Managing Refractive Laser Surgery Complications: Tips for Ophthalmology Residents

Refractive surgery is one of the most rewarding and gratifying fields in ophthalmology. The majority of patients are very satisfied postoperatively, and they have the convenience of no longer having to use glasses or contact lenses in their everyday life. In fact, excimer laser treatments have become incredibly consistent and reliable procedures; patients report very high satisfaction rates.

Complications of refractive laser surgery (i.e., LASIK and PRK) can occur, and it is necessary to be able to identify them early on in order to provide prompt treatment and preservation of vision. This article highlights the basic steps of both LASIK and PRK, important preoperative screening and counseling points, as well as examples of where things can go wrong, and how to handle them—at time of surgery as well as days to months to even years postoperatively.

PRK

Invented in 1987, Photorefractive keratectomy (PRK) is a successful means for treatment of refractive error in select patients.^1-6 In general, the steps of the procedure involve debridement of the epithelium, which can be done manually or via use of the excimer laser itself (transepithelial PRK), followed by excimer laser ablation of the stromal bed and placement of a bandage contact lens. Some surgeons also use mitomycin C from 12-20 seconds following ablation to prevent stromal haze and regression.^7-10

Some advantages of PRK include avoidance of creating a lamellar flap, as in LASIK—which may be best for patients with anterior corneal dystrophies (e.g. anterior basement membrane dystrophy), as well as those with thinner corneas.^5,6 By leaving thicker residual stroma than LASIK, PRK may be considered to be “less risk” in the development of postoperative ectasia and therefore can be considered the technique of choice for patients with thinner corneas or perhaps even those patients who are more at risk for trauma, like athletes or pilots.^5,10-12

LASIK

Laser Assisted In-Situ Keratomileusis (LASIK) was approved by the FDA in 1995.¹³ In comparison with PRK, it offers a quicker recovery with less pain. In general LASIK involves 3 steps: creation of a lamellar corneal flap, lifting the flap and ablation of the stromal bed, and finally replacing the flap to original position. It is most common for refractive surgeons now to use a femtosecond laser to create a corneal flap, followed by excimer laser ablation of the stromal bed (similar to PRK). Creation of a corneal flap allows for a quicker recovery time, but may come with its own risks, as outlined below.

When performing any laser vision correction (LVC) procedure, pristine preoperative evaluation is crucial. Patients who may not be good candidates for surgery include those with autoimmune disease (e.g. Sjogren’s Syndrome), severe dry eye (e.g. Schirmer test <5mm), history of corneal scarring (e.g. those patients who may be candidates for corneal transplant), and corneal ectasia (e.g. keratoconus). In addition, careful management and review of patient expectations is important. While LVC can be incredibly successful, it is important to go over risks, benefits and alternatives to surgery in order to properly prepare patients for visual expectations as well as what to expect in the postoperative period.

Patient education

Prior to considering refractive surgery, patients need to be fully informed about the benefits and risk of available procedures and be counseled on all available treatment options. Essential factors to be considered in patient education include the following:^{1,9-11,13-23,26}

Realistic expectations: LVC is considered an elective procedure, typically not covered by insurance. There is a chance, based on refractive error of needing refractive enhancement later on. Patients with unrealistic expectations (such as achieving vision better than 20/20 or never needing to use reading glasses) must be identified and properly counseled.
Normal symptoms and possible side effects of surgery: Discomfort, dry eye, fluctuating vision, halos or glare at night (may last 4-6 weeks), and foreign body sensation may occur.
Risk of complications: Albeit rare, intraoperative problems, abnormal healing, corneal haze, loss of best corrected visual acuity, higher order aberrations (HOAs), infection, and other surgical complications (e.g. corneal ectasia) can occur.
Presbyopia: The aging eye will experience increased dependence on reading glasses in later years when both eyes are surgically corrected for distance. This may become more evident after LVC.
Postoperative care: Patients should be counseled on the importance of ocular lubrication, instillation of drops, use of oral medications (if necessary), avoidance of eye rubbing, follow up visits, as well as reporting of concerning symptoms.

Proper preoperative evaluation

It is imperative that a scrutinous preoperative evaluation is performed on all potential refractive surgery candidates. There are several things to consider:⁹

Unstable refractive error: LVC should not be performed until there is no longer active change to eyeglass prescription for at least 6-12 months. This may not occur until the age of 21 in many patients.
Corneal thickness: Careful consideration should be paid to patients who have predicted postoperative corneal thickness less then 300µm (Calculated ablation depth is based on optical zone diameter, blend zone and refractive error (~15µm per diopter treated)). Thinner corneas are at much higher risk for ectasia.
Systemic disease: Uncontrolled diabetes, rheumatoid arthritis or other uncontrolled autoimmune conditions may be contraindications for LVC.
Large pupils: Patients with larger pupils, especially in dim illumination, may be at greater risk of observing higher order aberrations. The surgeon should measure pupillary diameter under both photopic, mesopic and scotopic conditions and document for dim illumination.
Corneal topography: It is essential to evaluate corneal contour to determine potential of early keratoconus/ectasia. If present, LVC should not be performed.
Keratometry: Preoperative corneal curvature (“K reading”) and dioptric (D) value of refractive error predict postoperative K readings. A cornea that is too flat or too steep may lead to postoperative visual dissatisfaction. Predictive K readings for myopic eyes less than 36D may result in poor postoperative optics, and for hyperopic eyes, predicted K readings greater than 49D may result in greater dry eye symptoms and ectasia.
Refraction: Manifest and cycloplegic refraction should be performed. Measurement of refractive error (myopia, hyperopia, astigmatism) is needed to ensure against overcorrection. In addition, there should not be a large discrepancy between manifest and cycloplegic refraction, as this could lead to an inability to determine exact refractive error to be treated as well as a resultant suboptimal visual result.
Ocular alignment: A cover-uncover test can be used to rule out strabismus. Patients with intermittent strabismus may not tolerate monovision corrections.
Evaluate for ocular disease: It is important to exclude patients with keratoconus/pellucid marginal degeneration, cataracts, glaucoma with manifesting visual field defects, Fuchs dystrophy, other anterior corneal dystrophies that result in recurrent erosion (e.g. map-dot dystrophy), and/or granular or lattice dystrophy that may be better served with other corneal procedures. Central/dense corneal scars are considered contraindications to LASIK/PRK, in that they may result in an irregular ablation and poor visual satisfaction. In addition, large pingueculae may increase difficulty of proper suction during LASIK flap creation.
Severe dry eye: Significant dry eye may delay healing and decrease visual acuity. Surgeons should seriously consider not performing LVC on patients with refractory dry eye (e.g. 3+ corneal staining not responding to therapy and/or Schirmer test <5mm).
Untreated lid disease (Blepharitis, meibomian gland dysfunction): These patients are more likely to experience dry eye and have more postoperative symptoms. They should be treated with lid hygiene, and topical antibiotics as indicated pre-and-perioperatively.
Keratitis: Neurotrophic keratitis and history of herpetic keratitis are relative contraindications to laser vision correction procedures
Dilated fundus exam: Just as in any other ocular surgery, a thorough exam prior to LVC is recommended to rule out retinal thinning, holes or partial detachments that could lead to potential problems during and after surgery.

What can go wrong? (And what to do!)

Fortunately, complications related to LVC are not very common. However, refractive surgeons should be aware of possible adverse events related to surgery and ensure proper preoperative counseling and patient understanding. Below, I outline several possible adverse outcomes that should be reviewed and explained to any LVC patient prior to undergoing surgery (and how to manage!).

Pain

Pain post-LVC is usually transient. However, the patient needs to be informed of this as part of preoperative counseling.^9,13 Pain and discomfort usually lasts approximately 4-6 hours post-LASIK, and may persist for 1-3 days post-PRK.^9,13 This being said, patients should be advised to contact their surgeon with any concerns of increasing pain, redness or discharge postoperatively. Management is typically symptomatic and the patient can be advised to use cool compresses (applied gently), artificial tears, and oral analgesics as needed.

Fluctuating vision

Fluctuations in vision may occur in the early postoperative period. Surgeons should educate their patients that this may occur in the very beginning and that they should experience a gradual increase in vision. In addition, visual fluctuations may take longer to resolve with PRK vs. LASIK.^9,13

Dry eye

Dry eye is a common cause of patient dissatisfaction and one of the most common complications after PRK and LASIK.^{9,13,19,21,23-26} Tear production, as shown by the Schirmer test, has been shown to be lower following LASIK vs. PRK. Both techniques impair corneal innervation, crucial for ocular surface homeostasis, and can also cause ocular surface inflammation.^{9,13,19,21,23-26}

Dry eye must be promptly recognized and addressed, as the tear film contributes to refraction and therefore visual acuity. It should be the goal of the refractive surgeon to maximize tear film stability preoperatively and minimize dry eye postoperatively. As discussed earlier, careful preoperative assessment of the eyelid, tear breakup time, corneal staining, esthesiometry, and Schirmer test should be performed. Post-surgery, patients may experience foreign body sensation, blurry vision and excessive tearing. Symptoms may persist up to 3 months for PRK and 6 months for LASIK.^{9,13,19,21,23-26} Initial management of dry eye may involve frequent use of preservative free artificial tears as well as treatment of preexisting lid disease (e.g. blepharitis, meibomian gland dysfunction). Additionally, use of topical cyclosporine or lifitegrast eye drops may be effective.^{9,13,19,20,21,23-26}

Risk of corneal haze

Corneal opacity/haze is a particular (albeit low) risk of PRK.^{7-10,14,16,18,27} Limiting haze formation is important in improving visual outcomes in surface ablation techniques; when it develops patients may experience decreased vision, refractive regression and glare.^{7-10,14,16,18,27} Two types of haze have been described: type I tends to appear 1-3 months after surgery and then disappear after 1 year; type 2 (“late onset”) appears after three months and can persist for more than 3 years.¹⁶ It is thought that the wound healing response caused by ablation of the central Bowman layer and anterior stroma can, in some cases, lead to subepithelial haze formation and/or regression of the initial refractive treatment.^9,16 Early haze formation usually peaks at 1-2 months post-PRK and usually decreases by 6-12 months post-surgery. It is felt that this fluctuation in haze is due to abnormal deposition of glycosaminoglycans and nonlamellar collagen in the anterior stroma with increased keratocytes.^9,16 Stromal surface irregularities created during PRK may also promote passage of transforming growth factor-beta (TGF-ß), which is involved in myofibroblast proliferation. As the cornea heals and the epithelial basement membrane is restored, levels of TGF- ß decrease, myofibroblasts undergo apoptosis and the cornea regains its transparency. This process can last weeks to several months.^{7-10,14,16-18,27}

Risk factors that may lead to increased formation of corneal haze include high preoperative myopia and astigmatism, smaller ablation zones, increased age and high exposure to ultraviolet (UV) radiation.^{7-10,14,16-18,27} UV radiation has also been associated with an increased risk of late-onset corneal haze, suggesting that the use of UV-protective eyewear during the first year after surgery should be recommended.^9,18

Initial management of corneal haze post-PRK includes topical steroid eye drops. This treatment may be able to prevent corneal haze for the first 3 months, but has not been shown to be effective in preventing late onset haze, except in eyes with high myopia.^{7-10,14,16,18,27}

High grade corneal haze can be treated with epithelial debridement and even phototherapeutic keratectomy (PTK), although success of these procedures may depend on haze morphology and individual wound healing response. In addition, following manual debridement, mitomycin C (MMC) can be applied to prevent recurrent haze development.^{7-10,14,16,18,27} MMC modulates the corneal wound healing process by blocking keratocyte activation and proliferation, as well as myofibroblast differentiation.^{7-10,14,16-18,27} However, it is important to note that despite multiple management techniques available to treat corneal haze, dense corneal haze unresponsive to treatment may ultimately require corneal transplantation.^{7-10,14,16,18,27}

Risk of infection

Risk of infection with laser vision correction can occur but is exceedingly low, with incidence reports ranging from 0.2-0.5% (~1/1000 cases).^22,28,29 Infectious keratitis may be due to Staphylococcus aureus (including methicillin resistant S. Aureus (MRSA)), Streptococcus pneumoniae, Strep viridans, atypical mycobacterium, Nocardia asteroides and fungi.^22,28,29 It is recommended that corneal cultures and sensitivity be performed on all cases of infection, as this can help guide antibiotic choice and response later in treatment.

Risk of infection post-LVC is heightened in patients with dry eye, diabetes, autoimmune conditions, and active smokers.^22,28,29 Early identification of infection is critical as it may lead to vision threatening consequences, such as corneal scarring, and even (rarely) endophthalmitis in severe cases.^22,28,29

Post-PRK infection

Risk of infection post-PRK may be linked to creation of epithelial defect at time of surgery and use of a bandage contact lens for (at least) several days postoperatively. These patients require very close follow up for epithelial closure, and proper preoperative counseling regarding hand hygiene and use of topical antibiotics in the postoperative period.^22,28,29

Post-LASIK infection

Although infection rate is quite low post-LASIK, it can follow a bimodal occurrence, in that early infections may involve typical gram-positive pathogens (e.g. S. aureus, S. viridans), and in later infections, atypical mycobacteria. Management of infection risk starts with prevention: sterile technique at the time of surgery as well as prophylactic antibiotics such as fourth generation fluoroquinolones (e.g. gatifloxacin, moxifloxacin) that may be given at time of surgery and after.^22,28,29

Early identification is essential as well. Steroid use should be stopped immediately, as it has the potential to worsen infection. If an infection of the LASIK flap/interface is identified, the surgeon will need to lift the flap, culture, irrigate with antibiotics and possibly amputate the flap (in severe cases).^22,28,29 LASIK flap infections may be due to atypical mycobacteria, which is typically treated by compounded amikacin and/or clarithromycin. However, it is important to note that culture and sensitivity results should help guide individual treatment.^22,28,29

LASIK flap complications

Flap dislocation

Flap dislocation may occur very early in the postoperative period (usually within the first week due to traumatic forces) and has a 1.4% incidence.^30-34 It is important to identify this complication as early as possible to avoid potentially permanent disturbances in the flap itself as well as the flap interface. Aside from patient education (NO eye rubbing!), treatment involves lifting and replacing (“refloating”) the flap using balanced saline solution, as well as monitoring for the presence of epithelium under flap (which can prove troublesome later on).

LASIK flap striae

LASIK flap striae, or folds in the LASIK flap itself, is associated with increased irrigation at the time of surgery, thinner flaps, deep ablations, and traumatic flap dislocation.^30-34 Striae are usually noted within the first week after surgery (95%), with 56% of cases noted within 1 day of surgery. Striae may be divided into 2 forms: macrostriae and microstriae.

Macrostriae are full thickness stromal folds due to initial flap malposition and/or postoperative flap slippage. This may lead to decreased visual acuity as well as multiplopia if central in location. At time of exam, under direct illumination, macrostriae are seen as broad furrows with parallel or radial converging lines; a widened flap gutter may be seen.^30-34 A negative staining pattern may be observed upon fluorescein instillation (can appear as “wrinkles in skewed carpet”). Topography may show disruption over striae as well. Management of macrostriae involves lifting the flap, moving the gutter into realignment and stroking out the corneal folds (“like stretching out a bedsheet”). Usually, a bandage contact lens is placed for several days following treatment, as well as use of topical antibiotics and steroids. In severe cases, a running suture may be used to suture and stretch the flap into correct position.^30-34

Microstriae are fine optical irregularities in Bowman’s layer due to mismatch of the flap to the new stromal bed and/or flap contracture.^30-34 Under direct illumination on exam, fine folds will be seen in Bowman’s layer; the gutter here is usually symmetric. Retroillumination can make folds more obvious—they may resemble “dried cracked mud” in their pattern.^30-34 Topography may be normal or slightly disrupted—mires on Placido disc images may show fine irregularity. Patients may have subtle decreased visual acuity or multiplopia if clinically significant.^30-34 Microstriae may or may not need treatment. If there is no apparent visual compromise and the LASIK flap is otherwise well positioned, the patient may be monitored closely. If there is potential visual compromise due to central striae, smoothing out the flap (as for macrostriae) is indicated.^30-34

Diffuse lamellar keratitis (DLK)

DLK is a nonspecific anterior stromal sterile inflammation in response to mechanical or toxic insults within the flap interface.^31-36 It is important to differentiate DLK from infectious keratitis. DLK is confined to the interface alone, versus infectious keratitis which usually spreads beyond the flap interface.^34-36 DLK is also typically observed within the first 24 hours, begins at the flap periphery, and moves centrally with increasing grade of inflammation (vs. infectious keratitis which is seen in the first 1-2 days and typically does not remain within the flap interface, nor follow a specific pattern).^34-36

DLK is divided into stages, with Stage 1 being the mildest, and consisting of peripheral faint white blood cells with a granular appearance.^34-36 Stage 2 shows progression to central scattered white blood cells in the flap interface.^34-36 Treatment of Stage 1 and 2 involves intensive topical steroids (usually every hour) until resolution is seen, followed by a slow taper.^34-36 Stage 3 DLK involves a dense central accumulation of white blood cells in the visual axis; stage 4 can involve flap melting and permanent scarring. Treatment of Stage 3 and 4 usually involve lifting the flap, irrigating with balanced saline solution, and oral steroids in addition to topical steroids.^34-36

Pressure induced stromal keratopathy (PISK)

PISK prevents as a diffuse stromal and interface opacity due to increase in intraocular pressure (IOP) associated with a fluid cleft and edema within the flap interface.⁹ It can also be associated with use of steroids (usually topical). PISK typically occurs within 10-14 days of surgery (vs. DLK which occurs within 24 hours and does not have increased IOP).⁹ Here, it is essential to check IOP centrally and peripherally as central flap edema may lead to inaccurate IOP reading. Treatment of PISK involves lowering IOP by rapidly tapering topical steroids and use of anti-ocular-hypertensive (glaucoma) eye drops.⁹

Epithelial ingrowth

Epithelial ingrowth post-LASIK is most commonly seen with poor surgical techniques where epithelial cells are inadvertently implanted onto the interface.^30-36 This occurs in less than 3% of eyes, is more common in patients older than 50 years, those with persistent corneal epithelial defects, undiagnosed corneal dystrophies and patients with previous incisional surgery (e.g. radial keratotomy).^30-36 This condition is typically diagnosed within the first few weeks following LVC. If noted to be peripheral and not visually significant, no acute treatment is necessary. However, if central in nature, or associated with decreased visual acuity or flap decompensation (i.e. flap melt), lifting the flap and scraping the epithelium on both surfaces is indicated. If recurrence occurs, re-lifting the flap is recommended, and in this case, it may be necessary to secure the flap in position with suture or fibrin glue.^30-36

Interface debris

Interface debris may be present post-LASIK (e.g. fibers of a surgical sponge) and intervention is indicated if an inflammatory reaction ensues. Management of this includes flap lifting, irrigation of the interface and/or manual removal of the foreign object.^30-36 Ideally, this should be prevented at the time of surgery by checking for presence of foreign material prior to the end of the case (i.e. after replacement of the flap and irrigation).

Ectasia

Corneal ectasia develops when the corneal biomechanical integrity is reduced beyond its functional threshold.^10-12,37 This leads to bulging of the corneal tissue, irregular astigmatism, and resultant decrease in visual acuity.^10-12,37 It is very important to rule out post-refractive surgery ectasia when it comes to deciding for enhancement treatment; only small topographical changes may be seen, especially in the initial stages, and these can be mistaken for regression.^10-12,37 Risk factors for ectasia include young patient age, thin cornea, high myopic correction, high number of laser corrections, and not maintaining at least 250µm of stromal tissue under flap ablation.^10-12,37 Some studies report that PRK has a less frequent incidence of ectasia vs. LASIK, which may be related to overall reduced ablation volume of stromal tissue.^9-12,37 Treatment of corneal ectasia involves corneal collagen crosslinking (CXL), intracorneal ring segments, contact lenses (soft, scleral, and gas-permeable are options), and in severe cases, corneal transplant.^10-12,37

Visual disturbances

Refractive surgery can sometimes induce higher order aberrations (HOAs), especially spherical aberrations and coma, as well as glare and halos, which can decrease quality of vision. It is reported that visual aberrations can occur after PRK but are less common than post-LASIK treatment, especially in patients with greater pupillary diameters. Risk factors for visual disturbances include smaller ablation zones, higher preoperative prescription, and decentered ablations.

Decentered ablations

When performing any LVC procedure, it is imperative to achieve excellent centration of the planned treatment. Off-axis and decentered treatments can not only lead to suboptimal visual results, but also visual aberrations such as glare and halos.^6,9,37-41,44 Risk factors for decentered ablations include inexperience, hyperopia and high preoperative prescription. In general disturbance of visual acuity occurs when decentration is more than 0.5mm from the visual axis.^6,9,34,37-41

Management of decentered ablations and the resultant visual disturbances may include customized excimer laser treatments designed to minimize HOAs.^{6,9,30,34,37-42} Several studies have shown that wavefront-guided retreatments can reduce HOAs and corneal spherical aberrations and therefore improve visual acuity. By measuring how the optical system alters a wavefront of light entering the eye, wavefront aberrometry can detect subtle irregularities of the eye.^31,41,42 This can also help improve nighttime glare and halo symptoms. Thus, retreatment using ablations based on corneal customization or topography guidance is an option to consider to restore quality of vision.^6,9,34,37-41

Missed refractive target: considerations for retreatment

Although the accuracy of refractive surgical procedures is excellent, it may be necessary to consider retreatment after LVC when there is a residual refractive error, such as over/under correction or regression of treatment. As some patients may adapt to small amounts of residual refractive error, the main indication to consider retreatment (or “enhancement”) is patient dissatisfaction with visual acuity. It is suggested to perform treatment at 3 months postoperatively at the earliest, as many patients achieve stability at 6 months post-LVC.^6,9,34,37-42

When evaluating refractive outcomes post-LVC, it is important to note that in the very early healing phase, there may be a slight overcorrection of refractive error during the first month due to calculated laser nomograms that anticipate a natural regression of effect. In addition, there may be induced astigmatism, due to corneal remodeling, epithelial remodeling (i.e. post-PRK) or tear film disruption.^9,42,43

Enhancement can be performed with a second PRK or LASIK procedure; LASIK enhancement after PRK is also considered safe, predictable and effective. Here, the surgeon must use precautions to prevent corneal haze, which can develop from increased keratocyte reactivation as a result of loss of Bowman layer and prolonged wound healing with previous PRK surgery.^{6,9,16-18,34,37-41}

Topographically-guided excimer laser photoablation, in which individual patient corneal topography is measured and converted to a custom ablation profile, can be effective and safe for the treatment of residual myopia or hyperopia after primary myopic or hyperopic LVC.^37,39,44 Here, reliable detection of corneal irregularities is required to permit the laser to perform customized corneal ablation. Topography guided treatment has been shown to be an effective option for patients who underwent prior eye surgery that resulted in decentered ablation, even post-keratoplasty astigmatism.^37,39,44

As with any surgery, the most important management of complications is prevention. Here are some steps refractive surgeons can take to prevent–or at least decrease the rate of—retreatments:

Overcorrection

Overcorrection can be due to stromal dehydration prior to treatment (more stromal tissue ablated per pulse). The key here is to control humidity and temperature within the laser suite, as well as to not allow too much time to pass between lifting the flap and stromal ablation for LASIK cases.^{3,4,6,31,38,39,40,43,44} Overcorrection is also more common in older individuals, and is thought to be due to less vigorous healing and the cornea ablating more rapidly.^{3,4,6,31,38-40,43,44} It is slightly more difficult to manage, but with approval of hyperopic laser treatment, it has become much more forgiving. Prior to enhancement, the patient should be off topical steroid eye drops; refractive stability is essential.^{3,4,6,13,31,39,40,43,44}

Undercorrection

Primary under-correction also depends on the epithelial and stromal healing response. It is much more common in higher myopic attempted ablations, especially greater than - 10D.^{3,4,6,31,39,40,43,44}

Regression

Refractive regression is defined as the gradual, partial, or complete loss of the attempted correction. Regression is thought to be due to epithelial hyperplasia and stromal remodeling. It usually occurs in the first 3-6 months post-surgery, and is more common with higher preoperative refractive errors.^{3,4,6,31,38-40,43,44} Most cases of regression develop over the first 3 months after surgery, with only slight change after the first 3 months and up to 10 years.^{3,4,6,31,38-40,43,44} Regression can also occur with abrupt discontinuation of steroids in certain PRK cases.

Conclusions

Many variables should be considered when approaching a potential LVC patient. Comprehensive preoperative counseling and examination is key in preventing possible complications and need for additional treatment.

Understanding of the mechanisms of potential LVC complications will allow for proper management, and most importantly, prevention!

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