Juan J. Pérez-Santonja, MD; José L Bueno, MD; Miguel A. Zato, MD
BACKGROUND: Implanting an anterior chamber intraocular lens in a phakic eye is an effective surgical procedure for the correction of high myopia. However, the potential risks on the anterior segment structures are not well-known. We conducted a prospective study to evaluate the effectiveness, predictability, and safety after Worst-Fechner lenses were implanted to correct high myopia.
METHODS: We studied 32 eyes with preoperative myopia from -9.50 to -27.00 diopters (D) (-16.60 + 6.29 D). All 32 eyes were studied by clinical specular microscopy, and the endothelium was analyzed for cell density. Twenty eyes were additionally examined by fluorophotometry for lens transmittance changes. Thirty eyes were additionally examined using the flare mode of a laser flare cell photometer for anterior chamber !inflammation; the patients were divided into three subgroups of ten eyes each according to when the postoperative flare measurements were done: 12 months, 18 months, and 24 months. Thirteen phakic eyes with myopia greater than -6.00 D were used as a control group for the flare study. The mean follow-up was 18.3 + 8 months (range 6 to 24 mo).
RESULTS: Fifty-seven per cent of eyes (16 of 28) had an uncorrected visual acuity of 20/40 or better 12 months after surgery, and 58% (10 of 17 eyes) at 24 months. Spectacle-corrected visual acuity unproved: 0.15 at 12 months and 0.16 at 24 months (0.1 = one line) from preoperative values. Visual acuity was stable after 3 months. Eighty per cent of eyes (25 of 31) at 6 months, 75% (21 of 28) at 12 months, and 76.5% (13 of 17) at 24 months had been correctly planned to within +1.00 D of emmetropia. The refractive results were stable 3 months after surgery. The mean endothelial cell loss was 7.2% at 3 months, 10.6% at 6 months, 13% at 12 months, and 17.6% at 24 months after surgery. The mean lens transmittance loss was 0.62% at 3 months, 0.72% at 6 months, 0.82% at 12 months, and 1.03% at 18 months after surgery. Flare values were significantly higher for eyes implanted with WorstFechner lenses than were those of the control group in all periods under consideration (MannWhitney test, ? < 0.05). A decentration greater than 0.5 mm was present in 43% of eyes (14 of 32), and halos in 56% (18 of 32). In three eyes (9.3%), fixation of the lens to the iris was not stable.
CONCLUSIONS: Our results for the WorstFechner myopia lens confirm earlier findings on the effectiveness of the refractive results. However, our study showed a continual decrease in endothelial cell density, a decrease in lens transmittance, and a chronic subclinical inflammation after the implantation of these lenses. Moreover, decentration was common, and the fixation of the IOL to the iris was not stable in some eyes. [J Refract Surg 1997;13:268-284]
The implantation of an anterior chamber intraocular lens (IOL) in a phakic eye to correct high myopia, first developed and later abandoned in the 1950s by Strampelli1 and Barraquer2, was recently revived by Fechner et al3 with an iris claw lens, and by JoIy et al4 with an anglesupported lens derived from the Kelman multiflex implant. This procedure achieves better optical results than other procedures for the correction of high myopia5 7, although its long-term complications are poorly known.7"9 In 1986, Worst and Fechner changed an existing iris claw lens used in cataract surgery into a negative biconcave lens for the correction of high myopia.3,10 Since then, this biconcave Worst-Fechner lens has provided accurate, predictable, and stable refractive results, and a low rate of early complications.7·8,11,12 Implanting an anterior chamber intraocular lens in phakic eyes raises many questions concerning the long-term potential risks to corneal endothelium, lens, anterior uvea, and other eye structures. In this prospective study, we evaluate the effectiveness, predictability, and potential risks after the implantation of Worst-Fechner lenses.
Figure 1 : Worst-Fechner lens. The temporal haptic is well enclavated but the nasal haptic enclavation is poor (arrow).
PATIENTS AND METHODS
Patient Selection and Examination
We studied prospectively 32 eyes (19 patients) hi whom a Worst-Fechner biconcave iris fixated lens to correct myopia (Ophtec BV, Groningen, The Netherlands)(Fig 1) was implanted by the same surgeon (M.A.Z.) between September 1990 and December 1993 at Jiménez-Díaz Foundation, Madrid, Spain.
Patient selection criteria were: age greater than 20 years; stable myopia greater than -9.50 D; unsuccessful attempt to wear contact lenses; refusal to wear spectacles because of severe psychological inhibition; normal anterior segment with an anterior chamber depth greater than 3.2 mm; endothelial cell density greater than 2300 cell/mm2; normal peripheral retina or treated with photocoagulation when necessary; no general health problems. The risks of this operation were fully explained to the patients, in accordance with the Helsinki declaration.
In this main group of 32 eyes, patient age ranged from 27 to 51 years (mean 36.12 ± 7.9 yrs). There were three males (five eyes) and 16 females (27 eyes). Preoperative refractive error ranged from -9.50 to -27.00 D (mean -16.60 ± 6.29 D). Examination before and after surgery included visual acuity, manifest and cyclopegic refraction, slit-lamp microscope examination, applanation tonometry, endothelial specular microscopy, and indirect ophthalmoscopy. Postoperative examinations were conducted at 1, 3, 6, 12, 18, and 24 months. A questionnaire was used to evaluate night halos 6 months after surgery. The mean follow-up was 18.3 ± 8 months (range 6 to 24 mo).
We used both parametric and nonparametric statistical analyses, based on the distribution of the data under consideration. Group differences for continuous variables were tested using the paired Student's ¿-test (two groups) or two-way analysis of variance (more than two groups) for normally distributed data and the Wilcoxon test for nonnormally distributed data. Differences for categorical variables were tested using the chi-square (x2) test for independence. Correlations between continuous variables were obtained using Pearson's correlation coefficient. Differences were considered statistically significant when the ? value was less than 0.05.
Corneal endothelium- The 32 eyes of the main group were studied by clinical specular microscopy Specular microscopy was performed with a video specular microscope (LSM 2000C wide field corneal contact specular microscope, Bio-Optics, Inc., Arlington, Mass) adapted to a video digitization image analysis system (Bio-Optics Thumper Video Digitization Image Analysis System, Bio-Optics, Inc., Arlington, Mass). Between two and three specular microscopic images of the central portion of each cornea were taken using the specular microscope video camera and sent to the image analysis system for digitization. Between 150 and 250 cells were digitized and analyzed for each cornea using the BioOptics Thumper video image analysis software. Using the "cell count vf" program, the endothelium was analyzed for cell density (cells/mm2) and was calculated automatically by the computer.
The paired Student's ¿-test and analysis of variance (two-way) were employed. Differences were considered statistically significant when the ? value was less than 0.05.
Lens transmitt ance -Twenty eyes of the main group were additionally examined by fiuorophotometry for lens transmittance changes. Although all patients of the main group were asked to have fluorophotometry, not all patients agreed to do so. Preoperative and postoperative fluorophotometric results were compared. Postoperative examinations were conducted at 1, 3, 6, 12, and 18 months.
A fluorophotometer (FM-2 Fluorotron Master, Coherent Radiation, Palo Alto, Calif)13 was used and the scan was performed automatically and displayed on a screen in concentration units versus distance from the retina. A reading was obtained for each discrete step, starting at a position posterior to the retina and ending at a position anterior to the cornea. Each measurement was calibrated by an automatic reading of an internal fluorescent glass. In our instrument, the in vitro lower limit of detection was 0.5 ng/ml, the axial resolution was 1.5 mm, and the error of measurement was 10% for concentrations of approximately 1 ng/ml. In this study, two steps per milimeter and 130 ms of exposure time per step were used.
We evaluated the anterior and posterior lens autoüuorescence and used the Van Best method14,15 to determine lens transmittance (the square root of the ratio of the posterior lens autofluorescence to the anterior lens autofluorescence). Although an anterior chamber lens can decrease lens autofluorescence, both anterior and posterior lens autofluorescence would be affected equally, hence the lens transmittance result would remain unchanged.16
The paired Student's i-test and analysis of variance (two-way) were applied and differences were considered statistically significant when the ? value was less than 0.05.
Anterior chamber inflammation- Thirty eyes of the main group were additionally examined using the flare mode of a laser flare cell photometer for anterior chamber inflammation. The patients were divided into three groups according to the follow-up period during which flare measurement was performed: ten eyes at 12 months, ten eyes at 18 months, and ten eyes at 24 months.
A group of 13 normal eyes (without implants) with myopia greater than -6.00 D, age and sex matched with the problem group, was used as a control group.
Anterior segment inflammation was measured with a laser flare cell meter (Kowa FC-1000, Kowa Electronics and Optics, Tokyo, Japan). The instrument measures the intensity of back-scattered light produced in the anterior chamber by a constantpower helium-neon laser beam.17 Flare intensity is proportional to the content and size of aqueous humor proteins, reflecting blood-aqueous barrier disruption.17,18 We chose to express aqueous flare in photon counts per millisecond (photons/ms), rather than convert the values into traditionally reported bovine albumin equivalent values expressed in milligrams per milliliter.19 The laser flare cell meter also counts cells (particle mode) in a volume of 0.075 mm3. Because the instrument is more sensitive and reproducible, and has better correlation with slit-lamp grading for anterior chamber flare measurements than for cell measurements20,21, we evaluated only flare data. Five measurements were taken for each eye, obtaining the mean and the standard deviation. The pupil was not dilated. Our laser flare cell meter device was regularly and continuously calibrated.
Data were processed for statistical analysis with the Mann- Whitney test (two independent groups) and the Kruskal- Wallis test (more than two independent groups) because of the limited number of eyes in our study. Differences were considered statistically significant when the ? value was less than 0.05.
Worst-Fechner Biconcave Lens, Surgical Technique, and Medication
The features of the Worst-Fechner iris fixated biconcave lens were described by Fechner and coauthors.3,7,8,12 The IOL is made of one-piece polymethylmethacrylate (PMMA). The total length of the lens is 8.5 mm with an optic diameter ranging from 4 to 5 mm, depending on the lens power (the greater the IOL power, the lower the optic diameter). The total height of the lens does not exceed 0.93 mm, regardless of power. The lens powers range from -5.00 to -20.00 D and it is manufactured in 1.00-D steps. The two diametrically opposed haptics fixate the lens on the iris by enclavation of midperipheral iris stroma.
Intraocular lens power was calculated using van der Heijde's formula.22
One hour before surgery, the pupil was constricted with pilocarpine 2%, and 100 mg of 6-methylprednisolone were intravenously administered. All procedures were done under general anesthesia.
A fornix-based flap was prepared from 10 to 2 o'clock. Then three corneoscleral incisions were made: one incision from 10:30 to 1:30 o'clock, and two small incisions 2.0 mm-long in the 3 and 9 o'clock positions, respectively. Then, the anterior chamber was washed with acetylcholine and filled with viscous material, usually hyaluroic acid 1% (Healon, Kabi Pharmacia, Barcelona, Spain). The IOL was then inserted from the 12 o'clock large incision and rotated with two hooks into a horizontal position over the pupil. A lens fixation forceps was inserted through the large incision and one haptic of the lens was grasped. The anterior chamber was entered through the ipsilateral small wound with iris forceps, and a 1-mm iris fold was picked up and pulled through the slit in the haptic. The maneuver was then repeated on the other side with the aim of achieving perfect centration of the IOL. Finally, all the viscoelastic material was carefully removed with balanced salt solution, and the large incision was closed with a running 10-0 nylon suture.
Figure 2: Time course of uncorrected visual acuity (UCVA), and spectacle-corrected visual acuity (SCVA) (mean ± standard deviation). Numbers in parentheses indicate number of eyes studied at each time period.
All patients received a 4 mg subtenon's injection of dexamethasone at the end of the procedure. On the first postoperative day, 100 mg of prednisone was administered orally. The eyes numbered from 12 to 32 received 500 mg of acetazolamide orally 6 hours after surgery. Drops containing 0.10% fluorometholone were administered five times a day for 3 weeks, then reduced in frequency for 1 additional week. Patients were given topical cyclopentolate 1% three times a day during the first two postoperative weeks. Antiglaucomatous medication was administered when required.
To evaluate visual acuity we must take into account the reduced levels of uncorrected and spectacle-corrected visual acuity in patients with high myopia due to myopic chorioretinal degeneration.
Preoperative mean uncorrected visual acuity was 0.016 ± 0.008 in 32 eyes, and after surgery, mean uncorrected visual acuity increased to 0.41 ± 0.22 at 1 months, 0.52 ± 0.20 at 3 months, 0.52 ± 0.20 at 6 months, 0.49 ± 0.20 at 12 months, 0.44 ± 0.19 at 18 months, and 0.44 ± 0.22 at 24 months (Fig 2). No patient had an uncorrected visual acuity of 0.5 (20/40) or better before surgery. However, 62% of eyes (20 of 32 eyes) had an uncorrected visual acuity of 0.5 (20/40) or better 3 months after surgery, 57.2% (16 of 28 eyes) at 12 months, and 58.8% (10 of 17 eyes) at 24 months. No patient had an uncorrected visual acuity of 1.0 (20/20) before or after surgery. Postoperative uncorrected visual acuity was significantly better than preoperative values at all follow-up points (Wilcoxon test,p<0.001 at 1, 3, 6, and 12 months; ? < 0.01 at 18 and 24 months). There were no statistically significant differences in uncorrected visual acuity after 3 months (analysis of variance, p>0.05).
Preoperative mean spectacle-corrected visual acuity was 0.47 + 0.18, and after surgery, spectacle-corrected visual acuity increased to 0.55 ± 0.19 at 1 month, 0.63 ± 0.18 at 3 months, 0.63 ± 0.18 at 6 months, 0.62 ± 0.20 at 12 months, 0.58 ± 0.19 at 18 months, and 0.59 ± 0.19 at 24 months (Fig 2). Spectacle-corrected visual acuity improved 0.15 at 12 months, and 0.16 at 24 months (0.1 = one line) with regard to preoperative values. Postoperative spectacle-corrected visual acuity was significantly better than preoperative values at all follow-up points (paired Student's ¿-test,p<0.001). There were no statistically significant differences in spectacle-corrected visual acuity after 3 months after surgery (analysis of variance, p>0.05). Only one eye (3.1%) lost two lines of spectacle-corrected visual acuity, probably because of progression of myopic macular degeneration.
Postoperative uncorrected visual acuity was equal to or better than preoperative spectaclecorrected visual acuity in 64% of eyes (18 of 28 eyes) at 12 months, and 71% (12 of 17 eyes) at 24 months. However, these differences were not significant (paired Student's ¿-test, p=0.54 preoperative spectacle-corrected visual acuity vs. 12-month postoperative uncorrected visual acuity; p=0.67 preoperative spectacle-corrected visual acuity vs. 24month postoperative uncorrected visual acuity).
Figure 3: Refractive results in eyes where full correction was attempted (mean ± standard deviation). Numbers in parentheses are number of eyes studied at each time period.
Our data show an improvement in both uncorrected and spectacle-corrected visual acuity after insertion of Worst-Fechner lenses, and stability in visual acuity 3 months after surgery.
We did not try to achieve emmetropia in all eyes. Because the IOL was available in powers up to -20.00 D, eyes with myopia higher than -22.00 D could only be undercorrected (six eyes). The IOLs were not available in all the desired strengths (two eyes).
In eyes where full correction was attempted, we still could not achieve emmetropia, since the IOL was available only in 1.00-D steps. In 24 eyes of the main group, we tried to achieve full correction, and they constituted the emmetropia group. For this group, mean preoperative spherical equivalent refraction was -14.24 ± 3.12 D, decreased to -0.04 ± 0.90 D 1 month after surgery, +0.28 ± 0.61 D at 3 months, +0.16 + 0.60 D at 6 months, +0.15 ± 0.62 D at 12 months, -0.22 + 0.80 D at 18 months, and -0.08 ± 0.77 D at 24 months (Fig 3). The difference between preand postoperative values was statistically significant for all follow-up points (paired Student's ¿-test, p<0.001). There were no statistically significant differences when postoperative values after 3 months were compared (analysis of variance, p>0.05), indicating stability in refractive outcome. In 91% of eyes (21 of 23 eyes) at 6 months, 85% (18 of 21 eyes) at 12 months, and 81% (9 of 11 eyes) at 24 months, the postoperative spherical equivalent was within +1.00 D. All eyes were within ±_2.00 D of emmetropia.
To assess the accuracy of the correction, including those eyes in which emmetropia had not been the aim, we calculated the expected correction with lens implantation for all eyes, as well as the difference between the calculated and achieved correction.
Preoperative mean spherical equivalent was -16.60 + 6.29 D, and after surgery, mean deviation of the achieved from the calculated correction was +0.41 ± 1.03 D at 1 month, +0.68 ± 0.94 D at 3 months, +0.62 ± 1.06 D at 6 months, +0.54 ± 0.95 D at 12 months, +0.11 ± 0.91 D at 18 months, and +0.22 + 0.99 D at 24 months (Fig 4). There was no significant difference between 3 and 12 months (analysis of variance, p>0.05), although a slight significant myopic shift was noted at 24 months after surgery (p<0.05, 12 vs. 24 months). Eighty percent of eyes (25 of 31 eyes) at 6 months, 75% (21 of 28 eyes) at 12 months, and 76.5% (13 of 17 eyes) at 24 months had been precalculated correctly to within ± 1.00 D. Moreover, 45% of eyes (14 of 31 eyes) at 6 months, 53% (15 of 28 eyes) at 12 months, and 53% (9 of 17 eyes) at 24 months, had been precalculated correctly to within + 0.50 D. Only 9.5% of eyes at 6 months, 7% at 12 months, and 6% at 24 months deviated by more than 2.00 D from the calculated correction.
Our study shows good predictabüity after insertion of Worst-Fechner lenses, and stability of refractive results, although a minimal myopic shift was observed during the second year after surgery.
Figure 4: Deviation of the achieved from the calculated correction (mean ± standard deviation). Numbers in parentheses indicate number of eyes studied at each time period.
Figure 5: Time course of endothelial cell density after Worst-Fechner lens implantation (mean ± standard deviation). Numbers in parentheses indicate number of eyes studied at each time period.
Preoperative mean cell density was 2433 + 174 cells/mm2 and after surgery, mean cell density decreased to 2258 + 209 cells/mm2 at 3 months, 2158 ± 243 cells/mm2 at 6 months, 2104 ± 257 cells/mm2 at 12 months, and 1972 + 296 cells/mm2 at 24 months (Fig 5). Postoperative endothelial cell density was significantly lower than preoperative values in at all follow-up points (paired Student's ¿-test, p<0.001, preoperative vs, 3, 6, 12, and 24 month postoperative values). There was also a statistically significant difference when 3 vs. 12 month, and 12 vs. 24 month postoperative cell densities were compared (analysis of variance, ? <0.05, 3 vs. 12 months, p<0.05, 12 vs. 24 months).
Endothelial cell loss was 7.2% at 3 months, 10.6% at 6 months, 13% at 12 months, and 17.6% at 24 months after surgery.
Our data show a continual decrease in endothelial cell density after insertion of Worst-Fechner lenses, and an unstable cell loss between 1 and 2 years after surgery.
Figure 6: Time course of lens transmittance after Worst-Fechner lens implantation (mean ± standard deviation). Numbers in parentheses indicate number of eyes studied at each time period.
Preoperative mean lens transmittance was 0.973 + 0.009 and after surgery, mean lens transmittance changed to 0.970 ± 0.009 at 1 month, 0.967 ± 0.007 at 3 months, 0.966 ± 0.009 at 6 months, 0.965 ± 0.007 at 12 months, and 0.963 ± 0.008 at 18 months (Fig 6). At 1 month after surgery, lens transmittance was not significantly lower than it was preoperatively (paired Student's i-test, p=0.088). However, a decrease in lens transmittance was noted at 3, 6, 12, and 18 months after surgery (paired Student's i-test used to compare preoperative vs. postoperative lens transmittance, p=0.003 at 3 months, p<0.001 at 6 months, p=0.005 at 12 months, and p=0.005 at 18 months). There was also a statistically significant difference between 1 and 6 months (analysis of variance, p<0.05), between 1 and 12 months (p<0.05), and between 1 and 18 months (p<0.05). The difference was not significant when 3 and 6-month (p>0.05), 6 and 12-month (p>0.05), and 12 and 18month (p>0.05) postoperative lens transmittance values were compared.
Lens transmittance loss was 0.62% at 3 months, 0.72% at 6 months, 0.82% at 12 months, and 1.03% at 18 months after surgery.
Our results show a decrease in lens transmittance after 3 months from the implantation of Worst-Fechner lenses. Although a continual decrease in lens transmittance was noted postoperatively, the change was small.
Anterior Chamber Inflammation
Postoperative flare results were 27.05 + 19 photons/ms (range 11.3 to 70.9 photons/ms) at 12 months; 18.09 ± 17.38 photons/ms (range 5 to 60 photons/ms) at 18 months; and 31.03 ± 28.8 photons/ms (range 11.94 to 110 photons/ms) at 24 months after surgery (Fig 7).
Flare results in the control group were 4.24 ± 2.8 photons/ms (range 0 to 10.5 photons/ms). Flare values were significantly higher for eyes implanted with Worst-Fechner lenses than for those of the control group at all follow-up points (Mann-Whitney test, p<0.05). There were not statistically significant differences among 12, 18 and 24-month postoperative flare values in eyes implanted with WorstFechner lenses (Kruskal-Wallis test,p>0.05).
Our data show a chronic subclinical inflammation between 1 and 2 years after implantation of Worst-Fechner lenses.
There is a significant relationship between the flare values and endothelial cell density: the higher the flare values, the lower the cell density (Pearson's correlation coefficient r=-0.38, p<0.05). The longer the follow-up, the stronger the correlation between intraocular inflammation and endothelial cell loss (r=-0.18 at 12 months, r=-0.33 at 18 months, and r=-0.38 at 24 months), although the number of eyes in groups was too small to produce a significant correlation.
Figure 7: Flare values in eyes implanted with Worst-Fechner lenses, and in a control group (mean ± standard deviation).
Figure 8: Correlation between flare and endothelial cell density (r = Pearson's correlation coefficient).
Our results show a relationship between intraocular inflammation and endothelial cell loss; chronic intraocular inflammation may play a role in the decline of endothelial density in eyes implanted with Worst-Fechner lenses (Fig 8).
Giant papillary conjunctivitis- Ocular itching and giant conjunctival papillae were present in three eyes (9.3%). In two eyes, it appeared at 3 months, and in one eye at 6 months after surgery. All cases were related to exposed nylon sutures. Removal of sutures and cromolyn sodium 4% eye drops were successful in all eyes.
Postoperative uveitis- All clinical signs of anterior chamber inflammation disappeared between 2 and 5 weeks after surgery. In three eyes (9.3%) an inflammatory response was observed during follow-up: one eye at 3 months, one eye at 6 months, and one eye at 24 months. All eyes improved with corticosteroid eye drops.
Figure 9: In this eye, the nasal haptic escaped from the iris fold 6 months after surgery, and the lens dislocated into the inferior angle.
Corneal pigment deposition- Six eyes (18.7%) developed pigment deposition on the corneal endothelium in a vertical pattern. This pigment deposition appeared between 6 and 18 months after surgery, and suggests a pigment release from the iris induced by the IOL. None of these eyes developed high intraocular pressure.
Cystic wounds- Six eyes (18.7%) developed a subconjunctival fistula between 1 and 4 weeks after surgery that required resuturing of the wound in two eyes. None of these eyes developed flattening of the anterior chamber.
Elevated intraocular pressure- Presumably, steroid induced elevated intraocular pressure (IOP > 22 mmHg) complicated the postoperative course in five eyes (15.6%) during the first month after surgery. After the corticosteroids were discontinued, the elevated intraocular pressure resolved. In none of the operated eyes did the rise of intraocular pressure persist more than 6 weeks after surgery.
Decentration and halos- Decentration was calculated as the distance between the center of the IOL and that of the pupil by means of slit-lamp microscopy, using visual inspection and slit-lamp beams of 0.2, 0.5 and 1 mm. Based on this method, we found 31% of eyes (10 of 32 eyes) with a decentration between 0 and 0.25 mm, 25% of eyes (8 of 32 eyes) between 0.26 and 0.50 mm, 28% (9 of 32 eyes) between 0.51 and 0.75 mm, and 15% (5 of 32 eyes) between 0.76 and 1 mm.
In 56% of eyes (18 of 32 eyes), halos were present after surgery. In the eyes with a decentration between 0 and 0.25 mm, only 10% of patients complained of halos; in eyes with a decentration between 0.26 and 0.50 mm, 50% of patients complained of halos; in eyes with a decentration between 0.51 and 0.75 mm, 88% complained of halos; and in eyes with a decentration between 0.76 and 1.00 mm,100% complained of halos. There is a significant relationship between decentration and halos: the greater the decentration, the higher the incidence of halos (X2 test=16.44, p<0.001; Contingency coefficient = 0.58 [0.70 = the highest relationship]).
Fixation of IOL- Three eyes (9.3%) did not show atrophy in the area of fixation, three eyes (9.3%) showed atrophy in the area of fixation on one side, and 26 eyes (81%) showed atrophy on both sides.
In one eye (3%) the nasal haptic escaped from the iris fold 6 months after surgery (Fig 9). Another surgery was required to put the lens in place. In the other two eyes (6.2%), the iris claw itself perforated the iris fold (in one eye at 12 months, and in the other eye at 24 months) causing a lens displacement and halos.
Lens opacities- No contact was noted between the IOL and the natural lens, either with a narrow or a wide pupil. One eye (3%) developed an anterior subcapsular opacity postoperatively, although the visual axis was not involved. This opacity did not progress during the follow-up period.
Funduscopy- The visualization of the peripheral fundus through a dilated pupil was more difficult than in eyes without anterior chamber lenses. No patient developed retinal detachment after surgery.
Refractive correction of high myopia is a controversial and difficult clinical problem. High myopia spectacles are thick and induce optical aberrations and limitations in the visual field, as well as poor cosmetic appearance. Contact lenses offer better visual results than spectacles, but a number of patients cannot tolerate these lenses. At the present time, there is not a completely satisfactory surgical procedure for the correction of high myopia. The upper limit of correction that can be achieved with radial keratotomy is generally thought to be -8.00 D.23 Epikeratoplasty for myopia has not proven to be accurate.24"26 Intracorneal lenses have not yet proven to be safe and effective.27·28 Clear lens extraction and low power IOLs have not gained wide acceptance due to complications such as retinal detachment29·30 and accommodation loss.31 Keratomileusis for myopia (traditional technique) offers moderate predictability32·33, although the complexity of the procedure and the frequent irregular astigmatism (9 to 28%) have limited its use.32·34 Keratomileusis in situ for myopia has not improved the traditional technique results.35,36 Excimer laser photorefractive keratectomy (PRK) offers good predictability, efficacy, and safety in low to moderate myopia37·38; however, poor predictability, regression of effect and corneal haze appear in high myopia.39·40 Multizone PRK has been suggested to increase the predictability of higher myopic corrections with less haze.41·42 However, no major differences were reported when single-zone treatment was compared with multizone treatment.41,43 In recent years, laser in situ keratomileusis (LASIK) has generated high expectations among refractive surgeons for the correction of high myopia44"46, although it is still under clinical investigation.
Implanting a phakic anterior chamber lens in high myopic eyes has generated a renewed interest because it is one of the most satisfactory surgical techniques for the correction of high myopia.59 Nevertheless, its long-term potential risks to the corneal endothelium, lens, and anterior uvea are not well-known.
Clinical results following refractive surgery are evaluated according to efficacy, predictability, stability, and safety. Uncorrected visual acuity is the main criterion used to assess the effectiveness of a refractive procedure.47 Several studies5·48·49 reported that between 46 and 64% of eyes have an uncorrected visual acuity of 20/40 or better after surgery, regardless of the type of phakic anterior chamber lens used. Concerning predictability, several authors5,8,12·48,49 have arrived at similar conclusions, regardless of the type of lens used; between 63 and 77% of eyes have a final refraction within 1.00 D of emmetropia. Long-term stability of the refractive effect achieved by phakic intraocular lenses has also been reported5,8,9,12,49. Additionally, Fechner et al8 reported that in 78% of eyes, spectacle-corrected visual acuity increases by one or two lines. These results have been confirmed by Baikoff and Colin6,9 for angle-supported lenses. The gain in visual acuity is caused by an enlargement of the retinal image due to the magnification effect of myopic intraocular lenses.50·51 Our results concerning effectiveness, predictability, stability, and improvement of spectaclecorrected visual acuity confirm the findings of these investigations on phakic anterior chamber lenses. The decrease in spectacle-corrected visual acuity in one eye of our series could be related to progression in myopic macular degeneration.
Therefore, if one considers optical improvements, the implantation of an anterior chamber intraocular lens in a phakic eye is probably the most satisfactory surgical procedure currently available for correcting high myopia. However, the long-term safety of this technique has yet to be determined. The potential hazard of the anterior chamber lens for the fragile surrounding ocular tissue in the anterior chamber was worrisome in all previous studies. The main issues concerning phakic anterior chamber lens safety are corneal endothelial damage, chronic iridocyclitis, and postoperative complications.
Concerning the corneal endothelium and sequential endothelial cell loss after the implantation of Worst-Fechner biconcave lenses, Fechner et al7 in their series of 65 eyes with a mean follow-up of 1 year reported that endothelial cell density decreased to approximately 1500 cells/mm2 in two eyes (3.2%) after implantation of Worst-Fechner lenses. Except for these two eyes, the authors did not find a continuous loss of endothelial cells during the follow-up period. In that study, the non-contact Karickhoff method was used for monitoring endothelial cell density, although this method has been considered inadequate for monitoring endothelial cell counts in a study that proposed to demonstrate the safety of a technique which is an obvious potential threat to the endothelium.52 Fechner et al8, in a series of 109 eyes with Worst-Fechner lenses and a mean follow-up of 2 years, found endothelial damage related to operative difficulties in 4% of eyes, and endothelial damage unexplained by surgery in 4% of eyes. Four eyes (3.2%) developed corneal decompensation. This study was also based on the Karickhoff method for monitoring endothelial density. These authors suggested that the closeness of the intraocular lens to the endothelium and the temporary IOL-endothelial contact induced by eye rubbing may play a role in the decline of endothelial density. Harto et al48, in their series of 25 eyes implanted with Worst-Fechner lenses and a mean follow-up of 5.3 months, did not find endothelial damage by non-contact specular microscopy. Landesz et al53, in a study concerning the new Worst-Fechner convex-concave lens, found an endothelial cell loss of 5.3% (n=32) and 9% (n=17) at 6 and 12 months after surgery, respectively. They found a significant increase in endothelial cell loss between 6 and 12 months. One patient developed corneal guttata in both eyes postoperatively.
Our study shows a continual decrease in endothelial cell density after Worst-Fechner lens implantation, with an endothelial cell loss of 13% at 12 months and 17.6% at 24 months after surgery, and an unstable cell loss at least 2 years after surgery.
Surgical trauma itself may induce endothelial cell loss after the implantation of Worst-Fechner lenses54, however, because the endothelial loss is higher for this type of lens than for the last generation of angle-supported phakic anterior chamber lenses55, and it is also higher than for routine anterior segment techniques, such as phacoemulsification;56 other long-term factors may be involved in inducing more cell loss in eyes implanted with Worst-Fechner lenses. The likelihood of intermittent touch between the IOL optic edge and the corneal midperiphery, basically when the patient rubs his/her eyes, has also been suggested as a mechanism of endothelial damage in anterior chamber lenses for phakic eyes.8,57 However, the long distance between the optic edge and the endothelium in the Worst-Fechner lens along with the advice to patients not to rub their eyes, reduce the chance of temporary contact between the IOL and the endothelium9, and the resulting endothelial loss. Therefore, other causes should be suggested to explain the long-term behavior of the corneal endothelium in eyes with Worst-Fechner lenses.
Several studies58"60 about the effects of intraocular lens implantation after cataract surgery suggest that implants, particularly those causing iris damage, are associated with progressive endothelial cell loss, and that chronic uveitis might be a possible mechanism for this loss. Our study shows a significant correlation between the flare values and the decrease in cell density: the higher the flare values, the lower the cell density. This relationship between intraocular inflammation and endothelial cell loss was stronger at longer follow-up points, although the number of eyes in separated groups was too small to produce a significant correlation. Our results show a relationship between intraocular inflammation and endothelial cell loss, and suggest that chronic intraocular inflammation might play an important role in the decline of endothelial density after the implantation of Worst-Fechner lenses.
If we assume that at age 35 (the age when eyes commonly undergo phakic anterior chamber lens surgery4·8·48), we have an endothelial cell density of roughly 2500 cells/mm2 and the normal 0.57% per year loss of endothelial cells occurs56·61·62, then the remaining cell population at age 85 would show a density of 1790 cells/mm2. If a patient at age 35 undergoes the implantation of a Worst-Fechner lens, then at age 85 endothelial cell density would be 1495 cells/mm2. If, instead of the normal 0.57% per year drop in cells, an increase to 1% per year occurred, ie, in a lens design which caused chronic inflammation/endothelial cell loss, then at age 85, the patient would be left with 1070 cells/mm2, which would probably sustain corneal clarity. However, if we assume that a cataract operation will be performed in these patients during their elderly years, the endothelial density could decrease to levels lower than those necessary to maintain corneal clarity.
Reporting mean endothelial cell loss alone does not reflect complete assessment of the damage or functional reserve of the corneal endothelium. Cell density, coupled with the coefficient of variation in cell size and the percentage of hexagonal cells is more complete.63,64 The coefficient of variation in cell size and hexagonality may disclose more subtle changes in the corneal endothelium before there is a significant reduction in cell count.63,64 However, the importance of these parameters decrease when there is a clear reduction in cell density.
Laser flare cell meter measurement is an objective, quantitative, sensitive, and reproducible method for in vivo evaluation of anterior segment inflammation.17·18 Fechner and coauthors8, using a laser flare cell meter, did not find anterior segment chronic inflammation in 68 eyes with a WorstFechner lens at 13 or more months after an operation; iris fluorescence angiography performed on 23 eyes showed a complete lack of vascular leaks in the iris. However, Alió and coworkers65 found flare values of 722 ± 639 photons/ms at 1 year after surgery in nine eyes with Worst-Fechner lenses, and values of 42 ± 91 photons/ms at 1 year after surgery in nine eyes implanted with Baikoff ZB5M lenses. The difference between these groups was statistically significant. Nevertheless, values as high as 722 photons/ms correspond to a clinical flare (slit-lamp) of 4+21·66, when it has been well-established that clinical flare is rare in eyes with Worst-Fechner lenses.3,7,8,65 Thus, the flare values found by Alió and coworkers suggest that some artifact was present when measuring with the laser flare cell meter, eg, a greater amount of dispersed light from the lens surface. Sawa and associates17 emphasized the importance of minimizing the light dispersion effect induced by anterior chamber structures on measurement values. Pérez-Santonja and associates67, using fluorophotometry, reported an increase in bloodaqueous barrier permeability after the implantation of Worst-Fechner lenses, which consistently increased between 3 and 14 months postoperatively. Our study shows a chronic subclinical inflammation between 1 and 2 years after surgery in eyes implanted with Worst-Fechner iris fixated lenses, but lower than those reported by Alió and coauthors65, probably because great care was taken in flare measurements outside the lens optic, thus avoiding contamination by laser light reflected from the lens surface. Changes in the permeability of the blood-aqueous barrier and subclinical inflammation may cause chronic endothelial cell loss.68,69 Our study shows a relationship between subclinical inflammation and endothelial cell loss, and suggests that an ongoing inflammatory response creates a progressive endothelial cell loss in eyes implanted with WorstFechner lenses. Anterior chamber inflammation could induce lens metabolic disturbances, as in uveitis and diabetes70"72, which could produce faster cataract development.
Yoshida and associates71 used fluorophotometry and observed an increase in lens autofluorescence in monkey eyes with induced axial myopia, when compared with the contralateral emmetropic eyes. Taking into account the results of Yoshida and associates and the bilateral implantation of lenses in some patients, we oriented our study to compare pre- and postoperative results.
Fluorophotometry is an objective and accurate method for in vivo evaluation of lens transmittance.14,16 Lens transmittance 1 month after surgery was not statistically different from preoperative values, indicating that measurement artifact from the presence of an anterior-chamber implant was not a problem.
Our study shows a continual decrease in lens transmittance 3 months after surgery, and a lens transmittance loss of 0.82% at 12, and 1.03% at 18 months after surgery. A decrease in lens transmittance indicates a greater decrease in posterior lens autofluorescence than anterior lens autofluorescence, and, therefore, a greater loss of light in the lens medium.16 A decrease in lens transmittance means a drop in lens transparency, probably due to changes in physical qualities. Van Best and associates14, using fluorophotometry and based on the same method we used, observed that lens transmission decreases slowly with age up to about 55 years and thereafter decreases rapidly. They observed a lens transmission loss of approximately 1% during 10 years, between age 30 and 40 years. Our study shows a similar loss (1.03%), but only in 18 months.
The decrease of lens transmittance could be related to the procedure or to changes in the permeability of the blood-aqueous barrier. Although we are not able to preclude a decrease in lens transmittance induced by the operation, we believe that changes in the permeability of the blood-aqueous barrier could induce lens metabolic disturbances70'72, which would produce a decrease in lens transmittance.
Several postoperative complications have been reported after the implantation of Worst-Fechner lenses. Early postoperative iridocyclitis has been reported in 6.4%8 to 16%48 of eyes. In our series, no patient developed severe iridocyclitis in the early postoperative period, but in 9.3% of eyes, an inflammatory reaction was observed during the follow-up. Corneal pigment deposition has not been reported in eyes implanted with Worst-Fechner lenses. However, we found pigment deposition in 18.7% of eyes, which suggests a pigment release from the iris induced by the IOL. Cystic wounds, presumably steroid-induced, have been reported in 8% of eyes8; we found this complication in 18.7% of eyes. Temporary ocular hypertension has been described in 16% of eyes7,8, and a similar value was found in our series. Concerning decentration and halos, Harto et al48 reported decentration in 4% of eyes, and Pérez-Torregrosa et al73, using a digital system for measuring decentration, found a decentration with respect to the center of the pupil greater than 0.5 mm. in 41% of eyes. Our study shows a decentration greater than 0.5 mm in 43% of eyes, and halos in 56% of eyes. A relationship between decentration and halos could be established; a wellcentered lens is rarely accompanied by halos, and the optic size of this lens is large enough to prevent halos. Fechner et al7,8 reported that the fixation of the IOL to the iris is stable, and they found no evidence of iris atrophy in the area of fixation. However, in our study, 81% of eyes showed iris atrophy in the area of fixation on both sides, and in three eyes (9.3%) the fixation of the lens was not stable. Fechner et al8, Harto et al48, and Worst et al12, did not find lens opacities after implanting WorstFechner lenses; we found this complication in one eye (3%). Retinal detachment has been reported in 0 to 0.8% of eyes after implantation of Worst-Fechner lenses8,48, although the relationship between phakic anterior chamber lenses and retinal detachment has not been established. No patient developed retinal detachment in our series. Giant papillary conjunctivitis has not been reported, but we found this complication in 9.3% of eyes- related to exposed nylon sutures. Removal of sutures was successful in all eyes. Other complications reported after implantation of Worst-Fechner lenses, such as Urrets-Zavalia syndrome (1.6%)7,8 and corneal edema (3.2%)8, were not found in our study.
The implantation of an anterior chamber IOL in a phakic eye to correct high myopia is a technique recently revived.3,4 If one considers optical improvements, this is probably the most satisfactory surgical procedure available for correcting high myopia.5' 8 However, long-term potential risks to the corneal endothelium, lens, and anterior uvea are not known. Our results for the Worst-Fechner myopia lens confirm the earlier findings of effectiveness of the refractive results. However, our study shows a continual decrease in endothelial cell density, a decrease in lens transmittance, and a chronic subclinical inflammation after the implantation of Worst-Fechner lenses. Decentration is common and the fixation of the IOL to the iris was not stable. These and other potential hazards8,52,67·74 of WorstFechner lens implantation should restrict the application of this method to patients under controlled clinical investigation until long-term results concerning its safety are evaluated.
Research on implantation of IOLs in phakic myopic eyes should not be abandoned, because this technique gives optical results far superior than other procedures. Other implants, with a different fixation system, could decrease the risks and complications found with Worst-Fechner lenses.
From the Department of Ophthalmology, Jiménez-Díaz Foundation, Autonomous University of Madrid, School of Medicine, Madrid, Spain.
The authors have no proprietary interest in the materials in this article.
Correspondence: Juan J. Pérez-Santonja, Sorolla 32-3, 03420Castalla, Alicante, Spain. Fax: 34-6-590 3488.
Received: March 11, 1996
Accepted: August 22, 1996
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COMMENT BY JORG KRUMEICH, MD (BOCHUM, GERMANY)
This article contradicts the findings we published in the Journal of Refractive Surgery (Krumeich JH, Daniel J, Gast R. Closed-system technique for implantation of iris-supported negative-power intraocular lens. J Refract Surg 1996;3:334-340).
The authors conclude that endothelial cell loss is inherently present with the Worst-Fechner irissupported lens and that it is progressive.
We think the paper confirms our conclusions that the implantation technique itself is the cause of most of the problems encountered by the authors. The description of the surgical technique shows a poor method of implantation which probably produced the endothelial cell loss. We demonstrated endothelial cell loss using "closed system implantation." I think the paper shows how the surgical technique should not be performed- by means of a three-incision technique or when implant fixation is done while the anterior chamber is open.
Negative consequences such as iris atrophy, flare, lens opacification, iris perforation, lens decentration or small iris fixation- well documented in this paper- must be seen in connection with the technique of implantation and not as a result of the lens design itself. It is little suprise that the authors came to their negative conclusions- similar to earlier reports in the literature that followed the same path.
COMMENT BY JOSÉ L. MENEZO, MD, PHD (VALENCIA, SPAIN)
This article leads to the conclusion that the authors did not have sufficient experience with this type of refractive surgery procedure, the implantation of an iris stromal-supported Worst Lobster claw lens. This is evidenced by the problems they describe at the moment of lens implantation as well as by the number of complications.
We have implanted more than 350 of these lenses, including bilateral implantation in more than 65 eyes, with more than 6 years of follow-up. We affirm the following results.
Both refractive and optical results of these lenses are excellent and superior to other refractive techniques for correction of high myopia.
The surgical technique requires extensive experience in intraocular lens implantation, especially with the first design of these lenses that had thicker edges to the optic. Although the implantation is done under viscoelastic protection, it is a difficult technique and we think that not all ophthalmic surgeons are capable of doing it correctly, especially the step of anchoring the lens haptic to iris stroma; it is very important to place it in the proper site and to grasp sufficient iris tissue for stability to avoid endothelial touch with the lens haptic postoperatively.
Lens centration over the pupil is very important and placement has to be accurate at the time of surgery. In fact, one of the advantages of IOL correction of myopia is that the technique is reversible, intraoperatively; if the lens is not centered, the surgeon can release the iris pinch and replace the lens, properly centered.
This flexibility is not available with corneal surgical techniques as excimer laser in situ keratomileusis or photorefractive keratectomy where decentration gives rise to postoperative optical and refractive complications, such as undercorrection, glare, halos and loss of spectacle-corrected visual acuity. We have noticed that mild decentration of 1 or 2 mm of the Lobster claw implants do not produce significant clinical refractive problems.
The authors observed a decrease in lens transmittance using fluorometric techniques greater than the loss related to age. In our experience, there has been no clinical or refractive effect on the crystalline lens; on the contrary, 46% of our patients have gained one or two lines of spectacle-corrected visual acuity compared to that preoperatively.
Regarding endothelial cell loss, our more than 3 years of follow-up shows mean endothelial cell loss between 8 and 10%. However, some patients have an endothelial cell loss between 20 and 30%; we studied these individuals and they had high risk factors favoring endothelial cell loss including contact lens wear of more than 25 years, epikeratoplasty performed early in our learning curve with more surgical trauma, and reoperations (two due to lens subluxation and one due to error in lens power calculation).
We conclude that the implantation of an anterior chamber phakic Lobster-claw lens for correction of high myopia is a valid and practical technique. I have not observed, after 6 years of follow-up, any significant corneal or crystalline lens alteration and I do not think that this slow endothelial cell loss will affect the transparency of the cornea. This opinion is partly supported by the evolution in design of claw lens implants for aphakia during 17 years: in secondary implantation, primary senile cataract, and traumatic aphakia in adults and children without significant corneal alteration or chronic inflammation-even subclinical, as mentioned by PérezSantonja and colleagues. If this type of lens produces chronic inflammation, we would have seen many eyes with corneal problems. We have also used specular microscopy of the endothelium to demonstrate that the coefficient of variation of cell size and the percent of hexagonal cells stabilize after 6 months, indicating that despite mild endothelial loss, the morphology of the endothelium remains stable and endothelial function remains good.
COMMEMT BY MICHAEL J. LYNN, MS (ATUNTA, GEORGIA)
Concerning the statistical analysis of the relationship between flare and cell density in this article, Figure 8 presents the most meaningful information, because the authors have wisely used a scattergram to represent all their data.
For most eyes, the flare value was within the range of 5 to 40, but two eyes had values of 90 and 110 (approximated from the graph data). When all of the eyes are analyzed, these two outlier points heavily influence the results, creating a correlation coefficient of -0.378 with a ? value of less than .05 - statistically significant. However, if both of these outlier eyes are removed, the correlation coefficient falls to -0.223 with a ? value of .15- not statistically significant, and if only the farthest outlier (110) is deleted, the correlation coefficient falls further to -0.158 with a ? value of .23- also not statistically significant. With little data for flare values greater than 40, the extreme points (90 and 110) exert a great influence on the correlation coefficient and the slope of the regression line.
The authors' conclusion that flare is associated with endothelial cell loss is not supported by the overall data- the conclusion that cell density is related to flare is heavily dependent on whether the two outlier points are included, and therefore, the statistical analysis in the paper is suspect.
RESPONSE BY AUTHORS
We appreciate all the experts' comments. Their comments emphasize the fact that the implantation of an anterior chamber phakic Worst-Fechner lens for correction of high myopia is an important topic and remains controversial.
Dr. Krumeich remarks that many negative consequences after this surgery must be seen in connection with a three-incision technique of implantation, and not as a result of the lens design itself. The technique used in our study was the standard technique described by the designers of the lens when it was first introduced1, and our results emphasize the need for independent long-term controlled trials to evaluate new refractive techniques or devices, before widespread use. Moreover, we believe that some complications such as chronic subclinical inflammation, chronic endothelial cell loss, transmittance loss, unstable fixation, or lens decentration could not be surgery-related. Our study and other articles show that such complications could be connected to the lens design or to the fixation mechanism.2'7 On the other hand, the new closed-system technique, described by Krumeich et al8, could be less harmful to anterior segment structures, although publication of long-term results concerning safety are necessary.
We agree with Dr. Menezo that the implantation technique is difficult, and not all refractive surgeons will be able to do it properly. For this reason, its use will be limited. Dr. Menezo also remarks that one of the advantages of this IOL is that the technique is reversible during surgery, allowing proper centration. However, Dr. Menezo and colleagues5, using a digital system for measuring decentration in eyes implanted with these lenses, found a decentration greater than 0.5mm with respect to the center of the pupil in 41% of eyes. Similar data were found in our study (43% of eyes).
Concerning Mr. Lynn's comments, our study shows a significant relationship between flare values and endothelial cell density; the higher the flare values, the lower the cell density (r = -0.378, p< 0.05). The longer the follow-up, the stronger the relationship between intraocular inflammation and endothelial cell loss, although the number of eyes in separate groups was too small to produce a significant correlation. It is obvious that if we change the data, the results will also change. If we added two eyes with high flare values and low cell density, the correlation would be stronger and the ? value lower. However, the data are those presented in Figure 8, and we should stick to the data. We should not forget that several studies4,9,10 concerning the effects of IOL implantation after cataract surgery suggest that implants, particularly those that cause iris damage, are associated with progressive endothelial cell loss, and that chronic uveitis might be a possible mechanism for this loss.
We abandoned implantation of Worst-Fechner biconcave iris-fixated lenses several years ago. At present, we use angle-supported phakic lenses for the correction of severe myopia (more than -16.00 D).
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