) in 30 eyes to the Baïkoff ZB 5M angle supported lens (Domilens, Lyon, France) in 28 eyes. The authors found progressive endothelial cell density loss in both groups. The cell loss in the Worst-Fechner lens group was 7.3% at 3 months, 10.6% at 6 months, 13.0% at 12 months, and 17.6% at 24 months. The cell loss in the Baïkoff ZB 5M lens group was 7.5% at 3 months, 10.9% at 6 months, 12.2% at 12 months, and 12.2% at 24 months. The measurements were statistically significantly decreased in both groups for all time points except between the 12and 24-month time point in the Baïkoff group. The Baïkoff lens group appeared to have a stable cell density after 1 year.11

Without longer follow-up, it is difficult to speculate why cell loss stabilized in the Baïkoff group, while the cell loss was progressive in the Worst-Fechner lens group. It has been speculated that the close proximity between the lens and the cornea could cause endothelial loss secondary to intermittent lens-to-cornea touch potentially occurring due to eye rubbing.12 There have been additional suggestions that a chronic low grade uveitis may be associated with progressive endothelial cell loss.13,14 This study did not evaluate the size or shape of the endothelial cells; it described density alone.

A study using a laser flare-cell meter evaluated the flare in the anterior chamber of patients that had the WorstFechner IOL or the Baïkoff ZB 5M lens and found that the postoperative flare was higher in the Worst-Fechner lens group. Although the study found chronic subclinical inflammation at all time points (12, 18, and 24 months), the flare was greater in the Worst-Fechner group. None of the points had a statistically significant difference between groups.14

32 Chapter 4

A later study with a longer follow-up evaluated both endothelial density and morphometric change, and it appeared as though the loss of endothelial density was related more to the surgical procedure itself. Menezo et al conducted a study that involved 111 eyes that underwent phakic IOL implantation with a Worst iris-claw lens.15 Although cell loss was documented, it was less than in earlier studies. Mean cell loss at 6 months was 3.9%, 12 months was 6.6%, 2 years was 9.2%, 3 years was 13.4%, and 4 years was 13.4%. Cell loss was greater in eyes with a shallower anterior chamber depth. In addition, there was a greater loss of cells in those eyes implanted with a higher power lens. Both of these findings were significant at the 6-month visit only; these variables were less significant in the late postoperative period. This suggests that it is possible to have the lens come into greater contact with the endothelium with a shallow anterior chamber, especially if the lens is of a larger diameter.

Interestingly, in the Menezo et al study, the polymorphism and polymegathism were near preoperative levels at the 2-year postoperative visit. At 4-years postop, there was no statistical significant difference between preoperative and postoperative values in cell shape or size.15 According to Shaw et al,16 the morphology of the corneal endothelial cell is the critical factor contributing to the functional reserve of the cornea. It is the shape and size of the endothelial cell that give the most sensitive indication of cell damage rather than cell density alone.16

Lastly, the Menezo et al study suggests that there is no chronic uveitis present with the Worst lens. Iris angiography was completed in 15 eyes at 6 months postop and no blood-aqueous barrier breakdown was seen.15 These findings continue to suggest that the reported endothelial cell loss is a consequence of the surgery itself and not the continued presence of the anterior chamber lens in place.

POSTERIOR CHAMBER

INTRAOCULAR LENS EFFECT

ON CORNEAL ENDOTHELIUM

There are similar reports of documented cell loss associated with implantation of a posterior chamber phakic IOL in addition to reported cell loss associated with implant of an anterior chamber phakic IOL.

In a study conducted by Jimenez-Alfaro et al,17 20 eyes underwent implantation of the STAAR posterior chamber phakic IOL (PCPIOL) (STAAR Surgical AG, Nidau, Switzerland). Several factors were evaluated to determine the safety of the procedure. The authors found that central endothelial cell density decreased significantly after the surgery. One limitation of this study is that the patients were only followed for 2 years. Cell loss was 4.4% at 3 months, 4.8% at 6 months, 5.2% at 12 months, 5.5% at 18 months, and 6.6% at 24 months.17

Dejaco-Ruhswurm et al conducted a similar study evaluating long-term changes to the corneal endothelium with a STAAR PCPIOL with similar findings. Cell loss was 1.8% at 3 months, 4.2% at 6 months, 5.5% at 12 months, 7.9% at 2 years, 12.9% at 3 years, and 12.3% at 4 years. This study also evaluated morphometric changes, including polymorphism (hexagonal cells) and polymegathism (coefficient of variation), both of which remained stable over the entire 4-year period.18

ENDOTHELIAL CELL

LOSS ASSOCIATED

WITH PHACOEMULSIFICATION

AND INTRAOCULAR LENSES

In both of the more comprehensive long-term studies of anterior chamber phakic IOLs and posterior chamber IOLs, it again appears that the endothelial cell loss is surgically induced rather than induced later by the phakic lens. It is well known that after any anterior segment surgery procedure endothelial cell loss occurs proportional to the length and type of surgery.19 It becomes important to compare and contrast the data given for the phakic IOLs to a surgical procedure that we are much more familiar with in terms of long-term results. There are several published studies documenting endothelial cell loss after phacoemulsification. The reports vary in different studies ranging from 4% to 13% endothelial cell loss.20-23 This reported density loss is very similar to the cell density loss reported for a phakic IOL implant.

SULCUS MEASUREMENTS

The ciliary sulcus measurement is a very important factor in determining the size of the PCPIOL selected for the patient. It is this factor that determines the vault (ie, the amount of separation between the Implantable Contact Lens [ICL] [STAAR Surgical AG, Nidau, Switzerland] and the natural lens). A current limitation of the PCPIOL is that we do not have extremely accurate and reproducible methods for determining this variable. If the lens diameter chosen is too large, this can result in greater vault than desired, resulting in increased distance between the ICL and the natural lens. This can result in increased contact between the posterior surface of the iris and the ICL, leading to pigment dispersion and potentially putting the patient at higher risk for developing glaucoma. If the ICL diameter chosen is too small, the opposite occurs: the ICL and the natural lens are in closer proximity, increasing risk for visually significant cataract development. Ideally, the ICL would vault forward enough to provide adequate space from the crystalline lens but not vault too much to cause iris chaff and pigment release.24

Typically, surgeons have determined sulcus size using the white-to-white limbal measurement. The phakic ICL size is then the white-to-white plus 0.5 mm for myopes and white-to-white minus 0.5 mm, or the total white-to- white measurement, for hyperopes.25 This method is indirect and, therefore, not an accurate measurement of ciliary sulcus diameter.24

Pop et al26 conducted a study to predict sulcus size with the use of ocular measurements, including ultrasound biomicroscopy to measure sulcus size, axial length, anterior chamber depth, lens thickness, limbus size, and pachymetry. The authors did not find that sulcus size significantly correlated with limbus size, suggesting that this is an inadequate means to measure the sulcus diameter. The authors did find that sphere and mean corneal power most significantly correlated to the sulcus size compared to all other measurements. Utilizing multiple regression analysis, the authors derived an equation relating sulcus size to other ocular variables:

Sulcus size = 18.9 + -0.023 x sphere + -0.15 x mean keratometry

This resulted in 24% total variance, statistical correlation of 0.89, and an estimated standard error of 0.5 mm.26

Although the method described by Pop et al26 may be an improvement over the traditional method of measuring sulcus diameter by white-to-white, it is still potentially limited due to the high probability of variation and the fact that it has not been tested in a prospective fashion in another set of eyes. With more accurate methods of sulcus measurement, this potentially could improve surgical outcomes when using an ICL.

SUMMARY

Although the use of phakic IOLs is certainly very exciting for the correction of high refractive error, the lack of long-term results continues to remain a concern. The later long-term studies are promising with regard to stabilization of endothelial cell loss. However, this will continue to remain a concern simply due to the lack of ability for the corneal endothelium to regenerate. A more accurate reproducible method for determining ciliary sulcus size is needed. Refinements in the techniques should allow continued improvements in safety and efficacy.

REFERENCES

1.Leibowitz HM, Laing RA. Specular microscopy. In: Leibowitz HM, ed. Corneal Disorders: Clinical Diagnosis and Management. Philadelphia, Pa: WB Saunders; 1984:123-163.

2.Chang SW, Hu FR, Lin LL. Effects of contact lenses on corneal endothelium—a morphological and functional study. Ophthalmologica. 2001;215:197-203.

3.Lee JS, Park WS, Lee SH, et. al. A comparative study of corneal endothelial changes induced by different durations of soft contact lens wear. Graefes Arch Clin Exp Ophthalmol. 2001;239:1-4.

4.Setala K, Vasara K, Vesti E, Ruusuvaara P. Effects of longterm contact lens wear on the corneal endothelium. Acta Ophthalmol Scand. 1998;76:229-303.

5.Esgin H, Erda N. Corneal endothelial polymegathism and pleomorphism induced by daily-wear rigid gas-permeable contact lenses. CLAO J. 2002;28:40-43.

6.Mustonen RK, McDonald MB, Srivannaboon S, et al. Normal human corneal cell populations evaluated by in vivo scanning slit confocal microscopy. Cornea. 1998;17:485492.

7.Abib FC, Barreto J. Behavior of corneal endothelial density over a lifetime. J Cataract Refract Surg. 2001;27:1574-1578.

8.Bentez BA, Diaconu E, Bowlin SJ, et al. Comparison of corneal endothelial image analysis by Konan SP8000 noncontact and bio-optics Bambi systems. Cornea. 1999;18:6772.

9.Vecchi M, Braccio L, Orsoni JG. The Topcon SP 1000 and Image-NET systems. Cornea. 1996;15:271-277.

10.Landesz M, Worst JGF, van Rij G. Long-term results of correction of high myopia with an iris-claw phakic intraocular lens. J Refract Surg. 2000;16:310-316.

11.Perez-Santonja JJ, Iradier MT, Sanz-Iglesias L, et al. Endothelial changes in phakic eyes with anterior chamber intraocular lenses to correct high myopia. J Cataract Refract Surg. 1996;22:1017-1022.

12.Mimouni F, Colin J, Koffi V, Bonnet P. Damage to the corneal endothelium from anterior chamber intraocular lenses in phakic myopic eyes. Refract Corneal Surg. 1991;7:277-281.

13.Rao GN, Stevens RE, Harris JK, Aquavella JV. Long-term changes in corneal endothelium following intraocular lens implantation. Ophthalmology. 1981;88:386-397.

14.Perez-Santonja JJ, Iradier MY, Benitez del Castillo JM, et al. Chronic subclinical inflammation in phakic eyes with intraocular lenses to correct myopia. J Cataract Refract Surg. 1996;22:183-187.

15.Menezo JL, Cisneros AL, Rodriguez-Salvador V. Endothelial study of iris-claw phakic lens: four year followup. J Cataract Refract Surg. 1998;24:1039-1049.

16.Shaw EL, Rao GN, Arthur EJ, Aquavella JV. The functional reserve of corneal endothelium. Ophthalmology. 1978;85: 640-649.

17.Jimenez-Alfaro I, Benitez del Castillo JM, Garcia-Feijoo J, et al. Safety of posterior chamber phakic intraocular lenses for the correction of high myopia. Ophthalmology. 2001; 108:90-99.

18.Dejaco-Ruhswurm I, Scholz U, Pieh S, et al. Long-term endothelial changes in phakic eyes with posterior chamber intraocular lenses. J Cataract Refract Surg. 2002;28:15891593.

Pseudophakic bullous keratopathy. Relationship to preoperative corneal endothelial status. Ophthalmology. 1984;91: 1135-1140.

20.Dick HB, Kohnen T, Jakobi EK, Jakobi KW. Long-term endothelial cell loss following phacoemulsification through a temporal clear corneal incision. J Cataract Refract Surg. 1996;22:63-71.

21.Hayashi K, Hayashi H, Nakao F, Hayashi F. Corneal endothelial cell loss in phacoemulsification surgery with silicone intraocular lens implantation. J Cataract Refract Surg. 1996;22:743-747.

22.Zetterstrom C, Laurell CG. Comparison of endothelial cell loss and phacoemulsification energy during endocapsular phacoemulsification surgery. J Cataract Refract Surg. 1995;21:55-58.

et al. Endothelial damage with cataract surgery techniques.

J Cataract Refract Surg. 1998;24:951-955.

24.Trindade F, Pereira F. Exchange of a posterior chamber phakic intraocular lens in a highly myopic eye. J Cataract Refract Surg. 2000;26:773-776.

25.Rosen E, Gore C. STAAR collamer posterior chamber pha-

kic intraocular lens to correct myopia and hyperopia.

J Cataract Refract Surg. 1998;24:596-606.

26.Pop M, Payette Y, Mansour M. Predicting sulcus size using ocular measurements. J Cataract Refract Surg. 2001;27: 1033-1038.

INTRODUCTION

Over the past 50 years, the goal of refractive surgery has been to eliminate the refractive error of the eye in order to achieve emmetropia. The measures of outcome have included the uncorrected Snellen visual acuity, the residual refractive error, incidence of retreatments, and complications. These measures are no longer sufficient with modern refractive surgery.1

Recent developments in the instrumentation and analysis of wavefront technology have provided the tools to analyze the optical elements of the eye independently and collectively as a system.2-6 Studies using these new instruments have demonstrated that the optical performance of the human eye is much better in the young and that there is a predictable, progressive decrease in the performance of the eye with age.7-13 Most of the degradation in image quality is due to changes in the crystalline lens.14-18

These studies have shown that the cornea and crystalline lens are optically coupled in a way in which the sum of the elements is better than either element performing independently. The cornea is prolate with an average Q-value in the population of approximately -0.26 (Figure 5-1).19 The Q-value of a sphere is zero and the Q-value of the perfect single surface for eliminating spherical aberration is -0.50, a parabola. Because the average cornea has a Q-value midway between the sphere and the parabola, the cornea has about half of the spherical aberration of a true sphere. Because the cornea is not a simple single refracting surface, the exact Q-value to eliminate spherical aberration is -0.52.

The crystalline lens, however, is dynamic and changes with increasing spherical aberrations throughout life. The crystalline lens has a negative spherical aberration in the young that is almost equal and opposite to the remaining positive spherical aberration in the cornea (Figure 5-2).15 The young eye is very well corrected, but as the crystalline lens begins to age, the lens spherical aberration goes from negative to positive, crossing zero at about age 40. The result is a progressive increase in the total ocular spherical aberration of the eye, with age starting shortly after birth (Figures 5-3 and 5-4).

DEFINING OPTICAL

QUALITY OF THE HUMAN EYE

The optical quality of the eye can be evaluated by high contrast Snellen acuity, wavefront analysis, and contrast sensitivity. Other factors, such as color vision and visual fields, are also important to visual function but are not considered clinical measures of optical quality.

Optically, high contrast Snellen acuity is the limiting resolution of the eye. Although standard visual acuity testing involves recognition, which is more complex than simple resolution, it is still considered the limiting resolution of the eye in clinical terms. Wavefront devices objectively measure the quality of the wavefront entering (ie, patient’s view) or leaving (ie, measurement view) the eye. The difference from the perfect spherical wavefront is a measure of the quality of the optical system. The data from the wavefront can be transformed into point spread func-

Figure 5-1. The cornea is prolate with an average Q-value in the population of ~0.26 (reprinted from J Cataract Refract Surg, 25(5), Holladay JT, Dudeja DR, Chang J, Functional vision and corneal changes after laser in situ keratomileusis determined by contrast sensitivity, glare testing, and corneal topography, pp. 663-669, with permission from the American Society of Cataract and Refractive Surgery and The European Society of Cataract and Refractive Surgery).

Figure 5-3. The young eye has almost no spherical aberration.

tion (PSF) and modulation transfer function (MTF), which are used to describe the quality of any optical system, such as cameras, microscopes, and telescopes.

Contrast sensitivity is a subjective measure of the patient’s visual system. This test actually determines the “threshold” of the lowest contrast optotype that can be detected. The size of the optotype (spatial frequency) is usually described in degrees so it can be related to a visual angle. Testing may be done with any optotype, but the primary tests that have been used historically are low contrast letters and sinusoidal gratings. The scientist prefers the sinusoidal gratings because it is a pure frequency and it is easy to make transformations and perform analyses. The low contrast letters are preferred by clinicians because

Figure 5-2. The crystalline lens has a negative spherical aberration in the young that is almost equal and opposite to the remaining positive spherical aberration in the cornea.

Figure 5-4. The older eye has significant spherical aberration.

they are similar to standard acuity testing and easily understood by the patient. The letters have higher order spatial frequencies (the corners of the letters) and require “recognition” of the letter, which complicates the idea of threshold detection. Snellen visual acuity and contrast sensitivity are the main subjective measurement outcomes of the entire visual system (optical and sensory), and wavefront the objective measure of the optical component of the visual system.

OPTICAL QUALITY OF

PHAKIC INTRAOCULAR LENSES

Phakic intraocular lenses (IOLs) are implanted in three locations: anterior chamber angle, iris supported, and poste-

rior chamber. The primary problem with the slow acceptance of phakic lenses into the refractive market is related to the surgical complications rather than any optical problems.

The angleand iris-supported lenses have the same problems as lenses supported by uveal tissue (ie, iritis, glaucoma, and ovalization of the pupil). Optical problems with these two lenses have been related to the size of the optic. When the optic is less than 5.0 mm in diameter, many patients complain of glare. When the lens is larger than 6.0 mm, endothelial cell loss becomes a problem. For patients with 5.5 mm pupils or less, these lenses provide good optical quality when they are well-centered and not tilted. For patients with larger pupils, light travels around the lens and through the pupil, causing secondary images and edge glare. If the lenses are tilted or decentered, astigmatism and coma aberrations are induced into the optical system, reducing visual performance.

Phakic IOLs in the posterior chamber (ie, intraocular contact lens [ICL] and phakic refractive lens [PRL]) are optically excellent, but surgical problems, such as pupillary block, anterior subcapsular cataract, and pigmentary dispersion, have prevented wide-spread use. If none of these surgical problems arise, high contrast visual acuity, contrast sensitivity, and wavefront analysis remain virtually unchanged after implantation, except for induced spherical aberration when the surfaces are spherical. In the near future, modified prolate aspheric phakic IOLs will be available, reducing or eliminating the induced and preoperative spherical aberration of the eye.20,21

PHAKIC INTRAOCULAR

LENSES AS AN ALTERNATIVE

TO KERATOREFRACTIVE SURGERY

Phakic IOLs provide an attractive alternative to keratorefractive surgery, particularly for larger refractive errors (>12 diopters [D]). The only common, presently used keratorefractive procedure that can achieve corrections at or above this range is laser in-situ keratomileusis (LASIK). The optical quality of the vision in these high myopic cases has been less than desirable. The primary reason for the marginal optical performance is due to the small optical zone, extreme oblate aspheric shape, and microirregularities (increase root mean square [RMS] surface values) that occur following the procedure.

Although improvements with scanning lasers, custom ablations, and improved algorithms for reshaping the cornea will certainly improve these results, the physical limitations of corneal thickness prevent this procedure from ever reshaping the cornea to the original prolate aspheric shape with the original optical zone and surface regularity. Because of this physical barrier for LASIK, phakic IOLs offer an attractive alternative.

Phakic IOLs have several advantages. They do not change the characteristics of the normal cornea and offer the potential of maintaining or possibly improving the optics of the eye. Because the phakic IOLs are nearer the pupil, the optical zones can be proportionately smaller than corresponding corneal treatments to obtain the same effective optical zone. The smooth surfaces of phakic IOLs are well above the optical limit of the eye and, therefore, provide no reduction in the RMS (surface regularity) optical quality of the retinal image, unlike the microirregularities induced in the cornea by LASIK. Furthermore, the procedure is reversible by removing or exchanging the lens.

As with any procedure, there are always tradeoffs. For phakic IOLs the disadvantages include the risk of an intraocular procedure with endothelial cell loss; possible infection; and contact with the crystalline lens, causing a cataract. Although removal and exchange are possible, it re-exposes the patient to another intraocular procedure and all of the risks associated with the procedure. Anterior chamber phakic IOLs contact uveal tissue and have the potential of inducing chronic iritis; pupillary distortion; endothelial cell loss; secondary glaucoma; and related posterior changes, such as cystoid macular edema. Posterior chamber phakic IOLs (ie, ICLs) do not contact uveal tissue, but may contact the anterior crystalline lens, which can cause a cataract. When the lens is vaulted properly over the crystalline lens, it may contact the posterior iris, causing pigment dispersion, transillumination defects in the iris, and pigmentary glaucoma. A larger vault can be created by increasing the diameter to avoid contact with the crystalline lens, but it may cause chaffing of the zonules, ciliary processes, or the sulcus, which may lead to a pseudoexfoliation syndrome or uveitis. ICLs may also lead to a pupillary block if the peripheral iridectomies are not patent or absent, which can lead to extremely high pressure and result in the same damage to the eye as an acute narrow angle attack: “blown” pupil and ischemia of the optic nerve and retina, causing blindness.

Because phakic IOL complications have been extremely rare and the quality of the optics of the eye are preserved, increasing numbers of phakic IOLs are being implanted throughout the world. Understanding the clinical and theoretical basis for IOL power calculations in these cases is extremely important.

NECESSARY MEASUREMENTS

FOR PHAKIC AND

PSEUDOPHAKIC INTRAOCULAR

LENS CALCULATION FORMULAS

Several measurements of the eye are helpful in determining the appropriate IOL power to achieve a desired refraction. These measurements include central corneal