Laser in situ keratomileusis (LASIK) is an effective option and currently one of the most commonly applied surgical techniques for the correction of refractive errors such as myopia, hyperopia, and astigmatism. Nevertheless, after LASIK, the stroma is exposed to infectious organisms. Infectious keratitis after LASIK as a sight-threatening complication is reported to be as rare as 1 in 1000 procedures. However, any infectious keratitis remains potentially devastating.1 In addition, contamination during surgery by microorganism is responsible for diffuse lamellar keratitis (DLK). Several studies using animal models have shown that endotoxins can cause DLK.2–4
The purposes of this study were to measure the rate of corneal interface contamination during surgery, determine probable sources of the contamination, and evaluate how the cornea reacts to contamination.
PATIENTS AND METHODS
This case series included 207 eyes of 109 patients. None of the study participants had been diagnosed as having an active ocular infection before surgery. Patients taking topical and systemic antibiotics were excluded.
Patients had LASIK for myopia, myopic astigmatism, or hyperopia. The ablation zone diameter was 5.5 to 6.0 mm in myopic eyes and 7.0 to 7.5 mm in hyperopic eyes. All eyes were operated on by the same surgeon (K.J.) using the same technique, the Keracor Technolas 217 Z Zyoptix 100 laser, and the Hansatome microkeratome (Bausch & Lomb).
After instillation of proparacaine hydrochloride 0.5%, cultures were taken from the upper and the lower eyelid margins and the inferior fornices using an alginate swab. Thereafter, povidone–iodine 10% solution was used to prepare the eyebrow and skin of the eyelids for 1 minute and the eyes were washed out with 20 cc of a balanced salt solution. After laser ablation of the corneal bed and before the corneal flap was replaced, a sample was taken from the corneal bed and the instrument (irrigation cannula used to wipe out the interface) with an alginate swab. The samples were collected under the direct supervision of a microbiologist and strictly adhered to the protocol; sterile technique was used at all times. All samples were incubated in enriched blood culture broth. The media were cultured at 37°C for 14 days under aerobic and anaerobic conditions. Bacteria from positive cultures were isolated and identified by biochemical procedures to determine the species of the organisms.
Postoperatively, all patients were treated with chloramphenicol 0.5% eyedrops 4 times a day for 2 weeks and betamethasone 0.1% eyedrops 4 times a day for 2 weeks and every 8 hours for another 2 weeks.
Postoperative examinations were performed 1 day, 1 week, and 1 month after surgery. Another ophthalmologist (S.F.) who was not aware of the results of the cultures performed the postoperative examinations.
Seven eyes were excluded because of flap complications (eg, incomplete flap, buttonhole). Therefore, 200 eyes remained in the study. The mean age of the participants was 28.15 years ± 7.2 (SD) (range 19 to 49 years). Ninety-four eyes were in men, and 106 eyes were in women. The mean spherical equivalent (SE) was −2.725 ± 1.9 diopters (D) (range −12.25 to +4.75 D).
One hundred ninety-three eyes with a mean SE of −3.75 ± 1.6 D (range −1.50 to −12.25 D) had LASIK for myopia or myopic astigmatism. Seven eyes with a mean SE of +2.42 ± 1.8 D (range +1.25 to +4.75 D) were treated for hyperopia.
Forty-nine cultures (24.5%) of the samples from the corneal bed were positive. The most commonly retrieved organism was Staphylococcus epidermidis (43 cases, 87.7%). Other species were Staphylococcus saprophyticus, Staphylococcus aureus, Bacillus species, Pseudomonas aeruginosa, and Streptococcus nongroup A (Table 1).
Twenty-six contaminated corneal interfaces were in men and 23 were in women. The difference between sexes was not statistically significant (P = .33).
In 19 (38.8%) of 49 contaminated cases, cultures of the eyelid margins, conjunctiva, and instruments were negative. Therefore, the sources of contamination in these cases could not be determined. Microorganisms cultured from the corneal interface were the same as the results of cultures from the instruments in 15 cases (30.6%), lid margins in 4 cases (8.2%), conjunctiva in 2 cases (4.1%), conjunctiva and the lid margins in 2 cases (4.1%), conjunctiva and instruments in 1 case (2%), and lid margins and instruments in 1 case (2.0%). In 5 cases (10.2%), although there were positive cultures from the instruments, lid margins, or conjunctiva in addition to the corneal interface, there was no correlation between the retrieved microorganisms (Table 2).
None of the contaminated or the noncontaminated cases developed a corneal ulcer; however, 2 eyes (#26 and #49) developed grade 2 DLK. Both eyes were in the contaminated group, and the microorganisms causing the DLK were S epidermidis and S saprophyticus. The eyes were treated successfully by frequent application of topical corticosteroids.
Although several studies have evaluated contamination of the anterior chamber during intraocular surgery and the outcomes, there is no similar study of corneal contamination during LASIK. To our knowledge, ours is the first study that showed corneal interface contamination during LASIK and the ability of the cornea to clear microorganisms introduced to the corneal interface.
Contamination of the surgical site occurs in all procedures, both extraocular and intraocular. The rate of contamination of the anterior chamber during intraocular surgery varies from 0% to 1.5% after phacoemulsification5,6 up to 29% after extracapsular cataract surgery.7
A study by Detorakis et al.8 evaluated the extent of the contamination of bandage soft contact lenses used in laser refractive surgery. The contamination rate was 18.3%, and the only microorganism isolated was S epidermidis.
In our study, the rate of contamination of the corneal interface during LASIK was 24.5%. As in other studies of contamination during intraocular surgery,9–12S epidermidis was the most common organism (87.7%) isolated. This is expected because it is a normal inhabitant of the eyelids, eyelashes, and conjunctiva11 and it is believed that bacteria that cause postoperative complications originate from the eyelids and conjunctiva.13
We could not find a source of contamination in 38.8% of cases. Although we strictly adhered to sterile techniques at all times, we cannot rule out contamination during handling of the samples. The most probable source of contamination was the instruments (30.6%). However, because we did not take samples from the instruments before surgery, we cannot determine whether they were contaminated at the beginning of surgery or whether they were contaminated during surgery after coming in contact with ocular tissues such as the corneal interface. In the other cases of contamination, the corneal bed results were compatible with the results from the lid margins and conjunctiva.
Several factors play a role in the evolution from contamination to actual infection. They include the load of inoculated microorganisms and the virulence of the organism.14,15 The ability of the tissue to clear organisms is another factor. For example, the anterior chamber may clear small numbers of bacteria without overt signs of infection.16 Our study showed the corneal stroma has the same capability to clear microorganisms introduced during surgery because no case with contamination developed corneal ulcers. However, because we routinely used a topical antibiotic in all cases, this capability is likely the result of the combination of the clearance ability of the cornea and the antibacterial effect of the topical antibiotic. The ability to clear organisms was also shown in a study by Detorakis et al. 8 The authors found that although some soft bandage contact lenses used after photorefractive keratectomy were contaminated, no overt bacterial keratitis occurred.
Diffuse lamellar keratitis, or the sands of Sahara syndrome, is a well-recognized complication of lamellar surgery. The incidence is reported to be 0.2%, although it is believed to be much higher.17 The exact etiology of this noninfectious syndrome remains unknown. Factors that have been implicated include toxic insult from organic esters, lubricants, and machine oil; particulate matter on the microkeratome blade; release of endotoxin from bacterial growth on reusable instruments after autoclaving; traumatic insult from the microkeratome; hemorrhage from a micropannus; the heating effect of the laser on the cornea; meibomian gland secretion; povidone–iodine; debris from gloves; absorbent sponges; and particles from an adhesive catheter dressing used as a drape.18,19
The rate of DLK in our study was 1%. The 2 eyes that developed DLK were in the contaminated group; thus, the probable role of microorganisms and their derivatives in the pathogenesis of DLK is highlighted. However, in 1 eye, the contaminating organisms on the cornea and the instrument were different. Therefore, we cannot confirm a statistical association between contamination of the corneal interface and DLK. Further studies are necessary to draw logical conclusions.
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