Ординатура / Офтальмология / Английские материалы / LASIK and Beyond LASIK Wavefront Analysis and Customized Ablation_Boyd_2001
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Chapter 27
Figure 27-7. Diffuse lamellar keratitis extending over the pupil.
Punctate Epithelial Keratopathy
Punctate epithelial keratopathy is not uncommon after LASIK. Mild cases are usually asymptomatic, but more severe cases can cause poor uncorrected and best corrected vision. Preexisting dry eye or blepharitis may be contributory. In fact, many patients choose to have refractive surgery because of contact lens intolerance resulting from dry eyes. The corneal nerves are severed at the time of LASIK and this may increase the susceptibility to keratopathy. Corneal sensation returns more quickly, however, after LASIK than PRK(12).
Treatment involves frequent lubrication of the ocular surface with artificial tears. Nonpreserved tears may be required in more advanced cases. Management of any lid disease with lid hygiene, antibiotic ointment, or oral tetracyclines may also be of benefit. In refractory cases, punctal occlusion with silicone plugs, argon laser, or thermal cautery may be required. When ocular surface disease is recognized preoperatively, some of these measures may be started prior to surgery as a preventative measure.
Diffuse Lamellar Keratitis (Sands of
Sahara)
Diffuse lamellar keratitis (DLK), also known as Sands of Sahara, is an interface inflammatory process that occurs in the early postoperative period fol-
Figure 27-8. Infectious keratitis after LASIK.
lowing LASIK. Patients are asymptomatic and often have no visual impairment, particularly in the early stages. The eye remains white and quiet. A fine granular appearing infiltrate that looks like dust or sand typically presents initially in the interface periphery. The inflammation, if left untreated, can progress through several stages. The cells can spread centrally to cover the pupil (Figure 27-7). Next, they may clump and, with the release of inflammatory mediators, can result in a stromal melt. The cause of DLK is likely multifactorial but its exact etiology is uncertain. Bacterial toxins or antigens, debris on the instruments, eyelid secretions, or other unknown factors may play a role. Treatment involves frequent topical steroids. In rare cases where inflammation continues to progress, the flap must be lifted and the interface irrigated.
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Infectious Keratitis
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Infectious keratitis is extremely rare after LASIK with a reported incidence of 1 in 5,000 (13) (Figure 27-8). The presence of an epithelial defect in the early postoperative period may increase the risk. Presumed microbial keratitis after LASIK should be cultured and treated with frequent broad spectrum topical drops. A fluoroquinolone, such as ofloxacin, or a combination of fortified antibiotics, such as vancomycin 33 mg/ml and tobramycin 15 mg/ml, should be used. Hourly drops around-the-
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clock are necessary. In certain cases, this may require hospitalization to ensure compliance. If the keratitis is resistant to treatment, the flap should be lifted, debrided, and irrigated with antibiotic solution. Oral and subconjunctival antibiotics are of no value. Careful intraoperative and postoperative sterility is important. Patients should be instructed to wash their hands before touching their lids. Swimming in lakes or Jacuzzis should be avoided in the first month.
Overcorrection and Undercorrection
Overcorrection or undercorrection may result from an inaccurate refraction, improper surgical ablation, decentration, beam inhomogeneity, abnormal corneal hydration status, or an excessive or inadequate healing response. Consistent and uniform stromal hydration during the ablation is crucial. If desiccation of the corneal tissue occurs, it will be relatively more compact, and more tissue will be removed per pulse of the laser. This result will be an overcorrection. If the stroma is overly hydrated, then less tissue per pulse will be ablated, resulting in undercorrection. Each surgeon should attempt to standardize the time between anesthetic administration, lid speculum insertion, flap creation, and laser application to reduce the variability of the hydration status. Attempted versus achieved results should continuously be analyzed to modify personal nomograms and improve predictability. Such nomograms are dependent on laser type, individual surgical technique, humidity, temperature, and geographic location. Patient age may also be a factor (14).
An enhancement may be performed once refractive stability is achieved. However, a visually significant undercorrection may be treated earlier, particularly if the patient had a low to moderate amount of myopia preoperatively.
Epithelial Ingrowth
Epithelium can grow in the interface between the cap and the stromal bed. This appears as small cysts or pearls of epithelial cells at the flap edge (Figure 27-9). Most often, the epithelial cells remain confined to the periphery and do not progress. Rarely,
Figure 27-9. Small pearls of epithelial cells in interface of flap periphery.
however, growth may progress toward the central visual axis causing irregular astigmatism and loss of best corrected acuity. In some cases, the epithelial cells in the interface will block nutritional support for the overlying stroma and lead to a flap melt.
Epithelial ingrowth occurs in 2 to 3% of myopic LASIK surgeries, most commonly after enhancements (15). In relifting the flap, epithelial cells may gain access to the interface because of irregularities that may result from dissection of the flap edge. Because of this, epithelial tags at the edge of the flap bed should be pushed back with a sponge prior to repositioning the flap. The risk of epithelial ingrowth is even higher after hyperopic LASIK, possibly because the ablation strikes the epithelium at edge of the flap cut and stimulates cellular proliferation.
Prevention of this complication is not always possible. Even with careful irrigation of the interface, epithelial ingrowth may still occur. An epithelial defect at the time of surgery can lead to stromal edema with poor adherence of cap to the underlying stromal bed. This allows an avenue for epithelial cells to transit under the flap.
Epithelial ingrowth should be treated when it extends more than 2 mm from the flap edge, when
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Chapter 27
Figure 27-10. Peripheral microstriae that were not visually significant.
there is documented progression in size, or when it threatens the visual axis. Other indications for removal include an altered residual refractive error, induced astigmatism, reduced uncorrected or best corrected visual acuity, or a stromal melt.
Treatment involves relifting the flap. The location of the ingrowth should be noted preoperatively. The edge of the flap should be marked with a sterile fine 27 or 30 gauge needle at the slit lamp. Under the microscope, the flap should then be lifted. Using a PRK spatula or a surgical spear, both the stromal bed and the undersurface of the flap should be debrided. Typically the cells come off in a single sheet. Spears should be discarded with each pass to avoid re-implantation of cells. The peripheral stromal bed should then be cleared of epithelial tags and the flap replaced. Irrigation beneath the flap should then be performed and the flap allowed to dry adequately. A bandage contact lens may be placed if the epithelium is disrupted. In aggressive or recurrent cases of epithelial ingrowth, some surgeons advocate using 70 or 100% alcohol.
Flap Striae
Microstriae are not uncommonly seen after LASIK, particularly if the flap is carefully examined
Figure 27-11. Nonsignificant peripheral haze where Bowman’s membrane was cut in creating the flap.
with retroillumination. Most cases of microstriae are visually insignificant, especially when the folds lie outside of the visual axis (Figure 27-10). Epithelial hyperplasia occurs over these irregularities, smoothing out the refractive surface. Nevertheless, when microstriae occur over the pupil or when macrostria exist, irregular astigmatism with visual aberrations and monocular diplopia may result. In such cases, the flap should be relifted, hydrated, and stretched back into position as described above in ‘Flap Displacement.’
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Haze
Haze under the flap is extremely uncommon
after LASIK. There is consistently a circular haze in Help ? the region where the microkeratome cut Bowman’s
layer (16) (Figure 27-11). Haze can occur if the detergent used to sterilize the instruments and equipment is not completely removed. Frequent topical steroids reduce the inflammatory response and minimize the long-lasting effects of this complication.
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Ectasia
The general consensus among refractive surgeons is that 200 to 250 mm should remain in the stromal bed at the completion of the ablation in order to avoid problems with ectasia. The Munnerlyn formula calculates the ablation depth based on the magnitude of the refractive error and size of the optical zone. In patients with higher refractive errors, the surgeon may reduce the size of the optical zone in order to limit the amount of tissue removed. However, this increases the likelihood of visual side effects such as glare and halos. In such cases, other refractive surgical options, such as phakic intraocular lenses or natural lens extraction, should be considered.
Visual Aberrations
Visual aberrations can occur because of irregular astigmatism after LASIK. Small optical zones or a large pupil can result in halos from refraction of light off the transition zone. Monocular diplopia can result from a wrinkled flap, decentered ablation, or a central island. Visual aberrations are more common in higher corrections, although these patients are more likely to experience visual aberrations with other forms of correction, such as spectacles and contact lenses. Large pupils can lead to reduced contrast at night as well as glare and halos.
Conclusion
Complications are much less likely to lead to visual loss if handled promptly and properly. Proper knowledge and careful use and maintenance of the microkeratome can reduce the incidence of complications. Overall, LASIK is a relatively safe operation in experienced hands.
REFERENCES
1.Burato L, Ferrari M, Genisi C. Myopic keratomileusis with the excimer laser: One year follow-up. Refract Corneal Surg 9: 1219, 1993.
2.Brint SF, Ostrick M, Fisher C, et al. 6 month results of the multi-center phase I study of excimer laser myopia keratomileusis. J Cataract Refract Surg 20: 610-615, 1994.
3.Pallikaris IG, Siganos DS. Excimer laser in situ keratomileusis and photorefractive keratectomy for correction of high myopia. J Refract Corneal Surg 10: 498-510, 1994.
4.Trokel SL, Srinivasan R, Branen R. Excimer laser surgery of the cornea. Am J Ophthalmol
96:710-715, 1983.
5.Burato L, Ferrari M. Photorefractive keratectomy or keratomileusis with excimer laser in surgical correction of severe myopia: Which technique is better? Eur J Implant Refr Surg 5: 183-186, 1993.
6.Slade SG. Abnormal induced topography. Central islands. In: Machat JJ, ed. Excimer Laser Refractive Surgery. Practice and Principles. Thorofare, NJ: Slack, Inc; 1996: 399.
7.Burato L, Ferrari M, Rama P. Excimer laser intrastromal keratomileusis. Am J Ophthalmol
113:291-295, 1992.
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8.Seiler T, Kahle G, Kriegerowski M. Excimer laser (193 nm) myopic keratomileusis in sighted and blind human eyes. Refract Corneal
Surg 6: 165-173, 1990. |
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9.Pallikaris IG, Patzanaki ME, Stathi Ez, et al. Laser in-situ keratomileusis. Lasers Surg Med
10:463-468, 1990.
10.Burato L. Excimer laser intrastromal keratomileusis: Case reports. J Cataract Refract Surg 18: 37-41, 1992.
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11.Martines E, John ME. The Martines enhancement technique for correcting residual myopia following laser assisted in situ keratomileusis. Ophthalmic Surgery & Lasers 27: S512-516, 1996 (suppl 5).
12.Lin DT, Sutton HF, Berman M. Corneal topography following excimer photorefractive keratectomy for myopia. J Cataract Refract Surg 19: 149–154, 1993 (suppl).
13.Slade SG. LASIK complications and their management. In: Machat JJ, ed. Excimer Laser Refractive Surgery. Practice and Principles. Thorofare, NJ: SLACK Inc.; 1996: 359.
14.Spivack LD. Results of LASIK using a New Nomogram. (Abstract #10). In American Society of Cataract and Refractive Surgery, Symposium on Cataract, IOL, and Refractive Surgery, 1998, p. 37.
15.Maloney RK. Epithelial ingrowth after lamellar refractive surgery. Ophthalmic Surg Lasers. 116; 27 (5 pl): S535.
16.Campos M, Wang XW, Herzog J, et al. Ablation rates and surface ultrastructure of 193 nm excimer laser keratotomies. Invest Ophthalmol Vis Sci 34: 2493, 1993.
Elizabeth A. Davis, M.D.,
Minnesota Eye Consultants, P.A.
710 East 24th St. Suite 105
Minneapolis, MN 55404
Fax: 612-813-3601
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316 SECTION IV
VITREORETINAL COMPLICATIONS OF REFRACTIVE SURGERY
Chapter 28
VITREORETINAL COMPLICATIONS OF
REFRACTIVE SURGERY
Steve Charles, M.D.
PREOPERATIVE EXAMINATION
It is unknown what examination methods are sufficient when a refractive surgery candidate is referred to a retinal consultant before refractive surgery. Options include: indirect ophthalmoscopy with or without 360-degree scleral depression and/ or 3-mirror contact lens examination. In view of the common notion of “clearing” patients for refractive surgery, it is essential that the retinal consultant perform a very careful examination while explaining to the patient that “clearing” or a “guarantee” against retinal detachment is not possible.
INDICATIONS FOR PROPHYLAXIS OF RETINAL BREAKS AND DEGENERATIONS
The efficacy of laser or cryopexy prophylaxis in preventing detachment by treating retinal breaks prior to refractive procedures is assumed, but has not been proven. The majority of retinal breaks in retinal detachment failure cases are located immediately posterior to areas of cryopexy leading to the conclusion that only definite holes/tears/breaks, not “peripheral changes” should be treated. Pattern, scatter, barrage, PRP, and “new ora” concepts are unwarranted by today’s standards.
Which retinal breaks should be treated is not known. Some retinal consultants stress that only symptomatic breaks should be treated 1-3. The author has seen several asymptomatic patients with significant retinal detachments discovered during preLASIK screening. It is probable that all surgeons would recommend treatment of these retinal
detachments even though the patients had no symptoms. Patients vary widely in their reporting of symptoms caused by PVD, retinal breaks and detachment. It is clear that symptoms are highly dependent on attitudes, level of activity, denial, comorbidity, and other societal and psychological factors. Relaying solely on symptoms is insufficient to address the real issue of safety.
Most surgeons recommend treating all breaks outside lattice but not those within the lattice. It is unknown whether upcoming clear lens extraction, phakic IOL implantation, PRK, or LASIK should change these treatment indications. Similarly, no recognized expert recommends treatment of lattice without retinal breaks. It is again unknown if refractive surgery means that this concept should change although most experts have recommended no change in treatment indications when refractive surgery is planned.
There is no evidence that degenerations other than lattice should be treated with laser. White without pressure is a generic term that is used to describe peripheral microcystoid (a degenerative retinoschsis precursor), the normal vitreous which is often visible in highly pigmented patients and a variety of other “changes”, none of which need retinopexy.
The term “atrophic” break is often used but unfortunately is ill-defined. To some ophthalmologists, “atrophic” implies that prophylactic retinopexy is not indicated, but this has not been proven. Although superior retinal breaks are probably more likely to result in clinical retinal detachment, location is seldom cited as a criterion for retinopexy. All surgeons treat horseshoe tears, any break/hole/ tear with apparent traction, and symptomatic tears.
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Most surgeons are more likely to treat borderline pathology in patients with a family history of retinal detachment or a history of detachment in the other eye. Personal history of retinal detachment in the same or eye is a relative contraindication for refractive surgery. If a decision is made to perform refractive surgery on such patients, careful peripheral retinal examination and prophylactic treatment of breaks/holes/tears is mandatory.
There is significant controversy about whether extensive peripheral retinopexy (PRP, scatter, barrage) is effective in preventing retinal detachment in giant break “other eyes”, proliferative vitreoretinopathy (PVR), and clear-lens extraction patients.
THEORETICAL MECHANISMS RESULTING IN RETINAL BREAKS AND DETACHMENT
Anterior Chamber Shallowing
Anterior movement of lens and anterior vitreous causes “traction” forces on peripheral retina and traction induced retinal breaks. Microperforation is a significant cause of anterior chamber shallowing during radial keratotomy, astigmatic keratotomy, and occasionally the microkeratome step in LASIK or the
placement of intrastromal rings (Figure 28-1). Improved pachymetry, depth adjustments on diamond knives, microkeratomes and other precautions have reduced, but not eliminated, microperforation.
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Figure 28-1. Microperforation of the cornea can lead to ante- |
Figure 28-2. Lens displacement during clear-lens extraction |
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Vitreoretinal Complications of
PRK & LASIK
Laser-tissue interaction creates acoustic pressure waves, which propagate through the vitreous and theoretically could cause retinal breaks. The concave surface of the ocular interior will focus the acoustic energy, significantly increasing local acoustic power density. Photorefractive keratectomy (PRK) and laser-in-situ-keratomileusis (LASIK) produce high-energy acoustic waves, which have the potential of producing significant forces on the vitreous and retina. The author has seen a patient that developed a macular hole instantaneously during a YAG (yttrium-aluminum-garnet) laser capsulotomy. A careful and experienced surgeon used normal power settings and a low number of pulses and the patient had a excellent vision and glare complaints preoperatively. It is probable that an acoustic pressure wave jerked on the posterior vitreous cortex attached to the macula.
There are few articles on vitreoretinal complications of LASIK and PRK. Many anecdotal case reports have been obtained from refractive surgeons and retinal consultants. The incidence of vitreoretinal complication appears to be quite low in the few series published. A low incidence could theoretically be explained by observer bias, short follow-up intervals, lack of a control group, and poor study design but it is probable that the incidence of vitreoretinal complications is low.
Retinal Detachment After PRK
Ruiz-Moreno JM, Artola A, and Alio JL reported on retinal detachment in myopic eyes after photorefractive keratectomy. They analyzed the incidence and characteristics of retinal detachment (RD) in myopic patients who had photorefractive keratectomy (PRK). The incidence of RD in 5936 consecutive eyes that had PRK to correct myopia was studied. Mean follow-up was 38.5 months +/- 17.4 (SD). They found that retinal detachment occurred in 5 eyes (0.08%); 2 in women and 3 in men. The mean interval between PRK and RD was 21.00 +/- 15.89 months (range 9 to 48 months). The
mean best-corrected visual acuity (BCVA) after PRK and before RD development was 20/81 (range 20/ 200 to 20/25). After RD repair, the mean BCVA was 20/460 (range 20/2000 to 20/29). In 4 of the 5 eyes, BCVA after RD was within 1 line of the preoperative value; in 1 eye, it decreased from 20/40 to 20/2000. The mean spherical equivalent (SE) before RD treatment was -1.35 +/- 1.08 diopters (D) (range 0 to -3.00 D) and after RD treatment, -2.95 +/- 0.83 D (range -2.00 to -4.00 D). Differences between SE before and after RD treatment were statistically significant (P =. 01, paired Student t test). They concluded that the incidence of RD after PRK to correct myopia was 0.08%. In 4 of 5 eyes, there was little or no visual loss; but in the group as a whole, there was a significant increase in myopic SE.
Retinal Detachment After LASIK
Ruiz-Moreno JM, Perez-Santonja JJ, and Alio JL reported in a study of retrospective study of retinal detachments observed in 1,554 consecutive eyes (878 patients) undergoing laser-in-situ keratomileusis for the correction of myopia (followup, 30.34+/-10.27 months; range, 16 to 54). Mean patient age was 33.09+/-8.6 years (range, 20 to 60). Before treatment with laser-in-situ keratomileusis, all patients had a comprehensive examination, and detected lesions predisposing to retinal detachment were treated before performing the laser-in-situ keratomileusis procedure. They found that retinal detachment occurred in four (0.25%) of 1,554 eyes of four (0.45%) of 878 patients. All four patients who developed retinal detachment in one eye were women. Degree of preoperative myopia was -13.52+/-3.38 diopters (range, -8.00 to -27.50). The time interval between refractive surgery and retinal detachment was 11.25+/-8.53 months (range, 2 to 19 months). In all cases retinal detachment was spontaneous. In all eyes the retina was reattached successfully at the first retinal detachment surgery. Mean best-corrected visual acuity after laser-assisted in situ keratomileusis and before retinal detachment development was 20/43 (range, 20/50 to 20/30). After retinal detachment repair, best-corrected visual acuity was 20/45 (range, 20/50 to 20/32). Differences between
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best-corrected visual acuity before and after reattachment were not statistically significant (P = .21, paired Student t test). A myopic shift was induced in three eyes that had retinal detachment repaired by scleral buckling, from -0.58+/-0.72 diopter (range, +0.25 to -1.00) before retinal detachment and -2.25+/-1.14 diopters (range, -1.00 to -3.25) after retinal detachment surgery (P = .03, paired Student t test). They concluded that laser-in- situ keratomileusis for correction of myopia is followed by a low incidence of retinal detachment. Conventional scleral buckling surgery was successful in most cases and did not cause significant changes in the final best-corrected visual acuity. A significant increase in the myopic spherical equivalent was observed after scleral buckling in these patients.
Several reports have appeared concerning retinal detachment after LASIK 4-12. Arevalo et al state in a discussion of an article Ruiz-Moreno and associates 11 that ”The authors are to be commended for reporting the results of a retrospective study to analyze the incidence and characteristics of retinal detachment in myopic patients treated by laserassisted in situ keratomileusis. Dr Ruiz-Moreno and associates conclude: ‘’Our study reported a large number of eyes consecutively corrected by laserassisted in situ keratomileusis for the correction of myopia (1,554 eyes of 878 patients), with a follow up of 30.34 ± 10.27 months and with a 0.25% incidence of retinal detachment.’’We agree that retinal detachment after laser in situ keratomileusis is infrequent and recently studied the incidence and characteristics of rhegmatogenous retinal detachment after laser-in-situ keratomileusis (Arevalo JF, unpublished data, 1999). We found 20 eyes (17 patients) with rhegmatogenous retinal detachment after laser-in-situ keratomileusis, for an incidence of 0.06% (20/31,739 eyes). Patients were followed for a mean of 36 months (range, 3 to 48 months), and rhegmatogenous retinal detachment occurred between 1 and 36 months (mean, 13.9 months) after laser-in- situ keratomileusis. Eyes that developed a detachment had from -1.50 to -16.00 diopters of myopia (mean, - 7.35 diopters) before laser in situ keratomileusis. Retinal detachment characteristics in our study showed that most rhegmatogenous retinal detachments and retinal breaks occurred in the temporal quadrants (71.4%). This is a very interesting
finding; because the surgical microkeratome used to create the corneal flap in laser in situ keratomileusis has a temporal handle that may be responsible for extra pressure on that side of the eye.
Rhegmatogenous retinal detachment (RRD) following laser-in-situ keratomileusis (LASIK) is uncommon(8) according to a recent report. Arevalo studied 24,890 myopic eyes that underwent the surgical procedure. The clinical files of five refractive surgeons from four institutions were reviewed for instances of RRD. All eyes in the study underwent LASIK for correction of myopia ranging from –0.75 to –29.00 diopters (D) (mean, -6.19 D). RRD occurred in 13 eyes from 12 patients between one and 36 months (mean, 12.6 months) after LASIK. The incidence of RRD was .05 percent at a mean of 24 months after surgery. Vitrectomy, cryopexy, scleral buckling, argon laser retinopexy or pneumatic retinopexy techniques were used to manage RRD. Myopia before surgery ranged from –1.50 to –16.00 D (mean, -6.96 D) in eyes that later developed RRD. Although the study did not reveal a cause-effect relationship between the corrective procedure and retinal detachment, the researchers recommended that “patients scheduled for refractive surgery undergo a thorough dilated indirect fundus examination with scleral depression and treatment of any retinal lesions predisposing them to the development of retinal detachment before LASIK surgery is performed.” The incidence of retinal detachment after PRK appears to be very low although there is little data 13.
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Macular Hemorrhage Secondary to Choroidal Neovascularization After LASIK and PRK
Macular hemorrhage secondary to choroidal |
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neovascular membranes occurs in many myopic |
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hemorrhage during or within days after cataract or filtering surgery. It is probable that the same mechanism could occur in any refractive procedure that transiently lowers the IOP. It is possible that any membrane that bled would have done so without surgery but this has not been proven. Many choroidal neovascular membranes have a self-limited course in myopic patients and never hemorrhage. It should be assumed that some patients will develop a submacular hemorrhage as a result of refractive surgery that otherwise would have stabilized without bleeding. These patients would have a worse visual outcome than a patient without bleeding. It is probable that the incidence of this complication is very low 15.
A careful history and Amsler ’s grid assessment should be performed preoperatively to determine if the patient has subjective evidence of choroidal neovascular membrane. Any suspicious changes indicate the need for fluoroscein angiography. Any active, untreatable membranes should probably be treated with PDT if subfoveal, PDT or laser if subfoveal is juxta-foveal or observed until inactive before any refractive procedure is performed.
Ruiz-Moreno and colleagues 15 reported on Choroidal neovascularization in myopic eyes after photorefractive keratectomy. They evaluated the incidence, characteristics, and results of treatment of choroidal neovascularization (CNV) in 5936 consecutive eyes that had PRK for the correction of myopia myopic eyes corrected by photorefractive keratectomy (PRK). Mean follow-up was 38.5 months +/- 17.4 (SD). This study had one patient that developed CNV. Extrafoveal CNV developed in the right eye of a 44-year-old woman 26 months after PRK for the correction of -12.00 diopters (D) of myopia. The follow-up after PRK was 38 months. Best corrected visual acuity (BCVA) before PRK was 20/40 (spherical equivalent [SE] -12.00 D). After PRK, BCVA was 20/32 SE -1.75 D). The CNV was treated by direct argon-green laser photocoagulation and did not recur in the subsequent 12 months). After CNV treatment, BCVA was 20/32 (SE -2.25 D). The incidence of CNV after PRK for myopia was low. Choroidal neovascularization is a possible complication in myopic eyes, and the risk exists
before PRK. After PRK, the risk of CNV in myopic patients did not increase
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Nerve Fiber Layer Damage
Nerve fiber layer damage can be caused by increased IOP during suction cup usage before LASIK. A recent paper demonstrates reduction of this effect by the use of Brimonidine in a randomized, controlled clinical trial.
Endophthalmitis
Endophthalmitis can occur anytime an incision is made into the eye. There are few reports of endophthalmitis after refractive surgery, but the results can be devastating in at least 50 percent of the patients. Few patients are informed about this potential complication before surgery is performed. One case has been reported after phakic IOL implantation 16.
Dislocated Intraocular Lenses
Posterior dislocation of a plate haptic IOL into the vitreous cavity immediately after LASIK has been observed. Acoustic effects or suction cup application most likely cause this complication.
Retinal Detachment After Phakic IOL
Implantation
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Moreno et al 17 studied retinal detachments in 166 consecutive eyes (98 patients) that underwent implantation of angle-supported phakic anterior
chamber intraocular lenses (models ZB5M and Help ? ZB5MF; Domilens; Lyon, France) for the correction
of severe myopia (follow-up ± SD, 45.26 ± 14.65 months; range, 20 to 84 months). Their results were as follows: Retinal detachment occurred in eight eyes (4.8%); four eyes belonged to men and four to women. The time between implanting surgery and retinal detachment was 17.43 ± 16.4 months (range, 1 to 44 months).
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