PURPOSE
To analyze the effects of variations in femtosecond
laser energy level on corneal stromal cell death and inflammatory cell influx
following flap creation in a rabbit model.
METHODS
Eighteen rabbits were stratified in three different
groups according to level of energy applied for flap creation (six animals per
group). Three different energy levels were chosen for both the lamellar and
side cut: 2.7 µJ (high energy), 1.6 µJ (intermediate energy), and
0.5 µJ (low energy) with a 60 kHz, model II, femtosecond laser
(IntraLase). The opposite eye of each rabbit served as a control. At the
24-hour time point after surgery, all rabbits were euthanized and the
corneoscleral rims were analyzed for the levels of cell death and inflammatory
cell influx with the terminal uridine deoxynucleotidyl transferase dUTP nick
end labeling (TUNEL) assay and immunocytochemistry for monocyte marker CD11b,
respectively.
RESULTS
The high energy group (31.9±7.1 [standard error of mean (SEM) 2.9]) had significantly more
TUNEL-positive cells in the central flap compared to the intermediate
(22.2±1.9 [SEM 0.8], P=.004), low
(17.9±4.0 [SEM 1.6], P<.001), and control
eye (0.06±0.02 [SEM 0.009], P<.001) groups. The
intermediate and low energy groups also had significantly more TUNEL-positive
cells than the control groups (P<.001). The
difference between the intermediate and low energy levels was not significant
(P=.56). The mean for CD11b-positive cells/400x field at the flap edge was 26.1±29.3 (SEM 11.9),
5.8±4.1 (SEM 1.6), 1.6±4.1 (SEM 1.6), and 0.005±0.01 (SEM 0.005) for
high energy, intermediate energy, low energy, and control groups, respectively.
Only the intermediate energy group showed statistically more inflammatory cells
than control eyes (P=.015), most likely due to variability between eyes.
CONCLUSIONS
Higher energy levels trigger greater cell death
when the femtosecond laser is used to create corneal flaps. Greater corneal
inflammatory cell infiltration is observed with higher femtosecond laser energy
levels. [J Refract Surg. 2009;25:869-874.]
doi:10.3928/1081597X-20090917-08
AUTHORS
From Cleveland Clinic, Cole Eye Institute, Cleveland, Ohio
(de Medeiros, Kaur, Agrawal, Chaurasia, Hammel, Dupps, Wilson); and the
Department of Ophthalmology, University of São Paulo, São Paulo,
Brazil (de Medeiros).
Supported in part by US Public Health Service grants EY10056
and EY15638 from National Eye Institute, National Institutes of Health,
Bethesda, Md; and Research to Prevent Blindness, New York, NY. Dr Wilson is the
recipient of a Research to Prevent Blindness Physician-Scientist Award.
The authors have no proprietary or financial interest in the
materials presented herein.
Correspondence: Steven E. Wilson, MD, Cole Eye Institute,
Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195. Tel: 216.444.5887;
E-mail: wilsons4@ccf.org
Received: February 5, 2008; Accepted: September 23, 2008
Posted online: October 31, 2008
