CASE CONSULTATION. Grand Rounds. Edited by Jaime Aramberri, MD & Alfredo Castillo, MD

CASE CONSULTATION Grand Rounds Edited by Jaime Aramberri, MD & Alfredo Castillo, MD A 40-year-old woman described a myopic shift in the OS 3 years ago. She underwent surgery for 7 D of myopia in both eyes by LASIK in 1998, with a good visual outcome until the present episode. She wishes to assess the possibility of retreating the refraction in the OS. She does not have any relevant history of interest and says that she does not rub her eyes. Eye examination: OD: 0.90 with 0.50 cylinder at 180 : 1.00 OS: 0.40 with 1.25 sphere, 0.50 cylinder at 180 : 1.00 Biomicroscopy (both eyes): Anterior pole normal. 9 mm LASIK flap with no significant abnormalities. Intraocular pressure (IOP): OD: 11 mmhg; OS: 11 mmhg. Eye fundus (both eyes): Posterior pole and periphery normal. Ocular response analyzer (ORA). Corneal hysteresis (CH): OD: 7.5 mmhg; OS: 8.00 mmhg. Corneal Resistance Factor (CRF): OD: 8.5 mmhg; OS: 8.5 mmhg. Graphs with normal peaks. Scheimpflug tomography: OD: Centered myopic ablation. No significant abnormalities on the posterior side or pachymetric topography. OS: Images attached. Corneal OCT: OD: No significant abnormalities; OS: Image attached. ANTERIOR SAGITTAL Figure 1. Anterior cornea sagittal topography. Normalized scale. OS ELEVATION MAP (ANTERIOR) Figure 2. Anterior cornea elevation map. Best fit toric ellipsoid. Normalized scale. OS In a patient who underwent surgery for mediumhigh myopia 15 years ago, at the age of 25, who reports a myopic shift in her OS, the differential diagnosis includes: (1) regression of the effect of the LASIK surgery, (2) corneal ectasia, (3) lens myopia (incipient nuclear cataract) and (4) progression of the axial myopia. In order to discard (1), the current topographic maps would have to be compared with those of the early post-operative period (which we do not have). Ectasia (2) seems to be ruled out due to the limited astigmatism, absence of suggestive elevation or topographical changes (although the axial is somewhat irregular), and the fact that it has been 3 years since she noticed the myopic shift without it having progressed. The low ORA values are irrelevant after LASIK. Changes in the lens (3) appear to be ruled out by the statement normal anterior pole and the age. However, these could be subtle and would merit a more detailed examination. Axial growth (4) seems to be most likely, given the degree of original myopia, the age at which she underwent surgery and the time elapsed. In order to confirm this, the current biometry would have to be compared with a pre-lasik one (something that we include in our protocol). With respect to treatment, if axial growth or partial regression of the effect without ectasia is confirmed (apart from weighing the usefulness of mild unilateral myopia at an age when presbyopia is approaching), if the patient prefers to recover emmetropia, the central residual pachymetry (511 μm) indicates that it is possible to perform a retouch, using either PRK or LASIK. The old flap may be lifted, although it would be good to measure its thickness with an OCT. Rafael I. Barraquer, MD, PhD Barcelona (Spain) 2013 SECOIR Sociedad Española de Cirugía Ocular Implanto-Refractiva ISSN: 2171-4703 153

154 CLINICAL CASE PRESENTATION ELEVATION MAP (POSTERIOR) Figure 3. Posterior cornea elevation map. Best fit toric ellipsoid. Normalized scale. Scheimpflug device. OS CORNEAL THICKNESS Figure 4. Pachymetry topography. Normalized scale.scheimpflug device. OS Figure 5. Total and epithelial pachymetry topography. Cornea OCT device. OS The case presented is consistent with a diagnosis of grade 1 corneal ectasia following LASIK. The definition of ectasia is not uniform in the literature, so its diagnosis in incipient or mild cases such as the one in question does not always meet classically accepted criteria with respect to the magnitude of the changes found. Nevertheless, the combination of various clinical signs, even if mild, may point to this diagnosis, which is more likely the more signs are combined 1,2. The characteristics of ectasia include a myopic refractive error with increased astigmatism, worse corrected visual acuity, increased corneal toricity with topographic abnormality and progressive thinning1. A recent study has proposed grading ectasia based on the visual limitation. The topography of the left eye shows an area of curvature in the inferotemporal area of the ablation, with elevation of the anterior and posterior side coinciding with that area. The area of curvature would stand out even more if a tangential topographic map had been selected instead of an axial map, as the former provides a more accurate location of these abnormalities. The elevations of the anterior and posterior sides refer to a sphero-toric best fit, which is the ideal fit for better detection of incipient elevations. The Scheimpflug total pachymetry and OCT map show a regular normal pattern with lower pachymetry values in the central area corresponding to the ablation. The differences in total pachymetry between both instruments are due to the different technology used; the pachymetry measured by OCT provides lower values than ultrasound

CLINICAL CASE PRESENTATION 155 or Scheimpflug pachymetry. However, in the OCT pachymetry map, we can observe epithelial thickening in the T, I and IT paracentral areas, which are the same areas that present a lower total pachymetry (except for the central one), which indicates reduced stromal thickness at the periphery of the ablation in the inferotemporal area, the area of curvature and the elevations. OCT pachymetry is thus useful for detecting areas of stromal thinning which are being masked by epithelial thickening in the total pachymetry. The central total corneal thickness is relatively good but it does not exclude a diagnosis of ectasia2. Analysis of the lens thickness by OCT, as well as the pre-operative topographies, would be useful for analyzing the cause of the ectasia 1,2. In summary, there is a thinner area of curvature coinciding with the highest area of the anterior and posterior side and with the paracentral area, all of which suggests an ectatic type abnormality. The differential diagnosis of the topographical abnormality could be raised with a superiorly decentered ablation. However, in this case, the posterior elevation as well as the area of thinning would not coincide with the area of curvature and the vision would have been poor from the immediate post-operative period. The patient s refractive defect is not the classical ectasia defect, as the existence of astigmatism is more typical of this 1,2. However, incipient or mild ectasia can present a spherical defect without a large astigmatism, so this clinical finding does not exclude the diagnosis either 2. Moreover, as this is a case of grade 1 ectasia, a decrease in the corrected visual acuity is not detected at present either. The pattern of epithelial thickness post-lasik evaluated by ultrasound biomicroscopy shows central lens thickening, which we did not find in this case 3. A recent study has found variable, unpredictable patterns of epithelial thickness in post-lasik ectasias 4. The pattern of thinning on the highest area and thickening over the thinnest area has been specifically described in some cases. In this case, the epithelium is thinner over the flattest area of the cornea and thickens over the area of the elevation. However, there is no pathognomonic pattern of epithelial thickness in cases of ectasia 4. As regards the result of the ORA examination, the CH and CRF values are low with respect to normal corneas, but they are within the values described in corneas operated on using LASIK 5 with stable results, and they are similar to those of the contralateral eye which does not present problems. The normal results of this examination do not exclude the diagnosis of ectasia, since its specificity and sensitivity for the detection of sub-clinical cases of keratoconus has been shown to be low 6 ; it has also been shown that the values do not show changes after the application of crosslinking 7. Another useful examination in this patient would be corneal aberrometry, where an increased coma would be detected. Although vertical coma may be useful in the diagnosis of sub-clinical keratoconus, a high coma could have its origin in a decentered ablation and is not pathognomonic of ectasia. In any case, it would be interesting to know its value for treatment of the refractive defect, and it could explain symptoms of poor vision quality despite corrected visual acuity of logmar 0.0. Regardless of the definition of ectasia, inherent in the description is the existence of a progression or difference with respect to the post-operative situation on discharge 1,2. In the case in question, the progressive nature of the abnormality is provided by the progressive myopic shift, although it would be more useful to be able to compare the current topographic maps with those of previous years or at discharge post-surgery. In order to attribute the myopic shift to the ectasia with certainty, the mean dioptric power of the cornea would have to be confirmed and an increase in the axial length excluded (unlikely at 40 years of age). Lens nuclear sclerosis would also have to be excluded; although it can occur in some high myopes from the age of 40, I assume it has been ruled out in this case, as the biomicroscopy has been reported as normal. Once the diagnosis of incipient ectasia has been established, the treatment has a dual objective: First and foremost is to stop its progression, and secondly, to try to correct the refractive defect generated. The only procedure that has been shown to be effective in reaching the first objective is the application of crosslinking 8. Like the diagnosis, this treatment requires documented evidence of progression 8. In such a case, if we do not have previous post-operative topographies with which to compare the current maps, in my opinion, the progressive myopic shift would be sufficient to indicate treatment, once other causes have been eliminated. The stromal pachymetry is appropriate, hence another advantage of having an epithelial thickness map: a thickened epithelium may mask areas of thinner stromal thickness. With respect to correction of the refractive defect, unlike crosslinking in keratoconus in which slight flattening of the mean corneal power has been described, we cannot expect such an obvious effect after crosslinking in ectasia according to the results of a recent study8, although certain flattening may occur in some cases. Thus it would be advisable to wait a few months after the crosslinking to check its effect on the residual refraction. If it was the same ( 1.25 0.5 cyl 180 ), the pre-presbyopic patient should be informed of the possible advantages of monovision, which would be a reasonable option if they agree. If they wish to have total correction of the refractive defect, contact lens wear could be indicated. However, since this is a patient who has already undergone LASIK and who has come to the clinic requesting repeat surgery, this alternative would probably not be satisfactory. Intracorneal segment implantation is not indicated in mild ectasia without loss of corrected visual acuity, as we would probably generate more astigmatism even if we correct the coma, and there is a risk of loss of lines of the CDVA 9. Another option would be topography-guided surface ablation together with crosslinking 10. Series have been published with

156 CLINICAL CASE PRESENTATION good results, but they are few and with short follow-up. However (and this is my personal opinion), I am not in favor a priori of ablating more tissue from an already weakened cornea. Should a surgeon decide to choose for this option, it would be very useful to have the epithelial pachymetry map to plan the treatment, another use of OCT pachymetry. In my opinion, if the patient wishes to have surgical correction of the residual refractive defect, I would prescribe implantation of an ICL 6 months after crosslinking, assuming that the patient meets the necessary requirements (including ACD from endothelium 3 mm), making the incision in the most curved axis. In addition, we should not forget to plan exhaustive follow-up of the right eye, with topographic and refractive check-ups every 6 months, in order to perform crosslinking in the OD as soon as there is the slightest evidence of onset of ectasia. 1. Twa MD, Nichols JJ, Joslin CE, Kollbaum PS, et al. Characteristics of corneal ectasia after LASIK for myopia. Cornea. 2004;23:447 457. 2. Brenner LF, Alió JL, Vega-Estrada A, Baviera J, Beltrán J, Cobo- Soriano R. Clinical grading of post-lasik ectasia related to visual limitation and predictive factors for vision loss. J Cataract Refract Surg. 2012;38:1817 1826. 3. Reinstein DZ, Archer TJ, Gobbe M. Change in Epithelial Thickness Profile 24 Hours and Longitudinally for 1 Year After Myopic LASIK: Three-dimensional Display With Artemis Very High-frequency Digital Ultrasound. J Refract Surg. 2012;28:195-201. 4. Rocha KM, Pérez-Straziota E, Stulting RD, Randleman JB. SD-OCT analysis of regional epithelial thickness profiles in keratoconus, postoperative corneal ectasia, and normal eyes. J Refract Surg. 2013;29:173-179. 5. Chen MC, Lee N, Bourla N, Hamilton DR. Corneal biomechanical measurements before and after laser in situ keratomileusis. J Cataract Refract Surg. 2008;34:1886 1891. 6. Touboul D, Benard A, Mahmoud AM, Gallois A, Colin J, Roberts CJ. Early biomechanical keratoconus pattern measured with an ocular response analyzer: Curve analysis. J Cataract Refract Surg. 2011;37:2144 2150. 7. Sedaghat M, Naderi M, Zarei-Ghanavati M. Biomechanical parameters of the cornea after collagen crosslinking measured by waveform analysis. J Cataract Refract Surg. 2010; 36:1728 1731. 8. Richoz O, Mavrakanas N, Pajic B, Hafezi F. Corneal collagen cross-linking for ectasia after lasik and photorefractive keratectomy long-term results. Ophthalmology. 2013;120:1354 1359. 9. Brenner LF, Alió JL, Vega-Estrada A, Baviera J, Beltrán J, Cobo- Soriano R. Indications for intrastromal corneal ring segments in ectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2012; 38:2117 2124. 10. Kanellopoulos AJ. Comparison of sequential vs same-day simultaneous collagen cross-linking and topography-guided PRK for treatment of keratoconus. J Refract Surg. 2009;25:S812-8. Victoria de Rojas, MD, PhD A Coruña (Spain) The diagnosis is mild myopia and astigmatism in the OS (EE 1.50 D). The distance UCVA in the OS is not optimal (0.4). Based on the other data from the eye examination, ocular hypertension and predisposing retinal lesions suitable for prophylactic treatment can be ruled out. The appearance of a myopic defect can be considered a possible finding after a long time period in high defect M-LASIK 1. The differential diagnosis should be made with: a. Ectasia. This is ruled out with the keratometric and topographical data. Streak retinoscopy could be performed to rule out the presence of scissoring retinoscopy reflex, although in this case we shall assume that it is negative. b. Myopic regression. It is impossible to confirm this hypothesis as we do not know the keratometric data at discharge after the initial myopic treatment. c. Index myopia (nuclear lens opacity). Ruled out by the biomicroscopy. d. Appearance of new myopia due to growth of the axial length. We cannot say either that this is the precise cause of the long-term myopic shift, as we do not know the values of this parameter. It would be advisable to request the patient data from the initial procedure, both pre-operative and on discharge to clarify the diagnosis. As we have no record of the refractive stability, we should probably reassess the patient in one year. There are essentially two therapeutic alternatives and prognoses: The first approach is retreatment of the myopic defect in the OS (objective: emmetropia), with the aim of achieving a distance UCVA of logmar 0.0. It has a good visual and refractive prognosis in distance vision. There are several surgical options for carrying out this retreatment, including: 1. ReLASIK with lift-flap. This has three disadvantages: 1) Difficulty in lifting the primary flap after 12 years since its creation 2. 2) Possibility of epithelial growth in the interface. This possibility increases in retreatments, especially when they are long term 3. 3) Finding an insufficient stromal bed for a new stromal ablation: - We do not know the thickness of the original flap. From the date of the original procedure (1998), we can assume that this is a flap larger than 100 micrometers (with the microkeratomes used at that time, it was usual to obtain lens 120 to 160 micrometers thick) 4,5. - We disregard the thickness of the residual stromal bed. Applying the technique used in those years (usually an optical area of 5.5 to 6 mm and micrometer consumption around 123), according to mathematics of LASIK, we should find a stromal bed of 451 micrometers (taking into account that the current

CLINICAL CASE PRESENTATION 157 central pachymetric value is 511 micrometers, the epithelial thickness 61 micrometers and the estimated flap thickness around 160 micrometers) 6. - It could happen that we are faced with the finding of a thick flap together with an insufficient bed (less than 300 micrometers or less than 60% of the total thickness of the original cornea), in which case we could suggest performing the retreatment on the stroma of the posterior side of the flap 7,8. 2. To create a new flap with an automatic microkeratome or with femtosecond, with two disadvantages: 1) Obtaining an irregular flap, which would complicate the process 9, and 2) Finding a nonviable stromal bed for a new stromal ablation. 3. Perform PRK on the original flap. Its main disadvantage would be the appearance of corneal haze, so mandatory use of mitomycin C would be prudent 10. The second alternative is not to perform any retreatment, maintaining the myopic defect in the OS (objective: monovision). For this approach, assessment of the monocular and binocular UCVA, near refraction and study of the sensory and motor dominance is missing in the examination. The ocular dominance should be evaluated, both motor (the hole-in-thecard test) and sensory dominance (the +1.50D blur test), as it is important when it comes to establishing a prognosis in the aspect of visual adaptation (presence or not of blurred vision) in a state of monovision. It is also essential to complete the anamnesis with data such as: type of professional activity, driving, hobbies, level of demand and expectations. However, several remarks should be made on monovision, also called blended vision: a) it is possible to have good binocular near vision; b) it permits optimal intermediate vision (70 cm);c) it allows acceptable binocular distance vision to be achieved; d) the distance vision is limited (it decreases the sensitivity to contrast and stereopsis) in low lighting conditions, at night-time or driving, obviously due to the myopia in one of the eyes; e) the contact lens test can be done (although not on all occasions, it allows a prognosis to be established); and f) there is a possibility of failure to adapt to monovision. In my opinion, the option in this case is based on primum non nocere, i.e. our second objective: monovision. We have a 40-year-old patient, myopic (who has always enjoyed good near vision), for whom we do not have relevant personal data for refractive surgery (profession, work activity, hobbies, personality), who currently has natural monovision (OD close to emmetropia and OS with a myopic defect of EE 1.50 D). The goal of the proposal should be explained very carefully and the patient involved: e. Explain to the patient what presbyopia is, its cause and evolution. f. Define her current situation and the visual expectations for the short/mid-term future: having useful vision to be able to carry out activities such as walking, watching TV, driving during the day, reading the newspaper, reading messages on the mobile. Explain the visual disadvantages in extreme vision : distance (such as driving at night, golf) and near (sewing, building models) 11. g. The intermediate vision is usually adequate for office work 12. h. Monovision has an expiry date, as the presbyopia will continue to increase over the years, and at some point, the monovision will no longer compensate for that presbyopia. 1. Dirani M, Couper T, Yau J, et al. Long-term refractive outcomes and stability after excimer laser surgery for myopia. J Cataract Refract Surg. 2010; 36:1709 17. 2. Hardten DR, Lindstrom M, Samuelson TW, Lindstrom RL. LASIK enhancements: a comparison of lifting to recutting the flap. Ophthalmology. 2002;109:2308-13. 3. Henry CR, Canto AP, Galor A, Vaddavalli PK, Culbertson WW, Yoo SH. Epithelial ingrowth after LASIK: clinical characteristics, risk factors, and visual outcomes in patients requiring flap lift. J Refract Surg. 2012;28:488-92. 4. Donnenfeld E, Sandoval HP, Al Sarraf O, et al. Flap thickness accuracy: comparison of 6 microkeratome models. J Cataract Refract Surg. 2004;30:964-77. 5. Randleman JB, Hewitt SM, Lynn MJ, Stulting RD. A comparison of 2 methods for estimating residual stromal bed thickness before repeat LASIK. Ophthalmology. 2005; 112: 98-103. 6. Flanagan GW, Binder PS. The theoretical vs. measured laser resection for laser in situ keratomileusis. J Refract Surg. 2005; 21: 18-27. 7. Machat JJ. Mathematics of laser in situ keratomileusis for high myopia. J Cataract Refract Surg. 1998;24:190-5. 8. Maldonado MJ. Undersurface Ablation of the Flap for Laser In Situ Keratomileusis Retreatment. Ophthalmology. 2002;109:1453 64. 9. Guell JL, Elies D, Gris O, Manero F, Morral M. Femtosecond laser-assisted enhancements after laser in situ keratomileusis. J Cataract Refract Surg. 2011; 37:1928 31 10. Liu A, Manche EE. Visually significant haze after retreatment with photorefractive keratectomy with mitomycin-c following laser in situ keratomileusis. J Cataract Refract Surg. 2010; 36:1599 601. 11. Steinert RF. Patient selection for monovision laser refractive surgery. Curr Opin Ophthalmol. 2009;20:251-4. 12. Arias A, Gómez de Liaño P, et al. La monovisión como corrección de la presbicia. En: Arias A. Cirugía de la Presbicia. Madrid: SECOIR; 2010:89-109. Fernando Llovet, MD, PhD Madrid (Spain)

158 CLINICAL CASE PRESENTATION First of all, the origin of this late post-lasik myopic shift must be analyzed, but may be due to three causes: 1) Axial myopic shift due to an increase in the axial length of the eyeball. Since we do not know the current axial length and the length prior to Lasik, this cannot be assessed. I do not think that axial elongation, although possible, is a likely cause in this case; 2) Index myopic shift due to an increase in the refraction index of the lens, generally due to the development of nuclear cataracts. In this case, there is no mention of significant changes in the anterior segment examination, so this can also be ruled out; and 3) Myopic shift due to a corneal cause. In this situation, changes would be observed in the shape of the cornea between the post-lasik and current examination. Under this heading, the most important process to rule out is the late development of corneal ectasia, which would substantially alter the case management. On the sagittal map of the anterior side of the cornea, a well-centered ablation pattern can be observed with asymmetry due to increased curvature in the inferior treatment area. This could be the manifestation of corneal ectasia coinciding with the presence of an increase in the curvature of the anterior side of the cornea on the previous altimetry map. However, against this diagnosis is a pachymetric map within normal for a post-lasik case, a normal elevation map of the posterior side and absence of epithelial thinning in the area of the supposed corneal ectasia. In contrast, on the epithelial map, epithelial thickening can be observed in the area coinciding with the increased curvature of the anterior side. Therefore, this is a patient with increased curvature in the inferior area of the treated region of the anterior side of the cornea coinciding with local epithelial thickening. It is known that epithelial hyperplasia may be responsible for regression after PRK and Lasik in the treatment of myopia 1-4. As a first measure, I would recommend that the patient undergo an observation period of 4 to 6 months to check the evolution of the process; meanwhile, I would prescribe an ocular lubricant and distance optical graduation for certain activities (e.g. night driving, TV, etc.). If the patient wishes to have a more short-term corrective measure, I would recommend epithelial debridement, observing how corneal re-epithelialization takes place. If its thickness returns to normal, this could mean a reduction in her myopic defect, and may be sufficient to avoid repeat laser ablation. As a final measure (if the previous approach did not resolve the problem), I would suggest PRK with a standard aspheric pattern. I would not consider the topography-guided pattern to be suitable, as the topographic irregularities would disappear with the deepithelialization prior to the laser treatment. 1. Lohmann CP, Güell JL. Regression after LASIK for the treatment of myopia: the role of the corneal epithelium. Semin Ophthalmol. 1998;13:79 82. 2. Lohmann CP, Reischl U, Marshall J. Regression and epithelial hyperplasia after myopic photorefractive keratectomy in a human cornea. J Cataract Refract Surg. 1999;25:712 15. 3. Spadea L, Fasciani R, Necozione S, Balestrazzi E. Role of the corneal epithelium in refractive changes following laser in situ keratomileusis for high myopia. J Refract Surg. 2000;16:133 39. 4. Reinstein DZ, Sabong Srivannaboon S, Gobbe M, et al. Epithelial Thickness Profile Changes Induced by Myopic LASIK as Measured by Artemis Very High-frequency Digital Ultrasound. J Refract Surg. 2009; 25: 444 50. Luis Cadarso, MD Vigo (Spain) Here we have a case of myopic regression following Lasik surgery. These symptoms present us with a twofold problem to resolve: on one hand, to determine the cause of the regression and on the other, depending on the cause, to respond to the patient s demand for visual improvement. The appropriate way to proceed should include a rigorous clinical and visual examination of the patient and its analysis together with the tests required in these cases, such as topographic, pachymetric and biomechanical studies. The patient s topographical images show a pattern typical of central myopic ablation, although its homogeneity is not ideal. The good vision achieved by the patient after correction with spectacles indicates that she has the corneal regularity and focusing ranges that we expect after Lasik surgery. The posterior side of the cornea does not show signs of suspected iatrogenic ectasia that might be considered to induce the residual refraction. The biomechanical study performed on the patient agrees with the topographical or pachymetric findings, as it shows CH and CRF values within normal for post-lasik patients, and rules out the existence of obvious biomechanical deterioration. Although the IOP values measured by the ORA are not reported, the patient s biomechanical CH and CRF values and the TAG reported would indicate an IOPcc 3-4 mmhg higher than the Goldmann. The development of lens nuclear sclerosis is a common cause of myopic regression in patients with high myopia aged over 40 years. In this case, the biomicroscopic examination of the patient rules out the existence of a cataract that could induce index myopia. Once the above conditions have been ruled out, we should consider an increase in the axial myopia

CLINICAL CASE PRESENTATION 159 (uncommon at the patient s age) or other causes of myopic regression. The mechanism of myopic regression is complicated, it has not been completely elucidated and it may have several etiologies that we must consider, among which are the corneal forward shift due to the effect of the IOP, the development of new stromal collagen and epithelial hyperplasia. In this case, as in most cases who attend the clinic for late post-lasik regression, patients come from other centers or ophthalmologists, so we do not have topographies from the early post-operative period. These would allow us to compare the values, to rule out an increase in the corneal curvature. Confirming that the curve remains the same would suggest the effect of epithelial hyperplasia or an increase in the axial length as a cause of the regression, which would allow us to suggest re-treatment with somewhat more confidence. However, in this patient, we have total and epithelial pachymetry images, in which the existence of areas of hyperplastic epithelium can be observed, in an attempt to return the anterior side of the cornea to normal. The epithelial thickness in the areas of hyperplasia exceeds 60 micrometers, so it could induce much of the regression in the patient. A small central island can be observed that affects the visual axis, so I am inclined to think that it could be the cause of the myopic regression. As regards surgical maneuvers or treatments recommended in order to be successful: This is a patient who aspires to have a better VA without any compensatory optical measure, and who does not have any signs of ectasia or lens sclerosis, so repeat surgery could be considered. However, if we consider the patient s age (close to presbyopia), the high previous myopia corrected with laser and the low unilateral residual refraction, my recommendation is not to perform surgery. I would recommend the application of topical hypotensive drops on a temporary basis. If a reduction in the myopic defect is obtained with this temporary treatment, I would continue the therapy indefinitely. I would also explain to the patient the benefits of their defect ahead of their impending presbyopia and I would confirm her near vision with her defect corrected and her uncorrected binocular distance vision. I would propose the options to follow without optical correction or consider the use of daytime or night-time contact lenses. Epithelial hyperplasia is a common cause of regression that is suitable for surgery. Until the arrival of equipment capable of measuring the epithelial pachymetry, its existence was assumed in patients with regression. Its presence is common in cases of old, deep ablations with smaller diameters and sudden transitions, as in this patient. Cases of a forward shift in the cornea have been described as a factor responsible for regression following Lasik, due to the effect of the IOP on the weakened central cornea. Moreover, various studies have shown that the topical application of drugs for reducing the IOP is effective for correcting the refractive regression. This presumably results from the backward movement of the cornea and applanation of the curvature after Lasik. Although the refractive effect of this treatment is mild (approximately 0.5 D), it should be tried first, before suggesting a retouch, especially in eyes without much regression. Kamiya K, Aizawa D, Igarashi A, Komatsu M, Shimizu K. Effects of antiglaucoma drugs on refractive outcomes in eyes with myopic regression after laser in situ keratomileusis. Am J Ophthalmol. 2008; 145(2):233-238. Mª Angeles del Buey Sayas, MD Zaragoza (Spain)