Corneal ectasia after laser in situ keratomileusis (LASIK) is a keratoconus-like biomechanical disorder characterized by a progressive distortion of corneal shape and optical quality. Current treatment options mainly include rigid gas permeable contact lenses, corneal cross-linking, intracorneal ring implantation, and keratoplasty.1 Recently, intrastromal lenticule implantation has been considered a potential alternative to regularize the cornea and improve refractive ability by thickening the cornea. Its safety and efficacy has been reported in clinical studies up to 22 months and presented as a promising technique for ectasia or keratoconus after LASIK.2–4
It is of interest to further investigate the corneal wound healing process in the recipient cornea and in implanted lenticules after allogenic intrastromal lenticule implantation to determine the viability and predictability of the procedure. Corneal nerves provide trophic and protective functions, and damage of innervation may alter epithelial function, worsen tear film, and delay wound healing.5,6 Keratocytes are also thought to play a central role in corneal wound contraction and tissue remodeling following refractive surgery or injury.7,8 Therefore, both innervation of the lenticule and changes in keratocytes are vital for donor lenticule in the recipient cornea, as well as the safety of this technique. However, these indicators have not been reported after the procedure.
Confocal biomicroscopy helps to elucidate alternations in the cornea at the cellular level, at a resolution of 1 µm in living humans. Therefore, in this prospective case series, we first investigated microscopic changes in implanted lenticules and in recipient corneas at various depths using in vivo confocal microscopy (IVCM) with a follow-up period of up to 3 years.
Patients and Methods
In this prospective study, 8 patients with a diagnosis of ectasia after LASIK were enrolled from 2015 to 2018 at the Department of Ophthalmology, Eye and ENT Hospital of Fudan University (Shanghai, China). All patients underwent a comprehensive ocular examination, including uncorrected (UDVA) and corrected (CDVA) distance visual acuity, manifest refraction, slit-lamp examination, and corneal topography. The inclusion criteria were: (1) age 18 years or older; (2) ectasia after LASIK with or without documented evidence of progression, where progression was defined as an increase in maximum keratometry reading of 1.00 diopter (D) in 1 year, or a change in mean central keratometry reading of 1.50 D or greater, or a decrease in mean central corneal thickness of 5% or greater in three consecutive topographies in the previous 6 months9; (3) intolerance to rigid gas permeable contact lens; (4) transparent cornea; (5) normal endothelial cell density; and (6) willingness to undergo the procedure.
Patients were excluded from our study if one of the following exclusion criteria was met: (1) history of herpetic keratitis, active infections of the cornea, or preexisting autoimmune diseases; (2) severe dry eye; (3) presence of apical scar; (4) other ocular diseases such as glaucoma, cataracts, or vitreoretinal disorders; and (5) pregnancy or lactation.
This study was approved by the Ethical Committee of the Eye and ENT Hospital of Fudan University Review Board (ChiCTR-ONC-16008300) and conducted in accordance with the tenets of the Declaration of Helsinki. Signed informed consent was obtained from all patients after the risks, benefits, and alternatives to surgery were completely explained.
With the exception of case 1, 7 of the 8 eyes had either a history of accelerated (45 mW/cm2) transepithelial corneal cross-linking (CXL)10 before lenticule implantation (cases 2 to 5) or both transepithelial CXL and lenticule implantation simultaneously (cases 6 to 8, the detailed procedure is described below). Cases 2, 4, and 5 underwent CXL 1.5 years before lenticule implantation, and case 3 underwent CXL 2.5 years before lenticule implantation. The detailed procedures were outlined in our previous study.10
All surgeries were performed successfully by a single, skilled surgeon (XZ). The lenticules were created through small incision lenticule extraction (SMILE) in hyperopic donors' eyes. Before the SMILE procedure, donors were screened for human immunodeficiency virus, hepatitis B and C viruses, and Treponema pallidum by serum testing and any positive donors were excluded. Blood glucose was also examined. A hyperopic SMILE procedure was scheduled with the VisuMax femtosecond laser (Carl Zeiss Meditec) using the standard technique.11 For all eyes, the following settings were applied: repetition rate of 500 kHz, pulse energy of 130 nJ, and lenticule diameter of 5.3 to 6.5 µm. The thickness of the intended lenticule ranged from 20 to 25 µm centrally and 71 to 119 µm peripherally. The side incision created to access the lenticule was set at 90°. The lenticule was separated and extracted through the incision. To correct for astigmatism, crystal violet was used to stain the edge of the lenticule at 90° once extracted. The extracted lenticules were then washed and cryopreserved at −80 °C.
For the recipients' eyes, lenticules were selected based on the degree of spherical equivalent in the recipient eye to improve refractive status. Following standard sterile draping and speculum insertion, a Sinskey hook was used to open and lift the inferior edge of the microkeratome flap. The preserved donor lenticule was immediately transferred onto the exposed stromal bed with the axis of maximum refraction set to the axis of minimum refraction in the recipient eye and then spread until flat. The details regarding rotation were described previously.12 In the last step, the flap was repositioned. In all patients, bandage soft contact lenses were applied for 1 day after surgery.
For cases 6 to 8, after the flap was lifted, the extracted lenticule from the SMILE donor was soaked in VibeX Xtra (Avedro, Inc; containing 0.25% riboflavin-5-phosphate) for 2 seconds and then transferred onto the exposed stromal bed with steepest part of the astigmatic axis of the lenticule matched to the flattest astigmatic axis of the recipient eye and then spread until flat. Finally, the flap was repositioned and an accelerated transepithelial CXL (ATE-CXL) procedure was performed using the KXL system (Avedro) with pulsed illumination for 1 second at 45 mW/cm2, delivering a surface dose of 7.2 J/cm2. The ultraviolet treatment procedure lasted for 5 minutes and 20 seconds.
Postoperative topical medications used were dexamethasone, 0.5% levofloxacin, 0.1% fluorometholone, and a tear supplement.
All IVCM images were collected using the Heidelberg Retina Tomograph III (HRT III; Heidelberg Engineering) equipped with a 60× water-immersion objective (Olympus Europa GmbH) using a 670-nm diode laser as a light source. Images were examined for microscopic morphological changes. The details of our microscopy methodology have been described in our previous study.13 Briefly, the scanning area was 384 × 384 pixels, corresponding to an area of 400 × 400 µm, with a transverse optical resolution of 2 µm and a longitudinal optical resolution of 1 µm. For topical anesthesia before examination, a drop of 0.4% oxybuprocaine hydrochloride (Benoxil; Santen Pharmaceutical Co., Ltd) was instilled in the lower conjunctival sac.
Microscopic examination was completed along the sagittal axis of the central cornea for consecutive visualization of the corneal epithelium, subepithelial neural plexus, anterior stroma, posterior stroma, and endothelium. The edge of the flap and the edge of the lenticule were examined in the same manner as the patient gazed up. To observe reinnervation and modification of the corneal architecture, the central cornea and inferior flap margins were scanned three to five times at each visit.
Nerve fiber bundles were visualized as bright and well-defined linear structures. The stromal interface junctions were identified by the simultaneous lack of keratocytes and the presence of small particles of varying brightness.14
The patient demographics and refractive outcomes are presented in Table 1. One eye was examined using confocal microscopy at postoperative week 1 (case 6), 5 eyes at postoperative month 1 (cases 4 to 8), 3 eyes at postoperative month 3 (cases 3, 6, 7, and 8), 4 eyes at postoperative month 6 (cases 3, 5, 6, and 7), 4 eyes at postoperative year 1 (cases 1, 3, 5, and 7), 3 eyes at postoperative year 2 (cases 1 to 3), and 2 eyes (cases 1 and 2) at postoperative year 3.
Patient Demographics and Refractive Data
Subbasal Nerve Fibers in the Central Recipient Cornea and Nerve Fibers in Implanted Lenticules
No subbasal nerve fibers were observed in all eyes at postoperative week 1. Sparse nerve fibers were observed in 1 of 5 eyes at postoperative month 1, 1 of 3 eyes at postoperative months 3, 3 of 4 eyes at postoperative months 6, and 3 of 4 eyes at postoperative year 1. Many thick and tortuous nerve fibers were visible in all observed eyes at the postoperative year 2 and 3 visits (Figure 1).
Subbasal nerve fibers in the central recipient corneas (red arrows). (A) Postoperative week 1 (case 6). (B) Postoperative month 1 (case 4). (C) Postoperative month 3 (case 3). (D) Postoperative month 6 (case 4). (E) Postoperative year 1 (case 3). (F) Postoperative year 2 (case 3). (G) Postoperative year 3 (case 1). Field size: 400 × 400 µm (the same below).
Regenerated and branched nerve fibers were detected in case 1 at the postoperative 2-year visit (Figure 2). No nerve fibers were observed in the implanted lenticules in other cases.
Regenerated and branched nerve fibers (red arrow) at postoperative 2-year visit (case 1).
Stromal Changes in the Recipient Cornea
“Activated” keratocytes, which are characterized as enlarged, highly reflective objects in which cell bodies and processes can be seen,15 were observed in the anterior stroma (from the Bowman's layer to the anterior boundary of the lenticule) and posterior stroma (from the posterior boundary of the lenticule to Descemet's layer) until postoperative month 3 in all cases except case 3 (Figure 3). In case 3, activated keratocytes were observed, at postoperative month 3, month 6, year 1, and year 2 follow-up visits (Figure 4).
Stromal keratocyte changes in the recipient corneas. Activated keratocytes (red arrows) were visible in anterior stroma at postoperative (A) week 1, (B) month 1, and (C) month 3. Quiescent keratocytes presented with visible and clear keratocyte nuclei at (D) month 6.
Activated keratocytes (red arrows) were observed throughout the follow-up in case 3 at month 3 (A: anterior stroma, E: posterior stroma), month 6 (B: anterior stroma, F: posterior stroma), year 1 (C: anterior stroma, G: posterior stroma), and year 2 (D: anterior stroma, H: posterior stroma) postoperative visits.
Stromal Changes in the Implanted Lenticule
Both the anterior (Figure 5) and posterior (Figure 6) lenticule interface showed an absence of keratocytes, as well as scattered high-contrast microdots of various brightness together with fibrotic healing reaction. We observed bright microdots in all treated eyes that decreased with time, but they were still visible at the postoperative year 3 visit.
At the anterior lenticular interface, there was an absence or reduction in keratocytes and the presence of small particles of varying brightness (red arrows) (A: case 1, postoperative year 3; B: case 2, postoperative year 3; C: case 3, postoperative year 2; D: case 4, postoperative month 1; E: case 5, postoperative year 1; F: case 6, postoperative month 6; G: case 7, postoperative year 1; H: case 8, postoperative month 3).
At the posterior lenticular interface, small particles with varying brightness were present (red arrows) (A: case 1, postoperative year 3; B: case 2, postoperative 3 years; C: case 3, postoperative 2 years; D: case 4, postoperative month 1; E: case 5, postoperative year 1; F: case 6, postoperative month 6; G: case 7, postoperative month 12; H: case 8, postoperative month 3).
The keratocyte nucleus was not clearly observed in all cases until the year 1 postoperative visit. The keratocyte nucleus was detectable at postoperative year 1 in 4 (cases 1, 2, 3, and 5) of 5 cases. The keratocyte nuclei in the implanted lenticules exhibited an elongated and deformed morphology (Figure A, available in the online version of this article), which were bright objects with regular morphology (quiescent keratocytes).
Changes in lenticular keratocytes after implantation are shown using confocal microscopy. Keratocytes (red arrows) were detected in the lenticules at year 1 (A: case 5), year 2 (B: case 3), and year 3 (C–D: cases 1 and 2) postoperative visits. The keratocyte nuclei exhibited an abnormal, elongated shape.
Lenticule and Flap Edges
An obvious epithelial plug was detected at the gap between the flap and peripheral cornea in all cases at all visits (Figure B, available in the online version of this article). In addition, a distinct cicatricial reaction indicative of a wound healing process was observed at the edge of the flap periphery (Figures BB and BD), as well as a hyperreflective adjacent stroma with irregularly arranged fibrils.
Slit-lamp photographs and in vivo confocal microscopy (IVCM) images of the flap periphery at the postoperative year 3 visit, case 2. An irregular fibrotic wound (red arrows) (A, B, and D) was visualized at the peripheral edges of the flap, and an epithelial plug (red arrowhead) was present (C).
The endothelium showed no particular change in all cases at all visits.
Changes in Case 1 Across 3 Years Postoperatively
Case 1 received IVCM examination at postoperative years 1, 2, and 3 (Figure C, available in the online version of this article). At the postoperative year 2 and 3 visits, regenerated and branched nerve fibers were detected. Keratocytes in the anterior stroma showed a gradual increase in number from postoperative year 1 to year 3, whereas keratocytes in the posterior stroma showed no obvious changes in number or morphology. Keratocytes in the implanted lenticule were still rare but showed a gradual increase in number. Both anterior and posterior interfaces appeared to have an acellular structure with hyperreflective particles. The hyperreflective particles decreased with time.
Changes in the layers of the cornea, case 1. A1–A6 represents the subbasal layer, anterior stroma, anterior interface, lenticule, posterior interface, and posterior stroma at postoperative year 1. B1–B6 represents the subbasal layer, anterior stroma, anterior interface, lenticule, posterior interface, and posterior stroma at postoperative year 2. C1–C6 represents the subbasal layer, anterior stroma, anterior interface, lenticule, posterior interface, and posterior stroma at postoperative year 3. Red arrows indicate subbasal nerve fibers (B1 and C1), keratocytes (A2, B2, C2, A4, B4, C4, A6, B6, and C6), and scattered high-contrast microdots of various brightness (A3, B3, C3, A5, B5, and C5).
Difference Between Cryopreserved and Fresh Lenticules
In the current study, five cases used cryopreserved lenticules (cases 3, 4, 5, 6, and 8) and the other 3 cases used fresh lenticules (cases 1, 2, and 7). We further investigated the differences in the corneal wound healing process between corneas using cryopreserved and fresh lenticules. No obvious differences were detected between these two groups.
Allogenic intrastromal lenticule implantation has been proved clinically to be safe and effective for hyperopia16 and corneal ectasia.4 To elucidate the duration and biological process of wound healing response after the implantation, our study reports microscopic changes in implanted lenticules and recipient cornea during a 3-year follow-up period.
Keratocyte nuclei were rarely detected in either the cryopreserved or fresh lenticules in the first 6 months postoperatively. This could be attributed to keratocyte necrosis and apoptosis triggered by laser-related damage. Several reports have shown that the density of keratocytes decreased immediately after corneal refractive surgery.17–19 For other types of keratoplasty (eg, deep anterior lamellar keratoplasty), the residual donor keratocytes can contribute to immune-mediated graft rejection.20 In contrast, the implanted lenticule is almost acellular and farther from the limbal vessels, so the recipient may be at lower risk of postoperative graft rejection, which is consistent with our results, in which none of the eyes showed evidence of rejection throughout the follow-up period. At postoperative year 1, the keratocyte nuclei reappeared with elongated and deformed morphology, indicating the repopulation and partial morphological recovery of keratocytes in the lenticules. Although the role of normally quiescent keratocytes remains unclear, it has recently been postulated that the adherence of keratocytes to extracellular matrix is critical for maintaining corneal homeostasis and structural integrity.21 Also, during stromal wound healing, they can be activated again to proliferate and finally restore the corneal transparency.22 Thus, recovery observed here suggests the implanted lenticule can restore the protection offered by keratocytes, which ensures the maintenance of corneal health in the long term.
In the recipient cornea, we detected “activation” of keratocytes in anterior and posterior stroma near the lenticule interface at postoperative month 3. This may result in haze formation and inferior visual outcomes unless a clinical intervention is made. This finding implies the need for prolonged postoperative topical corticosteroid treatment. Interestingly, keratocytes stayed “activated” only in case 3 for 2 years until the end of follow-up. The UDVA, CDVA, manifest refraction, slit-lamp examination, and corneal topography indicate that corneal ectasia of this patient was progressive (Table A, available in the online version of this article). Keratocyte activation in keratoconus has been verified through histopathological examination23; therefore, we believe the lasting activation in case 3 was related to the progression of keratoconus.
Case 3 Data as Measured by Pentacam
In this study, subbasal nerve fibers in recovery were observed to be thin and sparse at year 1 and abnormally tortuous at the postoperative year 2 and year 3 visits. The corneal reinnervation was much slower than expected, and we only detected nerve fiber in the lenticules in one case within postoperative 3 years. A possible explanation is the pathogenesis and natural progression of the disease.24 Several reports have reported the diminishment of nerve density and alteration of nerve morphology in keratoconic corneas compared with normal corneas.25–27
In regard to the origin and pathologies of the particles of various brightness seen on confocal microscopy, the appearance of these small particles is common following corneal refractive surgeries. There are various hypotheses for this. Use of a microkeratome blade,28 presence of ocular surface debris such as lipid products, implanted corneal epithelial cells, and retained synthetic materials such as sponge particles and powder from surgical gloves, inflammatory cells,28,29 stress fiber bundles in migratory keratocytes, extracellular empty spaces filled with fibrillar material, histiocytes filled with vacuoles full of fibrillar material, or clear vacuoles in activated keratocytes30 are all possible explanations for the particles seen on confocal microscopy.
A limitation of this study is the relatively small sample size. However, the incidence of corneal ectasia after LASIK is 0.06% to 0.4%,31 and that of patients who underwent the implantation is even rarer. An additional uncontrolled factor is follow-up. Unfortunately, some patients were lost to follow-up before the full 3-year postoperative period. Admittedly, during the IVCM examination, a plastic cap comes in contact with the cornea and patients may at times refuse the examination due to the discomfort.
This is the first study that has characterized the long-term wound healing response at the cellular level after allogenic intrastromal lenticule implantation for corneal ectasia after LASIK. Although the current study is based on a small sample size, the findings suggest there is gradual recovery in the density and morphology of keratocytes and regrowth of subbasal nerves after an initial decrease and deformation at the interface of the recipient cornea and implanted lenticule. Additional research using controlled trials is needed to investigate the effect of the progression of corneal ectasia on the postoperative healing response. The lenticule obtained by SMILE for hyperopia is valuable material, and lenticule banks should be established in the future to benefit more patients.
- Romero-Jiménez M, Santodomingo-Rubido J, Wolffsohn JS. Keratoconus: a review. Cont Lens Anterior Eye. 2010;33(4):157–166. doi:10.1016/j.clae.2010.04.006 [CrossRef]
- Bilgihan K, Ozdek SC, Sari A, Hasanreisoglu B. Microkeratome-assisted lamellar keratoplasty for keratoconus: stromal sandwich. J Cataract Refract Surg. 2003;29(7):1267–1272. doi:10.1016/S0886-3350(02)02055-2 [CrossRef]
- Mastropasqua L, Nubile M, Salgari N, Mastropasqua R. Femtosecond laser-assisted stromal lenticule addition keratoplasty for the treatment of advanced keratoconus: a preliminary study. J Refract Surg. 2018;34(1):36–44. doi:10.3928/1081597X-20171004-04 [CrossRef]
- Jin H, He M, Liu H, et al. Small-incision femtosecond laser-assisted intracorneal concave lenticule implantation in patients with keratoconus. Cornea. 2019;38(4):446–453. doi:10.1097/ICO.0000000000001877 [CrossRef]
- Araki K, Ohashi Y, Kinoshita S, Hayashi K, Kuwayama Y, Tano Y. Epithelial wound healing in the denervated cornea. Curr Eye Res. 1994;13(3):203–211. doi:10.3109/02713689408995778 [CrossRef]
- Niederer RL, Perumal D, Sherwin T, McGhee CNJ. Corneal innervation and cellular changes after corneal transplantation: an in vivo confocal microscopy study. Invest Ophthalmol Vis Sci. 2007;48(2):621–626. doi:10.1167/iovs.06-0538 [CrossRef]
- Stramer BM, Zieske JD, Jung J-C, Austin JS, Fini ME. Molecular mechanisms controlling the fibrotic repair phenotype in cornea: implications for surgical outcomes. Invest Ophthalmol Vis Sci. 2003;44(10):4237–4246. doi:10.1167/iovs.02-1188 [CrossRef]
- Nakamura H, Riley F, Sakai H, Rademaker W, Yue BYJT, Edward DP. Histopathological and immunohistochemical studies of lenticules after epikeratoplasty for keratoconus. Br J Ophthalmol. 2005;89(7):841–846. doi:10.1136/bjo.2004.054684 [CrossRef]
- Mastropasqua L. Collagen cross-linking: when and how? A review of the state of the art of the technique and new perspectives. Eye Vis (Lond). 2015;2(1):19. doi:10.1186/s40662-015-0030-6 [CrossRef]
- Shen Y, Jian W, Sun L, et al. One-year follow-up of changes in corneal densitometry after accelerated (45 mW/cm2) transepithelial corneal collagen cross-linking for keratoconus: a retrospective study. Cornea. 2016;35(11):1434–1440. doi:10.1097/ICO.0000000000000934 [CrossRef]
- Pradhan KR, Reinstein DZ, Carp GI, Archer TJ, Dhungana P. Small incision lenticule extraction (smile) for hyperopia: 12-month refractive and visual outcomes. J Refract Surg. 2019;35(7):442–450. doi:10.3928/1081597X-20190529-01 [CrossRef]
- Li M, Li M, Sun L, Ni K, Zhou X. Predictive formula for refraction of autologous lenticule implantation for hyperopia correction. J Refract Surg. 2017;33(12):827–833. doi:10.3928/1081597X-20171016-01 [CrossRef]
- Li M, Li M, Sun L, et al. In vivo confocal microscopic investigation of the cornea after autologous implantation of lenticules obtained through small incision lenticule extraction for treatment of hyperopia. Clin Exp Optom. 2018;101(1):38–45. doi:10.1111/cxo.12595 [CrossRef]
- Sonigo B, Iordanidou V, Chong-Sit D, et al. In vivo corneal confocal microscopy comparison of intralase femtosecond laser and mechanical microkeratome for laser in situ keratomileusis. Invest Ophthalmol Vis Sci. 2006;47(7):2803–2811. doi:10.1167/iovs.05-1207 [CrossRef]
- Hovakimyan M, Falke K, Stahnke T, et al. Morphological analysis of quiescent and activated keratocytes: a review of ex vivo and in vivo findings. Curr Eye Res. 2014;39(12):1129–1144. doi:10.3109/02713683.2014.902073 [CrossRef]
- Ganesh S, Brar S, Rao PA. Cryopreservation of extracted corneal lenticules after small incision lenticule extraction for potential use in human subjects. Cornea. 2014;33(12):1355–1362. doi:10.1097/ICO.0000000000000276 [CrossRef]
- Li M, Niu L, Qin B, et al. Confocal comparison of corneal reinnervation after small incision lenticule extraction (SMILE) and femtosecond laser in situ keratomileusis (FS-LASIK). PLoS One. 2013;8(12):e81435. doi:10.1371/journal.pone.0081435 [CrossRef]
- Erie JC, Patel SV, McLaren JW, Hodge DO, Bourne WM. Corneal keratocyte deficits after photorefractive keratectomy and laser in situ keratomileusis. Am J Ophthalmol. 2006;141(5):799–809. doi:10.1016/j.ajo.2005.12.014 [CrossRef]
- Lee SJ, Kim JK, Seo KY, Kim EK, Lee HK. Comparison of corneal nerve regeneration and sensitivity between LASIK and laser epithelial keratomileusis (LASEK). Am J Ophthalmol. 2006;141(6):1009–1015. doi:10.1016/j.ajo.2006.01.048 [CrossRef]
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- Brookes NH, Loh I-P, Clover GM, Poole CA, Sherwin T. Involvement of corneal nerves in the progression of keratoconus. Exp Eye Res. 2003;77(4):515–524. doi:10.1016/S0014-4835(03)00148-9 [CrossRef]
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Patient Demographics and Refractive Data
|Case No.||Gender/Age (y)||Preop U DVA||Preop Refractiona||Lenticule Parameters||Maximum LT (µm)||Lens Diameter (mm)||Cryo Length (Days)||Visits With IVCM (Months)||Last Visit (Months)||Last Visit U DVA||Last Visit Refraction||Changes in CDVA|
|1b||M/29||0.01||−13.50 −6.00 × 10° (0.3)||+5.75 −0.50 × 5°||116||6.7||0||12, 24, 36||36||0.5||−3.50 −2.00 × 10° (0.6)||3|
|2c||F/32||0.01||−4.00 −4.25 × 70° (0.4)||+5.00 −1.00 × 160°||112||6.8||0||24, 36||36||0.05||−1.00 −3.00 × 45° (0.3)||−1|
|3b,c||M/28||0.1||−11.25 −8.75 × 140° (0.4)||+3.50 −0.50 × 5°||71||7.3||50||3, 6, 12, 24||24||0.15||−11.25 −6.00 × 145° (0.6)||2|
|4c||M/42||0.01||−12.75 −4.50 × 130° (0.3)||+8.00 −2.00 × 165°||116||7.5||27||1||24||0.4||−3.25 −8.50 × 120° (0.4)||1|
|5b,c||M/25||0.04||−10.00 −2.75 × 180° (0.3)||+6.11 −1.95 × 145°||119||8.2||21||1, 6, 12||12||0.1||−7.00 −5.50 × 15° (0.5)||2|
|6c||F/50||0.04||−17.00 −0.50 × 135° (0.3)||+4.75||76||7.3||42||1 week, 1, 3, 6||12||0.1||−11.75 −0.50 × 160° (0.5)||2|
|7c||M/41||0.05||0.50 −4.50 × 110° (0.2)||+3.00 −0.25 × 80°||79||8.5||0||1, 6, 12||12||0.2||−0.00 −3.50 × 115° (0.3)||1|
|8c||F/29||0.04||−18.50 −5.50 × 180° (0.5)||+5.45 −2.75 × 160°||104||6.2||42||1, 3||3||0.06||−10.5 −4.50 × 135° (0.4)||−1|
Case 3 Data as Measured by Pentacam
|Parameter||Preop||Postop Day 1||Postop Month 1||Postop Month 3||Postop Month 6||Postop Year 1||Postop Year 2|
|Mean anterior K reading, D||53.90||52.60||54.90||56.60||56.50||54.60||53.60|
|Mean posterior K reading, D||−8.40||−8.10||−8.50||−8.90||−8.70||−8.20||−7.90|
|Thinnest corneal thickness, µm||400||484||463||462||476||428||416|
|Posterior corneal elevation, µm||60||77||80||101||105||146||153|