Laser-assisted in situ keratomileusis (LASIK) has become a well-acceptedand effective procedure for the treatment of a wide range of refractive errors.Microbial keratitis is a potential complication of LASIK with causative organisms,including gram-positive bacteria, atypical mycobacteria, fungi, and viralpathogens.1 Direct ocular trauma and exposurekeratopathy in severely ill patients in intensive care units are risk factorsfor microbial keratitis. We describe the first cases, to our knowledge, ofinfectious keratitis in donor corneas harvested from cadavers with a pasthistory of LASIK. Slitlamp, specular microscopy, and histopathologic findingsare presented. These donors would likely have suffered vision loss if theyhad survived their illnesses. This article illustrates the importance of eyecare by intensive care personnel managing patients with a past history ofLASIK.
Case 1. In December 2002, a healthy 22-year-oldman underwent uncomplicated myopic LASIK in both eyes. Two days later, hewas involved in a high-speed motor vehicle crash; he sustained diffuse braininjury. He was maintained on life support for 1 week and was evaluated fororgan donation. During his hospitalization, the patient received tobramycinand dexamethasone drops. Death-to-preservation time for in situ corneal excisionwas 6 hours 48 minutes. The donor corneas were placed in Optisol-GS corneastorage media (Chiron Ophthalmics, Irvine, Calif) and sent to the New MexicoLions Eye Bank (Albuquerque), using protocols established by the Eye BankAssociation of America.2
On slitlamp examination, the right donor cornea had an obvious LASIKflap with localized flap dehiscence and folds (Figure 1A). This cornea had evidence of an infiltrate with featheryedges (Figure 1B). The left donorcornea also had a poorly healed LASIK flap edge and a more extensive cornealinfiltrate (Figure 2). Specularmicroscopy performed 4 days after death revealed central endothelial cellcounts of 2008/mm2 in the right cornea and 2159/mm2 inthe left cornea. Highly reflective particles were seen in both donor corneaswhen the specular microscope was focused in the region of the stroma correspondingto the LASIK interface.
The donor corneas were then placed in 10% neutral buffered formalinand processed for permanent sections. Sections were stained with hematoxylin-eosin,periodic acid–Schiff, Brown and Brenn, and Gomori methenamine silver.Histologic examination of the right donor cornea revealed missing epitheliumover the inferior lamellar interface wound with mild chronic nongranulomatousinflammatory cells in the anterior stroma. No incriminating organism was found.Histologic examination of the left eye revealed similar findings, with thenoted difference of a moderate anterior stromal infiltrate. Additionally,the Gomori methenamine silver stain showed the presence of multiple yeastorganisms on the affected corneal surface, with some invading the anteriorstroma (Figure 3A and Figure 3B).
Case 2. A 61-year-old man with a medical historyremarkable for metastatic colon cancer had undergone LASIK in both eyes atan unknown date. He was placed in hospice care in October 2001. Ten days later,the patient died. The patient's body was refrigerated for 2 hours postmortem.Death-to-preservation time for in situ corneal excision was 12.5 hours. Thedonor corneas were placed in Optisol-GS cornea storage media and sent to theNew Mexico Lions Eye Bank, using established Eye Bank Association of Americaprotocols.
Slitlamp examination of the right donor cornea failed to reveal a LASIKflap edge; however, there was a dense corneal infiltrate presumably involvingthe lower one third of the cornea (Figure4). The left donor cornea had a subtle LASIK flap edge with smallerperipheral corneal infiltrates, revealed by slitlamp examination. Specularmicroscopy performed 2 days after death revealed central endothelial celldensity of 1721 in the right eye and 1531 in the left eye. Both donor corneashad highly reflective stromal particles by specular microscopy in the regioncorresponding to the LASIK interface.
The right donor cornea was placed in 10% neutral buffered formalin andprocessed for permanent sections using hematoxylin-eosin, periodic acid–Schiff,Brown and Brenn, and Gomori methenamine silver stains. Histologic examinationrevealed the presence of a LASIK lamellar flap with missing epithelium overthe entire flap and the cornea inferior to it. The latter region of the corneahad an ulcer, inferior to the LASIK flap wound, with a moderate chronic nongranulomatousinflammatory cell infiltrate in the anterior stroma (Figure 5A). Brown and Brenn stain revealed a small focus of gram-positivecocci on the surface of the ulcer (Figure5B).
These case reports represent the first description of infectious keratitisidentified during eye bank screening of corneoscleral tissue from donors withLASIK history. Microbial keratitis is considered a rare complication followingLASIK, varying from 0.1% to 1.2%.3-5 Althoughsome of the reported infections after LASIK are interface infections, thesecases seem to represent surface corneal ulceration. Laser-assisted in situkeratomileusis severs the branches of the trigeminal nerves that enter fromthe limbus centripetally to enervate the stroma and epithelium of the centralcornea.6 Regeneration of corneal nervesusually occurs within 1 year after LASIK.7 However,1 study reported that LASIK results in decreased corneal and conjunctivalsensitivity even at 18 months after the procedure.8 Thisstudy also reported that the decreased ocular sensitivity is accompanied bya decrease in aqueous tear production, punctate epithelial erosions, and adecrease in tear fluorescein clearance probably due to a decreased blink rate.8 Intubated or sedated patients are at risk for lagophthalmosand exposure-related keratitis. The post-LASIK neurotrophic status of thesepatients may further predispose them to infectious keratitis.
The first case represents, to our knowledge, the earliest post-LASIKhuman histopathologic finding (9 days post-LASIK). The neurotrophic corneawould certainly be a risk factor in the immediate postoperative period. Thefirst patient had evidence of probable traumatic displacement of the LASIKflaps, which may have contributed to the development of keratitis (Figure 1A and Figure 3A). Late traumatic displacement of LASIK flaps occurringmore than 2 years after the procedure, complicated by diffuse lamellar keratitis,has been reported.9 Late post-LASIK fungalkeratitis related to trauma has also been reported.10 Basedon the well-healed scar of the second case, the neurotrophic status of thecornea may predispose the cornea to infection even months after the LASIKprocedure. Postmortem microbial contamination of the donor corneas is unlikelygiven the chronic inflammatory cell response documented by histopathologicexamination.
These cases suggest that intensive care unit personnel consider addinga refractive surgery query to the eye history taken from family members oftrauma patients and other obtunded patients. Intubated and sedated patientswho have had LASIK surgery require close monitoring for exposure keratopathyand prompt diagnosis of keratitis. These patients would probably benefit fromaggressive lubrication and prophylactic antibiotic ointment.
The authors have no relevant financial interest in this article.
This study was presented in part at the 41st annual meeting of the EyeBank Association of America, Ponte Vedra Beach, Fla, June 22, 2002.
The study was supported in part by the Dedicated Health Research Fundsof the University of New Mexico School of Medicine, Albuquerque.
We thank Tissue Banks International (Baltimore, Md) for coordinatingthe collection of donor corneas. We also thank Edward Otero, BA, and ChrisMiguel-Nathan, BA, for their assistance with manuscript preparation.
Correspondence: Dr Mootha, Department of Surgery/Division of Ophthalmology,2211 Lomas Blvd NE, 2-ACC, Albuquerque, NM 87131 (vmootha@salud.unm.edu).
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