Nd:YAG Laser Posterior Capsulotomy

NOV 04, 2013

Author: Roger F. Steinert, MD

Figures and portions of the text were previously published in Steinert RF, Puliafito
CA: The Nd:YAG laser in ophthalmology: principles and clinical applications of
photodisruption, Philadelphia, 1985, WB Saunders.

Introduction
The neodymium:yttrium-aluminum-garnet (Nd:YAG) laser is a solid-state laser
with a wavelength of 1064 mm that can disrupt ocular tissues by achieving optical
breakdown with a short, high-power pulse. Optical breakdown results in ionization,
or plasma formation, in the ocular tissue. This plasma formation then causes
acoustic and shock waves that disrupt tissue.

The development of the Nd:YAG laser as an ophthalmic instrument and its

application in discussion of the posterior capsule coincided with the conversion
from intracapsular to extracapsular surgical techniques in cataract surgery. Before
the introduction of the Nd:YAG laser, only surgical cutting or polishing of the
posterior capsule could manage opacification of the posterior capsule following
extracapsular cataract extraction. Nd:YAG laser posterior capsulotomy introduced
a technique for closed-eye, effective, and relatively safe opening of the opacified
posterior capsule, and laser capsulotomy rapidly became the standard of care.

Capsular Opacification
Postoperative opacification of initially clear posterior capsules occurs frequently in
patients after extracapsular extraction of senile cataracts. Time to opacification is
highly variable. Time from surgery to visually significant opacification varies from
months to years in adults. Almost 100% opacification occurs within 2 years after
surgery in younger groups. Rate of opacification declines with increasing age.

The incidence of posterior capsule opacification varies with different studies.

Sinskey and Cain reported that 43% of their patients require discission, with an
average follow up of 26 months and a range from 3 months–4 years. Another
study found opacification in 28% of their patients with 2–3 years of follow-up.
Opacification after 3–5 years has been reported to be approximately 50%.
Incidence of opacification is lower if a posterior chamber intraocular lens (IOL) is
inserted with a convex posterior configuration in close apposition to the posterior
capsule. Phacoemulsification is associated with lower rates of opacification than
extracapsular cataract extraction.

A study of posterior capsule opacification in 5416 postmortem pseudophakic eyes

identified 6 factors associated with reduced posterior capsule opacification:

• Hydrodissection-associated cortical cleanup

• In-the-bag IOL fixation

• Continuous circular capsulorhexis diameter slightly smaller than the IOL

optic

• IOL material associated with reduced cellular proliferation: Hydrogel IOLs

are associated with the highest rate of posterior capsule opacification.
Polymethylmethacrylate (PMMA) is intermediate and silicone and acrylic
optic material is the lowest.

• Maximal IOL optic to posterior capsule opacification

• IOL optic geometry with a square, truncated edge

Diabetes mellitus may reduce the rate of posterior capsule opacification compared
with nondiabetic patients. Posterior capsule opacification occurs as a result of

• Formation of opaque secondary membranes by active lens epithelial

proliferation;

• Transformation of lens epithelial cells into fibroblasts with contractile

elements; and

• Collagen deposition. Anterior lens epithelial cells proliferate onto the

posterior capsule at the site of apposition of the anterior capsule flaps to
the posterior capsule. The contraction caused by the myoblastic features
of the lens epithelial cells produces wrinkling of the posterior capsule.

Collagen deposition results in white fibrotic opacities. Mitotic inhibitors instilled into
the anterior chamber after extracapsular cataract extraction dramatically reduce
capsular opacification. Pharmacologic inhibition of capsular opacification has yet
to be successfully introduced into clinical practice.

Posterior capsule opacification results from lens epithelial cells proliferating onto
the posterior capsule at the site of apposition of the anterior capsule flaps,
explaining the inability of polishing the capsule at surgery to delay the onset or
reduce the frequency of late capsular opacification. Polishing the posterior
capsule cannot remove the epithelial cells from the anterior capsule flaps. A
peripheral ring in the capsular bag may reduce opacification.

Clinical evidence has been presented that a convex posterior chamber IOL can
inhibit posterior capsule opacification and close apposition of peripheral anterior
and posterior capsule flaps leads to posterior capsule opacification. An unusual
form of early central posterior capsule fibrosis occurred when a posteriorly vaulted
biconvex optic IOL was positioned with the optic anterior to a capsulorhexis
opening smaller than the optic diameter. This positioning, usually with haptic
fixation in the ciliary sulcus, allowed the anterior capsule flaps to be apposed to
the posterior capsule and the IOL not to be in close apposition to the central
posterior capsule. Migration of lens epithelial cells onto the posterior capsule then
resulted in early central opacification.

The edge profile of the IOL is considered the dominant factor in the rate of
posterior capsule opacification. Truncated edge design has been associated with
reduced rates of posterior capsule opacification for both silicone and acrylic IOL
optics. Several studies indicate posterior capsule opacification rate is lower when
the anterior capsulorrhexis edge overlies the the optic for 360 degrees,but not all
studies have shown this. A sharp-edge truncated optic increases the risk of
undesireable optical phenomena after surgery.

Optical degradation of initially clear posterior capsules takes several forms

clinically.

• Fibrosis connotes a gray-white band or plaquelike opacity that may be

recognized in the early postoperative period or may occur later.

• Fibrosis present in the first days to weeks postoperatively likely represents

cortical lamellae left at the time of surgery (Figure 1).

• Fibrosis that develops months to years postoperatively is caused by

migration of anterior lens epithelium, fibroblastic metaplasia, and collagen
production.

• Figure 2 shows a dense fibrinous plaque. Heavy fibrosis occurs frequently

at the edge of a posterior chamber IOL placed in the bag with apposition
of anterior and posterior capsules (Figure 3).
Figure 1. Fine fibrosis of the posterior capsule seen at the second postoperative
examination represents cortical lamellae left at the time of surgery. The fibrosis is
evident with oblique slit lamp illumination (A) but is optically insignificant when
viewed with a red reflex (B). Fine fibrosis (C) may also develop months or years
after cataract surgery on an initially clear capsule. This eye is shown 2.5 years
after phacoemulsification cataract extraction with implantation of a one-piece
polymethylmethacrylate IOL within the capsular bag. From Steinert RF, Puliafito
CA: The Nd:YAG laser in ophthalmology: principles and clinical applications of
photodisruption, Philadelphia, 1985, WB Saunders, p 74.

Figure 2. Heavy diffuse fibrosis of a posterior capsule behind a posterior chamber

IOL. (From Steinert RF, Puliafito CA: The Nd:YAG laser in ophthalmology:
principles and clinical applications of photodisruption, Philadelphia, 1985,
WB Saunders, p 74.)
Figure 3. Dense fibrosis at the edge of a posterior chamber IOL optic placed in
the bag (arrow) in which an anterior capsular flap is apposed to the posterior
capsule. (From Steinert RD, Puliafito CA: The Nd:YAG laser in ophthalmology:
principles and clinical applications of photodisruption, Philadelphia, 1985,
WB Saunders, p 75.)

The second major form of opacity, formation of small Elschnig pearls and bladder
cells, (Figure 4) occurs months to years after surgery. Lens epithelial cells
proliferate, which can form layers several cells thick.

Figure 4. Red reflex view shows formation of multiple small epithelial pearls after
anterior epithelial cells migrate centrally from peripheral areas of apposition of
anterior capsular flaps to the posterior capsule. (From Steinert RF, Puliafito CA:
The Nd:YAG laser in ophthalmology: principles and clinical applications of
photodisruption, Philadelphia, 1985, WB Saunders, p 75.)

Capsular wrinkling can have two manifestations:

• Broad undulations of clear capsule are common in the early postoperative

period before the capsule tenses. Posterior chamber lens haptics may
induce broad wrinkles along the axis of the haptic orientation. A posterior
chamber lens may also flatten broad wrinkles if the optic body presses on
the capsule. Fibrotic contraction can also induce wrinkles (Figure 5).
Broad, undulating wrinkles of clear capsule are rarely visually disturbing.
On occasion, a patient may perceive linear distortion or shadows that
correspond to the wrinkles and that are relieved by capsulotomy.

• Fine wrinkles or folds in the capsule, caused by myoblastic differentiation

on the migrating lens epithelial cells, can result in marked optical
disturbance (Figure 6).
Figure 5. Broad wrinkles of the clear posterior capsule (arrow) are seen on red
reflex, with numerous small epithelial pearls. (From Steinert RF, Puliafito CA: The
Nd:YAG laser in ophthalmology: principles and clinical applications of
photodisruption, Philadelphia, 1985, WB Saunders, p 76.)

Figure 6. Fine wrinkles in the posterior capsule are evident on red reflex
(arrowheads). These wrinkles alone can be visually disturbing and can reduce
acuity by several lines or cause Maddox rod light streaks. (From Steinert RF,
Puliafito CA: The Nd:YAG laser in ophthalmology: principles and clinical
applications of photodisruption, Philadelphia, 1985, WB Saunders, p 76.)

If the iris forms synechiae to the capsule, reactive pigment epithelial hyperplasia
and migration onto the capsule may occur. Adhesions occur if large amounts of
cortex are left at the time of surgery, which is particularly common with traumatic
cataracts. Figure 7 shows dense melanin deposition on a pupillary membrane
after an old traumatic cataract. Localized pigmented precipitates on the capsule
and IOL can occur spontaneously or after hemorrhage or inflammation.
Figure 7. Pigment from proliferating uveal melanocytes has covered a large
portion of this dense pupillary membrane, which formed after a traumatic cataract
40 years previously. The border of the pigment has a sharp scalloped
configuration (arrow). (From Steinert RF, Puliafito CA: The Nd:YAG laser in
ophthalmology: principles and clinical applications of photodisruption,
Philadelphia, 1985, WB Saunders, p 77.)

Posterior Capsulotomy
Indications
Nd:YAG laser capsulotomy is indicated for treatment of opacification of the
posterior capsule resulting in decreased visual acuity or visual function, or both,
for the patient. Confirmation that posterior capsule opacification is the cause of
decreased visual acuity is necessary. Patients may complain of glare despite the
appearance of minimal capsular opacification. Glare testing can be helpful in
validating these symptoms.

Contraindications
Nd:YAG laser capsulotomy is contraindicated if

• Corneal scars, irregularity, or edema preclude adequate visualization of

the target aiming beam or degrade the Nd:YAG laser beam optics,
preventing reliable and predictable optical breakdown.

• The patient cannot fixate adequately, with the threat of inadvertent

damage to adjacent intraocular structures.

• A glass IOL is involved due to the possibility of a complete fracture in the

glass optic. The merits of surgical discission should be carefully weighed.

• Known or suspected active cystoid macular edema (CME), given evidence

regarding a beneficial effect of the barrier function of an intact posterior
capsule and rare cases of clinical CME that occur after Nd:YAG laser
capsulotomy. Avoidance of capsulotomy in an eye with active inflammation
 is suggested until the visual impairment becomes functionally
unacceptable to the patient.

• Though rare, Nd:YAG laser posterior capsulotomy may be complicated by

a retinal tear or detachment. Clinical data establishing a correlation
between the number or energy level of laser pulses and retinal
detachment is lacking.

For eyes at high risk for retinal detachment, the least amount of energy and the
lowest possible number of shots should be used to accomplish the capsulotomy,
and only a small opening should be made (Table 1). Repolishing the capsule may
be considered in high-risk patients.

Table 1. Contraindications to laser capsulotomy.

Absolute Contraindications Relative Contraindications

• Corneal scars, irregularities, or edema that • Glass intraocular lens
interfere with target visualization or make
• Known or suspected cystoid macular edema
optical breakdown unpredictable
• Active intraocular inflammation
• Inadequate stability of the eye
• High risk for retinal detachment

Technique
Preoperative Assessment

All patients require a complete ophthalmic history and examination before

treatment.

The contribution of a capsular opacity to a patient's overall visual deficit may be

difficult to judge. Table 2 lists useful techniques. Capsular opacities generally
cause little visual difficulty. Capsular opacities may be impressive in oblique slit-
lamp illumination but insignificant against the red reflex. Direct ophthalmoscopy is
the most reliable technique for assessing capsular opacity. The surgeon's view of
retinal details generally correlates with what the patient sees. Retinoscopy and the
red reflex also reveal significant optical disturbances. The fundus view with the
Hruby lens or 90-diopter lens may allow accurate assessment of capsular
clouding. Indirect ophthalmoscope can penetrate significant capsular opacity.

Table 2. Assessment of significance of capsular opacity.

• Direct ophthalmoscopic visualization of fundus structures
• Retinoscopy
• Red reflex evaluation by slit-lamp exam, direct/indirect
ophthalmoscopic exam
• Hruby lens view of fundus
• Laser interferometer evaluation
 • Potential acuity meter evaluation
• Fluorescein angiography

Laser interferometer and the potential acuity meter should penetrate mild to
moderate capsular opacity and predict macular function. Both instruments may
give false-positive ("good") acuity prediction in the presence of CME,which is the
most common cause of postcataract visual impairment besides capsular opacity.
False-negative acuity predictions may also occur because of diffuse posterior
capsule opacification, poor pupillary dilation, poor patient posture at the slit-lamp
examination, communication problems, alphabet illiteracy, nystagmus, tremor,
senility, poor patient cooperation, and fatigue.

Adequate visualization may be present for fluorescein angiography or angioscopy.

Posterior segment optical coherence tomography is possible in mild levels of
posterior capsule opacification but more advanced levels may disrupt the scan to
clinically unacceptable levels. To avoid unnecessary capsulotomy, CME should be
considered for patients where capsular opacity seems inadequate to explain the
quality of vision.

Preparation of the Patient

Explain the purpose and nature of the procedure and obtain informed consent.
Remind the patient that

• The procedure is painless.

• Small clicks or pops may be heard, but the patient is to maintain steady
fixation.

• The procedure is completed in a matter of minutes.

Brimonidine, apraclonidine, or a beta-blocking agent should be administered in the

eye immediately on completion of the Nd:YAG laser posterior capsulotomy to
minimize a postoperative intraocular pressure (IOP) spike. If contraindicated, a
topical or systemic carbonic anhydrase inhibitor, prostaglandin analogue, or, in a
case of an extremely vulnerable optic nerve, oral hyperosmotic agent may be
used to prevent or treat any IOP elevation following laser therapy.

Dilation of the pupil facilitates visualization of the capsule over a broad expanse.
Dilation is helpful for inexperienced surgeons, except in cases of an iris-clip lens.
In the absence of a miotic pupil, dilation may be omitted for an experienced
surgeon.

Sketch the landmarks of the pupillary zone of the capsule before dilating the pupil.
Pupils are often eccentric or may dilate eccentrically, as shown in Figure 8.
Inattention may result in an eccentric capsulotomy, necessitating a second laser
session. Before dilation, and a single "marker" shot can be placed in the capsule
near the middle of the pupillary axis. When the pupil is dilated, the marker shot is
a reminder of the patient's true visual axis.
Figure 8. (A) Typical capsular opacity before dilation. (B) Capsulotomy appears
eccentric because of uneven pupillary dilation caused by posterior synechia to the
capsule (arrow). The capsular opening is properly centered for the undilated pupil.
(From Steinert RF, Puliafito CA: The Nd:YAG laser in ophthalmology: principles
and clinical applications of photodisruption, Philadelphia, 1985, WB Saunders,
p 81.)

A single drop of 2.5% phenylephrine is recommended for routine dilation. Weak

dilation prevents iris capture of a posterior chamber IOL (Figure 9), which may be
difficult to properly reposition. If inadequate, a drop of 0.5% or 1% tropicamide
may be added.
Figure 9. Iris capture of a ciliary sulcus–fixated planar haptic posterior chamber
IOL. This phenomenon can occur after wide dilation for posterior capsulotomy. If
dilation is necessary at all, weak mydriatics and cycloplegics should be employed.
(From Steinert RF, Puliafito CA: The Nd:YAG laser in ophthalmology: principles
and clinical applications of photodisruption, Philadelphia, 1985,
WB Saunders, p 81.)

Capsulotomy generally does not require anesthesia unless a contact lens is used.
If a contact lens is used, a drop of topical anesthetic is applied to the cornea
immediately before the procedure. A retrobulbar injection to establish akinesia
may be helpful in rare circumstances, such as nystagmus. If a topical anesthetic is
applied in advance of the procedure, instruct the patient to keep their eyes closed
during the interim to maintain the surface integrity and optical quality of the
corneal epithelium.

The patient must be seated comfortably with properly adjusted stool, table, and
chin rest heights and a footrest when appropriate. A strap that passes from the
headrest behind the patient's head counteracts a patient's tendency to move back
during the treatment. Surgeon's visualization of the target is usually improved in a
darkened room. If a patient is expected to fixate with the other eye, an illuminated
fixation target should be provided. Table 3 summarizes the steps in patient
preparation.

Table 3. Preparation of the patient.

Before Treatment Session
• Complete ophthalmic history and examination
• Discussion of proposed procedure, including
risks, benefits, and alternatives; signing of
informed consent form
• Apraclonidine or beta-adrenergic blocking agent
• Pupillary dilation (optional)
• Determination of visual axis and normal
pupillary size: sketch and preliminary laser
At the Laser
• Review of the procedure, the expected pop or
click, and the importance of fixation
• Application of topical anesthetic if contact lens
is to be used
• Adjustment of stool, table, chin rest, and
footrest for optimal patient comfort
• Application of head strap to maintain forehead
position
 marker shot • Darkening of the room (optional)
• Weak mydriatic and cycloplegic agents: 2.5% • Provision of fixation target for fellow eye
phenylephrine or 0.5% or 1% tropicamide
• Illumination of target if room is darkened

Procedure

A Peyman or central Abraham contact lens may be used to stabilize the eye,
improve the laser beam optics, and facilitate accurate focusing. The Abraham
Nd:YAG laser:

• Increases the convergence angle to 24 degrees from 16 degrees.

• Decreases the area of laser at the posterior capsule to 14 µm from 21 µm.

• Increases the beam diameter at both the cornea and the retina.

Use the Abraham Nd:YAG laser lens with care because it is a modified posterior
pole lens. If the Nd:YAG laser is not sent through the lens button, but rather the
peripheral "carrier" portion of the lens, the Nd:YAG laser may be focused on the
retina and cause damage.

The minimal amount of energy necessary to obtain breakdown and rupture the
capsule is desired. With most lasers, a typical capsule can be opened by using
1 to 2 mJ/pulse.

The capsule is examined for wrinkles that indicate tension lines. Shots placed
across tension lines result in the largest opening per pulse because the tension
causes the initial opening to widen.

Figure 10 shows an actual capsulotomy, photographed sequentially and drawn

from the photographs, showing the opening as it develops and the location of the
next laser shot. Table 4 outlines the basic technique.
Figure 10. Artist drawing based on sequential capsulotomy photographs. The
capsulotomy is developed in a cruciate pattern. (A) The first shot is made
superiorly in the location of some fine tension lines. (B) The second shot is aimed
inside the inferior edge of the initial opening. (C) The next shot again is made at
the 6 o'clock position of the capsulotomy border. (D) The fourth shot is made
across inferior tension lines to allow the capsulotomy to widen. (E) The opening is
nearly 3 mm wide. It is widened by a shot at the 3 o'clock capsulotomy margin. (F)
The opening now needs to be directed to the left, with a shot at the 9 o'clock
position. (G) The cruciate opening has been accomplished, but a triangular flap
extends into the pupillary space from the 7:30 region in the left inferior pupil. A
shot is applied to the flap both to cut it and to push it toward the periphery. (H) The
capsulotomy is complete, and the pupil will be clear of capsule after the dilation
wears off. From Steinert RF, Puliafito CA: The Nd:YAG laser in ophthalmology:
principles and clinical applications of photodisruption, Philadelphia, 1985,
WB Saunders, pp 84–85.

Table 4. Posterior capsulotomy technique.

• Use minimum energy: 1 mJ if possible.
• Identify and cut across tension lines.
• Perform a cruciate opening: Begin at 12 o'clock in
the periphery, progress toward 6 o'clock, and cut
across at 3 and 9 o'clock.
• Clean up any residual tags.
• Avoid freely floating fragments.

Create a cruciate opening, beginning superiorly near the 12 o'clock position and
progressing downward toward the 6 o'clock position.

Unless a wide opening has already developed, shots are then placed at the edge
of the capsule opening, progressing laterally toward the 3 and 9 o'clock positions.

If any capsular flaps remain in the pupillary space, the laser is fired specifically at
the flaps to cut them and cause them to retract and fall back to the periphery. The
goal is to achieve flaps based in the periphery inferiorly. Free-floating fragments
should be avoided because they may remain and cause visual interference.
Cutting in a circle ("can-opener" style) tends to create large fragments that may
not sink from the visual axis or that may settle against the endothelium or angle
structures. A large "vitreous floater" of residual capsule may bother the patient.

Beginning the cruciate opening in the superior periphery has several advantages:

• If the patient startles and an adjacent IOL is marked, the mark appears in
the periphery.

• Both patient and surgeon are more relaxed before the critical central area
is treated.

• As the flaps develop, gravity aids in pulling them toward the inferior
periphery. It can be difficult to cause a flap that is hanging down from
above to retract.

An IOL may be marked in the course of the capsulotomy. This is particularly true
for posterior chamber lenses for which there is little or no separation of the
capsule from the IOL. Figure 11 shows a capsulotomy without damage to an
overlying posterior chamber IOL.
Figure 11. Posterior capsulotomy performed on a capsule in direct apposition to a
lathe-cut posterior chamber IOL. Figure 6 is the pretreatment photograph of the
same eye. Note the eccentric location of the optic caused by the displacement of
the inferior haptic in the bag and the superior haptic in the ciliary sulcus. The
capsulotomy is properly located in the visual axis, but care is taken not to extend
the opening beyond the edge of the optic to avoid vitreous herniation around the
optic (arrow). (From Steiner RF, Puliafito CA: The Nd:YAG laser in ophthalmology:
principles and clinical applications of photodisruption, Philadelphia, 1985,
WB Saunders, p 86.)

Visually significant pits and cracks can be minimized and avoided through careful
techniques, as outlined in Table 5. The minimal amount of energy must be
employed. With a typical capsule and careful focusing, 1 to 2 mJ is usually
adequate.

Table 5. Minimizing IOL laser marks.

• Use minimum energy. • Identify any areas of intraocular lens–capsule
separation and begin treatment there.
• Use contact lens to stabilize the eye, improve
laser beam optics, and facilitate accurate focusing. • Use deep focus techniques: Optical breakdown
occurs in the anterior vitreous. The shock wave
• If lens making is occurring, make a Christmas-
radiates forward and ruptures the capsule. Higher
tree opening from 12 o’clock to 4:30 and from
energy (2 mJ or more) must be used.
12 o’clock to 7:30 without placing any shots in
the central optical zone.

The capsule should be carefully examined for an area of separation from the IOL
in which to begin the capsulotomy. Once the capsulotomy has begun, further
areas of separation usually develop.

Beginning the capsulotomy in the 12 o'clock periphery gives an indication of the

tendency for IOL marking in a noncritical area.

If there is a tendency for unavoidable repeated marks, the usual cruciate pattern
should be modified. Instead of progressing from the 12 o'clock to the 6 o'clock
position across the visual axis, the cut should be made nasally and temporally,
staying in the periphery of the optical zone. The capsule can be opened
"Christmas-tree" fashion, based inferiorly, without any shots in the central visual
axis.

To avoid IOL marks, the laser can be intentionally focused posterior to the
capsule, causing optical breakdown in the anterior vitreous. The shock wave
radiates forward and ruptures the capsule. Optical breakdown just at the capsule
and IOL surface, with resultant IOL marking, is avoided. The breakdown threshold
is higher in the anterior vitreous than at an optical interface so higher energy,
usually a minimum of 2 mJ, is required. Focus consistently at an area posterior to
the capsule so the breakdown is not allowed to come up to the back of the IOL,
which would result in a larger mark. This technique traumatizes the vitreous, so
preference is to reserve the deep focus technique for cases in which IOL marks
are occurring with focus directly on the capsule.

In aphakic eyes, deliberate focus anterior to the capsule has been advocated as a
mechanism for opening the capsule while leaving the anterior hyaloid intact.

Capsulotomy Size

The capsulotomy should be as large as the pupil in isotopic conditions, such as

driving at night, when glare from the exposed capsulotomy edge is most likely. A
small opening might be preferred for a patient at high risk of retinal detachment. A
small opening in a dense membrane results in excellent optics, analogous to
those of a small pupil (Figure 12).
Figure 12. (A) Dense retropupillary membrane after complicated extracapsular
cataract extraction. (B) An adequate membrane opening is well centered on the
pupillary axis. (From Steinert RF, Puliafito CA: The Nd:YAG laser in
ophthalmology: principles and clinical applications of photodisruption,
Philadelphia, 1985, WB Saunders, p 92.)

When the capsule is only hazy and transmits images to the retina, a small opening
is an improvement but is still suboptimal. The hazy membrane continues to
transmit a poor quality image that mixes at the retina with the image transmitted
through the clear opening. The patient may experience symptoms of blur, glare, or
decreased contrast sensitivity.

Figure 13 shows an example of a posterior capsulotomy performed without

dilation. As the patient looks up, down, left, and right, the laser can be applied to
capsular edges behind the sphincter so that the capsulotomy can be perfectly
centered. Slit-lamp illumination should be with a narrow beam, angled obliquely, to
minimize miosis and indicate average pupillary size with ambient dim lighting.
Figure 13. Posterior capsulotomy performed without pupillary dilation. (A) Hazy
capsule before treatment. (B) After laser application, the pupillary zone is clear.
Two tags of capsule at the edge of the pupil can be seen (arrows). These could be
easily exposed to the laser by having the patient look up and down. From Steinert
RF, Puliafito CA: The Nd:YAG laser in ophthalmology: principles and clinical
applications of photodisruption, Philadelphia, 1985, WB Saunders, p 82.

Capsulotomies may spontaneously enlarge postoperatively. Capsulotomies may

increase in mean area by 32% within 6 weeks with capsular enlargement tending
toward sphericity with capsular tag retention. Tension created by contractile
properties of myofibroblastic lens epithelial cells, IOL haptics, or both, may cause
this alteration in capsulotomy contour.

A capsule with residual haze impairs vision and produces glare. A clinical study of
glare after extracapsular cataract extraction substantiated the deleterious effect of
capsular opacification. Glare and haze remain a problem for 1- and 2-mm
capsular openings, decrease with a 3-mm opening, and fully resolve only with a
4-mm capsular opening.

Postoperative Care

After Nd:YAG laser posterior capsulotomy in all patients, brimonidine,

apraclonidine, or a beta-blocker should be administered topically to minimize any
IOP increase. For high-risk patients, IOP may be measured again 1 hour following
laser treatment. IOP should be remeasured at 4 hours for patients with significant
preexisting glaucomatous disc damage or if the IOP is increased 5 mm Hg or
more at 1 hour.

Increased IOP may be treated with brimonidine, apraclonidine, topical beta-

adrenergic antagonists, prostaglandin analogue, topical pilocarpine, topical or
systemic carbonic anhydrase inhibitor, or hyperosmotic agents. Patient's medical
history, allergies, and current ocular therapy should be reviewed before
determining the appropriate acute antiglaucoma therapy. Continue antiglaucoma
therapy for at least 1 week to prevent a delayed pressure elevation. Measure IOP
again about 1 week after laser surgery and sooner if indicated by a pressure
increase or preexisting glaucomatous optic nerve damage or visual field loss.
Treatment following laser therapy (Table 6) with topical steroids and cycloplegic
agents varies based on the individual surgeon's experience. Many patients require
no therapy following laser treatment. For patients with iritis, topical steroids can be
used four times daily for one or more postoperative weeks. Some patients may
require a tapered dosage.

Table 6. Care following capsulotomy.

Medication Minimual Suggested Follow-Up Protocol
• Apraclonidine immediately following • 1 hour–4 hours
capsulotomy
• Pressure rise to 5 mm Hg: Treatment should be
• Optional additional antiglaucoma therapy (beta- given at 1 day, 1 week, 1 month, 3 months, and
adrenergic antagonist, pilocarpine, carbonic 6 months.
anhydrase inhibitor, hyperosmotic agents) as
needed for IOP control
• Optional: cycloplegics (1% cyclopentolate at time
of treatment); steroids (1% prednisolone or 0.1%
dexamethasone 4 times a day tapered as needed)

Results

Nd:YAG laser posterior capsulotomy results in improved visual acuity in 83% to

96% of eyes.

Failure of vision to improve is often due to preexisting ocular disease, including

age-related macular degeneration, CME, other macular disease, retinal
detachment, corneal edema, glaucoma, ischemic optic neuropathy, and
amblyopia.

Complications

Complications causing decreased vision are uncommon but include elevated

extraocular pressure, CME, retinal detachment, IOL damage, endophthalmitis,
iritis, vitritis, macular holes, and corneal edema.

Intraocular Pressure Elevation

Elevated IOP is the most common, although usually transient, complication

following Nd:YAG laser capsulotomy. IOP elevations greater than 10 mmHg have
been observed in 15% to 67% of eyes. IOP typically begins to rise immediately
after the laser capsulotomy, peaks at 3 to 4 hours, decreases but may remain
elevated at 24 hours, and usually returns to baseline at 1 week. Rarely, IOP
remains persistently elevated, causing visual field loss requiring glaucoma
surgery, or both. Acute IOP increase may cause loss of light perception vision.

Elevated IOP has been associated with preexisting glaucoma, capsulotomy size,
lack of a posterior chamber IOL, sulcus fixation of a posterior chamber IOL, laser
energy required for the capsulotomy, myopia, and preexisting vitreoretinal
disease.
Reliable in-the-bag fixation of posterior chamber IOLs has vastly reduced the
incidence of clinically significant elevation of IOP after Nd:YAG laser capsulotomy.

Increased IOP following Nd:YAG laser capsulotomy is associated with a reduced

facility for aqueous humor outflow. This reduction has been attributed to capsular
debris, acute inflammatory cells, liquid vitreous, and shock-wave damage to the
trabecular meshwork. Acute inflammatory cells and capsular debris cause
increased IOP by demonstrating pigment granules, erythrocytes, fibrin,
lymphocytes, and macrophages within the trabecular meshwork after laser
capsulotomy. Glaucomatous eyes may have increased frequency and magnitude
of IOP elevation as they already have a reduced outflow facility.

Liquid vitreous as the cause of outflow obstruction is supported by the clinical

association between increased IOP following laser treatment and myopia,
preexisting vitreoretinal disease, lack of a posterior chamber IOL, and sulcus-
fixated posterior chamber IOLs. A capsule-fixated posterior chamber IOL and a
smaller capsulotomy may provide a barrier effect, preventing liquid vitreous from
reaching the anterior chamber and trabecular meshwork. Liquid vitreous injected
into the anterior chamber in owl monkey eyes was found to increase IOP.

Nd:YAG laser–induced shock waves causing increased IOP resulting in damage

to the trabecular meshwork has been supported clinically by the association
between increased IOP and higher total laser energy used to create the
capsulotomy. Photodisruption pulses in the aqueous of the midanterior chamber
have not been associated with increased IOP, nor has there been microscopic
evidence of damage to the trabecular cords.

Prevention of the IOP increase is appropriate. Apraclonidine, brimonidine, timolol,

levobunolol, and pilocarpinedecrease the frequency and magnitude of IOP
increases. Apraclonidine is most effective. Apraclonidine, timolol, levobunolol, or
other beta-adrenergic antagonists are administered 1 hour before the procedure
and again following the procedure. Pilocarpine should be administered only
postoperatively due to its miotic effect.

Patients at high risk for IOP elevation or with vulnerable optic nerves should be
carefully monitored following the procedure as prophylactic therapy may not
prevent late IOP increases.

IOP following Nd:YAG laser capsulotomy may also be elevated by vitreous

obstruction of a sclerostomy, the development of neovascular glaucoma, or
pupillary block glaucoma.

Patients with existing glaucoma or where high IOP developed acutely after
capsulotomy may have long-term elevated IOP.

Cystoid Macular Edema

CME develops in 0.55% to 2.5% of eyes following Nd:YAG laser posterior

capsulotomy. CME may occur between 3 weeks and 11 months after the
capsulotomy. Incidence of new CME is low following laser capsulotomy, although
some patients may acquire CME at a later date. Risk of CME could be lowered by
a longer interval between extracapsular cataract extraction and laser capsulotomy,
although other studies have not confirmed this. Treatment of CME following
Nd:YAG laser posterior capsulotomy is identical to its treatment following cataract
extraction and is discussed in Phototherapeutic Keratectomy.

Retinal Detachment

Retinal detachment may complicate Nd:YAG laser posterior capsulotomy in 0.08%

to 3.6% of eyes.

Retrospective review of Medicare claims found the cumulative probability of retinal

detachment over 36 months following cataract surgery was 1.6% to 1.9% in
patients who had laser capsulotomy versus 0.8% to 1% in patients undergoing
cataract surgery alone. This review could not distinguish if the same or fellow eye
had cataract surgery, capsulotomy, and retinal detachment, nor could it determine
the sequence.

Retinal detachment may occur early after the laser capsulotomy or more than a
year later. Asymptomatic retinal breaks were found at a rate of 2.1% within 1
month of posterior capsulotomy in one study. Myopia, a history of retinal
detachment in the other eye, younger age,and male sex are risk factors following
Nd:YAG laser posterior capsulotomy.

In uncomplicated phacoemulsification and PC IOL implantation, a rate of retinal

detachment after laser capsulotomy of 0 to 0.4% over 1 to 8 years has been
reported in 2 series. In one of these series, no retinal detachments occurred in
eyes with axial lengths under 24.0 mm. A study found no increased risk of retinal
detachment after Nd-YAG laser capsulotiomy in eyes that did not have a posterior
capsule tear at the time of cataract surgery.

Intraocular Lens Damage

Pitting of IOLs occurs in 15% to 33% of eyes during Nd:YAG laser posterior
capsulotomy. Pitting is usually not visually significant, although rarely the damage
may cause sufficient glare and image degradation that the damaged IOL must be
explanted.

The type and extent of lens damage depend on the material used in the IOL.
Glass IOLs may be fractured by the Nd:YAG laser. PMMA IOLs sustain cracks
and central defects with radiating fractures. Molded PMMA IOLs are more easily
damaged than higher-molecular-weight lathe-cut lenses. Damage to silicone
lenses is characterized by blistered lesions and localized pits surrounded by
multiple tiny pits. The damage threshold is lowest for silicone, intermediate for
PMMA, and highest for acrylic materials.

Frequency of damage depends on IOL style. IOLs designed with a ridge

separating the posterior capsule from the IOL sustain less damage than lenses
with a convex posterior surface and close apposition between the posterior
chamber IOL and the posterior capsule.

Endophthalmitis
Propionibacterium acnes endophthalmitis has been reported following Nd:YAG
laser posterior capsulotomy. Patients have decreased vision caused by posterior
capsular opacification and an otherwise quiet eye. Following laser capsulotomy,
the eyes developed significant uveitis and loss of vision. The capsulotomy is
presumed to have created opportunity for organisms within the capsule to reach
the vitreous and develop into endophthalmitis.

Other Complications

Other complications include

• Iritis persisting for 6 months after laser capsulotomy has been reported in
less than 1% of eyes.

• Macular holes have rarely been reported to develop after capsulotomy.

• Specular microscopic studies have reported corneal endothelial cell loss

of 2.3% to 7% following Nd:YAG laser posterior capsulotomy.

Suggested Reading
1. Aron-Rosa D, Aron JJ, Griesemann M, Thyzel R. Use of the neodymium-
YAG laser to open the posterior capsule after lens implant surgery: a
preliminary report. J Am Intraocul Implant Soc. 1980;6(4):352-354.

2. Baratz KH, Cook BE, Hodge DO. Probability of Nd:YAG laser capsulotomy
after cataract surgery in Olmsted County, Minnesota. Am J
Ophthalmol. 2001;131(2):161-166.

3. Kraff MC, Sanders DR, Lieberman HL. Total cataract extraction through a
3-mm incision: a report of 650 cases. Ophthalmic Surg. 1979;10(2):46-54.

4. Frezzotti R, Caporossi A. Pathogenesis of posterior capsular opacification.

Part I. Epidemiological and clinico-statistical data. J Cataract Refract
Surg. 1990;16(3):347-352.

5. Apple DJ, Peng Q, Visessook N, et al. Surgical prevention of posterior

capsule opacification. Part 1: Progress in eliminating this complication of
cataract surgery. J Cataract Refract Surg. 2000;26(2):180-187.

6. Wang MC, Woung LC. Digital retroilluminated photography to analyze

posterior capsule opacification in eyes with intraocular lenses. J Cataract
Refract Surg. 2000;26(1):56-61.

7. Roy FH. After-cataract: clinical and pathologic evaluation. Ann

Ophthalmol.1971;3(12):1364-1366

8. Cobo LM, Ohsawa E, Chandler D, Arguello R, George G. Pathogenesis of

capsular opacification after extracapsular cataract extraction. An animal
model. Ophthalmology.1984;91(7):857-863.
9. Clark DS, Emery JM, Munsell MF. Inhibition of posterior capsule
opacification with an immunotoxin specific for lens epithelial cells: 24
month clinical results. J Cataract Refract Surg. 1998;24(12):1614-1620.

10.Nishi O, Nishi K. Preventing posterior capsule opacification by creating a

discontinuous sharp bend in the capsule. J Cataract Refract
Surg. 1999;25(4):521-526.

11.Buehl W, Findl O, Menapace R, et al. Long-term effect of optic edge

design in an acrylic intraocular lens on posterior capsule opacification. J
Cataract Refract Surg.2005;31(5):954-961.

12.Georgopoulos M, Menapace R, Findl O, Petternel V, Kiss B, Rainer

G. After-cataract in adults with primary posterior capsulorhexis:
comparison of hydrogel and silicone intraocular lenses with round edges
after 2 years. J Cataract Refract Surg.2003;29(5):955-60.

13.Hollick EJ, Spalton DJ, Ursell PG, Meacock WR, Barman SA, Boyce
JF. Posterior capsular opacification with hydrogel, polymethylmethacrylate,
and silicone intraocular lenses: two-year results of a randomized
prospective trial. Am J Ophthalmol.2000;129(5):577-584.

14.Mester U, Fabian E, Gerl R, et al. Posterior capsule opacification after

implantation of CeeOn Edge 911A, PhacoFlex SI-40NB, and AcrySof
MA60BM lenses: one-year results of an intraindividual comparison
multicenter study. J Cataract Refract Surg.2004;30(5):978-985.

15.Prosdocimo G, Tassinari G, Sala M, et al. Posterior capsule opacification

after phacoemulsification: silicone CeeOn Edge versus acrylate AcrySof
intraocular lens. J Cataract Refract Surg. 2003;29(8):1551-1555.

16.Sacu S, Menapace R, Findl O, Kiss B, Buehl W, Georgopoulos M. Long-

term efficacy of adding a sharp posterior optic edge to a three-piece
silicone intraocular lens on capsule opacification: five-year results of a
randomized study. Am J Ophthalmol.2005;139(4):696-703.

17.Li N, Chen X, Zhang J, et al. Effect of AcrySof versus silicone or

polymethyl methacrylate intraocular lens on posterior capsule
opacification. Ophthalmology.2008;115(5):830-838.

18.Davison JA. Positive and negative dysphotopsia in patients with acrylic

intraocular lenses. J Cataract Refract Surg. 2000;26(9):1346-1355.

19.Keates RH, Steinert RF, Puliafito CA, Maxwell SK. Long-term follow-up of
Nd:YAG laser posterior capsulotomy. J Am Intraocul Implant
Soc. 1984;10(2):164-168.

20.Dickerson DE, Gilmore JE, Gross J. The Abraham lens with the
neodymium-YAG laser.J Am Intraocul Implant Soc. 1983;9(4):438-440.

21.Stark WJ, Worthen D, Holladay JT, Murray G. Neodymium:YAG lasers: an

FDA report.Ophthalmology. 1985;92(2):209.
 22.Richter CU, Arzeno G, Pappas HR, Steinert RF, Puliafito C, Epstein
DL. Intraocular pressure elevation following Nd:YAG laser posterior
capsulotomy. Ophthalmology.1985;92(5):636-640.

23.Schubert HD. Vitreoretinal changes associated with rise in intraocular

pressure after Nd:YAG capsulotomy. Ophthalmic Surg. 1987;18(1):19-22.

24.Vine AK. Ocular hypertension following Nd:YAG laser capsulotomy: a

potentially blinding complication. Ophthalmic Surg. 1984;15(4):283-284.

25.Schubert HD, Morris WJ, Trokel SL, Balazs EA. The role of the vitreous in
the intraocular pressure rise after neodymium-YAG laser
capsulotomy. Arch Ophthalmol.1985;103(10):1538-1542.

26.Richter CU, Arzeno G, Pappas HR, Arrigg CA, Wasson P, Steinert

RF. Prevention of intraocular pressure elevation following neodymium-
YAG laser posterior capsulotomy.Arch Ophthalmol. 1985;103(7):912-915.

27.Weinreb RN, Wasserstrom JP, Parker W. Neovascular glaucoma following

neodymium-YAG laser posterior capsulotomy. Arch
Ophthalmol. 1986;104(5):730-731.

28.Winslow RL, Taylor BC. Retinal complications following YAG laser

capsulotomy.Ophthalmology. 1985;92(6):785-789.

29.Liesegang TJ, Bourne WM, Ilstrup DM. Secondary surgical and

neodymium-YAG laser discissions. Am J Ophthalmol. 1985;100(4):510-
519.

30.Koch DD, Liu JF, Gill EP, Parke DW 2nd. Axial myopia increases the risk
of retinal complications after neodymium-YAG laser posterior
capsulotomy. Arch Ophthalmol.1989;107(7):986-990.

31.Shah GR, Gills JP, Durham DG, Ausmus WH. Three thousand YAG lasers
in posterior capsulotomies: an analysis of complications and comparison
to polishing and surgical discission. Ophthalmic Surg. 1986;17(8):473-477.

32.Bath PE, Hoffer KJ, Aron-Rosa D, Dang Y. Glare disability secondary to

YAG laser intraocular lens damage. J Cataract Refract
Surg. 1987;13(3):309-313.

33.Keates RH, Sall KN, Kreter JK. Effect of the Nd:YAG laser on
polymethylmethacrylate, HEMA copolymer, and silicone intraocular
materials. J Cataract Refract Surg.1987;13(4):401-409.

34.Piest KL, Kincaid MC, Tetz MR, Apple DJ, Roberts WA, Price FW
Jr. Localized endophthalmitis: a newly described cause of the so-called
toxic lens syndrome. J Cataract Refract Surg. 1987;13(5):498-510.

Aftercare

After a laser capsulotomy, the patient will remain in the office for one to four hours so that the pressure in the eye
can be evaluated. The patient can then resume normal everyday activities. After surgery, pressure-lowering
eyedrops may be used for a week, if the intraocular pressure is raised significantly after the procedure.
Cycloplegic agents to keep the pupil dilated and to prevent spasm of the muscles in the iris, and steroids to
reduce inflammation may also be prescribed for up to a week. Follow-up visits are scheduled at one day, one
week, one month, three months, and six months after capsulotomy.

Risks

One risk of laser capsulotomy is damage to the intraocular implant. Factors that determine the extent of damage
to the IOL include the inherent resistance of a particular IOL to damage by the laser, the amount of energy used
in the procedure, the position of the IOL within the lens capsule, and the focusing accuracy of the surgeon. The
thicker the opacification of the lens capsule, the greater the amount of energy needed to remove it. The accuracy
of the surgeon is improved when there is less opacification on the lens capsule.
In addition, during laser capsulotomy the IOL can be displaced into the eye's vitreous. This happens more often
in eyes with a rigid implant, rather than with acrylic or silicone IOLs, and also if a larger implant is used. If the
posterior capsule ruptures during extraction of the primary cataract, risk of lens displacement is also increased.
Displacement risk is also increased if the area over which the laser capsulotomy is done is large. The most
serious complication of a capsulotomy would be IOL damage so extensive that extraction would be required.
This is a rare complication.
Another risk of this surgery is the re-formation of Elschnig's pearls over the opening created by the capsulotomy.
This occurs in up to 80% of patients within two years of laser capsulotomy. Most of time, these PCOs will
resolve over time without treatment, but 20% of patients will require a second laser capsulotomy. This secondary
opacification by Elschnig pearls represents a spatial progression of the opacification that caused the initial
secondary cataract.
Other risks to take into account when considering a posterior capsulotomy are macular edema, macular holes,
corneal edema, inflammation of the iris, retinal detachment, and increased pressure in the eye, as well
as glaucoma. These risks escalate with increased laser energy and with increased size of the capsulotomy area.
Retinal detachments are usually treated with removal of the vitreous behind the lens capsule. Macular edema is
treated by application of topical anti-inflammatory drops or intraocular steroid injections. Steroids control iritis
(inflammation of the iris), either topically or intraocularly. Macular holes are also treated by removal of the
vitreous (the substance that fills the main area of the eyeball), followed by one to three weeks of facedown
positioning. Elevated intraocular pressure and glaucoma are treated with anti-glaucoma drops or glaucoma
surgery, if necessary.
Finally, increased glare at night may result when the size of the capsulotomy is smaller than the diameter of the
pupil during dark conditions.

Normal results

Within one to two days after surgery, maximum visual acuity will be attained by almost 99% of patients. Once
the opacification is removed, most patients will not need a change in spectacle prescription. However, patients
who have undergone implantation of a rigid IOL may experience an increase in hyperopia, or far-sightedness,
after a capsulotomy. For a few weeks after surgery, the presence of visual floaters, which are pieces of the
excised capsule, is normal. But, the presence of floaters months after this timeframe, especially if accompanied
by flashes of light, may signal a retinal tear or detachment and require immediate attention. Also, if vision
suddenly or gradually worsens after an initial improvement, further follow-up to determine the cause of a
decrease in visual function is imperative.

Morbidity and mortality rates

The probability of a retinal detachment after capsulotomy is 1.6–1.9%. This represents a two-fold increase of
retinal detachment over the rate for all patients undergoing cataract surgery, regardless if a posterior capsulotomy
was done or not. Macular edema occurs in up to 2.5% of patients who undergo a laser capsulotomy and is more
likely to occur when the capsulotomy is performed soon after cataract extraction, or in younger individuals.
Rarely does glaucoma develop after laser capsulotomy, although as many as two-thirds of patients will
experience transient increased intraocular pressure.

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