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Chronic dry eye and regression after laser in situ keratomileusis for myopia

Albietz, Julie M PhD*; Lenton, Lee M FRANZCO, FRACS; McLennan, Suzanne G

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Journal of Cataract & Refractive Surgery: March 2004 - Volume 30 - Issue 3 - p 675-684
doi: 10.1016/j.jcrs.2003.07.003
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Laser in situ keratomileusis (LASIK) is considered a safe and effective procedure to correct low to moderately high (up to −15 diopters [D]) myopia.1,2 Refractive stability is generally achieved 1 to 3 months after LASIK.1,3 However, regression of the refractive result can occur in up to 10% of eyes that have had LASIK to correct low to moderate myopia.2,4,5 The incidence of regression after LASIK increases to approximately 40% in eyes with moderate to high myopia.5,6 As with other refractive surgery procedures, regression is dependent on the amount of myopic correction attempted; higher myopic corrections have a greater incidence and magnitude of myopic regression.5,7

Recent studies highlight that LASIK can cause sustained dysfunction of the integrated ocular surface/lacrimal gland functional unit, resulting in chronic dry eye.8,9 In a 2001 survey of members of the American Society of Cataract and Refractive Surgeons, the most common complication of LASIK was dry eye.10

Clinically, we have identified a subset of LASIK patients who experience chronic dry eye after LASIK and regression of the refractive result. Several studies report an association between refractive regression and dry-eye symptoms and signs before and/or after refractive surgery in patients with myopia who have had radial keratotomy11 or photorefractive keratectomy (PRK)12 and in patients with hyperopia who have had LASIK.9 However, other studies do not support an association between refractive regression and dry-eye symptoms or signs before myopic PRK13,14 or after LASIK.15

In this study, we analyzed our clinical patient database to compare patients with and without chronic dry eye after LASIK. The purpose of the analysis was to determine the effect of chronic dry eye on the refractive outcome and refractive regression after LASIK for myopia and identify potential risk factors for developing chronic dry eye and regression after this procedure.

To reinforce the clinical relevance of the analysis findings, we present several case studies and guidelines for managing LASIK patients with chronic dry eye.

Patients and Methods

The study was a retrospective analysis of 565 eyes (565 patients) that had LASIK for correction of low to moderate myopia at a private ophthalmology practice (Excimer Laser Vision Centre, Brisbane, Australia) between August 1998 and May 2002. Our database tracks surgical outcomes in all primary myopic LASIK procedures. The database contained 1602 LASIK procedures, of which 1475 were primary LASIK procedures in 771 patients. Of these, 565 patients met the inclusion criteria and had complete data for at least 1 eye for 12 months. Data analysis was based on these 565 patients. In cases in which a patient had surgery in both eyes, met the inclusion criteria, and had complete data for both eyes, only right-eye data were analyzed. All patients gave written informed consent. The Queensland University of Technology Biomedical Ethics Committee approved the study protocol.

The eligibility criteria used in the study were no autoimmune or metabolic disease, uncontrolled intraocular disease, degenerative or neurotrophic corneal disease, preoperative use of topical medications other than those prescribed for LASIK pretreatment, or previous ocular surgery or trauma within 6 months of the LASIK procedure; not pregnant or lactating; stable refraction for at least 12 months before LASIK; stable keratometry and pachymetry following cessation of contact lens use; compliance with prescribed tear-film and ocular-surface management schedule and required visit schedule before and after surgery; no intraoperative LASIK complications (eg, complete or incomplete flaps, significant epithelial defects, allergic reactions); no LASIK primary refractive undercorrection, overcorrection, or induced astigmatism of greater than 0.5 D; no lenticular opacities identified before or after surgery that were thought to have a significant effect on the refractive outcome; and no LASIK astigmatism corrections greater than 2.0 D, mixed astigmatism, or pure astigmatism corrections.

All LASIK procedures were performed by the same experienced LASIK surgeon (L.M.L.) using the standard laser ablation nomograms. The lamellar flaps were created using an Automated Corneal Shaper (Chiron) and an excimer laser (Nidek EC-5000). The flaps were 8.5 mm wide and 130 μm thick with an optical zone of 5.3 to 6.3 mm and a transition zone of 7.5 mm.

After surgery, all eyes received a standard treatment of nonpreserved chloramphenicol 0.5% 4 times a day for 3 days and a combination of fluorometholone acetate 0.1% (Flucon®) 4 times a day, tapered 1 drop per week over 1 month. All patients were instructed to use nonpreserved artificial tears (Cellufresh® [sodium carboxymethylcellulose 0.5% in nonpreserved lactate buffer] and/or Bion® Tears [hydroxypropyl methylcellulose 0.3% and dextran 70 0.1% in bicarbonate buffer]) at least 4 times a day for the first 6 months after surgery. Pretreatment of the tear film and ocular surface was also performed on indication when specific tear film and ocular surface problems were identified before LASIK. Pretreatment measures included nonpreserved artificial tears 4 times a day for at least 1 week before LASIK, nonpreserved steroid (prednisolone sodium phosphate 0.5%) for up to 2 weeks for lid margin and/or ocular surface inflammation, punctal plugs for tear deficiency unresponsive to artificial tears alone, and lid hygiene procedures for lid disease.

After LASIK, patients were instructed to use nonpreserved artificial tears (Cellufresh and/or Bion Tears) 4 times a day or more frequently for 12 months. The patients were also instructed to use sodium carboxymethylcellulose 1.0% in nonpreserved lactate buffer (Celluvisc®) for at least 1 week as a nighttime lubricant, and if long-term nighttime lubrication was required, Celluvisc and/or nonpreserved carbomer gel (Polygel) and/or nonpreserved paraffin plus lanolin ointment (Polyvisc).

Silicone punctum plugs (FlexPlug, Eagle Vision) were inserted in the inferior puncta on indication after LASIK when aqueous tear deficiency was diagnosed and could not be controlled with the lubricant therapy described above.


The following assessments were performed in each patient before surgery and 2 weeks and 1, 3, 6, and 12 months post-LASIK with the results recorded in the clinical database: (1) Fluorescein breakup time (FBUT), a measure of tear film stability, was performed using the method described by Cho and Douthwaite.16 (2) Phenol red-thread tear test (PRT) (Zone Quick, Menicon Co. Ltd.), a measure of tear secretion, volume, and turnover,17 was performed using the methods previously described.18 A PRT value of <11.0 mm over 15 seconds was diagnostic of tear-deficient dry eye.18 (3) Ocular surface staining to grade the severity of fluorescein corneal staining on a scale of 0 to 15, as recommended by Lemp.19 (4) Central corneal sensation measured using the Cochet-Bonnet esthesiometer.20 (5) Dry-eye symptoms were assessed using the McMonnies Dry Eye Symptom Survey, a validated dry-eye symptom survey.21 Patients were classified as having “dry eye symptoms” (either before or after surgery) if they reported experiencing 1 or more of the primary symptoms in the survey (soreness, scratchiness, dryness, grittiness, burning) “often” or “constantly.” (6) Ocular Surface Disease Index (OSDI), a validated 12-item questionnaire, assessed the symptoms of ocular irritation with dry eye and the impact on visual functioning.22,23 The OSDI scores range from 0 to 100 with 0 as asymptomatic and 100 as severe debilitating dry-eye disease. (7) Refractive outcome, defined as the difference between the spherical equivalent (SE) refraction and the target SE refraction. (8) Regression, defined as a refractive outcome of ≥1.00 D of myopia.

Patients were also questioned about their history of contact lens use. Patients were classified as contact lens users before surgery if they wore lenses on a regular basis (minimum mean wearing time of 30 hours per week) and had worn contact lenses for at least the past year. Occasional or intermittent contact lens users were regarded as non-contact lens users in this study.

Patients were diagnosed as having “dry eye” before or after surgery if they experienced 1 or more of McMonnies dry-eye primary symptoms occurring “often” or “constantly,” the FBUT value was less than 10 seconds, and they had a fluorescein corneal staining score of greater than 3/15 and a PRT value of <11 mm/15 seconds.

Patients were diagnosed as having “chronic dry eye” after surgery if they had dry eye (according to the definition above) for a period of 6 months or more after surgery. The 6-month cutoff point was chosen because by 6 months, most studies indicate that the following variables have returned to preoperative levels: dry-eye symptoms,24 tear-film stability,24, 25 ocular surface staining,8, 24 tear volume,24 tear secretion,8, 25 and corneal sensation.26

Statistical Analysis

Parametric tests were used to analyze the refraction data. Other ocular variables were analyzed using nonparametric tests because of the non-normal distribution of the data. Comparisons between groups and between variables were made using the Pearson chi-square test for categorical data and the analysis of variance (ANOVA) or the Kruskall-Wallis ANOVA test for continuous data. Differences were considered significant when P was less than 0.05.


Patient Characteristics

The mean age of the 565 patients was 36 ± 10 years (range 18 to 72 years); 249 patients (44%) were men.

The mean SE refraction was −4.00 D ± 2.26 (SD) (mean sphere −3.84 ± 2.36 D [range −0.50 to −16.50 D], mean cylinder −0.68 ± 0.59 D [range 0.00 to −2.00 D]). The mean ablation depth was 58 ± 27 μm (range 10 to 166 μm).

Before LASIK, dry eye was diagnosed in 40 patients (7%). An additional 102 patients (18%) reported dry-eye symptoms but did not have significant dry-eye signs. After surgery, 45 patients (8%) were affected by chronic dry eye. Regression was observed in 46 patients (8%) over the 12-month test period.

Baseline characteristics for patients with and without chronic dry eye after surgery are presented in Table 1.

Table 1
Table 1:
Baseline characteristics (before LASIK) of patients with and without chronic dry eye after LASIK surgery.

Effect of Chronic Dry Eye on Regression

Regression after LASIK was related to chronic dry eye. Regression occurred in 12 (27%) of 45 patients with chronic dry eye and in 35 (7%) of 520 patients without (P< .0001).

Patients with chronic dry eye had more myopic outcomes than those without. Statistically significant differences between the 2 groups were found 1, 3, 6, and 12 months after surgery (Figure 1). The between-group differences (approximately 0.25 D more myopic in the chronic dry eye group at the various time points) were not highly clinically significant.

Figure 1.
Figure 1.:
(Albietz) Refractive outcome (median difference in spherical equivalent refraction from target) after LASIK in patients with chronic dry eye (CDE) and without chronic dry eye (No CDE). Significant between-group differences (denoted by *) were detected at 1 (P = .02), 3 (P = .01), 6 (P = .004), and 12 (P = .008) months.

Risk Factors for Chronic Dry Eye

Patients developing chronic dry eye after LASIK were significantly more likely to be female and have more dry-eye symptoms before surgery; longer use of contact lenses was borderline significant (P = .05) (Table 1). The group that developed chronic dry eye also exhibited significantly greater presurgical ocular surface staining, lower FBUT values, and reduced presurgical corneal sensation. The lower PRT times in the chronic dry eye group were borderline significant (P = .05). The chronic dry-eye group was had a significantly higher attempted refractive correction and a greater ablation depth. Chronic dry eye was also associated with reduced central corneal sensation 12 months after surgery (3.4 ± 1.9 cm in chronic dry eye patients and 5.0 ± 1.1 cm in all other subjects [P = .007]) but not at any of the earlier time points after surgery.

Risk Factors for Regression

To further examine the relationship between regression and ocular variables, patients were subdivided into 2 groups: those with regression (n = 46) and those without (n = 519). The 2 groups did not differ before surgery in FBUT, PRT, ocular surface staining, corneal sensation, dry-eye symptoms, and OSDI. The regression group had significantly higher presurgical refractive corrections (preoperative SE refractive target −5.57 ± 2.19 D in regression group and −3.88 ± 2.16 D in no-regression group [P< .001]) and larger refractive ablations (71 ± 34 μm and 57 ± 27 μm, respectively [P< .001]). Between 3 and 12 months after surgery, between-group differences in ocular surface staining, dry-eye symptoms, and OSDI became apparent (Table 2).

Table 2
Table 2:
Differences in ocular variables between patients with and without regression.

No significant between-group differences in age, sex, or contact lens use were found before LASIK. Regression was associated with the length of time of contact lens use (regression group, 15 ± 10 years; no-regression group, 11 ± 8 years [P = .04]). There was no significant association between regression and central corneal sensation at any time after surgery.

Risk Factors for Experiencing Chronic Dry Eye and Regression

Highly significant differences in a number of demographic and clinical characteristics were detected between patients who developed chronic dry eye and regression after LASIK and those who did not (Table 3).

Table 3
Table 3:
Baseline characteristics (before LASIK) of patients with chronic dry eye and regression.

Case Studies of Chronic Dry Eye and Regression

The clinical relevance of the findings of our database analysis was evident in a number of patients managed in our practice. Two cases highlight the association between chronic dry eye and regression after LASIK and how management of chronic dry eye can elicit improvement in refractive outcome. The third case illustrates how the evidence from our research and that of others has influenced our presurgical management of potential LASIK candidates with dry eye and the selection of suitable candidates for LASIK.

Case 1. A 23-year-old white woman had uneventful LASIK to correct myopia (right eye −5.00 −0.50 × 16 [20/20] and left eye −5.25 −0.50 × 24 [20/20]). The preoperative tear function and ocular surface health were good. One month after surgery, the uncorrected visual acuity (UCVA) was 20/20 in both eyes and the refraction was +0.25 (20/20) in the right eye and +0.50 (20/20) in the left eye; mild bilateral inferior ocular surface staining was evident and corneal sensation was 0 mm in both eyes. The patient was advised to continue using nonpreserved artificial tears at least every 4 hours and nonpreserved gel at bedtime.

After failing to return for scheduled 3-month and 6-month reviews, the patient presented at 9 months with sore dry eyes, admitted to intermittent use of topical lubricants only, and had experienced reduced vision at night for approximately 2 weeks. Significant findings were inferior fluorescein corneal staining greater in the right eye (Figure 2), FBUT 2 seconds in both eyes, PRT 11 mm/15 seconds in the right eye and 17 mm/15 seconds in the left eye; a Schirmer test without anesthetic agent was 7 mm/5 min in the right eye and 9 mm/5 min in the left eye. Corneal sensitivity was still significantly reduced (right eye 1.5 mm, left eye 3.0 mm). She was diagnosed with chronic post-LASIK dry eye. The UCVA was 20/80 in the right eye and 20/25 in the left eye, and the refraction was −1.25 D (20/25) and −0.50 D (20/20), respectively. She was treated with an intense regimen of Cellufresh every 2 hours and Polygel at night; blink training was provided and semipermanent punctal plugs (FlexPlug) were inserted in the inferior puncta.

Figure 2.
Figure 2.:
(Albietz) Chronic post-LASIK dry eye (Case 1).

After 1 month of intense ocular surface management, the refraction improved to −0.50 D in the right eye and plano in the left eye; it remained stable over the next 18 months. Tear function, ocular surface health, and corneal sensation returned to preoperative levels by 12 months. Punctal plugs were removed, and lubricant therapy was reduced to a maintenance regimen of Cellufresh 3 times daily.

Case 2. A 33-year-old white woman who had had bilateral LASIK at another center to correct myopia (right eye −4.00 −1.00 × 170 [20/25]) and left eye (−4.50 [20/20]) experienced complications (intraoperative epithelial defects and interface inflammation), which had been treated with a protracted course of preserved topical steroids and antibiotics. She was referred for assessment 3 months after LASIK. She had experienced dry-eye symptoms from 1 month after LASIK and was using nonpreserved lubricants on indication. She complained of a foreign-body sensation on waking that was stronger in the right eye than in the left eye and reported recent deterioration in vision stronger in the right eye than in the left. The right eye had been particularly sore and blurry on waking that morning.

The UCVA was 20/100 in the right eye and 20/80 in the left eye and the refraction, −1.25 −1.00 × 165 (20/30) and −1.25 (20/30), respectively. Dry eye was confirmed on examination, and bilateral epithelial basement membrane anomalies, an acute corneal erosion in the right eye, and mild central ocular surface staining in the left eye were noted (Figures 3 and 4). Corneal sensation was reduced to 2.5 mm in the right eye and 3.0 mm in the left eye. Prescribed treatment was artificial tears (Bion Tears) every 2 hours, nonpreserved ointment (Polyvisc) and moisture shields at bedtime, and insertion of inferior punctal plugs and hypertonic saline drops on waking and at bedtime. (Hypertonic saline ointment is unavailable in Australia.)

Figure 3.
Figure 3.:
(Albietz) Acute corneal erosion 3 months after LASIK (Case 2, right eye).
Figure 4.
Figure 4.:
(Albietz) Epithelial basement membrane disturbance 3 months after LASIK (Case 2, left eye).

After 6 months of intense ocular surface management, recurrent erosion symptoms and dry-eye symptoms had ceased and the UCVA was 20/30 in the right eye, 20/20 with −0.50 −0.75 × 170, and 20/25 in the left eye, 20/20 with −0.50. The patient was satisfied with the UCVA. Spectacles were prescribed for night driving.

Case 3. A 54-year-old Eurasian woman presented for preoperative LASIK assessment to correct myopia (−8.00 DS [20/20] in the right eye and −9.50 DS [20/20] in the left eye). She had worn hard contact lenses for approximately 20 years before becoming contact-lens intolerant. She was now able to wear soft contact lenses only intermittently. She was currently using a selection of preserved topical artificial tears and decongestants to control symptoms of ocular irritation and redness. She was taking estrogen-progesterone hormone replacement therapy but had no other significant medical history. A Schirmer test without anesthetic was 2 mm/5 min in the right eye and 4 mm/5 min in the left eye; PRT was 10 mm/15 seconds and 13 mm/15 seconds, respectively. Meibomian gland dysfunction, inhibited tear clearance, and conjunctival inflammation were evident. Blink frequency and completeness were poor. Grade 3 bilateral interpalpebral and inferior ocular surface fluorescein staining were evident, and tear-film stability was poor. Corneal sensation was 3.0 mm in the right eye and 3.5 mm in the left eye. The patient was advised that she was not a good candidate for LASIK as she had numerous risk factors predisposing to chronic post-LASIK dry eye (preoperative dry eye symptoms, ocular surface staining, higher refractive correction, female sex). Concerns about the association between post-LASIK dry eye and regression were high. Because of the patient's dry eye and presbyopic status, refractive lensectomy was advised as an alternative refractive surgery procedure. After treatment the dry eye was treated with nonpreserved lubricants, a short course of nonpreserved steroid, use of lid hygiene procedures, and insertion of inferior punctual plugs, the patient had successful refractive lensectomy procedures.


This study demonstrated that patients who develop chronic dry eye after LASIK for low to moderate myopia had a significantly increased risk for refractive regression. It also identified probable risk factors for chronic dry eye and for regression.

The increased risk for regression observed in patients with chronic dry eye after LASIK for myopia is supported by our previous research on LASIK for hyperopia. In that study,9 we noted a strong association between refractive regression and chronic dry eye. Our results are supported by other studies in different populations and with different surgical techniques that report an association between dry eye and regression.11,12

Similar to the results in recent studies, our results highlight that dry eye after LASIK can be a chronic problem.8,27,28 In our study, dry-eye symptoms before surgery were a strong predictor of chronic dry eye after surgery, as was female sex. The same risk factors were identified in our earlier study on dry eye after LASIK for hyperopia.9 Based on the current evidence, LASIK should be approached cautiously in patients with preexisting dry eye, particularly as dry eye and associated contact lens intolerance are significant motivating factors for patients to consider refractive surgery.12,13 Patients with chronic dry-eye symptoms after surgery also have less satisfaction with surgery.28 The higher incidence of dry eye that we observed in women is supported by findings from other researchers. Postmenopausal women on hormone replacement therapy are reported to have significantly inferior refractive outcomes after PRK surgery compared to age-matched controls.29 Recently, a significant correlation between female sex and the occurrence of corneal punctate epitheliopathy after LASIK was reported (G.L. Mayo, MD, T. Starck, MD, “LASIK-Induced Neurotrophic Keratopathy (LINK): Incidence and Associated Risk Factors,” presented as a poster at the annual meeting of the Association for Research in Vision and Ophthalmology, Ft. Lauderdale, Florida, USA, May 2002). These results highlight the strong influence of hormone levels on the ocular surface/lacrimal gland function unit.30

Laser in situ keratomileusis disrupts the normal organization of corneal innervation and induces a corneal anesthesia or hyposthesia that lasts up to 6 months.25,31–33 Corneal sensory denervation has been proposed as a major driving mechanism for dry eye after LASIK. 8,15 In the current study, we observed that chronic dry eye was associated with lower levels of corneal sensation before and 12 months after surgery. Consistent with our results, other studies show that a delay in the return of corneal sensation to levels achieved before surgery can be associated with dry eye before LASIK,32 extended contact lens wear,8 and deeper ablations.33,34 The return of corneal sensation to levels observed before surgery appears to take up to 6 months. Although we acknowledge the inherit inadequacies of the highly subjective nature of the Cochet-Bonnet esthesiometer, our results provide support for neurotrophic damage being a significant contributing factor to sustained dry eye after LASIK. Further clinical studies will be required to identify strategies for preventing or minimizing the severity and duration of the post-LASIK loss of corneal sensation.

The reported associations between dry eye after LASIK and refractive regression in this study provide sufficient impetus for a systematic investigation of the contribution of dry eye to refractive regression. As ablation depth was significantly greater in the chronic dry eye group and there are strong associations between ablation depth and refractive regression,5–7 we cannot conclude that chronic dry eye is a causative factor of regression. However, based on current evidence, dry eye could play a key role in the 2 mechanisms proposed to explain refractive regression, epithelial hyperplasia and stromal remodeling.

Epithelial hyperplasia has been linked to myopic refractive regression in PRK and LASIK patients.35–37 Wilson and coauthors38 report that epidermal growth factor levels are increased in the lacrimal gland following corneal epithelial scrape injury. Recently, Lohmann et al.39 reported that the concentration of epidermal growth factor before surgery was higher in eyes that experienced regression after LASIK. We propose that in dry eye, chronic mechanical trauma occurs due to the shearing effects of blinking across the poorly lubricated ocular surface. This trauma increases the expression of epidermal growth factor, causing epithelial hyperplasia and regression. The associations we observed between regression and higher fluorescein ocular surface staining provide indirect support for our hypothesis.

The other mechanism proposed for regression is apoptosis-induced anterior stromal remodeling.40 Helena and coauthors41 propose that keratocyte apoptosis is an initiating factor in the wound-healing response after corneal trauma, including refractive surgical procedures. The injured epithelium releases cytokines capable of inducing apoptosis.41,42 Wilson15 has also suggested that dry eye after LASIK is related to apoptosis of stromal keratocytes and lack of innervation to the corneal flap. We propose that in chronic post-LASIK dry eye patients, ocular surface damage due to loss of corneal innervation causes the release of inflammatory cytokines, which induce apoptosis and lead to regression. Our results provide indirect support for this hypothesis as fluorescein staining (proof of epithelial injury) was associated with regression. Serial confocal microscopy, including epithelial and stromal pachymetry, would be required to determine whether the 2 proposed mechanisms for myopic regression occur in patients with sustained dry eye after LASIK.

While dry eye is now recognized as a common complication of LASIK,10 our results raise the additional concern that chronic dry eye after LASIK for myopia increases the risk for refractive regression. Treatment of dry eye may minimize the risk of regression. Our case studies highlight the benefits of intensive ocular surface management for at least some patients who experience chronic dry eye and regression after LASIK. We are not suggesting that all cases of refractive regression are due to dry eye nor are we suggesting that ocular surface management can reverse regression in all cases of chronic dry eye and refractive regression. However, we do suggest that intensive ocular surface management may be the preferred initial management strategy in eyes with chronic dry eye and regression. The alternative management strategy, LASIK enhancement surgery, carries many of the same risks as the initial LASIK surgery, including prolongation of dry-eye symptoms and signs. The 3 cases illustrate that LASIK regression in chronic dry eye can be managed effectively by ocular surface management (without enhancement) to the satisfaction of patient and surgeon.

Toda and coauthors33 recently published a prospective study examining the efficacy and safety of LASIK in patients with preoperative dry eye. Although the study differed from our study in design, both studies show that patients with dry eye before surgery are more likely to experience dry eye symptoms and signs after LASIK. Similar to the dry-eye group in our study, the preoperative dry-eye group in the Toda and coauthors' study had a greater attempted correction than the non-dry-eye group (−7.24 ± 2.38 D versus −6.82 ± 2.85 D, respectively; P value not reported). The refractive outcome in the group with dry eye before surgery was approximately 0.25 D more myopic than in the group that did not have dry eye before surgery (P = 0.01) at 3 months but not at 1, 6, and 12 months.

Based on the results of our study and those of Toda and coauthors33 and others,8 we believe the following guidelines should be considered by LASIK surgeons and potential patients:

  1. Patients with dry eye before LASIK should be advised that they have a significantly increased risk for developing chronic post-LASIK dry eye despite comprehensive ocular surface management before, during, and after surgery. There is also an association between chronic dry eye and poorer refractive outcomes. Other refractive management strategies should be discussed.
  2. Women and patients requiring higher refractive corrections have an increased risk for developing chronic dry eye and regression. Again, alternative refractive correction options should be discussed.
  3. If LASIK surgery is performed, the ocular surface and tear film must be managed with the best available treatment options and for a sufficient period of time. Unfortunately, corneal sensory denervation hinders the ability to detect and treat symptoms. Therefore, routine postoperative review in the first year after LASIK is advocated, even in asymptomatic patients.
  4. Ocular surface management strategies may accelerate the recovery of ocular surface/lacrimal gland dysfunction after LASIK and improve visual quality. Therefore, we advocate routine use of nonpreserved artificial tears in the first 6 months after LASIK.
  5. Failure to identify and treat early signs of ocular surface/lacrimal gland dysfunction may permit a vicious cycle to occur with reduced ocular surface sensation leading to ocular surface damage, reduced tear secretion, and sustained reduction in corneal sensation. Regression of the refractive result may also occur as a consequence of this chronic post-LASIK integrated ocular surface/lacrimal gland dysfunction.
  6. Enhancement surgery may exacerbate chronic post-LASIK dry eye and, hence, may be contraindicated in patients with chronic ocular surface dysfunction.

Given the increasing popularity of LASIK, the prevalence of chronic post-LASIK dry eye, and the association of chronic dry eye with refractive regression, further research into the mechanisms and management of chronic post-LASIK dry eye is clearly warranted.


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