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Journal Français d'Ophtalmologie
Volume 36, n° 1
pages 82-86 (janvier 2013)
Doi : 10.1016/j.jfo.2012.03.004
Received : 15 February 2012 ;  accepted : 30 Mars 2012
Traumatic flap dislocation 10 years after LASIK. Case report and literature review
Dislocation du flap dix ans après LASIK. Rapport de cas et revue de la littérature
 

Z. Khoueir a, , N.M. Haddad b, c, A. Saad b, c, E. Chelala a, E. Warrak d, e
a Hôtel-Dieu de France, Ophthalmology department, rue Alfred-Naccache, Beirut, Lebanon 
b Rothschild Foundation, 25, rue Manin, 75019 Paris, France 
c Center for Expertise and Research in Optics for Clinicians (CEROC), 25, rue Manin, 75019 Paris, France 
d Advanced Eye Care Hospital, Antelias, Naccache, Lebanon 
e University of Balamand, Deir El-Balamand, Al-Kurah, Lebanon 

Corresponding author.
Summary

We report a case of traumatic partial flap dislocation 10 years after uneventful laser in situ keratomileusis (LASIK). The patient was treated bilaterally for hyperopia and astigmatism with LASIK. A superior-hinged corneal flap was created using the Moria M2 microkeratome (Moria SA, Antony, France) and the surgery was uneventful. Ten years later, partial flap dislocation was diagnosed after mild trauma. This case suggests that flap dislocations can occur during recreational activities up to 10 years after surgery. Full visual recovery is achievable if the case is managed promptly. Further studies should evaluate the potential protective role of an inferior hinge during LASIK.

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Résumé

Nous rapportons le cas d’une dislocation de capot de Laser in situ keratomileusis (LASIK) dix ans après une chirurgie pour correction d’hypermétropie et astigmatisme bilatérale réalisée au microkératome Moria M2 (Moria SA, Antony, France) avec une charnière supérieure. Ce cas suggère qu’une dislocation du capot est possible dix ans après la chirurgie et qu’une récupération visuelle est possible si un traitement est instauré rapidement. Des études complémentaires pourraient évaluer le rôle protecteur potentiel d’une charnière inférieure au cours d’un LASIK.

The full text of this article is available in PDF format.

Keywords : Laser in situ keratomileusis (LASIK), LASIK flap dislocation, Late-onset, Inferior hinge

Mots clés : Laser in situ keratomileusis (LASIK), Dislocation du flap, Complication tardive, Charnière inférieure


Introduction

Lasik in situ keratomileusis (LASIK) is increasingly used worldwide to correct a wide range of refractive errors. LASIK consists of creating a corneal flap by using a microkeratome or a femtosecond laser. Once the flap is created and lifted, laser excimer stromal ablation reshapes the corneal tissue to correct the refractive error and the flap is repositioned at the end of the surgery.

Flap creation represents additional intraoperative and postoperative risks in comparison to more superficial ablation techniques, such as photorefractive keratectomy and laser subepithelial keratomileusis [1, 2]. Postoperative flap dislocations occur in approximately 1% to 2% of patients, usually within the first 24hours after surgery [3, 4] and mostly because of eye-rubbing or eyelid motion. Those cases of early flap slippage have been reported in various studies but the duration of time in which the flap remains vulnerable to traumatic dislocation is not currently known. In comparison, late traumatic dislocation is a less frequent occurring later than 1 week after the surgery. Several reports have described cases of late-onset LASIK flap dislocation up to 7 years following surgery and they have all showed concern about the strength of the adhesion between the flap and the stromal bed (Table 1). The purpose of this article is to report a case of late-onset traumatic dislocation occurring 10 years after surgery. This case represents the longest reported interval between initial surgery and traumatic flap displacement.

Case report

A 35-year-old man with a manifest refraction of +3.50 (+3.00×85) in the right eye and +3.50 (+2.00×20) in the left eye and best spectacle-corrected visual acuity (BSCVA) of 20/25 in the right eye and 20/40 in the left eye underwent uneventful bilateral LASIK for full correction of hyperopia and astigmatism in December 2000. He had mild cortical opacities in his left eye due to an old trauma.

The Moria M2 microkeratome (Moria SA, Antony, France) was used to create a superior-hinged corneal flap and the Nidek EC-5000 excimer laser (Nidek Co., Ltd., Japan) was used for the ablation. His topography and preop pachymetry were suitable for the Lasik procedure and did not show any abnormality. His central corneal thickness was 562μm in his right eye and the steep and flat axis showed a keratometric value of 41 and 38 diopters respectively. He had a smooth postoperative course; the flaps were well-positioned with a clean interface in both eyes. There were no micro- or macrostriae. He was followed on a yearly basis. His last follow-up was in 2009 where his best corrected visual acuity (BSCVA) was 20/25 with a refraction of plano (+1.25×80) in the right eye.

Ten years after the original LASIK procedure, in April 2010, he was struck on the right eye with a stick while playing with his 2-year-old kid resulting in immediate pain, tearing, and blurred vision. He was examined 5hours after the injury and had a UCVA of 20/200. Slit-lamp examination revealed avulsion of the corneal flap and epithelial abrasion. There was a double eversion of the flap superonasally and a large portion of the stromal bed was exposed nasally (Figure 1). No corneal or anterior chamber inflammation was observed. The flap was immediately elevated and unfolded in the operating room by hydrating it with salt saline solution in order to induce its swelling and facilitate the procedure. Then, it was hydrated again with balanced salt solution in order to bring it back to its original thickness. The mottled epithelium was debrided on all borders of the flap and the interface was cleaned so the flap could be applied again. A bandage contact lens was placed and a regimen of ciprofloxacin eyedrops (Ciloxan; Alcon, Fort Worth, TX) every 4hours for 10 days and prenisolone acetate (Pred Forte, Allergan Irvine CA) every 3hours then tapered over a period of 3 weeks was instituted. The Bandage lens was removed 5 days after the procedure and his BCVA was 20/25 10 days postoperatively. The last follow-up was 3 weeks later. No diffuse lamellar keratitis (DLK) was noted and the flap remained in good position (Figure 2).



Figure 1


Figure 1. 

Eversion of the flap superonasally with and a large portion of the stromal bed exposed nasally.

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Figure 2


Figure 2. 

Three weeks after flap repositioning.

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Discussion

Flap complications, including dislocations are one of the most frequent LASIK complications [4]. Flap dislocation occurs in the early postoperative period and to a lesser extent weeks to months after surgery secondary to mechanical trauma. It is a common belief among ophthalmologists that the corneal surface will eventually return to its preoperative integrity by a slow mechanism of adhesion that may take years in certain patients [5]. The case reported in this article shows that the corneal flap remains susceptible to trauma as late as 10 years after surgery and therefore integrity is never fully restored after the creation of the flap as if “the flap never heals”.

Postulated mechanisms for early flap adherence consists of capillarity, fiber interlacing, intracorneal suction, endothelial pumping, intracorneal molecular attraction, and ionic bonding [6, 7, 8]. On the other hand, the exact mechanism for long-term adhesion remains ill-defined.

Maurice and Monroe demonstrated in an animal model that after creation of a lamellar corneal dissection, the adhesive force of the healed stromal lamellae approximated one-quarter to one-half of normal [7]. Kato et al. [9] studied corneal wound healing in an animal model. Their work on immuno-histochemical staining and electron microscopy following LASIK showed that up to 9 months after the procedure, wound healing continued to be disorganized and delayed at the interface region. Philipp et al. analyzed human eyes and found a slight increase of staining of dermatan sulfate proteoglycan within the stromal interface adjacent to the lamellar flap, furthermore only a few collagen lamellae were documented crossing between the stromal bed and the flap, accounting for the weak adherence between flap and stroma [10].

In rabbit corneas, the post-LASIK healing reaction takes place only at the flap border, leaving a clear central optical zone [11, 12]. Similar findings have been described in human eyes after LASIK [13] and it has been proven that the interface was found to be free from cellular response or collagenase activity [14].

Dawson et al. [15, 16, 17] found in human eyes that keratocyte-mediated production of a thick lamellar corneal stromal scar occurs and that it results in two different types of scars. The hypercellular fibrotic reaction at the wound margin is usually visible clinically and holds the flap in place surrounding the more central hypocellular primitive scar which is not visible clinically and allows easy lifting of the flap postoperatively. These findings have been confirmed by confocal studies that show that post-LASIK remodeling mainly takes place at the edge of the flap [18].

Schmack et al. [19] found that, the LASIK flap wound margin heals by producing peripheral hypercellular fibrotic stromal scar that averages 28.1% as strong as normal corneal stromal. The central and paracentral hypocellular primitive stromal scar is 10 times weaker and averages 2.4% as strong as normal corneal stroma. As stromal remodeling appears to follow a regional distribution it seems quite logical that this leads to a weakening of the cornea in the setting of eye trauma. Mechanical trauma creates sheering forces causing a break in the scar tissue at the edges of the flap. This can also be performed iatrogenically during LASIK enhancements using a Sinskey hook by dissection of the fibrous adhesions along the edge of the flap in some cases up to 36 months or longer after a primary myopic LASIK procedure [20, 21].

The case reported in this article shows that the corneal flap remains susceptible to trauma as late as 10 years after surgery and therefore integrity is never fully restored after the creation of the flap as if “the flap never heals”. Late-onset traumatic flap dislocation is an ophthalmological emergency where prompt management is essential to achieve a good visual outcome. Treatment consists of carefully lifting the flap to expose the stromal interface. Foreign bodies, epithelial sliding and debris should be scraped off the interface which is then thoroughly irrigated to decrease the risk of epithelial ingrowth.

The flap is then stretched and repositioned without excessive manipulation to avoid unnecessary trauma and subsequent edema. Careful stretching of the flap and realignment of the wound will minimize irregular wound healing. Once the flap is in place, the peripheral epithelium beyond the flap margin can be removed with forceps. Optimal adhesion is then achieved by eliminating excess interface fluid by stroking the flap with a cyclodialysis spatula and sterile surgical sponge can be used to remove fluid from the edge of the flap. The eyelid speculum can be left in place for 5minutes to allow the cornea to deturgess under the influence of the strong negative osmotic pressure generated by the active transport system of the endothelial pump. Optimal adherence is then confirmed by the absence of independent movement of the flap when depressing the adjacent cornea external to the flap [22].

A bandage lens is applied to protect the flap and topical steroids and antibiotics are prescribed to prevent DLK and infectious complications.

DLK is a potential complication that can be diagnosed during follow-up or even initially before flap repositioning. It is the result of inflammation due to the trauma itself or the exposure of the interface to the ocular surface environment and other potential etiologic iatrogenic agents such as talc from the surgeon’s glove, povidone-iodine or chemicals used to treat surgical equipment. Occurrence of DLK in the setting of a traumatic flap dislocation is most probably related to the extent of stromal exposure, the duration of the exposure, the trauma itself and the initiation of the topical steroids. Therefore profuse irrigation to eliminate potential etiologic agents, prompt surgical repositioning and aggressive steroids are essential in reducing the risk of DLK occurrence.

The lifetime prevalence of blunt ocular trauma has been estimated to be 52.7 per 1000 individuals [23]. Patients undergoing LASIK are often active individuals and are therefore at risk for ocular trauma. As LASIK has been increasingly used, cases of traumatic flap dislocations are expected to become more common. Emergency doctors should be aware of the fact that all post-LASIK patients with a history of ocular trauma should have an eye exam regardless of symptoms to rule out a flap dislocation and general ophthalmologists should be familiar with optimal ways to manage those cases since prompt repair, topical treatment and adequate monitoring can avoid loss of BSCVA and therefore provide a good visual prognosis. Retinals surgeons should also be aware of the risk of intraoperative flap displacement, especially with epithelial debridement.

It is also crucial that all patients undergoing LASIK should be aware of the persistent vulnerability of the flap. The fact that their flap can be dislocated in the setting of a trauma, even 10 years after surgery, should be discussed in all patient consent to avoid medicolegal issues. Some studies suggested that young patients who are at high risk of sustaining glancing corneal injuries should be encouraged to choose a non-lamellar refractive procedure such as PRK [24, 25, 26]. Our review (Table 1) shows that the majority of dislocation cases did not occur in high risk activities but mainly because of accidents in routine daily activities. The average age did not suggest that younger and more active patients are at a higher risk of developing flap dislocations. Patients should be encouraged to wear protective eyewear during any domestic and sporting activity that could increase the risk of ocular trauma.

A very important reflex takes place in the setting of an eye trauma. Bell’s phenomenon is a protective outward and upward rotation of the globe with eyelid closure. The Bell’s reflex helps protect against corneal injury and it can be postulated that by closing the lid and rotating the globe upward and outward only the inferior part of the cornea is left exposed. LASIK with an inferior hinge presents the advantage of leaving a strong untouched corneal tissue inferiorly. The hinge remains the most solid corneal area after LASIK and this could help protect inferior-hinged patients from a flap dislocation in the setting of an eye trauma since the flap is displaced by sheering forces applied to the point of impact. Our review (Table 1) did not show any case of traumatic flap dislocation with an inferior hinge. Cosar et al. showed that laser in situ keratomileusis with an inferior hinge is safe and effective in a series of 46 eyes [27]. Further studies on mechanical models should help to evaluate the impact of hinge position and its potential protective effect.

Disclosure of interest

The authors declare that they have no conflict of interest concerning this article.

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