Flap and interface complications in LASIK
Michael C. Knorz, MD
Flap complications using first-generation microkeratomes,
such as the Automated Corneal Shaper, were reported in
2.5% (27 of 1,062 eyes). With modern microkeratomes, such
as the Hansatome, keratotomy-related complications dropped
to 0.16% (46 of 28,201 eyes). Postoperative flap
complications, such as flap slippage, occurred in 1.42% (21 of
1,418 eyes), most of them during the first hour after surgery.
Interface complications are a new diagnostic entity as the
interface between flap and stroma presents an empty space
where fluid or cells can accumulate. Diffuse lamellar keratitis
usually occurs within the first postoperative days but may also
develop later on, triggered, eg, by recurrent corneal erosion.
Epithelial ingrowth is a rare complication caused rather by
postoperative invasion than by intraoperative implantation,
which suggests that the quality of the flap edge and its
apposition are very important. Interface fluid is a rare but
important phenomenon related to steroid-induced glaucoma
but presenting with falsely low tonometry readings. Curr Opin
Ophthalmol 2002, 13:242–245 © 2002 Lippincott Williams & Wilkins, Inc.
University of Heidelberg, Faculty of Clinical Medicine, Mannheim, Germany.
Correspondence to Prof. Dr. Michael C. Knorz, Klinikum Mannheim, Theodor
Kutzer Ufer 1–3, Mannheim 68167 Germany, e-mail: knorz@eyes.de
Current Opinion in Ophthalmology 2002. 13:242–245
ISSN 1040–8738 © 2002 Lippincott Williams & Wilkins, Inc.
242
LASIK has rapidly become the most frequently per-
formed surgical procedure. This review will analyze the
complications associated with the LASIK flap and the
interface between the flap and the stromal bed. The
review is predominantly based on the literature pub-
lished between February 2001 and February 2002, but in
some instances older publications were also cited be-
cause of their impact or because of the lack of more
recent work.
Microkeratome-related flap complications
These complications occur during the microkeratome
cut and represent the largest group of flap complications.
There is clearly a historical trend that shows improve-
ment of the rate of complications in modern microkera-
tomes. In a study by Stulting et al. [1], the rate of com-
plications in 1,062 consecutive eyes operated with the
Automated Corneal Shaper by 14 surgeons between May
1995 and December 1996 was reported. Twenty-seven
eyes (2.5%) had flap complications during primary sur-
gery, 17 of them could not be ablated at the time of
primary surgery. Of the 27 flap complications, there were
eight incomplete flaps, six buttonholes, five normal free
flaps, five small free flaps, one thin, one thick, and one
bilevel flap. Two of the buttonhole-flaps resulted in a
loss of two or more lines of spectacle-corrected acuity,
one of them had been ablated at the time of primary
surgery. In a study by Gimbel et al. [2] on the first 1,000
consecutive cases operated between April 1995 and Feb-
ruary 1997 using the Automated Corneal Shaper by one
surgeon, 19 (1.9%) microkeratome-related complications
were observed. Twelve of them were incomplete flaps,
three thin flaps, three buttonholes, and one free flap.
None of these eyes lost two or more lines of spectacle-
corrected visual acuity. The incidence of microkera-
tome-related complications showed a clear learning
curve, with 4.5% during the first one hundred cases and
0.5% between case 800 and 1,000 [2].
In a more recent study of 3,826 eyes operated between
November 1996 and August 1998, microkeratome-
related flap complications occurred in 27 eyes (0.68%)[3].
Both the Automated Corneal Shaper and the Hansatome
were used in this study, and the authors did unfortu-
nately not evaluate the incidence for each of the respec-
tive microkeratomes. Only one eye lost two or more lines
of spectacle-corrected visual acuity. In 16 eyes, ablation
was not possible, and another microkeratome cut was
performed after three months. Two of the 16 eyes
(12.5%) had a microkeratome-related flap complication
DOI: 10.1097/01.ICU.0000020342.12033.D3

again, but none of the 16 eyes lost two or more lines of
visual acuity. This suggests that making another micro-
keratome cut after three months is generally safe [3].
However, it does not mean that a re-cut should be used
in all enhancements. Re-cutting should rather be limited
to cases with microkeratome-related flap complications,
as presented by Rubinfeld, who reported on nine cases
with significant visual loss caused be irregular astigma-
tism due to tissue loss after a re-cut (Rubinfeld RS:
American Academy of Ophthalmology Subspecialty Day
2001 Refractive Surgery, New Orleans).
Pallikaris et al. [4] reported microkeratome-related flap
complications in 14.37% (48 of 334 consecutive eyes)
operated between September 1997 and November 1998
by one surgeon using the Flapmaker, a disposable mi-
crokeratome. Their study is interesting because the au-
thors performed laser ablation in 37 of these eyes despite
the flap complication. The ablation resulted in central
corneal scars, haze, irregular astigmatism, and loss of one
line of spectacle-corrected visual acuity in many of the
eyes. The reviewer feels that based on that data it is
strongly recommended never to perform laser ablation at
the time a microkeratome-related flap complication oc-
curs. It should be standard practice to replace the abnor-
mal flap and retreat the eye between two and six months
later by re-cutting it using a thicker flap, if possible, but
never a thinner one.
One of the largest and most recent studies reports the
incidence of microkeratome-related flap complications in
84,711 eyes operated by 640 surgeons in 28 national
open-access laser facilities between November 1998 and
May 2000 [5] using both the Automated Corneal Shaper
and the Hansatome. Microkeratome-related flap compli-
cations occurred in 256 eyes (0.302%). There were 84
(0.099%) partial flaps, 74 (0.087%) thin or irregular flaps,
59 (0.074%) buttonholes, 29 (0.034%) failures to achieve
intraocular pressure, and 10 (0.012%) free flaps. In a sub-
set of data between December 1999 and May 2000, the
authors were also able to compare the Automated Cor-
neal Shaper and the Hansatome. They found a high in-
cidence of 6.38% (21 of 329 eyes) for the Automated
Corneal Shaper and a very low incidence of 0.16% (46 of
28,201 eyes) for the Hansatome [5]. Part of this signifi-
cant difference is most likely due to the unfamiliarity of
the staff with the Automated Corneal Shaper because of
its infrequent use, as the authors also state [5]. However,
in accordance with the reviewer the authors state that the
low rate of microkeratome-related complications reflects
a significant improvement in microkeratome technology.
Other flap complications
These include postoperative flap slippage and folds.
Other complications, such as flap melt, are included in
the chapter on interface complications. Flap slippage and
folds were reported by Stulting et al. [1] using the Auto-
Flap and interface complications in LASIK Knorz 243
mated Corneal Shaper in 13 of 1,062 eyes (1.2%). Seven
of them showed partial slippage, four showed total slip-
page, and two showed flap folds. One eye (flap folds) lost
two or more lines of spectacle-corrected visual acuity.
The study by Gimbel et al. [2] reported 18 (1.8%) slipped
or folded flaps using the same microkeratome. Twelve of
them had shifted, four showed micro-wrinkles, and two
edge folds. One eye (slipped flap) lost two or more lines
of spectacle-corrected visual acuity.
In a more recent study, Recep et al. [6] reported flap
slippage in 21 (1.42%) of 1,481 eyes operated between
January 1997 and May 1998 using a Moria microkera-
tome. Flap slippage was detected at one hour in 15 eyes,
at one day in two eyes, and at one week in three eyes.
One eye had a slipped flap both at one day and at one
week. The authors reported interface haze at six months
in two of the eyes, which had slipped flaps after one
week. No other complications were observed after six
months, leading to the conclusion that flap slippage is a
benign complication, especially when occurring early [6].
Accidental self-removal of a flap was reported as a rare
complication which occurred while a patient tried to re-
move a soft contact lens inserted ten days after sur-
gery [7].
Incidence of flap complications in
different microkeratomes
Based on the above analysis of flap complications, we
may also compare the incidence by microkeratome used.
Flap complications occurred in 0.16% with the Hansa-
tome [5], in 6.38% with the Automated Corneal Shaper
[5], and in 14,37% with the Flap Maker, a disposable mi-
crokeratome [4]. Unfortunately, there are no data available
on other microkeratomes, which limits the comparison.
Summarizing the data on flap complications, it may be
stated that microkeratome-related flap complications are
extremely rare today. There are, however, microkera-
tomes available which exhibit a far above average rate of
complications and should therefore no longer, or not at
all, be used.
Interface complications
Ultrastructural studies of the human cornea using scan-
ning and transmission electron microscopy in one corneal
button removed six months after LASIK during kerato-
plasty revealed no detectable wound repair at the
flap/bed interface [8]. The stromal surface and the un-
dersurface of the flap were smooth and devoid of cells
adjacent to the interface. No electron-dense layer, sug-
gesting thermal damage, was found on the ablated
stroma, and the orientation of the collagen fibrils was
preserved [8]. This indicates that the interface repre-
244 Refractive surgery
sents a space which can be filled by fluid or cells even
months after LASIK.
Using confocal microscopy, keratocyte apoptosis could
be confirmed adjacent to the interface, while keratocyte
activation occurred in the posterior stroma, indicating
some wound healing response. Six months after LASIK,
keratocyte activity had returned to normal levels [9].
There are a variety of complications that can occur at the
interface. The most frequent one is diffuse lamellar
keratitis (DLK). Epithelial ingrowth, infection and ab-
scess, and fluid accumulation are other complications
which are located at the interface.
Diffuse lamellar keratitis
Diffuse lamellar keratitis is a non-specific response to an
insult to the cornea. In rabbits, it was shown that as little
as 50 endotoxin units cause grade 2 of diffuse lamellar
keratitis [10]. The authors also found endotoxin in tap
water, distilled water, filtered water and in the reservoir
of the autoclaves, suggesting water as a possible means of
transfer [10]. Clinically, diffuse lamellar keratitis
presents as a diffuse or multifocal infiltrate defined to
the interface, usually one to six days after LASIK. It is
a diagnostic entity that can be observed after LASIK
only as it requires the space within the anterior stroma
created by the keratotomy. Within this space, granu-
locytes and other inflammatory cells accumulate [11].
Confocal microscopy can be a useful tool to identify
these cells [11,12]. Treatment consists of potent topical
steroids hourly and daily exams. It is important to in-
tervene early in the postoperative course. In stage 3
(diffuse lamellar infiltrate with snowball-like cell con-
densate) or deterioration of stage 2 (diffuse mono-
layered lamellar infiltrate), re-intervention and irrigation
of the interface should be performed immediately. In
contrast, should stromal melting or even scarring already
be present, it seems advisable not to lift the flap and
irrigate as the course cannot be improved [13], and scar-
ring might even be more pronounced due to tissue loss
during re-intervention.
Diffuse lamellar keratitis occurs more frequently if epi-
thelial defects are present. It is usually confined to the
interface area underlying the epithelial defect. It is ex-
tremely important to diagnose it and to use steroids de-
spite the epithelial defects as corneal melting and scar-
ring may develop otherwise. Diffuse lamellar keratitis
may also develop without any direct flap manipulation.
Harrison and Periman [12] presented a case report of a
patient who had a recurrent corneal erosion three months
after LASIK and developed diffuse lamellar keratitis.
Another case of late-onset diffuse lamellar keratitis was
reported by Probst and Foley [14]. These cases indicate
that diffuse lamellar keratitis has several causes. Most
frequently, it seems to be induced by some toxins or
allergenic agents introduced during surgery. It can also
be caused by trauma to the cornea, eg, epithelial erosions,
even months after LASIK. In these cases the interface
seems to provide an empty space where the inflamma-
tory cells can accumulate [12].
Epithelial ingrowth
Epithelial ingrowth requiring surgical removal was re-
ported to occur in 35 (0.92%) of 3,786 eyes by Wang and
Maloney [15]. In 42 of the 43 eyes, the ingrowth was
continuous with the surface epithelium, suggesting a
postoperative invasion rather than intraoperative implan-
tation of epithelial cells. Fourteen of the 43 eyes had a
postoperative epithelial defect and six of the 43 eyes had
loose epithelium intraoperatively, suggesting a higher in-
cidence of epithelial ingrowth in the presence of an ab-
normal epithelium. The authors also found a higher in-
cidence of epithelial ingrowth after re-treatments (eight
(1.7%) of 480 eyes)[15].
Microbial keratitis
Microbial keratitis [16,17,18,19] is fortunately a rare (1 in
5,000 to 10,000 cases)[17] but vision-threatening compli-
cation. A review by Alio et al. [17] presents an excellent
overview of most of the cases reported, the appropriate
therapy, and their clinical outcome.
Mycobacterium species recently emerge as a leading
pathogen in microbial infections after LASIK [16].
These infections are characterized by a late onset (mean
20 days, range 11 days to six weeks) and a prolonged
clinical course despite treatment, frequently requiring
amputation of the flap [16] or even penetrating kerato-
plasty [19].
Interface fluid
The occurrence of interface fluid presents a new diag-
nostic entity which can be observed after LASIK only. As
the collagen fibrils do not appear to heal, the lamellar cut
creates a space within the anterior stroma [8], which can
be filled by fluid or other matter. There are some case
reports describing interface fluid accumulation [20,21]. It
is caused by steroid-induced glaucoma leading to corneal
edema, and fluid accumulation in the interface. Appla-
nation-tonometry on the flap will show low or normal
readings, the glaucoma may not be diagnosed and even-
tually cause optic atrophy (Najman-Vainer J, Smith RJ,
Maloney RK: Interface fluid after LASIK: misleading
tonometry can lead to end-stage glaucoma (letter). J
Cataract Refract Surg 2000, 26:471). It is important that
the rare condition of interface fluid becomes known to all
ophthalmologists. It usually follows or is associated with
diffuse lamellar keratitis. The keratitis is treated with
steroids, which in turn leads to glaucoma in steroid-
responders, and the interface fluid accumulates. It is im-
portant to diagnose this condition by performing tonom-
etry off the flap or at the limbus, and to initiate proper

treatment. Steroids, which are needed to control the dif-
fuse lamellar keratitis, should be tapered off as soon as
possible, and anti-glaucoma medication must be added.
Summarizing interface complications, it can be stated
that the interface presents a new space created by the
keratotomy that allows the accumulation of cells or fluid,
creating new diagnostic challenges. Infections are ex-
tremely rare but the few cases reported suggest that strict
antisepsis of the surgical field could avoid most of them.
Diffuse lamellar keratitis must be aggressively treated to
avoid permanent scarring. Should interface fluid become
visible, steroid-induced glaucoma should be suspected.
Epithelial ingrowth seems to be caused predominantly
by invasion, suggesting that the quality of the flap edge
and its apposition are very important.
References and recommended readings
Papers of particular interest, published within the annual period of review,
have been highlighted as:
• Of special interest
•• Of outstanding interest
1 Stulting RD, Carr JD, Thompson KP, et al.: Complications of laser in situ
keratomileusis for the correction of myopia. Ophthalmology 1999,
106:13–20.
2 Gimbel HV, Andersen Penno EE, van Westenbrugge JA, et al.: Incidence and
management of intraoperative and early postoperative complications in 1000
consecutive laser in situ keratomileusis cases. Ophthalmology 1998,
105:1839–1848.
3 Tham VM, Maloney RK: Microkeratome complications of laser in situ ker-
atomileusis. Ophthalmology 2000, 107:920–924.
4 Pallikaris IG, Katsanevaki VJ, Panagopoulou SI: Laser in situ keratomileusis
• intraoperative complications using one type of microkeratome. Ophthalmol-
ogy 2002, 109:57–63.
This paper reports the outcome of 14.37% (n=48) flap complications with the
Flapmaker microkeratome of which 37 eyes were ablated at the time of initial sur-
gery despite of the complication. The poor results show an excellent example of
what should not be done.
5 Jacobs JM, Taravella MJ : Incidence of intraoperative flap complications in
• laser in situ keratomileusis. J Cataract Refract Surg 2002, 28:23–28.
This paper reports a retrospective analysis of flap complications in 84,711 proce-
dures performed by 640 surgeons in 28 national open-access laser facilities. With
an overall incidence of 0.3% (n=256), partial flaps were most common (0.099%).
6 Recep OF, Cagil N, Hasiripi H: Outcome of flap subluxation after laser in situ
Flap and interface complications in LASIK Knorz 245
keratomileusis: results of 6 month follow-up. J Cataract Refract Surg 2000,
26:1158–1162.
7 Sridhar MS, Rapuano CJ, Cohen EJ: Accidental self-removal of a flap–a rare
complication of laser in situ keratomileusis surgery. Am J Ophthalmol 2001,
132:780–782.
8 Rumelt S, Cohen I, Skandarani P, et al.: Ultrastructure of the lamellar corneal
wound after laser in situ keratomileusis in human eye. J Cataract Refract Surg
2001, 27:1323–1327.
9 Pisella PJ, Auzerie O, Bokobza Y, et al.: Evaluation of corneal stromal changes
in vivo after laser in situ keratomileusis with confocal microscopy. Ophthal-
mology 2001, 108:1744–1750.
10 Peters NT, Iskander NG, Anderson Penno EE, et al.: Diffuse lamellar keratitis:
isolation of endotoxin and demonstration of the inflammatory potential in a
rabbit laser in situ keratomileusis model. J Cataract Refract Surg 2001,
27:917–923.
11 Buhren J, Baumeister M, Kohnen T: Diffuse lamellar keratitis after laser in situ
keratomileusis imaged by confocal microscopy. Ophthalmology 2001,
108:1075–1081.
12 Harrison DA, Periman LM: Diffuse lamellar keratitis associated with recurrent
corneal erosions after laser in situ keratomileusis. J Refract Surg 2001,
17:463–465.
13 Parolini B, Marcon G, Panozzo GA: Central necrotic lamellar inflammation
• after laser in situ keratomileusis. J Refract Surg 2001, 17:110–112.
Case report presenting the course of diffuse lamellar keratitis without and with
belated surgical treatment.
14 Probst LE, Foley L: Late-onset interface keratitis after uneventful laser in situ
keratomileusis. J Cataract Refract Surg 2001, 27:1124–1125.
15 Wang MY, Maloney RK: Epithelial ingrowth after laser in situ keratomileusis.
Am J Ophthalmol 2000, 129:746–751.
16 Solomon A, Karp CL, Miller D, et al.: Mycobacterium interface keratitis after
• laser in situ keratomileusis. Ophthalmology 2001, 108:2201–2208.
Good description of these rare complications and the appropriate treatment.
17 Alio JL, Perez-Santonja JJ, Tervo T, et al.: Postoperative inflammation, micro-
• bial complications, and wound healing following laser in situ keratomileusis. J
Refract Surg 2000, 16:523–538.
This review article gives an excellent overview of microbial keratitis, its diagnosis
and treatment and the reported clinical course. It also addresses diffuse lamellar
keratitis.
18 Sridhar MS, Garg P, Bansal AK, et al.: Aspergillus flavus keratitis after laser in
situ keratomileusis. Am J Ophthalmol 2000, 129:802–804.
19 Kouyoumdjian GA, Forstot SL, Durairaj VD, et al.: Infectious keratitis after
laser refractive surgery. Ophthalmology 2001, 108:1266–1268.
20 Portellinha W, Kuchenbuk M, Nakano K, et al.: Interface fluid and diffuse cor-
neal edema after laser in situ keratomileusis. J Refract Surg 2001, 17(Sup-
pl):S192–195.
21 Fogla R, Rao SK, Padmanabhan P: Interface fluid after laser in situ keratomi-
• leusis. J Cataract Refract Surg 2001, 27:1526–1528.
Good case report describing steroid-induced glaucoma as the etiology of the in-
terface fluid.