Ординатура / Офтальмология / Английские материалы / Jaypee Gold Standard mini Atlas Series Lasik_Aragawal, Jacob_2009
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complications such as irregular astigmatism or threatening to cause stromal necrosis or flap melt. Treatment is also indicated in case of symptomatic ingrowth. Numerous techniques have been described for the management of epithelial ingrowth. Techniques for removal include scraping of epithelial ingrowth and excimer laser phototherapeutic keratectomy (PTK). The flap is reflected and the ingrowth is removed by peeling off as a sheet using fine forceps (Figures 3.1 A to D) or by scraping from both the stromal bed as well as the undersurface of the flap. The bed is then irrigated well before replacing the flap. Excimer laser PTK may also be used to remove the epithelial cells. Adjuncts such as cryotherapy, cocaine, Nd:YAG laser, mitomycin C, and sutures may lead to a decreased incidence of recurrence. Some authors have reported success with ethanol and laser therapy for recurrences. The major bugbear in the management of epithelial ingrowth is the high incidence of recurrences even after treatment. Recurrence of epithelial ingrowth after treatment has been reported to be as high as 44%.
Recurrence of ingrowth can be caused due to improper adhesion of the flap to the bed which leaves behind a potential space for the cells to grow into. It has been suggested to place interrupted sutures with just enough
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tension to oppose the flap to the bed without inducing striae at the site of ingrowth after epithelial removal. The sutures can be removed after 1 month.
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Figure 3.2A
Figure 3.2B
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Figure 3.2C
Figure 3.2D
Figures 3.2A to D: Post-LASIK infections (Courtesy: Nibaran Gangopadhyay). (A) Corneal ulcer with hypopyon after LASIK;
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(B) Corneal defect staining with fluorescein; (C) Status Postpenetrating keratoplasty and (D) Reinfection with hypopyon after penetrating keratoplasty
Laser in situ keratomileusis (LASIK) has become a very common refractive procedure today and is generally considered very safe. The incidence of sight threatening complications after LASIK still remains low. In this backdrop, post-LASIK infections can threaten to be a disastrous complication for the patient who is very often just undergoing a cosmetic procedure and usually has very high expectations (Figure 3.2). Infection occurring after photorefractive keratectomy (PRK) may be secondary to the defect in the epithelium as well as the use of therapeutic contact lenses. Unlike photorefractive keratectomy (PRK), the integrity of Bowman’s membrane and the corneal epithelium is maintained intact after LASIK, hence the risk for microbial keratitis after LASIK is considered lower than other procedures. Despite this, the occurrence of keratitis after LASIK is a reality and numerous case reports testify this. During surgery, the corneal stroma may come into contact with infectious agents coming from the patient’s own body or from contaminants present on the instruments. The surgeon and the operating room may also act as a source. Breaks in the epithelial barrier and
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excessive surgical manipulation are other risk factors. Other factors in the postoperative period such as delayed postoperative re-epithelialization of the cornea, the use of topical steroids and therapeutic contact lenses as well as the decreased corneal sensitivity and the dry eye situation may all contribute to post-LASIK infections.
Infectious keratitis generally presents later than diffuse lamellar keratitis with which it is often confused. It traditionally presents at least one week after surgery and often months later. Fungal keratitis usually has a late onset (two weeks after surgery), though S. epidermidis and Mycobacterium may also present late. A focal area of infiltrate associated with diffuse or localized inflammation, which may extend throughout the corneal thickness is generally seen. It may extend into the untreated area of the cornea and outside the flap. The flap may begin to melt. There may be associated ciliary congestion, secondary iritis, hypopyon and secondary glaucoma. There is a loss in best corrected visual acuity (BCVA) as well as uncorrected visual acuity (UCVA). The patient may have symptoms such as pain, irritation, lacrimation, photophobia, etc. Atypical organisms such as fungi and mycobacteria often are responsible and there may therefore be no response to the usual antimicrobial
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therapy. Simultaneous or sequential bilateral involvement of both eyes and infection after flap lift enhancement have also been described.
Infectious post-LASIK keratitis has also got to be differentiated from sterile corneal infiltrates which have been described after PRK and LASIK. Sterile infiltrates also present with symptoms similar to infectious keratitis. Subepithelial white infiltrates which may be associated with immune rings are seen in the first few postoperative days. Smears and cultures are negative, and it responds to topical steroids. It may result in stromal scarring and loss of BCVA. Numerous etiologies have been proposed for this including staphylococcal-immune mediation, secondary to the use of topical NSAIDs without concomitant use of topical steroids and contact lens-induced hypoxia .
Early diagnosis and institution of appropriate therapy is of prime importance in the treatment of post-LASIK infections. Any focal infiltrate should be considered infectious until proven otherwise. Flap elevation and culturing should be performed as early as possible in all cases where post-LASIK infectious keratitis is suspected. Smears help in deciding on immediate treatment which is then changed according to the culture and sensitivity reports. Polymerase chain reaction tesing is also helpful in
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diagnosis. A corneal biopsy may be required in some cases. Empiric therapy is not helpful as opportunistic and atypical organisms with unusual antimicrobial sensitivities are common and these do not respond to conventional therapy.
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Figure 3.3: Collagen cross-linking with riboflavin (C3-R treatment). In this an application of 20%riboflavin in dextrane solution on the cornea is done, followed by irradiation of the cornea with UVA (365-370 nm, 3 mw/cm2) at a distance of 1 cm for 30 min
The anterior cornea is the major stress-bearing layer of the cornea as it is composed of alternating collagen fibrils with a more complicated interwoven structure than the deeper stroma. The flap used for LASIK is made in this layer and thus results in a weakening of that strongest layer of the cornea that contributes maximum to the biomechanical stability of the cornea. This cornea is not able to withstand the normal intraocular pressure of the eye and becomes progressively ectatic at the weakest area
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leading to worsening myopia and irregular astigmatism. The process is irreversible once it begins. Corneal ectasia occurs insidiously after ablative refractive surgery and may be seen months after an originally uncomplicated refractive procedure.
Two well-known contributing factors are an excessively deep ablation and LASIK in a previously undiagnosed forme fruste keratoconus. The lamellar cut in the cornea as well as the decreased residual bed thickness or RBT, both contribute to the decreased biomechanical stability of the cornea after LASIK. Larger ablation diameters result in lesser RBT postoperatively and also result in a larger area of thin cornea. The RBT should not be less than 250 mm to avoid subsequent iatrogenic keratectasia. Factors like drying of the stromal bed may result in an ablation depth more than intended. The normal intraocular pressure (IOP), inadvertent excessive eye rubbing, prone position sleeping, and the normal wear and tear of the cornea all play a role in the progression of ectasia.
Patients with thin corneas less than 500 microns, primary posterior corneal elevation and forme fruste keratoconus are at greater risk for post-LASIK ectasia. In some cases, no preoperative risk factor can be identified. Structural rigidity of the individual cornea and IOP may
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