Lamellar corneal transplantation.

Penetrating keratoplasty (PK) has been the gold standard for the surgical treatment of most corneal pathologies; lamellar keratoplasty that only replaces the diseased corneal layers has recently evolved as an alternative, however. Innovations in surgical technique and instrumentation provide visual outcomes comparable to PK. We review the indications and outcomes of various techniques of anterior lamellar surgery developed to treat stromal disorders. Similarly, we discuss posterior lamellar keratoplasty techniques such as Descemet stripping automated endothelial keratoplasty and Descemet membrane endothelial keratoplasty. Posterior lamellar keratoplasty provides faster visual rehabilitation than PK in cases of Fuchs endothelial dystrophy and pseudophakic bullous keratopathy. In addition, for medically unresponsive infectious keratitis, therapeutic anterior lamellar keratoplasty yields similar graft survival to PK without an increased risk of disease recurrence.

Endothelial survival after Descemet-stripping automated endothelial keratoplasty in eyes with retained anterior chamber intraocular lenses: two-year follow-up.

PURPOSE: To evaluate endothelial cell survival 2 years after Descemet-stripping automated endothelial keratoplasty (DSAEK) for the treatment of endothelial dysfunction in the presence of an anterior chamber intraocular lens (AC IOL). SETTING: LSU Eye Center, New Orleans, Louisiana, and Florida Eye Microsurgical Institute, Boynton Beach, Florida, USA. DESIGN: Case series. METHODS: This study comprised eyes with endothelial failure that had DSAEK in the presence of an AC IOL. Donor central endothelial cell density (ECD) was recorded 6 months, 1 year, and 2 years postoperatively and compared with preoperative ECD eye-bank values. RESULTS: The study evaluated 25 eyes; data from 20 eyes were available up to 2 years postoperatively. The mean preoperative ECD was 2606 cells/mm(2). At 1 year, the mean ECD was 1943 cells/mm(2) ± 266 (SD), representing a mean cell loss from preoperative measurements of 24% ± 12%. At 2 years, the mean ECD was 1831 ± 291 cells/mm(2), representing a 28% ± 13% cell loss from preoperative values. The additional cell loss between the first and second postoperative years was not statistically significant (P=.265). CONCLUSIONS: Descemet-stripping automated endothelial keratoplasty grafts in the presence of a well-centered AC IOL with an AC IOL-to-endothelial depth greater than 3.0 mm had a mean postoperative donor endothelial cell loss of 24% at 1 year and 28% at 2 years. There was no significant difference in cell loss in this series compared with ECD loss in DSAEK surgeries in the presence of a posterior chamber IOL. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.

Endothelial cell survival after descemet stripping with automated endothelial keratoplasty with retained anterior chamber intraocular lens.

PURPOSE: To evaluate the donor endothelial cell loss in the first year after Descemet stripping endothelial keratoplasy (DSAEK) for the treatment of endothelial dysfunction in the presence of an anterior chamber (AC) intraocular lens (IOL). METHODS: We performed a retrospective study of a surgical case series of 25 patients who underwent DSAEK in the presence of an AC IOL. The donor central endothelial cell density (ECD) was recorded at 6 months and 1 year postoperatively and then compared with the preoperative eye bank values. RESULTS: The average and SD ECD at 6 months was 1876 ± 286 cells per square millimeters representing a mean cell loss from preoperative ECD measurement of 37% ± 13%. At 1 year postoperatively, ECD was 1793 ± 311 cells per square millimeters that correspond to a 40% ± 11% cell loss from preoperative ECD measurement. The increased cell loss between 6 months and 1 year was not significant statistically (P = 0.365). CONCLUSIONS: DSAEK in the presence of a well-centered AC IOL and an AC depth greater than 3 mm has a mean donor endothelial cell loss of 37% at 6 months and 40% at 12 months postoperatively. We found no difference in cell loss in our series compared with previous ECD loss in DSAEK surgery alone. Emphasis in a surgical technique that minimizes tissue manipulation and reduces the risk of graft-AC IOL touch should be considered to maximize the endothelial graft survival in these cases.

Role of platelet-activating factor in cell death signaling in the cornea: A review.

Platelet-activating factor (PAF) is a potent bioactive lipid generated in the cornea after injury whose actions are mediated through specific receptors. Studies from our laboratory have shown that PAF interactions with its receptors activate several transmembrane signals involved in apoptosis. Continuous exposure to PAF during prolonged inflammation increases keratocyte apoptosis and inhibition of epithelial adhesion to the basement membrane. As a consequence, there is a marked delay in wound healing, which is not countered by the action of growth factors. While apoptosis of stroma cells is rapid and potent, epithelial cells as well as myofibroblasts, which appear in the stroma during the repair phase, are resistant to apoptosis. However, PAF accelerates apoptosis of corneal epithelial cells exposed to oxidative stress by stimulating phospholipase A2, producing an early release of cytochrome C from mitochondria and activating caspase-3. In myofibroblasts, PAF has a synergistic action with tumor necrosis factor-alpha (TNF-alpha), increasing apoptosis of the cells to 85%. PAF antagonists block the effects of PAF and could have a therapeutic role in maintaining a healthy and transparent cornea.

Immunofluorescence of rabbit corneas after collagen cross-linking treatment with riboflavin and ultraviolet A.

PURPOSE: To assess ultrastructural modifications in keratocytes and inflammatory cell response in rabbit corneas after riboflavin and ultraviolet A exposure using immunofluorescence microscopy. METHODS: Twenty adult New Zealand albino rabbits weighing 2.0­3.0 kg were used in this study. Two rabbits served as controls.The animals had their epithelia removed and were cross-linked with riboflavin 0.1% solution (10 mg riboflavin-5-phosphate in 10 mL of 20% dextran-T-500) applied every 3 minutes for 30 minutes, and exposed to ultraviolet A (360 nm, 3 mW/cm2) for 30 minutes. Four rabbits were humanely euthanized at each time point of 1, 3, and 11 days and at 3 and 5 weeks after the procedure. Immunohistochemistry studies of thin sections of each cornea were performed using terminal deoxynucleotyl transferase­mediated uridine triphosphate biotin nick-end labeling staining, alpha smooth muscle actin (a-SMA),CD-3, myeloperoxidase antibodies, and 4',6-diamidino-2-phenylindole(DAPI) counterstaining. In another experiment, 6 additional rabbits were treated as above, and after 10 days of cross-linking, 5 mL of lipopolysaccharide endotoxin (1 mg/mL) was injected in the midstroma. RESULTS: Cross-linked corneas showed early stromal edema. By 5 weeks, complete resolution of the edema and a pronounced highly-organized anterior 200-mm fluorescent zone was observed. Terminal deoxynucleotyl transferase mediated uridine triphosphate biotin nick-end labeling staining showed keratocyte death by both necrosis and apoptosis between days 1 and 3 after cross-linking. At day 1,the limbal area close to the cross-linking zone showed some inflammatory cells and a-SMA­positive cells, indicative of the presence of myofibroblasts. By day 3, some myofibroblasts had migrated to the area beneath the cross-linked stroma. Between days 3 and 5 weeks, there was an increase in a-SMA staining in the area surrounding the cross-linked stroma. The area of cross-linking remained acellular up to 5 weeks. CONCLUSIONS: Collagen cross-linking results in early edema,keratocyte apoptosis, and necrosis, appearance of inflammatory cells in the surrounding area of treatment and transformation of surrounding keratocytes into myofibroblasts. Compaction of anterior stroma fibers, keratocyte loss, and displacement of cell nuclei including inflammatory cells may have clinical implications in the long-term risk of further corneal thinning in keratoconus and in the cross-linked corneal immune response.

Safety of DSAEK in patients with previous glaucoma filtering surgery.

PURPOSE: To report 4 cases of Descemet stripping automated endothelial keratoplasty (DSAEK) in the presence of previous glaucoma filtering surgery. DESIGN: Observational case series. METHODS: Review of clinical data of 4 patients who underwent DSAEK successfully performed in the presence of previous glaucoma filtering surgery with endothelial survival rates comparable with larger series published previously and good postoperative intraocular pressure (IOP) control. RESULTS: The endothelial cell loss was 36% and 39% mean cell loss at 6 months and 1 year postoperatively. The IOP remained well controlled within target levels in all patients. No complications were reported in any of the 4 cases. CONCLUSIONS: Corneal endothelial failure can be successfully managed with DSAEK in glaucoma patients with previous filtering surgery with good endothelial survival rates and IOP control.

Bilateral reversible corneal edema associated with amantadine use.

PURPOSE: In this article, we report a case of bilateral severe reversible corneal edema caused by amantadine therapy. CASE: A 39-year-old women was referred to us for evaluation of bilateral corneal edema. Her past medical history was significant for multiple sclerosis, anorexia, and seizures. She developed painless progressive bilateral loss of vision for the past 6 months. She was evaluated by several ophthalmologists elsewhere who felt that the patient's visual loss was secondary to a nutritional deficiency as opposed to related to multiple sclerosis. She was started on vitamin B-12 medication without improvement in her symptoms. She was then evaluated by neuro-ophthalmology. The examination revealed severe bilateral corneal edema and was referred to our corneal service for further evaluation of her corneal condition. Our examination revealed best corrected visual acuity of 20/400 bilaterally. Corneal thickness was 940 microm in the right eye and 802 microm in the left. Color vision was intact. Conjunctivas were white bilaterally. Cornea evaluation revealed diffuse stromal edema and Descemet's folds and microcystic subepithelial edema with to guttae noted. Anterior chambers were deep and quiet. A specular microscopy revealed significant pleomorphism and polymegathism with an endothelial cell count of 1,504 cells in the right eye and 1,596 in the left eye. RESULTS: Review of the patient's medical information revealed therapy with amantadine 2 months prior to the appearance of the patient's symptoms as a means to control the patient's tremors. The patient experienced rapid resolution of the corneal edema within the next 2 months after discontinuation of the agent with recovery of best corrected visual acuity of 20/40 in the right eye and 20/30 in the left. CONCLUSIONS: In cases of unexplained corneal edema and in the absence of any identifiable ocular cause, a review of toxic effects of systemic medications should be performed. Early diagnosis may prevent irreversible endothelial damage. Amantadine can cause endothelial failure and needs to be considered as part of the differential diagnosis of corneal edema.

Effect of the shape of the endothelial graft on the refractive results after Descemet's stripping with automated endothelial keratoplasty.

OBJECTIVE: To investigate the magnitude and the possible causes of the refractive changes after Descemet's stripping with automated endothelial keratoplasty (DSAEK). In this article we describe the changes in corneal power after DSAEK and correlate them with the shape, diameter, and thickness of the endothelial graft obtained. STUDY DESIGN: Retrospective chart review. PARTICIPANTS: 17 consecutive patients who underwent DSAEK at the Rand Eye Institute in 2007. METHODS: The preoperative and post-DSAEK corneal power was determined using Gaussian optics and correlated with the DSAEK graft diameter and central, paracentral (P1), and peripheral (P2) graft thickness using images obtained from the Pentacam Scheimpflug. RESULTS: During DSAEK there is addition of corneal tissue in the posterior layers of the cornea, which reduces the radius of curvature of the posterior layer of the cornea and also the total corneal power. The mean anterior:posterior corneal radius of curvature ratio after DSAEK is 72.3% (SD 4.63%). In consequence, the keratometry values calculated after DSAEK using the Gaussian optics method are less than those measured by manual keratometry after surgery. A strong correlation was observed between the postoperative Gaussian keratometric power and the ratio of the central corneal DSAEK graft thickness (C) to the mean P2 measured at 7 mm optical zone (C:P2) (r2 = 0.63, p< 0.01). CONCLUSIONS: DSAEK induced a mean hyperopic shift of 1.05 (SD 0.76) D. The mean anterior:posterior corneal radius of curvature ratio decreased to 72.3%. Despite a great variability, the ratio between the central DSAEK graft thickness and the graft thickness at the 7 mm optical zone (C:P2 ratio) was correlated with the magnitude of the change in corneal power and induced hyperopia, which produces a steeper posterior corneal surface. No correlation between the DSAEK graft diameter and change in corneal power was noted. Customization in the shape of the donor graft lenticle might reduce the hyperopic shift noted after DSAEK.

Immunohistological evaluation of the healing response at the flap interface in patients with LASIK ectasia requiring penetrating keratoplasty.

PURPOSE: To evaluate the healing response at the flap interface in corneas with LASIK ectasia that required penetrating keratoplasty (PK). METHODS: Corneas of five patients who developed corneal ectasia after LASIK (range: 2.5 to 5 years postoperative) were collected after corneal transplant surgery. The corneas were bisected and processed for conventional histologic analysis and immunofluorescence. RESULTS: Light microscopy showed a hypocellular fibrotic scar at the wound margin compared with the adjacent corneal stroma in all eyes. All corneas had positive staining for alpha-smooth muscle actin (SMA), a myofibroblast marker. In one eye, alpha-SMA cells were located in the fibrotic scar region in the area of the semicircular ring of haze along the margin of the LASIK flap corresponding to an area of epithelial ingrowth. In all other eyes, alpha-SMA positive cells were fewer and mainly located in the superficial stroma under the epithelial wound margin surface. Type III collagen was minimal or absent in the central zone and wound margin of all corneas except for the cornea with epithelial ingrowth present in the hypercellular fibrotic scar region. Chondroitin sulfate was stronger in the periphery of the flap wound coinciding with a higher presence of alpha-SMA-positive cells in that region. Positive staining for matrix metalloproteinase 9 (MMP-9) in the paracentral wound margin scar was seen. CONCLUSIONS: A wound-healing process characterized by absence of significant fibrosis and myofibroblasts at the wound edge in the flap interface was noted in all keratectatic eyes. However, changes in the composition of collagen and the presence of MMP-9 at the wound edge several years after LASIK indicates active wound remodeling that may explain the ongoing loss of tissue and tendency of the cornea to bulge.

A novel platelet activating factor receptor antagonist reduces cell infiltration and expression of inflammatory mediators in mice exposed to desiccating conditions after PRK.

PURPOSE: To study the contribution of a novel PAF receptor antagonist LAU-0901 in the modulation of the increased inflammatory response in mice exposed to dessicating conditions (DE) after PRK. METHODS: Eighty 13-14 week old female Balb/C mice were used. They were divided into two groups: One group was treated with LAU-0901 topical drops. The other group was treated with vehicle. In each group ten mice served as controls and ten were placed in DE. The other twenty mice underwent bilateral PRK and were divided in two additional groups: ten mice remained under normal conditions (NC) and the other ten were exposed to DE. After 1 week all animals underwent in vivo confocal microscopy, immunostaining and western blotting analysis. RESULTS: Confocal microscopy showed an increased number of reflective structures in the corneal epithelium after PRK and exposure to DE in eyes treated with vehicle as compared to eyes treated with LAU-090). Significant decrease of COX-2 and Arginase I expression and reduced alpha SMA cells was observed after PRK and exposure to DE in eyes treated with LAU-0901. DISCUSSION: Exposure of mice to a DE after PRK increases the epithelial turnover rate. PAF is involved in the inflammatory cell infiltration and expression of inflammatory cytokines that follow PRK under DE.

Novel therapeutic approach in the management of band keratopathy using amniotic membrane transplantation with fibrin glue.

A 91-year-old man with advanced glaucoma, status post trabeculectomy, and pseudophakia had a symptomatic recurrent band and bullous keratopathy in his left eye. Three previous ethylenediaminetetraacetic acid chelations with immediate recurrence of the calcic band keratopathy with frequent breakdown produced recurrent painful corneal epithelial defects. The calcified lesions were removed surgically, resulting in a smooth ocular surface. An 8-mm, 100-micron trephination was performed and a 360 degrees corneal lamellar peripheral dissection pocket was created. After covering the denuded corneal surface, the edges of the amniotic membrane were introduced into the pocket and secured using fibrin sealant. Additional amniotic membrane was glued to the nasal en temporal corneal areas and a collagen shield was applied. Wound healing was completed in 10 days and a stable ocular surface was restored without pain or inflammation. During the follow-up period, no recurrence of the band keratopathy was observed.

Cystoid macular edema in a pseudophakic patient after switching from latanoprost to BAK-free travoprost.

PURPOSE: The aim of this study was to report a case of cystoid macular edema (CME) in a pseudophakic patient after switching from latanoprost to BAK-free travoprost. METHODS: This study is presented as an interventional case report. RESULTS: Clinical examination showed the development of CME, proven by ocular coherence tomography, after institution of BAK-free travoprost in a patient that was previously treated with Latanoprost. Ocular signs and symptoms responded to stopping travoprost and treatment with topical prednisolone and non-steroidal anti-inflammatory medicines. The intraocular pressure was successfully controlled with brimonidine tartrate 0.15%. CONCLUSIONS: CME is a known adverse effect of all prostaglandin analogs. However, our patient developed this complication after being switched from latanoprost to BAK-free travoprost. This may be due to exacerbation of a previously undiagnosed CME or to the ionic-buffered preservative system (sofZia) alone or in combination with travoprost unique to this product. It is prudent to exercise caution in the use of prostaglandin analogs and prostamides especially in high-risk eyes.

Autogenous lamellar scleral graft in the treatment of scleral melt after pterygium surgery.

BACKGROUND: We report a case series of three patients who developed scleral melting 18-26 months after pterygium removal with beta-irradiation that refused to use any donor tissue. CASE SERIES: All patients presented with constant pain, redness and foreign body sensation on their eye. RESULTS: Initial evaluation revealed the presence of an area of scleral melt and epithelial defect with an underlying calcific plaque over the necrotic area in the nasal conjunctiva. Fluorescein staining and pooling was present at the base of the defect, indicating epithelial loss, in two patients. No signs of infection were present, and screening for associated systemic risk factors for melting was negative in all cases. The patients refused to use any kind of donor tissue to cover the area of melting. An autogenous lamellar scleral graft harvested from the superotemporal quadrant and an advancement of the nasal tenon was used. CONCLUSION: The use of autologous sclera and tenon has been described in the treatment of avulsive corneoscleral wounds and corneal fistulas. This case series describes the successful management of scleral melting with autogenous tissues.

Comparative in vivo high-resolution confocal microscopy of corneal epithelium, sub-basal nerves and stromal cells in mice with and without dry eye after photorefractive keratectomy.

BACKGROUND: The present study compares, using a new-generation high-resolution in vivo confocal microscope, the epithelial morphology, sub-basal nerves and stroma in two groups of mice: one exposed to normal conditions (NC) and the other to a desiccating environment (DE), following photorefractive keratectomy (PRK) with mechanical epithelial scraping. METHODS: Twenty-four 4- to 8-week-old female Balb/C mice were used in this study. Twenty mice underwent bilateral corneal epithelial scraping using an electric brush prior to PRK. Then, the mice were divided in two groups: 10 mice were placed in NC. The other 10 mice were exposed to a DE for 2 weeks. Four mice served as controls. Corneas were analysed in vivo using the Rostock Cornea Module of the Heidelberg retina tomograph II. For all eyes, 20 confocal microscopic images of each layer, that is, the superficial and basal corneal epithelium, Bowman's layer, anterior and posterior stroma and the endothelium, were recorded. Epithelial and stromal cell densities and sub-basal and stromal nerves were measured and compared. RESULTS: There was a higher density of superficial epithelial cells in the DE group (693 +/- 148 cells/mm(2) in NC group and 443 +/- 128 cells/mm(2) in DE group; Mann-Whitney U-test; P = 0.05). Higher number of basal cells were observed in the DE group. Its density was 986 +/- 198 cells/mm(2) in NC and 1598 +/- 280 cells/mm(2) in DE group (Mann-Whitney U-test; P < 0.05). Significantly higher number of reflective structures were noted within the stroma without clearly visible nuclei in the DE group compared with the NC eyes. Additionally, higher number of beads, nerve sprouts and higher tortuosity of sub-basal nerves were observed in the DE group. No difference was observed in the endothelial cell density between the groups. CONCLUSION: Exposure of corneas to a DE after PRK with previous mechanical epithelial scraping increases epithelial turnover and is associated with a higher number of reflective structures in the stroma. Additionally increased nerve beading, nerve sprouts and tortuosity of sub-basal nerves were observed in the DE group, possibly directed to repair the alterations observed at the epithelial level.

Safety and stability of laser in situ keratomileusis for myopic correction performed under thin flaps.

BACKGROUND: To determine the safety and long-term refractive stability of laser in situ keratomileusis (LASIK) performed under thin flaps (<110 microm) and to compare them with those of conventional thicker flaps (>110 microm). METHODS: This retrospective study consisted of 120 myopic eyes of 68 patients who underwent LASIK performed with the use of the Moria M2 microkeratome and the Technolas Keracor 117C excimer laser. Indicators of efficacy, predictability, and long-term stability were followed for 1 year after surgery and were compared among 3 groups of patients that varied according to the flap thickness used: thin (<110 microm, n = 29), medium (111-139 microm, n = 47) and thick (>140 microm, n = 44). RESULTS: One year after myopic LASIK, the mean spherical equivalent refraction for the thin-flap group A was -0.37 (standard deviation [SD] 0.44) diopters (D); medium-flap group B was -0.48 (SD 0.55) D; and thick-flap group C was -0.43 (SD 0.45) D. The percentage of eyes with spherical equivalent refraction within SD 0.50 D and SD 1.00 D of emetropia was 84% and 92% for group A, 82% and 91% for group B, and 79% and 90% for group C, respectively. Buttonholes were encountered in 3% of eyes in group A compared with 0% in the other 2 groups. Epithelial ingrowth and peripheral flap striae occurred in 7% and 7% in group A, 2% and 2% in group B, and 2% and 0% in group C, respectively. INTERPRETATION: Thin-flap LASIK (<110 microm) produces more intra- and early post-operative complications compared with thick-flap LASIK (>110 microm). However, if a thin flap is created and there are no complications, or if the complications are successfully managed, there does not appear to be any difference in the long-term refractive results.

New surgical approach for superior conjunctivochalasis.

PURPOSE: To show poor adhesion between the conjunctiva and the sclera in eyes with superior conjunctivochalasis (CCh) and to introduce a new surgical approach by reinforcing adhesion between the conjunctiva and the sclera for correcting this deficiency. METHODS: After conjunctival peritomy and removal of the loose Tenon remnants, "Tenon reinforcement" for conjunctival adhesion to the underlying sclera was achieved by transplantation of cryopreserved amniotic membrane with fibrin glue (group A, 9 eyes of 6 patients) or 10-0 nylon sutures (group B, 8 eyes of 6 patients) in 17 eyes of 12 patients with refractory superior CCh. RESULTS: The mean age of patients was 68.2 +/- 9.8 years (range, 54-80 years). Superior CCh was associated with a superior limbic keratoconjunctivitis (SLK)-like clinical feature before surgery and found to exhibit dissolved Tenon capsule during surgery in all patients. During a mean follow-up of 3.7 +/- 1.9 months after surgery, all eyes achieved smooth conjunctival surface without any sign of CCh. Complete resolution of symptoms was seen in 9 eyes (52.9%) and significant resolution in 8 eyes (47.1%). There was no significant difference between groups A and B in improvement of symptoms and signs. No complications related to surgery were noted during follow-up. CONCLUSIONS: We propose that loose and dissolved Tenon tissue is correlated with the development of superior CCh, which may result in an SLK-like appearance by blink-related microtrauma. Reinforcement of conjunctival adhesion onto the sclera by amniotic membrane with either fibrin glue or sutures is effective in alleviating symptoms and signs in eyes with superior CCh.

Healing process at the flap edge in its influence in the development of corneal ectasia after LASIK.

PURPOSE: Post-laser in situ keratomileusis (LASIK) corneal ectasia is a progressive deformation of the gross corneal anatomy that occurs after surgery. However, this is a rare event even after deep lamellar keratoplasty. We hypothesize that the strength of the lamellar keratoplasty wound is derived from the sutures that enhance the wound edge healing response. This study compares, in a rabbit model, the stability of previously sutured and unsutured microkeratome flaps. METHODS: Unilateral 160-micro m-thick LASIK flaps using a mechanical microkeratome was performed in 20 rabbit eyes. Animals were then divided in two groups: In group A, the flap was left without sutures. In group B, the flap was sutured with 12 interrupted 10/0 nylon stitches that were removed after 3 weeks under general anesthesia. Six weeks after surgery, all rabbits had corneal topographies performed at their baseline intraocular pressure (IOP) (14 mmHg) and at two artificially increased pressures (25 and 45 mmHg) using an anterior chamber maintainer implanted in the inferior limbal area. The animals were humanely euthanized, and immunohistological analysis of the corneas was performed. RESULTS: A delta K1 value, which indicates the difference in the simulated keratometric value at baseline and the one measured at 25 mmHg, was calculated for all eyes. It showed a mean steepening effect of 2.74 D +/- 0.38 D in group A compared with 1.08 D +/- 0.27 D in group B (p < 0.05). Similarly, a delta K2 value, which indicates the difference in the simulated keratometric value at baseline and the one obtained at 45 mmHg, was registered. It showed a mean steepening effect of 3.02 D +/- 0.87 D in group A compared with 0.75 D +/- 0.44 D in group B (p < 0.05). Six weeks after surgery, the peripheral flap interface in group B consisted of 14.3% +/- 4.15% of positive monoclonal mouse anti-alpha smooth muscle actin (alpha-SMA) cells compared with 4.18 +/- 3.76% in group A (p < 0.05). CONCLUSIONS: The addition of sutures in the corneal flap after LASIK appears to reduce the amount of corneal steepening when the IOP is artificially increased up to 25 mmHg in this rabbit model. Our results suggest that an increase in the amount of myofibroblastas induced by the sutures may be responsible for this behavior. Corneal ectasia may be related to the clinically observed lack of corneal wound-healing at the edge of the flap that allows the cornea to bulge. By stimulating a stronger wound-healing response at the edge of the flap, the cornea may better resist steepening under increased IOP conditions and improve the long-term stability of LASIK surgery in borderline thin corneas.

A new surgical technique for anterior segment ectasia: tectonic lamellar sclerokeratoplasty.

A 41-year-old patient with severe anterior segment ectasia and a previous history of failed corneal graft was treated by placing a 14-mm tectonic corneoscleral allograft in the eye to support both the corneal and the scleral thinning. Nylon 10-0 interrupted sutures were used at the sclero-scleral junction. The host conjunctiva, including the limbal area, was carefully sutured to the donor limbal area. Three months postoperatively, the graft was stable with no progression of the ectasia. The suturing of a corneoscleral graft over a severely ectatic cornea may be an acceptable technique for providing tectonic tissue support and stabilizing eyes with severe anterior segment ectasia.

Surgical correction of hyperopia.

Surgical attempts to correct hyperopia have yielded varying results over the last 130 years. These techniques include the reshaping of the cornea through incisions, burns, or lamellar cuts with removal of peripheral tissue; the addition of central inlays; laser ablations; and the replacement of the crystalline lens. By examining the success of each surgical technique, the refractive surgeon may be able to make an informed decision on its indications and limitations, based on the specific patient's characteristics. Reporting the outcomes and complications of hyperopic surgery will help refine our approach to the management of an increasingly hyperopic and presbyopic population.

Wound-healing response and refractive regression after conductive keratoplasty.

PURPOSE: To characterize the histological changes that occur after conductive keratoplasty (CK) using a rabbit model. SETTING: LSU Eye Center and Neuroscience Center of Excellence, Louisiana State University Health Sciences Center, School of Medicine, New Orleans, Louisiana, USA. METHODS: Conductive keratoplasty was performed on 24 eyes of 12 New Zealand albino rabbits. In each eye, 24 spots were placed in a cross-corneal manner using 3 optical zones at 6.0, 7.0, and 8.0 mm. Eyes were assessed with corneal topography weekly. Rabbits were humanely killed 2, 4, 6, and 8 weeks postoperatively. The eyes were then enucleated and processed for histopathology and immunohistochemical analysis. RESULTS: All eyes showed an initial mean steepening of the corneal curvature of 2.24 diopters (D) 2 weeks postoperatively. Corneal topography revealed a 26%, 36%, and 39% regression of the refractive results at 4, 6, and 8 weeks, respectively. Immunohistochemical analysis demonstrated keratocyte apoptosis, myofibroblast appearance, and upregulation of chondroitin sulfate, MMP-1, and collagen III in the area surrounding the tip in each spot. CONCLUSION: The histological changes that occur after CK may be responsible for the well-established regression of its refractive effect. A better understanding of the wound-healing response after CK is necessary to improve the long-term stability of the procedure.