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18 July 2008

Laser refractive surgery

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Laser in situ keratomileusis (Lasik) is the most commonly performed laser refractive procedure due to its predictability and safety,1 with the first procedure being performed in 1990.2

The Lasik procedure consists of two important parts - the creation of a corneal flap (with a mechanical microkeratome or femtosecond laser) and laser ablation (with an excimer laser). Complications are infrequent but when they do occur they can be sight threatening. Optometrists are becoming increasingly involved in preoperative assessment and postoperative aftercare of refractive surgery patients, hence an understanding of the potential intraoperative and postoperative complications are necessary.

Operative complications

Flap-related (microkeratome)

Incomplete flap

This occurs when the microkeratome halts during the creation of the corneal flap, with a reported incidence between 0.3-1.2 per cent.3,4 The main causes are due to either mechanical obstacles (lids, lashes, drape, loose epithelium, precipitated salt) or electrical failure (loss of suction).5 The management depends primarily on how far the microkeratome has advanced. In most cases the microkeratome is removed and the flap replaced with the procedure being deferred. In some cases, if the microkeratome has advanced past the visual axis, the remaining flap may be created manually with extreme caution.

Buttonhole flap

A buttonhole flap occurs when the microkeratome advances more superficially than intended, during the flap creation.6 This may be partial thickness (dissecting Bowman's layer) or full thickness (exiting the through the epithelium). The incidence of buttonhole flaps is between 0.3-0.56 per cent.3,7 Many theories exist as to the potential cause such as anatomically steep corneas, microkeratome dynamics and previous ocular surgery.8 Steep corneas can be compared to a tennis ball that would buckle centrally when applanated, resulting in a missed area by the microkeratome blade. The safest method to employ when prompted with this complication is to abort the procedure without lifting the flap. A bandage contact lens is fitted and most cases usually heal successfully. However, there is a risk of sub-epithelial scarring and epithelial ingrowth.

Free cap

This is the result of a complete dissection of the corneal flap, with an incidence of 0.1-1 per cent.9 Patients with flat corneas are more at risk of developing a free cap as it is dependent on the amount of cornea protruding above the superior plane of the suction ring. However, the use of a larger suction ring will reduce the risk in flat corneas as there will be more tissue above the suction ring. Inadequate suction can also increase the risk of a free cap. Ablation may be performed if the diameter of the exposed stroma is greater than the ablation diameter. The free cap should be stored in a moist chamber to prevent desiccation (epithelial side down) until it is replaced. Replacement of the flap with the proper orientation is key to preventing induction of astigmatism this is facilitated by careful preoperative marking on the cornea to transect the flap edge. A bandage contact lens may be useful in some cases and sutures are rarely needed. The patient needs be instructed to take extra care to avoid postoperative flap dislocation with the use of protective eyewear.

Anterior chamber penetration

This devastating complication ranges from corneal perforation to iris and/or lens damage. It is often managed with suturing, but if damage has occurred to the iris or lens, further management is required.11,12

Decentred flap

In the case of a decentred flap, treatment may be possible if the ablation zone is still within the flap. If not, it is best to abort the procedure by replacing the flap and re-treating in three months.13

Oedematous flap

Prolonged manipulation of the flap during the procedure can lead to an oedematous flap which can hinder flap adhesion. This can lead to flap decentration or dislocation known as 'floating flap phenomenon'. The management is both surgical and with the use of postoperative topical steroids.14

Epithelial defect

Epithelial defects can be caused by microkeratome head passage over a dry or a weaken epithelium following excessive anaesthetic use.9 Occasionally, a complete epithelial defect may occur in which case it needs to replaced and a bandage contact lens fitted. Antibiotic cover is also required. These steps will minimise pain, promote flap adherence and avoid infection and ingrowth.15 Patients with pre-existing recurrent corneal erosion syndrome are at higher risk of developing epithelial defects after Lasik and would be better candidates for surface treatment procedures such as Lasek or PRK.16

Corneal bleed

Corneal bleeding may occur as a result of damage to limbal vessels by the microkeratome usually in the scenario of a decentred flap or in the presence of corneal pannus. Sponging is applied with pressure to halt bleeding. The sponge is sometime soaked in phenylephrine 2.5 per cent, a vasoconstrictor, but this can cause pupillary dilation which can affect the laser eye-tracking and treatment centration.17

Ablation-related

Decentred ablation

Laser refractive surgery ablation is usually centred on the pupil centre. In cases were the laser beam decentres before the ablation procedure (shift) or the eye drifts during the procedure (drift), a decentred ablation can result.18 Drift may occur with higher magnitudes of refractive error due to poor uncorrected vision of the patient and also in longer treatment duration as this requires more concentration from the patient. Drift is less of an issue with more modern excimer laser systems that have eye-trackers. With these systems, if a patient makes a small shift in fixation, the laser will follow the eye to the new position and continue the ablation. If the eye makes a large shift in fixation, the laser will stop the ablation temporarily. However, even with these systems, shift may still occur, resulting in a decentred ablation. To ensure shift does not occur, following the flap creation and before the eye-tracker is initiated, the eye is repositioned. Decentration can induce irregular astigmatism causing many visual symptoms such as glare, halos, monocular diplopia and reduced best corrected visual acuity (BCVA) which will be dependent of the degree of decentration. Treatment is usually difficult, but reasonable results have been reported with topographic-linked ablations (Topolink).19

Central islands

Central islands are characterised by steep areas on cornel topography which are either 2mm in diameter or 3D in dioptric height.9 There are thoughts on the potential causes of central islands such as shielding by pulverised tissue plume, acoustic shock waves, central fluid collection and laser degradation.20 However, they are rarely seen with flying-spot excimer lasers. Each case needs to be monitored closely because approximately 25 per cent resolve by six months. There is less of a tendency for central islands to resolve following Lasik compared to PRK which is probably due to minimal epithelial remodelling after Lasik.21 Treatment is often in the form of laser ablation and only performed if the central islands exist for more than six months.

Interface debris

Debris in the flap interface should be differentiated from infectious or inflammatory responses. In essence, debris is typically inert, with no known visual effects unless a large quantity exists. The debris may be metallic fragments or oil from the microkeratome,22 meibomian gland secretions, powder from gloves, air bubbles or lint fibres.23

Flap folds

This may occur intraoperatively or in the early postoperative period and can induce irregular astigmatism. In the case of intraoperative flap wrinkling, it may be difficult to detect during the operation with the surgical microscope and hence the need for immediate slit-lamp examination following surgery using retro-illumination techniques. Subtle wrinkles can sometimes be more easily picked up with fluorescein staining. The overall incidence of flap folds is 0.2-1.5 per cent and is more common with greater degrees of refractive error.22 Management of intraoperative wrinkles is to replace the flap in the proper position, ensuring no fluid remains in the flap interface. This often requires a short period of air drying before the flap in replaced and the dryness also helps with adhesion.

Postoperative wrinkling can be caused by eye rubbing or heavy blinking and is often managed in the same way. However, the prognosis reduces the longer the wrinkling is left as epithelial hyperplasia may develop.24 When the flap is lifted and refloated it requires extra smoothing to remove the wrinkling and a bandage contact lens is usually fitted. In some cases suturing is required to stretch the flap into its optimal position, but this may induce unwanted astigmatism. Other reported treatment options include epithelial incisions, epithelial debridement, flap hydration or removal of the corneal cap.9

Postoperative complications

Dislocated flap

This may occur at any stage postoperatively but is more likely to occur in the first day after Lasik. It is imperative that the flap is repositioned to prevent infection, folds and epithelial ingrowth.25 The reported incidence varies between 1.1-2 per cent.26 Dislocation may occur due to lid action on the flap, especially if the ocular surface is dry and with other forms of physical trauma, such as eye rubbing. This complication is more likely to occur with large diameter and thin flaps.8 The management involves lifting the flap and scraping the stroma bed to remove any debris or epithelial cells. A bandage contact lens is usually fitted following flap replacement.

Flap loss

If the flap completely detaches, management options depend on whether the flap is found or not. If it is found it may be oedematous and difficult to distinguish the stromal and epithelial side of the flap. The flap is cleaned to remove debris and ingrowth. When it is replaced it is unlikely that it will adhere without sutures.9 However, if the flap is not found, the patient is managed in a similar fashion as per post-surface treatment. A bandage contact lens is placed on the eye and the cornea is allowed to re-epithelialise. An alternative procedure is the immediate suturing of a lamellar homograft.27

Diffuse lamellar keratitis (DLK)

DLK is also known as 'sands of the Sahara', which is a proliferation of sterile inflammatory cells within the Lasik interface with an incidence of 0.2-3.2 per cent.4,7,8 There is a great deal of variability in the presenting symptoms and clinical appearance. Symptoms may be in the form of photophobia, tearing and discomfort to pain. Inflammation may occur as soon as 24 hours after surgery or delayed a few days.28 The typical infiltrate characteristics are shown in Table 1.9

Infectious keratitis

This is a sight-threatening rare complication with an incidence of 0.1-0.2 per cent.29 There have also been case reports of bilateral infectious keratitis after Lasik.30 Studies have indicated a variety of contamination sources such as the ocular flora, instruments, surgeons' hands and airborne contaminants.31 The patient may complain of photophobia, ocular pain, reduced vision and tearing. On examination, signs may include stromal infiltrate, ciliary injection, anterior chamber reaction and hypopyon. Early diagnosis is of prime importance to enable appropriate treatment. The culture scrape is taken once the flap is lifted and most cultures indicate the causes to be Gram-positive bacteria and mycobacteria.9

Epithelial ingrowth

The incidence of postoperative epithelial ingrowth is 4.3 per cent.32 It occurs when epithelial cells grow into the lamellar interface, usually from the edge of the flap. The epithelial cells are seen as tongues or pearls under the flap. This ingrowth can induce refractive changes including irregular astigmatism and hence reduced BCVA. Epithelial cell nests may occur which should be monitored but in most cases they disappear due to the limited proliferative life of the cells. Ingrowth that is contiguous with the flap edge is more serious. This ingrowth can progress towards to the visual axis and there is the possibility of stromal melting.34 Tables 2 and 3 indicate the methods of ingrowth entry to the interface and the slit-lamp signs.

Treatment is required if the ingrowth encroaches the visual axis (2mm from the flap edge). The flap is lifted and the stromal bed along with the underside of the flap are irrigated and scraped and the flap is replaced.35 Alternatively the ingrowth can be removed with the excimer laser on the phototherapeutic keratectomy (PTK) mode, 50 per cent ethanol or mitomycin C.34,36 Preventive measures to avoid this complication should be followed at all times in terms of surgical technique and preoperative assessment. Patients with a history of recurrent corneal erosions may be more susceptible to ingrowth due to poorly adhering epithelium,37 in which case would be better suited to a surface treatment procedure (PRK or Lasek). There are reports of an increased risk of ingrowth following flap lift re-treatments,38 and again certain surgical steps are taken to minimise this.

Overcorrection/undercorrection

Many factors may cause an over- or undercorrection of the refractive error such as variable corneal wound healing, inaccurate refraction, atmospheric pressure, humidity, ambient temperature, ablation algorithm, inaccurate nomogram, magnitude of refractive error and age.8,39,40 The management of overcorrection and undercorrection depends on a number of factors. It may be possible to re-treat the patient if the refractive error has stabilised (after approximately three months) and there is sufficient corneal tissue remaining.

Regression

Regression is defined as a return of the refractive error towards the preoperative refractive error. It is more common with higher magnitudes of refractive error and also more common with hyperopia.41 Following hyperopic ablation, as the epithelial grows from the periphery towards the centre, it approaches an area of depression and hence this area is filled with a hyperplastic response reducing the steepened peripheral cornea. This, therefore, reduces the positive corneal shape, causing regression.41 Regression is managed similarly to over- and undercorrections however, iatrogenic keratectasia must be ruled out before re-treatment is performed.

Ectasia

Corneal ectasia is a serious complication resulting from a weakening of the corneal biomechanical strength. The key issue with postoperative ectasia is the residual stroma thickness. The industry standard 250µm of residual stroma must remain after surgery to avoid the development of iatrogenic keratectasia.42 It is imperative in the preoperative assessment that keratoconus suspects or forme fruste keratoconus is detected by an appropriate examination. Ectasia can induce irregular astigmatism and decreased vision. Figure 2 shows a case of Lasik-induced ectasia. This complication may occur at any time postoperatively as there have been reports as early as one week and as late as two years.9 Management options include contact lenses, intracorneal ring segments, corneal cross-linking, lamellar grafting and penetrating keratoplasty.

Dry eye

Lasik has been known to result in decreased corneal sensation, resulting in dry-eye related symptoms.43 Many patients present with postoperative superficial punctate keratopathy.17 It has been proposed that reduced blinking and lacrimal secretion may result from reduced sensation caused by nerve dissection from the microkeratome. In addition, it has been proposed that this condition is rather due to loss of trophic sensory support to the cornea, known as Lasik-induced neuroepitheliopathy (LINE).44 The hallmark of LINE is the presence of corneal staining confined to the flap and sparing the hinge region.

There is very limited data to indicate the extent of the problem of induced dry eye states. Prevalence studies have demonstrated differing levels of dry eye dependent on the methods of diagnosis up to 59 per cent at one month after Lasik.45 The rate of dry eye appears greatest initially but some studies demonstrate that it still may not reach baseline levels by one year postoperatively.43 Most cases do resolve by six months possibly due to the regeneration of corneal nerves. In cases of Lasik induced dry eye it is important to determine the cause to develop a treatment plan. A recent study investigated whether measurable preoperative characteristics predispose patients to chronic dry eye after Lasik.46 This study found that the preoperative tear volume (Schirmer test) may affect recovery of the ocular surface after Lasik and reduced levels may increase the risk of chronic dry eye.

Halos and glare

Visual symptoms such as halos, glare and night vision disturbances affect many patients after Lasik. Typically, the symptoms decrease with time but the mechanism is unknown. Symptoms are more evident with increased pupil size (at night) due to increased peripheral aberrations and light entering outside the treatment zone. Induced spherical aberration has been described as the main cause of halos and glare after refractive surgery.47 Other reasons suggested are wide area ablation profiles, subclinical decentration and dry eye.50,51

Femtosecond laser complications

The femtosecond laser delivers short bursts of pulses lasting approximately 10-15 seconds (at about 1,000nm) in the creation of a Lasik flap. They have a variety of theoretical advantages over mechanical microkeratomes, such as the reduced risk of intraoperative flap complications. The femtosecond laser can create the flap with a lower intraocular pressure increase, which reduces the risk of damage to the optic nerve head. However, the femtosecond laser procedure is of longer duration and some studies have suggested a higher incidence of diffuse lamellar keratitis along with other complications.50 They have also introduced a new set of complications such as vertical and horizontal gas breakthrough,51 opaque bubble layer52 and transient light sensitivity syndrome (TLSS).53 However, little is known about these complications and hopefully future research will provide such information.

Conclusion

No surgical procedure is complication free and a sound understanding of the potential complications is essential for eye care practitioners working in this area. Careful preoperative evaluation is required to reduce the potential risks along with careful postoperative examination to enable early diagnosis and management.

References

  1. Wilson SE. Use of lasers for vision correction of nearsightedness and farsightedness. N Engl J Med, 2004 351(5): 470-475.
  2. Pallikaris IG, Papatzanaki ME, Siganos DS, et al. A corneal flap technique for laser in situ keratomileusis. Human study. Arch Ophthalmol, 1991 109: 1699-1702.
  3. Gimbel HV, Anderson Penno EE, van Westenbrugge JA, et al. Incidence and management of intraoperative and early postoperative complications in 1000 consecutive laser in situ keratomileusis cases. Ophthalmol, 1998 105: 1839-1848.
  4. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol, 1999 127 129-136.
  5. Filatov V, Vidaurri-Leal JS, Talamo JH. Selected complications of radial keratotomy, photorefractive keratectomy, and laser in situ keratomileusis. Int Ophthalmol Clin, 1997 37: 123-48.
  6. Wilson SE: Lasik: management of common complications. Laser in situ keratomileusis. Cornea, 1998 17: 459-67.
  7. Stulting RD, Carr JD, Thompson KP, et al. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmol, 1999 106: 13-20.
  8. Melki SA, Azar DT. Lasik complications: etiology, management, and prevention. Surv Ophthalmol, 2001 46: 95-116.
  9. Farah SG, Ghanem RC, Azar DT. Lasik complications and their management. In: Azar DT. Refractive surgery. Second edition. Mosby Elsevier. 2007.
  10. Kim EK, Choe CM, Kang SJ, et al. Management of detached lenticule after in situ keratomileusis. J Refract Surg, 1996 12: 175-9.
  11. Ansari EA, Morrell AJ, Sahni K. Corneal perforation and decompensation after automated lamellar keratoplasty for hyperopia. J Cataract Refract Surg, 1997 23: 134-6.
  12. Arevalo JF, Ramirez E, Suarez E, et al. Incidence of vitreoretinal pathologic conditions within 24 months after laser in situ keratomileusis. Ophthalmol, 2000 107: 258-262.
  13. Lam DS, Leung AT, Wu JT, et al. Management of severe flap wrinkling or dislodgement after laser in situ keratomileusis. J Cataract Refract Surg, 1999 25: 1441-1447.
  14. Buratto L, Brint S. Complications of Lasik. In: Buratto L, Brint S, eds. Lasik: surgical techniques and complications. Thorofare, NJ, Slack, 2000 177-263.
  15. Oliva MS, Ambrósio R Jr, Wilson SE. Influence of intraoperative epithelial defects on outcomes in Lasik for myopia. Am J Ophthalmol, 2004 137: 244-249.
  16. O'Brart DP, Muir MG, Marshall J. Phototherapeutic keratectomy for recurrent corneal erosions. Eye, 1994 8: 378-383.
  17. Davidorf JM, Zaldivar R, Oscherow S. Results and complications of laser in situ keratomileusis by experienced surgeons. J Cataract Refract Surg, 1998 14: 114-122.
  18. Mulhern MG, Foley-Nolan A, O'Keefe M, et al. Topographical analysis of ablation centration after excimer laser photorefractive keratectomy and laser in situ keratomileusis for high myopia. J Cataract Refract Surg, 1997 23: 488-494.
  19. Knorz Mc, Jendritza B. Topographically-guided Lasik to treat corneal irregularities. Ophthalmol, 2000 107: 1138-1143.
  20. Johnson JD, Azar DT. Surgically induced topographical abnormalities after Lasik: Management of central islands, corneal ectasia, decentration, and irregular astigmatism. Curr Opin Ophthalmol, 2001 12: 309-317.
  21. Rachid MD, Yoo SH, Azar DT. Phototherapeutic keratectomy for decentration and central islands after photorefractive keratectomy. Ophthalmol, 2001 108: 545-52.
  22. el Danasoury MA, el Maghraby A, Klyce SD, et al. Comparison of photorefractive keratectomy with excimer laser in situ keratomileusis in correcting low myopia (from -2.00 to -5.50 diopters). A randomized study. Ophthalmol, 1999 106: 411-420.
  23. Stein HA: Powder-free gloves for ophthalmic surgery. J Cataract Refract Surg, 1997 23: 714-717.
  24. Lyle WA, Jin GL. Results of flap repositioning after laser in situ keratomileusis. J Cataract Refract Surg, 2000 26: 1451-1457.
  25. Melki SA, Talamo JH, Demetriades AM, et al. Late traumatic dislocation of laser in situ keratomileusis corneal flaps. Ophthalmol, 2000 107: 2136-9.
  26. Recep OF, Cagil N, Hasiripi H: Outcome of flap subluxation after laser in situ keratomileusis: results of 6 month followup. J Cataract Refract Surg, 2000 26: 1158-62.
  27. Pallikaris I, Siganos D. Lasik complications and management. In: Cornea, 2nd ed. Thorofare, NJ, Slack. 1999.
  28. Smith RJ, Maloney RK. Diffuse lamellar keratitis: a new syndrome in lamellar refractive surgery. Ophthalmol, 1998 105: 1721-1726.
  29. Kouyoumdjian GA, Forstot SL, Durairaj VD, et al. Infectious keratitis after laser refractive surgery. Ophthalmol, 2001 108: 1266-1268.
  30. Garg P, Bansal AK, Sharma S et al. Bilateral infectious keratitis after laser in situ keratomileusis: a case report and review of the literature. Ophthalmol, 2001 108: 121-125.
  31. Detorakis ET, Siganos DS, Houlakis VM, et al. Microbiological examination of bandage soft contact lenses used in laser refractive surgery. J Refract Surg, 1998 14: 631-5.
  32. Brint SF, Ostrick DM, Fisher C, et al. Six-month results of the multicenter phase I study of excimer laser myopic keratomileusis. J Cataract Refract Surg, 1994 20: 610-615.
  33. Castillo A, Diaz-Valle D, Gutierrez AR, et al. Peripheral melt of flap after laser in situ keratomileusis. J Refract Surg, 1998 14: 61-3.
  34. Helena MC, Meisler D, Wilson SE, et al. Epithelial growth within the lamellar interface after laser in situ keratomileusis (Lasik). Cornea, 1997 16: 300-5.
  35. Lim JS, Kim EK, Lee JB, et al. A simple method for the removal of epithelium grown beneath the hinge after Lasik. Yonsei Med J, 1998 39: 236-9.
  36. Haw WW, Manche EE. Treatment of progressive or recurrent epithelial ingrowth with ethanol following laser in situ keratomileusis. J Refract Surg, 2001 17: 63-68.
  37. Dastgheib KA, Clinch TE, Manche EE, et al. Sloughing of corneal epithelium and wound healing complications associated with laser in situ keratomileusis in patients with epithelial basement membrane dystrophy. Am J Ophthalmol, 2000 130: 297-303.
  38. Walker MB, Wilson SE. Incidence and prevention of epithelial growth within the interface after laser in situ keratomileusis. Cornea, 2000 19: 170-3.
  39. Huang D, Stulting RD, Carr JD, et al. Multiple regression and vector analyses of laser in situ keratomileusis for myopia and astigmatism. J Refract Surg, 1999 15: 538-549.
  40. Ditzen K, Handzel A, Pieger S. Laser in situ keratomileusis nomogram development. J Refract Surg, 1999 15(suppl): S197-S201.
  41. Chayet AS, Assil KK, Montes M, et al. Regression and its mechanisms after laser in situ keratomileusis in moderate and high myopia. Ophthalmol, 1998 105: 1194-9.
  42. Probst LE, Machat JJ. Mathematics of laser in situ keratomileusis for high myopia. J Cataract Refract Surg, 1998 24: 190-5
  43. Toda I, Asano-Kato N, Komai-Hori Y, et al. Dry eye after laser in situ keratomileusis. Am J Ophthalmol, 2001 132: 1-7.
  44. Wilson SE. Laser in situ keratomileusis-induced (presumed) neurotrophic epitheliopathy. Ophthalmol, 2001: 108: 1082-7.
  45. Yu EY, Leung A, Rao S, et al. Effect of laser in situ keratomileusis on tear stability. Ophthalmol, 2000 107: 2131-5.
  46. Konomi K, Chen L, Tarko RS, et al. Preoperative characteristics and a potential mechanism of chronic dry eye after Lasik. Invest Ophthalmol Vis Sci. 2008 49: 168-174.
  47. Pop M, Payette Y. Risk factors for night vision complaints after Lasik for myopia. Ophthalmol, 2004 111: 3-10.
  48. Mrochen M, Kaemmerer M, Mierdel P, et al. Increased higher-order optical aberrations after laser refractive surgery: a problem of subclinical decentration. J Cataract Refract Surg, 2001 27: 362-9.
  49. Vinciguerra P, Azzolini M, Airaghi P, et al. Effect of decreasing surface and interface irregularities after photorefractive keratectomy and laser in situ keratomileusis on optical and functional outcomes. J Refract Surg, 1998 14: S199-203.
  50. Gil-Cazorla R, Teus MA, de Benito-Llopis L, et al. Incidence of diffuse lamellar keratitis after laser in situ keratomileusis associated with the IntraLase 15 kHz femtosecond laser and Moria M2 microkeratome. J Cataract Refract Surg, 2008 34(1):28-31.
  51. Srinivasan S, Herzig S. Sub- Epithelial Gas Breakthrough During Femtosecond Laser Flap Creation for Lasik. BJO. 2007 91: 1373
  52. Kaiserman I, Meresky HS, Bahar I, et al. Incidence, possible risk factors, and potential effects of an opaque bubble layer created by a femtosecond laser. J Cataract Refract Surg, 2008 34(3): 417-23.
  53. Muñoz G, Albarrán-Diego C, Sakla H, et al. Transient light-sensitivity syndrome after laser in situ keratomileusis with the femtosecond laserIncidence and prevention. J Cataract Refract Surg, 2008 32(12): 2075-2079.

● Colm McAlinden is an optometrist currently undertaking a PhD in Refractive Surgery with the University of Ulster, Coleraine and Professor Jonathan Moore is a Consultant Ophthalmic Surgeon at the Mater Hospital, Belfast, Visiting Professor at the University of Ulster and Director of the Leeson Eye Institute, Dublin and Cathedral Eye Clinic, Belfast




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