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have reported different hydraulic behaviours between stromal bed and LASIK flap in human eye bank corneas, in 2 experimental models of interface fluid syndrome.
We present a case of transient corneal edema after cataract surgery, confined to the LASIK flap. This would confirm, in vivo, the different hydraulic behaviour of the LASIK flap compared with the stromal bed and the rest of the cornea.
A 58-year-old male was referred to our clinic for cataract surgery in his left eye. Seven years before he had had an uneventful femtosecond LASIK surgery to correct a refractive error of –4.00, –0.75 × 90° in his left eye with plano result. He had a nuclear cataract, 2530 endothelial cells/mm2, and the central corneal thickness was 520 μm measured by ultrasonic pachymeter. He had neither signs nor family history of glaucoma. An uneventful phacoemulsification technique was performed, and a monofocal intraocular lens was implanted. The patient was instructed to apply topical antibiotic and steroid drops every 6 hours.
On postoperative day 1, the uncorrected distance visual acuity was 20/80. The slit-lamp examination showed corneal edema circumscribed to the LASIK flap (Fig. 1); the underlying residual stromal bed and cornea surrounding the flap limits were clear. The intraocular pressure (IOP) was 25 mm Hg and the lens was correctly positioned in the capsular bag. No fluid was detected in the interface between the flap and the stromal bed with the anterior segment optical coherence tomography (Fig. 2). Topical timolol maleate twice a day and hyperosmotic eye drops 3 times daily were prescribed in addition. One week later, the UCVA improved to 20/25, the flap edema was completely resolved, and IOP was 16 mm Hg.
Corneal hydration is determined by factors such as endothelial pump, epithelial barrier, water evaporation, IOP, and stromal swelling pressure, mainly because of keratan and chondroitin sulfate.
It seems that the anatomical and biomechanical changes that occur in the cornea after a LASIK flap creation might alter the balance between the factors that define the corneal hydration or the response to an acute hydraulic stress. In fact, Dawson et al.
evaluated the behaviour of human eye-bank donor corneas that had undergone LASIK surgery years before, using 2 models that caused cornea edema. The authors found that the fluid tends to accumulate within the flap and in the flap–stroma interface, thus proving that the flap has different properties, from the hydraulic conductivity point of view, than the rest of the cornea.
Interestingly, in our case, no fluid was found in the interface, but a corneal edema confined to the LASIK flap developed, suggesting a different hydraulic behaviour of the flap compared with the stromal bed “in vivo.”
It is accepted that the flap creation changes the corneal biomechanical properties. Therefore, the superficial corneal lamellae of the LASIK flap may be less strongly attached to the peripheral cornea than the posterior lamellae within the stromal bed,
found a significant decrease of the keratocyte density in both the stromal flap and the stromal bed months after LASIK, although the average cell density throughout the whole cornea was not decreased. Keratocytes are involved in the synthesis of collagen molecules and glycosaminoglycans, both crucial in maintaining stromal homeostasis. In fact, the specific distribution of the different proteoglycans, which have different water affinity, may play a role in the establishment of water gradients across the cornea (i.e., keratan sulfate, more hydrophilic, is predominantly located in the posterior stroma, whereas dermatan sulfate, less hydrophilic, is predominantly located in the anterior stroma).
Therefore, LASIK-induced changes in the keratocyte density might modify the normal distribution of proteoglycans throughout the cornea, thus explaining the peculiar distribution of water seen in acute corneal edema in these eyes.
Finally, the stronger adhesion that a femtosecond laser-created flap seems to have to the stromal bed in comparison with mechanical microkeratome flaps
may modify the response of the flap to an acute hydraulic stress. An increased IOP or a transient endothelial dysfunction that commonly happen after cataract surgery might have caused the corneal edema confined to the LASIK flap in our case.