Download Postrefractive surgery dry eye

Postrefractive surgery dry eye
Guilherme G. Quinto, Walter Camacho and Ashley Behrens
The Wilmer Ophthalmological Institute, The Johns
Hopkins University School of Medicine, Baltimore,
Maryland, USA
Correspondence to Ashley Behrens, MD, The Wilmer
Eye Institute, 600 North Wolfe St., 255 Woods
Building, Baltimore, MD 21287-0005, USA
Tel: +1 410 502 0461;
e-mail: [email protected]
Current Opinion in Ophthalmology 2008,
19:335–341
Purpose of review
To report the recently published literature on ocular surface changes after refractive
surgery, as well as the outcomes of treatment modalities on postrefractive surgery dry
eye.
Recent findings
Cyclosporine, the first US Food and Drug Administration approved agent to treat the
underlying pathological mechanism of chronic dry eye, has demonstrated promising
results in dry eye patients. Further, there may be an additive effect of topical
cyclosporine and punctal occlusion. Femtosecond lasers for corneal flaps in laser in-situ
keratomileusis seem to induce fewer signs and symptoms of dry eye and may be
attributed to the creation of thinner flaps.
Summary
Dry eye is one of the most common complications after photorefractive keratectomy and
laser in-situ keratomileusis. Keratorefractive surgery is known to cause damage to the
corneal sensory nerves. Several studies have demonstrated a decrease in corneal
sensation, tear secretion, and tear film stability several months after keratorefractive
surgery. For patients with preoperative dry eye, the ocular surface must be treated
accordingly prior to surgery.
Keywords
dry eye syndrome, laser in-situ keratomileusis, management, ocular surface,
photorefractive keratectomy
Curr Opin Ophthalmol 19:335–341
! 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
1040-8738
Introduction
One of the most common complications of photorefractive
keratectomy (PRK) and laser in-situ keratomileusis
(LASIK) is dry eye syndrome [1,2!!]. Although dry eye
after refractive surgery is usually transient, some patients
complain of severe symptoms, which may negatively
influence their satisfaction with the outcome of the procedure [3,4]. Both keratorefractive procedures have been
reported to perturb the ocular surface homeostasis by
causing a decrease in corneal sensitivity, tear film instability, decreased aqueous tear production, and corneal and
conjunctival epitheliopathy [5]. This review summarizes
the recently published literature on the ocular surface
changes after keratorefractive surgery and its treatment
modalities.
gathered to elaborate diagnostic and treatment guidelines
for dry eye syndrome using a Delphi consensus technique
[3]. One of the recommendations of the panel was that the
term ‘dry eye syndrome’ be replaced with ‘dysfunctional
tear syndrome’ to reflect current understanding of the
pathophysiology of the disease [3].
DEWS Definition and Classification Subcommittee [7!]
provided a contemporary definition of dry eye disease
supported within a comprehensive classification framework. A new definition of dry eye was developed to
reflect current understanding of the disease, and the
committee recommended a three-part classification of
dry eye, based on etiology, mechanism, and disease
stage. These guidelines are not intended to override
the clinical assessment and adjustment of an expert
clinician in individual cases.
Dry eye syndrome
Dry eye syndrome encompasses diverse etiologies and
varies greatly in severity. In addition, correlations between
symptoms, clinical signs, and diagnostic test results are
variable, making the diagnosis and treatment of this condition challenging [6!]. Due to this need, an International
Task Force consisting of 17 dry eye expert clinicians was
Dry eye syndrome is defined as a disorder of the tear film
caused by tear deficiency or excessive tear evaporation,
which causes damage to the interpalpebral ocular surface
and is associated with symptoms of ocular discomfort
[8–10]. Diagnosis is made after analyzing patients’ complaints, objective signs, and abnormal results of dry eye
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336 Refractive surgery
tests [11]. The symptoms are usually described by
patients as burning, dryness, or foreign-body sensation,
often associated with ocular pain, blurred vision, photophobia, and visual fatigue. The clinical signs of dry eye
include positive vital staining of ocular surface, decreased
tear film breakup time and Schirmer tests, reduced
corneal sensitivity, and decreased functional visual acuity
[11].
The quality of life can be significantly affected by dry eye
symptoms, as documented by several validated survey
instruments [12]. The psychological impact of this
chronic condition is suggested by a utility assessment
of patients’ willingness to trade years at the end of life for
an opportunity to be free of dry eye, which found that the
utility of moderate dry eye was similar to that of moderate
angina [13].
Etiology
The pathophysiologic definition of dry eye was changed
to a dysfunction of the integrated ocular surface-secretory
glandular functional unit [14]. Communication between
the ocular surface and lacrimal glands occurs through a
sensory autonomic neural reflex loop. The sensory nerves
innervating the ocular surface connect with efferent
autonomic nerves in the brain stem that stimulate
secretion of tear fluid and proteins by the lacrimal glands.
Ocular surface sensitivity has been found to decrease as
aqueous tear production and clearance of tears from the
ocular surface decrease. This decrease in surface sensation exacerbates dry eye because sensory stimulated
reflex tearing is decreased, resulting in decreased ability
of the lacrimal glands to respond to ocular surface insults.
Thus, a self-perpetuating cycle between the lacrimal
gland and the ocular surface is created [14]. Adequate
aqueous tear production and clearance with normal
mucous gland function are finely controlled by balancing
the innervation of the ocular surface and the tearsecreting glands to prevent surface dryness. The dry
eye from keratorefractive surgery results mostly from
damage to the corneal sensory nerves. Inflammation plays
an important role as well in the pathogenesis of dry eye,
and it has been elucidated over the past decade [15].
Decreased tear production and tear clearance lead to
chronic inflammation of the ocular surface. This inflammatory response consists of cellular infiltration of the
ocular surface by activated T lymphocytes, with
increased expression of adhesion molecules and inflammatory cytokines, increased concentrations of inflammatory cytokines in the tear fluid, and increased activity of
matrix degrading enzymes such as matrix metalloproteinase MMP-9 in the tear fluid. Significant positive correlation has been observed between the levels of inflammatory cytokines in the conjunctival epithelium and the
severity of symptoms of ocular irritation, corneal fluor-
escein staining, and severity of conjunctival squamous
metaplasia in patients with Sjögren’s syndrome keratoconjunctivitis [15].
Tear secretion and tear film instability
Keratorefractive surgery seems to cause tear-deficient dry
eye by a neural-based mechanism. Since the usual standard method to evaluate reduced tear volume and tear flow
is the Schirmer test, studies have consistently included
these data when reporting dry eye incidence [8]. Several
recent studies have demonstrated the decrease on corneal
barrier, tear secretion, and tear film stability. Polunin et al.
[16] showed that the corneal barrier function decreased
after PRK and LASIK treatments, and the recovery was
more delayed after LASIK than after PRK. Yu et al. [17]
investigated the effect of LASIK on tear function in 96
eyes of 58 patients for the correction of myopia. LASIK
significantly altered the tear break-up time, Schirmer test
values, and basal tear secretion. They also concluded that
patients with preexisting tear flow abnormality measured
with Schirmer test values less than 10 mm was a significant
risk factor for experiencing dry eye symptoms at 1 month
after surgery.
Lee et al. [18] compared tear secretion and tear film
instability following PRK (36 eyes of 21 patients, ranging
from "2.50 to "6.00 D) and LASIK (39 eyes of 25 patients,
ranging from "3.25 to "9.75 D). At 3 months following
surgery there was significantly decreased tear secretion and
tear film stability in LASIK patients compared with PRK
patients. Although not statistically significant at 6 months,
tear secretion and tear film stability were still decreased in
LASIK and these values never reached preoperative
levels. Nejima et al. [19] evaluated corneal barrier function,
tear secretion, and tear stability after PRK (28 eyes of
15 patients) and LASIK (115 eyes of 59 patients). Both
procedures decreased epithelial barrier function, reduced
tear secretion, and deteriorated tear film stability
(P < 0.05). Increases in corneal epithelial permeability
were, again, more prolonged after LASIK than after
PRK. A significant intergroup difference in permeability
was observed 1 month after surgery (P < 0.05). In their
study, tear break-up time was significantly shorter in the
LASIK group than in the PRK group up to 3 months after
surgery (P < 0.045).
Konomi et al. [20] have shown recently that preoperative
tear volume may affect the recovery of the ocular surface
after LASIK, increasing the risk of chronic dry eye. In this
study, patients were classified into two main outcome
groups: the nondry eye group and the chronic dry eye
group, on the basis of dry eye status 9 months after
surgery. All parameters, except rose bengal staining, were
significantly deteriorated after surgery but returned to
preoperative levels within 3–9 months. The chronic dry
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Postrefractive surgery dry eye Quinto et al. 337
eye group had significantly lower preoperative Schirmer
test values, both with and without anesthesia, and showed
delayed recovery in goblet cell density, rose bengal
staining, Schirmer test values without anesthesia, and
tear break-up time after surgery. Results of preoperative
Schirmer tests without anesthesia positively correlated
with tear break-up time 9 months after surgery. Preoperative Schirmer test values without anesthesia appeared to
be predictive of the development of chronic dry eye after
LASIK.
Corneal sensation
Corneal sensitivity is essential for the maintenance of
normal corneal structure and function [21]. Inevitably,
surgical procedures such as PRK and LASIK induce loss
of normal sensitivity which may compromise the protective blink reflex, delay epithelial wound healing, and
even induce neurotrophic keratitis or sterile corneal melts
[22,23]. In PRK, the damage is to the sensory nerve
endings that terminate in the corneal epithelium that
is removed by mechanical scraping during the procedure
[8]. In both PRK and LASIK, there is additional damage
to the nerves in the stroma removed by the laser procedure and the greater the myopic correction, the greater
the dry eye symptoms [8]. In LASIK, the superior hinged
corneal flap is made through the stroma, transecting
the posterior corneal nerve trunks that enter the cornea
at the 3 and 9 o’clock positions and provide the sensory
innervation to the cornea [24]. Several studies have
compared PRK and LASIK in terms of their influence
on corneal sensation.
Campos et al. [25] reported that in a series of 14 eyes that
had undergone PRK, patients with preoperative myopia
of less than "6.50 D recovered 95.7% of central corneal
sensitivity after 3 months, whereas patients with severe
myopia (more than "9.00 D) recovered 86.2% of the
original corneal sensitivity at the same time period.
Chuck et al. [26] evaluated 28 eyes of 18 patients (range
1.50–11.25 D) who underwent LASIK. Preoperative and
postoperative corneal sensation at the nasal flap hinge, at
the central cornea and within the temporal flap edge
was measured before and after LASIK for a 3-week
period using the Cochet-Bonnet esthesiometer. Corneal
sensation initially decreased in all three positions of the
flap measured after LASIK and the greatest decrease was
in the central cornea. Near preoperative corneal sensation
returned by 3 weeks. Furthermore, the degree of sensation
loss did not appear to correlate with the ablation depth.
Pérez-Santoja et al. [22] evaluated the recovery of postoperative corneal sensitivity after LASIK (17 eyes of
17 patients, ranging from "3.25 to "6.75 D) and PRK
(18 eyes of 18 patients, ranging from "3.12 to "7.00 D) for
correction of low myopia. Corneal sensitivity was tested at
the center of the cornea, and in four additional central
points 2 mm from the corneal center. They showed that
corneal sensitivity after LASIK was reduced at the ablation
zone during the first months (P < 0.05), and, only after
6 months, it returned to its preoperative values. In the
PRK group, corneal sensitivity recovered its preoperative values 1 month after surgery (P > 0.05) except for the
central corneal point which took 3 months to recover.
Comparing both groups, corneal sensitivity was more
compromised after LASIK than PRK during the first
3 months (P < 0.05), except for the nasal central point,
although no differences were found between both
groups at 6 months (P > 0.05).
Matsui et al. [23] compared the effects of PRK (22 patients,
ranging from "2.00 to "7.75 D) and LASIK (13 patients,
ranging from "4.38 to "11.00 D) on corneal sensation.
After PRK, corneal sensitivity was decreased slightly at
3 days, began to recover at 1 week, and returned to preoperative values at 3 months, but none of the changes was
statistically significant (P > 0.05). After LASIK, corneal
sensation was significantly decreased at 3 days, 1 week
and 1 month; it recovered slightly at 3 months, although
it remained significantly less than preoperatively.
Nejima et al. [19] have demonstrated that LASIK induces
greater and more prolonged damage to corneal sensation
than PRK. After PRK, corneal sensation was significantly
deteriorated compared with the preoperative level up to
6 months postoperatively. After LASIK, corneal sensation
did not return to the normal level throughout the
12 months postoperatively.
Use of intraoperative mitomycin C
Recently, encouraging results have been reported in
reducing haze after high myopic PRK corrections by
administering a single intraoperative application of diluted
mitomycin C (MMC) solution [27]. Bedei et al. [28]
evaluated the prophylactic use of MMC to reduce haze
formation and refractive regression after PRK for high
myopic defects (over "5.00 D). The application of
MMC 0.02% solution immediately after PRK produced
lower haze rates and had better predictability and improved
efficacy 1 year after treatment. Kymionis et al. [29], however, reported a patient with dry eye after bilateral PRK
(–5.50 " 0.50 # 170 left eye and "5.00 " 1.00 # 180 right
eye) with MMC treatment in the left eye. The patient
developed dry eye symptoms and superficial punctate
keratopathy (SPK) in the eye treated with MMC for
15 months postoperatively whereas no evidence was noted
in the control eye, except for mild haze. Uncorrected visual
acuity was 20/20 in both eyes at 15 months.
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338 Refractive surgery
Femtosecond laser
The solid-state femtosecond laser creates variable thickness and size corneal flaps for LASIK. The femtosecond
laser seems to have advantages over mechanical microkeratomes including improved predictability of the flap
thickness and diameter, better flap uniformity, better
predictability of hinge position and size, astigmatic
neutrality, and reduced incidence of epithelial defects,
buttonholes, and cap perforation [30]. Mian et al. [2!!] have
reported dry eye after LASIK in 66 eyes (33 patients) with
the femtosecond laser (assessed by the Ocular Surface
Disease Index), with values of 22.9% after the first week
postoperatively, and 21.9% after the first month
(P < 0.00001). Overall, symptoms were mild and resolved
over the first month. The lower incidence of dry eye signs
and symptoms with the femtosecond laser may be attributed to the application of lower suction on the eye and
creation of thinner flaps, resulting in a greater residual
stromal bed and a decreased corneal denervation. They
also demonstrated that loss of central corneal sensation
persisted significantly longer than dry eye signs and symptoms and was, in fact, still present at the 1-year postoperative examination. Furthermore, they showed
that when performing LASIK with femtosecond laser,
either with superior hinge or nasal/temporal hinge position, there was no effect on either corneal sensation or dry
eye parameters. In fact, decreased corneal sensation and
LASIK-induced neurotrophic epitheliopathy [5] seemed
to correlate well with the degree of preoperative myopia,
depth of laser treatment, and flap thickness. Rodriguez
et al. [31!!] have studied the effect of the LASIK procedure
performed with femtosecond laser (34 eyes, preoperative
spherical equivalent "3.1 $ 3.1 D) and a manual microkeratome (30 eyes, preoperative spherical equivalent
"2.0 $ 3.8 D). All patients in both groups showed a
decrease in goblet cells after LASIK that recovered after
6 months. At 1 week, 1 month and 3 months, goblet cell
counts were lower with the femtosecond group than with
microkeratome group (P < 0.001). This finding is probably
explained because of the length of time that the suction
ring exerted pressure on the conjunctiva, which is
considerably larger in the femtosecond laser compared
with the microkeratome. These changes in the goblet cells
may contribute to the development of the ocular surface
syndrome after LASIK.
Preoperative dry eye
The efficacy and safety of refractive surgery is not necessarily affected by preexisting dry eye. Preexisting dry eye,
however, is a risk factor for symptomatic postkerat
orefractive surgery dry eye with measurable lower tear
function and supra-vital staining of the ocular surface.
Preoperative conjunctival staining represents a risk factor
for postoperative dry eye, and corneal staining is con-
sidered to be a relative contraindication of surgery until
the ocular surface has been stabilized. Patients with symptoms of dry eye but no signs of corneal or conjunctival
staining are generally good candidates for refractive
surgery. Patients who have dry eye symptoms with mild
conjunctival staining should be treated accordingly in
order to stabilize the ocular surface prior to surgery [15].
Many patients who want to have excimer laser refractive
surgery are not able to wear contact lenses because of
preexisting dry eye or secondary dry eye caused by longterm contact lens use. Commonly, these patients continue
to report dry eye symptoms after surgery, despite an
improvement in visual acuity following successful correction of the refractive error [18]. Patients with dry eye
syndrome are typically considered poor surgical candidates
because of an increased association with postoperative
complications, including severe dry eye, fluctuating vision,
abnormal wound healing, and persistent epithelial defects
which can predispose to an increased incidence of diffuse
lamellar and microbial keratitis [5,22,32,33].
Patients without preoperative dry eye may experience
symptoms and decreased tear function for several months
after keratorefractive surgery. Moreover, patients with
preoperative dry eye exhibited more severe symptoms
and ocular surface damage after keratorefractive surgery
compared with patients without preexisting dry eye,
although efficacy and predictability were comparable
between these groups [34].
A retrospective study was carried out by Toda et al. [33] in
which the patients were preoperatively categorized into
two groups – the dry eye group and the nondry eye group –
according to selected criteria for characterization of dry
eye. Subsequently, the incidence of complications, loss of
best corrected visual acuity (BCVA), and dry eye symptoms/tear function were compared in the two groups postoperatively. No difference was identified in the incidence
of intraoperative and postoperative complications and loss
of BCVA between groups. Dry eye symptoms and tear
function were more compromised in the dry eye group
preoperatively and also postoperatively, 1 year after the
surgery. Despite this, symptoms and tear function
returned to preoperative levels in both groups. The authors
suggest that these results may indicate that LASIK may
be performed safely and effectively in patients with
preoperative dry eye. Albietz et al. [32] examined the
relationship between chronic dry eye and refractive
regression after LASIK for myopia. The regression after
LASIK occurred in 12 (27%) of 45 patients with chronic dry
eye and in 34 (7%) of 520 patients without dry eye
(P < 0.0001). Patients with chronic dry eye had significantly worse outcomes than those without (6 months,
P ¼ 0.004; 12 months, P ¼ 0.008). The risk for regression
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Postrefractive surgery dry eye Quinto et al. 339
was associated with higher attempted refractive correction,
greater ablation depth, and dry eye symptoms after
LASIK.
Management
The majority of patients with dry eyes respond to
conventional treatment aimed at optimizing the ocular
surface microenvironment. The ecosystem of the ocular
surface depends on dynamic interactions of healthy
adnexae, adequate blink reflex, normal tear production,
and ocular surface tissue, consisting mostly of cornea and
conjunctiva. Conventional therapeutic options include
intensive tear supplements, punctal occlusion, contact
lenses, and an appropriate management of the adnexal
disease [35].
Artificial tears have been the primary treatment of the
postkeratorefractive surgery dry eye [36,37]. Despite
attempts to improve composition, artificial tears can
never replace those produced by the lacrimal gland. In
the last decade, it has been recognized that tears
with preservatives may be toxic to the ocular surface
epithelium. Therefore, it has been recommended to use
preservative-free artificial tears in some cases [9,37].
While artificial tears improve symptoms of dry eye, they
do not eliminate the underlying inflammatory process
[38].
Meibomian gland dysfunction is another common and
critical component of ocular surface inflammation.
Patients with meibomian gland dysfunction due to blockage of the glands may also benefit from warm compresses,
lid scrubs and massages that would help breaking up the
oils and open up the ducts within the glands [11,39]. This
particular problem is best controlled with systemic antibiotics, such as doxycycline for a period of 4–6 weeks or
more [39]. These antibiotics have shown the capacity of
thinning these glands secretions, to maintain the natural
flow of their secretions.
Anti-inflammatory therapy using topical corticosteroids
has also been reported to be an efficacious therapy for
patients with dry eye [36]. Marsh and Pflugfelder [40]
reported the efficacy of a topical administration of 1%
nonpreserved methylprednisolone for patients with severe
dry eye, demonstrating relief from irritation, a decrease in
fluorescein staining, and resolution of SPK. While topical
steroids may have the most rapid anti-inflammatory action,
treatment is not advisable for long-term management
because of the side effects of corticosteroids, especially
cataract formation and glaucoma [38].
In 2002, the Federal Drug Administration approved
cyclosporine for the treatment of dry eye. Cyclosporine
0.05% ophthalmic emulsion was the first treatment to
target the underlying pathological mechanism for chronic
dry eye: the immune-mediated inflammation. Cyclosporine has minimal side effects compared with steroids and
may be used for long periods of time without deleterious
effects in the eye [38,41,42]. In addition, cyclosporine
offers the advantage of immunomodulation without the
risk of corticosteroids’ side effects, as opposed to immunosuppression. This treatment has been shown to increase
tear production and reduce inflammation based on T-cell
recruitment as well as increasing goblet cell numbers, and
preventing lymphocyte infiltration within the lacrimal and
accessory glands and conjunctiva [43]. Salib et al. [44]
carried out a study to evaluate two treatments for dry
eye, and refractive outcomes in patients with dry eye
having LASIK. Forty-two eyes of 12 myopic patients
(ranging from –1.00 to –10.63 D) with dry eye were treated
with unpreserved artificial tears or cyclosporine 0.05%
ophthalmic emulsion twice a day beginning 1 month
before LASIK. Treatment with the study drug was
discontinued for 48 h following refractive surgery and then
resumed for three additional months. Statistically significant increases from baseline were found in Schirmer values
for artificial tears at 1 month (P ¼ 0.036) and cyclosporine
before surgery and 1 week, 1 month, and 6 months after
surgery (P < 0.018). Mean refractive spherical equivalent
in cyclosporine-treated eyes was significantly closer to the
intended target at 3 and 6 months after surgery than in
artificial-tear-treated eyes (P ¼ 0.007). Thus, treatment
with cyclosporine 0.05% provided greater refractive
predictability at 3 and 6 months after surgery than unpreserved artificial tears, according to this study.
Punctal plugs is another tool that appears to be a relatively
safe, effective, and reversible method of preserving
aqueous and artificial tears on the ocular surface to reduce
the signs and symptoms of dry eye [45]. Studies have
shown that dry eye patients may often decrease and sometimes eliminate the need for artificial tear preparations
[46]. Albietz et al. [47] reported that postoperative ocular
surface management, which included the use of punctal
plugs when indicated, improved symptoms and goblet cell
density in patients who had undergone PRK or LASIK.
Since punctal occlusion and topical cyclosporine treat dry
eye under different mechanisms, Roberts et al. [48!!]
carried out a study to examine their efficacy separately
and then in combination. They evaluated three treatment
regimens consisting of topical cyclosporine twice daily,
punctal plugs, and a combination of cyclosporine and plugs
over 6 months. As a result, all three treatment groups were
effective and increased tear volume to a similar extent over
the course of the study. At 1 and 3 months, however, groups
that included punctal plugs were superior to cyclosporine
alone in improving Schirmer scores. These results are
consistent with the known function of punctal occlusion
in physical conservation of existing tears. In summary,
although all the treatments in this study effectively treated
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
340 Refractive surgery
chronic dry eye, some trends regarding specific modalities
are evident. In the near term, punctal occlusion (alone or in
combination with cyclosporine) produced the most rapid
improvements in wetness, as assessed by Schirmer testing
and patient self-medication with artificial tears, consistent
with the tearing–conserving function of punctal plugs.
Over the longer term, the cyclosporine-containing regimen resulted in improvement in the same measures that
were statistically indistinguishable from, or were superior
to, the plugs-only regimen. Furthermore, only the cyclosporine-containing regimen significantly improved ocular
surface staining over time. These observations are consistent with the known roles of topical cyclosporine in
addressing the underlying immune pathophysiology of
chronic dry eye disease. There may be an additive effect
of topical cyclosporine and punctal occlusion, and patients
with punctal occlusion may also benefit from adjunctive
cyclosporine.
Autologous serum has also been used as a potential treatment for dry eye. It contains anti-inflammatory agents and
MMP inhibitors that are especially useful in patients with
autoimmune-associated inflammatory processes, such as
Sjögren’s [38,49]. The efficacy of autologous serum
application for the treatment of corneal transplantation
or other ocular surface disorders [50], such as superior
limbic keratitis [51], dry eye in graft-versus-host disease
[52], or Stevens-Johnson syndrome [50], has been
reported. These studies suggest that autologous serum
may improve almost all types of dry eye. Noda-Tsuruya
et al. [53] evaluated the efficacy of autologous serum eye
drops for dry eye after LASIK. The results showed that
break-up time test and vital staining were significantly
improved after LASIK in the autologous serum eye drops
group, whereas no change was reported in the artificial tear
group at 6 months postoperatively. These findings suggest
that autologous serum eye drops could be effective for
postoperative dry eye induced by LASIK. Toda et al. [34]
performed LASIK in three patients who suffered from
Sjögren’s syndrome and showed decreased reflex tearing.
They inserted punctal plugs and prepared the autologous
serum at the first visit of each patient. The LASIK procedure was scheduled to be undertaken after the ocular
surface damage was healed by the treatment. LASIK was
then performed uneventfully, and no complications were
observed in any of the patients. These results indicate that
LASIK may be safely performed on patients with severe
dry eye, if the ocular surface damage is energetically
treated before surgery.
Conclusion
LASIK and PRK may exacerbate preexisting dry eye, or
trigger a previously nonexistent dry eye. The symptoms
after keratorefractive surgery are usually transient but
may cause significant discomfort in patients. Attention
must be paid to dry eye in candidates undergoing
keratorefractive surgery, and appropriate methods of
management must be made available to these patients.
The incidence of postkeratorefractive procedure dry eye
may be reduced by identifying patients at risk for dry eye,
maximizing tear film stability preoperatively, and
minimizing dry eye through intra and postoperative
interventions, both pharmacological and surgical.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
!
of special interest
!! of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 366).
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