LASIK Complications

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Article initiated by:

Ladan Espandar, M.D., M.S., Majid Moshirfar, M.D.

All contributors:

Brad H. Feldman, M.D., Alex Kozak, Koushik Tripathy, MD (AIIMS), Vandana Reddy, MD, Riccardo Vinciguerra, MD, Bruno Battaglia, Anjali K. Pathak, M.D., Majid Moshirfar, M.D., Ladan Espandar, M.D., M.S., Brian Shafer, MD, Shaina N. Kumar, M.D.

Assigned editor:

Brian Shafer, MD

Review:

Assigned status Up to Date

 by Brian Shafer, MD on August 7, 2026.

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Contributing Editors:	add

Laser in situ keratomileusis (LASIK) is among the most commonly performed elective surgical procedures worldwide, with well-established safety, efficacy, and predictability. Nevertheless, complications—though uncommon—do occur and range from self-limited to sight-threatening. In a large contemporary retrospective series of 61,833 LASIK eyes, the total incidence of adverse events was 1.3% (1:79 eyes), with serious adverse events occurring in 0.4% (1:228 eyes). Loss of 2 or more lines of corrected distance visual acuity was recorded in 0.37% of eyes across combined LASIK and PRK cohorts.

LASIK complications can be categorized into intraoperative and postoperative complications.

Overview of LASIK Complications

The American Academy of Ophthalmology Refractive Surgery Preferred Practice Pattern enumerates the recognized side effects and complications of LASIK, which include symptomatic undercorrection or overcorrection, partial regression of effect, loss of BCVA, glare and starburst/halo effects, decreased contrast sensitivity, induced regular or irregular astigmatism, induced anisometropia, corneal haze or scarring, corneal infiltrates/ulceration/melting/perforation, corneal ectasia, dry eye and decreased corneal sensitivity, corneal neuralgia, recurrent corneal erosion, HSV keratitis reactivation, corticosteroid-induced complications, ptosis, artifactual reduction of IOP by applanation tonometry, interface debris, interface fluid accumulation (pressure-induced stromal keratitis), epithelial ingrowth, flap necrosis, early or late-onset diffuse lamellar keratitis, central toxic keratopathy, transient light sensitivity syndrome, rainbow glare, persistent flap edema, striae, and traumatic flap dislocation.

Intraoperative Complications

The intraoperative complication rate of LASIK has historically been reported between 0.7% and 6.6%. The most common are flap-related, occurring with either a traditional mechanical microkeratome or a femtosecond (FS) laser. Depending on the method of flap creation, meaningful differences in complication profiles exist.

Microkeratome-Related Flap Complications

Flap Buttonhole

Buttonholes occur when the microkeratome exits the epithelium prematurely and then re-enters the stroma, creating a central defect in the flap ("donut" configuration). Buttonholes are essentially exclusive to mechanical microkeratome LASIK and are among the most feared flap complications because of the risk of central irregular astigmatism and scarring.

Risk factors:

Suction loss

Steep corneas (>46 D)

Corneal scars or prior corneal surgery

Large diameter flap or thin flap settings

Decreased intraocular pressure

Defective or dull blade

Abnormal or uneven advancement of the blade

Management: Abort laser ablation and reposition the flap without lifting it further. A bandage contact lens may be placed temporarily and topical antibiotic/corticosteroid started. Any laser procedure should be delayed for several weeks to months until the cornea has stabilized topographically. Surface ablation (PRK), typically with mitomycin-C to reduce haze risk, is generally the preferred subsequent approach rather than re-lifting or recutting the flap.

Free Cap

A free cap occurs when the entire flap is dislodged from the cornea without a hinge. Risk factors include inadequate suction, a flat cornea (<40 D), thin corneas, defective blades, decentered suction ring placement, and improper ring height or stop value selection. Preventive measures include a larger suction ring, stop ring, appropriate hinge settings, and placement of asymmetric corneal epithelial reference marks before flap creation.

Management: Management depends on the regularity of the residual stromal bed and the integrity of the free cap. If the stromal bed is regular and the cap of normal thickness, laser ablation can be continued. The free cap should be placed epithelial side up on a drop of balanced salt solution to prevent desiccation, then replaced on the bed using pre-placed corneal markings for correct rotational orientation. A bandage contact lens is typically placed. If the bed is irregular, ablation should be aborted and the cap simply replaced.

Incomplete, Short, or Irregular Flaps

Incomplete flaps occur if the microkeratome stops prematurely, most often due to obstruction (lid speculum, drape, lashes), loss of suction, or mechanical failure. Predisposing factors include flat corneas, corneal scars, low intraocular pressure, and small palpebral fissures.

Management: Depending on the amount of exposed stromal bed and the location of the flap hinge relative to the visual axis, the surgeon should decide either to terminate the procedure or to continue with LASIK. If sufficient regular stroma is exposed and the flap edge/hinge lies beyond the visual axis, ablation may proceed. If the flap hinge encroaches on the visual axis, the ablation should be aborted, the flap repositioned, and the procedure deferred for at least 3 months, with subsequent surface ablation or a recut at a deeper plane.

Flap Tear

Flap tears may occur during flap lifting or repositioning, especially with thin flaps or in the setting of epithelial basement membrane dystrophy. Careful, even traction with a blunt instrument and adequate flap hydration reduce this risk. Torn flaps should be repositioned meticulously with attention to gutter symmetry, and a bandage contact lens applied.

Corneal Perforation

Perforation through the cornea is a rare but devastating complication. It has been reported with older models of mechanical microkeratomes that were improperly assembled or set to an inappropriate depth, or when the depth plate was absent. Other risk factors include extremely thin corneas. Sequelae may include iris prolapse, lens damage, and endophthalmitis.

Management: Immediately deactivate the suction, remove the microkeratome, and repair the perforation in a sterile manner (in the operating room if necessary). Intensive topical and systemic antibiotic prophylaxis should be administered given the risk of endophthalmitis.

Femtosecond Laser-Related Flap Complications

The femtosecond laser has substantially improved the predictability and safety of the lamellar incision, with flap thickness standard deviations of 4–18.4 µm and reduction in buttonholes, free caps, and irregular flaps. However, a distinct set of complications unique to femtosecond technology has emerged.

Suction Loss

Loss of suction during the femtosecond laser pass results in an incomplete lamellar dissection. Management depends on the percentage of the dissection completed and the timing of the suction break. If suction is lost early, an immediate re-treatment at the same or deeper plane may be attempted; if lost mid-dissection, the case should generally be aborted and rescheduled after several months, or converted to surface ablation.

Opaque Bubble Layer (OBL)

OBL results from the accumulation of cavitation gas bubbles (carbon dioxide and water vapor) within the corneal stromal lamellae adjacent to the dissection plane. OBL appears as a whitish opacity that can interfere with pupil tracking, iris registration, and applanation for subsequent procedures.

Risk factors: Higher laser energy settings, thicker flaps, smaller flap diameters, thick corneas, steep keratometry, and dense stromal architecture.

Management: OBL is generally self-limited and resolves within minutes to hours. Waiting several minutes before lifting the flap allows partial dissipation. If pupil tracking is compromised, manual centration or delaying the ablation briefly is appropriate.

Vertical Gas Breakthrough

Vertical gas breakthrough (VGB) is the escape of cavitation gas bubbles from the dissection plane anteriorly into the subepithelial space, producing a focal epithelial bleb. The cause is not fully established, but a thin flap setting, focal irregularity or break in Bowman's layer, or prior corneal surgery may be causative.

Management: If a large VGB is identified, the flap should not be lifted, as attempting to lift the flap through the breakthrough site can produce a buttonhole. The procedure should be aborted and converted to surface ablation at a later date. For small, peripheral breakthroughs, the flap may be lifted cautiously away from the affected area and ablation performed.

Anterior Chamber Gas Bubbles

The mechanism of gas bubbles entering the anterior chamber during FS laser-assisted flap creation is not fully known; one theory holds that gas escapes from the dissection plane into the trabecular meshwork and then into the anterior chamber. The incidence is very low, and risk factors are not well established. Anterior chamber bubbles can interfere with pupillary tracking and iris registration but are usually self-limiting and resolve over a short period.

Management: Lift the flap cautiously and perform laser ablation, using manual centration if pupil tracking is unreliable. Waiting for bubble resolution is an alternative.

Complications Common to Both Microkeratome and Femtosecond LASIK

Corneal Epithelial Defect

Epithelial defects occur intraoperatively at a rate of 0.6%–14%, with a substantially lower rate with femtosecond lasers than with mechanical microkeratomes.

Risk factors:

Older age

Steep cornea

Previous corneal trauma

Preoperative hyperopia

Diabetes mellitus

History of contact lens use

Increased corneal thickness

Epithelial basement membrane dystrophy (EBMD)

Type of microkeratome

Epithelial defects predispose to delayed healing, diffuse lamellar keratitis (DLK), epithelial ingrowth, flap striae, and infectious keratitis. Epithelial injury is the single most common trigger for DLK, releasing IL-1α, IL-1β, and TNF-α from the epithelium into the stroma, which chemotactically attract inflammatory cells from the limbal vasculature.

Prevention: Limiting toxic topical medications, minimizing use of topical anesthetics, frequent use of lubricating drops, preoperative inspection of the blade, meticulous microkeratome maintenance, and preoperative identification and management of EBMD (with consideration of surface ablation instead of LASIK in these patients).

Management: A bandage soft contact lens may be used for larger defects (>1 mm), with topical lubricants until re-epithelialization occurs. Topical antibiotics should be continued for infection prophylaxis, and corticosteroids used judiciously with close monitoring for DLK.

Limbal Bleeding

Limbal hemorrhage can occur secondary to the microkeratome blade or femtosecond laser transecting limbal vessels. Predisposing factors include large diameter flaps, hyperopic treatments, inappropriately sized or improperly positioned suction rings, and corneal pannus (as in chronic contact lens wearers). Limbal bleeding has been associated with delayed wound healing, sterile interface keratitis, and decreased contrast sensitivity and glare acuity. Retained blood in the interface is also a recognized trigger for DLK.

Management: Apply gentle pressure on the oozing vessels either directly with a dry sponge, or by pushing a fold of conjunctiva over the limbal feeder vessels. Remove any visible blood from the ablation zone prior to returning the flap to its original position. After replacing the flap, phenylephrine 2.5% may be used to constrict the vessels. Note that secondary iris dilation from topical phenylephrine 2.5% may interfere with pupil tracking and laser treatment.

Interface Debris

While creating and lifting the flap, debris can accumulate within the interface. Sources include meibomian gland secretions, particles from sponges, talc from gloves, metallic or plastic fragments from the microkeratome, red blood cells, epithelial cells, and tear film debris. Debris including microkeratome blade particles, glove talc, drape fibers, cleaning solutions, meibomian secretions, bacterial antigens, and endotoxins are all recognized DLK triggers.

Prevention: Use an aspirating speculum, operate in a lint-free environment, drape the lashes and eyelids, use powder-free gloves, and thoroughly irrigate the interface before flap repositioning.

Management: Most interface debris is inert and harmless. If an inflammatory reaction is elicited, or if the debris is visually significant or centrally located, the flap should be lifted and irrigated and the debris removed.

Decentered Ablation and Central Islands

Decentered ablation results from poor patient fixation, inadequate eye tracking, or improper centration reference. It may produce coma, irregular astigmatism, glare, halos, and loss of BCVA. Central islands—focal areas of relative undertreatment in the central ablation zone—present as a central steep area on topography with monocular diplopia or ghosting. Both are less common with modern broad-beam and flying-spot lasers with active eye tracking and iris registration. Management options include topography-guided or wavefront-guided retreatment when sufficient residual stromal bed is available.

Postoperative Complications

Undercorrection, Overcorrection, and Refractive Regression

Undercorrection is the most common refractive complication after primary LASIK, whereas overcorrection is most often seen after retreatment. Both relate to the ablation algorithm, surgeon nomogram, patient age, and magnitude of refractive error.

Refractive regression is a distinct and well-described long-term phenomenon. Proposed mechanisms include epithelial hyperplasia, stromal remodeling and keratocyte activation, corneal biomechanical changes, and continued axial elongation in myopes. In a 12-year follow-up study of LASIK for moderate to high myopia, most eyes showed approximately 10% myopic regression over time. Reported annual regression rates are approximately −0.12 ± 0.15 D for myopia up to −10.0 D and −0.25 ± 0.18 D for myopia over −10.0 D. At 15 years, mean regression of −1.66 ± 2.15 D has been reported in eyes with baseline myopia of −9.47 ± 3.26 D.

Risk factors for regression: Higher preoperative myopia or hyperopia, younger age, steeper preoperative keratometry, thinner residual stromal bed, and larger optical zone-to-pupil mismatch.

Management: A stable refraction is usually achieved by 3 months after surgery, though more time may be required for higher corrections. Retreatment (enhancement) should not be considered until refractive stability has been documented by repeat measurements. Before retreatment, a full eye evaluation including all relevant elements of the preoperative evaluation should be performed. It must be determined that the residual refractive error is not due to accommodation or to pathologic conditions such as cataract or corneal ectasia. Corneal topography/tomography and central corneal thickness should be obtained, and post-retreatment residual stromal bed thickness calculated. Anterior segment OCT or intraoperative pachymetry may be used to measure the residual stromal bed before repeat ablation.

Visual Aberrations and Night Vision Symptoms

Approximately 20% of patients report some form of visual change postoperatively. Flap creation alone induces higher-order aberrations, particularly spherical aberration and coma. Symptoms include glare, halos, starbursting around lights, haze, monocular diplopia, and decreased contrast sensitivity.

Risk factors: Large scotopic pupil diameter relative to the optical zone, high myopic corrections, decentered ablation, and small optical zones.

Visual disturbances tend to stabilize three to six months after the procedure. Persistent symptoms may be addressed with pilocarpine or brimonidine to reduce pupil size, wavefront-guided or topography-guided enhancement, or in rare cases specialty contact lenses.

Rainbow Glare

First described in 2008, rainbow glare is a femtosecond laser-specific optical phenomenon in which patients report colored bands radiating from white point light sources against a dark background. It is thought to result from a diffraction grating effect created by the regular microscopic pattern of laser spots on the undersurface of the LASIK flap.

Rainbow glare is distinguished from conventional glare and halos by its spectral (multicolored) quality. Most cases are self-limited and resolve over months. For persistent symptomatic cases, the surgeon can lift the flap and perform phototherapeutic undersurface ablation of the stromal bed or flap undersurface to disrupt the diffraction grating.

Transient Light Sensitivity Syndrome (TLSS)

TLSS is a femtosecond laser-specific complication characterized by severe photophobia in the setting of an essentially normal slit-lamp examination and good uncorrected visual acuity, typically presenting 2 to 8 weeks after surgery. It is thought to relate to a subclinical inflammatory response to keratocyte necrosis from femtosecond laser energy.

In a large retrospective series, the incidence of clinically significant TLSS was:

1.2% after myopic SMILE

5.3% after myopic LASIK

9.0% after hyperopic LASIK (P < .001 between all groups)

For myopic LASIK, TLSS incidence was dose-dependent on the refractive error treated (4.7% low, 5.8% moderate, 8.1% high myopia; P < .001), whereas for myopic SMILE and hyperopic LASIK it was independent of the degree of correction. Late TLSS occurring between 8 weeks and 6 months after surgery has also been described.

Management: Topical corticosteroids, often at high frequency with a slow taper, generally result in resolution. Lowering femtosecond laser energy settings reduces incidence.

Flap Fold or Striae

Risk factors for flap folds include:

Excessive irrigation of the flap during LASIK

Poor repositioning of the flap at the end of the procedure

Thin flaps

Deep and highly myopic ablation with flap-bed mismatch

Postoperative eye rubbing or squeezing

Older patient age

Flap folds are classified as macro- or microstriae.

Macrostriae

Macrostriae are full-thickness, rolling stromal folds that occur because of flap malposition or slippage. They are typically visible on broad-beam slit-lamp illumination and can cause substantial irregular astigmatism and loss of BCVA.

Management: If found early in the postoperative period, the flap should be immediately lifted, irrigated, and repositioned, with a bandage contact lens placed. After 24 hours, macrostriae may require refloating, de-epithelialization, hypotonic hydration (sterile water), stretching/stroking, and suturing. Antitorque or interrupted 10-0 nylon sutures can be considered in cases of recalcitrant striae. If folds are identified much later, surgical intervention may still be attempted, but if patients are asymptomatic and content with their vision, folds can be monitored.

Microstriae

Microstriae are fine folds in Bowman's layer, resulting from mismatch of flap to the new ablated bed, and are often visually insignificant. They are best visualized with retroillumination or fluorescein (negative staining).

Management: Observation with aggressive lubrication. If visually significant, perform refloating, stroking, and suturing.

In a series of 21,536 femtosecond LASIK eyes, the overall incidence of flap repositioning was 0.35%, with visually significant striae accounting for 64.3% of indications. After repositioning, final uncorrected distance visual acuity of 20/20 or better was achieved in 78% of eyes and 20/40 or better in 98%.

Flap Dislocation

Flap dislocation occurs most commonly within the first 24 hours following surgery, but it can also occur many months to years after surgery as a consequence of corneal trauma. In an analysis of 41,845 consecutive adults undergoing LASIK, the incidence of flap displacement over a 12-month period was 0.012% (10 in 81,238 eyes), with a higher rate after mechanical microkeratome surgery than after femtosecond laser flap creation.

Risk factors:

Excessive lid squeezing

Eye rubbing

Severe dry eye

Presence of epithelial abrasion

Poor intraoperative repositioning

Excessive irrigation of the flap

Trauma

High myopia (OR = 3.04, P = 0.001)

Age over 50 years (OR = 3.69, P = 0.001)

Prevention: Check adhesion of the flap at the end of the procedure (striae test, gutter symmetry), remind the patient not to squeeze or rub the eyes, and instruct wearing of a protective shield for the first 24 hours and every night for the first week.

Management: Reposition the flap promptly with interface irrigation, remove any epithelium from the interface and stromal bed, suture the flap in the event of persistent folds, and use lubricants and a bandage contact lens.

Outcomes: In a study of 66 eyes with late traumatic LASIK flap displacements, efficacy remained unchanged in 75% and safety in 90%; 100% achieved 20/40 or better and 70.3% achieved 20/20. Immediate surgical management led to better visual efficacy. Notably, the risk of developing epithelial ingrowth increased with the time interval between LASIK surgery and the traumatic displacement (OR 1.001; P < .001), making prompt repair essential.

Dry Eye

Dry eye is one of the most common side effects of LASIK, with a reported incidence of 60–70% in the early postoperative period. Flap creation transects afferent corneal nerves, disrupting the corneal-lacrimal gland and corneal-blink reflex arcs, which leads to reduced reflex tearing, altered blink dynamics, and ocular surface disease.

Prevention: Perform a thorough preoperative examination to identify signs of ocular surface disease and treat aggressively with topical lubrication, cyclosporine A, and systemic treatment with oral tetracyclines and oral omega-3 fatty acids. Optimization of the ocular surface before surgery improves both refractive predictability and patient satisfaction.

Management:

Mild: Frequent use of non-preserved artificial tears and gels; environmental modification.

Moderate to severe: Topical cyclosporine A, lifitegrast, short-course topical corticosteroids, oral tetracyclines, oral omega-3 fatty acids, and punctal occlusion.

Refractory: Autologous serum tears, scleral lenses, and evaluation for corneal neuropathic pain.

Persistent ocular discomfort disproportionate to clinical signs should raise suspicion for corneal neuralgia / neuropathic ocular pain, a recognized post-LASIK complication distinct from conventional dry eye.

Diffuse Lamellar Keratitis (DLK)

DLK is a noninfectious aggregation of inflammatory cells confined to the lamellar interface in an otherwise uninflamed eye, arising most commonly in the first few days after surgery. The eye shows little or no conjunctival hyperemia or anterior chamber inflammation, and the patient generally has no discomfort. It is initially characterized by a fine granular reaction in the interface, becoming more prominent if untreated and progressing to the "Sands of the Sahara" appearance. It is frequently more prominent in the periphery and does not extend anteriorly into the flap or posteriorly into the stroma. Reported rates range from 0.4% to 4.38%, and the incidence appears higher with femtosecond LASIK than with microkeratome LASIK.

Pathophysiology: DLK is most commonly triggered by epithelial injury during or after lamellar surgery, leading to release of IL-1α, IL-1β, and TNF-α from the epithelium into the stroma. These chemokines directly attract inflammatory cells from limbal blood vessels and bind to keratocyte and corneal fibroblast receptors, upregulating additional chemokines that recruit monocytes, macrophages, granulocytes, and lymphocytes. Other triggers include retained interface blood, endotoxins and other toxins, and excessive keratocyte necrosis caused by femtosecond lasers. Potential triggers also include interface debris from the microkeratome blade, gloves, drapes, cleaning solutions, meibomian gland secretions, and bacterial antigens.

Staging (conventional 4-stage classification):

Stage 1: Faint, peripheral granular white cells in the interface, sparing the visual axis. Occurs on postoperative day 1.

Stage 2: Diffuse white cells throughout the interface including the visual axis, typically on day 2–3.

Stage 3: Dense, clumped aggregation of cells in the central visual axis with relative clearing peripherally, occurring on day 2–3. Visual acuity declines and haze is reported.

Stage 4: Stromal melting, permanent scarring, and induced hyperopic shift with irregular astigmatism due to central stromal collapse.

Management: Stage 1 and 2 DLK is treated medically with intensive topical corticosteroids (e.g., prednisolone acetate 1% or difluprednate hourly) with close daily follow-up; oral corticosteroids may be added. Stage 3 and 4 DLK requires prompt flap lift with interface irrigation to remove inflammatory mediators and cells, followed by intensive topical corticosteroid therapy. Because central Stage 3–4 disease can progress to permanent scarring and hyperopic shift within 24 hours, urgent recognition is essential. See the discussion in the Diffuse Lamellar Keratitis article.

Late-onset DLK may occur months to years after LASIK, typically triggered by an epithelial defect, corneal abrasion, or intercurrent ocular surface insult. It responds to topical corticosteroids but requires exclusion of infectious keratitis.

Pressure-Induced Stromal Keratitis (PISK)

PISK—also termed interface fluid syndrome—is a late-onset interface opacity that mimics DLK but is caused by elevated intraocular pressure, most often from prolonged topical corticosteroid therapy. Fluid accumulates in the potential space of the lamellar interface, producing a visible optically clear fluid cleft rather than the granular inflammatory infiltrate of true DLK.

Critical diagnostic pitfall: Central applanation tonometry reads falsely low because the interface fluid cushion dampens applanation. IOP must be measured peripherally (over the paracentral or peripheral cornea outside the flap) or with a Tono-Pen/dynamic contour tonometer, otherwise the diagnosis is missed and corticosteroids are erroneously escalated—worsening the condition. Anterior segment OCT demonstrating an interface fluid cleft is confirmatory.

Management: Rapid tapering or cessation of corticosteroids and initiation of aqueous suppressant anti-glaucoma therapy to lower IOP. The interface fluid and opacity typically resolve as IOP normalizes.

Feature DLK PISK Infectious Keratitis Onset POD 1–3 (or late after epithelial defect) Typically 1–3+ weeks postoperatively POD 3–4 (bacterial); weeks (atypical) Interface finding Granular white cells, peripheral → central Optically clear fluid cleft, diffuse haze Focal, dense, often unilateral infiltrate IOP Normal Elevated (falsely low centrally) Normal or variable Pain/redness Minimal Minimal Prominent pain, photophobia, injection Laterality Often bilateral Often bilateral Usually unilateral Treatment Intensify steroids ± flap lift/irrigation Stop steroids, lower IOP Lift flap, culture, fortified antibiotics; stop steroids

Central Toxic Keratopathy (CTK)

CTK is a rare, noninflammatory, self-limited condition characterized by central corneal stromal opacification with striae, corneal thinning, and a significant hyperopic shift with irregular astigmatism, typically presenting within the first week after LASIK. Unlike DLK, CTK lacks a cellular inflammatory infiltrate and does not respond to corticosteroids, and unlike PISK, IOP is normal.

The etiology remains uncertain, with proposed mechanisms including keratocyte apoptosis, excimer laser–induced photothermal or photochemical effects, and toxic reactions to interface contaminants. Management is largely observational, as most cases improve spontaneously over 2 to 18 months with gradual resolution of the opacity and partial regression of the hyperopic shift. Flap lifting and irrigation are not beneficial and may worsen the process. Refractive correction should be deferred until stability is achieved. See the discussion in the Central Toxic Keratopathy article.

Infectious Keratitis

Although rare, infection under a LASIK flap is one of the most vision-threatening complications and must be differentiated from sterile DLK. Reported incidence ranges from approximately 0.02% to 0.2%.

Microbiology by timing:

Early (within first 2 weeks): Gram-positive organisms predominate—Staphylococcus aureus, coagulase-negative staphylococci, and Streptococcus species.

Late (2 weeks to months): Atypical organisms predominate—nontuberculous (atypical) mycobacteria (M. chelonae, M. abscessus, M. fortuitum), fungi (Candida, Aspergillus, Fusarium), Nocardia, and Acanthamoeba.

Symptoms and signs: Decreased visual acuity, pain, photophobia, redness, and a focal interface or stromal infiltrate. Unlike DLK (which presents on postoperative day 1–2, is often bilateral, and is relatively painless), infectious keratitis typically presents on day 3–4 or later and is usually unilateral with prominent pain and conjunctival injection.

Prevention: Adequate sterilization of instruments, preoperative treatment of blepharitis and dry eye syndrome, use of sterile surgical technique, avoidance of surgery in patients with active ocular surface infection, and postoperative topical antibiotic prophylaxis.

Management: Prompt flap lift with interface scraping/culture (bacterial, fungal, mycobacterial, and Acanthamoeba media) and irrigation with antibiotic solution. Topical corticosteroids should be discontinued or markedly reduced until infection is controlled. Start empirical fortified therapy:

Bacterial: Fortified vancomycin (50 mg/mL) plus fortified tobramycin (14 mg/mL) or a fourth-generation fluoroquinolone (gatifloxacin, moxifloxacin), given hourly.

Atypical mycobacteria: Topical amikacin (8 mg/mL), topical clarithromycin (10 mg/mL), and oral clarithromycin (500 mg twice daily); topical fourth-generation fluoroquinolones are also active.

Fungal: Topical natamycin 5% (50 mg/mL) for filamentous fungi, topical amphotericin B (1.5 mg/mL) or voriconazole 1% for yeasts; oral voriconazole for deep or severe infection.

In refractory cases, flap amputation may be required to improve antimicrobial penetration and remove the sequestered infectious nidus. Therapeutic penetrating keratoplasty is reserved for progressive melting or perforation.

Herpes simplex reactivation is a recognized post-LASIK complication; a history of ocular HSV warrants preoperative and perioperative oral antiviral prophylaxis.

Epithelial Ingrowth

Epithelial ingrowth is the most common interface complication, with reported incidence between 1% and 20% in the historical literature, though rates after primary femtosecond LASIK are considerably lower. It is markedly more common after flap-lift enhancement and after traumatic flap dislocation. Presentation is typically weeks to months after surgery.

Risk factors:

Poor adhesion of the flap edges

Epithelial abrasions at the flap margin

Buttonhole flap

Free cap

Ablation at the edge of the stromal bed

Epithelial irregularity at the flap edge

Introduction of epithelial cells during the cut or with instruments

Inadequate interface irrigation

Previous radial keratotomy (RK)

Reoperation / flap-lift enhancement

Epithelial basement membrane dystrophy

Older age

Delayed repair of traumatic flap displacement (OR 1.001 per unit time; P < .001)

Classification: Two morphologic types are recognized—isolated epithelial pearls or nests within the interface, and a contiguous sheet of epithelium growing centrally from the flap periphery. The Probst-Machat grading scale (grades 1–3) is commonly used, with grade 3 denoting thick ingrowth ≥2 mm from the flap edge with a rolled, whitened flap margin and associated flap melt.

Symptoms and signs: Reduced vision, monocular diplopia or ghosting, irregular astigmatism, foreign body sensation, and in severe cases progressive stromal melting of the overlying flap.

Prevention: Avoid epithelial defects, meticulously irrigate epithelial cells and debris from the interface, ensure good flap edge apposition and gutter symmetry at the conclusion of surgery, avoid an excessively wide ablation zone extending to the flap edge, and consider surface ablation rather than flap lift for enhancements in high-risk eyes.

Management: No treatment is necessary for asymptomatic, isolated, or peripheral nests, which frequently remain stable or regress; these should be monitored with serial photography and topography. If the patient is symptomatic, if the ingrowth is progressive or encroaches on the visual axis, or if there are findings of flap melt or irregular topography, the flap should be lifted to expose the affected area and the underside of the flap and the stromal bed mechanically scraped before repositioning. Adjuncts to reduce recurrence include:

Alcohol application or phototherapeutic keratectomy to the affected surfaces

Nd:YAG laser treatment for localized ingrowth

Flap edge suturing (interrupted or running 10-0 nylon)

Fibrin tissue glue at the flap margin

Bandage contact lens

In severe or recurrent cases with flap melt, flap amputation may be necessary.

Corneal Ectasia

Post-LASIK ectasia is progressive corneal steepening, thinning, and irregular astigmatism resembling keratoconus, occurring months to years after otherwise uncomplicated surgery. It is the most feared long-term complication of LASIK.

Risk factors: Abnormal preoperative topography/tomography (forme fruste keratoconus, pellucid marginal degeneration, asymmetric inferior steepening), low residual stromal bed thickness (generally <250–300 µm), high myopia, thin preoperative central corneal thickness, and young age. The Randleman Ectasia Risk Score System stratifies these variables.

Prevention: Careful preoperative screening with corneal tomography, adherence to residual stromal bed thickness limits, and selection of surface ablation or phakic IOL in borderline candidates.

Management: Corneal collagen crosslinking to halt progression, rigid gas permeable or scleral contact lenses for visual rehabilitation, intrastromal corneal ring segments, and keratoplasty in advanced cases. See the discussion in the Post-LASIK Ectasia article.

Recurrent Corneal Erosion

Recurrent corneal erosion may occur after LASIK, particularly in patients with underlying epithelial basement membrane dystrophy or prior intraoperative epithelial defects. Management follows standard principles: aggressive lubrication, hypertonic saline ointment, bandage contact lens, and consideration of anterior stromal puncture or phototherapeutic keratectomy for refractory cases.

Corticosteroid-Related Complications

Prolonged postoperative topical corticosteroid use may cause ocular hypertension, steroid-induced glaucoma, PISK/interface fluid syndrome, cataract formation, and increased susceptibility to infection. IOP should be monitored during any extended corticosteroid course, with the caveat that central applanation readings are falsely low after LASIK.

Artifactual Reduction of Measured Intraocular Pressure

LASIK reduces central corneal thickness and alters corneal biomechanics, resulting in artifactually low IOP measurements by Goldmann applanation tonometry. This has important implications for glaucoma screening and management in post-LASIK patients, who may harbor unrecognized ocular hypertension or glaucoma. Documentation of preoperative IOP and central corneal thickness is recommended, and alternative tonometry methods (dynamic contour tonometry, ocular response analyzer) may be considered.

Ptosis

Transient or persistent ptosis may follow LASIK, attributed to speculum-related trauma to the levator aponeurosis, suction ring pressure, or postoperative edema. Most cases resolve spontaneously within 3 to 6 months; persistent cases may require levator advancement.

Rare Complications

Ischemic optic neuropathy, retinal detachment, vitreous hemorrhage, posterior vitreous detachment, macular hemorrhage, and choroidal neovascularization are potential but very rare complications of LASIK, occurring in less than 0.1% of patients. Proposed mechanisms include the transient marked elevation of intraocular pressure (to >65 mmHg) during suction ring application, causing vascular compromise of the optic nerve head, and vitreoretinal traction. Highly myopic patients are at baseline elevated risk for retinal pathology independent of surgery, and a dilated peripheral retinal examination is recommended preoperatively.

Patient Satisfaction and Quality of Life

Despite the complications enumerated above, patient satisfaction with LASIK is consistently high. In the FDA-sponsored PROWL studies (PROWL-1, n=262; PROWL-2, n=312), less than 1% of participants experienced difficulty with or inability to perform usual activities without corrective lenses due to visual symptoms after LASIK. Dissatisfaction with vision was reported by 1–4% and dissatisfaction with the surgery by 1–2%.

However, PROWL also demonstrated that new visual symptoms are common:

Up to 45% of participants without preoperative symptoms reported at least one new visual symptom (glare, halos, starbursts, or ghosting) at 3 months.

A substantial proportion of patients with preoperative symptoms reported resolution of those symptoms after surgery.

Approximately 28% of participants with no preoperative dry eye symptoms reported new dry eye symptoms at 3 months.

These data underscore the importance of thorough preoperative counseling regarding the expected incidence of transient visual symptoms and dry eye, even in uncomplicated cases.

Prevention: The Role of Preoperative Screening

Most LASIK complications are best addressed through prevention. Key elements of preoperative evaluation include:

Corneal tomography (anterior and posterior elevation, pachymetry mapping) to exclude ectatic disease

Central corneal thickness with calculation of anticipated residual stromal bed thickness

Ocular surface assessment including tear breakup time, staining, Schirmer testing, and meibomian gland evaluation, with treatment of dry eye before surgery

Refractive stability documented over time

Slit-lamp examination for EBMD, corneal scars, and prior surgery

Dilated fundus examination, particularly in high myopes

Pupil size measurement under scotopic conditions

Review of systemic conditions and medications (autoimmune disease, diabetes, isotretinoin, amiodarone, immunosuppression)

History of herpetic eye disease

Preoperative optimization of the ocular surface in particular has been shown to improve refractive predictability, reduce postoperative dry eye severity, and increase patient satisfaction.

Conclusion

LASIK remains a highly safe and effective procedure, with serious adverse events occurring in approximately 0.4% of eyes in contemporary large series. The transition from mechanical microkeratomes to femtosecond lasers has largely eliminated the classic flap complications of buttonhole, free cap, and irregular flap, while introducing a distinct set of energy-related phenomena including opaque bubble layer, vertical gas breakthrough, rainbow glare, and transient light sensitivity syndrome. Rigorous preoperative screening—particularly corneal tomography to exclude ectatic disease and ocular surface optimization—remains the single most effective strategy for avoiding complications. Prompt recognition and correct differentiation among DLK, PISK, central toxic keratopathy, and infectious keratitis is essential, as their managements are divergent and, in the case of infection versus sterile inflammation, diametrically opposed.

Additional Resources

AAO Refractive Surgery Preferred Practice Pattern

FDA LASIK Information Page

AAO EyeSmart: LASIK Eye Surgery