Dry Eyes After Laser in situ Keratomileusis (LASIK)
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Introduction
Laser in situ keratomileusis (LASIK) is a safe and effective procedure for the treatment of myopia, hyperopia, and astigmatism. However, the most common adverse effect is dry eye disease (DED) following the procedure.[1] Post-LASIK dry eye is the most common postoperative dry eye after ophthalmic surgeries.[2] The clinical signs include positive vital staining of the ocular surface, decreased tear breakup time (TBUT) and Schirmer test values, reduced corneal sensitivity, and decreased functional visual acuity.[2] Although symptoms typically resolve within 3 to 6 months, a small proportion of patients continue to experience dry eye symptoms beyond one year postoperatively.[2] Understanding the pathophysiology, risk factors, and management of post-LASIK dry eye is essential to optimize patient outcomes and satisfaction.
Epidemiology
The reported incidence of post-LASIK dry eye varies widely depending on the definition used and the study population. An older estimate suggested approximately 4% of LASIK patients develop clinically significant dry eye syndrome.[1] However, using modern diagnostic criteria, the incidence has been reported to be as high as 60–70% in the early postoperative period.[3] In a large registry-based study of 48,892 eyes from the IRIS Registry, DED was documented in 16.1% of LASIK eyes over a 12-month follow-up period.[4]
Identified risk factors for developing or worsening post-LASIK dry eye include:
Pre-existing dry eye: Patients with preoperative dry eye disease or symptoms are at significantly higher risk of postoperative exacerbation.[2][5]
Female gender: Multiple studies have identified female sex as an independent risk factor for post-LASIK dry eye.[6][7]
Higher refractive correction: Greater spherical equivalent correction and deeper ablation depth correlate with increased risk.[8][7]
Contact lens wear: Particularly extended-wear contact lens use prior to surgery.
Medications: Antihistamines, hormone replacement therapy, and other anticholinergic medications can exacerbate dry eye.[9]
Meibomian gland dysfunction: Pre-existing evaporative dry eye from MGD increases susceptibility.[10]
Pathophysiology
The pathophysiology of post-LASIK dry eye is multifactorial, involving corneal denervation, disruption of reflex tear secretion, altered blink dynamics, goblet cell loss, and ocular surface inflammation.[2][11]
Corneal Nerve Transection
The primary mechanism of post-LASIK dry eye is the transection of corneal sensory nerves during flap creation.[2][12][13] These sensory nerves originate from the ophthalmic division of the trigeminal nerve (CN V1). The long ciliary nerves enter the cornea radially in the peripheral stroma, run in the middle third of the stroma, then branch anteriorly to form a dense subepithelial plexus. The nerve fibers then penetrate Bowman's layer and supply the epithelium via the subbasal nerve plexus.[3]
Flap creation severs these radial nerve fibers, resulting in corneal hypoesthesia and LASIK-induced neurotrophic epitheliopathy (LINE).[14] The loss of sensory innervation disrupts three critical reflex arcs:
Corneal-lacrimal gland reflex: Reduced afferent input decreases reflex aqueous tear secretion.
Corneal-blinking reflex: Impaired blink frequency and quality leads to increased ocular surface exposure and desiccation.
Blinking-meibomian gland reflex: Altered blink dynamics reduce meibomian lipid expression, contributing to evaporative tear film instability.[2]
Corneal Nerve Regeneration
Corneal nerve recovery after LASIK is characteristically slow and often incomplete. Subbasal nerve density decreases by more than 90% in the first month after LASIK.[15] Recovery of subbasal nerves begins by approximately 6 months, and by 2 years nerve density may approach preoperative levels, although nerve fiber numbers may subsequently decrease again and remain below 60% of pre-LASIK values at 3 years.[15] In contrast, the subbasal nerve plexus recovers within 5 to 8 months after photorefractive keratectomy (PRK).[14]
Importantly, even after more than 10 years, the subbasal corneal nerve plexus does not completely recover to its preoperative pattern following LASIK. A study with a mean follow-up of 13 years demonstrated that main nerve density and nerve branch density remained significantly lower compared with virgin corneas, although nerve length, tortuosity, and reflectivity normalized.[16]
Additional Contributing Mechanisms
Goblet cell loss: Flap creation and excimer laser ablation cause goblet cell damage and a reduction in mucin expression, contributing to tear film instability.[11]
Ocular surface inflammation: Surgical trauma induces cytokine release and inflammatory cell infiltration, perpetuating tear film disruption.[10]
Preservative toxicity: Preservatives in topical postoperative medications (e.g., benzalkonium chloride) may exacerbate epithelial damage and worsen dry eye symptoms.[10]
Altered corneal shape: Changes in corneal curvature after ablation may affect tear film distribution and stability.
Effect of Flap Parameters
Hinge Position
Classically, a superior hinge is created during LASIK, which results in the greatest transection of corneal nerves since a large proportion of nerves enter from the radial (temporal and nasal) aspects of the cornea. Alternating the hinge to the nasal or temporal aspect has been shown to reduce dryness and loss of corneal sensation up to 6 months postoperatively (p < 0.0001), although no difference persists beyond that time point.[12]
Flap Thickness
Thinner flaps created with femtosecond lasers have been shown to produce less disruption of corneal sensation and improved tear function tests compared with thicker flaps.[17][18]
Femtosecond Laser versus Mechanical Microkeratome
The use of femtosecond laser versus mechanical microkeratome for flap creation remains a topic of investigation. A Cochrane review of 11 trials (943 participants) found that evidence on dry eye was limited, but one included trial showed a potentially higher risk of dry eye in the mechanical microkeratome group compared with the femtosecond laser group.[19] A comparative study of thin-flap (100 µm) LASIK demonstrated that femtosecond laser flaps were associated with better TBUT, Schirmer I values, lower tear meniscus height and area measurements, and lower OSDI scores at both 3 and 6 months compared with mechanical microkeratome flaps.[18] However, some contralateral-eye randomized studies have found no statistically significant difference in self-reported dry eye symptoms between the two methods.[20]
Ablation Depth
The relative risk for dryness per diopter of myopia was approximately 0.88, which correlates with the laser-calculated depth of ablation (RR 1.01/µm for combined ablation depth and flap creation).[8]
Comparison with Other Refractive Procedures
SMILE
Small incision lenticule extraction (SMILE) avoids corneal flap creation and instead uses a small peripheral corneal incision through which a stromal lenticule is extracted. By preserving the anterior stroma and subbasal nerve plexus, SMILE is postulated to reduce postoperative corneal denervation and accelerate corneal nerve recovery relative to LASIK.[21]
Comparative studies support a reduced impact of SMILE on the ocular surface:
A prospective contralateral-eye randomized trial (80 eyes, 40 patients) demonstrated significantly greater corneal denervation after LASIK compared with SMILE at 1, 3, and 6 months postoperatively, though both groups returned to baseline corneal sensitivity by 12 months. Notably, there was no significant difference in self-reported dry eye symptoms (OSDI) between the two groups at any time point.[22]
A nonrandomized comparative study found significantly less dry eye at 6 months after SMILE compared with LASIK (overall severity score 0.2 ± 0.4 vs. 1.2 ± 1.1; P < 0.01), with higher subbasal nerve density and fewer DED-related symptoms.[23]
In vivo confocal microscopy has confirmed that SMILE has less impact on corneal nerve fiber density, branch density, and fiber length compared with FS-LASIK at 1 month postoperatively.[24]
Surface Ablation (PRK/LASEK)
Surface ablation procedures (PRK, LASEK) avoid deep stromal nerve transection and may be associated with different dry eye profiles. In a large registry study, PRK was associated with a higher incidence of DED during the 1 to 3 month postoperative interval compared with LASIK (IRR 0.8, 95% CI 0.7–0.9 favoring LASIK), but differences were not significant at later intervals.[4] At 6 months, LASIK was associated with a higher DEWS severity score than PRK or LASEK.[7] The subbasal nerve plexus recovers more rapidly after PRK (5–8 months) compared with LASIK (incomplete recovery at 3–5 years).[14][15]
Neuropathic Ocular Pain
Post-LASIK ocular surface pain is increasingly recognized as a distinct clinical entity from dry eye disease, possibly representing a form of corneal neuropathic pain.[2] This condition is thought to be induced by abnormal reinnervation, the formation of microneuromas, or neural sensitization of peripheral nerves and the central nervous system after LASIK.[2][25]
A comparative study of post-LASIK patients found that those with both neuropathic ocular pain (NOP) and dry eye, compared with those with dry eye alone, exhibited:
Greater symptom severity and more frequent use of ocular lubrication (P = 0.003)
Higher rates of anxiety and depression (P < 0.001)
Higher prevalence of central sensitization syndromes (P < 0.001)
Higher tactile corneal sensitivity after topical anesthesia (P = 0.002)
Lower subbasal nerve density (P = 0.049) and higher microneuroma density (P = 0.008) on in vivo confocal microscopy[25]
The diagnosis of neuropathic ocular pain should be considered in patients with persistent ocular discomfort disproportionate to clinical signs, particularly when conventional dry eye treatment fails.
Symptoms
For the majority of patients, dry eye poses limited long-term concern, as symptoms typically resolve within 3 to 6 months. The most common symptom associated with post-LASIK dry eye is fluctuation in vision, especially within the first 6 weeks. Other symptoms include:[1][26]
Irritation and foreign body sensation
Pain or burning
Redness
Photophobia
Slow epithelial healing
Refractive regression
Worsening astigmatism
Dry eye symptoms, although mild for some, can be the primary reason for patient dissatisfaction with LASIK, even in patients with excellent visual acuity outcomes.[27] In order to maximize surgical outcomes, it is imperative to optimize the ocular surface before performing any refractive surgical procedure.
Preoperative Screening and Optimization
A thorough preoperative evaluation of the ocular surface is the most critical step in preventing or reducing post-LASIK dry eye.[28][29] Although most refractive surgeons recognize the importance of DED on surgical outcomes, many are unaware of current guidelines and do not use modern diagnostic tests or advanced treatments preoperatively.[28]
The ASCRS Cornea Clinical Committee has developed a consensus-based diagnostic algorithm for ocular surface disease prior to refractive surgery.[28] Key elements of preoperative evaluation include:
Symptom assessment: Validated questionnaires such as the OSDI (Ocular Surface Disease Index) or DEQ-5 (Dry Eye Questionnaire).
Tear film stability: Non-invasive or fluorescein TBUT.
Tear production: Schirmer testing (with and without anesthesia).
Ocular surface staining: Fluorescein and lissamine green staining.
Meibomian gland evaluation: Lid margin inspection, gland expression, and meibography when available.
Tear osmolarity: When available, elevated tear osmolarity is a marker for tear film instability.
Medication review: A thorough review of systemic medications that may exacerbate dry eye, including antihistamines, allergy medications, hormone replacement therapy, anticholinergics, and over-the-counter cold remedies.[9]
Patients with clinically significant dry eye should be treated and their ocular surface optimized before proceeding with surgery. By treating ocular surface disease preoperatively, postoperative visual outcomes and patient satisfaction are significantly improved.[28][29]
Management
The management of post-LASIK dry eye follows a stepwise approach based on symptom severity, consistent with the American Academy of Ophthalmology Preferred Practice Patterns (PPP) for Dry Eye Syndrome.[9][30]
Mild Dry Eye
Conservative measures are appropriate first-line therapy:
Artificial tears: Preserved or non-preserved lubricating eye drops are the mainstay of initial treatment and can significantly reduce or eliminate symptoms. Non-preserved formulations are preferred for patients requiring frequent instillation (>4 times per day) to avoid preservative-related toxicity.
Lubricating ointments: Useful for nighttime symptoms. However, evening ointments should not be used during the initial postoperative period to avoid possible migration under the flap.[3]
Warm compresses and lid hygiene: To address any concurrent meibomian gland dysfunction.
Environmental modification: Humidifying the air in home and office environments, particularly in extreme hot or cold climates with air conditioning or heating systems that dry out the air.[9]
Medication review: Discontinuation or substitution of medications known to exacerbate dry eye when possible.
Moderate Dry Eye
For moderate symptoms unresponsive to conservative measures:
Topical anti-inflammatory therapy:
Cyclosporine A ophthalmic emulsion (0.05%): The most widely studied anti-inflammatory agent for post-LASIK dry eye. Two randomized controlled trials demonstrated that topical cyclosporine 0.05% consistently hastened flap sensitivity recovery (Δ+4 cm at 3 months) and improved 6-month ocular surface metrics (OSDI -5 points; TBUT +4 seconds; Schirmer +5.5 mm; P < 0.001).[31] Cyclosporine not only improves dryness and neurotrophic epitheliopathy, but may also reduce the time needed for faster visual recovery after LASIK.[13][32] Additional formulations now available include cyclosporine 0.09% (Cequa) and cyclosporine 0.1% in perfluorobutylpentane (Vevye), which offers a preservative-free, water-free vehicle with improved bioavailability.[33]
Lifitegrast 5% ophthalmic solution (Xiidra): An LFA-1 antagonist approved by the FDA in 2016 for the treatment of the signs and symptoms of DED. Lifitegrast blocks T-cell–mediated inflammation on the ocular surface. Improvement in both signs and symptoms has been observed as early as day 14, and the treatment is generally well tolerated, with dysgeusia as the most common adverse effect.[34][35]
Loteprednol etabonate 0.25% (Eysuvis): Approved for short-term treatment of DED flares; may be useful in the acute postoperative setting.
Punctal plugs: Temporary (collagen) or semi-permanent (silicone) punctal plugs reduce tear drainage and increase tear film residence time.
Omega-3 fatty acid supplements: Nutritional supplementation that has been proposed to reduce the viscosity of meibomian oils and decrease inflammation.[9] However, a Cochrane review noted that there is a paucity of high-quality RCT evidence for many DED treatments, and the role of omega-3 supplementation remains debated.[36]
Severe or Refractory Dry Eye
For severe symptoms unresponsive to the above measures:
Autologous serum eye drops: Contains growth factors, fibronectin, and other components that promote epithelial healing and may support corneal nerve regeneration.[2]
Nerve growth factor (NGF) therapies: Animal studies have shown that topical NGF significantly accelerates corneal subbasal and superficial stromal nerve recovery after LASIK, with improved corneal sensitivity and prolonged TBUT compared with standard lubricants.[37] Cenegermin (Oxervate), a recombinant human NGF, is FDA-approved for neurotrophic keratitis and is being evaluated in broader ocular surface applications.[38]
Meibomian gland-directed therapies: Thermal pulsation (LipiFlow), intense pulsed light (IPL) therapy, and lid exfoliation for concurrent meibomian gland dysfunction.[10]
Varenicline nasal spray (Tyrvaya): A cholinergic agonist approved for the signs and symptoms of DED; stimulates natural tear production via the trigeminal parasympathetic pathway.[38]
Perfluorohexyloctane ophthalmic solution (Miebo): A semifluorinated alkane approved for DED that reduces tear evaporation by supplementing the lipid layer.[38]
Scleral contact lenses: May provide ocular surface protection and symptom relief in refractory cases.
Summary of FDA-Approved Therapies
Currently, FDA-approved treatments for dry eye disease include topical cyclosporine (0.05%, 0.09%, and 0.1% formulations), lifitegrast 5%, loteprednol etabonate 0.25%, perfluorohexyloctane, and varenicline nasal spray. No direct head-to-head comparisons in prospective clinical trials are available in the literature, and none has been proven more effective than the other.[30]
Special Considerations
Hyperopic LASIK
The hyperopic population warrants special consideration. A retrospective evaluation found that post-LASIK dryness occurred mainly in females. In the same cohort, refractive regression occurred in 32% of individuals at 12 months after surgery.[39] Whether the regression is secondary to dry eye-related corneal surface changes or the inherent effects of the hyperopic ablation profile has not been definitively established.
LASIK Enhancement
LASIK enhancement by flap-lifting induces fewer dry eye symptoms and signs than the initial surgery, suggesting that factors other than neurotrophic effects alone may be involved in the mechanisms of post-LASIK dry eye (e.g., surgical stress, inflammation, and goblet cell loss associated with the initial procedure).[2]
Conclusion
Dry eye disease is the most common side effect encountered after LASIK. Its pathophysiology is multifactorial, with corneal nerve transection during flap creation being the primary mechanism. Although most patients experience symptom resolution within 3 to 6 months, a subset may develop chronic dry eye or neuropathic ocular pain. A stepwise management approach—beginning with artificial tears and progressing to anti-inflammatory agents, punctal plugs, and advanced therapies as needed—can effectively control symptoms. The advent of newer refractive procedures such as SMILE, which better preserves corneal innervation, may reduce the incidence of postoperative dry eye. Critically, thorough preoperative screening and optimization of the ocular surface remain the most effective strategies to improve patient outcomes and satisfaction following refractive surgery.
Additional Resources
AAO Preferred Practice Patterns for Dry Eye Syndrome
AAO EyeSmart: Eye Strain - How to Prevent Tired Eyes
References
- ↑ 1.0 1.1 1.2 Foster CS, Azar DT, Dohlman CH. Smolin and Thoft's The Cornea. 4th Edition. Philadelphia, PA. Lippincott Williams & Wilkins; 2005.
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Toda I. Dry Eye After LASIK. Invest Ophthalmol Vis Sci. 2018;59(14):DES109-DES115.
- ↑ 3.0 3.1 3.2 American Academy of Ophthalmology. Basic and Clinical Science Course. Section 13: Refractive Surgery. American Academy of Ophthalmology, 2011-2012.
- ↑ 4.0 4.1 Kang S, Persad LS, Woreta FA, Yoo SH. Temporal Incidence of Dry Eye Disease, Visual Disturbances, and Ocular Pain After Laser-Assisted in Situ Keratomileusis Versus Photorefractive Keratectomy. Am J Ophthalmol. 2026;268:51-60.
- ↑ Nair S, Kaur M, Sharma N, Titiyal JS. Refractive Surgery and Dry Eye - An Update. Indian J Ophthalmol. 2023;71(4):1104-1117.
- ↑ Shoja MR, Besharati MR. Dry eye after LASIK for myopia: Incidence and risk factors. Eur J Ophthalmol. 2007;17(1):1-6.
- ↑ 7.0 7.1 7.2 Yahalomi T, Achiron A, Arnon R, Stanescu N, Pikkel J. Dry Eye Disease Following LASIK, PRK, and LASEK: An Observational Cross-Sectional Study. J Clin Med. 2023;12(11):3691.
- ↑ 8.0 8.1 De Paiva CS, Chen Z, Koch DD, et al. The incidence and risk factors for developing dry eye after myopic LASIK. Am J Ophthalmol. 2006;141(3):438-445.
- ↑ 9.0 9.1 9.2 9.3 9.4 AAO. Preferred Practice Patterns. Dry Eye. 2011.
- ↑ 10.0 10.1 10.2 10.3 Spangler MD, Kirupaharan N, Sheppard JD. Ocular Surface Disease Following LASIK and Cataract Surgery: A Review of Their Interrelated Complications. Front Med. 2025;12:1527268.
- ↑ 11.0 11.1 Sharma B, Soni D, Saxena H, et al. Impact of Corneal Refractive Surgery on the Precorneal Tear Film. Indian J Ophthalmol. 2020;68(12):2886-2894.
- ↑ 12.0 12.1 Donnenfeld ED, Solomon K, Perry HD, et al. The Effect of hinge position on corneal sensation and dry eye after LASIK. Ophthalmology. 2003;110(5):1023-1029.
- ↑ 13.0 13.1 Ambrosio R Jr, Tervo T, Wilson SE. LASIK-associated dry eye and neurotrophic epitheliopathy: pathophysiology and strategies for prevention and treatment. J Refract Surg. 2008;24(4):396-407.
- ↑ 14.0 14.1 14.2 Eguchi H, Hiura A, Nakagawa H, Kusaka S, Shimomura Y. Corneal Nerve Fiber Structure, Its Role in Corneal Function, and Its Changes in Corneal Diseases. Biomed Res Int. 2017;2017:3242649.
- ↑ 15.0 15.1 15.2 Calvillo MP, McLaren JW, Hodge DO, Bourne WM. Corneal Reinnervation After LASIK: Prospective 3-Year Longitudinal Study. Invest Ophthalmol Vis Sci. 2004;45(11):3991-3996.
- ↑ Garcia-Gonzalez M, Cañadas P, Gros-Otero J, et al. Long-Term Corneal Subbasal Nerve Plexus Regeneration After Laser In situ Keratomileusis. J Cataract Refract Surg. 2019;45(7):966-971.
- ↑ Barequet IS, Hirsh A, Levinger S. Effect of thin femtosecond LASIK flaps on corneal sensitivity and tear function. J Refract Surg. 2008;24(9):897-902.
- ↑ 18.0 18.1 Abdel-Radi M, Abdelmotaal H, Anwar M. Thin-Flap Laser in Situ Keratomileusis-Associated Dry Eye: A Comparative Study Between Femtosecond Laser and Mechanical Microkeratome-Assisted Laser in Situ Keratomileusis. Eye Contact Lens. 2022;48(1):26-31.
- ↑ Kahuam-López N, Navas A, Castillo-Salgado C, et al. Laser-assisted in-situ keratomileusis (LASIK) with a mechanical microkeratome compared to LASIK with a femtosecond laser for LASIK in adults with myopia or myopic astigmatism. Cochrane Database Syst Rev. 2020;4(4):CD011952.
- ↑ Golas L, Manche EE. Dry Eye after laser in situ keratomileusis with femtosecond laser and mechanical keratome. J Cataract Refract Surg. 2011;37(8):1476-1480.
- ↑ Jacobs DS, Lee JK, Shen TT, et al. Refractive Surgery Preferred Practice Pattern. American Academy of Ophthalmology. 2023.
- ↑ Ma KK, Manche EE. Corneal Sensitivity and Patient-Reported Dry Eye Symptoms in a Prospective Randomized Contralateral-Eye Trial Comparing Laser in Situ Keratomileusis and Small Incision Lenticule Extraction. Am J Ophthalmol. 2022;241:155-163.
- ↑ Denoyer A, Landman E, Trinh L, et al. Dry Eye Disease After Refractive Surgery: Comparative Outcomes of Small Incision Lenticule Extraction Versus LASIK. Ophthalmology. 2015;122(4):669-676.
- ↑ Recchioni A, Sisó-Fuertes I, Hartwig A, et al. Short-Term Impact of FS-LASIK and SMILE on Dry Eye Metrics and Corneal Nerve Morphology. Cornea. 2020;39(7):851-857.
- ↑ 25.0 25.1 Vázquez A, Blanco-Vázquez M, Martínez-Plaza E, et al. Corneal Sensory Changes and Nerve Plexus Abnormalities in Chronic Neuropathic Ocular Pain and Dry Eye Postrefractive Surgery. Am J Ophthalmol. 2025;266:213-226.
- ↑ Azar DT, Gatinel D, Hoang-Xuan T. Refractive Surgery. 2nd Edition. China. Elsevier, Inc.; 2007.
- ↑ Levinson BA, Rapuano CJ, Cohen EJ, et al. Referrals to the Wills Eye Institute Cornea Service after laser in situ keratomileusis: reasons for patient dissatisfaction. J Cataract Refract Surg. 2008;34(1):32-39.
- ↑ 28.0 28.1 28.2 28.3 Starr CE, Gupta PK, Farid M, et al. An Algorithm for the Preoperative Diagnosis and Treatment of Ocular Surface Disorders. J Cataract Refract Surg. 2019;45(5):669-684.
- ↑ 29.0 29.1 Donaldson K, Parkhurst G, Saenz B, et al. Call to Action: Treating Dry Eye Disease and Setting the Foundation for Successful Surgery. J Cataract Refract Surg. 2022;48(5):601-613.
- ↑ 30.0 30.1 American Academy of Ophthalmology. Dry Eye Syndrome Preferred Practice Pattern. 2024.
- ↑ Alamoudi A, Aldahlawi AK, Alnabihi A, et al. Neuroprotective and Anti-Inflammatory Strategies for Corneal Nerve Regeneration and Ocular Surface Stability After Corneal Refractive Surgeries: A Systematic Review. J Cataract Refract Surg. 2026;52(5):540-548.
- ↑ Ursea R, Purcell TL, Tan BU, et al. The effect of cyclosporine A (Restasis) on recovery of visual acuity following LASIK. J Refract Surg. 2008;24(5):473-476.
- ↑ Akpek EK, Wirta DL, Downing JE, et al. Efficacy and Safety of a Water-Free Topical Cyclosporine, 0.1%, Solution for the Treatment of Moderate to Severe Dry Eye Disease: The ESSENCE-2 Randomized Clinical Trial. JAMA Ophthalmol. 2023;141(5):459-468.
- ↑ Holland EJ, Jackson MA, Donnenfeld E, et al. Efficacy of Lifitegrast Ophthalmic Solution, 5.0%, in Patients With Moderate to Severe Dry Eye Disease: A Post Hoc Analysis of 2 Randomized Clinical Trials. JAMA Ophthalmol. 2021;139(11):1163-1170.
- ↑ Li JX, Tsai YY, Lai CT, et al. Lifitegrast Ophthalmic Solution 5% Is a Safe and Efficient Eyedrop for Dry Eye Disease: A Systematic Review and Meta-Analysis. J Clin Med. 2022;11(17):5014.
- ↑ Downie LE, Ng SM, Lindsley KB, Akpek EK. Omega-3 and omega-6 polyunsaturated fatty acids for dry eye disease. Cochrane Database Syst Rev. 2019;12(12):CD011016.
- ↑ Gong Q, Zhang S, Jiang L, et al. The Effect of Nerve Growth Factor on Corneal Nerve Regeneration and Dry Eye After LASIK. Exp Eye Res. 2021;203:108428.
- ↑ 38.0 38.1 38.2 Patil S, Sawale G, Ghuge S, Sathaye S. Quintessence of Currently Approved and Upcoming Treatments for Dry Eye Disease. Graefes Arch Clin Exp Ophthalmol. 2025;263(2):315-336.
- ↑ Albietz JM, Lenton LM, McLennan SG. Effect of laser in situ keratomileusis for hyperopia on tear film and ocular surface. J Refract Surgery. 2002;18(2):113-123.
