TABLE 1. Excimer laser emission

Direct bond breakage by a high-energy photon is a photochemical laser–material interaction. The relative contribution of photochemical and thermal mechanisms to the UV ablation of organic polymers remains controversial.¹⁵ At the shortest laser wavelengths, such as 193 nm, the high photon energy may result in a purely photochemical process of ablative photodecomposition. At longer wavelengths, absorbed photon energy leads to a local rise in temperature that causes etching through a photothermal process. At longer wavelengths, coagulation of protein may be expected adjacent to the ablation zone. Short laser pulses delivered at a low repetition rate help to limit local heating.

Photochemical and photothermal effects of excimer laser wavelengths on the cornea result from absorption by solid elements. Water poorly absorbs wavelengths between 193 and 293 nm.¹ The carbon–nitrogen peptide bond is believed to be the source of a strong protein absorption peak at approximately 190 nm.¹⁷ Most of the corneal amino acids are nonaromatic, and they account for collagen absorption that begins to rise at wavelengths of less than 260 nm and particularly less than 240 nm.^18,19 Aromatic amino acids absorb more strongly at wavelengths of greater than 240 nm. A collagen absorption peak around 250 nm is attributed to a carbon–nitrogen enolized peptide linkage.¹⁷ The corneal glycosaminoglycans have similar absorption spectra, with peaks around 190 nm and minimal absorption at 248 nm.²⁰ Nucleic acids are limited to the occasional keratocyte in the stroma but are more important chromophores in the epithelium, with strong absorption at both 248 and 193 nm.^21,22Ascorbic acid, particularly concentrated in epithelial cells, has more absorption at 248 nm than at 193 nm.²³

Mutagenesis and carcinogenesis are concerns with UV radiation. Almost all carcinogens have been shown to be mutagens.²⁴ UV radiation-induced mutation parallels absorption by DNA.¹⁹ The low density of stromal keratocytes offers some protection against carcinogenesis resulting from stromal photoablation. In several studies, 193-nm irradiation did not cause mutagenic or carcinogenic cellular events. Nuss and colleagues examined unscheduled DNA synthesis, a measure of repair of pyrimidine dimers. Compared with a control incision made with a diamond knife, unscheduled DNA synthesis did not increase after 193-nm linear ablation; in contrast, a statistically significant increase occurred after 248-nm irradiation.²⁵ Possible mechanisms for the decreased toxicity at 193 nm include absorption of that wavelength by protein surrounding the nucleus (a protein shield), lack of cytotoxicity of DNA photoproducts produced by 193-nm light, DNA damage that can readily be repaired by the cells, or such lethal damage that potentially mutagenic repair processes are not possible.²⁶ In a skin model, DNA damage and subsequent cytotoxicity were least at 193 nm, intermediate at 308 nm, and greatest at 248 nm.

Corneal irradiation at 193 nm also results in fluorescence between 295 and 425 nm.²⁷ These emissions could be both mutagenic and cataractogenic; however, the highly attenuated energy of the fluorescence may not reach toxic levels.

In 1983, Trokel and coworkers first reported the precise and controlled etching of the cornea by an argon–fluorine (ArF) excimer laser.²⁸ Puliafito and colleagues compared the histopathologic effects of linear cornea ablation at 193 and 248 nm.²⁹ Both studies found excellent preservation of normal corneal stromal microstructure adjacent to the ablation zone at 193 nm (Fig. 1). The adjacent cornea remained optically clear. High-power transmission electron microscopy showed a submicron zone of electron density immediately adjacent to the ablation only. Kerr-Muir and associates first described a pseudomembrane that appears to seal cells and cellular nuclei transected by the laser beam.³⁰ In contrast, at 248 nm, disorganization of the collagen microstructure extended into the adjacent stroma for more than 10 νm.²⁹ The cornea immediately adjacent to the ablation showed a loss of transparency, which was indicative of thermal injury. Further, a study by Peyman and associates³¹ showed a significant coagulative effect from 308-nm excimer laser radiation with induced corneal necrosis, stromal opacification, and endothelial cell damage.

Krueger and associates quantitated ablation rates. Etch depth per pulse plotted against radiant energy density generated sigmoid curves.^32,33 The steep portion of the curve is approximately logarithmic; this finding corresponds to observations in simpler organic polymers. The inflection point of the curve is approximately 200 mJ/cm² for 193 nm, which represents the energy density yielding the most efficient ablation. Puliafito and colleagues postulated that ablation at the inflection points may be clinically undesirable; at the inflection point small changes in laser output could alter the ablation rate dramatically.³⁴ Ablation at higher energy densities, such as 400 to 600 mJ/cm² per pulse, where the ablation rate has the flattest slope, might be preferable in situations where ablation rate is critical. Krueger and coworkers³³ further observed that for wavelengths higher than 193 nm, the threshold for corneal ablation increases as the laser repetition rate decreases. At 193 nm, the threshold was constant despite varying repetition rates. This observation is consistent with the photochemical theory of excimer corneal ablation, in which the buildup of heat does not play an important role at 193 nm and thermal mechanisms of ablation are important for ablation at longer wavelengths.

The effect of radiation density on corneal smoothness remains controversial. Fantes and Waring showed improved corneal surface uniformity with their scanning system at higher laser energy density, especially with 500 mJ/cm² per pulse.³⁵ In contrast, Berns and coworkers observed that such high levels of energy can be associated with ridges on the corneal surface, damage to the endothelium, and the formation of small pits on the stromal surface inside the linear ablation zones.³⁶

Endothelial toxicity probably is minimal, although endothelial effects can be seen despite the nearly complete absorption of 193 nm photons within 1 microns of tissue. Dehm and coworkers found that in linear ablations, 193-nm incisions to 90% of corneal depth produced endothelial membrane disruption similar to that seen underlying diamond knife incisions at the same depth.³⁷ Frank loss of endothelial cells underlying the incision was observed at 248 nm. Hanna and coworkers observed the appearance of electron-dense granules in the endothelium after surface ablation of rabbit corneas at 193 nm.³⁸ These electron-dense granules migrated through Descemet's membrane over several weeks and then dissipated. The clinical significance of this observation is unclear. This phenomenon may be related to transient pressure injury to the endothelium. Zabel and colleagues measured pressures as high as 100 atm at the endothelium during ablation of the superficial stroma, but no frank disruption of the corneal endothelium occurred.³⁹

The fragments ejected from the corneal surface are visible several hundred nanoseconds after the laser exposure. For 193-nm irradiation, the particles travel at an initial velocity of approximately 400 m/sec for the first 500 nsec, but then rapidly decelerate. The ejection of the particles ends within 5 to 15 νsec as the decelerating particles form a mushroom-shaped cloud (Fig. 2). ⁴⁰ Increased exposure energy leads to increases in both the plume size and initial velocity of the ejected fragments. Analysis of the plume has identified numerous molecules that contain between 10 and 20 carbon atoms.⁴¹

The objective of PTK in the treatment of recurrent erosions is simply to remove enough of the superficial Bowman's layer to permit formation of a new basement membrane with adhesion structures; therefore, it is the most superficial of the PTK procedures. The usual technique is to debride the loose epithelium manually. In most cases, even if the area of clinical recurrent erosion is localized, the surgeon finds that the epithelium is poorly adherent over most or all of the corneal surface. With the use of a large spot size, such as 6.5 mm, the surgeon ablates the central superficial corneal surface.

Depending on the laser, varying techniques are used to expose the peripheral cornea outside the central zone. For example, with the VISX laser, a smaller spot is manually scanned around the periphery by moving the patient's head. With some smaller spot scanning lasers, the periphery can be treated by programming the scan to include these areas.

The amount of tissue to be ablated to maximize the effect with minimal refractive change has not been elucidated. Some investigators remove only 2 to 6 microns,^44–47 but others have found that removal of 10 microns results in fewer recurrences.⁴⁸ After the laser ablation, a drop of topical antibiotic, steroid, and sometimes nonsteroidal agent is applied, followed by placement of a bandage contact lens. Close follow-up is required until epithelialization is complete, at which time the contact lens is removed. Patients typically are instructed to continue aggressive lubrication, including nightly application of lubricating ointment, for several months after the procedure.

The results of clinical studies of PTK for recurrent erosions have been encouraging. Morad and coworkers⁴² treated 23 eyes for recurrent or persistent corneal erosion with PTK by ablating 2 to 6 νm of tissue after epithelial removal. Eighty-three percent of patients remained free of symptoms during the 12- to 60-month follow-up, and none experienced a significant refractive change. Cavanaugh and colleagues treated 36 eyes for recurrent erosion in the setting of anterior basement membrane dystrophy and found that 86.6% had no recurrence of symptoms after 12 months of follow-up.⁴⁹ The average change in refraction was +0.72 ± c1.26 diopters (D), and a positive correlation was found between the number of pulses applied and induced refractive change. Jain and Austin⁴³ reported that of 77 eyes treated with PTK for recurrent erosions, 69% were free of all symptoms after 6 to 55 months of follow-up and 100% were free of acute episodes after one or two treatments. It also was found that patients treated for recurrent erosions resulting from trauma had a better outcome than those whose symptoms were idiopathic or caused by a basement membrane dystrophy. Several other studies have shown a 60% to 100%^{44,45,50–56} cure rate with one or more PTK treatments for recurrent erosions. Quantitative studies indicate that the fundamental health of the corneal epithelium may be improved after PTK.⁵⁷

More studies are necessary to determine the optimal amount of tissue to be removed to minimize both recurrences and significant refractive changes. Sridhar, Rapuano, and coworkers found that diamond burr polishing was at least as effective although simpler and less costly than PTK for recurrent erosions.⁵⁸

In a similar mode, PTK has successfully reduced painful bullae in eyes with pseudophakic bullous keratopathy.^59,60

Many of these sources of surface irregularity also are associated with corneal opacities. In some cases, smoothing the optical surface alone significantly improves the patient's visual function without the hyperopic shift and potential scarring that can be associated with the deeper ablations often necessary for removal of opacities. Hard contact lens refraction can be helpful in determining what component of a patient's visual complaints is secondary to surface irregularity alone. The improvement in visual acuity with a hard contact lens is attributable to irregularity, and the remaining vision impairment with the hard contact lens in place is caused by the opacity.

Irregularities are not intrinsically removed by exposure to repeated pulses of the excimer beam. Photons that encounter an irregular surface do not discriminate between elevations and depressions, and tissue that is removed largely replicates the original irregularity (Fig. 3). Strategies have been devised to protect the deeper tissues (valleys) while exposing elevated pathology (peaks) to the ablating photons.

Epithelial hyperplasia commonly occurs in areas of corneal depression. Performing transepithelial ablation, where the thickened epithelium shields the valleys from the laser energy, therefore, can take advantage of the natural masking effect of the epithelium. As an example, one strategy for removing surface irregularities of Reis-Bucklers' dystrophy involves ablating through the epithelium that is intermixed with the abnormal substance until the epithelium is largely absent. This absence is determined by the disappearance of the fluorescence that occurs during epithelial ablation. Further ablation then is performed in conjunction with the use of masking fluids.

The most commonly used masking fluids are artificial tear substances, which are available in varying viscosity. Kornmehl and coworkers compared artificial tear substances of varying viscosity with saline and a nonfluid control in an experimental model of surface irregularity.⁶⁴ In a model in which the corneal surface initially was roughened with sandpaper, solutions of moderate viscosity yielded a smoother surface than more viscous artificial tears, and markedly better results than the nonviscous saline solution. All of these fluids outperformed the nonfluid control. A subsequent study found good results with a preparation of 0.25% sodium hyaluronate.⁶⁵ Figure 4 shows the theoretic concept that a fluid with inadequate viscosity tends to run off, providing insufficient protection for the valleys, whereas a substance that is too viscous drapes over the peaks, protecting the elevations, where ablation is desired.

In addition to the effect of viscosity, different solutions may have varying effectiveness in the absorption of 193-nm photons. A thin film of fluid must have adequate absorption to prevent ablation of the underlying tissue. Enhancing absorption at 193 nm may be one step toward the development of a more effective masking fluid for phototherapeutic keratectomy of an irregular surface. A substance such as a gel also could be applied uniformly over the cornea and molded into a new, smooth anterior surface. This gel would be ablated and, as ablation progresses, would expose the peaks while protecting the valleys without the need for repeated artful application of viscous fluids. For this gel to be fully effective, however, the ablation rate of the gel would have to match that of the pathologic tissue. Such a gel has yet to be implemented in clinical practice.^66,67

In the evaluation of a visually significant corneal opacity, it is critical to assess its depth. In some conditions, such as Reis-Bucklers' dystrophy, the location of the abnormality is limited to the anterior stroma. In lattice or granular dystrophy, the surgeon must examine the optically significant opacities in the visual zone and assess their depth. Postinflammatory scarring is more difficult to assess because the posterior extent of the opacity typically is ill defined and often is deeper than initially appreciated at slit-lamp examination. However, partial removal of the opacity may be adequate for the patient's visual needs. An optical pachymeter can be a useful adjunct in measuring the depth of the opacity, although the opacity itself may preclude accurate use of this device.⁷³

Visual impairment associated with these disorders often results from a combination of the opacity itself and accompanying corneal irregularity, both of which must be treated to obtain an optimal visual result. In addition, depending on its cause, the opacity may ablate at a different rate than the surrounding stroma. For example, the hyaline material in granular dystrophy ablates more slowly than the surrounding stroma. Therefore, even a surface that was smooth before surgery can become irregular after PTK if careful attention is not given to maintaining a smooth surface during the procedure. It is often effective to debride discrete elevated opacities such as Salzmann nodules or calcium deposits manually with a blade before PTK and then use masking agents to expose the elevated remaining irregularities during the ablation to create or maintain a smooth optical surface.⁷⁴

Depending on the excimer laser used and the surgeon's preference, ablation usually is performed as a planar disc ablation alone or followed by a hyperopic ablation. These approaches are intended to reduce the frequently induced hyperopic shift. Although the initial ablation may be planar and may retain the original anterior corneal curvature, remodeling after laser treatment with new collagen formation and epithelial hyperplasia at the periphery of the treatment zone may result in net flattening and a hyperopic shift of up to +8.00 D in some cases.⁵⁷ Amm and Duncker reported that, of 45 patients treated, all refractions remained stable after PTK for recurrent erosions, whereas after treatment for corneal scars, anterior stromal dystrophies, or surface irregularities, 40.6% of patients developed a hyperopic shift, 9% developed a myopic shift, and 40.6% remained stable.^75,76 Overall, it was found that deeper ablations were associated with a greater likelihood of hyperopic shift.⁷⁷ Katsube and coworkers have proposed that the fluid-filled porous nature of the cornea accounts for much of the tendency for the hyperopic shift after PTK.⁷⁸

In assessing suitability for PTK, the patient's refractive status is a major component. Unless the patient is moderately myopic before surgery, and either has bilateral disease or readily accepts contact lens correction in the fellow eye, the potential for unacceptable anisometropia is high. However, postoperative use of a hard contact lens often is of additional benefit to the patient by optically eliminating residual irregular and regular astigmatism.

In addition to the hyperopic shift, deeper ablation, particularly exceeding 50 to 100 μm, usually is accompanied by haze that can become visually significant at its extreme. It is unclear whether intensive steroid administration after laser treatment significantly retards scarring, and to what extent intensive steroid treatment leads to a more pronounced permanent hyperopic shift by retarding wound healing. The brief application of topical mitomycin-C immediately after the ablation also may reduce scar formation.⁷⁹

Although PTK may reduce the optical and surface disruption of anterior dystrophies, most dystrophies recur naturally, requiring a repeat PTK or transplantation.⁸⁰ However, Miller and co-workers reported a case of Reis-Bucklers dystrophy that experienced two rapid recurrences after conventional PTK but had 1 year without evidence of recurrence after a third PTK in conjunction with topical application of mitomycin-C. ⁸¹ Prolonged use of mitomycin-C has been reported to cause permanent corneal edema, however.⁸²

PTK does not impair the outcome of subsequent penetrating keratoplasty when surgical intervention is needed.⁸³

CENTRAL ISLANDS

Central islands, usually defined as at least 1.00 D of central steepening in the presence of overall flattening on corneal topography, are often evident after PRK and less commonly after LASIK (Fig. 8). Patients with symptomatic central islands may experience mild loss of best corrected visual acuity, multiplopia, ghost images, halos, glare, and increased astigmatism. The refraction usually is mildly myopic because of the central steep zone.

Preventing central island formation requires careful adherence to the manufacturer's recommendations. These include “anti-island” ablation treatments in which extra pulses are delivered to the center of the ablation zone. Some surgeons interrupt the treatment several times to dry the central stroma with a cellulose surgical sponge.

The natural history of central islands after PRK is that most resolve or become optically insignificant by 6 months after surgery.² Although histologic documentation of the healing mechanism of central islands remains unavailable, a common hypothesis is that the central island represents unablated stromal tissue and that the “healing” consists of a thickening of the epithelium in the midperiphery surrounding the island, which gradually envelops and covers the island.

After PRK, it is generally prudent to wait at least 6 months in patients with symptomatic central islands before considering retreatment. Some topographically evident central islands do not cause symptoms and should be ignored. When symptoms are present and unchanged after 6 months, and the topography and refractive status are stable, treatment should be considered. After LASIK, in contrast, surface remodeling is minimal. If a symptomatic central island is stable for at least 2 months, relifting the flap and treating the central island in the stromal bed can be considered.

Two treatment options for central islands after PRK have been advocated. In the first, the central epithelium is removed with a blade, exposing the central stromal island. The peak of the island is then treated either with a PRK algorithm, whose optical zone is set to the diameter of the central island and whose dioptric correction matches the height of the island, or with a PTK algorithm, again with the diameter set to the width of the island and the number of pulses calculated to create the dioptric flattening needed (approximately 12 pulses per diopter). In either case, the dioptric correction is based on the height of the island as detected on an early topography, usually the 1-month topographic analysis. By 3 to 6 months, the island may appear to be less elevated as a result of partial hyperplasia of the surrounding epithelium; therefore, retreatment will be incomplete.

An alternative treatment technique is to retain the epithelium and use a PTK disc ablation equal to the largest diameter of the island. The first area of stroma to be exposed is at the peak of the island if epithelial hyperplasia has occurred around the central island. This can be visualized as the “breakthrough” of the cobalt blue fluorescence that occurs with ablation of the epithelium; fluorescence readily visualized when the room lights and microscope lights are shut off. The ablation through the epithelium progressively exposes the island, whereas the thicker peripheral epithelium shields the surrounding stroma. When the central nonfluorescent stromal island reaches the width of the topographic island as it was seen at 1 month, the island ablation is complete. If the breakthrough of the transepithelial ablation does not occur centrally but rather simultaneously throughout the optical zone, then the surgeon employs PRK or PTK pulses, calculated as described in the preceding paragraph.

In either of these techniques, after removal of the tissue island, aggressive topical steroids should be used until stable healing and a stable refractive status are achieved to discourage any central scarring.

After LASIK, central islands are treated by lifting the pre-existing flap and ablating the central stroma with a diameter and depth corresponding to the width and height of the island on the topographic map. The authors' preference is to program a myopic correction for the dioptric value of the height of the island on topography. The width is programmed to match the topographic diameter of the island. In the United States, where Food and Drug Administration restrictions may not allow the surgeon to select a small optical zone in myopic corrections, the surgeon using a broad-beam laser can either manually stop the exposure when the ablation is observed to reach the desired size, or, more precisely, apply the number of pulses that correspond to a certain diameter (the laser manufacturer can supply a nomogram interrelating dioptric correction, diameter, and number of pulses).

Corneal Haze after PRK

After PRK, subepithelial corneal haze usually develops in several weeks, peaks within 1 to 2 months, and then resolves spontaneously during the next 6 to 12 months (Fig. 9). Haze is more prominent in eyes after treating higher degrees of correction, especially when using smaller ablation zones. It is often asymptomatic, being more noticeable to the examiner than the patient. However, sometimes haze can contribute to loss of contrast sensitivity or even loss of best corrected visual acuity.

Significant subepithelial haze may improve with increasing the frequency of topical steroids.⁸⁵ If visually significant haze persists without improvement after 6 to 12 months, surgical intervention may be indicated. Often haze formation is accompanied by regression, so that repeat excimer ablation can simultaneously treat both the regression and the haze. However, retreatment in patients with significant haze yields less predictable results than retreatment of patients with regression in the absence of haze.⁸⁶ Seiler and associates⁶⁶ used a combined PTK-PRK approach to treat 21 undercorrected eyes with corneal haze and found scar recurrence in four (19%). Pop and Aras⁶⁴ found that patients with greater haze had a 40% rate of overcorrection. To limit overcorrection, retreatment should be directed toward decreasing haze to a clinically insignificant level rather than eliminating it. A transepithelial approach often is used in PTK mode with a large ablation diameter. When using the PRK mode, it has been recommended to correct only 50% to 60% of the myopia to avoid overcorrection.^64,87

PTK has been successfully combined with amniotic membrane transplants in two cases of severe haze following PRK.⁸⁸

DECENTERED ABLATIONS

Decentered ablations can occur with PRK or LASIK secondary to initial improper positioning or loss of patient fixation with drift of an initially centered treatment (Figs. 10 and 11). During the ablation, the patient's head must be stabilized, typically by the surgeon's hands, and the patient and surgeon must monitor the fixation beams. Decentered ablations are more common after correction of higher degrees of refractive error, probably secondary to the longer fixation time required. They are more likely to be symptomatic with the use of smaller optical zones, because the edge of the ablation is then more likely to be within the pupillary margin. Mild decentrations may be asymptomatic but if greater than 1 mm are often associated with glare, halos, monocular diplopia, and occasionally loss of best corrected visual acuity.

Decentrations are difficult to treat; however, some success has been found with using the excimer laser to reapply an ablation.^89–92 In one approach, the epithelium is retained over the topographically flattened zone to act as a mask. The epithelium outside the ablation zone is removed either mechanically or with the excimer laser in PTK mode. A ridge at the border of the treatment zone can be ablated as necessary with a small optical zone PTK. A PRK treatment then is performed either centrally or decentered 180 degrees away from the first ablation, with the optical power guided by topography. The already flattened treatment zone is protected by the pre-existing epithelium and, if necessary, other masking agents such as high-viscosity artificial tear fluids or a methylcellulose sponge.⁹³

Pallikaris has described the treatment of decentered ablations without the use of the laser by using a limbal relaxing incision or arcuate keratotomy oriented 180 degrees opposite the decentration.⁹⁴ Studies are necessary to determine whether these incisions result in better outcomes compared with retreatment with the excimer laser.

Decentration usually results in large amount of the high order aberration known as coma. With the clinical introduction of wave front guided optics for primary treatment, the stage is set for development of therapeutic applications. These may be a more precise and effective method for correcting decentration.

LASIK FLAP COMPLICATIONS

When performing the keratectomy for LASIK, a flap of uniform thickness with a smooth interface is essential. When a thin, incomplete, or buttonholed flap is created, the flap should be replaced without applying the ablation. Unfortunately, irregular astigmatism and scarring with loss of best corrected vision or optical aberrations still can occur and are difficult to treat. PTK potentially can be used to treat the irregular surface in these cases. Kapadia and Wilson reported a case of a buttonholed flap that healed with superficial scarring associated with monocular diplopia and glare.⁹⁵ Transepithelial PTK followed by PRK for partial treatment of the refractive error was performed with resolution of the optical aberrations.

Leu and Hersh used PTK on the underside of the flap and on the stromal bed to resolve a case of recurrent diffuse lamellar keratitis (DLK) that was unresponsive to conventional treatment; ablation of inciting toxins was hypothesized to be the basis for the resolution of the DLK.⁹⁶

PTK can help resolve recurrent erosions and anterior basement membrane irregularities after LASIK, in a manner similar to the management of primary recurrent erosions as discussed in the preceding.⁹⁷

FLAP STRIAE

Large macrofolds that occur because of flap slippage in the early postoperative period should be treated with immediate repositioning. Long-standing macrofolds, however, are resistant to repositioning and manual smoothing, as are troublesome microstriae that disrupt the anterior corneal optics (Figs. 12 and 13). These complications are described in detail in Chapter 48 of this section. Steinert, Ashrafzadeh, and Hersh reported excellent results with PTK used to treat these irregularities.⁹⁸ Figure 14 schematically shows the concept of the PTK treatment of striae. The technique, as performed with the VISX broad-beam laser, is to use the PTK mode for planar ablation with the maximal 6.5 mm zone. With the tracker engaged, 200 pulses are applied to the cornea, performing transepithelial ablation. The epithelium acts as a masking agent for the PTK. (The elevated ridges of striae are exposed first, where the epithelium is thinnest, whereas the valleys between the ridges, where the epithelium is hyperplastic, are protected [Fig. 15]). Next, the tracker is turned off. The ring illuminator is turned on, generally revealing a large amount of striae resulting from the removal of the partially masking epithelium. At this point, the surgeon gently debrides any remaining epithelium, stroking with a minimally moist surgical spear sponge or, if needed, a back-tilted surgical blade in the direction away from the hinge. More laser pulses then are applied in short bursts of five or so pulses, with a wipe of masking fluid between each burst. A medium viscosity artificial tear usually is the best choice. The cornea should look slightly moist but not so much fluid that the striae disappear. If the masking fluid bubbles, or the laser pulses sound like a dull thud rather than a snap, too much fluid is present. The PTK procedure stops whenever the cornea looks smoother, but in any case no more than 100 further pulses (300 total) are applied, in order to avoid a major hyperopic shift. Used with this technique, the typical hyperopic shift is about 1 D on the average. In addition, if needed, PRK can be applied after PTK to correct any significant optical error. This will be less accurate than primary PRK due to the variable effect of the PTK, however. Applied with the technique described in the preceding, no optically significant haze was observed in the published series.

Fig. 15. Sequential operative photographs of the epithelial fluorescence pattern seen during phototherapeutic keratectomy (PTK) for microstriae. A. Initial perforation over most elevated region of striae. B. With successive pulses, epithelial fluorescence over most elevated striae disappears. C. With further pulses, the epithelium between the striae recedes, with further reduction in fluorescence. D. At the end of the transepithelial phase of the PTK, most of the epithelium is removed, with only minimal residual fluorescence in the areas of thickest epithelium between the striae. (Reproduced with permission from Steinert RF, Ashrafzadeh A, Hersh PS: Results of phototherapeutic keratectomy in the management of flap striae after LASIK. Ophthalmology 111:740, 2004)

Wiesinger-Jendritza and associates reported a series of 23 eyes treated with LASIK using topography-based ablations for irregular astigmatism after penetrating keratoplasty, trauma, or previous excimer laser surgery.⁹⁹ They found that 61.9% were partially corrected and 19.4% were fully corrected after the treatment. Improvements in this technique will likely be seen as topographic analysis becomes incorporated into the laser for real-time feedback on topographic changes during the ablation. Vinciguerra and Camesasca also have reported good results with a topography-based custom therapeutic treatment of highly aberrated eyes.^100,101 In 52 eyes, the percentage with BSCVA of 20/30 or better increased from a preoperative rate of 59% to 88% at one postoperative year, and BSCVA of 20/15 was reached by 25% of eyes compared to none preoperatively.

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