Ординатура / Офтальмология / Английские материалы / LASIK and Beyond LASIK Wavefront Analysis and Customized Ablation_Boyd_2001

3.Pachymetry – the elevation difference between anterior and posterior corneal surfaces.

4.Tangential curvature – also called instantaneous curvature, calculated from single plane and multiple axes. The plane runs from a central point radially to the periphery, as in the sagittal map, but the curvature is calculated by the tangent circle at each point along the plane.

5.Mean curvature, composite curvature – calculated from 3-D surface data. Composite curvature maps display curvature from all directions. Each map point is the mean of its curvatures in all directions.

How the Orbscan Helps Evaluating High Risk Cases for LASIK and FFK.

1.Pachymetry – The Orbscan gives a full corneal readout and in the preoperatory eye is probably more accurate than ultrasonic pachymetry. This especially true when you realize that the thinnest part of the cornea is often not central. Full corneal readouts are also important because the difference from the periphery to the thinnest area is also important. If there is a difference from the thickest to the thinnest of 200 microns, and a suspicious anterior surface (over 3D of asymmetrical astigmatism etc.) then one may be dealing with a high risk case.

2.Posterior Float – This measures the forward bulge on the posterior corneal surface. It is felt that this measurement can be used to evaluate risk factors for LASIK. The location of the steepest posterior float is also important, those that are paracentral can be more threatening than those that are central. Preoperatory values more than 50-65 microns are suspicious risks for ectasia. The posterior float almost always increases after surgery. In thin corneas when there is some question as to whether there is enough cornea to perform a LASIK the posterior float often is the deciding factor. Many people feel that the first sign

11.Seiler T. Iatrogenic keratectasia: academic anxiety or serious risk? J Cataract Refract Surg 1999;25:13071308.

12.Joo CK, Kim TG. Corneal ectasia detected after laser in situ keratomileusis for correction of less than –12 diopters of myopia. J Cataract Refract Surg 2000;26:292-295.

13.Vesaluoma M, Pérez-Santonja J, Petroll WM, Linna T, Alio J, Tervo T. Corneal stromal changes induced by LASIK. Invest Ophthalmol Vis Sci 2000;41:369376.

14.Maguire LJ, Bourne WM. Corneal topography of early keratoconus. Am J Ophthalmol 1989;108:107-112.

15.Maguire LJ, Lowry JC. Identifying progression of subclinical keratoconus by serial topography analysis. Am J Ophthalmol 1991;112:41-45.

16.Maeda N, Klyce SD, Smolek MK. Comparison of methods for detecting keratoconus using videokeratography. Arch Ophthalmol 1995;113:870874.

17.Srivannaboon S, Reinstein DZ, Sutton HFS, Holland SP. Accuracy of Orbscan total optical power maps in detecting refractive change after myopic laser in situ keratomileusis. J Cataract Refract Surg 1999;25:15961599.

18.Auffarth GU, Wang Li, Völcker HE. Keratoconus evaluation using the Orbscan Topography System. J Cataract Refract Surg 2000;26:222-228.

Leonardo P. Werner, M.D.

Department of Ophthalmology,

São Geraldo Eye Hospital,

Federal University of Minas

Gerais, and the “Instituto

Vizibelli”, Belo Horizonte,

Minas Gerais, Brazil.

Contents

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Section 2

Section 3

Section 4

Section 5

Section 6

Section 7

Subjects Index

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Contents

Section 1

Section 2

Section 3

Section 4

Section 5

Section 6

Section 7

Subjects Index

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Chapter 26

and the confinement of the infiltrate to the interface suggest a non-infectious etiology. An allergic or a toxic inflammatory reaction is the most likely cause of DLK, although the inciting agent is uncertain. Talc from gloves has been associated with interface infiltrates, although in many cases of DLK, talc-free gloves were used during the procedure10. Interface inflammation may be related to material that is present on the surface of the LASIK microkeratome blades, as cleaning the microkeratome blade before use can reduce the interface debris and inflammation14, although DLK can occur without the use of a microkeratome. For some surgeons, there is some evidence that oil or other substances coming out from the microkeratome motor during the LASIK procedure are involved as a cause of DLK in specific cases. Recently, Richard Sherin and John Doane, MD, (unpublished data) hypothesized the endotoxin contamination as a cause of SOS. Bacteria can contaminate the instruments after surgery, and subdivide quickly if the instruments are not sterilized promptly. If the instruments are autoclaved several hours later (i.e. one day after surgery), all the accumulated bacteria will release, in their death, lipopolysaccharide (LPS) (endotoxin) from their shells. This LPS is in no way detoxified by the autoclave, and coats the instruments. This LPS is well known to be extremely toxic to the corneal stroma. This theory can explain the cases of DLK following removal of epithelial ingrowth or LASIK enhancement, where neither the laser nor the microkeratome were used.

Other possible factors that may be associated with DLK in some cases are substances produced by the laser ablation, meibomian gland secretions, and povidone-iodine.

In conclusion, DLK is a nonspecific inflammatory response to one or several possible inciting agents that have not completely been elucidated.

Clinical Findings

Diffuse lamellar keratitis presents 1-6 days following LASIK, LASIK enhancement, removal of interface epithelium, keratomileusis in situ or related lamellar procedures with discomfort, mild to moderate pain, foreign body sensation, tearing, or photophobia10. Conversely, some cases are asymptomatic.

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Section 7

Subjects Index

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Chapter 26

Differential Diagnosis

The differential diagnosis for interface infiltrates in the early postoperative period includes DLK, infectious keratitis, epithelial cells, and interface opacities. All these interface disorders, that can be confusing for the ophthalmologist, should be ruled out before a suspected clinical diagnosis of diffuse lamellar keratitis is made.

In contrast to DLK, acute infectious keratitis presents with decreased visual acuity, pain and inflammation (redness). Infectious keratitis is characterized by a single or dominant focus with extension anteriorly into the flap and posteriorly into the stroma. Infectious keratitis does not respect the boundaries of the flap interface. There is also conjunctival/ciliary injection, epithelial defects over the infiltrate, and inflammatory cells in the anterior chamber. DLK can be distinguished from infectious infiltrates by clinical presentation and close followup. Patients with this syndrome should be spared the more invasive treatment of infectious keratitis.

Epithelial cells in the interface may be present in the early postoperative period, and they appear as a few scattered fine translucent cells in the interface without inflammation. The cells are more transparent, and there are fewer cells than would be present in diffuse lamellar keratitis. In addition, a small area is affected.

Non-infectious interface opacities are common within the first postoperative weeks, and are related to tear film debris, or foreign particles from the microkeratome, blade or sponge. Interface debris can also be caused by the powder of the gloves, or blood from cut pannus7,20. Usually, it is not difficult to recognize these interface opacities after lamellar refractive surgery. The foreign bodies are usually well tolerated but may be a nidus for infection or inflammation. If inflammation is present, then flap repositioning and foreign body removal could be considered.

Treatment

Once the diagnosis of DLK syndrome is made, and other causes of interface infiltrates are ruled out, a therapeutic plan is developed to most effectively manage the problem. The goals of therapy include

to decrease the acute polymorphonuclear inflammatory reaction, to prevent degranulation of the polymorphonucleocytes enzymes, and, sometimes, removal of the proteolytic enzymes along with the inciting agent. Many of these goals are best achieved by prompt initiation of steroid therapy8,10.

For patients with Stage 1 and 2 DLK, a therapy with prednisolone acetate 1% one drop every 1 to 2 hours is recommended. Most cases resolve with no sequelae over the course of the first postoperative month during which time the patient is weaned off corticosteroids. These patients should be followed closely because of the condition could worsen, and the high-dose topical steroid therapy could accelerate infectious keratitis.

If the infiltrate worsens, or for patients with Stage 3 and 4 DLK, the flap is lifted, the infiltrates are cultured and removed, the flap is replaced to its original position, and the interface is irrigated copiously with balanced salt solution. Approximately 4-6 hours after washout, an intensive therapy with prednisolone acetate 1% one drop every 1 to 2 hours should be established. Washing the interface is to washout the deposited proteolytic enzymes from neutrophilic cells, thus limiting tissue destruction, and also the inciting agent. The intensive steroid therapy is for preventing enzymatic release from the infiltrating cells, and for decreasing the number of polymorphonuclear cells (Table 2).

Prevention

Several possible inciting agents may contribute to diffuse lamellar keratitis following LASIK. Prevention of DLK following LASIK can be achieved by avoiding all involved agents, at least, until a definitive agent is identified.

The eyelids should be draped to cover completely the meibomian glands orifices as well as the eyelashes. Powder-free surgical gloves are recommended. The ocular surface should be irrigated copiously prior to keratomileusis in order to remove all debris. The microkeratome head and blades should be cleaned before use using distilled water, and the motor tip should be checked for oil contamination. Immediately after surgery, all instruments should be cleaned and sterilized. Never leave instruments stand-

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ing wet and unsterilized for an extended period of time. In this way, the count of dead bacteria is kept low and the production of clinically significant amounts of endotoxin is prevented. The interface should be irrigated under the flap with balanced salt solution, once the flap is replaced to its original position. In this way, all particles, debris, and inciting agents in the interface are removed, and, at the same time, the tear film debris are prevented to reach the interface. After surgery, topical corticosteroids should be used routinely four times per day for 5 to 7 days to prevent DLK, beginning 12-24 hours after the procedure.

Conclusions

Diffuse lamellar keratitis is a distinct syndrome of noninfectious inflammation of the lamellar interface following LASIK and related lamellar surgery. The inflammation can be identified on careful slitlamp examination and can be differentiated from other causes of interface infiltrates. DLK responds to corticosteroids, however if the inflammation does not respond as expected, if the inflammation is severe, or if there is a suspicion of infection, the flap should be lifted, the infiltrates cultured and removed, and intensive corticosteroids and/or antibiotics should be considered.

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Table 3

Clinical Signs of Infection in 16 Cases

Following LASIK 9,12,15-19,26-28

munocompetent individuals and 2 were HIV positive9, 12,15-19,26,27,28. The infection was unilateral in 10 patients and bilateral in 312,27,28. The HIV positive individuals developed bilateral staphylococcal keratitis27,28 . Patients ranged from 18 to 55 years of age, with a mean of 38.7 ± 11 years; 6 patients were females and 7 were males. Eight of the 16 infections were in the right eye and 8 in the left. Twelve patients developed infection within 3 weeks of LASIK, and 9 within the first week. The mean time of early onset keratitis was 5.3 ± 6 days (range, 1 to 21 days). Only 1 case had a late onset infection that developed infection 28 days after LASIK.

The symptoms of infectious keratitis after LASIK are similar in most patients, but may differ depending on the severity of the infection. The most common symptoms include decreased visual acuity, pain, photophobia, and redness. Other commonly encountered symptoms include discharge, foreign-body sensation, tearing, and eyelid edema9,12,15-19,26-28.

The most common signs of infectious keratitis after LASIK include9,15-19,26 ciliary and conjunctival hyperemia, and whitish stromal infiltrates in the interface (Table 3). Other signs include anteriorchamber reaction, hypopyon, stromal/flap edema, and flap melting. Stromal infiltrates may be single or multiple and begin anywhere in the stromal interface as a dense, gray-white abscess. The edges of the stromal infiltrate are usually indistinct and often

Figure 26-4.- Slit-lamp photograph showing a round interface abscess surrounded by stromal infiltration and satellite lesions 3 days after primary LASIK. An overlying epithelial defect that stains with fuorescein is present. (The culture was negative).

sessment of the depth of the stromal infiltration, appearance of the infiltrate borders, and anterior chamber reaction. Slit-lamp photography can be extremely helpful as a baseline and for documenting changes in the appearance of the corneal infiltrate29. This would help in assessing improvement after initiation of antibiotic therapy.

Causative Organisms

In the cases reported, the diagnosis was confirmed by cultures which were obtained either by scraping the corneal ulcer or by scraping the stromal interface after lifting the flap. Microorganisms were isolated from 10 (77%) of the 13 cultures. Three cultures were negative, but a bacterial infection was presumed, based on the clinical presentation and the response to therapy15,28. All 10 patients with positive cultures had bacterial isolates and no fungi were found.

Gram-positive cocci were isolated in 8 (61.5%) of the 13 cultures, gram-positive filamentous bacilli in 1 (7.7%) culture, and acid-fast bacilli in 1 (7.7%). Three cultures were negative. No gram-negative bacilli were isolated. All gram-positive bacterial cultures were isolated from infections occurring within the first 3 weeks of surgery. Only acid-fast bacilli

were isolated from late-onset infection cases (three weeks after surgery).

Gram-positive cocci included Staphylococcus aureus in 5 (38%) patients, Streptococcus viridans in 2 (15.4%), and Streptococcus pneumoniae in 1 (7.7%). Gram-positive filamentous bacillus was Nocardia asteroides in 1 (7.7%) patient. The acidfast bacilli infection was caused by Mycobacterium chelonei. Three cultures were sterile. (Table 4).

Table 4

The patient history and clinical examination are insufficient for making a definitive diagnosis of infectious keratitis. In patients with suspected infectious keratitis, obtaining corneal scrapings of the infiltrates is mandatory to confirm the diagnosis, to isolate the organism, and to determine the sensitivity to antibiotics. Broad spectrum antibiotic therapy may be initiated after obtaining corneal scraping specimens for culture and staining.

Chapter 26

The initial step should be obtaining culture material from the conjunctiva. The use of anesthesia in this procedure should be avoided because preservatives may decrease the yield of live isolates. Calcium alginate swabs or cotton swabs are used for this purpose. The swab should be moistened and the entire lower cul-de-sac should be wiped. The material obtained is placed directly onto culture plates. All conjunctival specimens should be plated directly onto blood agar, chocolate agar, MacConkey agar, Sabouraud’s agar, and thioglycolate broth. Growth from the conjunctival cultures is helpful only when the corneal cultures are all negative, especially when the one ipsilateral to the keratitis grows a pathogen not found in the other eye.

Then, following topical anesthetic eyedrops such as proparacaine hydrochloride (0.5%), the patient is aligned under the surgical microscope and a lid speculum is inserted. The corneal flap is marked with a marker at the cut edge. The corneal flap is lifted using a spatula or forceps, and the interface is exposed. A sterilized spatula is used for scraping the corneal stromal bed of the interface. Multiple scrapings are required, and each of them may be inoculated onto the surface of different culture media. Direct corneal scraping, without lifting the flap is not recommended because the corneal flap can be sloughed off in the process26. After corneal cultures are taken, the interface is irrigated with antibiotics or 5% povidone iodine12,15,19. Then, the flap is replaced and aligned to its original position, and the flap circular edge is dried with a microsponge12,15. The exudate and material obtained from the interface is placed on a microscope slide for Gram and Giemsa staining, and also directly onto blood agar, chocolate agar, MacConkey agar, thioglycolate broth, and Sabouraud’s medium9,29.

Gram and Giemsa staining results can be useful to guide the initial antibiotic therapy. The bacteria of most keratitis begin to grow on some media within 24 to 48 hours. Then, antibiotic sensitivity testing is begun even before the final species identification is made. This may allow rational adjustments in therapy when correlated with the clinical response29.