Severe Diffuse Lamellar Keratitis Following Laser <i>in Situ</i> Keratomileusis with an Iatrogenic Double Flap

doi:10.4236/ojoph.2012.22008

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Open Journal of Ophthalmology, 2012, 2, 34-36

http://dx.doi.org/10.4236/ojoph.2012.22008 Published Online May 2012 (http://www.SciRP.org/journal/ojoph)

Severe Diffuse Lamellar Keratitis Following Laser in Situ

Keratomileusis with an Iatrogenic Double Flap

Hidemasa Torii, Kazuno Negishi*, Murat Dogru, Kazuo Tsubota

Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.

Email: *[email protected]

Received January 18th, 2012; revised February 28th, 2012; accepted March 20th, 2012

ABSTRACT

We present a case of an iatrogenic double flap created during laser in situ keratomileusis using a femtosecond laser mi-

crokeratome that resulted in development of severe diffuse lamellar keratitis (DLK). The DLK occurred mainly in the

second interface, made by the spatula accidentally and not exposed to femtosecond or excimer lasers. Because of dif-

ferences in the severity of the interface inflammatory reactions between the two layers exposed to the same spatula, an

allergic reaction to detergent, bacteria, or other chemicals could not be assumed to be the main cause of DLK. Our ob-

servations in this case may suggest an important association of neural factors with DLK, because the inflammatory re-

action occurred mainly in the deep stromal layer at the thick corneal nerves.

Keywords: Laser in Situ Keratomileusis; Femtosecond Laser; Complications; Diffuse Lamellar Keratitis

1. Case History

A 35-year-old man who had undergone bilateral laser in

situ keratomileusis (LASIK) using a 15-KHz IntraLase

femtosecond laser microkeratome (Advanced Medical

Optics, Irvine, CA) 1 week previously was referred to

our clinic for a visual disturbance in his right eye. His

bilateral visual acuity was 20/63 that improved to 20/10

with a refractive correction preoperatively. The parame-

ters of the femtosecond laser procedure were a 110-µm

flap depth, hinge angle of 60˚ for a superior hinge, 9-mm

flap diameters, and 1.45 mJ of energy for the lamellar cut

and 1.3 mJ for the side cut. Intraoperatively, a spatula

used to lift the flap was inserted accidentally into a dif-

ferent deeper layer of corneal stroma in the right eye. The

surgeon noticed wide dehiscence in the wrong layer and

created the corneal flap again in the planned layer in the

right eye (see Figure 1). The excimer laser ablation was

performed as planned; the target refractions were (–2.25 -

0.50) × 90 and (–2.00 - 0.50) × 110 in the right and left

eyes, respectively.

At the initial examination in our clinic, the uncorrected

visual acuity (UCVA) was 20/160 in the right eye that

improved to 20/100 with a refractive correction of (–1.00

- 1.50) × 100. The UCVA in the left eye was 20/12.5. The

intraocular pressure was 10 mmHg bilaterally. Biomi-

croscopic examination showed corneal stromal edema

with a severe diffuse inflammatory reaction, mainly in

the deep stroma in the right eye, and no abnormal find-

ings in the left eye. The right eye was diagnosed with

severe stage 3 diffuse lamellar keratitis (DLK). The ante-

rior chamber, lens, vitreous, and fundus appeared normal

bilaterally. Pentacam (Oculus, Wetzlar, Germany) meas-

urements showed total central corneal thicknesses of 535

μm and 537 μm in the right and left eyes, respectively

(552 μm and 567 μm preoperatively), and there was a

layer of diffuse high pixel intensity in the deep stroma of

the right eye (see Figure 2(a)). The Pentacam did not

detect any abnormal findings in the left eye except for

the area of relatively high pixel intensity in the flap (see

Figure 2(b)). The DLK gradually improved with topical

steroidal treatment. The most recent examination 45

months postoperatively showed UCVA levels of 20/50

and 20/16 in the right and left eyes, respectively. A deep

stromal scar (see Figure 2(c)) was still apparent on

biomicroscopy.

Figure 1. Schema of the iatrogenic double flap. The con-

tinuous line indicates the actual flap interface. The dotted

line indicates the iatrogenic rupture line. Dots indicate dif-

fuse lamellar keratitis. At the first visit, corneal stromal

edema was seen in the shaded area.

*Corresponding author.

Severe Diffuse Lamellar Keratitis Following Laser in Situ Keratomileusis with an Iatrogenic Double Flap 35

Figure 2. (a) Scheimpflug photograph of the right eye (1

week postoperatively). There is a diffuse layer of high pixel

intensity (arrowheads). Relatively high pixel intensity area

also can be seen in a shallower layer that is assumed to be

the flap (arrows); (b) On a Scheimpflug photograph of the

left eye (1 week postoperatively), there is an area of rela-

tively high pixel intensity in a shallower layer that is as-

sumed to be the flap (arrows); (c) Biomicroscopy of the

right eye 3 years postoperatively shows a corneal scar in the

deep stroma (arrowheads).

2. Discussion

The femtosecond laser delivers thousands of micro-

photodisruptive pulses to a specific corneal plane to ob-

tain a smooth cut and create a stromal flap with parallel

anterior and posterior surfaces [1]. The femtosecond la-

ser microkeratome has achieved good refractive out-

comes with a low complication rate [1,2], although sev-

eral studies have reported complications related to in-

flammatory reactions including DLK [2,3]. We present a

complicated case of severe DLK that developed in an

iatrogenic double flap after LASIK using a femtosecond

laser.

We described a rare complicated case of femtosecond

laser-assisted LASIK with an iatrogenic double flap that

resulted in development of severe DLK.

The low complication rate associated with flap crea-

tion [4] is an advantage of the laser microkeratome.

Nonetheless, in the current case, the surgeon ruptured the

deep stromal layer that resulted in the iatrogenic double

flap.

DLK is characterized by an inflammatory response at

the flap interface after LASIK. Although the detailed

etiology is unknown [5], DLK has been attributed to

multiple etiologies including bacterial endotoxins, chem-

icals, or debris produced during autoclaving or by surgi-

cal gloves and drapes, marking pens, meibomian gland

secretions, atopy, iatrogenic epithelial defects, low mean

endothelial cell density, and wide palpebral fissure height

[5]. DLK currently is thought to be related to the manner

in which endogenous factors modulate the patient re-

sponse to exogenous exposures [5].

The development of DLK after LASIK performed with

a mechanical microkeratome is well recognized. In con-

trast, the incidence of DLK after LASIK performed with

a femtosecond laser has been reported previously [3-7].

The incidence rates of DLK after LASIK in which a laser

keratome is used vary considerably and are higher than

with a mechanical microkeratome. It also has been re-

ported that higher laser energy levels may result in higher

DLK rates.

In the current case, there was a layer of diffuse high

pixel intensity in the deep stroma of the right eye, which

was the layer into which the surgeon accidentally in-

serted the spatula (see Figure 2(a)). A Scheimpflug im-

age showed inflammation in the deep stromal layer

where dehiscence was present and not in the actual flap

layer. Stromal cell necrosis associated with a femtosec-

ond laser flap likely contributes to greater inflammation

after LASIK, especially with higher energy levels that

result in higher rates of keratocyte cell death [8]. It also

was hypothesized that accumulated gas bubbles and

femtosecond laser energy may increase the inflammatory

response in patients who might be more susceptible to

DLK [7]. However, in the current case, the DLK mainly

developed in the second interface that was not exposed to

femtosecond or excimer lasers. In addition, the associa-

tion with exogenous factors such as an allergic reaction

to detergent, bacteria, or other chemicals could not be

assumed to be the main cause of DLK in the current case

because of the differing severities of the interface in-

flammatory reactions between the two layers, despite

almost the same procedure with the same instruments

except laser ablation. Alio et al. reported that corneal

innervation probably is involved in both the immediate

inflammatory response and long-term healing after LA-

SIK and photorefractive keratotomy [9]. Previous studies

have shown that the ciliary nerves of the ophthalmic

branch of the trigeminal nerve radially penetrate the cor-

nea in the deep peripheral stroma and then course anteri-

orly and the diameter increases with increasing distance

from the anterior corneal surface [10]. In the current case,

we believe that there was an important association of

neural factors with DLK, because the inflammatory reac-

tion developed mainly in the deep stromal layer where

the thick corneal nerves were damaged mechanically.

Further studies on the mechanisms of inflammation in

Severe Diffuse Lamellar Keratitis Following Laser in Situ Keratomileusis with an Iatrogenic Double Flap

patients with DLK should be performed and hopefully

will provide invaluable information.

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