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Secondary glaucoma

Article in Clinical and Experimental Optometry February 2000

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 C L I N I C A L
OPTOMETRY
Secondary glaucoma
Anthony JH Hall MD FRACO FRACS
Department of Ophthalmology,
Royal Melbourne Hospital
Accepted for publication: 22 June 2000
Key words: corticosteroid, glaucoma, pigment dispersion, pseudoexfoliation, traumatic glaucoma.
Secondary glaucoma is an important cause
of ocular morbidity in our community,
occurring in around 0.2 per cent of Vic-
torians over the age of 40 years,' and an
even more common cause of glaucoma in
the developing world.' The secondary
glaucomas are a heterogeneous group of
conditions with a wide range of causes and
clinical manifestations requiring a variety
of treatment strategies. This article is not
intended to be a comprehensive review
but an introduction to the clinically im-
portant secondary glaucomas. Treatment
of secondary glaucoma is complicated and
must be individualised for every patient,
and differs markedly according to the
Clinical and Experimental Optometry 83.3 May-June 2000
A N D E X P E R I M E N T A L
Purpose: To review the common causes of secondary glaucoma.
Methods: Review of current literature.
Results: Secondary open and closed angle glaucomas are an important cause of ocular
morbidity and vision loss in our community. Secondary glaucoma occurs with acquired
ocular diseases (pigment dispersion, pseudoexfoliation, intraocular infection,
intraocular inflammation and retinal vascular disease), blunt anterior segment injury,
intraocular surgery (especially corneal grafting and congenital cataract surgery) and
topical corticosteroid use. The medical treatment of secondary glaucoma is different
from that of primary open angle glaucoma and must be tailored for the individual
patient. Surgical treatment of secondary glaucoma carries a higher risk of complica-
tions and a lower rate of success than does surgical treatment of primary open angle
glaucoma.
Conclusions: Secondary glaucoma occurs with a variety of intraocular conditions and
after a variety of intraocular insults. Awareness of patients at high risk should enable
early detection and referral for appropriate management.
(Clin Exp Optom 2000; 83: 3: 190-194)
aetiology of the secondary glaucoma. Gen-
eral guidelines for treatment will be given
After blunt trauma
for each type of secondary glaucoma. After prolonged or intermittent use of
This paper will not review secondary topical, inhaled or systemic steroids
glaucoma as a result of congenital malfor- In aphakic patients and after corneal
mations, that is, those associated with con- grafting
genital cataracts, aniridia a n d o t h e r After an attack of inflammation or infection,
congenital anterior congenital malforma- especially herpes simplex or zoster
tions. I will limit the scope of the paper to In patients who have had congenital
glaucoma associated with acquired ocular cataracts or any other congenital
disorders (Table 1) and especially those anterior segment abnormality
likely to be of clinical relevance to prac-
tising optometrists.
Table 1 . Important conditions in which
secondary glaucoma may be forgotten
190

PATHOLOGY
Different forms of secondary glaucoma
are associated with different types of angle
damage and different final pathways of
raised intra-ocular pressure.3 These
changes can be condensed essentially into
two basic types: secondary open angle
glaucoma and secondary angle closure
glaucoma.
Secondary open angle glaucoma has a
variety of underlying pathological causes.
They can be summarised as follows:
1 . Trabeculitis (inflammatory angle dam-
age) with secondary mechanical block-
age by plasma proteins, trabecular
damage mediated by cytokines released
by inflammatory cells, mechanical
blockage to outflow by inflammatory
cells o r sclerosis of the meshwork
associated with hyaline membrane
formation.
2. Obstruction of the intertrabecular
spaces by cellular material, for exam-
ple, macrophages in phacolytic glau-
coma, blood-filled macrophages in
hyphaema, erythroclastic or ghost cell
glaucoma, invasion by neoplastic cells
etcetera.
3. Obstruction of the outflow system by
abnormal extracellular materials, for
example, pigmentary glaucoma,
pseudoexfoliative glaucoma, silicon oil
glaucoma.
4. Changes in the metabolic activity of the
trabecular meshwork cells, for exam-
ple, steroid induced glaucoma.
5. Increases in episcleral venous pressure,
for example, carotid-cavernous fistula.
Si m i 1arl y, second a r y a n g 1e c 1o su r e
glaucoma has a variety of underlying
pathological causes:
Synechial angle closure caused by
abnormal new vessels, for example,
rubeotic glaucoma.
Synechial angle closure caused by
abnormal epithelial o r fibrous
downgrowth.
Synechial angle closure caused by
inflammatory infiltrate, for example,
post uveitis.
Non-synechial angle closure caused by
abnormal lens/iris diaphram anatomy,
for example, ciliary body swelling or
Clinical and Experimental Optometry 83.3 May-June 2000
detachment, abnormally thickened
lens et cetera.
The underlying final mechanism of
trabecular outflow obstruction is usually
obvious from the clinical situation and the
examination findings.
GLAUCOMA ASSOCIATED WITH
OCULAR DISEASE
Pigmentary glaucoma
Pigmentary glaucoma was initially de-
scribed over 50 years ago as a rare clinical
entity. Since then, pigmentary glaucoma
has become recognised as one of the most
common and important forms of second-
ary open-angle glaucoma. As with other
secondary glaucomas, pigmentary glau-
coma usually affects a much younger
patient population than primary open-
angle glaucoma. It has a special predilec-
tion for myopic males. The defining clini-
cal features of pigmentary glaucoma are
midperipheral iris transillumination de-
fects, Krukenberg spindles (characteristic
pigment deposits on the central corneal
endothelium in a vertical oval distribu-
tion) and a heavily pigmented trabecular
meshwork.
The mechanism of pigment dispersion
appears to be a rubbing between iris
pigment epithelium and packets of lens
zonules caused by a backwards concavity
of the iris diaphragm, possibly associated
with an i n h e r e n t abnormality of the
pigment epithelium. The mechanism of
aqueous outflow obstruction is believed to
involve accumulation of the pigment gran-
ules in the trabecular meshwork, followed
by denudation, collapse, and sclerosis of
the trabecular beams. There is evidence
to suggest that the presence of pigment
granules alone in the trabecular mesh is
not enough to decrease aqueous outflow.
Conventional management includes
standard anti-glaucoma drugs, laser
trabeculoplasty (which is particularly
effective in pigmentary glaucoma) and fil-
tering surgery. Studies performed looking
at anterior chamber morphology follow-
ing laser peripheral iridotomy in patients
with pigmentary glaucoma have demon-
strated flattening of the iris and a decrease
191
Secondary glaucoma Hull
in iris-lens contact while the lens position
remains constant. Future studies may
show a t h e r a p e u t i c benefit of laser
peripheral iridotomy in pigmentary
glaucoma.
PSEUDOEXFOLIATION
Pseudoexfoliation is an important cause
of secondary glaucoma and is covered
in another chapter in this issue of the
journal.
NEOVASCULAR GLAUCOMA
Neovascular (or rubeotic) glaucoma is
characterised by the growth of new vessels
on the iris and particularly in the angle,
and a secondary increase in intraocular
pressure. These new vessels may be obvi-
ous but often they are hard to discern
clinically. There are only a few common
clinically important causes of neovascular
glaucoma. Most neovascular glaucoma
occurs as a complication of either ischae-
mic central retinal vein occlusion or pro-
liferative diabetic retinopathy. Occasion-
ally, neovascular glaucoma develops as a
consequence of ocular ischaemia (oph-
thalmic or internal carotid artery occlu-
sion). Rubeotic glaucoma may uncom-
monly develop following rubeosis caused
by ocular inflammation or ocular tumours
(retinoblastoma o r m e l a n o m a ) . In
rubeosis associated with retinal ischaemia
(that is, diabetes, retinal vein occlusion
o r ophthalmic artery occlusion) the
neovascular stimulus is probably vascular
endothelial growth
In typical acute neovascular glaucoma
the eye is painful and photophobic with a
very high pressure, often in the 50s to 70s.
There is marked conjunctival injection
and corneal oedema. The iris new vessels
are usually visible through the cloudy cor-
nea. After acute treatment and corneal
clearing the angle is visible and charac-
teristically the picture is of a smooth
zipped-up line of iridocorneal adhesion.
Prior to this end stage and prior to final
angle closure, the new vessels may be vis-
ible climbing up from the iris across the
ciliary body and scleral spur to the trabecu-
lar mesh. It has long been taught that any
Secondary glaucoma Hall
vessels crossing the scleral spur onto the
trabecular mesh are ahnormaL7
The differential diagnosis falls into two
stages. The first is the differential of
abnormal-looking iris vessels. The second
is the differential of an acute increase in
IOP with cloudy cornea. With regard to
the first, the list is short: abnormal iris
vessels may be due to true ruheosis (from
any cause hut usually ischaemia), abnor-
mal iris vessels also occur in Fuch's
heterochromic iridocyclitis and pseudoex-
foliation. Abnormally prominent iris ves-
sels can occur with intraocular inflamma-
tion of any cause-but these vessels do not
cross the scleral spur onto the trabecular
meshwork. An acute presentation with
high IOP and cloudy cornea may he due
to rubeotic glaucoma, ordinary acute
angle closure glaucoma, hypertensive
iritis, phacolytic glaucoma or ghost cell
glaucoma.
The treatment is aimed at diagnosing
those eyes that are at risk of rubeotic glau-
coma before rubeosis develops, or as soon
as rubeosis develops, and preventing the
development of full-blown neovascular
glaucoma. All patients with central reti-
nal vein occlusion should be assessed to
determine the degree of ischaemia and
either treated with pan-retinal photoco-
agulation or followed closely to allow early
detection of iris neovascularisation, and
then treated.
Treatment after the development of
neovascular glaucoma, especially if the
angle is entirely closed, is much more dif-
ficult. In this situation, treatment is aimed
at lowering the pressure in the short term
enough to clear the cornea and allow pan-
retinal photocoagulation. After the reti-
nal ischaemia has been addressed, topi-
cal or oral glaucoma treatment may he
successful. If not, glaucoma surgery may
be attempted. Even if the iris neovas-
cularisation has been addressed a n d
treated, there is still a high rate of failure
of conventional glaucoma surgery and
Molteno tubes or cyclodestructive proce-
dures may be required. Surgical manage-
ment of neovascular glaucoma carries a
higher failure rate than surgical manage-
ment of other complicated secondary
glaucomas."
Clinical and Experimental Optometry 83.3 May-June 2000
UVEITIC/INFLAMMATORY
GLAUCOMA
Raised intraocular pressure is a common
and frequently serious complication of all
forms of uveitis. There are several mecha-
nisms at play in uveitic glaucoma." The
inflammatory c e 11s themselves , t h e
cytokines they release, the architectural
changes accompanying uveitis and the
corticosteroid therapy used to treat the
inflammation all can lead to or exacerbate
glaucoma. Inflammatory cells may clog
t h e trabecular mesh o r a n active
trabeculitis may impede outflow. After
prolonged inflammation p e r m a n e n t
changes may lead to irreversible mesh
damage, so-called trabecular sclerosis.
Peripheral anterior synechiae may form
and block outflow or posterior synechia
may cause pupil block and iris bomb6.
Although secondary glaucoma may
complicate any form of uveitis, it is much
more common in and, indeed, almost
characteristic of, several specific uveitic
conditions. The important underlying
uveitis diagnoses with uveitic glaucoma
are: herpetic (simplex and zoster) kerato-
uveitis, Fuchs' heterochromic iridocycli-
tis, juvenile rheumatoid arthritis associ-
ated iridocyclitis, Posner-Schlossman
syndrome, syphilitic uveitis, chorioretinal
toxoplasmosis and sarcoidosis.'"
As there are several mechanisms at play
in uveitic glaucoma, careful examination
is critical to determine the underlying
aetiology of the raised intraocular pres-
sure in each case. It is important to assess
the level of inflammation, the degree of
angle damage o r synechial closure, the
extent of posterior synechia a n d iris
bomb6 and importantly the evidence for
disc damage.
Diagnostic and therapeutic decisions
are guided by careful delineation of the
pathophysiology of each individual case.
The goal of treatment is to minimise per-
manent structural alteration of aqueous
outflow and to prevent damage to the
optic nerve head. Treatment is first and
foremost aimed at effective control of the
inflammation and in the majority of cases
controlling the inflammation alone will
control the pressure. In those cases, where
192
controlling the inflammation alone is not
enough to control the pressure, specific
anti-glaucoma treatment will be needed.
In general, in patients with uveitic glau-
coma, treatments that worsen inflamma-
tion, exacerbate posterior synechia forma-
tion or worsen macular oedema, are best
avoided. This means that prostaglandin
analogues (for example, latanoprost),
miotics and adrenaline are contraindi-
cated. The most commonly used topical
treatments for uveitis glaucoma are beta
blockers, alpha agonists (hut not adrena-
line) and topical carbonic anhydrase in-
hibitors. Oral carbonic anhydrase inhihi-
tors a r e used m o r e often in uveitic
glaucoma than in general glaucoma
practice because patients with uveitic glau-
coma tend to be younger and are worse
candidates for glaucoma surgery.
Those patients who fail medical treat-
ment for their uveitic glaucoma may be
candidates for surgical therapy. In these
patients, wherever possible, surgery
should he delayed until the inflammation
has been quiet for at least three months.
Oral carbonic anhydrase inhibitors may
he required to tide the patients over for
that period. Even with adequate control
of inflammation, surgery in these eyes is
difficult and conventional drainage sur-
gery is at increased risk of failure. In some
cases of uveitic glaucoma, Molteno tubes
may he the best surgical option." Laser
traheculoplasty carries an increased risk
of causing anterior synechiae and is con-
traindicated in uveitic glaucoma.
POST-TRAUMATIC GLAUCOMA
The incidence of significant angle dam-
age with rim microhyphaemas may he as
high as 20 per cent.12 The incidence of
secondary glaucoma after anterior seg-
ment injury is increased if there are other
signs of significant injury, such as trau-
matic cataract (especially cataract severe
enough to require surgerylg),iris damage,
angle recession of greater than 180 degrees
o r posterior dislocation of the lens.14Even
in these cases at high risk, secondary glau-
coma may not develop for many years after
the injury and patients at risk should be
followed life-long to detect glaucoma as

early as possible. The lifetime incidence
of glaucoma may be as high as eight per
cent in those with significant angle
damage.I5
In general, treatment of angle recession
glaucoma is best achieved with modalities
that reduce aqueous production (for ex-
ample, beta blockers) rather than improve
trabecular outflow (miotics or argon laser
trabeculoplasty) . The long-term success of
drainage surgery for angle recession glau-
coma is not as high as for uncomplicated
glaucoma.16 It may be that in medically
uncontrolled post-traumatic angle reces-
sion glaucoma, trabeculectomy with anti-
metabolite therapy is the most effective
primary surgical procedure.I7
GLAUCOMA ASSOCIATED WITH
OCULAR SURGERY
Glaucoma used to be a common compli-
cation of cataract surgery but with mod-
ern techniques it has become much less
common. There is a high incidence of
glaucoma after intracapsular cataract sur-
gery but the incidence is much lower after
modern phakoemulsification style cata-
ract surgery. In fact many authors have
suggested that on average intra-ocular
pressure falls (by up to 3 mmHg'') after
routine phakoemulsification surgery in
normal patients and those with ocular
hypertension and even in those with glau-
coma.Ig There are some forms of cataract
surgery that especially predispose the
patients to post-operative glaucoma.
Patients with anterior chamber lenses,
patients having had intracapsular cataract
extraction (and especially with vitreous in
the anterior c h a m b e r ) , patients who
develop epithelial downgrowth, and espe-
cially children who have cataract surgery
are all prone to post-operative glaucoma.
Aphakic patients and especially aphakic
o r pseudophakic children should be
followed in the long term for glaucoma.
Acute glaucoma is very common with
retained lens fragments after phakoemuls-
ification surgery ( u p to 36 per cent of
patients), but is usually effectively treated
with vitrectomy."
Treatment of post-cataract glaucoma
depends on the cause. As in the treatment
Clinical and Experimental Optometry 83.3 May-June 2000
of uveitic glaucoma, in many cases pros-
taglandin analogues, miotics and argon
laser trabeculoplasty may be contraindi-
cated. Patients with post-operative glau-
coma are at high risk of failure for con-
ventional drainage surgery a n d may
require adjunctive anti-metabolites.
Glaucoma after penetrating kerato-
plasty is a significant clinical problem. It
may occur early after corneal grafting and
the incidence of early glaucoma may be
as high as 20 per cent in those patients
having combined corneal grafting and
other intraocular surgery.?' The long-term
incidence of glaucoma after even uncom-
plicated penetrating keratoplasty may be
as high as 21 per cent."' Post-corneal graft
glaucoma is more common in patients
who a r e also aphakic o r have had a
vitrectomy or complicated anterior seg-
ment reconstruction along with their
corneal graft.2' There are a number of rea-
sons for glaucoma after even uncompli-
cated penetrating keratoplasty. There may
be underlying angle damage as part of the
reason that the cornea failed in the first
place; or there may be angle damage from
the graft surgery or some accompanying
surgery, the post-operative inflammation
or the use of post-operative steroids; and
all these may contribute to the pressure
rise. There is evidence that a reduction in
the use of post-operative steroids signifi-
cantly decreases the incidence of high IOP
post grafting, but unfortunately a reduc-
tion in the use of post-operative steroids
also increases the incidence of graft
rejection.24
It is critically important to follow for
glaucoma for the rest of their lives, all pa-
tients who have had penetrating kerato-
plasty. In the medical treatment of post-
corneal graft glaucoma any drugs that may
initiate or exacerbate rejection (for exam-
ple, prostaglandin analogues) or lead to
endothelial damage (for example, topical
carbonic anhydrase inhibitors) should be
avoided. No surgical procedure is ideal for
the management of medically uncon-
trolled post-corneal graft glaucoma and all
procedures are associated with late failure,
hypotony or visual loss in a proportion of
patients.25
The incidence of glaucoma after com-
193
Secondary glaucoma Hall
plicated retinal detachment repair and
silicon oil is as high as 18.5 per cent.2ti
Silicon oil may lead to permanent angle
damage and many of these patients re-
quire long-term glaucoma management.
GLAUCOMA ASSOCIATED WITH
SYSTEMIC DISEASE OR DRUGS
Steroid-induced glaucoma
There is much debate about the incidence
of steroid induced-glaucoma, but it seems
clear that the incidence of a steroid-
induced pressure rise is higher in patients
with glaucoma or a family history of glau-
coma.2i In the normal population, even
with short-term exposure, the incidence
of some pressure response may be as high
as 58 per cent. Around one-third of peo-
ple will have a moderate or marked in-
crease in intraocular pressure after expo-
sure to topical steroids.2xT h e r e are
important differences in the incidence of
steroid-induced pressure rise and glau-
coma between different topical steroids,
but even low potency topical steroids can
cause pressure rises." Systemic or inhaled
steroids are also implicated in producing
a rise in IOP, but not as frequently or as
reliably as topical steroids. The exact
aetiology of steroid-induced glaucoma
remains unclear, but it is possible to
demonstrate an in vitro change in the
metabolic a n d phagocytic activity of
trabecular mesh cells in the presence of
steroids. The onset of steroid-induced
pressure rise is variable but the pressure
rise generally resolves within weeks after
steroid withdrawal.'" In patients in whom
it is not possible to stop the topical ster-
oids, medical treatment of increased IOP
may be necessary.
There are a huge number of other
causes of secondary glaucoma that, while
important, are less common and shall not
be discussed in detail. These include pri-
mary and secondary malignant disease,"
raised episcleral venous pressure, a
number of forms of lens-induced glau-
coma and malignant glaucoma.
 Secondary glaucoma Hall
CONCLUSION
Secondary glaucoma is an i m p o r t a n t clini-
cal and public h e a l t h problem. It t e n d s
t o affect y o u n g e r patients t h a n primary
g l a u c o m a and early d e t e c t i o n is impor-
t a n t . Practising o p t o m e t r i s t s s h o u l d be
aware o f t h e patients w h o are a t risk of
secondary glaucoma a n d should screen
appropriately.
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