Late Traumatic Dislocation of Laser In Situ

Monday, October 20, 2014

Keratomileusis Corneal Flaps

Samir A. Melki, MD, PhD,1 Jonathan H. Talamo, MD,2 Anna-Maria Demetriades, BA,1 Nada S. Jabbur, MD,3 John P. Essepian, MD,4 Terrence P. O’Brien, MD,3 Dimitri T. Azar, MD1

Purpose: To report the management and outcome of late-onset traumatic dislocation of laser in situ keratomileusis (LASIK) flaps.

Design: Retrospective, observational case series.

Participants: Four patients with late-onset LASIK flap dislocation occurring after mechanical trauma at various intervals (10 days–2 months) after the procedure.

Intervention: In all cases of postoperative traumatic LASIK flap dislocation, the flap was refloated with scraping and irrigation of the underlying stromal bed within 12 hours of the injury. A bandage contact lens was placed, and a regimen including topical antibiotics and corticosteroids was instituted in all cases.

Main Outcome Measures: Best spectacle-corrected visual acuity and complications associated with the surgery were monitored.

Results: Postoperative follow-up ranged from 4 to 21 months. Nonprogressive epithelial ingrowth was noted in one patient and diffuse lamellar keratitis developed in another patient. All patients recovered pretrauma spectacle-corrected visual acuity.

Conclusions: Corneal LASIK flaps are prone to mechanical dislocation as late as 2 months after the procedure. Appropriate management results in recovery of optimal visual outcomes.

Ophthalmology 2000;107: 2136–2139 � 2000 by the American Academy of Ophthalmology.

Laser in situ keratomileusis (LASIK) is a relatively new ophthalmic procedure that represents a combination of previously used techniques in refractive surgery.1 It involves using a microkeratome to create a thin corneal flap, followed by excimer laser stromal ablation and repositioning of the flap.2 The creation of a corneal flap represents additional risks of intraoperative and postoperative complications as compared with laser ablation after epithelial removal alone, as in photorefractive keratectomy.3–5 These complications include incomplete, irregular, or buttonholed flaps; flap folds; epithelial ingrowth; and diffuse lamellar keratitis.6–8 Although early flap slippage has been reported in various studies, the vulnerability of the LASIK flap to late dislocation is still unclear.

In the first 24 hours after LASIK, flap dislodgment presumably occurs as a result of mechanical disruption (e.g., blinking, lid squeezing, eye rubbing). It is not known to what extent the flap is subject to traumatic dislocation later in the postoperative period. In this study, we report four cases of late-onset (.1 week after the surgery) traumatic LASIK flap displacement.

Patients and Methods

We performed a retrospective analysis of patients with flap dislodgment occurring more than 1 week after LASIK surgery between October 1996 and February 2000. Details of the mechanism of injury, repair, and postoperative follow-up were available on all patients. Follow-up ranged between 4 and 21 months.

Patient 1

A 28-year-old man with a cycloplegic refraction of 25.25 2 1.75 3 90 in the right eye and 24.00 2 2.25 3 115 in the left eye and best spectacle-corrected visual acuity (BSCVA) of 20/20 in the right eye and 20/25 in the left eye underwent uneventful bilateral simultaneous LASIK for full correction of myopia and astigmatism. On postoperative day 8, both uncorrected visual acuity (UCVA) and BSCVA were 20/20 in both eyes. Two days later, he was struck in the left eye with a basketball resulting in immediate decrease in vision. Slit-lamp evaluation revealed a radial tear of the LASIK flap at the nasal hinge with 50% of the hinge intact. The inferior portion of the flap was folded on itself with bare stroma exposed.

The patient was immediately taken to the operating room and the flap was refloated, irrigated, and flattened. Tobramycin and dexamethasone combination eyedrops (Tobradex, Alcon, Fort Worth, TX) were given four times daily for 1 week, followed by a tapering dose of fluorometholone 0.1% (FML, Allergan, Inc., Irvine, CA) for 1 month. After surgery, moderate striae and minimal epithelial ingrowth at the tear location were noted. The Originally received: May 9, 2000.

Accepted: July 5, 2000. Manuscript no. 200279. 1Massachusetts Eye & Ear Infirmary, Boston, Massachusetts. 2Cornea Consultants of Boston, Boston, Massachusetts. 3Wilmer Eye Institute, Johns Hopkins University, Baltimore, Maryland. 4Private practice, Fairfax, Virginia. Presented in part at the American Academy of Ophthalmology annual meeting, Orlando, Florida, October 1999.

The authors have no proprietary interest in any aspect of this article. Reprint requests to Dimitri T. Azar, MD, Corneal and Refractive Surgery Services, Massachusetts Eye & Ear Infirmary, Harvard Medical School, 243 Charles Street, Boston, MA 02114. 2136 � 2000 by the American Academy of Ophthalmology ISSN 0161-6420/00/$–see front matter Published by Elsevier Science Inc. PII S0161-6420(00)00405-X BSCVA steadily improved, reaching 20/20 (12.25 2 2.00 3 30) at 2 months after injury (UCVA, 20/30). There was no progression of the epithelial ingrowth, and the folds were not considered visually significant.

Patient 2

A 21-year-old white male with a manifest refraction of 28.25 2 3.25 3 020 in the right eye (BSCVA, 20/15) and 27.25 2 2.00 3 002 in the left eye (BSCVA, 20/15) underwent uneventful bilateral simultaneous LASIK for the correction of myopia and astigmatism. The corneal flap was created using a Hansatome (Bausch & Lomb) microkeratome (8.5-mm suction ring diameter, 160-mm thickness footplate). The UCVA was 20/25.

Twenty-four days after surgery he was injured in the right eye by a “finger flick.” He was examined 10 hours after the injury and had a UCVA of 4/200. Examination revealed a partially dislocated corneal flap with flap folds across the visual axis as well as epithelial migration over the exposed area of the stroma in the inferotemporal quadrant (Figs 1A–C). The flap was immediately repositioned after thorough scraping of the stromal bed and of the flap underside. A bandage contact lens was placed for additional protection. On postoperative day 1, his UCVA was 20/30. Mild diffuse lamellar keratitis subsequently developed and was treated with intensive topical prednisolone acetate 1% (Pred Forte, Allergan) as well as oral prednisone. One week later, the inflammation was resolved and his UCVA was 20/20.

Patient 3

A 61-year-old woman with a manifest refraction of 12.50 2 0.50 3 60 in the right eye and 12.50 2 0.75 3 160 in the left eye and BSCVA of 20/15 in both eyes underwent uneventful bilateral LASIK surgery resulting in BSCVA of 20/20 in the left eye (UCVA, 20/30). Six weeks after surgery she was struck in the left eye by a dog’s paw. She noted immediate decrease in vision, pain, and photophobia. Evaluation revealed counting fingers visual acuity (pinhole, 20/60), 21 conjunctival injection, and a dehisced corneal flap. The temporal 30% of the underlying stromal bed was exposed. The remaining portion of the nasal-hinged flap exhibited significant folds and debris. Centrally, vertical paw marks were noted with fluorescein staining.

Four hours after injury, the flap was refloated with scraping and irrigation of the underlying stromal bed. A bandage contact lens was placed and a regimen of trimethoprim sulfate and polymyxin B sulfate combination eyedrops (Polytrim, Allergan, Inc.) every 2 hours and prednisolone acetate 1% twice daily was instituted for 2 weeks. The BSCVA was 20/30 2 days after repair and returned to 20/20 at 5 weeks after the injury (UCVA, 20/20). At the 2-month follow-up, no other complications were noted except scattered inert debris in the flap interface.

Patient 4

A 38-year-old man with a preoperative manifest refraction of 28.50 2 1.00 3 130 in the right eye and 27.50 2 0.50 3 070 in the left eye underwent uneventful bilateral LASIK for full correction of myopia and astigmatism (nasal-hinged flap). Two months later his left eye was struck by a snowball. He noted eye pain and decrease in vision. A BSCVA of 20/60 was noted, and slit-lamp evaluation revealed an edematous dehisced corneal flap. The inferotemporal quarter of the underlying stromal bed was exposed. The central portion of the flap, however, did not exhibit significant folds.

Within hours of the injury, the flap was refloated with scraping and irrigation of the underlying stromal bed, a bandage contact lens was placed, and a regimen of ofloxacin 0.3% (Ocuflox, Allergan) four times daily for 5 days and tobramycin and dexamethasone combination eyedrops (Alcon) four times daily for 3 weeks was instituted. Spectacle-corrected and uncorrected visual acuity returned to the preinjury level of 20/20 2 weeks after repair. Visual acuity was 20/15 at 21 months after repair. No apparent flap abnormalities were noted.

Figure 1. A, B, C: color photograph of a dislocated laser in situ keratomileusis flap 24 days after surgery secondary to a “finger flick” to the right eye (patient 2). Note the severe folds across the visual axis (B) as well as the coverage of the exposed stroma by corneal epithelium (C) within 10 hours of the injury. Melki et al z Late Dislocation of LASIK Flaps 2137


A summary of the relevant clinical findings is presented in Table 1. All cases reported in this series resulted in recovery of pretrauma BSCVA. Epithelial ingrowth was noted only in one case after flap repair (patient 1). Diffuse lamellar keratitis occurred in another patient who responded well to topical and systemic steroid treatment (patient 2).


Keratorefractive surgery may be associated with a variety of complications.6,7 This includes loss of BSCVA, reduction in the quality of vision (secondary to glare, halos, and diminished contrast sensitivity), and other optical aberrations.9,10 The susceptibility of eyes undergoing refractive surgery to injury after blunt trauma deserves close attention, especially because one of the most common motivations for undergoing the procedure is to engage in sporting activities without the need for corrective (and protective) glasses.

Several studies reported early flap dislocation and most seem to be related to early postoperative slippage. Gimbel et al11 reported an incidence of 1.2% in a study of 1000 eyes. Lin and Maloney12 noted an overall incidence of 2.0% in 1017 eyes. Stutling et al13 documented an incidence of 1.1% in 1062 eyes. In the aforementioned studies, there are no reports of loss of BSCVA more than two lines from flap dehiscence. A recent report by Lam et al14 described management of four cases of flap slippage within the first 24 hours after the surgery.

The cases reported in this article indicate that the corneal flap remains susceptible to trauma as late as 2 months after LASIK. This is consistent with anecdotal and published reports relating the ease of lifting a LASIK corneal flap more than 1 year after the initial procedure. Other supporting evidence can be found in a case of partial flap infolding related to a bird’s peak injury as late as 11 months after uneventful LASIK.15 Similarly, LASIK and automated lamellar keratectomy (ALK) cap displacement has been reported as an intraoperative event during retinal surgery as late as 5 months after the procedure.16,17 Thus an eventual return of the corneal surface to its preoperative integrity may take years in certain patients.

The exact mechanism of long-term adhesion remains unclear. Postulated mechanisms of early flap adherence include endothelial pumping, capillarity, fiber interlacing, intracorneal suction, intracorneal molecular attraction, and ionic bonding.18–20 The relative strengths of such forces early in the postoperative period as compared with later in the postoperative period have yet to be elucidated. Wound healing occurring at the stromal interface is believed to be less than that of the surrounding epithelial rim, as evidenced by the surgical experience during retreatment. More difficulty is noted when lifting the flap at the time of enhancement in younger patients, presumably because of a faster healing rate (personal observation). It is not known if other factors such as race, amount of refractive error corrected, or underlying systemic diseases could influence the rate and strength of flap healing.

A displaced or subluxed flap should be regarded as an emergency. Immediate repositioning is crucial to prevent formation of fixed folds and epithelial ingrowth. Fixed folds probably occur secondary to epithelial hyperplasia within the fold crevices, rendering flap stretching more difficult. Initially, the flap should be reflected and the interface examined carefully for epithelial cells and debris. If present, we recommend aggressive scraping before repositioning of the flap. Application of a contact lens for a few days may provide added protection from further displacement. If a flap is completely detached from its bed, repositioning in the proper orientation becomes fairly difficult after the loss of surgical landmarks.21 Improper repositioning of the flap can result in irregular astigmatism and loss of BSCVA. Suturing of the flap may be necessary at times.22 In the event of a lost flap, the epithelium is simply allowed to heal. This, however, may lead to significant flattening, depending on the diameter and the thickness of the flap, and may induce a hyperopic shift. Despite appropriate surgical techniques, complications such as diffuse lamellar keratitis and epithelial ingrowth may still occur, as seen in two of our patients. In conclusion, traumatic displacement of corneal flaps after LASIK is a possible postoperative complication occurring weeks to months after the procedure. As more cases of late trauma emerge, we will learn more about the fragility of the attachment of the flap to the underlying stroma. At the same time, reports of cases of ocular trauma where the flap remains intact would provide additional information regarding the strength of the flap adhesion. Discussion of this potential complication should be included in the informed consent process, especially for patients at greater risk for blunt ocular trauma from occupational hazards (such as military or law enforcement personnel) or sporting activities.


1. Pallikaris IG, Papatzanaki ME, Stathi EZ, et al. Laser in situ keratomileusis. Lasers Surg Med 1990;10:463– 8.
2. Pallikaris IG, Papatzanaki ME, Siganos DS, Tsilimbaris MK. Table 1. Traumatic Laser In Situ Keratomileusis Flap Dislocation: Summary of Injury Characteristics and Outcomes

Patient No.
Mechanism of Injury
Time after Laser In Situ
Uncorrected Visual
Acuity before Trauma
Time of Repair
Final Uncorrected Visual
Acuity and Best Spectaclecorrected
Visual Acuity
Loss of Best
Visual Acuity

1 28/M Basketball 10 days Nasal 20/20 ,6 hrs 20/30, 20/20 No
2 21/M Finger 24 days Superior 20/25 12 hrs 20/20, 20/20 No
3 61/F Dog’s paw 6 wks Nasal 20/30 ,6 hrs 20/20, 20/20 No
4 38/M Snowball 2 mos Nasal 20/20 ,6 hrs 20/20, 20/20 No
Ophthalmology Volume 107, Number 12, December 2000 2138

A corneal flap technique for laser in situ keratomileusis. Human studies. Arch Ophthalmol 1991;109:1699 –702.

3. Trokel SL, Srinivasan R, Braren B. Excimer laser surgery of the cornea. Am J Ophthalmol 1983;96:710 –5.

4. McDonald MB, Frantz JM, Klyce SD, et al. Central photorefractive keratectomy for myopia. The blind eye study. Arch Ophthalmol 1990;108:799–808.

5. Azar DT, Farah SG. Laser in situ keratomileusis versus photorefractive keratectomy: an update on indications and safety [editorial; review]. Ophthalmology 1998;105:1357– 8. Comment on: Ophthalmology 1998;105:1512–22; discussion 1522–3.

6. 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.

7. Wilson SE. LASIK: management of common complications. Cornea 1998;17:459–67.

8. Smith RJ, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721– 6.

9. Pallikaris IG. Quality of vision in refractive surgery. Barraquer Lecture 1997. J Refract Surg 1998;14:549 –58.

10. Melki SA, Proano CE, Azar DT. Optical disturbances and their management after myopic laser in situ keratomileusis [review]. Int Ophthalmol Clin 2000;40:45–56.

11. Gimbel HV, Penno EEA, van Westenbrugge JA, et al. Incidence and management of intraoperative and early postoperative complications in 1000 consecutive laser in situ keratomileusis cases. Ophthalmology 1998;105:1839–47; discussion 1847–8.

12. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129– 36.

13. Stulting RD, Carr JD, Thompson KP, et al. Complications of laser in situ keratomileusis for the correction of myopia. Ophthalmology 1999;106:13–20.

14. Lam DSC, Leung ATS, Wu JT, et al. Management of severe flap wrinkling or dislodgment after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1441–7.

15. Leung ATS, Rao SK, Lam DSC. Traumatic partial unfolding of laser in situ keratomileusis flap with severe epithelial ingrowth. J Cataract Refract Surg 2000;26:135–9.

16. Chaudhry NA, Smiddy WE. Displacement of corneal cap during vitrectomy in a post-LASIK eye. Retina 1998;18:554–5.

17. Shakin EP, Fastenberg DM, Udell IJ, et al. Late dislocation of a corneal cap after automated lamellar keratoplasty and epithelial debridement for retinal surgery [letter]. Arch Ophthalmol 1996;114:1420.

18. Perez EP, Viramontes B, Schor P, Miller D. Factors affecting corneal strip stroma-to-stroma adhesion. J Refract Surg 1998; 14:460 –2.

19. Maurice DM, Monroe F. Cohesive strength of corneal lamellae. Exp Eye Res 1990;50:59–63.

20. Holly FJ. Biophysical aspects of epithelial adhesion to stroma. Invest Ophthalmol Vis Sci 1978;17:552–7.

21. Kim EK, Choe CM, Kang SJ, Kim HB. Management of detached lenticule after in situ keratomileusis. J Refract Surg 1996;12:175–9.

22. Pannu JS. Incidence and treatment of wrinkled corneal flap following LASIK [letter]. J Cataract Refract Surg 1997;23: 695–6. Comment on: J Cataract Refract Surg 1996;22:1391. Melki et al z Late Dislocation of LASIK Flaps 2139

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