Ординатура / Офтальмология / Английские материалы / Master Techniques in Cataract and Refractive Surgery_Hampton Roy, Arzabe_2004

risks are: dislodging the lens for all models, and the possible contact between the endothelium and the PRL in the case of angleor iris-fixated lenses. The management of the flap does not represent additional difficulty for the lens implantation and can easily be lifted any time after for the excimer laser application.

The anesthesia and other surgical conditions are determined by the technique used for the particular PRL to be used. The microkeratome pass could be done with topical, peribulbar, retrobulbar, or general anesthesia without major differences in the outcome. Let us say that in case of hyperopic bioptics, retrobulbar anesthesia could be advantageous as it “lifts” the globe from the orbit and could make the creation of the corneal flap in deep and small eyes easier.

The timing for the excimer laser ablation varies among surgeons. It is considered that the refraction is stable after 1 month of the PRL implantation in most cases so usually the laser is applied anytime after that.

PSEUDOPHAKIC BIOPTICS

Taking into account that nearly 6 million cataract surgeries are done each year worldwide and that cataract surgery is now considered a refractive procedure by itself, bioptics becomes a logic step in the search of plano or almost plano as a final result. According to Louis D. Nichamin, MD, standard cataract surgery represents a 50/50 chance for the patients to be free of glasses for most daily activities except reading, whereas with bioptics, the chance is over 95%.17 Even the most experienced cataract surgeons have cases that end with undesirable refractive results. As with PRLs, pseudophakic bioptics could be planned and unplanned.

Planned Pseudophakic Biopics

As a good refractive result becomes the expected outcome after cataract surgery, pseudophakic bioptics emerges as a way for ensuring such results. Among the advantages of bioptics is the fact that the learning curve is almost null for the average surgeon; there is no new technique to learn and even more important, the surgeon could be more tolerant about the incision placement and size in standard phacoemulsification surgery, as the astigmatic factor would be corrected by the excimer laser. The different available techniques to deal with preoperative astigmatism by means of incision placement or additional refractive incisions are not very precise and usually fail with astigmatisms over 3.00 D.17

Indications

As a general guide, planned pseudophakic bioptics is indicated when the preoperative astigmatic factor exceeds 2.00 D.

Technique

For planned pseudophakic bioptics, the corneal flap must be created before the lens surgery. Preference among surgeons varies, regarding the timing of the flap creation. The microkeratome can be passed the day before but there is not any good reason for this practice as the flap can be created as the first step of the cataract surgery and does not jeopardize the rest of the procedure even if epithelial defects are produced.

After the cataract surgery, the excimer laser application must be delayed at least 2 weeks. The refractive result of the implant surgery will be more reliable after 4 weeks and it could be more appropriate to wait this amount of time before proceeding to the ablation and even more so if a wavefront guided correction is going to be used. At the chosen time, the flap is just lifted and the excimer applied.

Unplanned Pseudophakic Bioptics

As LASIK is becoming a widely practiced surgery among cataract surgeons, bioptics would become routinely used to refine the results of the intraocular lens implantation. LASIK usually has fewer risks and is easier than other options like IOL exchange or piggyback implants.

INDICATIONS

Any uncomplicated cataract case that ends with an undesirable refractive result could be greatly improved with subsequent LASIK treatment for the residual refractive error. Pseudophakic bioptics has been used even with multifocal intraocular lenses as the Array (Advanced Medical Optics, Santa Ana, Calif).17

Jose Guell, MD, proposes another use of bioptics. He uses a bioptics approach in patients who want to try monovision along with the correction of high ammetropies. He adjusts the residual myopia with the excimer including the total correction in unsatisfied patients.17

Combined cataract surgery plus penetrating keratoplasty can be also complemented with late LASIK as a final step to reach a better refractive result.

Another interesting type of candidates are those patients requiring cataract surgery and who have previously had incisional corneal refractive surgery. Pseudophakic bioptics is particularly well suited to these patients as IOL calculation is difficult and less predictable and also because many of them have significant astigmatism.

Using a less strict definition, it could be said that CLE plus LASIK is another form of bioptics.

TECHNIQUE

The type of cataract surgery performed, the surgical incision, and the postoperative evolution are the major factors to be taken into account when unplanned pseudophakic bioptics is under consideration.

The stability of the incision used for the cataract surgery is by itself the main factor. For phacoemulsification patients with CCIs, it is considered that passing the microkeratome 1 month after the cataract surgery is safe. For limbal incisions, either phacoemulsification or other minimal incision techniques, opinion varies but 3 months must be the minimum lapse before constructing the flap being safer to wait up to the sixth month after the intraocular surgery.

In cases where penetrating keratoplasty has been practiced as a combined technique with IOL implantation, it is safer to wait more than 12 months to perform the LASIK procedure.

When the patient has had incisional corneal refractive surgery, it is very advisable to create the flap as an initial step and wait at least 4 weeks before proceeding to the laser applications as it is not unusual to find changes on the refractive error and axis shifting of the astigmatic portion.

COMPLICATIONS

Obviously bioptics, either with PRL or pseudophakic, shares all the known complications of implanting IOLs and those of LASIK.

The most important complications of bioptics use are related to the effect of passing the microkeratome when the IOL (PRL or even pseudophakic) is in place. Other complications are the dislodging of the IOL and the causing contact between the optic of the lens and the endothelium with damage of the later.

Special attention must be given to the epithelium in older patients as it could become very loose because of the age, and also, this group of population has proclivity to dry eye so corneal abrasions are more common and heals slowly.

SUMMARY

As a good refractive result has become of paramount importance for all types of IOL implantations (either PRLs or pseudophakic), bioptics as emerged as a very useful way to reach such results. Also, bioptics represents a safe method of correcting higher defects that are beyond the limits of LASIK alone.

Every refractive and cataract surgeon must consider bioptics among the options for treating his patients. Bioptics will become a routinely used approach as risks are low and custom ablation techniques will provide even more accurate results. Any innovation in LASIK, PRLs, and cataract surgery will improve bioptics consequently.

The beauty behind the concept of bioptics is that the surgeon can combine completely different methods of correcting the refractive defects (the keratorefractive and the intraocular), in such a way that the end result will be better than the one reached by either approach by itself.

REFERENCES

1.Zaldivar R, Davidorf J, Oscherow S, Ricur G, Piezzi V. Combined posterior chamber phakic intraocular lens and laser in situ keratomileusis: bioptics for extreme myopia. J Refract Surg. 1999;15:299-308.

2.Malecaze FJ, Hunlin H, Bierer P. A randomized paired eye comparison of two techniques for treating moderately high myopia: LASIK and the artisan phakic lens. Ophthalmology. 2002;109(9):1622-30.

3.Maloney RK, Nguyen LH, John ME. Artisan phakic lens for myopia: short-term results of a prospective, multicenter study. Ophthalmology. 2002;109(9):1631-41.

4.Arne JL, Lesueur LC. Phakic posterior chamber lenses for high myopia: Functional and anatomical outcomes. J Cataract Refract Surg. 2000;26:369-374.

5.Uusilato RJ, Aine E, Sen NH, Laatikainen L. J Cataract Refract Surg. 2002;28(1):29-36

6.Landesz M, van Eij G, Luyten G. Iris-claw phakic intraocular lens for high myopia. J Refract Surg. 2001;17(6):634-640.

7.Zaldivar R, Davidorf JM, Oscherow S. Posterior chamber phakic intraocular lens for myopia of -8 to -19 diopters. J Refract Surg. 1998;14:294-305.

8.Sanders DR, Brown DC, Martin RG, Sheperd J, Deitz M, DeLuca M. Implantable contact lens for moderate to high myopia: phase 1 FDA clinical study with 6 months follow-up.

J Cataract Refract Surg. 1998;24:607-611.

9.Pérez-Santoja JJ, Alió JL, Jiménez-Alfaro I, Zato M. Surgical correction of severe miopía with an angle-supported phakic intraocular lens. J Cataract Refract Surg. 2000;26:1288-1302.

10.Yoon H, Macaluso DC, Moshirfar M, Lundergan M. Traumatic dislocation of an Ophtec artisan phakic intraocular lens. J Refract Surg. 2002;18(4):481-483.

11.Sánchez-Galeana CA, Zadok D, Montes M, Cortés MA, Chalet AS. Refractory intraocular pressure increase after phakic posterior chamber intraocular lens implantation. Am J Ophthalmol. 2002;134(1):121-123.

12.Muzzi G, Cantú C. Vitreous hemorrhage following phakic anterior chamber intraocular lens implantation in severe myopia. Eur J Ophthalmol. 2002;12(1):69-72.

13.Henahan JF. A first look at the presbyopic phakic IOL. Available at: http://www.eyeworld.org/apr01/0401p76.html. Accessed October 15, 2003.

14.Gimbel HV, Ziemba SL. Management of myopic astigmatism with phakic intraocular lens implantation. J Cataract Refract Surg. 2002;28(5):883-886.

15.Cimberle M. Surgeon: toric artisan iol effective against astigmatism. Available at: www.osnsupersite.com. Accessed October 15, 2003.

16.Davidorf J, Zaldivar R, Oscherow S. Posterior chamber phakic intraocular lens for hyperopia of +4 to +11 diopters. J Refract Surg. 1998;14:306-311.

17.Lipner M. Bioptic vision: for 6 million like cataract results. Available at: http://www.eyeworld.org/nov01/1101p54.html. Accessed October 15, 2003.

INTRODUCTION

Surgical correction of hyperopia has always been more challenging to ophthalmologists than the correction of myopia.1-6 The results with lower amounts of baseline hyperopia are of particular interest, because 80% of adult hyperopes have refraction equal to or less than +3.00 D.7 Different methods and techniques have been used to treat hyperopia. However, their results have been variable and not always satisfactory.

Nonincisional approaches to refractive surgery have been explored in the quest of finding a satisfactory solution to hyperopia.1-6,8-19 Attempts to steepen the central cornea using thermal keratoplasty date back to the rabbit studies by Lans in the 19th century.1-3,8,10-13 During the 1980s, hot wire thermokeratoplasty, a technique developed in the Soviet Union, was used to produce thermal burns (up to 600° C) that penetrated to 95% of corneal depth in hyperopic eyes. Studies showed that it resulted in substantial overcorrection followed by marked regression.1,2,8,10

Conductive keratoplasty (CK) is a new, nonablative method for the correction of mild to moderate hyperopia that consists of an electrical current-based technique for shrinking stromal collagen. The technique delivers low energy, high-frequency (radio frequency, 350 kHz) current directly into the corneal stroma by means of a Keratoplast tip

(Refractec Inc, Irvine, Calif) inserted at 8 to 32 treatment points in the midperipheral cornea (Figures 6-1 and 6-2).8,9 CK uses the electrical properties of corneal tissue to generate heat in the cornea. Collagen within the treatment zone is heated in a gentle, controlled fashion as a result of the natural resistance of stromal tissue to the flow of current.1 Increasing dehydration of collagen increases resistance to the flow of the current, making the process self-limiting.1,2,20,21 A thermal model predicts protein denaturation at each treated spot that results in a cylindrical footprint approximately 150 to 200 mm wide and 500 mm deep extending to approximately 80% of the midperipheral cornea. Striae form between the treated spots, creating a band of tightening that increases the curvature of the central cornea, thereby decreasing hyperopia. Unlike Fyodorov’s original “hot needle keratoplasty” technique, the CK delivery needle stays cool as collagen is heated. This hyperopic correction is stable and

has little regression through time.1,2,8,9

Histopathologic analysis of 6 human corneas that had radio-frequency current applied showed thermal injury to the epithelium, an intact Bowman membrane with discrete shrinkage of its fibers, and a shrunken and edematous stroma. No severe necrosis or inflammatory cells were present indicating that the technique gives more stable results.8 A study reported to The American Society of Corneal and Refractive Surgery showed that the CK procedure did not

Figure 6-1. The conductive keratoplasty (CK) system (Viewpoint CK System; Courtesy of Refractec, Inc., Irvine, Calif).

significantly change endothelial cell counts in the central or peripheral cornea despite penetration of treatment to approximately 80% of the corneal depth.2

INDICATIONS AND

CONTRAINDICATIONS

CK is designed to treat spherical, previously untreated hyperopia of +0.75 to +3.00 D. Treatment of presbyopia, astigmatism, and residual hyperopia following LASIK or other refractive procedures is another potential application. The best candidate is over 35 years of age, with pachymetry readings of no less than 560 mm at the 6-mm optical zone. Patients not eligible for CK treatment are those with active ocular disease, corneal abnormality, progressive or unstable hyperopia, or other significant ocular or physical histo-

ry.1,2,8,9

SURGICAL TECHNIQUE

A complete ophthalmologic exam is necessary before treating any patient. This includes visual acuity, manifest and cycloplegic refraction, slit lamp biomicroscopy, tonometry, fundoscopic examination, keratometry, pachymetry, and computerized corneal topography.

The procedure is explained to the patient preoperatively and it is very important to advise the patient that for the first few weeks, he or she will have a myopic effect. This is normal because at first the patient is overcorrected, allowing for the predetermined amount of regression to take effect. During this time, the patient may require visual aid with glasses for far vision.1,2,8,9

This procedure may be performed under topical anesthesia with 1 drop of 0.5% tetracaine, administered 3 times at 5-minute intervals. A lid speculum is placed in the eye to be

Figure 6-2. Conductive keratoplasty (CK) treatment with the keratoplast tip. (Courtesy of Refractec, Inc., Irvine, Calif.)

treated to obtain maximal exposure and to provide the electrical return path. It is important to ensure that the lid drape (if used) does not prevent direct contact of the lid speculum and eyelid, which would disrupt the electrical current return path. The fellow eye is taped closed. The operating microscope can be positioned over or in front of the eye to be treated. There is no need to fixate the globe. As the patient fixated on the microscope’s light, the cornea is marked with a gentian-violet-dampened eight-intersection CK marker that creates a circle at the 7-mm optical zone and hatch marks at the 6-mm and 8-mm optical zones (Figure 6-3). The surface of the cornea is dried with a fiber-free sponge to avoid dissipation of the applied energy through a damp surface.

The Refractec corneal shaper system (Refractec Inc., Irvine, Calif) used to perform the CK procedure consists of a radio frequency energy-generating console. Attached to the probe is a single-use, sterile, penetrating tip, 90 mm in diameter and 450 mm long that delivers the current directly to the corneal stroma. At the very distal portion of the tip is an insulated stainless-steel stop (cuff) that assures correct depth of penetration (0.5 mm). The energy level default is 60% of 1 watt and the exposure time default is 0.6 seconds. These parameters are set on the console so that each foot pedal excursion delivers the same level and duration of energy to the keratoplast tip.1,2,8,9

The keratoplast tip is examined under the microscope to ensure that it is not damaged or bent prior to application. The appropriate treatment parameters are set on the console, and the eye is treated with the appropriate number of treatment spots, as specified in the nomogram. For example, to correct +1.00 D to +1.625 D of hyperopia, 16 treatment spots are placed: 8 at the 6-mm optical zone and another 8 at the 7-mm optical zone. When treating +0.75 D to +0.875 D, 8 treatment spots are applied only at the 7-mm optical zone. If astigmatism is present, greater amount of treatment will be needed in the flatter meridians to induce steepening in this area.1,2

Figure 6-3. Number, location, and application sequence of the treatment spots. (Reprinted from Ophthalmology, 109, McDonald MB, Davidorf J, Maloney RK, Manche EE, Hersh P, Conductive keratoplasty for the correction of low to moderate hyperopia. 1-year results on the first 54 eyes, 637-49, Copyright [2002], with permission from the American Academy of Ophthalmology.)

The surgeons place the keratoplast tip on the cornea at the treatment markings, attempting to place it perpendicular to the corneal surface. The cuff around the probe, which settles perpendicular to the cornea, helps to achieve perpendicular placement. Light pressure is applied until the tip penetrates the stroma to its insulator stop. After each treatment spot, the tip is carefully cleaned with a fiber-free sponge, removing any tissue debris. Keratometry is performed after the full circle of treatments had been completed to check for any induced cylinder. Depending on the epithelium drying and edema, the patient may be able to have very good near vision immediately.1,2,8,9

After treatment, 1 drop of topical ophthalmic antibiotic solution and 1 drop of an ophthalmic nonsteroidal antiinflammatory drug are administered and continued for 3 days. Topical corticosteroid is not used.

One hour after treatment, the opacities at each treatment spot are visible by slit lamp as small surface leukomas, with a band of striae connecting the treatment spots (Figure 6-4). Leukomas visible by slit lamp postoperatively are small because CK delivers energy deep into the stroma rather than on the surface. The striae between treatment zones remain visible at 3, 6, and 12 months, as reported by the United States CK clinical trial investigators, and suggest that the effect of treatment on the stroma is long lasting.1,2

COMPLICATIONS

Some treatment-related adverse events include corneal edema between 1 week and 1 month postoperatively. After this period we can find peripheral corneal epithelial defect, recurrent corneal erosion, foreign body sensation, pain, or

Figure 6-4. Slit-lamp view of treatment spot after CK showing bands of striae between spots. (Courtesy of Refractec Inc., Irvine, Calif).

ghosting/double images.1 Induced irregular astigmatism may be present when the application of the high frequency current is not done symmetrically on the entire treatment. Retreatment may be performed safely at the slit lamp.8

OUTCOMES

McDonald et al1 in a prospective multicenter study found encouraging results 1 year after CK (Figure 6-5). The predictability was good, but seemed to decrease with increased number of treatment spots. Regression after the CK procedure was low and decreased with time. The refraction appeared to stabilize at 6 months postoperatively. BSCVA was generally preserved after the procedure and incidence of induced cylinder is low.

Asbell et al,2 also in a multicenter clinical trial, reported that efficacy results exceeded all FDA guidelines for performance of refractive surgery procedures. Mendez et al8 reported an increased in postoperative visual acuity in all patients studied. The immediate postoperative refraction ranged from -1.50 D to -2.50 D, decreased to -1.00 D in 3 to 6 months, and reached plano at 1 year.

In an attempt to compare CK with laser techniques for the correction of hyperopia, we present a summary of the outcomes of well-known studies in Table 6-1. These preliminary results suggest that CK may be safer and more stable than PRK and as effective as LASIK for the treatment of low to moderate levels of hyperopia. The refractive correction after CK appears to be more stable for 1 year postoperatively than that after noncontact LTK. Conductive keratoplasty

may provide patients a full refractive correction that does not markedly regress.

As a nonexcimer laser technique for correcting hyperopia, CK preserves the central cornea, does not induce flap-relat- ed complications, and does not involve removal of any corneal tissue or cut corneal nerves. The decreased complexity of the procedure compared with LASIK results in the need for fewer staff members. The range of correction, however, is limited to low hyperopia, and the surgeon must turn

to other procedures for patients outside of the treatment range of CK.

It is still too early to claim that this procedure results in a stable postoperative refractive error. Predictability needs to be improved, particularly in the ± 0.50 D range, and stability needs to be more firmly established. Research is still being done to make this procedure even more efficient. Many developments are underway which will enhance the intrastromal conductive keratoplasty procedure.1,2,8

REFERENCES

1.McDonald MB, Davidorf J, Maloney RK, Manche EE, Hersh P. Conductive keratoplasty for the correction of low to moderate hyperopia. 1-year results on the first 54 eyes. Ophthalmology. 2002;109:637-49.

2.Asbell PA, Maloney RK, Davidorf J, Hersh P, McDonald M, Manche E. Conductive keratoplasty for the correction of hyperopia. Tr Am Ophth Soc. 2001;99:79-83.

3.Kohnen T. Advances in the surgical correction of hyperopia. J Cataract Refract Surg. 1998;24:1-2.

4.Pietilä J, Mäkinen P, Pajari S, Uusitalo H. Excimer laser photorefractive keratectomy for hyperopia. J Cataract Refract Surg. 1997;13:504-10.

5.Vinciguerra P, Epstein D, Radice P, Azzolini M. Long-term results of photorefractive keratectomy for hyperopia and hyperopic astigmatism. J Refract Surg. 1998;14:S183-5.

6.Esquenazi S, Mendoza A. Two-year follow-up of laser in situ keratomileusis for hyperopia. J Refract Surg. 1999;15:648-52.

7.Leibowitz M, Krueger DE, Maunder LR, et al. The Framingham eye study monograph. VIII: visual acuity. Surv Ophthalmol. 1980;24(suppl):472-9.

8.Mendez A, Mendez Noble A. Conductive keratoplasty for the correction of hyperopia. In: Sher NA, ed. Surgery for Hyperopia and Presbyopia. Philadelphia, Pa: Williams and Wilkins. 1997;163-71.

9.Mendez Noble A, Mendez A. Queratoplastia conductiva intraestromal para el manejo de la hipermetropia. In: Albertazzi R, Centurión V, eds. La Moderna Cirurgia Refractiva. Buenos Aires. 1997;243-5.

10.Souza L, Nosé W, Campos M, McDonnell PJ. Thermokeratoplasty for the treatment of hyperopia: a clinical follow-up. Arq Bras Oftal. 1997;60:136-45.

11.Eggink CA, Bardak Y, Cuypers MHM, Deutman AF. Treatment of hyperopia with contact Ho:YAG laser thermal keratoplasty. J Refract Surg. 1999;15:16-22.

12.Alió JL, Ismail MM, Sanchéz Pego JL. Correction of hyperopia with non-contact Ho:YAG laser thermal keratoplasty. J Refract Surg. 1997;13:17-22.

13.Koch DD, Abarca A, Villarreal R, et al. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. Clinical study with two-year follow-up. Ophthalmology. 1996;103:731-40.

14.Koch DD, Kohnen T, McDonnell PJ, et al. Hyperopia correction by noncontact holmium:YAG laser thermal keratoplasty. United States phase IIA clinical study with 2-year fol- low-up. Ophthalmology. 1997;104:1938-47.

15.Ismail MM, Alió JL, Pérez-Santonja JJ. Noncontact thermokeratoplasty to correct hyperopia induced by laser in situ keratomileusis. J Cataract Refract Surg. 1998;24:1191-4.

16.Daya SM, Tappouni FR, Habib NE. Photorefractive keratectomy for hyperopia. Six-month results in 45 eyes. Ophthalmology. 1997;104:1952-8.

17.Jackson WB, Mintsioulis G, Agapitos PJ, Casson EJ. Excimer laser photorefractive keratectomy for low hyperopia: safety and efficacy. J Cataract Refract Surg. 1997;23:480-7.

18.Argento CJ, Cosentino MJ. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg. 1998;24:1050-8.

19.Ditzen K, Huschka H, Pieger S. Laser in situ keratomileusis for hyperopia. J Cataract Refract Surg. 1998;24: 42-7.

20.Brinkmann R, Radt B, Flamm C, et al. Influence of temperature and time on thermally induced forces in corneal collagen and the effect on laser thermokeratoplasty. J Cataract Refract Surg. 2000;26:744-54.

21.Spörl E, Genth U, Schmalfuss K, Seiler T. Thermo-mechani- cal behavior of the cornea. Ger J Ophthalmol. 1997;5:322-7.

INTRODUCTION

The surgical correction of hyperopia and hyperopic astigmatism by altering the shape of the cornea has always been a greater challenge than the correction for myopia and myopic astigmatism. Early attempts with incisional keratorefractive surgery, hexagonal keratotomy, found limited success. The hyperopic refractive error could be reduced, but at the expense of corneal instability and a high incidence of irregular astigmatism. The development of the excimer laser and hyperopic photorefractive keratectomy has achieved a more acceptable success rate with fewer complications. The range of correction, however, is still somewhat limited and postoperative recovery prolonged.

This chapter is intended to compare 3 photoablative techniques: LASIK, PRK, and LASEK. The expectation is to challenge the reader to critically analyze their utilization of these procedures and optimize their application. A common and popular misconception has been that there is 1 “best” procedure to be used in all situations. The refractive surgeon maintaining the philosophy of providing a diversification of techniques and selecting the most appropriate will most certainly better serve his or her patients.

Corneal Anatomy and Physiology

There are numerous excellent references discussing corneal anatomy, physiology, and biomechanics.1-4 The intention of this section is simply to expose the reader to aspects of those areas that are pertinent to the correction of hyperopia and hyperopic astigmatism by 1 of these 3 photorefractive procedures. Our understanding of many of these considerations remains limited; however, it is important to at least recognize these limitations so as to guide our surgical decisions. Patient expectations must be realistic. Failure to acknowledge the uncertainties surrounding wound healing and individual tissue variability can definitely lead to false expectations by both the patient and the surgeon.

The excellent precision with which corneal tissue can be ablated using the excimer laser tends to overshadow the factors that work to decrease the precision of these hyperopic corrective procedures. Epithelial healing, the laser ablation profile and characteristics, and variability in stromal hydration are just a few of these factors to be considered. The enthusiasm being generated about “supervision” associated with the development of wavefront technology and custom ablation must be tempered with the understanding that the limitations of the results of these procedures are related to the above factors, not only on the precision of the laser or its

technology. We know that the changes made in the anterior curvature of the cornea do induce higher order optical aberrations. These ultimately limit the quality of postoperative vision. Our ability to be able to reduce or correct these should improve the level of visual functioning. Presently, poor control over individual tissue reactivity and wound healing has to raise concern over the claims of success being made for results obtained with wavefront refractions and custom ablations.

The cornea maintains 2 primary functions: to refract light rays onto the retina and to protect the intraocular contents. Excimer photorefractive procedures alter the anterior curvature of the cornea to change its ability to refract light. In accomplishing this, the transparency of the tissue as well as the strength and integrity must be maintained. The ability to alter the cornea’s shape to correct hyperopia has proven to be a greater challenge than that to correct myopia. It is much easier to flatten the cornea by removing central tissue than to steepen it. The cornea’s wound healing responses are much better at repairing the peripheral tissue removal, primarily through the epithelium’s ability to thicken and fill in the defect. Fortunately, the hyperopic ablation is less likely to alter the structural integrity to the cornea since it is removing tissue in the midperiphery where the cornea is normally much thicker. However, one must not get careless and forget to calculate the residual posterior stroma especially in higher hyperopic treatments as well as retreatments. Dr. Steven Slade has presented a hyperopic PRK case in which multiple retreatments led to complete corneal perforation.

The corneal epithelium is integrally involved in the attempts made to steepen the anterior corneal curvature with either surface or lamellar photorefractive procedures. The epithelium functions as a barrier to both mechanical forces as well as diffusion of fluids and substances. In addition, its ability to provide a smooth optical surface is imperative to good visual function. It is composed of 5 to 7 cell layers normally 30 to 50 µm in thickness.2 Each cell is approximately 7 µm in thickness, which can account for a half to threequarters of a diopter of refractive effect. Thus the epithelial response seen to the peripheral tissue removal can significantly affect the refractive result just with a single extra cell layer. After LASIK and PRK the corneal epithelium will thicken as much as 75 µm.1 It has been demonstrated that the epithelium thickens over areas of corneal thinning and especially over areas of irregularity in the LASIK flap.

The epithelium is composed of 3 types of cells: the surface squamous cells, middle polygonal wind cells, and regenerating basal cells. The glycoprotein layer in the plasma membrane of the squamous cell assists in protecting the cornea from infectious agents. Since LASIK does minimal damage to this layer, the risk of infection with lamellar procedures is significantly less than for surface ablative procedures. The polygonal cells have attachments to each other that are not destroyed by the 20% alcohol solution used in

LASEK and assist in permitting the epithelial flap to be detached in a single sheet. The basal cells are responsible for the regeneration of the epithelium. The accumulation of iron in these cells is the etiology for the iron lines seen after refractive surgery.

Not only does the structure of the epithelium participates in the results after photorefractive keratectomy, but its metabolism also plays an important role. Because the epithelium receives its oxygen supply from the tear film layer, during eyelid closure with sleep there is a reduction in the oxygen available. This results in anaerobic metabolism and increased lactic acid levels. The lactic acid will then lead to stromal swelling through increased osmolality and its toxic effects on the endothelium. Using a bandage soft contact lens in PRK and LASEK can increase the deleterious effect of this nocturnal hypoxia.

The basement membrane secreted by the epithelium assists in its attachment to the underlying stroma. It is postulated by Dr. Camellin that in LASEK, if the basement membrane is preserved, the re-epithelialization will be considerably faster.5 Dr. Singh has work to suggest that the basement membrane is responsible for directing the nature of the differentiation of the underlying stroma.6 Its presence may modify wound healing and eliminate the haze seen after surface ablative procedures.

The true function and value of Bowman’s membrane has continued to evade identification. This uncertainty is an underlying factor in the controversy between surface (PRK and LASEK) and lamellar (LASIK) photorefractive procedures. Because Bowman’s layer cannot regenerate, surface ablation greater than 1.00 D of correction will remove this layer exposing the underlying stroma. The interaction between the epithelium and this denuded stroma can lead to “haze” formation. This opacification is due to subepithelial and/or stromal wound repair.7 As LASIK spares Bowman’s and does not disturb its natural relationship to the epithelium and epithelial basement membrane, haze is rarely, if ever a consideration. One must not forget that LASIK does affect Bowman’s layer as the incision does disrupt its integrity and biomechanical forces. If Bowman’s layer has a role in maintaining the corneal shape, one would expect the LASIK flap to affect the surface topography. Indeed studies have shown that the simple construction of the lamellar flap can alter corneal topography.8 More definite is the change in wavefront evaluation seen with flap construction.

It is not simply Bowman’s layer that demonstrates this biomechanical weakening response. The underlying corneal lamellae are also under tension in the dome shape of the cornea. The LASIK flap relieves the strain in the anterior lamellae both peripheral to and central to the cut. The collagen fibers unwind and water moves into the tissue. This results in peripheral corneal thickening and central fiber uncoiling seen clinically as microstriae.4