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    Microbial keratitis after LASIK enhancement poses risk

    In spite of intensive topical therapy, lamellar flap amputation needed, followed by penetrating keratoplasty


    Editor's Note: Daniel H. Chang, MD, of Emory University, Atlanta, was named the winner of the first Ophthalmology Times Resident Writer's Award Program-presented during the American Academy of Ophthalmology annual meeting in Anaheim, CA. Dr. Chang's winning submission is featured here. He was nominated by R. Doyle Stulting, MD, PhD, chairman,department of ophthalmology, Emory University, Atlanta.

    For the names of the other winners and program participants, see "Winners of first Resident Writer's Award Program announced" on Page 18. The program was presented and sponsored by Advanced Medical Optics (AMO).

    Daniel H. Chang, MD, received his BS degree in chemistry with honors from the California Institute of Technology, where his investigational career began with a summer undergraduate research fellowship. He obtained his MD degree from Duke University, where he served as a research analyst. Dr. Chang is currently chief resident in ophthalmology at Emory University and will pursue a fellowship in cornea and external disease next year. Dr. Chang's research activities have included investigations of the free electron laser and corneal transplantation.

    -R. Doyle Stulting, MD, PhD, professor of ophthalmology, Emory University, Atlanta

    Figure 1 The slit-lamp examination reveals moderate conjunctival injection, multiple patches of white infiltrate under the flap, and 1+ anterior chamber cells. A diagnosis of infection versus diffuse lamellar keratitis was made and the patient was treated with topical ofloxacin (0.3%) and prednisolone acetate (1%).
    Abstract A 36-year-old man developed decreased vision and white interface opacities 2 weeks following uneventful LASIK enhancement of his left eye. Staining of corneal scrapings revealed acid-fast bacilli, and the treatment was started with topical amikacin, levofloxacin, and clarithromycin. Microbiological studies revealed Mycobacterium abscessus. In spite of intensive topical therapy, the lamellar flap was amputated 16 days after presentation. The keratitis gradually resolved over 2 months and formed a vascularized scar. Penetrating keratoplasty 5 months later gave a final best-corrected visual acuity (BCVA) of 20/20. A discussion about this unusual but increasingly reported and potentially devastating LASIK complication is presented.

    History A 36-year-old man was referred to Emory Eye Center for blurred vision of his left eye. Sixteen days prior, he had undergone uneventful LASIK enhancement of that eye with a LADARVision 4000 excimer laser (Alcon). His course was benign until 2 weeks postoperatively, when he began to notice blurred vision. Examination by the referring physician demonstrated a BCVA of 20/63. Slit-lamp examination revealed white "floral-like spots" in the flap interface. A diagnosis of infection versus diffuse lamellar keratitis (DLK) was made. Treat-ment was started with topical ofloxacin (0.3%) and prenisolone acetate (1%) and the patient referred to Emory Eye Center.

    The patient presented to Emory Eye Center the next day with continued blurred vision and new redness and light sensitivity of his left eye. His ocular history was significant for uneventful bilateral primary LASIK 10 months prior. Initial planned enhancement at 3 months was deferred due to dry eyes, which were treated with artificial tears and punctal plugging.

    Examination On presentation, uncorrected visual acuity (UCVA) was 20/20 in the right eye and 20/30 in the left eye. Pupils, IOP, and motility were normal. Slit-lamp examination of the left eye revealed mild conjunctival injection. There were multiple areas of a white infiltrate under the flap. The anterior chamber had 1+ cells.

    Discussion and diagnosis The differential diagnosis of whitish opacities in the lamellar interface following LASIK includes DLK, epithelial ingrowth, and microbial keratitis. DLK is a culture-negative inflammatory infiltrate that appears within days of the procedure. It appears as a white diffuse granular infiltrate limited to the interface that starts peripherally (grade I), spreads centrally (grade II), and may form clumps (grade III) with anterior chamber reaction (grade IV). Epithelial ingrowth causes more smooth discrete-appearing peripheral patches with no associated inflammation. Microbial keratitis typically has a single dominant focus that invades the flap and stromal bed with significant conjunctival and anterior chamber reaction. It is usually bacterial or fungal.

    Figure 2 The flap was lifted, scraped, and irrigated, and cultures taken. The initial stains indicated acid-fast bacilli. More intensive topical therapy was instituted. However, an epithelial defect formed and the infiltrate worsened. At 12 days after presentation, the flap was again lifted, cultured, and irrigated. The cultures grew Mycobacterium abscessus.
    Microbial keratitis is a rare (1 in 1,000 to 5,000 cases) but potentially devastating complication of LASIK. Causative organisms include Staphylococcus aureus, coagulase-negative staphylococcus, Streptococcus viridans, Streptococcus pneumoniae, Pseudomonas aeruginosa, and several atypical organisms, including mycobacteria, norcardia, fungus, and even Acanthamoeba. The nature and course of these infections are dependent on the pathogenicity of the causative organism and are similar to cases of keratitis in unoperated eyes. Dry eyes and blepharitis may increase the risk of postoperative infection.1

    Given the subacute presentation of this case, a differential diagnosis of mycobacterial versus fungal keratitis was made. The flap was lifted, scraped, and irrigated. Cultures were taken on chocolate agar, Sabouraud's dextrose agar, Lýstein-Jensen media, thioglycollate broth, and Middlebrook 7H9 broth. Initial stains were positive for acid-fast bacilli and negative for other bacteria and fungus. Treatment was started with intensive topical amikacin (10 mg/ml), levofloxacin (0.5%), clarithromycin (10 mg/ml), and prednisolone acetate (1%).

    Following an initial improvement in the infiltrate, an epithelial defect formed, and the infiltrate worsened. Twelve days after presentation, the flap was again lifted, irrigated, and cultured. At this time, the initial cultures grew Mycobacterium abscessus sensitive to amikacin, clarithromycin, and kanamycin and resistant to ofloxacin, levofloxacin, tobramycin, and doxycycline. Levofloxacin was discontinued, and kanamycin (40 mg/ml) was added.

    Sixteen days after initial presentation, the dense infiltrate and epithelial defect persisted. The flap was therefore amputated. Topical amikacin and clarithromycin concentrations were increased to 2%. Five days later, a hypopyon was noted. Corneal neovascularization also increased, so loteprednol (0.5%) was added gradually. Repeated scrapings demonstrated scant organisms. Over the next 2 months, the epithelial defect slowly closed, forming a vascularized scar. Seven months after initial presentation, the patient underwent uneventful penetrating keratoplasty for visual rehabilitation with a final BCVA of 20/20.

    Figure 3 Sixteen days after initial presentation, the dense infiltrate and epithelial defect persisted and the flap was amputated. (Figures courtesy of Daniel H. Chang, MD, and R. Doyle Stulting, MD, PhD)
    Mycobacteria are ubiquitous in nature and are found in places such as soil, foodstuffs, and tap water. The family Mycobacteriaceae consists of approximately 50 species of acid-fast, aerobic organisms, including M tuberculosis and M leprae. The remaining species are considered nontuberculous or atypical mycobacteria. The Runyon classification groups mycobacteria based on rate of growth and pigment production with respect to light stimulation. Group IV consists of the rapid-growing mycobacteria M chelonae, M fortuitum, and M abscessus (formerly classified as a subspecies of M chelonae). These are the most commonly reported mycobacterial organisms causing infectious keratitis.

    Prior to the first report of mycobacterial keratitis following LASIK in 1998,2 only 88 cases of this unusual infection had been reported, with M chelonae (48 of 88) and M fortuitum (25 of 88) being the most common.3 To date, 54 cases of mycobacterial keratitis following LASIK have been reported, with 80% (43 of 54) due to M chelonae or M abscessus.4-7

    Clinically, mycobacteria cause an indolent infection, with onset typically 2 to 8 weeks following the corneal insult. On slit-lamp biomicroscopy, the infiltrates are white with focal and diffuse components. They may be round or crystalline-appearing with margins that are feathery or well demarcated, giving a "snowflake" or "cracked windshield" appearance. Epithelial defects may form over the infiltrate.2,7


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