Today’s PRactice Bonus Feature
The Vitreomacular
Interface After LASIK
Epiretinal membranes and macular holes may occur, although rarely, after refractive surgery.
By Hugo Quiroz-Mercado, MD; and Miguel Paciuc-Beja, MD
C
omplications from refractive surgery are related
mostly to refractive outcomes. Retinal complications after LASIK can include retinal tears, retinal
detachment, choroidal neovascularization, subretinal hemorrhage, epiretinal membrane, and macular
hole. Fortunately, such complications are rare; the incidence of vitreoretinal complications after LASIK has been
estimated to be between 0.06% and 0.36%.1
It is not easy to relate vitreomacular pathology directly
to LASIK surgery. When we perform LASIK, we do not
typically think about its potential effect on the vitreomacular interface (VMI). Additionally, there may be
weeks or even months between the time LASIK is performed and the occurrence of vitreomacular symptoms.
It is difficult to know whether the LASIK surgery or the
patient’s myopia is the root cause; the aforementioned
complications, although uncommon, occur at a higher
incidence in patients with myopia—the majority of
patients undergoing LASIK.
POSTERIOR VITREOUS DETACHMENT
Availability of optical coherence tomography (OCT)
has changed the way we visualize the retina, the vitreous,
and the VMI, in the same way that corneal topography
and pachymetry changed the way we see the cornea.
Vitreomacular complications observed after LASIK share
a common pathophysiology: posterior vitreous detachment (PVD). With the help of OCT and ultrasonography,
we can see that the incidence of PVD is higher in patients
who have undergone LASIK compared with the expected
incidence in patients with similar characteristics in whom
the procedure was not performed. That is to say, there is
a cause-and-effect relationship between LASIK and PVD.
Ultrasonography has shown that, after myopic
microkeratome-assisted LASIK, 14% of eyes had PVD.
Another study showed an incidence of post-LASIK
PVD of 9.5%, and B-scan ultrasonography demonstrated that 16% of eyes had PVD 48 hours after LASIK
in which a femtosecond laser was used to create the
30 Cataract & Refractive Surgery Today Europe January 2014
Figure 1. Case No. 1: Color fundus photograph of the left eye.
The macular region shows macular folds and distortion of
the normal architecture of the juxtafoveal vessels. Nasal and
inferior to the fovea, there is evidence of epiretinal fibrous
tissue, which is likely due to the presence of an epiretinal
membrane.
flap. Numerous studies are consistent with an incidence
of post-LASIK PVD of greater than 10%.2-4 According to
autopsy studies, PVD is present in less than 10% of individuals younger than 50 years.5
It has been suggested that post-LASIK PVD may be
caused either by deformation of the eye secondary to
increased intraocular pressure (IOP) with the application of the corneal suction ring or by trauma as a
result of the shockwave induced by the excimer laser.
Deformation of the eye theoretically occurs when the
suction ring induces an increase in IOP, which can rise
above 80 mm Hg. The suction and the increase in IOP
could elongate the eye along the anteroposterior axis
and, in turn, cause a contraction in the horizontal axis.
This combination of events may push the lens anteriorly
and cause vitreoretinal traction at the vitreous base and
the posterior pole, facilitating PVD.
Today’s PRactice Bonus Feature
A
B
Figure 2. Case No. 1: Time-domain OCT of the left eye shows
complete distortion of internal and external architecture of
the retina nasal and inferior to the fovea. Over the retina,
there is a highly reflective membrane, which makes contact
with the retina in the central part of the projection. The nerve
fiber layer shows a characteristic saw-like configuration.
There is a substantial increase in retinal thickness.
Could trauma caused by the excimer laser shockwave
induce PVD? Stress wave amplitudes of up to 100 atm,
6.2 to 7.3 mm behind the endothelium, have been measured during experimental LASIK. At the retinal plane,
23 mm behind the endothelium, the stress wave amplitude fell to approximately 10 atm, which seems to be
insufficient to cause a significant retinal lesion.6
PVD has been widely associated with the occurrence
of epiretinal membrane (ERM). Separation of the vitreous from the inner retinal surface usually occurs due to
the aging process and is more common in myopic eyes.
It may also occur as a consequence of trauma or inflammation at any age. PVD has been shown to cause small
breaks in the internal limiting membrane, through which
glial cells may grow and proliferate on the retinal surface.
With PVD progression, residual vitreous is often left
on the inner retinal surface. Residual vitreous remains
on the surface of the retina in nearly half of eyes with
PVD.7 This is called vitreoschisis. ERMs are composed of
Take-Home Message
• Vitreomacular complications observed after LASIK
share the common pathophysiology of PVD.
• PVD, which occurs in about 10% of patients after
LASIK, can cause vitreomacular traction.
• Macular OCT is advisable in patients with unexplained visual symptoms after LASIK.
Figure 3. Case No. 2: Seven months after successful LASIK,
a 21-year-old woman presented with sudden onset of
metamorphopsia. OCT showed an inner segment ellipsoid
band loss at the subfoveal area in the patient’s right eye (A).
One month later, OCT revealed a stage 3 macular hole (B).
glial cells that attach to vitreous cortex remnants on the
inner retinal surface.
CASE REPORT NO. 1
A 29-year-old man underwent uneventful LASIK in
both eyes. Cycloplegic refraction was -2.50 D sphere in
each eye. Corneal pachymetry was 549 µm in the right
eye and 530 µm in the left. Dilated funduscopy was
unremarkable, and no PVD was noted. LASIK was performed using the Hansatome microkeratome (Basuch +
Lomb) with a 160-µm flap and the Visx Star S4 excimer
laser (now Abbott Medical Optics Inc.). Visual acuity was 20/20 OU after 6 months. Dilated funduscopy
revealed PVD in both eyes. Eighteen months after surgery, visual acuity remained 20/20 OU, but the patient
complained of metamorphopsia in his left eye. In this
eye, funduscopy revealed an ERM with thin macular
folds (Figure 1). Stratus OCT (Carl Zeiss Meditec) of the
macula showed a hyperreflective line partially in contact
with the retinal surface, folds in the interior layers of the
retina, retinal thickening, and distortion of the normal
retinal architecture (Figure 2).
(Continued on page 37)
January 2014 Cataract & Refractive Surgery Today Europe 31
Today’s PRactice Bonus Feature
(Continued from page 31)
CASE REPORT NO. 2
A 21-year-old woman was seen in our retina clinic
because of sudden onset of metamorphopsia in her right
eye. Visual acuity was 20/25 OD and 20/20 OS. The
patient had no history of trauma or ocular inflammation. She reported having undergone successful LASIK
7 months earlier. Fundus examination of the right eye
showed PVD, Amsler grid testing showed a central area
of metamorphopsia, and Spectralis OCT (Heidelberg
Engineering) showed loss in the inner segment ellipsoid
band at the subfoveal area (Figure 3A). There were no
abnormal findings in the left eye.
One month later, she complained of a sudden
decrease in visual acuity in her right eye and a large central scotoma. Her BCVA was 20/200 OD and 20/20 OS.
Funduscopy showed a full-thickness macular hole, and
OCT revealed a stage 3 macular hole (Figure 3B).
CONCLUSION
Excessive traction on the macula can lead to anatomic
changes in the contour of the foveal surface. OCT and
ultrasonography suggest that macular holes are caused
by tractional forces related to perifoveal vitreous detachment. Idiopathic macular holes can be viewed as a complication of early stages of PVD. In theory, a PVD caused
by vitreoretinal traction could lead to a macular hole.
Retinal complications, although uncommon, can
occur after LASIK. PVD occurs in about 10% of patients
after LASIK and can cause vitreomacular traction.
Macular OCT is therefore necessary to investigate
unexplained visual symptoms after LASIK. n
Hugo Quiroz-Mercado, MD, is a Professor at the
University of Colorado School of Medicine. Dr. QuirozMercado states that he has no relevant financial interests
to disclose.
Miguel Paciuc-Beja, MD, is an Associate Professor at
the University of Colorado School of Medicine. Dr. PaciucBeja states that he has no relevant financial interests to
disclose. He may be reached at tel: +303 602 8574; e-mail:
miguel.paciuc@dhha.org.
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2010;149(3):371-382.
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3. Mirshahi A, Schopfer D, Gerhardt D, Terzi E, Kasper T, Kohnen T. Incidence of posterior vitreous detachment after
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7. Duker J, Kaiser PK, Binder S, et al. The International Vitreomacular Traction Study Group classification of vitreomacular adhesion, traction, and macular hole. Ophthalmology. 2013;120(12):2611-2619.
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