Download Angle recession glaucoma

Focus on glaucoma
Marc B. Taub OD and Brian Gardner OD
Angle recession glaucoma
Case reports and literature review
O
ur understanding and management of glaucoma has
progressed immensely in the past few decades. Although
the true aetiology of glaucoma remains elusive, the
treatments and diagnostics have made leaps and bounds.
The introduction of the prostaglandin
analogues have made unmanageable cases
manageable, and have allowed us to
successfully avoid surgical intervention in
more of our patients. The Ocular
Hypertensive Treatment Study (OHTS)
identified multiple risk factors for
developing glaucoma, including decreased
central corneal thickness. Pachymetry has
emerged as the new standard of care in the
management of glaucoma patients. The
introduction of diagnostic equipment such
as the GDx nerve fibre analyser, optical
coherence tomography (OCT), and the
Heidelberg Retinal Tomograph II (HRT II)
have proven to be useful adjuncts.
The following cases describe the
evaluation, diagnosis and management of
angle recession glaucoma. Each patient
presented with unique clinical findings
and was successfully managed with various
therapies.
Case history one
A 45-year old Hispanic female was referred
by her optometrist for asymmetrical
cupping of the optic nerves, increased IOP,
and a perimacular scar in her right eye.
Her ocular history was positive for a
corneal abrasion in her left eye at nine
years of age and a car accident 11 years
ago, which resulted in the need for
reconstructive surgery to the right side of
her face and periocular area. The patient
did not report any ocular complaints. Her
past medical history was positive for
intermittent tension headaches. She took
no medications and had no allergies to
food or drugs.
Examination
Best corrected distance visual acuities were
6/9 RE and 6/6 LE. Her left pupil was
round and reactive, while her right
pupil was reactive with corectopia
(a displacement of the pupil). An afferent
pupillary defect was observed in her right
eye. Colour vision was normal with slower
responses in her right eye. Extraocular
motility was full and smooth with normal
confrontation fields in both eyes.
Anterior segment evaluation revealed
mild anterior and posterior blepharitis in
both eyes, with trace pigmentation of the
endothelium in the left eye. Corectopia of
the iris in the right eye was observed.
Goldmann applanation tonometry
revealed IOPs of 25mmHg RE and
28 | February 27 | 2004 OT
16mmHg LE. Gonioscopy showed ciliary
body in both eyes of 360˚ with angle
recession of the inferior angle in the right
eye from five to seven o’clock.
The optic nerves were asymmetric with
cup to disc ratios of 0.55/0.60 (H/V) with
superior temporal thinning in the right eye
and 0.35/0.35 in the left. Also noted was
pallor of the optic nerve head in the right
eye with a posterior vitreous detachment
(PVD). The macular area in the right eye
exhibited drusen and an epiretinal
membrane. A perimacular scar secondary
to a longstanding choroidal rupture was
also seen in the right eye. 24-2 SITA Fast
Humphrey visual field of the right eye
(Figure 1) indicated a nasal step with
other isolated missed points. There were
several non-specific missed points in the
left eye, which were noted to be evaluated
for repeatability on the next visit.
HRT II (Figures 2 and 3) showed
asymmetry of the cup/disc ratio, but were
within normal limits per Moorfield’s
regression analysis. GDx results (Figure 4)
showed significant asymmetry of the nerve
fibre layers between the two eyes.
Discussion
The patient was diagnosed with angle
recession glaucoma and treatment was
initiated with Alphagan P twice a day in
the right eye. The patient was instructed to
return for a follow-up after two weeks for
an IOP check and to repeat visual fields.
Also diagnosed were corectopia, PVD,
optic atrophy, and longstanding choroidal
rupture in the right eye – all presumably
secondary to trauma. Upon follow-up,
IOPs were 18mmHg RE and 17mmHg LE,
which represented a 28% decrease in the
right eye. Serial visual fields were not
performed at this visit due to patient time
constraints.
An interesting point concerning this
case was the comparison of the GDx and
HRT II results. Although asymmetry of the
cup/disc ratio was present, both eyes still
fell within normal limits on the HRT II.
GDx results showed general nerve tissue
loss in the right eye, consistent with the
optic nerve head atrophy and
glaucomatous axonal loss. Inter-eye
symmetry fell outside of normal limits.
The left eye showed normal range of nerve
fibre layer thickness values surrounding
the optic nerve, as shown by the TSNIT
(Temporal, Superior, Nasal, Inferior,
Temporal) graph and chart. With this
added information, the missed visual field
points in the left eye became questionable.
The contradiction of the two
instruments exemplifies why practitioners
must interpret test results for themselves,
rather than simply rely on the normative
database of each particular diagnostic
software analysis.
Case history two
A 54-year old black male presented for a
routine eye examination with a positive
history of primary open angle glaucoma.
He had discontinued his drops three years
earlier. His complaints included itching,
tearing, burning, flashing lights, and
floating spots in both eyes. His last eye
examination was three and a half years
ago. His ocular history included trauma in
the right eye as a child. His systemic
history was positive for arthritis and
post-surgical prostate cancer.
Examination
Best corrected visual acuities at distance
and near were 6/6 in both eyes. Pupils
were equal, round and reactive to light
with no afferent defect. Colour vision and
confrontation fields were normal.
Extraocular muscles were full and smooth,
and blood pressure was 136/82.
Anterior segment revealed a corneal
scar in the right eye, along with
pinguecula, papillae and capped
meibomian glands in both eyes.
Goldmann applanation tonometry
revealed IOPs of 26mmHg RE and
17mmHg LE. The optic nerves showed
asymmetry, RE>LE with cup to disc ratios
of 0.6/0.75 and 0.25/0.25 respectively.
Gonioscopy revealed recession of the angle
nasally in the right eye. SITA Std 24-2 SITA
Standard Humphrey visual fields (Figures
5 and 6) indicated possible superior
arcuate scotoma in both eyes. Fields were
repeated two months later and indicated
less extensive defects in both eyes. GDx
(Figure 7) revealed normal nerve fibre in
the left eye with significant defects in the
right eye.
Discussion
Treatment was initiated with Lumigan
once a day at night in the right eye only.
Goldmann applanation tonometry was
taken at a two-month follow-up and
showed IOPs of 19mmHg RE and
20mmHg LE. This represented a 27.6%
reduction in the right eye. The patient was
advised to continue to return for follow-up
every three months.
At first glance, the visual field did not
reveal a large difference between the eyes.
Focus on glaucoma
Figure 1
Figure 2
Right visual field shows a nasal step and
other isolated missed points
Right HRT II shows a larger cup/disc ratio
but within normal database limits
Figure 3
Figure 4
Left HRT II shows a smaller cup/disc ratio
within normal database limits
Right GDx (left side) shows diffuse nerve fibre layer loss with
abnormal TSNIT values. Left GDx (right side) shows normal nerve
fibre layer thickness with normal TSNIT values
29 | February 27 | 2004 OT
Focus on glaucoma
Marc B. Taub OD and Brian Gardner OD
Figures 5 and 6 Visual fields show a possible arcuate scotoma with GHT outside of normal limits in both eyes
When the GDx was brought into the mix, the nerve fibre layer
defect in the right eye jumped off the page. The visual field defect
in the left eye was believed to be an artifact because a nerve fibre
layer defect was not present on the GDx. Both eyes were noted for
close monitoring in the future with continued follow-ups.
When comparing the first and second visual fields, it must be
kept in mind that there was most likely a learning curve. The
glaucomatous defects did not resolve with treatment – the patient
worked out how to take the test. One bad field does not represent
glaucoma; several must be performed to truly diagnose this
disease.
Background
Approximately 1.8-5.6 per thousand Americans over the age of 40
suffer ocular injuries. The annual incidence of ocular trauma
requiring in-patient hospital treatment is 13.2 per 100,000 per
year. Trauma to the eye, face and head is generally due to several
activities. With regard to age, ocular trauma occurs in a bimodal
distribution. The maximal risk occurs in young children and
adults over the age of 70. The causes for the trauma also differ
among these age groups. Falling, leading to secondary open globe
trauma, is the most common cause among the over-70
population, while assault, car accidents and occupational hazards
are more common in young adults. Children suffer trauma due to
organised sports, domestic accidents, and from simply playing1.
The first description of angle recession was by Collins in 1892.
He described a split between the circular and longitudinal muscle
fibres in two patients2. Wolf and Zimmerman reviewed 300
traumatised eyes in 1962, pointing out the clinical association
among trauma, angle recession and glaucoma. They reported the
presence of six patients who suffered from unilateral glaucoma
and who had a history of blunt trauma with angle recession3.
Figure 7
GDx indicates a nerve fibre layer asymmetry in the right eye
(right side) versus the left eye (left side). TSNIT values are abnormal in
the right eye and normal in the left
30 | February 27 | 2004 OT
Aetiology
When a blunt object hits the cornea, a pressure wave is formed.
This wave causes the iris to strike the anterior surface of the lens,
closing the iris-lens diaphragm. Since the fluid is not able to
Focus on glaucoma
travel posteriorly, the only option is for the
fluid to move laterally into the anterior
chamber angle. This can cause a breakage,
or cleavage, between the circular and
longitudinal fibres of the ciliary body.
This shockwave also causes damage to
the trabecular meshwork, producing
micro-tears. Scarring of the trabeculum
results from these tears. While the scars
cannot be seen via gonioscopy, they have
been seen on histopathological
examination4.
Other mechanisms are also responsible
for decreasing outflow. Descemet’s
membrane may be stimulated to grow over
the trabeculum due to the trauma4,5.
Furthermore, the injury to the ciliary body
may lessen the ability of the longitudinal
ciliary body to apply tension to the
trabeculum4.
Epidemiology
It is unknown why some patients with
angle recession develop glaucoma and
others do not. Even the incidence of angle
recession following blunt trauma/
contusion injuries varies from 20% to
100%. Studies have shown that between
0-20% of patients with angle recession go
on to develop glaucoma6-12. The main risk
factor for the development of glaucoma in
individuals with angle recession is the
degree of recession. In studies, most
patients who ultimately develop glaucoma
had 240-360˚ of recession7. Those with less
than 180˚ have a very low risk to develop
glaucomatous changes11.
The lifetime risk of developing
primary open angle glaucoma in the
non-traumatised fellow eye may be as high
as 50%. A greater increase of IOP in the
fellow eye with steroid provocative testing
has been found6,7. One thing to keep in
mind is that even though the patient in
your chair has angle recession glaucoma in
one eye, it does not preclude them from
having POAG in both eyes. It is possible
that the injury merely accelerated the
glaucomatous changes in the traumatised
eye7.
Clinical findings
As we all know, a good examination
begins with a great case history. In some
cases, the trauma may be so long ago,
or not in the forefront of the patient’s
thoughts, that they forget about it. One
thing to keep in the back of your mind
when you have a patient who denies a
traumatic event is the emotional aspect.
They may have been, or are currently in,
an abusive relationship or the trauma may
be part of a bigger picture of which you
are unaware.
In addition to trauma to the angle,
other parts of the eye may also reveal
damage. Iris injuries include iris sphincter
tears, atrophy, iridogenesis, heterochromia
iridis and mydriasis. The cornea can show
signs of insult in the form of scars and
pigment on the endothelium. The lens
may form a cataract, most likely in the
anterior subcapsule, Vossius’ ring,
dislocation and phacodonesis7,14.
Retinal detachments or tears can also
occur13.
Performing gonioscopy is the gold
standard for evaluation of the angle.
Whether you use a one, three or
four-mirror lens makes no difference.
Whichever you choose, perform this
procedure on ‘normal’ patients to hone
your skills. The more you do, the better
you will become at picking up the subtle
differences. As is the case when looking at
a questionable optic nerve head, look at
the ‘normal’ eye angle first to better judge
the variations.
Depending on the force of the injury,
the view through a gonio-lens may vary.
Minor injuries may present as torn iris
processes or small tufts of uveal tissue
observed on the iris root, or on the
trabecular meshwork just above the scleral
spur.
Physical separation of the ciliary body
at the apex of the angle is present in more
severe cases. In these cases, the grey
portion of the ciliary body appears
broadened and the scleral spur is white
and prominent13,14. Small peripheral
anterior areas of synechiae can appear at
the lateral limits of the angle recession and
may extend into the peripheral areas of the
recession14.
A different clinical picture will be
present on gonioscopy years after the
initial assault. A marked, wedge-like
contour of the ciliary muscle will be
present due to the atrophying of inner
circular muscles which were separated
from the longitudinal fibres. The
trabecular meshwork undergoes
degeneration leading to atrophy, fibrosis
and hyalinization. Peripheral anterior
synechiae may also be present13.
Differential diagnosis
One angle anomaly which can be
confused with angle recession is
cyclodialysis. In contrast to the changes
found in angle recession, in which
cleavage is between the circular and
longitudinal fibres of the ciliary body, the
separation in cyclodialysis occurs between
the longitudinal muscle fibres of the ciliary
body and the sclera. Clinically, there will
be an area of white posterior to the scleral
spur. Iridodialysis, trabecular tears and
other abnormalities secondary to trauma
must be ruled out14.
Other forms of unilateral or
asymmetrical glaucoma must be
investigated as well. That list includes
pigmentary dispersion and
pseudoexfoliative syndromes, uveitic or
inflammatory glaucoma, lens induced
pressure changes, tumours of the iris or
ciliary body, and iris or angle
neovascularisation13. These various types of
glaucoma will be ruled out during the
examination and case history, which
includes a full medical and ocular
history14.
Treatment
Because glaucoma secondary to angle
recession can occur up to 50 years after the
initial insult, patients must be monitored
at least yearly. Gonioscopy should be
considered for all patients presenting with
history of ocular trauma regardless of
intraocular pressure. If greater than 180˚
of angle recession is present, closer
monitoring may be warranted. The
standard of treatment for angle recession
glaucoma is similar to that of primary
open angle glaucoma.
The first-line of treatment involves
topical medications which decrease
aqueous formation, such as beta-blockers,
carbonic anhydrase inhibitors and alpha
2-agonists. Prostaglandin analogues, such
as Xalatan, Lumigan and Travatan, which
increase uveoscleral output, may prove
useful13,14.
Surgical management can be quite
challenging in these cases. Argon laser
trabeculoplasty (ALT) usually fails to lower
IOP in this population. Traditional
trabeculectomy has a lower success rate in
this group. These patients require more
post-operative glaucoma medications,
develop more bleb fibrosis and have less
of a decrease in IOP versus primary open
angle glaucoma patients. The use of
mitomycin-C or 5-florouracil and other
metabolites appear to increase the success
rate of this procedure. While filtering
implants have shown some success, they
too are prone to failure14.
Conclusion
Despite the incidence of ocular trauma,
very few patients will go on to develop
angle recession glaucoma. Even with this
evidence, patients who have recessed
angles require close monitoring of not
only the traumatised angle but also the
fellow eye. Determining if and what type
of glaucoma is present relies solely on the
abilities of the practitioner. In POAG and
NTG, making a diagnosis can be
straightforward at times, or very
challenging in cases where true
glaucomatous damage is questionable.
Secondary open angle glaucomas can
mimic POAG, but careful history and
evaluation of the anterior segment using
biomicroscopy and gonioscopy will help
to determine the true aetiology and type
of glaucoma present.
With your care and hard work, your
patients can continue to live their lives
seeing all the world has to offer.
References
For a full set of references, email
[email protected]
About the authors
Dr Marc B. Taub is a paediatric resident
at Nova Southeastern University in
Ft. Lauderdale, Florida. Dr Brian Gardner
is a primary care resident also at Nova
Southeastern University.
31 | February 27 | 2004 OT