|Year : 2002 | Volume
| Issue : 4 | Page : 265-282
Complications of laser-in-situ-keratomileusis
Mittanamalli S Sridhar, Srinivas K Rao, Rasik B Vajpayee, Murali K Aasuri, S Hannush, R Sinha
Cornea Center, All Institute of Medical Sciences, New Delhi, India
Mittanamalli S Sridhar
Cornea Center, All Institute of Medical Sciences, New Delhi
Laser-in-situ-keratomileusis (LASIK) has become a popular technique of refractive surgery because of lower postoperative discomfort, early visual rehabilitation and decreased postoperative haze. Compared to photorefractive keratectomy (PRK), LASIK involves an additional procedure of creating a corneal flap. This may result in complications related to the flap, interface and underlying stromal bed. The common flap-related complications include thin flap, button holing, free caps, flap dislocation and flap striae. The interface complications of diffuse lamellar keratitis, epithelial ingrowth and microbial keratitis are potentially sight threatening. Compared to PRK, there is less inflammation and faster healing after LASIK, but there is a longer period of sensory denervation leading to the complication of dry eyes. The refractive complications include undercorrection, regression, irregular astigmatism, decentration and visual aberrations. Honest and unbiased reporting is important to understand the aetiology and redefine the management.
Keywords: LASIK, complications, refractive surgery
|How to cite this article:|
Sridhar MS, Rao SK, Vajpayee RB, Aasuri MK, Hannush S, Sinha R. Complications of laser-in-situ-keratomileusis. Indian J Ophthalmol 2002;50:265-82
|How to cite this URL:|
Sridhar MS, Rao SK, Vajpayee RB, Aasuri MK, Hannush S, Sinha R. Complications of laser-in-situ-keratomileusis. Indian J Ophthalmol [serial online] 2002 [cited 2014 Nov 22];50:265-82. Available from: http://www.ijo.in/text.asp?2002/50/4/265/14766
The predictability and safety of refractive surgery have improved significantly in recent years. We practise an era where 6/6 visual acuity is considered the standard for success. New laser technologies like wavefront are helping us achieve postoperative uncorrected visual acuity better than pre-operative best spectacle corrected visual acuity. However, it is necessary to understand the aetiology, pathophysiology, visual safety implications and management of complications following refractive surgery. This understanding will help surgeons obtain more consistent and predictable outcomes. This review aims to help in understanding potential complications of LASIK surgery.
The various complications of LASIK surgery are shown in [Table - 1]
Gulani, proposed a three-level classification of postoperative complications as LASIK tissue components comprise three basic levels [Figure - 1]. They are: corneal section (Level I), interface (Level II), and ablation bed (Level III). Each corneal complication of LASIK has been assigned to its respective level. While this approach provides a fairly comprehensive overview of the possible complications during the surgical procedure, it does not address the complication of corneal ectasia seen in some eyes. This does not also address the occurrence of tear film dysfunction, and the inaccuracies in measuring the intraocular pressure (IOP) and keratometry. Gimbel et al, have suggested that LASIK complications should be classified on the basis of time of occurrence, i.e., intraoperative or postoperative. The preventive strategies, presentation and management in each case will differ such as a shifted flap detected intraoperatively might be managed with a simple repositioning, whereas a shifted flap that may present 48 hours later may require more complex care. In a study of 1019 eyes by Lin et al, 88 (8.6%) of 109 eyes had flap-related complications. But, there was no loss of best spectacle-corrected visual acuity with proper management of complications. They concluded that flap complications decrease with the surgeon's experience. A significant learning curve in the use of microkeratome was also noted by Tham and Maloney.
| Flap-related Complications|| |
When the microkeratome head stops in the middle of a pass and does not complete its full excursion across the cornea, an incomplete cut results, producing a partial or incomplete flap. An incomplete flap is reported in up to 3% of cases.
There are several causes. Physical obstruction to the smooth passage of the microkeratome can result from the lid speculum or drapes, eyelashes or other debris, a fold of conjunctiva or crystallisation of salt from intraoperative use of balanced salt solution (BSS). Another significant cause of incomplete pass is intraoperative loss of suction, since most of the newer microkeratomes stop cutting on loss of suction. Other causes include electrical failure (addressed in most newer microkeratomes which allow a completion of the cut even in the event of power failure), blockage of foot pedal or accidental interruption of its motion, accidental release of the vacuum by the surgeon or assistant activating the footswitch inadvertently during the procedure, damage to the microkeratome during handling or transport, and improper assembly or cleaning. "Galling" is another microkeratome-related problem. This is the metal-to-metal transfer caused by the frictional hot spots created by a combination of pressure, lack of sufficient lubrication and speed. A defective blade that is too thick or has a high spot (surface flaw) causes galling in the microkeratome head. This results in increased resistance during blade oscillation and can cause incomplete excursion of the microkeratome. Eyes with scleral buckling surgery and dense conjunctival scarring are at high risk of not being able to develop a sufficient suction and IOP elevation for creation of a good flap with the microkeratome.
The prevention of incomplete flap would require meticulous attention to microkeratome assembly, cleaning, handling, and storage. Intraoperative care includes careful choice of speculum, draping of lid margins and lashes, and avoiding obstruction to the smooth translation of the microkeratome head. During surgery the use of a protected power supply and creation of protective housing for the vacuum footpedal can help avoid the inadvertent release of vacuum. Routine inspection of microkeratome blades under the operating microscope prior to instrument assembly to detect any flaws in the blades help reduce galling. Regular half yearly servicing of the instrument is recommended. It is important to run the microkeratome through a complete cycle prior to every use to ensure its smooth functioning.
The management depends on the extent of uncut flap and location of the hinge of the reflected flap. If the reflected flap hinge is at the periphery of the planned treatment zone, one can proceed with laser if the flap hinge can be shielded with a moist sponge during ablation. However, this approach can result in flattening and irregular astigmatism adjacent to the hinge., A tethering effect of the hinge on the adjacent cornea is the probable cause. Reducing the optic zone of ablation may also be considered to fit this smaller treatment space; but if the patient's scotopic pupil size is larger than the ablation zone, the result is not gratifying. It is suggested to continue with manual dissection of the flap to its full extent using a lamellar dissection blade, of course with great care to maintain the same lamellar plane. The ablation may then be performed with the originally planned optic zone or one that is slightly smaller. However, this is technically difficult and can result in irregular astigmatism. If the hinge is in the central 5-6mm of the cornea, the most appropriate option is to reposit the flap and postpone laser ablation.
Various studies have discussed the timing of retreatment after a partial flap and most suggest a two-three month delay before retreatment, [3, 4, 9, 10] A greater delay might increase the safety of retreatment, but may not be acceptable to the patient, especially when the other eye has received LASIK, resulting in anisometropia. In one of the authors study (SKR), retreatment after a partial flap was suggested a month after the initial procedure, provided the corneal flap had healed and the refraction was stable. A thicker corneal flap was advised during retreatment. A delay up to 3 months was suggested in patients with a thin cornea and/or high myopia, in whom a thicker flap is not appropriate during retreatment. It also appears that a smaller flap during retreatment is safer as any slivers of tissue would remain in the recut host bed, rather than in the flap where there is a greater chance of being dislodged and lost.
A free cap is a free corneal flap without a hinge. Failure to ensure a proper fit of the stop mechanism of the microkeratome may lead to the formation of a free cap. Currently available microkeratomes have a built-in stop mechanism that seldom gives rise to a free cap. All the same, free caps can occasionally occur with these instruments due to anatomic reasons. Gimbel et al described occurrence of free cap during surgery in eyes with very flat (<41D) corneal curvature. A smaller area of the cornea is usually exposed to the microkeratome blade in these cases, resulting in a free cap. Reduced intraoperative
IOP during flap creation can also produce this complication. A free cap that results from loss of suction is very thin and different from an even-thickness free cap caused by a defective stop mechanism. Rarely, lifting of the suction ring with the dehydrated flap adherent to it, can result in total detachment of the flap from the cornea.
The free cap should be kept covered in the microkeratome or carefully placed in an anti-desiccation chamber with the epithelial side down, on a drop of BSS, and the anti-desiccation chamber closed. The stromal bed ablation is performed as usual and then the flap is carefully replaced with the use of Barraquer perforated spatula using the reference marks to guide its relocation with the stromal side down. Gimbel et al advocate the routine use of double-circle markings with different size circles to aid in realignment, if a free cap occurs. Free flaps usually position well if carefully handled but it may be prudent to wait at least 5 minutes to ensure adequate adherence of the flap to the stromal bed. The patient should be reexamined at the slitlamp after 2 hours to ensure that there is no flap displacement. In some patients, a bandage contact lens may be used for the first 2-3 days to promote re-epithelialisation and flap adherence. In patients with very oedematous flaps or in the event of flap displacement, a continuous 8-bite anti-torque nylon suture should be placed. Rarely an external compression type suture is needed. If the flap is lost, the epithelium is simply allowed to heal, but this is likely to lead to significant stromal scarring and a hyperopic shift in refraction. In this event, a donor flap can be created from a donor eye using the microkeratome and this can be sutured to the recipient stromal bed.
Thin flaps and buttonholes
Thin flaps and buttonholes can result from application of inadequate suction, loss of suction during the procedure, irregular corneas, poor blade quality or its reuse, and machine malfunction. [6,12] Corneas that are steeper than average (>48D) may be prone to buckling when excess tissue is compressed beyond applanation by the footplate of the microkeratome. The microkeratome may perform a complete pass, but the resultant flap may have a central thinning or a full thickness hole [Figure - 2]. Use of a poor quality blade or the presence of debris that interferes with blade movement may form narrow ridges on the stromal bed. Conjunctival chemosis and oedema caused by repeated applications of the suction ring to achieve optimal corneal centration, can contribute to loss of suction during the cut. Alteration in the speed of advancement of the microkeratome along the track, insufficient elevation of IOP, small lid fissure and uncontrolled blinking by the patient are other risk factors responsible for such a complication.
The occurrence of this complication can be reduced by proper preventive maintenance of the microkeratome. Care should also be taken during evaluation. Patients with very steep corneas or those in whom LASIK is being performed after an earlier PRK should be cautioned about the increased risk of this complication in such eyes. A separate assembly if used for each eye might also prevent formation of thin flap.
Gimbel et al, suggested that in presence of a full thickness hole, the ablation should be deferred. The flap should be carefully replaced and retreatment scheduled 3 to 6 months after stabilization of the corneal surface. During retreatment, a different depth plate is used to create a thicker flap. In the case of a thin flap without full thickness hole, but has faint ridges on the bed, an alternative approach is to proceed with the ablation if the ridges are outside the 5mm to 6mm zone. A thin flap, which is irregular, can lead to an irregular astigmatism and can also increase the risk of epithelial ingrowth. In such cases, laser ablation should be aborted, the flap replaced and a re-cut planned with a thicker depth plate 3 months later.
An alternate approach is "transepithelial keratectomy" suggested by Wilson et al. In this procedure, surface PRK is done, without mechanical removal of the corneal epithelium. Ideally, this procedure is best performed within a month of the flap hole. When performed after complete healing of the buttonhole and scarring of the edges results in increased corneal haze and suboptimal outcome.
Up to 2% of flap dislocation or subluxation is reported in different studies.,,, In dislodged flaps, the corneal flap is almost always in contact with the underlying bed. Poor flap adherence can lead to decentration or irregularity in the flap surface. If the patient squeezes the eyelids while the drapes and speculum are removed, it can lead to a shifted flap. Flap dislocation usually occurs following trauma. In the first 24 hours after LASIK, flap dislodgement presumably occurs as a result of mechanical disruption due to blinking, lid squeezing, eye rubbing, etc.Flap dislodgment as a late event can occur following a variety of injuries. Both late occurrence and late repair usually lead to poor outcome. Speaker has proposed a classification of LASIK-related corneal flap complications and management based on the time of presentation following the original procedure [Table - 2].
A displaced or subluxated flap should be considered an emergency. The flap should be repositioned as early as possible to prevent formation of fixed folds and epithelial ingrowth. The flap should be lifted and its undersurface and the stromal bed thoroughly examined for epithelial cells and debris.Three to four minutes of drying time should be allowed to ensure good adherence. Application of a contact lens for a few days may provide added protection against further displacement. In a completely detached flap, repositioning might be difficult once the surgical landmarks are lost and such situations may warrant suturing of the flap. Improper repositioning of the flap can result in irregular astigmatism. Prolonged drying, use of a compression bandage and routine use of an eye shield on the first postoperative day may reduce the rate of subluxation of the LASIK flap.
A corneal perforation during creation of the flap is a devastating intraoperative complication. It can result from improper seating of the thickness plate or failure to install it. The microkeratome blade without the restraint of the thickness plate can perforate the cornea during the pass. Because the IOP is high during this particular manueovre, this could result in expulsion of intraocular contents, including lens and vitreous. This can also be seen in corneal ectatic disorders. Inadvertent corneal perforation is not usually seen with newer microkeratomes that have a pre-assembled fixed thickness plate. Corneal perforation has also been reported during laser ablation.This could result either from improper calculation of the depth of the stromal bed or excessive dehydration of the bed, leading to compaction of the stromal lamellae.
Once the cornea is perforated, the suction should be turned off immediately and the procedure terminated. Depending on the severity of complication, repair may include suturing of the cornea, reconstruction of the anterior chamber or a lensectomy/vitrectomy. Small corneal perforations can be managed with conservative means. Soft contact lens is placed on the perforation and the eye is patched, topical antibiotics and oral carbonic anhydrase inhibitor prescribed for one week. In a rabbit model, the corneal wound healing pattern following corneal perforation during LASIK surgery was found similar to that after an uncomplicated LASIK procedure.
Corneal epithelial defect
Corneal epithelial defects during LASIK results from overuse of topical anaesthetic drops, trauma by the corneal markers, the suction ring, passage of the microkeratome over the corneal surface, dehydration and drying of the flap, or minor trauma induced by forceps or spatula. These require prompt management to prevent prolonged exposure of the underlying stromal tissue, which could lead to stromal melting and infection. Such problems may also be seen in eyes that have manifest or subclinical basement membrane dystrophy abnormalities. Should an epithelial defect occur towards the peripheral part of the flap the risk of stromal oedema increases. This in turn may reduce flap adherence and predispose to epithelial ingrowth locally. These eyes also have greater risk of developing interface inflammation. Late onset diffuse lamellar keratitis (DLK) is often associated with epithelial defects and it has been found that epithelial defects of any size increases the risk of DLK.
Lubrication of the area before the microkeratome pass helps prevent epithelial defects. The use of preoperative topical anaesthetics should be minimal and careful screening for anterior basement membrane dystrophy is mandatory.
Intensive use of preservative-free lubricants with antibiotics is optimum if the epithelial defect is less than 3 mm. Smirennaia et al. recommend use of bandage soft contact lens in eyes with epithelial defect of more than 3 mm in size. Bandage soft contact lens can be used for smaller epithelial defects as well, as it brings comfort to the patient and enhances healing of the epithelial defect. After the epithelial defect heals, it is critical to support the corneal surface with preservative-free lubricants (eye drops 6 to 8 times during the day and ointment at bedtime) to allow the hemidesmosomal attachments to form. Failure to do this can lead to the development of a recurrent corneal erosion syndrome with its attendant complications.
The incidence of flap striae after LASIK reported in various series ranges from 1.1 to 3.5%. [4, 13, 23, 31, 32] Flap striae are classified into two types. Macrostriae appear as multiple, parallel straight lines on retroillumination and are a result of flap dislocation. These striae can cause reduction of vision. Microstriae are related to the flap setting, not slipping. Slitlamp examination with retroillumination is extremely useful in detecting the striae [Figure - 3]. Faint striae not visible on retroillumi-nation can be detected by the uneven pooling of tear film with cobalt filter examination after instilling fluoroscein. Horizontal striae are more commonly seen with nasally hinged flaps, and vertical folds are characteristic of superior hinges. Visual acuity is usually reduced by 2 or 3 lines and may be partially improved by artificial tears or a contact lens.
The variety of causes of flap striae include misalignment of the corneal flap after flap replacement, flap desiccation and contraction during laser ablation, flap wrinkling during stretching, movement of the corneal flap on the first postoperative day, or the tenting effect of the corneal flap over the ablated stromal bed During the reflection of the flap, care must be taken to preserve the convexity of the flap. With a superior hinge, the reflected flap is placed with the epithelial surface in contact with the superior bulbar conjunctiva. Since the curvature of the epithelial surface is convex and the superior globe also has the same curvature, approximation of the two surfaces is produced by bending the flap against its natural curvature. This can theoretically result in damage to the architecture of the Bowman's layer and the anterior stromal lamellae in the flap, which may increase the chances of striae formation. To decrease the incidence of this problem, a Chayet ring can be placed at the limbus after the flap is cut. When the flap is reflected, it will then rest against the sponge, thereby preserving its curvature. Misalignment of the flap can occur when the flap is initially repositioned after the laser treatment or if the flap is moved in the early postoperative period. Even a properly positioned flap may move while removing the drapes, eye speculum or when the patient rubs the eye. Striae are more common with unusually thin or thick flaps, irregular flaps, free caps or epithelial defects. When the flap is reflected back in preparation for ablation, the flap may dry out resulting in wrinkles and shrinkage. Flap stretching can occur with excessive manipulation of the flap as it is repositioned.
Despite attention to all the above details, two factors inherent to the procedure may predispose the eye to flap striae formation. The creation of a stromal ablation in the bed in highly myopic patients results in a central depression. When the flap is reposited, it has to seat itself over this depression, and this may produce striae due to alteration of normal anatomy. Obviously, this would be more pronounced in a deeper ablation, as done in high myopia. There is also a tendency for the cut flap to retract towards the hinge and this may also lead to striae formation.
Gentle flap manipulation can decrease the incidence of striae. The flap must be reflected back carefully during the ablation and hydration. While repositioning, the flap has to be realigned carefully at the marks. Adequate time, from 30 seconds to 5 minutes, should be allowed for the flap to adhere. The blink and striae test will help determine whether the flap has adequately settled. To prevent dislocation of the flap while removing the eyelid speculum and drapes, it is helpful to have the patient look straight and not to squeeze the eyelids. Various instruments to compress and applanate the flap at the end of the procedure to reduce the incidence of striae have been developed, although their efficacy is variable.
Care must be taken to ensure a minimal peripheral gutter at the flap margins, as this ensures proper positioning of the flap. Stroking the flap with a wet weck cell sponge would 'iron out' the flap and ensure good apposition. The use of a 12 to 6 o'clock movement would be ideal in the case of a superiorly hinged flap, to ensure 'macro' flap alignment. Further stroking of the flap, using a radial centrifugal movement, at different meridians across the flap edge would perhaps provide greater 'micro' flap alignment.
It is often considered that the movement of the lid against the reposited flap provides the most physiological approach to flap repositioning. It is suggested that the flap be floated into position, and minimally stroked with a wet sponge to squeeze out interface fluid. After about 30 - 45 seconds, the speculum is removed and the lid is used to massage the flap against the stromal bed to achieve good apposition. Some surgeons feel that a soft contact lens applied at the end of the procedure helps reduce the incidence of striae, whereas others feel that it increases the risk of wrinkles.
Central striae or any striae that affect visual acuity, quality of vision or cause irregular astigmatism are indications for treatment. Striae should be treated early as delay causes considerable difficulty. If they are identified on the first postoperative day the flap should be lifted, refloated and repositioned. Striae not treated with this technique or that have been present for longer than 24 hours, may require additional techniques.
Probst and Machat recommend careful identification of the extent and direction of the striae using retroillumination. The flap edge is then marked to ensure that the realigned flap is not in the same position as before repositioning. The flap is dissected free of the stromal bed, and the undersurface of the flap is hydrated with balanced salt solution. The hydration effect causes the flap to expand and oedematous, that makes it malleable for removal of flap striae. The flap is floated back into position and allowed to adhere for 3-5 minutes. The side of a blunt forceps is used to stretch the striae in a perpendicular direction with a downward and outward motion. This must be carried out for several minutes and performed on both sides of the striae. The eye is taped shut and the cornea examined after 20 minutes. Pannu has suggested a technique where the reflected flap is not hydrated. It is smoothened with a Caro iron and is then floated back into position. A therapeutic soft contact lens is placed on the eye and the eye is not taped shut.
Hypotonic saline (1: 1 mixture of saline and water) or deionised water is used to hydrate the flap before it is repositioned without stretching. Gimbel et al described suturing the flap and leaving the sutures in place until adequate flap stromal adhesion has occurred. Steinert believes that the microstriae represent folds in the Bowman's layer that fibrose progressively, therefore becoming more difficult to remove with time. Sterile distilled water is placed on the cornea and the epithelium over the striae can be wiped off with Merocel sponge [Figure - 4]. After application of additional distilled water to the denuded areas of the cornea, the striae usually resolve. Forceps may be used to break the fibrosis in Bowman's membrane by applying force across the striae. Occasionally the flap is lifted to break the fibrosis, but it is not hydrated.
| Epithelial Ingrowth|| |
The mechanisms by which the epithelial cells migrate to the interphase are 1) microkeratome blade mechanically dragging the cells into the interphase during keratectomy; 2) irrigation of the stromal bed after ablation carrying the floating epithelial cells into the interphase; 3) the cells of the surface epithelium growing into the lamellar interface at the junction of the flap; and 4) outgrowth from epithelial plugs in eyes with previous incisional keratotomy.,
The risk of epithelial ingrowth is higher after hyperopic LASIK, particularly when the ablation strikes the edge of the cut flap and after enhancement surgery. Important risk factors for epithelial ingrowth include peripheral epithelial defects, poor flap adhesion, perforated corneal flap and free cap. Poor or improper adhesion of the flap will encourage migration of the epithelial cells into the interface. The various risk factors for epithelial ingrowth include anterior basement membrane dystrophy, postoperative epithelial defects, postoperative inflammation, postoperative flap slippage, previous radial keratotomy, previous corneal surgery and history of ingrowth in the fellow eye.
Although isolated nests of cells will disappear without consequences, ingrowth that is contiguous with the flap edge can progress to involve the visual axis and result in flap melting. A combination of nutritional and inflammatory mechanisms have been proposed as a mechanism for flap melting in epithelial ingrowth. Flap necrosis may occur due to interference with the supply of glucose to the epithelial cells and keratocytes in the superficial corneal layers. Additionally, following a complicated LASIK procedure, cytokines released by epithelial cells induce corneal fibroblasts to produce plasminogen, collagenases, or other proteases in significant amounts and this can cause keratolysis of the flap.
The typical appearance of an epithelial ingrowth is that of a tongue or peninsula extending from the cap edge in a whorl or finger-like pattern [Figure - 5]. Connection to the outside epithelium might be conspicuous or undetectable at the slitlamp. Most isolated nests will disappear without consequences. Of greater concern is the epithelial ingrowth that is continuous with the flap edge. This can progress to involve the visual axis with irregular astigmatism and overlying flap melting. Epithelial ingrowth at the interface is more common after enhancement procedures as lifting of the flap can induce adjacent epithelial abrasions with increased cell proliferation.,.
If detected early, epithelial ingrowth is seen as faint gray line extending less than 2 mm from the flap edge best detected by direct focal tangential slitlamp illumination. It is white to gray in colour with white to gray areas of stromal haze, accompanied with irregular fluorescein staining or pooling. Surface irregularities may be seen on topography. In nasal flaps, the epithelium is usually seen in superior and inferior temporal regions whereas in cases of superior hinge they are seen temporally, inferiorly or along the hinge. The patient may have mild foreign body sensation or reduction in vision. Haze and scarring from the ingrowth which extends near the visual axis can be associated with the complaints of glare, ghosting and halos.
Stages of epithelial ingrowth
Grade 1 :-Thin ingrowth, usually one to two cells thick, non-progressive limited to within 2 mm of the flap edge and often difficult to detect.
Grade 2 : Thicker ingrowth, discrete individual cells, easily detected by slitlamp, and usually more than 2mm in extension. Grade 2 requires non- urgent treatment within 2-3 weeks.
Grade 3 : Very pronounced and thickened ingrowth, several cells deep, white geographic areas of necrotic epithelial cells. Progression will result in large areas of flap melting. Confluent haze develops peripheral to the flap egde, as the flap pulls away leaving the exposed stromal bed in contact with surface epithelium. Urgent treatment is required as abnormal flap edges invite recurrence of epithelial ingrowth and reinitiate the cycle.
The risk of epithelial ingrowth can be decreased by taking the following precautions during surgery: 1) use of suction (aspirating) lid speculum; 2) careful irrigation of the interface and sponging of the surface; 3) use of bandage contact lens to prevent flap dislodgement, since partial lifting or microtrauma to the flap edge by the lids during the early healing period may be one source of epithelial ingrowth into the interphase; 4) lifting the flap edge with a forceps rather than extensive edge dissection around the flap circumference using a spatula or similar instrument. Such a procedure, termed 'rhexis of the flap' will also provide a more even epithelial margin on the flap and stromal bed, avoiding the irregular edges that often result after blunt dissection; 5) treatment of epithelial defects with the bandage contact lens especially when the defects are adjacent to the flap; 6) preservation of the integrity and health of the epithelium. Minimal use of local anaesthetic and adequate lubrication when the microkeratome pass is made, would help protect the epithelium; 7) production of sufficient suction before microkeratome pass. If the suction is not sufficient, then a sharp edge that could serve as a barrier to the epithelial ingrowth may not be obtained; 8) lastly, one should consider PRK rather than LASIK in patients with a history of poorly adherent epithelium (history of recurrent erosions), or there is history of epithelial defect occurring during LASIK in the first eye, especially if the myopia is less than 4 to 5D.
Indications for treatment are documented progression of epithelial ingrowth, disturbance of the corneal flap and loss of best corrected visual acuity. Grade 2 and 3 epithelial ingrowths should be treated as soon as possible to avoid progression and stromal melting. These flaps are easy to lift because of the presence of the epithelium. Non-progressive isolated epithelial cells should be monitored. Hyperopic shift is an early indication of possible underlying stromal melt. The treatment consists of the following modalities.
- 1. Scraping the bed and the flap with a number 15 blade on Bard Parker knife or with a special instrument like Yaghouti LASIK polisher. Sharp debridement is preferred. A dry surgical spur is useful to scrub the stromal surfaces. The edges of the flap and along the periphery of the stromal bed are the primary sites to clear the epithelial remants. A bandage contact lens may be required if the surrounding epithelium has been denuded during the debridement
- 2. In small peripheral ingrowths with no flap abnormality, a spreader can be used with the patient seated at the slitlamp to try milk the cells out under direct visualisation.
- 3. If epithelial ingrowth recurs, short pulses of excimer laser (5 to 10 pulses) PTK can be used to ablate both surfaces and any nests of epithelial cells not removed by scraping. Once a flap melt has occurred treatment is often not necessary as the epithelium trapped underneath the flap has broken through the corneal surface, and hence further progression will not occur. LASIK enhancements by lifting the flap after a flap melt are considerably more difficult, as the flap is extremely adherent in the area where the flap melt has occurred.
- 4. After denuding the epithelial remnants, both the bed and undersurface of the cap are treated with absolute alcohol soaked in a merocel sponge for 30 seconds. The flap is then replaced and floated. Haze may be seen. Recently, Domniz et al, have cautioned against the use of 100% alcohol that can cause photophobia and inflammation resulting in scarring and cap melting. Instead they advised use of 10% alcohol on a foam surgical spear in cases of recurrent epithelial ingrowths.
| Diffuse Lamellar Keratitis (DLK)|| |
In diffuse lamellar keratitis (DLK), a diffuse infiltrate is seen under the flap without signs of microbial infection [Figure - 6]. Usually it occurs within a week of surgery. Isolated cases occurring in the late postoperative period have been reported., It was first described as a distinct entity by Maddox (ASCRS 1997 meeting). The first published report appeared in 1998 by Smith and Maloney. They described the condition as a peculiar noninfectious inflammatory reaction in the lamellar interface occurring in the first week after LASIK. In their initial report of 13 eyes the condition disappeared spontaneously in a few, while in others it caused scarring. This condition is also known as "Shifting Sands" or "Sands of Sahara" syndrome, because of the white granular appearance with waves of increasing density. Cellular reaction is evident within the first 24 hours and the white granular appearance is more prominent in the periphery.
DLK can occur sporadically or as a cluster of cases. The various causes for DLK in the early postoperative period include talc from gloves, oil, wax, metallic fragments, silicates, bacterial endotoxins, epithelial defects, substances produced by laser ablation, particles from eye drape, Meibomian gland More Details secretions and povidone iodine. Kaufman et al demonstrated that cleaning off the deposits from microkeratome blade with acetone prevent DLK. The infiltration of cells is due to accumulation of mononuclear cells and granulocytes in the flap interface.
Bacterial endotoxins are also associated with the development of DLK. Endotoxins released by gram-negative bacteria like Burkholderia picketii are present widely in water supplies and in operating room environment. They are stable to short cycles of steam sterilisation, as is used with most LASIK procedures. Steriliser reservoirs represent an ideal environment for the creation of biofilms on the inner linings and tubes. Bacteria released from the biofilms in the steriliser reservoir are killed with the sterilisation process, but the endotoxins may persist and coat instruments. Introduction under the LASIK flap can incite an inflammatory response. Meibomian gland debris has a glistening oily appearance, unlike the flat, white granular appearance of DLK. Late cases of DLK are associated with epithelial defects.
[TAG:2]Stages of DLK[/TAG:2]
Stage 1- White granular cells in the periphery of the lamellar flap, outside the visual axis.
Stage 2- White granular cells involving the visual axis. This is more frequently seen on day 2 or 3 and is the result of central migration of cells. It leads to the "Sands of Sahara" syndrome.
Stage 3- Dense, white, clumped cells in the visual axis with relative clearing of the periphery. There is decrease in visual acuity by 1 or 2 lines. The cellular reaction may settle inferiorly because of gravity. If left untreated, scarring could occur.
Stage 4- Severe lamellar keratitis. Stromal melting and permanent scarring is the likely result.
| Treatment|| |
Stage 1 and 2 are treated with prednisolone eye drops every hour and corticosteroid ointment at bedtime. Intensive corticosteroid therapy should be given for at least 3 days. Follow-up in 24 to 48 hours will identify the minority of cases which progress to stage 3. Stage 3 is treated by lifting the flap and debulking the inflammatory response. Caution has to be exercised here as the flap is inflamed and friable. The bed and the undersurface of the flap should be carefully irrigated on day 2 or 3 with BSS on a blunt canula. Washing the interface cleans out the proteolytic enzymes deposited by neutrophils, thus limiting tissue destruction, and also removes the inciting agent. Topical corticosteroids need to be continued.
In stage 4 DLK, aggregation of inflammatory cells and release of collagenases result in fluid collection in the central lamellae with overlying bullae formation and stromal volume loss. Central tissue loss may lead to the appearance of corrugated mud cracks resulting in hyperopic shift. Lifting of the flap and irrigation is of little benefit at this point as additional stromal volume loss can occur with aggressive tissue manipulation. Stromal collagen becomes boggy, gelatinous and easily damaged with even moderate manipulation. Early identification of stage 3 and appropriate management can prevent this severe keratitis.
Anecdotal reports describe use of systemic corticosteroids and immunomodulators such as methotrexate with limited success. DLK associated with epithelial defects is treated with topical antibiotics and topical corticosteroids
The following precautions help prevent DLK: 1) Eyelids should be draped to cover meibomian gland orifices and eyelashes completely. 2) Powder-free surgical gloves are recommended. 3) Microkeratome head and blades should be cleaned with distilled water. 4) Motor tip should be checked for oil contamination. 5) The flap edge should be dried before lifting. 6) Immediately after surgery, all instruments should be cleaned and sterilised. 7) After the flap is replaced, the interface should be irrigated with BSS to remove particles, debris and inciting agents. 8) Prevent tear film debris from reaching the interface. In order to achieve this, a suction wire speculum can be used to constantly remove tear film debris from the ocular surface. In addition, use of a Chayet sponge at the limbus, prior to lifting the flap helps, prevent migration of such debris on to the stromal bed and interface. 9) Topical corticosteroids are given starting 12 to 24 hours after surgery for 5-7 days.
The differential diagnosis of DLK includes acute microbial keratitis, epithelial cells in the interface and non-microbial interface opacities. Acute microbial keratitis is usually associated with pain, redness and decreased vision. Epithelial defect with inflammatory cells in the anterior chamber is the rule.
| Dry Eyes|| |
It is now believed that the ocular surface (cornea, conjunctiva, accessory lacrimal glands, and meibomean glands), the main lacrimal gland, and the interconnecting neural reflex loops comprise a functional unit whose parts act together. The coordinated functioning of the various components described above results in normal tear function, vital to the health and comfort of the eye. Corneal innervation is considered essential for normal tear secretion which is in part, if not wholly, reflexive. Sensory loss causes decreased tear secretion and, when bilateral, reduces the blink rate. Corneal refractive surgical procedures can result in marked postoperative hypoesthesia, thus interfering with tear function.
Contradictory reports exist in literature regarding the effect of excimer laser surgery on corneal sensitivity. There are reports of both hyperaesthesia and hypoaesthesia., Recovery of corneal sensation is reportedly better following LASIK than PRK. Studies in the rabbit cornea indicate that at 5 months after LASIK, the epithelial, subepithelial, and anterior stromal innervation attain an almost normal nerve density and architecture. All studies also have documented a decrease in tear secretion following PRK and LASIK though the tear film stability appears unaltered. Myopic patients with poor preoperative tear function (Schirmer test values less than 10 mm) have a significantly greater risk (relative risk: 1.58) of experiencing dry eye symptoms one month after LASIK surgery.
The probable causes of tear film abnormalities after PRK and LASIK include corneal denervation in the ablation zone, operative trauma to the epithelium, toxicity from topical eye drops, inflammatory response to surgery with release of cytokines and inflammatory mediators,, poor blink rate, altered corneal contour, poor quality thin lipid layer, and alterations in tear evaporation rate and osmolarity.
Since the tear secretion system (the conjunctival tear secreting glands and the lacrimal gland) is not affected by LASIK, most of the changes should stem from the alteration in the afferent arc of the tear secretion pathway. Both PRK and LASIK damage the corneal nerves in the region of the ablation (central 6 to 7 mm of the cornea). There are two fundamental differences between LASIK and PRK. They are (1) deeper corneal ablation (130-180 μm: usually 160 μm) and (2) creation of hinged corneal flap in LASIK procedure. The peculiar arrangement of corneal nerves beneath the Bowman's layer, explains greater loss of corneal sensitivity in LASIK (deeper transection) procedure. But this is partly compensated with the preservation of nerve function in the uncut portion of the hinged corneal flap. Since a significant amount of corneal sensation is preserved due to the intact nerves in the hinge of the corneal flap, it could be debated whether a nasally hinged flap is better than a superiorly hinged flap, since the long ciliary nerves enter the corneal stroma at 3 and 9 o'clock meridians. The effects of corneal denervation on the ocular surface are even less clear. Preoperative tear insufficiency has been postulated to be a risk factor for overcorrection and haze formation after PRK. The role of the precorneal tear layer as a permeability barrier that is essential for maintaining a smooth quality optical surface is well documented, and hence eyes with significant tear dysfunction after LASIK are less likely to achieve optimal visual function. The altered central corneal contour after myopic laser refractive surgery is less efficiently resurfaced by the lid blink mechanism and, in conjunction with altered tear function, this can further compromise corneal epithelial health and function.
Diffuse punctate staining of the LASIK flap is the usually seen clinical sign [Figure - 7]. With our current understanding of alterations in tear function after PRK and LASIK for myopia, it appears reasonable to recommend the use of non-preserved tear substitutes in the postoperative period after surgery. In patients who have severe symptoms after surgery and or those in whom significantly decreased tear function is noted preoperatively, punctual occlusion may improve patient comfort and optimise visual function. The cornea and ocular surface seem capable to adapt to above mentioned postsurgical alterations. The changes themselves are temporary, although the exact time for restoration of normal anatomy and physiology are yet unknown.
| Corneal Ectasia|| |
Corneal ectasa as a postoperative complication of LASIK manifests as an area of non-inflammatory, progressive corneal
thinning in the area of ectasia with unstable topographical steepening. It is associated with reduction of unaided or spectacle-aided visual acuity.
Iatrogenic keratectasia is the most serious late complication following LASIK. Altered biomechanics of the cornea following lamellar refractive surgery predispose it to ectasia despite normal IOP. The strength of cornea following LASIK is determined by the residual stromal bed thickness. While the minimal residual stromal bed thickness required to withstand ectasia varies from individual to individual, a range of 250-300μm is recommended by most surgeons. The two most common risk factors predisposing to ectasia following LASIK are treating forme fruste keratoconus, and not adhering strictly to minimal residual stromal bed thickness, particularly in high myopes. Thin corneas, eyes with abnormal corneal topography, or a combination of both also seem to be factors involved in corneal ectasia.
A computer simulated corneal model and an eye bank study, are also available. Based on these studies it was concluded that the area of corneal ectasia is larger with smaller optical zones and vice versa. Geggel and Talley have studied the histopathological features of the ectatic cornea without keratoconus; the light microscopy did not reveal any inflammation, suggesting a biomechanical weakening as the cause for ectasia.
Three intraoperative pachymetry readings: before raising corneal flap, after raising the corneal flap and after stromal ablation seems helpful. This enables the surgeon to modify the laser ablation parameters in order to leave behind the desired minimal residual stromal bed. This is particularly relevant since there are considerable variations in the actual flap thickness obtained using a microkeratome.
In the view that the patients have undergone LASIK to avoid spectacle and contact lens wear, management of corneal ectasia is difficult. All the same, the first choice in the management of corneal ectasia following LASIK is rigid gas permeable contact lens wear. Spherical and toric soft contact lenses may be tried in selected cases. Penetrating keratoplasty is recommended in rare situations where contact lenses cannot provide clear vision or cannot be stabilised due to the stromal irregularity.
Although the reports on corneal ectasia following LASIK are rare, there is a growing concern regarding the biostability of the cornea in the late postoperative period. Also, the introduction of new topographic tools have enabled us to observe the posterior corneal curvature changes following LASIK. Seitz et al have reported posterior corneal curvature changes suggestive of mild "keratectasia" in the early postoperative period even in eyes with residual bed thickness of greater than 250μm. This raises concern about the long-term safety of LASIK and a possibility of creating an epidemic of "iatrogenic keratoconus". High-frequency ultrasono-graphic corneal analysis will probably offer a better tool to evaluate cases of poor postoperative visual function with unexpected ectasia.,
In view of the above, it may be prudent to avoid LASIK in high refractive errors when the corneal thickness is reduced. In such patients, alternatives such as phakic IOL, refractive lensectomy with IOL implantation or combination of LASIK with other procedures (Bitorics) in order to limit significant corneal tissue loss, may be considered.
| Ablation Problems in LASIK|| |
Successful outcome following LASIK is not just achieving a unaided visual acuity of 6/6. Quality of vision can be impaired by loss of contrast sensitivity, halos, night vision problems, uniocular diplopia and other optical aberrations. Improved patient satisfaction can be achieved through a better understanding and management of these optical problems.
| Irregular astigmatism|| |
Broadly, the irregular astigmatism can be categorised into preoperative (preexisting), peroperative (induced) and postoperative causes. Patients with keratoconus, high myopia and corneal scars have preexisting irregular astigmatism and are best avoided from treatment with the existing technology. Intraoperative causes include poor laser optics, irregular hydration of stromal bed, central islands, ablation decentration and flap-related problems, flap decentration, hinge ablation, poor flap alignment (buttonholes, lost flap, etc.). Postoperative irregular astigmatism may result from corneal ectasia or flap displacement (folds and wrinkles). A significant percentage of patients undergoing LASIK may have loss of BCVA secondary to irregular astigmatism. Treatment is directed to the underlying cause.
| Decentration|| |
Misalignment of the laser treatment over the patient's entrance pupil or involuntary eye movement of the patient during the laser treatment can result in ablation decentration.
Although current active eye-tracking systems overcome the effects of patient eye movement to a large extent, studies have shown that patient cooperation during the procedure is essential for well centered ablation. Irregular astigmatism, monocular diplopia, ghosting and night vision problems can result from decentration, best measured by tangential topography. Decentration is visually significant only when it is greater than 0.3mm. Administration of miotics or fitting rigid gas permeable contact lenses may be helpful in some patients. Retreatment with a small diameter (3-4mm) ablation zone at the edge of the original optical zone, decentered in the opposite direction, is useful in treating mild forms of decentration. Astigmatic keratotomy, with incisions placed outside the flap edge in the steeper meridian can reduce symptoms. Increasing the overall ablation zone diameter, after masking the original ablation zone with a modulating agent, originally described for PRK, is an alternative technique. This technique has a lower refractive effect and is hence useful in patients with minimal or residual refractive error after the initial treatment. Topography-linked or wavefront guided laser ablations could be options for the future.
| Central islands|| |
Central islands are well-circumscribed areas of higher refractive power located in the central cornea. It is better demonstrated by computerised videokeratography. Krueger and co-authors have defined topographic central islands as areas of 1.5mm in diameter and steepening of at least 3.0 D. However, most surgeons believe that any area of excessive central steepening can adversely affect visual acuity, and hence are indeed the central islands. Incidence of visually-significant central islands are reportedly greater with PRK than LASIK,, though the ones following PRK could resolve spontaneously due to epithelial remodeling. The incidence of central islands following LASIK has been reported at 5.7% with only 25% resolving over a 6-month period.
While there are many theories to explain central islands, they are primarily due to factors such as laser ablation pattern, laser software and surgical technique. Irregular profile of the delivery beam is an important cause. Older software in broad beam laser systems are particularly prone and it is rarely seen with the newer flying spot or scanning slit laser systems. Debris on the stromal bed, uneven stromal hydration or any obstruction to laser energy can result in central islands. Large ablation diameters and higher diopteric corrections increase the chances of central island formation.
Patients with central island experience ghosting, glare, uniocular diplopia and undercorrection. Corneal topography reveals a peninsula pattern with a "hot" color surrounded by a sea of "cool" colors. It is advisable to observe the patient for 3-6 months prior to undertaking any surgical intervention. At two-weekly intervals serial topographic evaluations and repeat refractions should be performed till stability is achieved although this may not be logistically feasible. Miotics are often unhelpful, while rigid gas permeable lenses may help selected patients regain lost visual acuity. If a true central island does not regress spontaneously, surgical intervention is required. Comparing the patients refractive error with the size and power of the central island on topography will decide whether Munnerlyn's equation could be used (Ablation depth = S2χ D/3; S=diameter of island in millimeters; D=desired correction in diopters). Should the power of the central island correlate with the refraction, the above equation can be used. If the power of the central island does not match the manifest refraction, the initial treatment should be based upon refractive data. If the refractive error persists despite the elimination of the central island, further ablation should be considered 3-6 months after the initial treatment. PTK may be needed in selected cases, associated with possible hyperopic shift. Currently, trials are underway to estimate the efficacy of topography-linked laser treatments. In future, wavefront analysis may play an important role in the management of various optical aberrations.
| Undercorrection and Overcorrection after Myopic LASIK|| |
Despite the current safety of LASIK procedures a tendency for under or overcorrection is not uncommon following treatment of myopic eyes. Most studies have used the manifest spherical equivalent (MSE) after LASIK as a measure of failure to achieve the intended correction. While the undercorrection is defined as MSE ≥ -1.0D at first postoperative week the overcorrection is not precisely defined. Regression is defined as a 0.25D or greater myopic shift occurring between follow-up visits.
The incidence of undercorrection and regression after myopic LASIK is generally more than overcorrection. It varies from 5% to 51%. This wide variations owes to the definition chosen and methodology adopted in various studies. The rate of regression appears to be greater with higher myopia. The incidence of overcorrection after LASIK varies between 3% and 7%.,, While overcorrections tend to trouble the patients more than residual myopia, possibly because of the increased accommodative demand, many of these eyes tend to regress towards myopia during the first year after surgery.
Pre-operative factors. The eyes of older patients could be prone to overcorrection. Regression is strongly correlated with the magnitude of the preoperative refraction and therefore, the attempted correction and ablation depth. A greater regression after primary treatment was noted in eyes with higher preoperative myopia. Most of the regression occurs within 6 months, though delayed regression up to 2 years is not uncommon. Curiously, refractive stability is apparently better after LASIK revision than after primary treatment., It is reported that eyes with flatter preoperative keratometry (< 43.50 D) tended to have greater undercorrection than eyes with similar myopia and steeper corneas (> 44.50 D).
Intraoperative factors. An association between higher humidity level in the treatment room and a greater likelihood of regression has been described. [84,90] It has been suggested that greater hydration of the stromal bed, in a higher humid environment, results in less effective ablation of tissue per unit of laser energy. However, the laser room temperature is not known to affect the outcome of the LASIK procedure.
The importance of understanding the efficacy of the individual laser system and nomogram used for treatment has been repeatedly stressed in different studies. [80,87] Programming of algorithms depending on the degree of myopia is the key to success. The newer generation laser systems incorporate fairly stringent pretreatment test protocols to ensure a stable beam profile and performance.
Postoperative factors. The undercorrection following LASIK may be due to masking and vaulting effect of the LASIK flap. The masking effect is analogous to the effect of a soft contact lens over an irregular corneal surface, which modifies the surface contour to some extent. Vaulting has been described as a tendency of the flap to retain its original curvature. If the flap does not conform to the altered stromal contour, some amount of the refractive effect would be lost. This phenomenon would be more pronounced in eyes that undergo higher refractive corrections. Recent studies have indicated that there is considerable variation in the flap thickness created by microkeratome. [91,92] This could possibly influence the refractive outcome. Severe form of DLK is related to an increased risk of regression after myopic LASIK. Central corneal ectasia is a more worrisome anatomical change noted in some eyes after myopic LASIK. The principal reason is destabilisation of the cornea by the deep lamellar cut.
Undercorrections. The undercorrections are generally treated between 6 weeks and 3 months after the primary procedure, and relies mostly on treatment of the stromal bed., One of the theoretical advantages of LASIK is the ease with which the flap can be lifted and the stromal bed retreated. However, there is an increased risk of complications like flap edge scarring, interface haze and inflammation, epithelial ingrowth and flap striae or folds following such procedures.
The preferred technique of relifting the flap is to disengage a short section of the flap using a needle or a Sinskey hook.
This may be performed just before repeat LASIK with the patient seated on a slitlamp. During retreatment, the lifted edge is held with non-toothed forceps and bent back, creating a sharp demarcation line in the epithelium.
Despite these precautions, the risk of epithelial ingrowth remains high in eyes with a history of inflammation after the first procedure. So as to avoid epithelial ingrowth, Lyle and Jin have suggested to recut rather than lift the flap.
However, recutting a flap of the same or different diameter, at the same or different thickness, using a similar or different microkeratome can theoretically produce slivers of stromal tissue due to disparity between the first and the second cut. Using individual nomograms for residual myopia after LASIK, various authors have amply demonstrated the safety and efficacy of retreatment.,
An alternative approach is the "intraepithelial photorefractive keratectomy". In this technique photoablation is performed directly on the epithelium without damage to Bowman's membrane though the amount of correction possible with this technique is limited.
Overcorrection. Overcorrection after myopic LASIK has been treated using a variety of approaches. Since most patients undergo the primary procedure to get rid of their dependence on external aids, spectacles and/or contact lens, the solutions are often unsatisfactory. Non-contact thermokeratoplasty using Ho:YAG laser, and hyperopia LASIK, are suggested treatment modalities for overcorrected myopic LASIK. Both the procedures were found safe and effective. A more conservative approach is intentional undercorrection of all myopic patients, followed by retreatment of the residual myopia, This avoids overcorrection following the first procedure.
Prevention of under or overcorrection after myopic LASIK should be the aim. Paying attention to preoperative patient parameters like estimation of the refractive error and contact lens warpage, and using a meticulous, consistent surgical technique would appear to help in decreasing unpleasant postoperative surprises.
| Microbial Keratitis|| |
Though rare, infection following LASIK is a potentially vision-threatening complication. The incidence of infection after LASIK is estimated to be 1 in 5,000. Perez-Santonja et al reported the first case of corneal infection after LASIK. This was caused by Nocardia asteroides. Subsequently various authors reported cases of bacterial and fungal infections following LASIK. [Table - 3]. Bilateral infection has been associated with human immunodeficiency virus infection. It can occur both in the early and late postoperative periods. There is a possibility of microbial contamination of the bed during surgery from eyelids, eyelashes, conjuctiva and microkeratome. The various predisposing factors for infection after LASIK includes blepharitis or dacryocystitis, dry eye, extended wear soft contact lens, HIV infection, entropion and trichiasis, iatrogenic (topical corticosteroids), anaesthetic abuse, use of contaminated drops and epithelial defects.
The usual presenting symptoms are increased light sensitivity, pain, redness and loss of vision. The clinical signs include stromal infiltrates, epithelial defects, hypopyon, odema of corneal flap and corneal flap melt. Focal inflammation beneath the flap with or without inflammatory cells in the early postoperative period should be considered an infective infiltrate. Usually the diagnosis is confirmed by lifting the flap and scraping the bed. The material is sent for microbiological investigations which include microscopy and, culture-sensitivity. Lifting the flap provides samples from the infection site with the greatest chance of obtaining a positive culture and permits irrigation of the bed with antibiotics during debulking of infected tissue.
Management of infection following LASIK is difficult because of the deep inoculation of the causative organism into stromal bed, and sequestration away from tear film. This contributes to lower therapeutic levels of antibiotics. The situation is worse in fungal infection. Culture and sensitivity is mandatory because of the high risk of resistant organisms.
After obtaining samples for microbiological investigations, the stromal bed is usually irrigated with antibiotics. Intensive fortified antibiotics and antifungal therapy is initiated. Amikacin, clarithromycin and ciprofloxacin are useful in mycobacterial infection; natamycin and amphotericin B are effective in fungal infection. In cases of resistant bacterial infection, flap removal and intensive medical therapy has been found useful. In cases of resistant fungal infection, an aggressive approach consisting of amputation of the flap, daily debridemant of the bed, intensive topical and systemic antifungals may be required Eyes not responding to medical therapy and those presenting late with large infiltrates may need therapeutic penetrating keratoplasty. Therapeutic penetrating keratoplasty possibly controls infection and restores useful vision in patients with mycobacterial and fungal infections.,, Antibiotic prophylaxis after surgery may be useful in preventing the infection.
| Interface Debris|| |
Interface debris may result from metal fragments from blade shattering during the dissection, oil material from the microkeratome, powder from gloves, air bubbles, sponge fibres, meibomian secretions or lint fibres. Lint fibers are released from clothes, eye patches used to cover the unoperated eye, and gauze close to the operative field. Interface debris may remain even after aggressive irrigation. A slit-beam attachment in the operating microscope would be very helpful in identifying such interface debris at the conclusion of the procedure. If this in not available, slitlamp examination 15-20 minutes after surgery is a suitable alternative. These particles rarely incite inflammation or affect vision. If significant amounts are present in the visual axis, the flap needs to be relifted, and the debris irrigated. If an inflammation is suspected the flap should be lifted and copious irrigation applied.
Operating in a lint-free environment, using nonfragmenting sponges, powder-free gloves, draping of the eyelashes, applying fibrocellulose ring (Chayet ring) and careful irrigation can limit this complication. Lint fibers can be minimised by the use of scrub suits by the surgical team and by having the patient wear a scrub like cover over their clothes to minimise floating fibers in the atmosphere. Moistening any gauze material in the surgical field will achieve similar result.
| Loss of Best Spectacle Corrected Visual Acuity|| |
The reported incidence of loss of two or more lines of the best spectacle corrected visual acuity (BSCVA) after LASIK is 4.8%. It is frequent with correction of large refractive errors and with compound astigmatism compared to spherical corrections. It has been associated with flap complications and hyperopic treatment., Most complications discussed in this review will potentially affect BSCVA either temporarily or permanently. Early recognition and adequate management is needed.
| Visual Aberrations|| |
Visual aberrations can permanently affect the quality of vision. The main causes for higher order abberrations resulting in glare and haloes are subclinical decentration and wide-area laser ablation profiles. Similarly when pupils dilate leading to a larger diameter than the optical treatment zone, rays of light refracted by the untreated peripheral cornea are not focused at the same position as the central rays and result in blurred circles. These symptoms are more pronounced after treatment of cylindrical errors due to oval shape of laser treatment.
In addition, correction of higher refractive errors is associated with increased aberrations due to larger refractive differential between the ablated and intact cornea. Irregular astigmatism due to flap folds, topographic abnormalities, residual myopia, dry eyes and irregular epithelial surface can also result in these symptoms.
Pupil size under photopic, mesopic and scotopic conditions should be measured preoperatively preferably with a pupillometer. Patients with pupil diameter of more than 6mm should be informed of the risk of night vision disturbances after LASIK. Larger ablation zone diameters have been associated with decreased incidence of night glare. In future, development of software allowing effective larger ablation diameter and measures to prevent decentration and central islands will also reduce the incidence of these symptoms. Enlargement of ablation zone by means of wavefront or topography-guided lasers will significantly reduce the complication of optical aberrations. These symptoms can be conservatively managed with mild miotics, which can help for driving during night. Topical brimonidine is found useful. Tinted contact lenses with artificial pupils may provide significant relief. Adequate surface lubrication may be of help. A well-centred rigid gas permeable contact lens will enlarge the optical zone and could be helpful in selected conditions.
To conclude, complications following LASIK though rare, can be sight threatening. The demand for safety for this surgery is mandated because of the fact that relatively healthy eyes are placed at risk every time the procedure is performed. Knowledge, experience, careful use and maintenance of the microkeratome can largely reduce the incidence of these complications. It is necessary not only to periodically analyse one's surgical data, but also to honestly report the complications.
| References|| |
|1.||Gulani AC. LASIK corneal complications (letter).Ophthalmology 1999;106:1457. |
|2.||Gimbel H, Penno EA. LASIK corneal complications (In reply). Ophthalmology 1999; 106:1457-58. |
|3.||Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129-36. |
|4.||Tham VM, Maloney RK. Microkeratome complications of laser in situ keratomileusis. Ophthalmology 2000;107:920-24. |
|5.||Farah SG, Azar DT, Gurdal C, Wong J. Laser in situ keratomileusis: Literature review of a developing technique. J Cataract Refract Surg 1998;24:989-1006. |
|6.||Gimbel HV. Flap complications of lamellar refractive surgery. Am J Ophthalmol 1999;127:202-24. |
|7.||Rao SK, Padmanabhan P, Sitalakshmi G, Rajagopal R, Lam DS. Timing of retreatment after a partial flap during laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1424-25. |
|8.||Rao SK, Padmanabhan P, Sitalakshmi G, Rajagopal R. Partial flap during laser in-situ keratomileusis: Pathogenesis and timing of treatment. Indian J Ophthalmol 2000;48:209-12. |
|9.||Wilson SE. LASIK: Management of common complications. Cornea 1998;17:459-67. |
|10.||Stulting RD, Carr JD, Thompson KP, Waring GO 3rd, Wiley WM, Walker JC. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999;106:13-20. |
|11.||Gimbel HV, Anderson Penno EE. Intraoperative complications. In: Gimbel HV, Anderson Penno EE, editors.LASIK Complications: Prevention and Management. Thorofare, NJ: SLACK Incorporated, 1998:47-79. |
|12.||Lam DSC, Cheng ACK, Leung ATS. LASIK complications (letter). Ophthalmology 1999;106:1455-56. |
|13.||Gimbel HV, Anderson Penno EE, van Westernbrugge JA, et al. Incidence and management of intraoperative and early postoperative complications in 1000 consecutive laser in situ keratomileusis cases. Ophthalmology 1998;105:1839-48. |
|14.||Slade SG. Lasik complications and their management. In Machat JJ, editor. Excimer Laser Refractive Surgery: Practice and Principles. Thorofare, NJ: Slack 1996;360-96. |
|15.||Probst LE, Machat J. Removal of flap striae following laser in situ keratomileusis. J Cataract Refract Surg 1998;24:153-55. |
|16.||Recep OF, Cagil N, Hasiripi H. Outcome of flap subluxation after laser in situ keratomileusis: Results of 6 months follow-up. J Cataract Refract Surg 2000;26:1158-62. |
|17.||Melki SA, Talamo JH, Demetriades AM, Jabbur NS, Essepian JP, O'Brien TP et al. Late traumatic dislocation of laser in situ keratomileusis corneal flaps. Ophthalmology 2000;107:2136-39. |
|18.||Lombardo AJ, Katz HR. Late partial dislocation of a laser in situ keratomileusis flap. J Cataract Refract Surg 2001;27:1108-1110. |
|19.||Lemley HL, Chodosh J, Wolf TC, Bogie CP, Hawkins TC. Partial dislocation of laser in situ keratomileusis flap by air bag injury. J Refract Surg 2000;16:373-74. |
|20.||Iskander NG, Peters NT, Penno EA, Gimbel HV. Late traumatic flap dislocation after laser in situ keratomileusis. J Cataract Refract Surg 2001;27:1111-114. |
|21.||Chaudhry NA, Smiddy WE. Displacement of corneal cap during vitrectomy in a post-LASIK eye. Retina 1998;18:554-55. |
|22.||Speaker MG. Prevention and management of flap dislocation. Presented at the Refractive Surgery Subspecialty Meeting, in Dallas, Texas, USA. Oct., 2000. |
|23.||Pannu JS. Incidence and treatment of wrinkled corneal flap following LASIK (letter). J Cataract Refract Surg 1997;23:695-96. |
|24.||Pallikaris IG, Siganos DS. Laser in situ keratomileusis to treat myopia; Early experience. J Cataract Refract Surg 1997;23:39-49. |
|25.||Joo CK, Kim TG. Corneal perforation during laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1165-67. |
|26.||Hori Y, Wantanabe H, Maeda N, Inoue Y, Shimomura Y, Tano-Y. Medical treatment of operative corneal perforation caused by laser in situ keratomileusis. Arch Ophthalmol 1999;117:1422-23. |
|27.||Chang SW, Ashraf FM, Azar DT. Wound healing patterns following perforation sustained during laser in situ keratomileusis. J Formos Med Assoc 2000;99:635-41. |
|28.||Smirennaia E, Sheludchenko V, Kourenkova N, Kashnikova O. Management of corneal epithelial defect following laser in situ keratomileusis. J Cataract Refract Surg 2001;17 (2 suppl.): S196-99. |
|29.||Haw WW, Manche EE. Late onset diffuse lamellar keratitis associated with an epithelial defect in six eyes. J Cataract Refract Surg 2000;16:744-48. |
|30.||Shah MN, Misra M, Wihelmus KR, Koch DD. Diffuse lamellar keratitis associated with epithelial defects after laser-in-situ-keratomileusis. J Cataract Refract Surg 2000;26:1312-18. |
|31.||Gimbel HV, Basti S, Kaye GB, Ferensowicz M. Experience during the learning curve of laser in situ keratomileusis. J Cataract Refract Surg 1996;22:542-50. |
|32.||Kulatza PV, Stark WJ, O'Brien TP. Management of flap striae. IOC 2000;40:87-92. |
|33.||Rabinowitz YS, Rasheed K. Fluorescein test for the detection of striae in the corneal flap after laser in situ keratomileusis. Am J Ophthalmol 1999;127:717-18. |
|34.||Munoz G, Alio JL, Perez santonja JJ, Attia WH. Successful treatment of severe wrinkled corneal flap after laser in situ keratomileusis with deionized water. Am J Ophthalmol 2000;129:91-92. |
|35.||Steinert RF. LASIK. Intraoperative and post-operative flap striae. In:Buratto L, Brint S editors. LASIK: Surgical Techniques and Complications. Thorofare, NJ: Slack, 2000:563. |
|36.||Helena MC, Meisler D, Wilson SE: Epithelial growth within the lamellar interface after laser in situ keratomileusis(LASIK). Cornea 1997;16:300-5 |
|37.||Melki SA, Azar DT. Lasik complications: Etiology, Management, and prevention. Surv Ophthalmol 2001;46:95-116. |
|38.||Maloney RK. Epithelial ingrowth after lamellar refractive surgery. Ophthalmic Surg Lasers 1996;116:27 S 535 |
|39.||Castillo A, Diaz-Valle D, Gutierrez AR, Toledano N, Romero F. Peripheral melt of flap after laser in situ keratomileusis. J Refract Surg 1998;14:61-68. |
|40.||Perez-Santonja JJ, Ayala MJ, Sakla HF, Ruiz-Moreno JM, Alio JL. Retreatment after laser in situ keratomileusis.Ophthalmology 1999;106:21-28. |
|41.||Wang MY, Maloney RK. Epithelial ingrowth after laser in situ keratomileusis. Am J Ophthalmol 2000;129:746-51. |
|42.||Domniz Y, Comaish IF, Lawless MA, Sutton GL, Eckshtein R, Collins MB, et al. Epithelial ingrowth: Causes, prevention and treatment in 5 cases. J Cataract Refract Surg 2001;27;1803-11. |
|43.||Godinich AC, Steinert RF, Wu HK. Late occurrence of diffuse lamellar keratitis after laser in situ keratomileusis. Arch Ophthalmol 2001;119:1074-76. |
|44.||Keszei VA. Diffuse lamellar keratitis associated with iritis 10 months after laser in situ keratomileusis. J Cataract Refract Surg 2001;27;1126-27. |
|45.||Smith RJ, Maloney RK. Diffuse lamellar keratitis: A new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721-26. |
|46.||Kaufman SC, Maitchouk DY, Chiou AG, Beuerman RW.Interface inflammation after laser in situ keratomileusis. Sands of Sahara syndrome. J Cataract Refract Surg 1998;24:1589-93. |
|47.||Buhren J, Baumeister M, Kohnen T. Diffuse lamellar keratitis after Laser in situ keratomilusis imaged by confocal microscopy. Ophthalmology 2001;108:1075-81. |
|48.||Holland SP, Mathias RG, Morck DW et al. Diffuse lamellar keratitis related to endotoxins released from steriliser reservoir biofilms. Ophthalmology 2000;107;1227-33. |
|49.||Linebarger EJ, Hardten Dr, Lindstrom RL. Diffuse lamellar keratitis: Diagnosis and management (review). J Cataract Refract Surg 2000;26;1072-72. |
|50.||Stern ME, Beuerman RW, Fox RI, Gao J, Mircheff AK, Pflugfelder SC. The pathology of dry eye: The interaction between the ocular surface and lacrimal glands. Cornea 1998;17:584-89. |
|51.||Kanellopoulos AJ, Pallikaris IG, Donnenfeld ED, Detorakis S, Koufala K, Perry HD. Comparison of corneal sensation following photorefractive keratectomy and laser in situ keratomileusis. J Cataract Refract Surg 1997;23:34-38. |
|52.||Perez-Santonja JJ, Sakla HF, Cardona C, Chipont E, Alio JL.Corneal sensitivity after photorefractive keratectomy and laser in situ keratomileusis for low myopia. Am J Ophthalmol 1999;127:497-504. |
|53.||Kim W-S, Kim J-S. Change in corneal sensitivity following laser in situ keratomileusis. J Cataract Refract Surg 1999;25:368-73. |
|54.||Patel S, Perez-Santonja JJ, Alio JL, Murphy PJ. Corneal sensitivity and some properties of the tear film after laser in situ keratomileusis. J Refract Surg 2001;17:17-24. |
|55.||Linna TU, Perez-Santonja JJ, Tervo KM, Sakla HF, Alio y Sanz JL, Tervo TM. Recovery of corneal nerve morphology following laser in situ keratomileusis. Exp Eye Res 1998;66:755-63. |
|56.||Aras C, Ozdamar A, Bahcecioglu H, Karacorlu M, Sener B, Ozkan S. Decreased tear secretion after laser in situ keratomileusis for high myopia. J Refract Surg 2000;16:362-64. |
|57.||Yu EY, Leung AT, Rao SK, Lam DS. Effect of laser in situ keratomileusis on tear stability. Ophthalmology 2000;107:2131-35. |
|58.||Lee JB, Ryu CH, Kim J-H, Kim EK, Kim HB. Comparison of tear secretion and tear film instability after photorefractive keratectomy and laser in situ keratomileusis. J Cataract Refract Surg 2000;26:1326-31. |
|59.||Vesaluoma MH, Tervo TT. Tenascin and cytokines in tear fluid after photorefractive keratectomy. J Refract Surg 1998;14:447-54. |
|60.||Vesaluoma M, Teppo AM, Gronhagen-Riska C, Tervo T.Platelet derived growth factor - BB (PGDF - 88) in tear fluid: A potential modulator of cornea wound healing following photorefractive keratectomy. Curr Eye Res 1997;16:825-31. |
|61.||Tuunanen TH, Tervo TMT. Schirmer test values and the outcome of photorefractive keratectomy. J Cataract Refract Surg 1996;22:702-8. |
|62.||Dursun D, Monroy D, Knighton R, Tervo T, Vesaluoma M, Carraway K, et al. The effects of experimental tear film removal on corneal surface regularity and barrier function.Ophthalmology 2000;107:1754-60. |
|63.||Barraquer J. Querato mileusis y queratofaquia. Bogota, Colombia:Instituto Barraqquer de America, 1980:342. |
|64.||Seiler T, Koufala K, Richter G. Iatrogenic keratectasia after laser in situ keratomileusis. J Cataract Refract Surg 1998;14:312-17. |
|65.||Seiler T, Quurke AW. Iatrogenic keratectasia after LASIK in a case of forme fruste keratoconus. J Cataract Refract Surg 1998;24:1007-1009. |
|66.||Argento C, Cosentino MJ, Tytiun A, Rapetti G, Zarate J.Corneal ectasia after laser in situ keratomileusis. J Cataract Refract Surg 2001;27:1440-48. |
|67.||Geggel HS, Talley AR. Delayed onset keratectasia following laser in situ keratomileusis. J Cataract Refract Surg 1999;25:582-86. |
|68.||Binder PS, Moore M, Lambert RW, Seagrist DM.Comparison of two microkeratome systems. J Cataract Refract Surg 1997;13:142-53. |
|69.||Seitz B, Torres F, Langenbucher A, Behrens A, Suarez E.Posterior corneal curvature changes after myopic laser in situ keratomileusis. Ophthalmology 108;4:666-73. |
|70.||Reinstein DZ, Silverman RH, Sutton HF, Coleman DJ. Very high-frequency ultrasound corneal analysis identifies anatomic correlates of optical complications of lamellar refractive surgery: anatomic diagnosis in lamellar surgery.Ophthalmology 1999;106:474-82. |
|71.||Allemann N, Chamon W, Silverman RH, Azar DT, Reinstein DZ, Stark WJ et al. High-frequency ultrasound quantitative analysis of corneal scarring following excimer laser keratectomy. Arch Ophthalmol 1993;111:968-73. |
|72.||Azar DT, Yeh PC. Corneal topographic evaluation of decentration in photorefractive keratectomy: treatment displacement vs. intraoperative drift. Am J Ophthalmol 1997;124:312-20. |
|73.||Alkar N, Genth U, Seiler T. Diametral ablation-a technique to manage decentered photorefractive keratectomy for myopia. J Cataract Refract Surg 1999;15:436-40. |
|74.||Salah T. Reoperation following LASIK. In:Pallikaris IG, Siganos D, Editors. LASIK. Thorofare, NJ: SLACK Incorporated, 1998:307. |
|75.||Talamo JH, Wagoner MD, Lee SY. Management of ablation decentration following excimer photorefractive keratectomy. Arch Ophthalmol 1995;113:706-7. |
|76.||Knorz MC, Jendritza B. Topographically-guided laser in situ keratomileusis to treat corneal irregularities.Ophthalmology 2000;107:1138-43. |
|77.||Krueger RR, Saedy NF, McDonnell PJ. Clinical analysis of steep central islands after excimer laser photorefractive keratectomy. Arch Ophthalmol 1996;114:377-81. |
|78.||McGhee CNJ, Bryce IC. Natural history of central topographic islands following excimer laser photorefractive keratectomy. J Cataract Refract Surg 1996;22:1151-58. |
|79.||Tsai Y, Lin JM. Natural history of central islands after laser in situ keratomileusis. J Cataract Refract Surg 2000;26:853-58. |
|80.||Chayet AS, Assil KK, Montes M, Espinosa-Lagana M Castellanos A, Tsioulias G. Regression and its mechanisms after laser in situ keratomileusis in moderate and high myopia. Ophthalmology 1998;105:1194-99. |
|81.||Febbraro JK, Buzard KA, Friedlander MH. Reoperations after myopic laser in situ keratomileusis. J Cataract Refract Surg 2000;26:41-48. |
|82.||Martines E, John ME. The Martines enhancement technique for correcting residual myopia following laser assisted in situ keratomileusis. Ophthalmic Surg Lasers 1996;27:S512-16. |
|83.||Hersh PS, Brint SF, Maloney RK, Durrie DS, Gordon M, Michelson MA, et al. Photorefractive keratectomy versus laser in situ keratomileusis for moderate to high myopia. A randomized prospective study. Ophthalmology 1998;105:1512-23. |
|84.||Lyle WA, Jin GJC. Retreatment after initial laser in situ keratomileusis. J Cataract Refract Surg 2000;26:650-59. |
|85.||El Maghraby A, Salah T, Waring GO III, Klyce S, Ibrahim O. Randomized bilateral comparison of excimer laser in situ keratomileusis and photorefractive keratectomy for 2.50 to 8.00 diopters of myopia. Ophthalmology 1999;106:447-57. |
|86.||El Danasoury MA, El Maghraby A, Klyce SD, Mehrez K.Comparison of photorefractive keratectomy with excimer laser in situ keratomileusis in correcting low myopia (from-2.00 to -5.50 diopters); A randomized study. Ophthalmology 1999;106:411-20. |
|87.||Ditzen K, Handzel A, Pieger S. Laser in situ keratomileusis nomogram development. J Refract Surg 1999;15:S197-201. |
|88.||Serdaveric ON. Laser in situ keratomileusis: results, complications, and comparison with photorefractive keratectomy for low and moderate myopia. In: Brightbill FS, editor. Corneal Surgery; Theory, Technique, Tissue, 3rd ed.St. Louis, MO, Mosby 1999;807-19. |
|89.||Rao SK, Cheng AC, Fan DS, Leung AT, Lam DS. Effect of preoperative keratometry on refractive outcomes after laser in situ keratomileusis. J Cataract Refract Surg 2001;27:297-302. |
|90.||Duncker GIW, Amm M, Schroder E. The problem of undercorrection after laser in situ keratomileusis: an explanation (letter). J Refract Surg 1996;12:454. |
|91.||Yi WM, Joo CK. Corneal flap thickness in laser in situ keratomileusis using an SCMD manual microkeratome. J Cataract Refract Surg 2000;26:1103-4. |
|92.||Naripthaphan P. Vongthongsri A. Evaluation of the reliability of the Nidek MK-2000 microkeratome for laser in situ keratomileusis. J Refract Surg 2001;17:S255-58. |
|93.||Alio JL, Perez-Santonja JJ, Terro T, Tabbara KF, Vesaluoma M, Smith RJ, et al. Post-operative inflammatory, microbial complications and wound healing following laser-in-situ-keratomileusis. J Refract Surg 2000:16;523-38. |
|94.||Kohnen T. Retreating residual refractive errors after excimer surgery of the cornea: PRK versus LASIK (editorial). J Cataract Refract Surg 2000;26:625-26. |
|95.||Peters NT, Iskander NG, Gimbel HV. Minimizing the risk of recutting with a Hansatome over an existing automated corneal shaper flap for hyperopic laser in situ keratomileusis enhancement. J Cataract Refract Surg 2001;27:1328-32. |
|96.||Guell JL, Lohmann CP, Malecaze FA, Junger J, Muller A, Denueville S. Intraepithelial photorefractive keratectomy for regression after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:670-74. |
|97.||Ismail MM, Alio JL, Perez-Santonja JJ. Noncontact thermokeratoplasty to correct hyperopia induced by laser in situ keratomileusis. J Cataract Refract Surg 1998;24:1191-94. |
|98.||Lindstrom RL, Linebarger EJ, Hardten DR, Houtman DT, Samuelson TW. Early results of hyperopic and astigmatic laser in situ keratomileusis in eyes with secondary hyperopia. Ophthalmology 2000;107:1858-63. |
|99.||Jacobs JM, Sanderson MC, Spivack LD, Wright JR, Roberts AD, Taravella MJ. Hyperopic laser in situ keratomileusis to treat overcorrected myopic LASIK. J Cataract Refract Surg 2001;27:389-95. |
|100.||Machat J. Lasik complications and their management. In: Macha J, editor. Excimer laser refractive surgery: practice and principles. Thorofare, NJ:Slack,1996:359-400. |
|101.||Perez- Santonja JJ, Sakla HF, Abad JL, Zorraquino A, Esteban J, Alio JL. Nocardial keratitis after laser in situ keratomileusis. J Refract Surg 1997;13:314-17. |
|102.||Garg P, Bansal AK, Sharma S, Vemuganti GK. Bilateral infectious keratitis after laser in situ keratomileusis. A case report and review of literature. Ophthalmology 2001;108:121-25. |
|103.||Watanobe H, Sat S, Maeda N, Inoue Y, Shimomura Y, Tano Y. Bilateral corneal infection as a complication of laser in situ keratomileusis case report. Arch Ophthalmol 1997;115:1593-94 |
|104.||Karp KO, Hersh PS, Epstein RJ. Delayed keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2000;26:925-28 |
|105.||Chung MS, Goldstein MH, Driebe WT, Schwartz BH.Mycobacterium chelonae keratitis after Laser in situ keratomileusis successfully treated with medical therapy and flap removal. Am J Ophthalmol 2000;129:382-84. |
|106.||Chung MS, Goldstein MH, Driebe WT, Bruce S. Fungal keratitis after laser in situ keratomileusis: A case report.Cornea 2000;19:236-37. |
|107.||Kouyoumdjian GA, Forstot SL, Durairaj VD, Damiano RE.Infectious keratitis after Laser refractive surgery. Ophthalmology 2001;108:1266-68. |
|108.||Gelender H, Carter HL, Bowman B, Beebe W, Walters GR.Mycobacterium keratits after Laser in situ keratomileusis. J Refract Surg 2000;16:191-95. |
|109.||Sridhar MS, Garg P, Bansal AK, Sarma S. Fungal keratitis after laser in situ keraomileusis. J Cataract Refract Surg 2000;26:613-15. |
|110.||Sridhar MS, Garg P, Bansal AK, Gopinathan U. Aspergillus flavus keratitis after laser in situ keratomileusis 2000;129:802-4. |
|111.||Webber SK, Lawless MA, Sutton GL, Rogers CM.Staphylococcal infection under a LASIK flap. Cornea 1999;18;361-65. |
|112.||Kim HM, Song JS, Han HS, Jung HR. Streptococcal keratitis after myopic laser in situ keratomilusis. Korean J Ophthalmolol 1998;18:108-11. |
|113.||Dada T, Sharma N, Dada VK, Vajpayee RB. Pnuemococcal keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2000;26:460-61. |
|114.||Kuo IC, Margolis TP, Cevallos V, Hwang DG. Aspergillus fumigatus keratitis after laser in situ keratomileusis. Cornea 2001;20:342-44. |
|115.||El Danasoury MA, El Maghraby A, Klyce SD, Mehrez K: Comparison of photorefractive keratectomy with excimer laser in situ keratomileusis in correcting low myopia (from -2.00 to -5.50 diopters). A rendomised study. Ophthalmology 1999;106:411-20. |
|116.||Stulting RD, Carr JD, Thompson KP, Waring GO III, Wiley WM, Walker JM.Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999;106;13-20. |
|117.||Davidorf JM, Zaldivar R, Oscherow S: Results and complications of laser in situ keratomileusis by experienced surgeons. J Refract Surg 1998;14;114-22. |
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7]
[Table - 1], [Table - 2], [Table - 3]
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