Our role in refractive surgery involves not only patient selection and education, but also diagnosis and management of post-op complications. Here, we'll explore some of the problems that follow LASIK, how to manage them and when to refer patients for surgery.

Nuisances vs. Complications
We must educate patients on the distinction between a nuisance problem and surgical complication. For example, blurred vision is the most common complaint after LASIK. Residual spherocylindrical refractive error usually underlies this symptom. Without proper education, some patients mistakenly equate residual refractive error to a surgical complication instead of a nuisance.

This underscores the importance of reviewing patients' expectations before the procedure. Emphasize that visual outcomes vary due to individual differences in healing. Rather than use the terms "over-correction" and "under-correction," discuss the cornea's "over-response" and "under-response." If you demonstrate the targeted outcome with contacts or a trial frame, make sure your patient understands that the simulated vision may differ from the end result.

Patient education continues through the recovery period. For example, proactively advise patients with post-LASIK subconjunctival hemorrhages that these red spots are normal, have no adverse effect on visual outcome and generally resolve within 10-14 days.

Otherwise, the patient may think she has developed a complication.

Epithelial Irregularity
Epithelial defects (figure 1) and sloughing occur in 1.6% of LASIK procedures, with a greater frequency with advancing age.¹ That's because with advancing age, the epithelium can become less adherent to the rest of the eyeball.

With epithelial defects, surgeons apply a bandage soft contact lens to improve comfort and promote epithelial healing. When the epithelium has closed, often by the next day, you can remove the contact lens after copious lubrication. If the epithelial defect has not closed, keep the bandage lens in place until it does (usually within 48 hours). Never replace the bandage lens with a pressure patch. This risks flap displacement.

It can take months for the epithelium to smooth after defects and sloughing (figure 2). You can prescribe Muro 128 5% drops qid and nighttime ointment to promote epithelial adhesion and minimize the risk of recurrent corneal erosions.

Raised epithelium within the visual axis (figure 3) can affect visual quality, much as a central island does. Recalcitrant cases that affect vision may require subsequent phototherapeutic keratectomy (PTK) so that the epithelium can adhere smoothly. This procedure carries the possibility of corneal haze and a hyperopic shift.

Patients with a prior corneal abrasion or epithelial basement membrane dystrophy are at risk for epithelial irregularity after LASIK. These patients should undergo photorefractive keratectomy (PRK) instead to achieve both therapeutic and refractive benefits.²

Patients who experience epithelial defects after LASIK are at greater risk for epithelial ingrowth due to actively migrating epithelium. A higher incidence of diffuse lamellar keratitis (DLK) has also been noted after epithelial defects, although we do not understand why.³

Irregular Astigmatism
The following may cause irregular astigmatism after LASIK:

• Central island and peninsulas (figures 4 and 5, respectively). These form when the ablation plume or fluid over the stromal bed impedes the excimer application. Ablation irregularities may subside over months as epithelium migrates to fill in relative depressions in topography.
  Local steepening on corneal topography is not enough to diagnose central islands. Tear debris, striae and raised epithelium in the center can cause a similar topographical appearance. Repeated findings on topography in conjunction with a normal slit lamp exam help you make the diagnosis.
• Decentered ablation (figure 6). This results if the patient does not fixate properly during the procedure, if the surgeon applies the laser off-center, or if an eye-tracking laser incorrectly designates the center of treatment (there are no published reports of this happening).
• Keratectasia. Excessive subtraction of corneal tissue after LASIK can lead to iatrogenic keratectasia (figure 7), with onset from weeks up to years after the procedure. Many surgeons believe that at least 250µm of untouched residual posterior stroma is required to prevent keratectasia. However, some patients have developed keratectasia with more than 250µm of residual bed.⁴ Patients with forme fruste keratoconus and corneas with preoperative central thickness of less than 500µm are also at risk for iatrogenic keratectasia. They should not have LASIK.
• Irregular epithelial responses. Epithelial irregularity is a cause of irregular astigmatism when within the visual axis, as discussed earlier.

Nighttime Glare and Haloes
"Glare" is light scattered by any media opacity, while uncorrected refractive error causes "haloes."^10,11 Perhaps the most publicized problems in post-LASIK patients, these terms are commonly interchanged. "Night vision disturbances" is the preferred description because it is somewhat more generic. Most LASIK patients who complain of "glare" don't have true glare (caused by loss of media transparency). Proper treatment of night vision disturbances hinges on the real cause of those symptoms.

There are several possible causes of persistent post-op night vision disturbances. Differential diagnosis is uncorrected spherocylindrical refractive error, irregular astigmatism, pupil enlargement beyond functional optical zone, reduction in media clarity and malingering. When the patient complains of persistent night problems that are greater than before LASIK, you need to systematically go through the differential diagnosis to offer the best treatment.¹²

First, perform your manifest refraction using a trial frame. Do this in dim lighting as the patient notes the "glare" and "halo" around a distant fixation light. If the patient experiences significant reduction of the disturbance, then uncorrected refractive error is the problem.

If not, place a pinhole over the trial lenses. If the pinhole reduces the "glare" and "halo," the patient may have irregular astigmatism. Potential causes include decentered or irregular ablation, flap striae, irregular microkeratectomy or flap keratolysis. Corneal topography, manual keratometry and biomicroscopy are all useful in determining the cause of the irregular astigmatism.

If the pinhole doesn't help, carefully perform biomicroscopy to confirm a change in media clarity. If there is no loss of media transparency, suspect malingering.

When irregular astigmatism is absent but the pinhole reduces the "glare" and "halo," the pupil is enlarging beyond the optical zone. To verify this, have the patient look at the distant fixation light in dim illumination. Shine a penlight into one eye and ask the patient if there is a reduction in visual disturbance from the fellow eye. Pupillary constriction from the consensual light response will reduce glare and halo symptoms due to large pupil size.

Some patients are satisfied understanding the cause of their night vision disturbance and knowing that their symptoms will reduce over time as the pupil size decreases with age. Others have symptoms so pronounced they do not feel safe driving at night. Treatment seeks to decrease pupil size or increase the functional optical zone size. Options include:

• Over-minused spectacles. These can stimulate enough accommodative miosis to reduce night vision disturbances.^13,14 Even a small amount of miosis can significantly reduce haloes.
  Because over-minusing is noninvasive, convenient and free of pharmocologic side effects, it is my treatment of choice for post-LASIK patients with night vision disturbances. These lenses do not work for everyone. Also, over-minusing can cause asthenopia if the accommodative reserve or compensatory divergence ranges are inadequate. If symptomatic esophoria is induced, decenter the optical centers of the lenses to achieve base-out prism.
• Driving with the car dome light on. Increasing ambient light can effect enough pupillary miosis to reduce symptoms. Vehicle codes in certain states may not allow this practice; check with your state.
• Miotic eye drops. Dapiprazole HCl 0.5% is an alpha-adrenergic blocking agent indicated for reversing pharmacological mydriasis. This drop can also constrict the pupil to a size smaller than the optical zone. However, patients may dislike it because it stings on instillation and causes temporary redness.
  Pilocarpine 0.25% also achieves pharmacologic miosis. However, it may cause accommodative spasm and increase the risk of retinal detachment.
  Brimonidine tartrate 0.2%, best known as an ocular hypotensive, also has a miotic effect with generally favorable patient tolerance.¹⁵ Ever more doctors are prescribing this for post-LASIK nighttime vision problems.
• Soft contact lens with an artificial pupil. Soft contact lenses are available with an artificial pupil that can be made smaller than the optical zone (figure 8). These lenses sometimes vault over the ablation zone. In such cases, neutralize the tear lens by adding minus power in the contact lens. You can also use the contact lenses to correct residual refractive error or deliberately over-minus.
• RGPs. Rigid contact lenses reestablish a functional optical zone that is larger than the entrance pupil. Reverse geometry lenses are usually required for optimal fit. New RGP wearers may find the lenses uncomfortable to wear.
• Optical zone enlargement. Surgical enlargement of the optical zone has successfully reduced night vision disturbances for some patients.^16,17 But it is the most invasive option. Future wavefront-guided excimer lasers may be more successful at increasing the functional optical zone.

Dry Eye Symptoms
Dry eye is common after LASIK, and most often affects patients who were symptomatic before the procedure. Mounting evidence supports the neurotrophic theory, which says that post-LASIK dry eye occurs when the microkeratome severs sensory nerve fibers involved in lacrimation.¹⁸ It can take months for these nerve fibers to regenerate, causing intermittent dry eye.

These patients demonstrate superficial punctate keratopathy (figure 9), and in severe cases, corneal filaments. A small percentage of patients experience protracted, irritating dryness. Any central epitheliopathy can degrade visual quality (figure 10).

Some patients with superficial epitheliopathy are asymptomatic due to reduced corneal sensitivity. Others complain of pronounced dryness, possibly due to spontaneous firing of the sensory fibers cut during microkeratectomy.¹⁹

For now, the primary therapy for reduced tear volume after LASIK is ocular lubrication with artificial tears, gels and ointments. Punctal occlusion may also help. An overlooked cause of post-LASIK dry eye symptoms: meibomian gland dysfunction.

Patients are told not to rub their eyes after LASIK to prevent flap shifting. A derivative effect is meibomian gland inspissation, which can lead to symptoms of dryness. Although aggressive lid hygiene and digital massage is not appropriate during the early recovery, you can prescribe oral doxycycline 100mg bid. Doxycycline inhibits normal eyelid flora from metabolizing meibomian secretions into irritating fatty acids.²⁰

Diffuse Lamellar Keratitis
DLK is a sterile accumulation of inflammatory cells in the lamellar interface. This is also called "Sands of the Sahara" to describe its white, granular appearance. Mild and self-limiting DLK can occur in one of 25 LASIK patients; severe, vision-threatening DLK may occur in one of 5,000 cases.²¹

The etiology of DLK remains mysterious, though numerous causes have been suggested. These include bacterial endotoxins, residual chemicals from the microkeratome blade, talc from gloves, meibomian gland debris and blood. However, cumulative evidence suggests no single causative agent. Rather, a multifactorial etiology is likely.²¹

Many patients with DLK are asymptomatic and present with a quiet, white eye. Careful slit lamp examination at day one post-op will almost always detect the presence of inflammatory interface cells. These cells migrate centrally from the limbal vasculature.

Sodium fluorescein can differentiate superficial epitheliopathy from non-staining interface inflammation. Unlike sequestered meibomian gland secretions, inflammatory cells do not have an oily and globular appearance.

Florid presentations (figure 11) can lead to severe vision loss if you don't refer the patient promptly for flap lifting and interface irrigation. Untreated, aggregates of inflammatory cells can release collagenase, leading to keratolysis and scarring (figure 12).

You can treat mild DLK with topical steroid drops.

In your differential diagnosis, consider infectious keratitis, which can also lead to interface inflammation. Unlike DLK, infectious keratitis causes pain, redness and photo- phobia. Infectious interface inflammation usually presents after one discontinues antibiotic prophylaxis.

Epithelial Ingrowth
Epithelium in the lamellar interface (figure 13) occurs to some degree in an estimated 10-30% of LASIK patients. In a study of 1,245 LASIK cases, there was a 14.7% rate of epithelial ingrowth and a 1.7% rate of clinically significant epithelial ingrowth.²² Epithelial ingrowth appears as a nest of cells, a thin sheet within the interface, or a combination of the two. The sheet-like presentation is sometimes difficult to visualize without indirect illumination.

Most instances of epithelial ingrowth are not clinically significant and require only observation. But in about 1% of cases, you'll need to refer the patient back to the surgeon to lift the flap and remove the epithelial cells to protect vision. Without intervention, visually significant ingrowth can disturb nutrient diffusion between the aqueous and flap tissue. Keratolysis can occur with the release of collagenase in a similar fashion to severe DLK.

Stable epithelial ingrowth less than 2.0mm from the flap edge generally is not clinically significant. Consider referring patients with intrusion beyond 2.0mm for ingrowth removal. Progressive epithe- lial ingrowth can induce astigmatism by flattening the same meridian where epithelium is located while concurrently steepening the meridian 90° away.

Risk factors for epithelial ingrowth include epithelial defects and excessive flap edema after LASIK. Ingrowth originates from the epithelial cells near the limbus, where they migrate centrally under the flap edge.

You cannot diagnose epithelial ingrowth the day after LASIK, but you can detect the potential for ingrowth. By instilling fluorescein, you can visualize areas of the flap gutter that haven't yet "zippered" with epithelium.

Epithelium implanted within the interface does not grow. This situation arises when the surgeon repositions the flap over epithelial debris. Implanted epithelium becomes absorbed and opacifies, so sequestered epithelial debris in the visual axis requires surgical removal.

Patients who have epithelial basement membrane dystrophies and recurrent corneal erosions are at highest risk for epithelial ingrowth. For them, PRK is advisable over LASIK.

Flap Striae
Flap striae (figure 14) may occur especially after treatments for large amounts of myopia. Striae can form after the flap conforms to the ablated stromal bed. The higher the myopic correction, the more the flap must bend to appose to the stromal bed. Less frequently, surgical technique or flap dislodgment introduce striae.

Most cases of striae are not clinically significant. However, about 1% of all LASIK procedures results in degraded visual quality when striae are within the visual axis. Visually significant striae require referral for flap lifting and striae removal. Striae are most easily removed shortly after surgery; removal becomes increasingly difficult with time.

O.D.s play an integral role when things don't go as expected after LASIK. Sometimes we must refer the patient for surgical management. In most cases, however, non-surgical management is a safer and more judicious approach. Teamwork with your surgeon can help ensure optimal LASIK outcomes and prevent the horror stories we hear about from becoming reality with our patients.

Dr. Chou completed a fellowship in refractive surgery management at the Jules Stein Eye Institute, University of California at Los Angeles School of Medicine, and is now in private practice in San Diego.

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