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Persistent Corneal Edema after Collagen Cross-Linking

for Keratoconus
ASHOK SHARMA, JENNIFER MARIE NOTTAGE, KANISH MIRCHIA, RAJAN SHARMA, KANWAR MOHAN,
AND VERINDER SINGH NIRANKARI
PURPOSE: To present a new complication of persistent
corneal edema after collagen cross-linking (CXL) in
keratoconus patients.
DESIGN: Retrospective case series of postoperative
corneal edema after CXL.
METHODS: STUDY POPULATION: All patients who underwent CXL treatment with subsequent corneal edema.
Patients with stromal haze were excluded. INTERVENTION:
The CXL treatments used the Dresden protocol with
corneal thickness of more than 400 m after epithelium
was removed. MAIN OUTCOME MEASURE: The resolution of
corneal edema after surgery.
RESULTS: Postoperative corneal edema was identified
in 10 (2.9%) of 350 patients who were followed up for
a mean of 14 4 months. The edema started on
postoperative day 1 (10/10) and increased for 3 weeks.
Additional findings included: deep vascularization (2
eyes; 20%), iris atrophy (6 eyes; 60%), pigment dispersion (5 eyes; 50%), persistent epithelial defect (3 eyes;
30%), and infectious keratitis (1 eye; 10%). Specular
microscopy was unsuccessful, but the fellow untreated
eyes had normal endothelial counts. Intraocular pressure
and lenticular evaluations were normal. Corneal edema
improved in 4 patients and resolved in 1 patient. In these
5 patients, the logarithm of the minimal angle of resolution best-corrected visual acuity was 0.5 0.18. Penetrating keratoplasty was offered to 5 patients when
improvement plateaued at 3 months, but only 2 patients
underwent penetrating keratoplasty.
CONCLUSIONS: CXL is a safe and effective procedure
with few known side effects. This case series reports the
possibility of corneal endothelial damage with visually
significant corneal edema after CXL treatment. Based on
the extent of endothelial damage, patients may require
penetrating keratoplasty. (Am J Ophthalmol 2012;
154:922926. 2012 by Elsevier Inc. All rights
reserved.)

Accepted for publication June 6, 2012.


From the Cornea Centre, Chandigarh, India (A.S., K.Mo.); the
Cornea Service, Eye Consultants of Maryland, Owings Mills, Maryland
(J.M.N., V.S.N.); the Government Medical College and Hospital, Chandigarh, India (K.Mi.); the Maharishi Markandeshwar Institute of Medical
Science and Research, Haryana, India (R.S.); and the Department of
Ophthalmology, University of Maryland, Baltimore, Maryland (V.S.N.).
Inquiries to Verinder S. Nirankari, Cornea Service, Eye Consultants of
Maryland, 21 Crossroads Drive, Suite 425, Owings Mills, MD 21117;
e-mail: vnirankari@aol.com

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2012 BY

ERATOCONUS IS A BILATERAL, ASYMMETRIC, NON-

inflammatory, progressive ectatic degeneration resulting in stromal thinning and distortion of the
cornea. Depending on the severity and progression of the
disease, it can be treated with spectacles, rigid gas permeable contact lenses, intracorneal ring segments, deep anterior lamellar keratoplasty, or penetrating keratoplasty.15
Recently, collagen cross-linking (CXL) with riboflavin
drops has been reported to be effective in increasing the
biomechanical strength and stability of the cornea.6 8
CXL, if preformed according to standard protocols, has
been found to be a safe procedure.9,10 Despite the high
safety profile reported, there are a few reports of adverse
events after CXL. Persistent corneal haze is one of the
more frequently reported complications of CXL.1113 In
addition, a few cases of infectious keratitis after CXL have
been reported.14,15 Furthermore, Gokhale recently reported a single case of CXL-induced corneal endothelial
cell damage resulting in corneal edema.16 We observed
several cases of persistent corneal edema after CXL for
treatment of progressive keratoconus and have evaluated
this case series of 10 patients.

METHODS
AFTER APPROVAL FROM THE CORNEA CENTRE INSTITU-

tional Review Board, a retrospective chart review of all


patients treated with CXL for progressive keratoconus from
July 1, 2008, through June 30, 2011, was conducted. These
charts were reviewed for any complications of the treatment. Patients who were treated for persistent stromal haze
were excluded from the study. Patients in whom corneal
edema developed that persisted for more than 3 weeks were
included in the study.
Data acquisition included preoperative and postoperative best-corrected visual acuity, refraction, keratometry,
pachymetry, and corneal topography. Pachymetry readings
were obtained from a Pentacam (Pentacam Oculyzer;
Oculus Optikgerate GmbH, Heidelberg, Germany) to
eliminate the chance of missing the thinnest point in the
cornea that could be missed by ultrasonic pachymeter. The
details of the surgical procedure, including frequency of
riboflavin drops, total energy delivered, and any deviation
from the Dresden protocol, were recorded. The postoper-

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http://dx.doi.org/10.1016/j.ajo.2012.06.005

TABLE. Investigational Parameters for Patients in Whom Persistent Corneal Edema Developed after Collagen Cross-Linking
Treatment for Progressive Keratoconus
VA

Max K

CCT

Patient
No.

Age
(y)

Sex

Preoperative

Postoperative

Preoperative

Postoperative

Preoperative

3 Weeks
after
Surgery

1
2a
3a
4b
5
6b
7
8
9
10b

17
21
24
20
29
16
32
26
16
22

M
F
M
M
F
M
F
M
M
M

0.00
0.00
0.00
0.20
0.00
0.00
0.00
0.00
0.00
0.20

0.20
0.80
0.20
1.00
0.50
1.00
0.30
0.60
0.60
0.80

53.8
51.2
59.8
59.4
57.9
53.8
58.3
56.9
59.5
56.9

48.0
50.0
49.3
56.8
55.4
54.2
55.6
54.8
57.9
54.6

493
482
484
480
496
474
463
447
449
458

621
698
656
695
598
687
620
678
634
658

3 Months
after
Surgery

6 Months
after
Surgery

12 Months
after
Surgery

Follow-up
(mos)

596
693
645
685
587
659
582
674
626
632

586
682
594
663
585
633
571
628
597
609

565
664
585
657
572
585
569
590
575
584

22
12
18
8
10
15
16
14
16
12

CCT central or minimal corneal thickness; F female; M male; Max K maximum keratometry; mos months; VA visual acuity;
y year.
a
Patients who underwent penetrating keratoplasty after cross-linking.
b
Patients offered penetrating keratoplasty after cross-linking, but declined.

ative anterior segment findings and duration of symptoms


also were evaluated.
COLLAGEN CROSS-LINKING PROCEDURE:

The CXL
treatment was preformed as an outpatient procedure following the Dresden protocol by an experienced ophthalmologist (K.Mi.).17 The treatment was performed under
sterile conditions in an operating theater. After obtaining
informed consent, the ocular surface was anesthetized with
topical proparacaine hydrochloride 0.5% solution. An
eyelid speculum was inserted, and the corneal epithelium
was removed using a hockey stick blade (Grieshaber;
Alcon, Schaffhausen, Switzerland). The epithelium was
debrided to expose 80% to 90% of the central cornea. The
corneal thickness was measured after the epithelium was
removed to confirm a thickness of more than 400 m in all
cases. Next, isotonic riboflavin 0.1% drops (Medio-Cross;
Medizinprodukte GmbH, Neudorf, Germany) were instilled every 2 minutes for 30 minutes, concurrent with
instillation of topical proparacaine. The corneas then were
exposed to ultraviolet A light (UV-X System; Peschke
Meditrade GmbH, Huenenberg, Switzerland) for 30 minutes. Administration of additional isotonic riboflavin drops
occurred every 3 minutes during the ultraviolet A exposure. The parameters of emitted ultraviolet light included:
wavelength, 370 nm; irradiance, 3 mW/cm2; and diameter,
7.5 mm. A calibrated ultraviolet meter was used to confirm
the irradiance (3.0 mW/cm2) before each treatment session; however, the corneal thickness was not remeasured
during the ultraviolet exposure. After completion of ultraviolet A exposure, the eyelid speculum was removed and a
drop of moxifloxacin hydrochloride ophthalmic solution
0.5% (Cipla Ltd, Roorkee, India) was instilled. An eye pad
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PERSISTENT CORNEAL EDEMA

and shield then were applied. The standard postoperative


treatment included both moxifloxacin hydrochloride ophthalmic solution 0.5% and carboxymethyl cellulose (Allergan, Karnataka, India) 4 times daily. For pain control,
the patient also was prescribed Combiflam (combination
pill of ibuprofen and acetaminophen; Aventis, Akhleshwar, India) as needed for 2 to 3 days. After the corneal
epithelium healed, fluorometholone drops were added
twice daily for 2 weeks followed by a taper to once daily for
2 weeks. If the patient had a nonhealing epithelial defect,
then a bandage contact lens was placed.
Those patients in whom corneal edema developed were
prescribed prednisolone acetate 1.0% drops (Allergan) 3
times daily, carboxymethylcellulose 1% (Allergan) 4 times
daily, and homatropine 1% (Bell Pharma, Mumbai, India)
twice daily. Topical steroids were stopped after 6 weeks of
treatment.

RESULTS
OF THE 520 CHARTS OF PATIENTS WITH PROGRESSIVE KERA-

toconus that were reviewed, 350 consecutive patients received CXL from a referring ophthalmologist. Of these,
postoperative corneal edema developed in 10 (10/350; 2.9%).
Three patients (3/350; 0.9%) were excluded: 1 because of
stromal haze, 1 because of infectious keratitis without corneal
edema, and 1 because of corneal melt. No intraoperative
complications were noted at the time of CXL treatment. The
average age was 22 5 years (range, 16 to 32 years). Patients
were followed up for mean of 14 4 months (range, 8 to 22
months). Before surgery, the median logarithm of the minimal angle of resolution (logMAR) best-corrected visual acuAFTER

COLLAGEN CROSS-LINKING

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FIGURE 1. Photograph showing corneal edema and iris atrophy in a keratoconus patient after collagen cross-linking
treatment.

FIGURE 3. Photograph showing nonresolving corneal edema


after collagen cross-linking for progressive keratoconus treated
by penetrating keratoplasty with good visual results.

11%; Figures 1 and 2). The infectious keratitis occurred in


a patient with a persistent corneal epithelial defect.
Specular microscopy after CXL was attempted in all
cases, but was unsuccessful because of the degree of
edema or residual stromal haze. The fellow untreated
eye did not have any guttata on postoperative examination. Specular microscopy was performed on the nontreated eye with an average endothelial cell count of
2610 128 cells/mm2.
The median postoperative logMAR best-corrected visual acuity at the last follow up was 0.60 0.30 (P
.0001, MannWhitney U test). The postoperative vision
included patients who required penetrating keratoplasty
(PK) to obtain improved vision. The median postoperative
maximum keratometry at the last follow-up visit was
reduced to 54.7 3.36 diopters (P .0043, Mann
Whitney U test). The mean postoperative pachymetry
declined from 654.5 35.1 m at 3 weeks after CXL (P
.0001, MannWhitney U test) to 637.9 40.4 m at 3
months (P .0001, MannWhitney U test). It decreased
further to 614.8 36.2 m at 6 months (P .0001,
MannWhitney U test) and 595.7 37.7 m at 12
months (P .0001, MannWhitney U test). The 12month pachymetry excluded 1 patient who underwent PK
before this time point.
Corneal edema improved in 4 patients and resolved in 1
patient. The posttreatment logMAR visual acuity for this
group of patients was 0.5 0.18. One patient had
complete resolution of the corneal edema and was able to
resume rigid gas permeable contact lens wear without
sequelae. Surgical options were offered to patients when
improvement plateaued for 3 months. PK was recommended for 5 patients, but only 2 patients underwent PK at
8 and 13 months after CXL treatment (Figure 3). For the
2 patients who underwent PK, they had significant iris
atrophy, iris prolapse, and iris billowing in response to

FIGURE 2. Photograph showing corneal edema and peripheral


anterior synechiae after collagen cross-linking treatment for
progressive keratoconus.

ity was 0.00 0.08, the median maximum keratometry was


57.4 2.90 diopters, and the mean pachymetry was 472.6
17.5 m. Preoperative specular microscopy was not performed (Table).
In all cases, the onset of corneal edema occurred within
the first 24 hours after the procedure, and both the corneal
edema and anterior chamber inflammation increased for 2
to 3 weeks. Descemet membrane was not ruptured, nor was
intraocular pressure elevated after surgery in any cases. All
patients were phakic, and there were no lens opacities after
CXL. Additional anterior segment findings in the 10
patients included: marked deep corneal vascularization (2
eyes; 22%), iris atrophy (6 eyes; 67%), pigment dispersion
(5 eyes; 56%), corneal epithelial defect present for more
than 6 days (3 eyes; 33%), and infectious keratitis (1 eye;
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ordinary intraocular fluid currents. This condition resembled intraoperative floppy iris syndrome. These 2 patients
were not taking an -1-adrenergic blocker, and their
pathology reports showed only stromal scarring and inflammation. Their posttreatment logMAR visual acuities were
0.2 and 0.8. For the 3 patients with significant edema who
declined PK, their posttreatment logMAR visual acuity
was 1 0.12.

DISCUSSION
CXL HAS BEEN REPORTED TO BE A SAFE AND EFFECTIVE

treatment to increase the biomechanical strength of the


cornea in keratoconus patients.18,19 The combined use of
ultraviolet A irradiation with riboflavin decreases the
cytotoxic irradiance level to 10 times lower than that of
ultraviolet A irradiation alone.20 Studies have shown that
the standard surface ultraviolet A irradiance of 3 mW/cm2
penetrates human keratocytes up to a depth of 300 m.20
At the endothelial level, the irradiance is reduced to 0.15
mW/cm2, which is well below the threshold considered
cytotoxic (0.36 mW/cm2).13,20 24 Despite following these
guidelines, Gokhale reported one case of CXL-induced
corneal edema in a cornea thicker than 400 m before
surgery.16 To our knowledge, this case is the only previously reported incident of persistent corneal edema after
CXL for keratoconus.
It is difficult to speculate about the pathophysiologic
features of the corneal edema in our case series. Various
possibilities were entertained, including inadvertent delivery of excessive energy, intraoperative corneal thinning
resulting from corneal dehydration, inaccurate pachymetry
reading during surgery, acute hydrops, and pre-existing
Fuchs endothelial dystrophy.
Several safety factors were followed to prevent inadvertent delivery of excessive energy, including checking
the accuracy of the calibration device, confirming the
ultraviolet output, ensuring patient stability, consistent
focus of the ultraviolet light source, and verifying
pachymetry measurements of more than 400 m in all
cases. Despite these measures, it is always possible that
an excessive amount of energy was applied to the
corneas in this series.
Intraoperative corneal thinning resulting from corneal
dehydration from epithelial debridement is another possible cause of corneal endothelial damage during CXL. In a
recent study by Holopainen and Krootila, the corneal
thickness decreased from more than 400 m to 350 m in
80% of eyes over a 60-minute CXL treatment (30 minutes
of riboflavin instillation without a lid speculum in place
and 30 minutes of ultraviolet treatment).25 The study did
not report any cases of corneal edema or endothelial cell
damage. Corneal thinning in our patients may be higher
than that reported by Holopainen and Krootila because
the lid speculum was left in place for the 30-minute
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PERSISTENT CORNEAL EDEMA

riboflavin instillation period. The corneal thickness was


not rechecked during the ultraviolet exposure. It is possible
that extreme intra-CXL treatment corneal thinning occurring during CXL in our patients may be responsible for
corneal endothelial damage. Based on this potential cause
of ultraviolet light toxicity, we recommend removal of the
lid speculum during the riboflavin instillation and rechecking the pachymetry during the ultraviolet exposure period.
Pre-existing Fuchs endothelial dystrophy also may cause
corneal edema after CXL. Given the associated link between
Fuchs endothelial dystrophy and keratoconus,26 all study
corneas were evaluated before surgery for guttata by slit lamp.
Preoperative specular microscopy was not performed. Postoperative evaluation of the corneas with slit-lamp examination
and specular microscopy of the fellow eye also revealed a
normal endothelium and endothelial cell count.
Of the 2 patients who underwent PK, corneal button
specimens were available, and stromal scarring and inflammation were the only reported findings. These data did not
contribute to a viable reason that patients experienced
cornea edema after CXL.
In addition to corneal edema, many patients had other
anterior segment changes that could be attributed to excessive ultraviolet light exposure. These changes included corneal neovascularization, pigment clumps on the back of the
cornea, and iris atrophy. Two eyes had significant iris atrophy
and intraoperative floppy iris syndrome-like changes. Persistent epithelial defect in 1 patient extended beyond the
limbus, suggesting limbal stem cell damage. The intraocular
pressure and crystalline lens were not altered by the ultraviolet exposure. There were no cases of uveitis in our series.
Previous studies have proven that exposure to excessive
ultraviolet light can cause stromal haze, endothelial dysfunction, lenticular opacities, uveitis, iris changes, and retinal
phototoxicity.2730
Despite multiple anterior segment changes, half of the
study patients (5/10) recovered endothelial function
enough to reduce corneal edema and regain functional
vision. The best-corrected logMAR visual acuity at the last
follow-up in this subgroup was 0.60 0.30.
CXL is a well-known procedure that is gaining popularity as a treatment option for progressive keratoconus,
especially given its relatively safe side-effect profile. This
case series reports the possibility of corneal endothelial
damage with visually significant corneal edema after CXL
treatment. Although rare, corneal endothelial damage
with subsequent corneal edema is a possible complication.
Based on the extent of the endothelial damage, patients
may require PK to obtain optimal vision. Possible means of
prevention include: ensuring that the corneal thickness is
more than 400 m, removal of the lid speculum during
instillation of riboflavin drops to prevent excessive thinning secondary to evaporation, frequent equipment calibration, and frequent intratreatment checks of the corneal
thickness with readministration of hypotonic solution if
the thickness drops to less than 350 m.
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ALL AUTHORS HAVE COMPLETED AND SUBMITTED THE ICMJE FORM FOR DISCLOSURE OF POTENTIAL CONFLICTS OF
interest and none were reported. Involved in Design and conduct of study (A.S., J.M.N., K.Mi., R.S., K.Mo., V.S.N.); Collection, management, and
analysis of data (A.S.); and Preparation (A.S.) and review or approval (A.S., J.M.N., K.Mi., R.S., K.Mo., V.S.N.) of manuscript. This retrospective study
of patient data was approved by the Institutional Review Board from the Cornea Centre, Chandigarh.

15. Rama P, Di Matteo F, Matuska S, Paganoni G, Spinelli A.


Acanthamoeba keratitis with perforation after corneal crosslinking and bandage contact lens use. J Cataract Refract Surg
2009;35(4):788 791.
16. Gokhale NS. Corneal endothelial damage after collagen
cross-linking treatment. Cornea 2011;30(12):14951498.
17. Wollensak G, Spoerl E, Seiler T. Riboflavin/ultraviolet-ainduced collagen crosslinking for the treatment of keratoconus. Am J Ophthalmol 2003 May;135(5):620 627.
18. Spoerl E, Wollensak G, Seiler T. Increased resistance of
crosslinked cornea against enzymatic digestion. Curr Eye Res
2004;29(1):35 40.
19. Wollensak G, Wilsch M, Spoerl E, Seiler T. Collagen fiber
diameter in the rabbit cornea after collagen crosslinking by
riboflavin/UVA. Cornea 2004;23(5):503507.
20. Wollensak G, Spoerl E, Reber F, Seiler T. Keratocyte
cytotoxicity of riboflavin/UVA-treatment in vitro. Eye
(Lond) 2004;18(7):718 722.
21. Wollensak G, Spoerl E, Wilsch M, Seiler T. Keratocyte
apoptosis after corneal collagen cross-linking using riboflavin/UVA treatment. Cornea 2004;23:43 49.
22. Wollensak G, Spoerl E, Wilsch M, Seiler T. Endothelial cell
damage after riboflavin-ultraviolet: a treatment in the rabbit.
J Cataract Refract Surg 2003;29:1786 1790.
23. Spoerl E, Mrochen M, Sliney D, Trokel S, Seiler T. Safety of
UVA-riboflavin cross-linking of the cornea. Cornea 2007;
26(4):385389.
24. Wollensak G, Sprl E, Reber F, Pillunat L, Funk R. Corneal
endothelial cytotoxicity of riboflavin/UVA treatment in
vitro. Ophthalmic Res 2003;35(6):324 328.
25. Holopainen JM, Krootila K. Transient corneal thinning in
eyes undergoing corneal cross-linking. Am J Ophthalmol
2011;152(4):533536.
26. Lipman RM, Rubenstein JB, Torczynski E. Keratoconus and
Fuchs corneal endothelial dystrophy in a patient and her
family. Arch Ophthalmol 1990;108(7):993994.
27. Pitts DG, Cullen AP, Hacker PD. Ocular effects of ultraviolet radiation from 295 to 365 nm. Invest Ophthalmol Vis Sci
1997;16(10):932939.
28. Olsen EG, Ringvold A. Human cornea endothelium and
ultraviolet radiation. Acta Ophthalmol (Copenh) 1982;60(1):
54 56.
29. Glickman RD. Phototoxicity to the retina: mechanisms of
damage. Int J Toxicol 2002;21(6):473 490.
30. Dolin PJ. Ultraviolet radiation and cataract: a review of the
epidemiologic evidence. Br J Ophthalmol 1994;78(6):478
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Biosketch
Ashok Sharma is the Director of Cornea Centre in Chandigarh, India, where he has served on the faculty for 11 years.
He is also the founder and honorary secretary of Eye Bank Society, Chandigarh, India, and has over 80 peer-reviewed
publications. Dr Sharma also received the Achievement Award and the International Ophthalmologist Education Award
from the American Academy of Ophthalmology. His research interests include cornea and external diseases.

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