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Ординатура / Офтальмология / Английские материалы / Jaypee Gold Standard mini Atlas Series Lasik_Aragawal, Jacob_2009

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COMPLICATIONS/ 167

the anterior chamber partially obscuring the pupil and the patient’s view of the fixation light (Figure 3.12A). If the bubble(s) is large enough, it may prevent pupil margin tracking by the laser and inhibit the patient’s ability to fixate. The bubbles absorb into the aqueous humor in two to three hours and treatment may be completed. Often the bubble(s) are small and the edge of the pupil is not obscured and the patient is able to fixate around the bubble. In this event then the treatment may proceed without waiting for the bubbles to absorb. The gas bubbles are otherwise innocuous and do not cause any subsequent effect to the eye.

Gas Bubbles in the Cornea

Gas bubbles are routinely formed in the LASIK interface by femtosecond laser photodisruption (“opaque bubble layer, OBL”). These interface bubbles are released when the flap is lifted and therefore they do not interfere with treatment. However, sometimes the bubbles dissect into the superficial layers of the stromal bed during propagation of the laser interface (deep OBL) (Figure 3.12B). These deep bubbles are not released when the flap is lifted. Depending on the location of the deep OBL the pupil or iris landmarks may be obscured preventing either pupil

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localization for tracking and/or iris landmark-based iris registration. In addition if the bubbles are distributed confluently in the peripheral cornea adjacent to the limbus they, may form a false limbus and as a consequence decenter the laser treatment by excimer lasers (such as VISX) which use the limbal ring to center the treatment zone. These superficial stromal bed bubbles usually resolve within 30 to 45 minutes. If the OBL interferes in pupil tracking or iris registration then the laser treatment should be delayed until the OBL resolves.

Unliftable Flap

Occasionally the interface is insufficiently dissected and it is difficult or impossible to the separate the flap from the underlying stromal bed. Attempts to forcefully open the interface with spatulas and blades may lead to torn flaps or rough or irregular surfaces (Figure 3.12C). The etiology of the inadequate dissection is uncertain but appears to occur bilaterally in individual patients. When the ophthalmologist is actually able to forcefully elevate the flap there often is some keratocyte activation and associated interface haze. The haze is corticosteroid sensitive and resolves with treatment within three to four months. There is no effect on vision. If the flap appears difficult to

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lift then it is reasonable to abort the procedure and replace the already lifted edges of the flap to allow for healing over approximately a one month period. The procedure may be reattempted with a blade microkeratome set to cut the flap 50 microns deeper than the original femtosecond flap interface. If the flap were to be recut with the femtosecond laser then the plasma gas bubbles may percolate through to the level of the old unlifted interface preventing passage of the laser light through to the newly programmed interface level.

Non-dissected Islands

If gas bubbles dissect through the stroma anteriorally, the bubbles will come to lie between the applanation plate and the corneal surface. The bubbles will spread ahead of the advancing propagation of the laser raster pattern and block the focused femtosecond laser light. This blocking leaves an undissected zone wherever it occurs. The interface then is not separable in this area. Forceful attempts to delaminate the corneal collagen fibers in this area can result in a tear through to the surface leaving an isolated “island” of undissected tissue similar to the central islands that may occur with blade microkeratome created flaps. This phenomenon of dissection of gas bubbles

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through the anterior stroma can occur with thin flaps (anterior stromal component less than 50 microns), through incisions such as following radial keratotomy or penetrating keratoplasty, and through scars such as following previous microbial keratoplasty or conductive keratoplasty. A similar process may occur when there has been a previous surgical lamellar plane created in the cornea such as from previous LASIK or keratomilieusis. In this event the gas may dissect along this existing intralamellar plane anterior to the intended plane and block the laser. The new plane is not dissected under this area resulting in what amounts to a partial flap cut. Again the management in these cases is to not initially attempt to lift the flap, allow it to heal for six weeks and then recut the flap with a blade microkeratome at a level at least 50 micons deeper or more superficial to the original femtosecond laser plane.

Postoperative Complications

Transient Light Sensitivity

There are two minor complications which are encountered following LASIK with the IntraLase laser. The first is the transient light sensitivity (TLS) syndrome or good acuity – photophobia syndrome (GAPS) in which patients with

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good vision develop photophobia in the absence of any apparent finding on examination.3 Corticosteroid drops are prescribed and symptoms improve within one week of treatment. Invariably symptoms resolve with or without treatment leaving no residual abnormality or symptoms. Its etiology is unknown and speculation has varied among keratocyte activation to laser induced iritis, scleritis or neuritis. The majority of patients feel more comfortable wearing sunglasses during the two to six weeks that it takes to resolve. The incidence of this symptom is approximately 1 percent.

Keratitis

The second complication is intrastromal inflammation localized around the edge of the flap which occurs two to seven days following flap creation. The corneal stromal tissue becomes hazy or white along the side cut and there is associated cellular infiltration in the interface and in the superficial cornea in a narrow band along the edge of the flap. There may be some associated photophobia. Presumably this inflammation results from microscopic cornea tissue damage caused by the laser photo disruption perhaps exaggerated by exogenous inflammatory factors in the tear film. Although this process may share some

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features with the diffuse lamellar keratitis syndrome (DLK) it is differentiated by its later onset and the stromal inflammation outside of the edge of the flap. Treatment consists of frequent topical corticosteroid drops and adjunctive measures such as oral doxycycline. In mild to moderate cases the process resolves without sequelae. In rare cases the inflammation is severe and scarring may develop in the area of the side cut and haze in the interface. Since the majority of the inflammation occurs in the peripheral area of the flap outside the visual axis, there is typically minimal, if any, effect on visual acuity. The frequency of cases appears to have declined with lower side cut energies.

Diffuse Lamellar Keratitis

Typical diffuse lamellar keratitis (DLK) is occasionally observed in femtosecond laser created flaps but the clinical course is benign and self-limited. Treatment is with topical corticosteroids until resolution. Higher laser repetition rates such as 30,000 or 60,000 hertz and smaller spot energies (1.7millijoules) appear to decrease the incidence of both GAPS and DLK.

4

Miscellaneous

Topics

Phakonit

and

MicrophakonitAmar Agarwal

Soosan Jacob

Rahul Tiwari

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Figure 4.1A

Figure 4.1B

Figures 4.1A and B: Phototherapeutic keratectomy (Figure & Text Courtesy: Jes Mortensen) cornea with Groenow´s dystrophy preand postoperative after PTK

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In 1983, Professor Stephen Trokel suggested the use of the excimer laser in ophthalmic surgery. Since then, millions of patients have been treated successfully, mostly in the refractive area. The exact edging capability of the excimer laser has been found useful in treating superficial corneal opacities, corneal scars, dystrophies and irregularities. This part of the excimer laser use is commonly referred to as PTK or phototherapeutic keratectomy. PTK aims to change the corneal surface: To correct irregularities of the corneal surface or to change the refraction of the cornea, to make the epithelium adhere better to the basal membrane in recurrent erosions and in some superficial corneal dystrophies. Different techniques have been used to remove the epithelium: Scraping with a knife and later a brush. We prefer to loosen the epithelium by exposure to 30% alcohol for 20 seconds in a ring. After the treatment the epithelium is rolled back and covered by a silicon lens. We have found that this procedure reduces the postoperative pain the patient has to endure. In refractive cases such as anisometropia after previous ocular surgery, LASIK is the preferred technique. Removing the epithelium gives a better situation to accurately measure the degree of the irregularity of the corneal surface, as the epithelium always conceals the minor irregularities.

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Corneal dystrophies (Figures 4.1A and B) can be classified into pre-Bowman’s layer, Bowman’s layer, anterior stromal and stromal. The dystrophies are congenital and will recur, so the PTK treatment cannot be considered as a cure for the future problems caused by the dystrophies. This means that the procedure should offer the anatomy as little as possible, to allow for repeated treatment later. Generally, the problems most often seen with dystrophies are recurrent erosion and irregularity of the surface. Cloudiness of the stroma is a rarer cause for reduction of the visual acuity. Putting a hard contact lens on the cornea can give a good idea of what can be accomplished by the polishing of the irregular corneal surface, especially if some cloudiness is also a part of the picture.

Most eyes are treated transepithelially followed by 15 to 100 μm in the stroma; LaserVis®, methylcellulose or BSS was used as masking. Today LASEK is used followed by polishing by LaserVis®. PTK treatment of various corneal dystrophies often gives very good results, especially if the problem is due to recurrent erosion or moderate irregularity of the corneal surface.

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