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Title: La reticulación del colágeno corneal en Cirugía Refractiva
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Reticulación del colágeno corneal en cirugía refractiva Información Autor Departamento de Oftalmología, Albert Einstein Coll...



Reticulación del colágeno corneal en cirugía refractiva

Información Autor
Departamento de Oftalmología, Albert Einstein College of Medicine, del Centro Médico Montefiore, Bronx, Nueva York, EE.UU.
Correspondencia a Prabjot Channa, MD, Departamento de Oftalmología, Montefiore Medical Center, 111 E 210a Street, Edificio Centenario, 3 º piso, Bronx, NY 10467, EE.UU.. Tel: +1 914 413 3681, e-mail: pchanna@montefiore.org

Abstracto
Objetivo de la revisión: Describir el desarrollo y usos de reticulación del colágeno corneal (CXL) en asociación con los procedimientos querato así como en el tratamiento del queratocono progresivo y progresista postlaser in situ queratomileusis (post-LASIK) queratectasia.
Hallazgos recientes: CXL ha demostrado ser eficaz para retrasar, detener o revertir la ectasia progresiva tanto en el queratocono y progresiva post-LASIK queratectasia por medio de rigidización corneal. Por lo tanto, es la única opción de tratamiento disponibles en la actualidad que se refiere a la progresión subyacente de condiciones ectactic. Combinando CXL con querato procedimientos, tales como la implantación corneal intraestromal segmento de anillo y queratectomía fotorrefractiva, es una prometedora alternativa terapéutica a la queratoplastia penetrante o queratoplastia lamelar que en muchos casos puede mejorar la agudeza visual, estabilizar ectasia, y retrasar o incluso prevenir la necesidad de más invasivo procedimientos.
Resumen: El efecto de la rigidez del CXL ha convertido en una alternativa prometedora en el arsenal del oftalmólogo para el tratamiento del queratocono progresivo y progresista ectasia post-LASIK. Futuros estudios son necesarios para determinar la estabilidad a largo plazo de CXL, así como para hacer frente a las posibles complicaciones.
INTRODUCCIÓN
Reticulación del colágeno corneal (CXL), inicialmente descrita por Sporl et al. [1] en 1997 es una técnica cada vez más utilizado que utiliza riboflavina y luz ultravioleta A (UVA) para aumentar la estabilidad biomecánica y la resistencia de la córnea mediante la inducción de la reticulación entre el colágeno fibras.
.El queratocono progresivo y postlaser in situ queratomileusis (post-LASIK) queratectasia (PPLK) se caracterizan por corneal progresivo aumento de la pendiente y adelgazamiento estromal [2] . Las opciones terapéuticas para la rehabilitación visual, tales como lentes de contacto permeables al gas rígidas o segmentos de anillo intraestromales corneales (ICRS), aunque es eficaz en la mejora de la agudeza visual, no tratan la causa subyacente de progresivos cambios en la córnea. Cuando se produce la progresión o contactar desarrolla intolerancia a las lentes, la queratoplastia penetrante o queratoplastia laminar han sido tradicionalmente el siguiente paso. CXL se ha mostrado prometedora para frenar, detener o incluso revertir la progresión tanto en el queratocono y PPLK, retrasando o evitando la necesidad de procedimientos más invasivos.
CORNEAL COLLAGEN CROSSLINKING PROCEDURE AND BIOMECHANICS

CXL involves the use of riboflavin and UVA light to induce photooxidative collagen crosslinking. Blue light, although not used clinically, has also been shown to be effective in producing significant corneal stiffening in laboratory research [3]. Although there are slight variations, the fundamental technique is as follows: under topical anesthesia, riboflavin 0.1% drops are applied to the central 7 mm of the cornea either with an intact epithelium or after creating a similar sized epithelial defect. Riboflavin is allowed to permeate through the cornea and is periodically reapplied during the procedure to ensure adequate corneal absorption. Riboflavin acts as a photosensitizer for subsequent UVA irradiation with two UV diodes at the desired irradiance of 4 mW/cm2 (5.4 J/cm2) at a 1 cm distance for 30 min [4]. It is also thought to block UVA transmission beyond the corneal stroma, thus protecting the corneal endothelium and deeper intraocular structures such as the lens and retina from unwanted side effects [5▪]. Furthermore, the UVA intensity used during crosslinking is far below the damage threshold for the corneal endothelium, iris, lens, and retina[6].

Additional covalent binding between collagen molecules stabilizes the collagen scaffold and has been shown to increase corneal stiffness and enhance resistance against proteolytic enzymes [3,7–10]. The stiffening effect of CXL is heterogeneously distributed with more pronounced effect in the anterior 200–300 μm of the cornea [8,11,12]. The increased stiffness and rigidity of the cornea stabilizes the corneal ectasia [5▪].

Possible reported complications of CXL, although quite rare, include sterile infiltrates, stromal scars, transient stromal haze, corneal edema, diffuse lamellar keratitis, transient endothelial damage, and herpetic keratitis with iritis [5▪,13,14,15▪]. There has been increased interest recently in decreasing total stromal irradiation time by increasing the fluence of applied UVA light, thus possibly reducing stromal keratocyte loss. Kanellopoulos has shown similar results and adverse effects with use of higher fluence but shorter irradiation time compared to a standard CXL protocol. He has further theorized that the higher fluence protocol may have an additional ‘disinfective’ effect, reducing the risk of postoperative infectious keratitis [16▪].
INTRODUCTION
Corneal collagen crosslinking (CXL), initially described by Spörl et al.[1] in 1997 is an increasingly used technique that uses riboflavin and ultraviolet-A (UVA) light to increase the biomechanical stability and resistance of the cornea by inducing crosslinking between collagen fibers.
Keratoconus and progressive postlaser in-situ keratomileusis (post-LASIK) keratectasia (PPLK) are characterized by progressive corneal steepening and stromal thinning [2]. Therapeutic options for visual rehabilitation, such as rigid gas permeable contact lenses or intrastromal corneal ring segments (ICRS), although effective in improving visual acuity, do not address the underlying cause of progressive corneal changes. When progression occurs or contact lens intolerance develops, penetrating keratoplasty or lamellar keratoplasty have traditionally been the next step. CXL has shown promise in slowing, halting, or even reversing progression in both keratoconus and PPLK, thus delaying or preventing the need for more invasive procedures.

CORNEAL COLLAGEN CROSSLINKING PROCEDURE AND BIOMECHANICS

CXL involves the use of riboflavin and UVA light to induce photooxidative collagen crosslinking. Blue light, although not used clinically, has also been shown to be effective in producing significant corneal stiffening in laboratory research [3]. Although there are slight variations, the fundamental technique is as follows: under topical anesthesia, riboflavin 0.1% drops are applied to the central 7 mm of the cornea either with an intact epithelium or after creating a similar sized epithelial defect. Riboflavin is allowed to permeate through the cornea and is periodically reapplied during the procedure to ensure adequate corneal absorption. Riboflavin acts as a photosensitizer for subsequent UVA irradiation with two UV diodes at the desired irradiance of 4 mW/cm2 (5.4 J/cm2) at a 1 cm distance for 30 min [4]. It is also thought to block UVA transmission beyond the corneal stroma, thus protecting the corneal endothelium and deeper intraocular structures such as the lens and retina from unwanted side effects [5▪]. Furthermore, the UVA intensity used during crosslinking is far below the damage threshold for the corneal endothelium, iris, lens, and retina[6].
Additional covalent binding between collagen molecules stabilizes the collagen scaffold and has been shown to increase corneal stiffness and enhance resistance against proteolytic enzymes [3,7–10]. The stiffening effect of CXL is heterogeneously distributed with more pronounced effect in the anterior 200–300 μm of the cornea [8,11,12]. The increased stiffness and rigidity of the cornea stabilizes the corneal ectasia [5▪]

Possible reported complications of CXL, although quite rare, include sterile infiltrates, stromal scars, transient stromal haze, corneal edema, diffuse lamellar keratitis, transient endothelial damage, and herpetic keratitis with iritis [5▪,13,14,15▪]. There has been increased interest recently in decreasing total stromal irradiation time by increasing the fluence of applied UVA light, thus possibly reducing stromal keratocyte loss. Kanellopoulos has shown similar results and adverse effects with use of higher fluence but shorter irradiation time compared to a standard CXL protocol. He has further theorized that the higher fluence protocol may have an additional ‘disinfective’ effect, reducing the risk of postoperative infectious keratitis [16▪].

USE IN KERATOCONUS

Keratoconus is a progressive and bilateral noninflammatory corneal degeneration characterized by cone-like ectasia. Mild-to-severe visual loss results from induction of irregular astigmatism by progressive corneal steepening, apical thinning, and corneal scarring [17]. Its estimated incidence in the general population is one in 2000 [18]. The age of onset is usually at puberty, with 20% of cases eventually progressing to the degree to require penetrating keratoplasty [19]. Patients with keratoconus have significantly impaired quality of life that is comparable with that of patients with advanced age-related macular degeneration despite better visual acuity and younger age [20,21]. Although the exact pathophysiology of keratoconus is not clear, there is increasing evidence that altered enzymatic activity, such as increased levels of pepsin digestion and catalase activity, plays a significant role in degrading the stiffness of the cornea by decreasing cross links [22–25].

Therapeutic options in keratoconus initially involve spectacles or rigid gas permeable contact lenses. When contact lens intolerance, severe irregular astigmatism or stromal opacities develop in advanced cases, penetrating keratoplasty may be required. CXL has emerged as an important tool in these cases to slow, halt or sometimes reverse progression of keratoconus [4,5▪,8,26–28]. First introduced for use in keratoconus by Wollensak et al.[4] in 2003, numerous studies have supported its efficacy in significantly reducing keratometric values and mildly improving visual acuity in patients with progressive keratoconus[4,5▪,8,26–28]. Wollensak et al.[4] reported a mean decrease of 2.01 D in the maximum keratometric value and of 1.14 D in refractive error. Vinciguerra et al.[26] reported a 6.16 D decrease in maximum keratometric value, whereas Caporossi et al.[27] showed improvement or stabilization of keratoconus in 92% of the cases. Wittig-Silva et al.[28] demonstrated a mean decrease of 1.45 D in the maximum keratometric value in a treated group compared to a mean increase of 1.28 D in maximum keratometric value in a control group. Asri et al.[5▪]explored the long-term outcomes, including complications, of CXL in eyes with progressive keratoconus. They reported a significant improvement or stabilization in best corrected visual acuity in 87.6% of eyes with only a 3.5% complication rate leading to vision loss.
Although CXL has been shown to be efficacious in slowing or halting progression of keratoconus, the visual recovery, although statistically significant, is quite modest. As a result, there has been increasing amounts of attention paid to combining CXL with keratorefractive procedures to further improve vision. These surgical approaches include radial keratectomy, photorefractive keratectomy (PRK), asymmetric keratotomy, LASIK, lamellar keratoplasty and epikeratoplasty. Unfortunately, many of these alternatives are fraught with poor refractive predictability and poor stability [29–33].

Recently, use of ICRS for treatment of keratoconus has become more widespread [34–38]. Initially employed to correct low myopia [39–41], ICRS involves placement of two polymethyl methacrylate segments of various thickness in the corneal stroma to flatten the central cornea by an ‘arc-shortening’ effect [34,36]. Colin et al.[34] demonstrated a reduction in mean keratometric of 4.85 D and in spherical equivalent of 2.12 D by placement of ICRS in 10 patients with keratoconus. In a cohort of 74 eyes, Boxer Wachler et al.[37] demonstrated an improvement in visual acuity of two lines or more in 45% of eyes.

Although ICRS has been shown to be effective in decreasing corneal abnormality to improve visual acuity, it does not prevent progression of keratoconus. Alió et al.[38] evaluated the stability of ICRS in 13 keratoconic eyes and showed that between 6 and 36 months, there was an increase in keratometric of 1.67 D. CXL can be a useful adjunct in ICRS to both provide stability and deliver an additive effect on improving visual acuity and topographic characteristics [42–44,45▪,46▪]. Chan et al.[42] found improved outcomes when ICRS was combined with CXL over use of ICRS alone. There was greater flattening in the steep keratometric values and average keratometric values, as well as greater reduction in manifest cylinder. Ertan et al.[43] report a significant improvement in uncorrected visual acuity, best corrected visual acuity, and spherical values in patients undergoing CXL an average of 4 months following ICRS placement.

It is not clear which of the following sequence is most advantageous: simultaneous ICRS and CXL, CXL followed by ICRS, or ICRS followed by CXL. Coskunseven et al.[44] found that ICRS followed by CXL resulted in greater improvement in best corrected visual acuity and reduction in cylinder than vice versa. They hypothesize that the stiffer cornea produced by CXL decreases the flattening effect of ICRS implantation, thus limiting its maximal flattening potential. Additionally, El-Raggal [45▪] has shown that in eyes having undergone CXL 6 months prior to ICRS implantation, more energy was required for femtosecond laser channel creation for ICRS insertion, causing more severe and persistent corneal haze. In a separate study, El-Raggal[47▪] has shown that performing ICRS implantation and CXL on the same day resulted in greater decrease in keratometric compared to ICRS implantation followed by CXL 6 months later. More extensive studies are needed to ascertain the most ideal sequence of ICRS implantation and CXL.

Recently, Kymionis et al.[47▪] have also shown promising results combining PRK with CXL. They showed significant improvement in spherical equivalent refraction, uncorrected visual acuity, best corrected visual acuity, and mean keratometric values that remained stable throughout the follow-up period of up to 25 months. Additionally, none of the patients showed topographic or clinical signs of keratoconus progression during the follow-up period. However, as the authors note, this combination may be more appropriate for patients with early keratoconus because the thinner corneas of more advanced keratoconus would preclude the possibility of further tissue removal by topography-guided PRK.

USE IN PROGRESSIVE POSTLASER IN-SITU KERATOMILEUSIS KERATECTASIA

PPLK is a rare condition, first reported by Seiler et al.[48] in 1998, characterized by a progressive corneal steepening with accompanying refractive changes, loss of visual acuity and stromal thinning [15▪]. Generally occurring within 2 years after LASIK, its incidence in a large series was found to be 660 in 100 000 cases [49–51]. The underlying pathophysiology of PPLK is not well understood, but may in some cases involve worsening of an underlying unrecognized ectatic condition, such as forme fruste keratoconus or pellucid marginal degeneration. LASIK, in creating a corneal flap and subsequent tissue ablation, weakens the anterior stroma, which normally confers more biomechanical strength to the cornea than the posterior stroma [52]. Risk factors for its development are thin corneas, a thin residual stromal bed, deep ablations, enhancement treatments, and preoperative abnormalities such as forme fruste keratoconus. However, it may occur without any of the above factors [2,53,54].

Therapeutic options for PPLK are similar to those available for progressive keratoconus, namely rigid gas permeable contact lenses, ICRS implantation and penetrating keratoplasty. Also similar to keratoconus, CXL has become an increasingly recognized tool to treat PPLK. Kohlhaas et al.[2] first described the successful use of CXL to treat PPLK in 2005. Hafezi et al.[54] soon followed in 2007 in a case series of 10 patients, demonstrating clinically meaningful improvement in keratometric readings in five of 10 patients, reduction in cylinder in all patients, and improvement in best spectacle corrected visual acuity in nine of 10 patients. Salgado et al.[15▪] similarly showed regression of corneal ectasia with flattening of the cornea, as well as improvement of the spherical equivalent in a series of 22 patients up to the sixth postoperative month. Hersh et al.[55▪▪] have reported 1-year outcomes of a prospective, randomized controlled clinical trial on CXL use in both keratoconus and PPLK. Although the entire cohort showed significant improvements in best corrected visual acuity and reductions in maximum keratometric values, there were notable differences in response between keratoconus and PPLK patients. PPLK patients showed a significant improvement in best corrected visual acuity at 1 year compared to preoperative levels, but not at time points in between as was the case in keratoconus patients. Also, keratoconus patients had a significant reduction in maximum keratometric value of 2.0 D, whereas PPLK patients had a nonstatistically significant reduction of 1.0 D. The authors do note, however, that at baseline the PPLK cohort had flatter corneas than the keratoconus cohort, possibly partially accounting for the difference seen [55▪▪]. Biomechanical differences caused by the LASIK flap may also play a role in the less dramatic response to CXL in PPLK patients. CXL preferentially strengthens the anterior stroma, including the flap in PPLK patients, which does not contribute to the mechanical stability of the cornea. Other possible explanations include differences in riboflavin diffusion rate in post-LASIK corneas and intrinsic pathophysiologic differences between keratoconus and PPLK [55▪▪]. In a report of the same cohort published separately, four of seven topography indices (keratoconus index, minimum radius of curvature, index of surface variance, and index of vertical asymmetry) improved in the entire cohort with no significant difference between keratoconus and PPLK patients in terms of change in any topography index from baseline to 1 year, postoperatively [56▪▪].
Similar to progressive keratoconus, combining CXL with ICRS for PPLK has been advocated by some. Kamburoglu et al.[57] report a case of bilateral PPLK successfully treated with initial ICRS followed by CXL, resulting in improvement in visual acuity and reduction in keratometric values. Interestingly, there was a slight decrease in the effect of ICRS in the right eye when CXL was delayed for 1 month, whereas the left eye did not suffer such a decrease in ICRS when CXL was performed the day following ICRS implantation, highlighting the fact that only CXL addresses the underlying cause of progressive ectasia.

FUTURE APPLICATIONS

There are several other potential uses of CXL that are increasingly being promoted, including combined CXL–orthokeratology for keratoconus, combined LASIK–CXL to stabilize the effects of LASIK and possibly prevent subsequent ectasia, combined CXL–microwave thermal keratoplasty for mild myopia, and CXL alone for mild myopia. Thus far, there is limited peer-reviewed literature on the efficacy of the above combinations.

Orthokeratology involves the use of a specially designed rigid contact lens to reversibly alter corneal shape to improve mild refractive error[58]. Calossi et al.[59] proposed the novel use of orthokeratology to reduce corneal aberration in progressive keratoconus and evaluated the efficacy of CXL in stabilizing the orthokeratology molding effect. They found that orthokeratology temporarily improved corneal shape and reduced corneal aberration in five eyes with progressive keratoconus, but this effect was more transient than that found in nonkeratoconus eyes. Furthermore, CXL after orthokeratology did not stabilize the change in corneal shape, with topography and wave-front error returning to baseline levels 1 month after orthokeratology interruption. However, both uncorrected visual acuity and best spectacle corrected visual acuity maintained an improvement over baseline levels 1 year after orthokeratology–CXL [59].

There are no peer-reviewed publications examining CXL for mild myopia, combining CXL with LASIK, or combining CXL with microwave thermal keratoplasty. Kampik et al.[60] have shown that in enucleated porcine eyes previously treated with CXL, subsequent LASIK results in decreased refractive change and increased flap thickness. Further studies are needed to ascertain wheth

CONCLUSION

In summary, CXL is a powerful tool that can induce corneal stiffening in ectatic corneas. It has been shown to be effective in halting, and sometimes reversing the progression of both keratoconus and PPLK, while having a relatively low complication rate. Its use as an adjunct with keratorefractive procedures show promise in improving visual outcomes and possibly decreasing or delaying the need for penetrating keratoplasty. However, more long-term data are required to assess the stability of change as well as long-term complication rates. In addition, more studies are needed to ascertain whether PPLK and keratoconus respond differently to CXL. Lastly, further studies are needed to determine the efficacy of potential uses of CXL in combination with other keratorefractive procedures.


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