 |
|
Late Occurrence of Diffuse Lamellar Keratitis After Laser In Situ Keratomileusis
Arch Ophthalmol. 2001;119:1074-1076.
Diffuse lamellar keratitis (DLK) is a noninfectious inflammatory complication
associated with laser in situ keratomileusis (LASIK).1
Post-LASIK sterile interface keratitis has also been described as "sands of
the Sahara syndrome" and "central focal interface opacity after LASIK."2-3 The corneal infiltrates may be
focal or multifocal but remain confined to the lamellar interface without
extension, anterior chamber reaction, or associated epithelial defect. Common
to all previously reported cases is an onset within 1 month after LASIK treatment,
enhancement, or flap manipulation.1-4
We report 2 cases of DLK appearing after the immediate postoperative period
(2-7 months after LASIK), 1 of which had bilateral involvement.
Report of Cases
Case 1
A 48-year-old woman with euthyroidism and a treatment history of hypothyroidism
underwent bilateral sequential LASIK using a 180-µm Hansatome microkeratome
(Bausch and Lomb, Rochester, NY) and a Summit Apex Plus excimer laser (Summit
Technology, Waltham, Mass). Preoperative refraction of -4.75 +1.50 x
092 OD and -4.50 +1.75 x 085 OS yielded a best-corrected visual
acuity of 20/20 OU. Fifty percent epithelial flap defects in both eyes and
mild DLK in the left eye were present on postoperative day 1. The defects
healed with bandage soft contact lens wear and the DLK resolved after 1 week
of intensive fluorometholone treatment. One month postoperatively, uncorrected
visual acuity was 20/40 OD and 20/30 OS. Refraction of +0.25 +1.50 x
102 OD and -0.75 +0.75 x 037 OS yielded a best-corrected visual
acuity of 20/25 OU. The flaps were well healed with the exception of mild
interpalpebral punctate epithelial staining in both eyes. She was offered
bilateral lower punctal plugs, which she declined.
Two months postoperatively she complained of a sudden onset of redness
and a foreign body sensation in her left eye. Examination was remarkable for
an uncorrected visual acuity of 20/40 OS. Slitlamp biomicroscopy showed minimal
diffuse conjunctival hyperemia and a focal 2 x 2-mm nonsuppurative infiltrate
in the lamellar interface inferocentral to the pupil. Mild edema of the flap
without epithelial defects was noted. The anterior chamber was quiet. A regimen
of hourly topical ofloxacin was started. Examination 24 hours later revealed
a visual acuity of counting fingers. Slitlamp biomicroscopy showed severe
diffuse conjunctival hyperemia, diffuse stromal edema with a large central
epithelial defect, and a diffuse lamellar infiltrate without anterior or posterior
extension (Figure 1). The lamellar
flap was lifted and debrided of soft infiltrate. Scrapings were sent for aerobic,
anaerobic, atypical mycobacterial, and fungus staining and culturing. The
interface was irrigated with fortified vancomycin and tobramycin eye drops,
the flap was repositioned, and the bandage soft contact lens was applied.
Fortified vancomycin and tobramycin eye drops were administered hourly. One
day later, discrete granular infiltrates reappeared in the interface. Stains
and cultures revealed no organisms. Topical prednisolone acetate was given
every 2 hours to treat DLK and then hourly when cultures remained without
growth after 48 hours. On complete reepithelialization, the bandage soft contact
lens was removed and the dose of fortified antibiotics was decreased to 4
times per day. Prednisolone was taken hourly. On day 21, uncorrected visual
acuity was 20/60 OS. Refraction of plano +1.00 x 180 yielded a best-corrected
visual acuity of 20/30 OS. Slitlamp biomicroscopy showed mild interface scarring
centrally, 2+ granular infiltrates, and 1+ stromal flap edema (Figure 2).
|
|
|
|
Figure 1. Patient 1, left eye, 2 months
postoperatively. Slitlamp biomicroscopy reveals severe lamellar keratitis
with diffuse stromal edema, overlying epithelial defect, and diffuse lamellar
infiltrate without anterior or posterior extension. Visual acuity is counting
fingers.
|
|
|
|
|
|
|
Figure 2. Patient 1, left eye, 3 weeks after
treatment. Slitlamp biomicroscopy shows organized healing of interface keratitis.
Visual acuity is 20/30 OS with refraction of plano +1.00 x 180.
|
|
|
The left eye remained stable during the prednisolone dose taper. However,
3 months postoperatively, her right eye showed a small epithelial erosion
without keratitis. On follow-up day 3, slitlamp biomicroscopy of the right
eye revealed a healing erosion with few focal interface opacities and mild
diffuse granular infiltrates (Figure 3).
The keratitis resolved after a 5-day regimen of prednisolone acetate taken
hourly and ofloxacin taken 4 times per day.
|
|
|
|
Figure 3. Patient 1, right eye, 3 months
postoperatively. Slitlamp biomicroscopy shows mild lamellar keratitis with
few focal interface opacities and mild granular infiltrates centrally.
|
|
|
Case 2
A 51-year-old woman with myopic amblyopia currently taking thyroxine
for hypothyroidism underwent bilateral LASIK for treatment of high myopia.
She came for a second opinion regarding management of superior limbal keratoconjunctivitis
in the right eye 7 months postoperatively. Refraction of -1.75 yielded
a visual acuity of 20/40 OD. Slitlamp biomicroscopy was remarkable for mild
superior conjunctival hyperemia, redundancy, and rose Bengal staining. She
underwent superior conjunctival resection and was given tobramycin/dexamethasone
ointment to apply 4 times per day. Three days after resection, she complained
of worsening pain and decreased vision. On examination, her best-corrected
visual acuity was 20/80 OD. The superior conjunctival defect was healing well
without suppuration. Diffuse granular infiltrates were visible in the flap
interface without epithelial defects or anterior chamber reaction. Her regimen
was switched to ofloxacin taken 4 times per day and prednisolone acetate taken
hourly. Follow-up examination 48 hours later showed best-corrected visual
acuity to be 20/40 OD with completely resolved interface keratitis.
Comment
The causes of DLK are not clearly defined. A rare postoperative complication
of LASIK, with an estimated incidence of 3 in 400,2
DLK is thought to be a secondary inflammatory response to a variety of potential
agents within the space of the flap interface. Four clinical stages have been
described, ranging from non–visually significant focal infiltrates to
diffuse infiltrates with stromal necrosis.5
Known to occur within a week after either primary LASIK or enhancement procedures,
DLK has also been reported after epithelial flap debridement to reduce visually
significant basement membrane irregularities 1 month after LASIK enhancement.4
Unusual in our cases is the late onset of DLK. In the most severe case,
the lack of initial epithelial defect, confinement of infiltrate to the interface,
rapid progression despite hourly ofloxacin treatment, rapid improvement with
intensive topical steroids, and negative microbiology culture results strongly
support a diagnosis of DLK rather than infectious keratitis. One case series
review of infectious ulcerative keratitis following LASIK reported that all
cases had epithelial defects and none had infiltrate confined only to the
interface.6 Our case 1 had documented recurrent
epithelial erosions and typical DLK in the acute postoperative period. Case
2 had probable microdisruption of the superior corneal epithelium after manipulation
of the superior conjunctiva. We propose a mechanism whereby an inflammatory
reaction to corneal surface disruption occurs in the potential space of the
flap interface resulting in a clinical picture of lamellar keratitis.
We report these 2 cases to bring attention to the possibility of DLK
occurring beyond the immediate postoperative period, especially when the potential
for corneal surface disruption exists. As more patients undergo LASIK, more
cases of late-onset DLK will be seen. Care must be taken to exclude infectious
keratitis. However, the prognosis for recovery is good following intensive
topical steroid treatment.
AUTHOR INFORMATION
Supported in part by a grant from the Heed Ophthalmic Foundation, Cleveland,
Ohio (A.C.G.).
The authors have no proprietary interest in any of the companies mentioned.
Dr Steinert is a paid consultant for Summit Technology.
Corresponding author and reprints: Helen K. Wu, MD, Refractive Surgery
Center, Tufts University School of Medicine, New England Eye Center, 750 Washington
St, Box 450, Boston, MA 02111 (e-mail: helenkw{at}aol.com).
Anne Chang-Godinich, MD
Houston, Tex
Roger F. Steinert, MD;
Helen K. Wu, MD
Boston, Mass
REFERENCES
1. Smith RJ, Maloney RK. Diffuse lamellar keratitis: a new syndrome in lamellar refractive surgery. Ophthalmology. 1998;105:1721-1726.
FULL TEXT
|
ISI
| PUBMED
2. Kaufman SC, Maitchouk DY, Chou AGY, et al. Interface inflammation after laser in situ keratomileusis: sands of
the Sahara syndrome. J Cataract Refract Surg. 1998;24:1589-1593.
ISI
| PUBMED
3. Fraenkel GE, Cohen PR, Sutton GL, et al. Central focal interface opacity after laser in situ keratomileusis. J Refract Surg. 1998;14:571-576.
PUBMED
4. Steinert RF, McColgin AZ, White A, et al. Diffuse interstitial keratitis after laser in situ keratomileusis:
a nonspecific syndrome. Am J Ophthalmol. 2000;3:380-381.
FULL TEXT
5. Machat JJ. LASIK complications. In: Machat JJ, Slade SG, Probst LE, eds. The Art
of LASIK. 2nd ed. Thorofare, NJ: Slack Inc; 1999:392-396.
6. Quiros PA, Chuck RS, Smith RE, et al. Infectious ulcerative keratitis after laser in situ keratomileusis. Arch Ophthalmol. 1999;117:1423-1427.
FREE FULL TEXT
SECTION EDITOR: W. RICHARD GREEN, MD
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Relapsing Diffuse Lamellar Keratitis After Laser In Situ Keratomileusis Associated With Recurrent Erosion Syndrome
Jeng et al.
Arch Ophthalmol 2004;122:396-398.
FULL TEXT
Bilateral diffuse lamellar keratitis following bilateral simultaneous versus sequential laser in situ keratomileusis
McLeod et al.
Br. J. Ophthalmol. 2003;87:1086-1087.
ABSTRACT
| FULL TEXT
|
