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Cataract extraction in patients with glaucoma presents the
ophthalmic surgeon and the afflicted patient with many problems. One
of the most important is the misconception that “a cataract
extraction is a cataract extraction.” Society’s perception of
cataract surgery as a quick-fix operation with a rapid return of
splendid vision is often not true for glaucoma patients undergoing
“routine” cataract surgery. The management approach in the
patient who has both glaucoma and cataract must be in many ways
totally different from that of a person with cataract uncomplicated
by glaucoma. The failure to appreciate this difference may lead to
unnecessary morbidity and visual loss. In years past, patients with
both cataract and glaucoma frequently provided overwhelming surgical
challenges for the ophthalmologist. Fortunately, surgical techniques
for both diseases have improved greatly over the past decade, and
surgeons with up-to-date expertise in both subspecialties can
provide superior outcomes for their patients. The learning curve may
be steep at times, but the fusion of surgical skills slowly falls
into place as the surgeon constantly learns and upgrades his or her
skills.
The latest advances in small-incision cataract surgery include
continuous curvilinear capsulorhexis (CCC), improved management of
miotic pupils, divide-and-conquer nucleofractic phacoemulsification,
clear cornea lens extraction, and foldable intraocular lenses.
These techniques, in combination with antimetabolite-assisted
guarded filtration surgery (GFS) and postoperative sclera flap
suture lysis, dramatically improve outcomes for most glaucoma
patients with surgical cataracts. The ability to combine these two
procedures through one small incision and simultaneously modulate
would healing dramatically improves success rated, decreases
postoperative complications, improves cost-effectiveness, allows for
rapid visual recovery, and provides superior outcomes for glaucoma
patients.
Small-incision cataract surgery, however, is not appropriate for
every glaucoma patient. The surgeon must be facile and maintain
skill in all branches of cataract surgery, including intra-capsular
cataract extraction (ICCE), manual nuclear expression with
extra-capsular cataract extraction (ECCE), and phaco-emulsification
of soft and hard nuclei. A fusion of these skills is necessary
because a subluxated rock-hard nucleus may require ICCE, the nucleus
may be too dense for emulsification, thus requiring manual
expression, or the surgeon may find it necessary to convert to ECCE
techniques during small-incision surgery.
This page will provide a framework to help the surgeon caring for
a patient with both cataract and glaucoma decide when to perform a
cataract extraction alone, a glaucoma procedure alone, or a combined
cataract-glaucoma procedure. Furthermore, techniques that are
especially appropriate when performing cataract extraction in
patients with glaucoma will be presented in detail. The theme
running through these decisions is based on the following section on
guiding principles and on the concept that any additional surgical
step carries with it the increased risk of complication.
Guiding Principles
Glaucoma is a disease in which ocular tissues become damaged by
intraocular pressure (IOP) that is higher than the tissues can
tolerate. Glaucoma is not a single condition; the word encompasses a
wide variety of entities of different pathogenesis and different
intensity.
Knowledge of the basic principles related to the effects and side
effects of cataract extraction in patients with glaucoma is
essential of the surgeon is to choose a course that is most
appropriate for each individual case. Some of these principles are
known by all, and many are established but not known by all, and
many are established but not well appreciated. Some of the
principles that follow are neither well known nor well established
but are based on our personal experience or the experiences of those
whose clinical judgment appears to us to be sound. Principles not
given a supporting reference usually fall into this category.
Clinical Aspects of Optic Nerve Head Damage
Short-term, moderate elevation of intraocular pressure is not
likely to affect a healthy optic nerve.
Optic nerves vary in their ability to resist the damaging effects
of intraocular pressure. Healthy optic nerves of adults are not
usually damaged by intraocular pressures below the diastolic
ophthalmic artery pressure (around 30 to 35 mmHg) unless the
pressure persists for a minimum of at least 3 months. The exceptions
patients with sickle-cell disease. In addition, healthy optic nerves
in adults can withstand short-term (perhaps up to 2 weeks)
elevations of IOP below the systolic level of ophthalmic artery
blood pressure (average, 70 mmHg) without sustaining apparent damage
(with the exception of sickle-cell abnormalities). All optic nerves
are damaged permanently by intraocular pressures greater than
systolic retinal artery blood pressure when such an elevation
persists for more than a few minutes.
Glaucomatous optic nerves are likely to be damaged by elevated
intraocular pressure.
Optic discs already compromised by disease (glaucoma or
otherwise) are at greater risk for further damage and can be
permanently damaged by increases of IOP of relatively small
magnitude and short duration. Precise data are lacking, but pressure
elevations as small as a 50% increase (i.e., 20 to 30 mmHg) for 1
month can be expected to cause a permanent worsening of disc damage
in patients with serious disc damage present prior to the pressure
elevation.
Optic discs that are badly damaged by glaucoma (“sick discs”)
can be further damaged permanently by pressure elevations as short
as: 1 day or less when the pressure elevation is in the range of 50
mmHg or more; 1 day when intraocular pressure is 30 to 50 mmHg: or
several days when the spike is in the range of the diastolic
ophthalmic artery blood pressure. The visually damaging pressure
level of intraocular pressure can be estimated.
The pressure at which a patient has developed a hemorrhage of the
optic disc or at which progressive disc damage or visual field loss
has been noted to occur prior to cataract extraction gives a rough
estimate of the level of IOP the optic nerve is able to tolerate.
This pressure provides a baseline to use for predicting future
damage. For example, a patient whose intraocular pressures are
fairly consistent at about 15 mmHg and who develops an optic disc
hemorrhage with pressures in that range, is very likely to be at
risk for progressive optic disc deterioration with intraocular
pressures above 15 mmHg. In contrast, a patient who develops a disc
hemorrhage when intraocular pressures are averaging around 25 mmHg
probably has an optic disc that is more resistant to the damaging
effects of IOP and may tolerate a pressure up to 25 mmHg. These
factors help the comprehensive ophthalmologist decide how high and
how long a postoperative intraocular pressure spike is tolerable.
Pseudo-pits of the optic nerve are a sign of a pressure-sensitive
optic nerve.
Optic discs in which there is an acquired pit of the optic nerve
are probably damaged more rapidly by pressure elevations than are
optic discs without pits of the optic nerve.
Visual Field Loss and Its Relation to Cataract and Glaucoma Surgery
Visual field defects of a diffuse type are generally
characteristic of patients whose optic nerves are relatively
resistant to the damaging effects of intraocular pressure. Dense paracentral defects, however, are characteristic of patients whose
optic discs are more sensitive to the damaging effects of
intraocular pressure.
Factors affecting the likelihood of visual field
damage
Patients with visual field loss that extends into fixation are
more likely to have their visual acuity damaged by postoperative
pressure elevations than are patients whose field defects spare the
area of fixation. Appropriate preoperative planning, such as
combined or staged surgery to eliminate postoperative pressure
spikes, is essential for this group of patients. In addition,
patients with preoperative visual field defects that split into
fixation may experience a sudden decrease in acuity associated with
an otherwise uncomplicated intraocular surgery. This phenomenon of
wipeout occurs in 1% to 5% of cases. "Wipeout" also
appears to be related to severe postoperative hypotony and is more
common in patients whose postoperative intraocular pressure
measures less than 5 mmHg. This is an entity different from hypotony/maculopathy.
Any surgical procedure causing severe hypotony predisposes to
wipeout; thus, patients with split fixation having cataract
extraction followed later by a filtration procedure are twice as
likely to develop wipeout as patients undergoing a combined
cataract-glaucoma procedure.
Anterior-Segment Tissue Alterations Secondary to Glaucomatous
Disease
The anatomic and
physiologic alterations of glaucomatous eyes are protein
Recognition of these alterations facilitates
treatment of the disease process. Patients who have suffered an
acute-angle closure glaucoma attack with intraocular pressures of
60mmHg may develop significant corneal endothelial damage, posterior synechiae, and iris necrosis. All of these tissue alterations affect
the surgeon's type of cataract surgery. Corneal decomposition after
otherwise uncomplicated cataract extraction is common in patients
having sustained a severe attack of acute angle-closure glaucoma.
Surgeons contemplating cataract extraction in these eyes naturally
desire to avoid as much corneal trauma as possible.
The atonic pupil that follows a severe
angle-closure attack is fixed and dilated. This pupil alteration may
cause the surgeon to choose intraocular lens (IOL) with a larger
optic to prevent glare and monocular diplopia associated with the
larger pupil. Eyes with short axial lengths typically have a very
shallow anterior chamber. This makes it even more difficult for the
surgeon to work, especially when introducing any instrument into the
eye. In addition, eyes with short axial lengths (Less than 22mm)
require different IOL calculation formulas; otherwise, undesirable
postoperative hyperopia occurs. another example relates to patients
with the exfoliation syndrome who have abnormal zonules and an
abnormal capsule, predisposing to rupture.
The iris of glaucoma patients is usually abnormal
Widespread glaucomatous iris abnormalities
include abnormal blood vessels permeability, flaccid iris tone,
rigid or atrophic muscles, and friability. the iris of patients with
exfoliation syndrome is extremely tender and easily torn. Pigment
dispersion, breakdown of the blood-aqueous barrier, and hyphema at
the time of surgery and postoperatively are common in these eyes.
The lens capsule and zonules tend to be more fragile in patients
with glaucoma than in those without glaucoma. The problem is most
severe in those with the most advanced glaucoma who have been
treated most intensively. Surgery is extremely complicated in the
exfoliation syndrome because of zonular dehiscence and loose zonules,
and the cortex is unusually sticky and can be extremely difficult to
aspirate after nuclear removal. The lenses of patients with
long-standing glaucoma and advanced cataracts are often partially
"loose" even though they do not appear frankly dislocated.
The conjunctiva of patients with glaucoma is
often abnormal
Long-term parasympathomimetic drug therapy
produces leaky iris vessels with breakdown of the blood-aqueous
barrier, posterior synechiae, peripheral anterior synechiae, and
rigid miotic pupils. Inability to sufficiently dilate the pupil is a
leading cause of vitreous loss at the time of cataract surgery. The
final outcome of cataract extraction is worsened by preoperative
long-term use of parasympathomimetic drugs because the pupil does
not dilate well, the iris is more likely to bleed when traumatized
breakdown of the blood-aqueous barrier is excessive, and there is an
increased likelihood of vitro-retinal interface problems. The
tissues of patients with glaucoma who have been treated medically
for glaucoma are not as healthy as the tissue of patients who do not
have glaucoma. The conjunctiva undergoes several tissue alterations
due to topical anti-glaucoma therapy. These tissue alterations lead
to higher intra-operative complications and excessive filtration
failure.
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Glaucoma Associates of Texas
10740 N. Central Expressway, Suite 300
Dallas, TX 75231
Office: 214-360-0000
Fax: 214-360-0083
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