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Transient effect of suction on the retinal neurovasculature in myopic patients after small-incision lenticule extraction

Liu, Jiayan MD; Tonk, Rahul Singh MD; Huang, Amy Michelle MD; Han, Elaine MD; Karp, Carol L. MD; Zeng, Minzhi MD; Zou, Huyong MD; Zheng, Yu MD; Luo, Wei MD; Sha, Xiangyin MD, PhD; Liu, Zhiping MD, PhD

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Journal of Cataract & Refractive Surgery: February 2020 - Volume 46 - Issue 2 - p 250-259
doi: 10.1016/j.jcrs.2019.09.003
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Myopia is a common condition that affects a significant portion of the world's population.1,2 The prevalence of myopia is highest in Asia at approximately 50%. By 2050, myopia and high myopia will affect 4.95 billion (52%) and 0.93 billion (10%) of the world's population, respectively.3 High myopia can cause serious, sight-threatening retinal damage, such as myopic choroidal neovascularization and lacquer cracks, and carries an increased risk of developing glaucoma and cataracts.4,5 Interestingly, high myopic individuals have decreased retinal vessel caliber and decreased superficial and deep retinal microvasculature density.6–8

Corneal refractive surgery is an effective surgical option to correct myopia. Procedures include photorefractive keratectomy, laser in situ keratomileusis (LASIK), laser epithelial keratomileusis, femtosecond lenticule extraction, and small-incision lenticule extraction (SMILE).9,10 SMILE, first reported by Shah and Sekundo 2011,11,12 is a type of corneal refractive surgery that involves the use of a femtosecond laser to create an intrastromal lenticule followed by lenticule removal through a small peripheral corneal tunnel incision to reshape the cornea and correct refractive error.13,14 In contrast to LASIK, SMILE does not require a corneal flap. Thus, SMILE theoretically causes less morphological and biomechanical disruption of the corneal surface. Because of the safe, effective, and predictable quality of this surgical procedure, SMILE has gained widespread acceptance.

Clinically, it is well documented that there are significant increases in intraocular pressure (IOP) during refractive surgery. In a study with donated human eyes, mean IOP levels during flap creation with a 200 kHz femtosecond laser (Carl Zeiss Meditec AG), a 60 kHz femtosecond laser (Abbott Medical Optics, Inc.), and a microkeratome (Ziemer Ophthalmic Systems AG) were 81 ± 18 mm Hg (SD), 179 ± 14 mm Hg, and 220 ± 53 mm Hg, respectively. Although there was lower IOP elevation during the femtosecond laser flap creation than LASIK flap creation using microkeratomes, a longer procedure time is required than during microkeratome flap creation. The duration of the cutting phase was longest for procedures performed using the 200 kHz femtosecond laser (91 ± 9 seconds).15

The transient IOP spikes during the creation of corneal flaps or intrastromal lenticules may cause harm to the optic nerve and retina, particularly in myopic patients. First, spikes in IOP during refractive surgery may have an impact on optic nerve function. Myopia itself is a risk factor for open-angle glaucoma, and the effects of transient increases in IOP are of particular concern in these patients.16 Iester et al.17 demonstrated that a 45-second acute increase in IOP, such as during LASIK (microkeratome) suction, did not decrease the retinal nerve fiber layer (RNFL) thickness in normal eyes. However, the effect of IOP elevation after SMILE surgery on the RNFL and ganglion cell-inner plexiform layer (GCIPL) still remains largely unexplored. Second, the sudden elevation in IOP during LASIK has been reported to cause retinal tears, retinal detachments, and macular holes.18,19 Finally, the IOP elevation during corneal refractive surgeries may cause transient ischemia of the retinal and optic nerve.20 Previous studies have shown that during refractive surgery procedures in rabbit or porcine eyes, the IOP was elevated.21,22 Myopic individuals who already have morphologic changes in their retinal vasculature, such as reduced vessel density, may be more susceptible to ischemic events secondary to transient intraoperative increases in IOP. However, to date, no studies have specifically focused on the alterations in the retinal vasculature after refractive surgery in myopic individuals.

Although SMILE has been widely used to correct myopia and its predictability and stability have been documented in long-term follow-ups,23 a gap exists in the understanding of the immediate effect of IOP elevation during SMILE on the retinal neurovasculature. In this work, we aimed to bridge this gap using optical coherence tomography angiography (OCTA) to explore the effect of IOP elevation during SMILE on RNFLs and the vasculature. In addition, a new strategy was developed to evaluate retinal safety after SMILE based on the application of OCTA.



This study was approved by the Institutional Review Board for Human Research of the Second Affiliated Hospital of Guangzhou Medical University. Written informed consent was obtained from all patients. All patients were treated according to the tenets of the Declaration of Helsinki. The patients were enrolled at the Ophthalmic Center, the Second Affiliated Hospital of Guangzhou Medical University. The data were processed and analyzed in the Bascom Palmer Eye Institute, University of Miami Miller School of Medicine.

A total of 38 patients with myopia (−10 diopters [D] ≤ spherical equivalent < −1.0 D) were recruited. The inclusion criteria were age older than 18 years, central corneal thickness 480 µm or greater, and target of postoperative refraction of plano. Patients were excluded if they had a history of corneal trauma or surgery, suspicion of keratoconus, severe dry eye, glaucoma, progressive corneal degeneration, cataract, uveitis, retinal vessel occlusions, and systemic disease, such as autoimmune disease or diabetes mellitus. One eye of each patient was randomly selected if both eyes were eligible for this study. All patients underwent a comprehensive ophthalmic examination that included corrected distance visual acuity (CDVA), uncorrected distance visual acuity (UDVA), slitlamp examination, corneal tomography as measured by Pentacam Scheimpflug tomography (OCULUS Optikgeräte GmbH), and IOP as measured by a noncontact tonometer (Cannon TX-F), which was adjusted as corrected IOP (IOP) based on the corneal thickness as obtained by Pentacam at baseline preperatively (PRE), postoperative day (POD) 1, and POD 7.

Surgical Procedures

All surgeries were performed by one experienced surgeon (X.S.). The VisuMax femtosecond laser system (Carl Zeiss Meditec AG) was used for SMILE with a pulse energy of 130 nJ to 160 nJ and a repetition rate of 500 kHz. The intended SMILE parameters were cap thickness between 110 µm and 120 µm, lenticule diameter between 6.0 mm and 7.0 mm, and cap diameter 1.0 mm larger than the stromal lenticule. The refractive stromal lenticule was extracted using surgical forceps through a superior side cut with a circumferential length of 2.1 mm. Postoperative medications included levofloxacin 0.5% (Cravit) 4 times a day for 2 weeks, sodium hyaluronate 0.3% (Hialid) 4 times a day for 3 weeks, and tobramycin 0.3% and dexamethasone 0.1% (Tobradex) 4 times a day for 1 week, before switching to fluorometholone 0.1% (Flumetholon) 4 times a day for 1 week. Fluorometholone was then tapered to 2 times a day for 3 weeks.

GCIPL and RNFL Thickness Measurement

To measure the thickness of the GCIPL and the peripapillary retinal nerve fiber layer (pRNFL), the 512 × 128 scanning protocol was used in a high-definition optical coherence tomography (OCT) with an AngioPlex OCTA device (Carl Zeiss Meditec) (Figure 1). The GCIPL thickness was measured using an elliptical partition, and the pRNFL thickness was measured using a quadrantal partition; measurements were obtained from OCT reports. GCIPL and RNFL thicknesses were measured at baseline PRE, POD 1, and POD 7.

Figure 1.
Figure 1.:
Optical coherence tomography imaging protocols and partition methods for analyzing the thickness of the pRNFL and GCIPL. A, B: The pRNFL scan with a diameter of 3.4 mm was divided into 4 quadrants. Dimensions of an elliptical annulus (vertical inner and outer diameter of 1.0 mm and 4.0 mm, respectively; horizontal inner and outer diameter of 1.2 mm and 4.8 mm, respectively) centered on the fovea within the macular area scanned with a macular cube scan. C, D: The GCIPL thickness of the elliptical annulus was evaluated in 6 sectors (GCIPL = ganglion cell-inner plexiform layer; I = inferior; IN = inferior nasal; IT = inferior temporal; N = nasal; pRNFL = peripapillary retinal nerve fiber layer; S = superior;

Retinal Microvasculature Imaging

The retinal vessels were imaged using a 3 × 3 mm scan on a high-definition OCT device (Figure 2). It acquires the retinal vasculature using a scan rate of 68 000 A-scans per second with an optical source centered at a wavelength of 840 nm and a bandwidth of 90 nm. The OCTA images are generated by analyzing differences in both the intensity and phase information between a number of B-scan images acquired at the same locations. Angiographic images of the superficial vascular plexus (SVP) and deep vascular plexus (DVP) were exported for further processing. To measure the vessel area density (VAD), a custom Matlab (Mathworks, Inc.) software program was used to extract the vessels using a series of image-processing procedures as described previously.24–26 OCTA images were standardized, cropped, and binarized. In each binary image, large vessels were defined as vessels with a diameter of 25 µm or larger, whereas the remaining vessels were defined as small vessels. The small vessels of the SVP and DVP were analyzed. The annulus from 0.6 to 2.5 mm was analyzed. The VAD was calculated as a unitless proportion of the total image area occupied by the detected OCTA signal (binarized as white pixels) compared with the total area of the retina (the total number of pixels). Skeletonized images were created by iteratively deleting the pixels in the outer boundary of the binarized, white-pixelated vasculature unit 1 pixel remained along the width direction of the vessels. The vessel skeleton density (VSD) was calculated based on the skeletonized images. The vessel diameter index, which represents the average vessel caliber, was calculated by dividing the total vessel area in the binarized image by the total vessel length in the skeletonized image.27 Fractal dimension (Dbox) of each skeletonized image could then be calculated by using a fractal analysis toolbox (TruSoft Benoit Pro 2.0; TruSoft International, Inc.). OCTA images were measured at baseline PRE, POD 1, and POD 7. Images of poor quality were excluded from the current study.

Figure 2.
Figure 2.:
Image processing to extract large and small vessels in the retina. The raw optical coherence tomography angiography enface view image of the SVP (A) and DVP (B) with a field-of-view 3 × 3 mm2 was processed. A 2.5 mm diameter circle (red) centered on the fovea was analyzed. The images were converted to binary images (a, i), in which large vessel diameter 25 µm or larger (b, j) and the remaining small vessels (c, k) were separated. After acquiring the binary image, the vessel density (VD, %) was calculated. SVP and DVP binary images were skeletonized for fractal analyses (e, f, g, m, n, o). d, l: Merged SVP and DVP binary images of large and small vessels. h, p: Merged SVP and DVP skeletonized images of the large and small vessels. Blue: large vessels in the SVP; green: large vessels in the DVP; red: small vessels in the SVP/DVP (DVP = deep vascular plexus; SVP = superficial vascular plexus).

Statistical Analysis

Statistical analysis was performed using IBM SPSS Statistics for Windows software (version 25, IBM Corp.). The Shapiro-Wilks test was used to test the data normality. Generalized estimating equation models (repeated measures) were conducted to evaluate the variations in each group at different time points: PRE, POD 1, and POD 7. Pearson correlation coefficients were used to evaluate the linear correlation between changes in corrected IOP and retinal neurovasculature parameters. All data were presented as mean ± SD, and P values less than .05 were considered statistically significant.


Study Population and Baseline Clinical and Structural Parameters

Thirty-eight eyes of 38 myopic patients were included. The mean age of the patients was 28.1 ± 4.9 years. The mean spherical equivalent of the patients was −4.71 ± 1.50 D. Baseline demographic and clinical data are shown in Table 1.

Table 1.
Table 1.:
Demographics of patients at baseline.

Clinical and Structural Parameters After SMILE

All patients had a significant improvement in UDVA and no loss of CDVA at the final follow-up (POD 7). No patient experienced any serious adverse events. Slitlamp examination showed there was no clinically significant corneal edema at POD 1 and POD 7.

Compared to baseline, the patients had decreased Km (P < .05), decreased central corneal thickness (P < .05), and decreased corneal volume (P < .05) (Table 2). Although the cornea was slightly thicker at POD 1 than at POD 7, there was no significant difference in corneal volumes at POD 1 and POD 7. The patients showed an increase in the GCIPL thickness after SMILE at POD 1 and POD 7 (P < .05) (Figure 3). Compared to baseline, superior temporal, superior, superior nasal, inferior, and inferior temporal quadrants of the GCIPL thickness were significantly increased at POD 1 (Table 3). At POD 7, each quadrant of the GCIPL thickness reverted to the baseline level except the superior nasal quadrant (P < .05). As shown in Figure 4, the VAD, VSD, and Dbox of the SVP and DVP were decreased at POD 1 in both groups (P < .05), but not at POD 7. As shown in Figure 5, the VDI in total vessels of the DVP was increased at POD 7 (P < .05), and the VDI in small vessels of the SVP and DVP was decreased at POD 1 (P < .05). Compared to PRE, the VDI in big vessels of the DVP at POD 1 and POD 7 was decreased (P < .05). As shown in Figure 6, the Dbox of the SVP and DVP were decreased at POD 1 in both groups (P < .05), but not at POD 7. Representative patient images at various time points, PRE, POD 1, and POD 7, are shown in Figure 7.

Table 2.
Table 2.:
Clinical parameters of patients at baseline and after SMILE.
Figure 3.
Figure 3.:
Changes in the mean thickness of the pRNFL and GCIPL at baseline and after small-incision lenticule extraction (GCIPL = ganglion cell-inner plexiform layer; POD = postoperative day; pRNFL = peripapillary retinal nerve fiber layer).
Table 3.
Table 3.:
Changes in pRNFL and GCIPL thicknesses at baseline and after SMILE.
Figure 4.
Figure 4.:
Changes in the vessel area density and vessel skeleton density at baseline and after small-incision lenticule extraction in the patients. (DVP = deep vascular plexus; POD = postoperative day; SVP = superficial vascular plexus).
Figure 5.
Figure 5.:
Changes in the vessel diameter index at baseline and after small-incision lenticule extraction in the patients. (DVP = deep vascular plexus; POD = postoperative day; SVP = superficial vascular plexus).
Figure 6.
Figure 6.:
Changes in the fractal dimension (Dbox) at baseline and after small-incision lenticule extraction in the patients. (DVP = deep vascular plexus; POD = postoperative day; SVP = superficial vascular plexus).
Figure 7.
Figure 7.:
Representative images of changes in the vessel density at different time points in a 34-year-old woman. Top row and top tables showed the changes of the VAD, VSD, VDI, and Dbox in the SVP at PRE, POD 1, and POD 7. Bottom row and bottom tables showed the changes of the VAD, VSD, VDI, and Dbox in the DVP at PRE, POD 1, and POD 7 (Big = big vessels; DVP = deep vascular plexus; POD 1 = postoperative day 1; POD 7 = postoperative day 7; PRE = baseline; Small = small vessels; SVP = superficial vascular plexus; Total = total vessels; VAD = vessel area density; VDI = vessel diameter index; VSD = vessel skeleton density).

Correlations Between Clinical and Structural Parameters

Correlational analyses were performed between changes in clinical (corrected IOP and logarithm of the minimum angle of resolution) and structural OCTA (layer thickness, VAD, VSD, and Dbox) parameters at various time points, PRE, POD 1, and POD 7. Changes in corrected IOP were not significantly correlated with changes in the pRNFL thickness (r = 0.039, P = .738). Changes in corrected IOP were positively correlated with changes in the GCIPL thickness (r = 0.385, P = .001), negatively correlated with changes in the VAD of small vessels in the DVP (r = −0.300, P = .008), and negatively correlated with changes in the Dbox of total vessels in the DVP (r = −0.348, P = .002). Changes in corrected IOP were negatively correlated with the VSD of small vessels in the DVP (r = −0.231, P = .045). Changes in corrected IOP were negatively correlated with the VDI of big vessels in the SVP (r = −0.240, P = .037) and the VDI of small vessels in the DVP (r = −0.291, P = .011) (Table 4).

Table 4.
Table 4.:
Pearson correlation analysis of ∆CIOP with the changes in retinal neurovasculature parameters.


OCTA is a noninvasive imaging modality based on OCT that allows for the visualization of functional blood vessels in the eye by using the variable backscattering of light from different static structural tissues and moving particles (ie, red blood cells). The images obtained from OCTA are essentially motion-contrast images of such high-resolution that they approach a histological level of resolution. Because of the degree of high-resolution images that OCTA can provide, this imaging modality can provide in-depth information about the retinal neurovasculature. This unprecedented resolution coupled with the simple, fast, and noninvasive nature of this imaging platform has allowed a host of basic and clinical research applications.28

Studies have demonstrated that OCTA is subject to low intravisit and intervisit flow index variability as well as good repeatability of vessel density measurements.29,30 In the current study, OCTA was performed by the same technician who had been trained well. Patients with poor images were excluded. In addition, the vascular parameters were measured in a circular area (ϕ 2.5 mm) centered on the fovea, which decreases variability because of motion and macular area tilt between tests.30

This study quantitatively characterized the retinal neuro-vasculature in patients with myopia after SMILE using OCTA. To our knowledge, this is the first study to directly evaluate the transient fluctuations of the retinal neurovasculature after SMILE. All patients had a significant improvement in UDVA and no loss of CDVA at the final follow-up, which indicated that the patients had good visual acuity outcome and no serious adverse effect after SMILE surgery. In this study, we used OCTA to objectively measure retinal neural structures (GCIPL and the pRNFL) and retinal vascular perfusion in the SVP and DVP at baseline and up to a week after SMILE surgery.

Because of the various degrees of degenerative alterations in the retinas of myopic patients and the susceptibility of this population to chronic open-angle glaucoma, the risk of retinal complications of SMILE in myopic patients is increased. Most studies have focused on the effect of corneal refractive surgery on nerve fiber loss, particularly in the GCIPL and pRNFL (Table 5).31–37 However, studies to date have failed to demonstrate a significant decrease in the pRNFL or GCIPL thickness after refractive surgery when compared with baseline. In agreement with previous studies, our results confirmed previous findings that the transient IOP increase during the flap preparation was unlikely to create consequent loss of retinal nerve fibers. By contrast, our study found that the thickness of the GCIPL was transiently increased after SMILE surgery. It is possible that acute high IOP can cause axoplasmic flow disorder in retinal ganglion cells, causing cell dysfunction or death, which could cause the thickness of the GCIPL to transiently increase after SMILE surgery during the early stages.22,38

Table 5.
Table 5.:
Retinal neurovasculature alterations in patients with myopia after refractive surgery.

IOP fluctuations during refractive surgery, including LASIK, FS-LASIK, and SMILE,39–43 can cause ocular complications, especially in the retina. A potential source of damage to the vitreous and retina is from the pulsed energy applied to the cornea. When the suction ring induces an elevation in IOP that is then suddenly released, the anterior segment is quickly drawn into a vacuum chamber with subsequent rapid shape deformation. All structures posterior to the suction ring are also rapidly compressed and decompressed in sequence. Intraoperative vacuum suction caused by transient elevated IOP may cause optic nerve and retinal circulatory ischemia, and the sudden drop of IOP after stopping the suction may cause ischemia–reperfusion dysfunction.44,45 Transient changes in retinal hemodynamics may cause vascular endothelial spasm or dysfunction.17,38

Significant alterations in retinal hemodynamics after SMILE surgery appear to be mediated by fluctuation in IOP. Specifically, the vessel density (VAD, VSD, and Dbox) and vessel caliber (VDI) in the SVP and DVP were decreased at POD 1, likely in response to surgical factors such as IOP elevation during flap preparation. These effects appeared to be transient in nature at POD 1. During the capillary reperfusion procedure, the VDI of small vessels in both the SVP and DVP was increased at POD 7, and the VDI of big vessels in the DVP was decreased at POD 7. The dynamic regulation of the vessel density and vessel caliber between small and big vessels also demonstrated the retinal hemodynamics during transient ischemia–reperfusion spasm after suction.

Although the changes in the retinal neurovasculature were attributed to IOP changes during refractive surgery, other factors may also affect the retinal neurovasculature during and after SMILE. Liu et al. found that approximately 34% of eyes had corneal edema immediately after SMILE. However, all eyes in this series had a resolution of this edema within 6 hours to 24 hours.46 In agreement with this finding, the current study did not observe any operative corneal edema at POD 1 and POD 7. Although frank postoperative edema was not observed, the corneal thickness was slightly higher at POD 1 than at POD 7. In animal models, keratocyte death and proliferation, inflammatory infiltration, and extracellular matrix remodeling predominately take place during the first POD after refractive surgery.47,48 Compared to LASIK, the SMILE procedure elicits virtually identical and minimal keratocyte activation, cell death, and inflammation.49 During corneal wound healing, inflammation responses may affect corneal ultrastructure, which may cause the changes in densitometry of the cornea. Thus, inflammation responses during corneal wound healing may contribute to vessel density reduction at POD 1. Further studies may be necessary to more clearly elucidate the cause of these transient retinal neurovasculature changes.

As with all studies, our findings must be considered in light of its limitations. First, although the present study demonstrated reversible fluctuations in the retinal neurovasculature in myopic patients after SMILE, this should be repeated with a larger sample size. Second, the alterations in the corneal curvature and corneal edema might influence the accurate measurement of the retinal parameters. Third, we did not measure the intraoperative IOP or immediate postoperative IOP, which may have more significant clinical relevance of the changes in IOP between retinal neurovasculature parameters. The final limitation is the lack of longer follow-up to truly show return to baseline. Long-term alterations in the retina need to be further explored in the future.

In summary, this study demonstrated surgical-related fluctuations in the retinal neurovasculature in patients with myopia after SMILE. The transient reversible fluctuations in the retinal neurovasculature may represent a characteristic pattern of homeostasis in patients after refractive surgery. Our findings may lead to further validation for using the retinal neurovasculature in clinical research aimed at the detection and monitoring of the retinal neurovasculature after refractive surgery, which could provide a predictor model for evaluating the retinal safety of refractive surgery.


  • Myopia is projected to affect 50% of the world's population by 2050. Small-incision lenticule extraction (SMILE) has gained widespread acceptance. The effect of SMILE on the retinal neurovasculature remains unexplored.


  • There are transient retinal neurovasculature fluctuations after SMILE. Changes in the ganglion cell-inner plexiform layer thickness were positively correlated with changes in corrected intraocular pressure (IOP). Changes in the vasculature of the superficial vascular plexus and deep vascular plexus were negatively correlated with changes in corrected IOP.


1. World Health Organization. The impact of myopia and high myopia. Report of the Joint World Health Organization–Brien Holden Vision Institute Global Scientific Meeting on Myopia. University of New South Wales, Sydney, Australia. 2015:1–40.
2. Bourne RR, Stevens GA, White RA, Smith JL, Flaxman SR, Price H, Jonas JB, Keeffe J, Leasher J, Naidoo K, Pesudovs K, Resnikoff S, Taylor HR. Causes of vision loss worldwide, 1990-2010: a systematic analysis. Lancet Glob Health 2013;1:e339–e349
3. Holden BA, Fricke TR, Wilson DA, Jong M, Naidoo KS, Sankaridurg P, Wong TY, Naduvilath TJ, Resnikoff S. Global prevalence of myopia and high myopia and temporal trends from 2000 through 2050. Ophthalmology 2016;123:1036–1042
4. Vongphanit J, Mitchell P, Wang JJ. Prevalence and progression of myopic retinopathy in an older population. Ophthalmology 2002;109:704–711
5. Kim YM, Yoon JU, Koh HJ. The analysis of lacquer crack in the assessment of myopic choroidal neovascularization. Eye 2011;25:937–946
6. Li M, Yang Y, Jiang H, Gregori G, Roisman L, Zheng F, Ke B, Qu D, Wang J. Retinal microvascular network and microcirculation assessments in high myopia. Am J Ophthalmol 2017;174:56–67
7. Yang Y, Wang J, Jiang H, Yang X, Feng L, Hu L, Wang L, Lu F, Shen M. Retinal microvasculature alteration in high myopia. Invest Ophthalmol Vis Sci 2016;57:6020–6030
8. Li H, Mitchell P, Rochtchina E, Burlutsky G, Wong TY, Wang JJ. Retinal vessel caliber and myopic retinopathy: the Blue Mountains Eye Study. Ophthalmic Epidemiol 2011;18:275–280
9. Seiler T, Holschbach A, Derse M, Jean B, Genth U. Complications of myopic photorefractive keratectomy with the excimer laser. Ophthalmology 1994;101:153–160
10. Melki SA, Azar DT. LASIK complications: etiology, management, and prevention. Surv Ophthalmol 2001;46:95–116
11. Shah R, Shah S, Sengupta S. Results of small incision lenticule extraction: all-in-one femtosecond laser refractive surgery. J Cataract Refract Surg 2011;37:127–137
12. Sekundo W, Kunert KS, Blum M. Small incision corneal refractive surgery using the small incision lenticule extraction (SMILE) procedure for the correction of myopia and myopic astigmatism: results of a 6 month prospective study. Br J Ophthalmol 2011;95:335–339
13. Wang M, Zhang Y, Wu W, Young JA, Hatch KM, Pineda R, Elze T, Wang Y. Predicting refractive outcome of small incision lenticule extraction for myopia using corneal properties. Transl Vis Sci Technol 2018;7:11
14. Shetty R, Francis M, Shroff R, Pahuja N, Khamar P, Girrish M, Nuijts RMMA, Sinha RA. Corneal biomechanical changes and tissue remodeling after SMILE and LASIK. Invest Ophthalmol Vis Sci 2017;58:5703–5712
15. Vetter JM, Faust M, Gericke A, Pfeiffer N, Weingartner WE, Sekundo W. Intraocular pressure measurements during flap preparation using 2 femtosecond lasers and 1 microkeratome in human donor eyes. J Cataract Refract Surg 2012;38:2011–2018
16. Marcus MW, de Vries MM, Junoy Montolio FG, Jansonius NM. Myopia as a risk factor for open-angle glaucoma: a systematic review and meta-analysis. Ophthalmology 2011;118:1989–1994
17. Iester M, Tizte P, Mermoud A. Retinal nerve fiber layer thickness changes after an acute increase in intraocular pressure. J Cataract Refract Surg 2002;28:2117–2122
18. Qin B, Huang L, Zeng J, Hu J. Retinal detachment after laser in situ keratomileusis in myopic eyes. Am J Ophthalmol 2007;144:921–923
19. Arevalo JF, Mendoza AJ, Velez-Vazquez W, Rodriguez FJ, Rodriguez A, Rosales-Meneses JL, Yepez JB, Ramirez E, Dessouki A, Chan CK, Mittra RA, Ramsay RC, Garcia RA, Ruiz-Moreno JM. Full-thickness macular hole after LASIK for the correction of myopia. Ophthalmology 2005;112:1207–1212
20. Bashford KP, Shafranov G, Tauber S, Shields MB. Considerations of glaucoma in patients undergoing corneal refractive surgery. Surv Ophthalmol 2005;50:245–251
21. Vetter JM, Schirra A, Garcia-Bardon D, Lorenz K, Weingartner WE, Sekundo W. Comparison of intraocular pressure during corneal flap preparation between a femtosecond laser and a mechanical microkeratome in porcine eyes. Cornea 2011;30:1150–1154
22. Cheng W, Liu L, Yu S, Jing Y, Zuo T, Cui T, Zhang H, Ma J, Wei P, Hao W, Lap-Ki NA, Pak-Man CG, Chi-Pang WV, Chiu K, Wang Y. Real-time intraocular pressure measurements in the vitreous chamber of rabbit eyes during small incision lenticule extraction (SMILE). Curr Eye Res 2018;43:1260–1266
23. Han T, Zheng K, Chen Y, Gao Y, He L, Zhou X. Four-year observation of predictability and stability of small incision lenticule extraction. BMC Ophthalmol 2016;16:149
24. Lin Y, Jiang H, Liu Y, Rosa GG, Gregori G, Dong C, Rundek T, Wang J. Age-related alterations in retinal tissue perfusion and volumetric vessel density. Invest Ophthalmol Vis Sci 2019;60:685–693
25. Liu Z, Wang H, Jiang H, Gameiro GR, Wang J. Quantitative analysis of conjunctival microvasculature imaged using optical coherence tomography angiography. Eye Vis 2019;6:5
26. Wei Y, Jiang H, Shi Y, Qu D, Gregori G, Zheng F, Rundek T, Wang J. Age-related alterations in the retinal microvasculature, microcirculation, and microstructure. Invest Ophthalmol Vis Sci 2017;58:3804–3817
27. Kim AY, Chu Z, Shahidzadeh A, Wang RK, Puliafito CA, Kashani AH. Quantifying microvascular density and morphology in diabetic retinopathy using spectral-domain optical coherence tomography angiography. Invest Ophthalmol Vis Sci 2016;57:OCT362–OCT370
28. Kashani AH, Chen CL, Gahm JK, Zheng F, Richter GM, Rosenfeld PJ, Shi Y, Wang RK. Optical coherence tomography angiography: a comprehensive review of current methods and clinical applications. Prog Retin Eye Res 2017;60:66–100
29. Jia Y, Wei E, Wang X, Zhang X, Morrison JC, Parikh M, Lombardi LH, Gattey DM, Armour RL, Edmunds B, Kraus MF, Fujimoto JG, Huang D. Optical coherence tomography angiography of optic disc perfusion in glaucoma. Ophthalmology 2014;121:1322–1332
30. Lim CW, Cheng J, Tay ELT, Teo HY, Wong EPY, Yong VKY, Lim BA, Hee OK, Wong HT, Yip LWL. Optical coherence tomography angiography of the macula and optic nerve head: microvascular density and test-retest repeatability in normal subjects. BMC Ophthalmol 2018;18:315
31. Zivkovic M, Jaksic V, Giarmoukakis A, Grentzelos M, Zlatanovic M, Zlatanovic G, Miljkovic A, Jovanovic S, Stamenkovic M, Kymionis G. The effect of LASIK procedure on peripapillary retinal nerve fiber layer and macular ganglion cell-inner plexiform layer thickness in myopic eyes. Biomed Res Int 2017;2017:8923819
32. Zhao PF, Zhou YH, Zhang J, Wei WB. Analysis of macular and retinal nerve fiber layer thickness in children with refractory amblyopia after femtosecond laser-assisted laser in situ keratomileusis: a retrospective study. Chin Med J 2017;130:2234–2240
33. Zhang J, Zhou Y, Zheng Y, Liu Q, Zhai C, Wang Y. Effect of suction on macular and retinal nerve fiber layer thickness during femtosecond lenticule extraction and femtosecond laser-assisted laser in situ keratomileusis. J Cataract Refract Surg 2014;40:1994–2001
34. Zangwill LM, Abunto T, Bowd C, Angeles R, Schanzlin DJ, Weinreb RN. Scanning laser polarimetry retinal nerve fiber layer thickness measurements after LASIK. Ophthalmology 2005;112:200–207
35. Shpak AA, Kostenev SV, Mushkova IA, Korobkova MV. Effect of corneal refractive surgery on optical coherence tomography measurements. Vestn Oftalmol 2018;134:48–53
36. Sharma N, Sony P, Gupta A, Vajpayee RB. Effect of laser in situ keratomileusis and laser-assisted subepithelial keratectomy on retinal nerve fiber layer thickness. J Cataract Refract Surg 2006;32:446–450
37. Halkiadakis I, Anglionto L, Ferensowicz M, Triebwasser RW, van Westenbrugge JA, Gimbel HV. Assessment of nerve fiber layer thickness before and after laser in situ keratomileusis using scanning laser polarimetry with variable corneal compensation. J Cataract Refract Surg 2005;31:1035–1041
38. Tsai JC, Lin PW, Teng MC, Lai IC. Longitudinal changes in retinal nerve fiber layer thickness after acute primary angle closure measured with optical coherence tomography. Invest Ophthalmol Vis Sci 2007;48:1659–1664
39. Zhang Y, Shen Q, Jia Y, Zhou D, Zhou J. Clinical outcomes of SMILE and FS-LASIK used to treat myopia: a meta-analysis. J Refract Surg 2016;32:256–265
40. Huang Y, Li Z, van RN, Wang N, Pang CP, Cui Q. Different responses of macrophages in retinal ganglion cell survival after acute ocular hypertension in rats with different autoimmune backgrounds. Exp Eye Res 2007;85:659–666
41. Shen Z, Zhu Y, Song X, Yan J, Yao K. Dry eye after small incision lenticule extraction (SMILE) versus femtosecond laser-assisted in situ keratomileusis (FS-LASIK) for myopia: a meta-analysis. PLoS One 2016;11:e0168081
42. Shen Z, Shi K, Yu Y, Yu X, Lin Y, Yao K. Small incision lenticule extraction (SMILE) versus femtosecond laser-assisted in situ keratomileusis (FS-LASIK) for myopia: a systematic review and meta-analysis. PLoS One 2016;11:e0158176
43. Hamed AM, Heikal MA, Soliman TT, Daifalla A, Said-Ahmed KE. SMILE intraoperative complications: incidence and management. Int J Ophthalmol 2019;12:280–283
44. Arevalo JF. Posterior segment complications after laser-assisted in situ keratomileusis. Curr Opin Ophthalmol 2008;19:177–184
45. Takayama J, Tomidokoro A, Tamaki Y, Araie M. Time course of changes in optic nerve head circulation after acute reduction in intraocular pressure. Invest Ophthalmol Vis Sci 2005;46:1409–1419
46. Liu T, Dan T, Luo Y. Small incision lenticule extraction for correction of myopia and myopic astigmatism: first 24-hour outcomes. J Ophthalmol 2017;2017:5824534
47. Dong Z, Zhou X, Wu J, Zhang Z, Li T, Zhou Z, Zhang S, Li G. Small incision lenticule extraction (SMILE) and femtosecond laser LASIK: comparison of corneal wound healing and inflammation. Br J Ophthalmol 2014;98:263–269
48. Riau AK, Angunawela RI, Chaurasia SS, Lee WS, Tan DT, Mehta JS. Early corneal wound healing and inflammatory responses after refractive lenticule extraction (ReLEx). Invest Ophthalmol Vis Sci 2011;52:6213–6221
49. Luft N, Schumann RG, Dirisamer M, Kook D, Siedlecki J, Wertheimer C, Priglinger SG, Mayer WJ. Wound healing, inflammation, and corneal ultrastructure after SMILE and femtosecond laser-assisted LASIK: a human ex vivo study. J Refract Surg 2018;34:393–399
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