Intraocular Pressure Changes after Treatment for Graves’ Orbitopathy

Intraocular Pressure Changes after
Treatment for Graves’ Orbitopathy
Helen V. Danesh-Meyer, FRACO,1,2 Peter J. Savino, MD,1 Vincent Deramo, MD,1 Robert C. Sergott, MD,1
Andrew F. Smith, PhD3
Objective: To evaluate the change in intraocular pressure (IOP) in subjects with Graves’ orbitopathy (GO)
after orbital decompression, strabismus surgery, and orbital radiation.
Design: Retrospective case review.
Methods: The charts of 172 consecutive subjects from the Neuro-ophthalmology Service at Wills Eye
Hospital (Philadelphia, PA) with GO who underwent either orbital decompression, strabismus surgery, or orbital
radiation between 1994 and 1999 were analyzed. Subject age, gender, diagnosis of glaucoma in either eye, use
of systemic steroids or topical glaucoma medications, procedure performed, and the preoperative and postoperative IOP (in primary position and upgaze) were evaluated.
Results: Of 116 eyes that underwent orbital decompression, the mean preoperative IOP was 21.6 ⫾ 4.6
mmHg (standard deviation) in primary position and 27.9 ⫾ 6.8 mmHg in upgaze. The postoperative IOP was 17.5
mmHg ⫾ 3.0 mmHg in primary position and 20.1 ⫾ 4.7 mmHg in upgaze, a decrease in IOP of 18.9% in primary
position and 27.9% in upgaze (P ⬍ 0.001). Subjects taking glaucoma medication or who had IOP greater than
21 mmHg demonstrated a significantly (P ⬍ 0.001) greater reduction in IOP postoperatively. The mean preoperative IOP in the 32 subjects who had strabismus surgery was 18.5 ⫾ 2.8 mmHg (primary position), and 24.7 ⫾
4.3 mmHg (upgaze). Postoperative IOP was 16.1 mmHg (primary position) and 16.9 mmHg (upgaze), a decrease
of 2.4 mmHg (13.3%, P ⬍ 0.01 in primary position) and 7.8 mmHg (31.2%, P ⬍ 0.01 in upgaze). There was no
statistically significant reduction in IOP after orbital radiation.
Conclusions: In the selected subgroup of subjects with GO who required intervention, orbital decompression and strabismus surgery resulted in a significant reduction in IOP in the early postoperative period, especially
in subjects with preoperative IOP greater than 21 mmHg. Ophthalmology 2001;108:145–150 © 2001 by the
American Academy of Ophthalmology.
Thyroid disease may cause multiple ophthalmic problems,
including proptosis, diplopia, soft tissue and ocular surface
changes, and optic neuropathy. Elevated intraocular pressure (IOP) is one of the less commonly discussed problems
directly associated with Graves’ orbitopathy (GO). The
initial description of increased IOP in subjects with GO
appeared as early as 1897.1 The prevalence of ocular hypertension in subjects with GO is estimated to be between
5% and 24%.2–5
There are several theories on the possible causes of this
increased IOP in GO: increased episcleral venous pressure
Originally received: May 2, 2000.
Accepted: August 16, 2000.
Manuscript no. 200266.
1
Neuro-ophthalmology Service, Wills Eye Hospital, Thomas Jefferson
Medical College, Philadelphia, Pennsylvania.
2
Discipline of Ophthalmology, University of Auckland, Auckland, New
Zealand.
3
Medical Economics and Epidemiology Unit, Retina Service, Wills Eye
Hospital, Thomas Jefferson Medical College, Philadelphia, Pennsylvania.
Dr Deramo is supported by Heed Ophthalmic Foundation, Cleveland,
Ohio, and Ronald G. Michels Fellowship, Riderwood, Maryland.
Dr Deramo’s present address is Retina Service, Durham Hospital, Duke
University, Durham, North Carolina.
Reprint requests to H. V. Danesh-Meyer, FRACO, Neuro-ophthalmology
Service, Wills Eye Hospital, 900 Walnut Street, Philadelphia PA 19107.
© 2001 by the American Academy of Ophthalmology
Published by Elsevier Science Inc.
resulting from orbital congestion and venous outflow obstruction,6,7 increased resistance to trabecular outflow,3 restriction and compression of the globe by fibrotic and enlarged rectus muscles,10 a genetically linked predisposition
to glaucoma,8 or increased mucopolysaccharide deposition
in the trabecular meshwork.3,9,10
The purpose of this study was to assess the contribution
of orbital congestion and the tethering effect of fibrotic
extraocular muscles to IOP in subjects with GO by investigating the change in IOP in subjects who underwent orbital decompression (which predominantly relieves orbital
congestion), extraocular muscle surgery (which relieves restriction of fibrotic muscles), or orbital radiation therapy
(which decreases orbital inflammation).
Methods and Materials
The clinical charts of all subjects with GO examined in the
Neuro-ophthalmology Service at Wills Eye Hospital from January
1, 1994 to December 31, 1998, who underwent either orbital
decompression, extraocular muscle surgery, or orbital radiation
were retrospectively reviewed. Subjects were included in the study
if they had (1) undergone either orbital decompression, strabismus
surgery, or orbital radiation; (2) preoperative IOP measurements
within 2 weeks of surgery or the start of orbital radiation treatment;
and (3) IOP measurements within 2 to 6 weeks postoperatively for
ISSN 0161-6420/00/$–see front matter
PII S0161-6420(00)00477-2
145
Ophthalmology Volume 108, Number 1, January 2001
those who had orbital decompression or strabismus surgery or
between 6 and 12 weeks from the end of radiation treatment.
Subjects were excluded if there were changes to their medications
that could influence IOP (glaucoma medication and oral steroids)
or if there were incomplete preoperative or postoperative data in
the medical records.
Information that was collected from the medical record included subject age, gender, diagnosis of glaucoma in either eye,
use of systemic steroids or topical glaucoma medications, procedure
performed, and the preoperative and postoperative IOP. In all subjects, the IOP was recorded in the primary position and in upgaze.
All subjects who underwent orbital decompression had two
wall (medial and inferior) orbital decompression with an endonasal
approach to the medial wall. Extraocular muscle surgery consisted
of unilateral or bilateral inferior rectus muscle recession at times
combined with medial rectus muscle recessions. Strabismus surgery used adjustable suture technique in all inferior rectus muscle
surgery. Subjects who had orbital radiation had received a dose of
2000 cGy delivered in 10 200-cGy daily fractions.
Statistical Methods
Data were collected and entered into a computerized statistical
software package (SPSS Version 6.1) (SPSS Inc, Chicago, IL) in
a standard fashion. Analysis of the data consisted of deriving the
descriptive statistics, calculating the means, and tests for statistical
significance, including two-tailed Student’s t tests and the analysis
of variance, which measure differences in IOP readings between
the three intervention groups and between preoperative and postoperative IOP levels. Throughout, P value for significance was set
at 0.05.
Results
The charts of 172 subjects with GO treated with orbital decompression, strabismus surgery, or orbital radiation were reviewed;
132 subjects met the inclusion criteria, leaving 204 eyes for analysis. One hundred sixteen eyes (80 subjects) underwent orbital
decompression, 32 eyes (24 subjects) underwent strabismus surgery, and 56 eyes (28 subjects) underwent orbital radiation. Forty
subjects were excluded. Thirty subjects had inadequate follow-up
information, and 10 were excluded because oral steroids were
begun between the preoperative and postoperative visits. The
average age for the entire group was 50.5 years (range, 27–76
years). Most subjects (60%) were women.
Fifty-six subjects had a diagnosis of glaucoma and were taking
topical glaucoma medications at the time of referral to the Neuroophthalmology Service. Table 1 summarizes the demographic data
for each of the three groups.
Orbital Decompression
For all subjects who underwent orbital decompression, the mean
preoperative IOP was 21.6 ⫾ 4.6 mmHg (standard deviation) in
primary position and 27.9 ⫾ 6.8 mmHg in upgaze (Table 2). The
mean postoperative IOP was 17.5 mmHg ⫾ 3.0 mmHg in primary
position and 20.1 ⫾ 4.7 mmHg in upgaze. This was a mean
decrease in IOP postoperatively of 18.9% in primary position and
27.9% in upgaze. (P ⬍ 0.001)
The change in IOP after orbital decompression surgery was
further analyzed according to indication for surgery (Table 3) and
whether subjects were taking glaucoma medications (Table 4). The
indication for decompressive surgery was optic neuropathy in 80
eyes and proptosis in 36 eyes. Subjects with optic neuropathy
146
Table 1. Demographic Data (Number of Eyes ⫽ 204)
Characteristic
Decompression Strabismus Radiation
n
Age, mean (SD)
Female, n (%)
Indications for surgery, n (%)
Diplopia
Proptosis
Optic neuropathy
Inflammatory disease
On glaucoma medications,
n (%)
116
49.0 (10.6)
84 (72)
NA
36 (31)
80 (69)
NA
35 (30)
32
56
51.3 (9.4) 53.5 (11.2)
22 (69)
41 (74)
100
NA
NA
NA
13 (41)
NA
NA
38 (67)
18 (32.2)
8 (14)
SD ⫽ standard deviation.
showed a 21.6% (5.0 mmHg, P ⬍ 0.01) decrease in their IOP
postoperatively in primary position and 30.7% (9.2 mmHg, P ⬍
0.01) in upgaze. The decrease in IOP in the proptosis group was
9.5% (1.7 mmHg, P ⬍ 0.01). Thirty-five eyes were receiving
glaucoma medication; 19 were taking one topical antiglaucoma
agent, and 16 were taking two agents. Subjects who were taking
glaucoma medication had a significant decrease of 27.4% (7.1
mmHg, P ⬍ 0.001) in IOP postoperatively in primary position and
30% (9.1 mmHg, P ⬍ 0.001) in upgaze. Those who underwent orbital
decompression who were not on glaucoma medications had a smaller
decrease in IOP postoperatively of 13.9% (2.8 mmHg, P ⬍ 0.001) in
primary position and 27.2% (7.3 mmHg, P ⬍ 0.001) in upgaze.
Subjects (n ⫽ 51) who had preoperative IOP values of less than
21 mmHg (mean, 17.3 mmHg) had a decrease in IOP of 6.9% (1.2
mmHg, P ⬍ 0.01) postoperatively. Subjects with a preoperative
IOP greater than 21 mmHg (mean, 24.9 mmHg) experienced a
24.9% (6.2 mmHg, P ⬍ 0.01) decrease in their IOP postoperatively (Table 5).
Strabismus Surgery
Thirty-two eyes underwent strabismus surgery: 21 had inferior
rectus recessions alone and 11 had inferior and medial rectus
recessions simultaneously. The mean preoperative IOP in primary
position was 18.5 ⫾ 2.8 mmHg, and 24.7 ⫾ 4.3 mmHg in upgaze
(Table 2). Postoperative IOP in primary position was 16.1 mmHg
and 16.9 mmHg in upgaze. This is a decrease of 2.4 mmHg
(13.3%, P ⬍ 0.01) in primary position and 7.8 mmHg (31.2%, P ⬍
Table 2. Mean Intraocular Pressure Readings (mmHg)
Characteristic
Preop IOP, mean (SD)
Primary position
Upgaze
Postop IOP, mean (SD)
Primary position
Upgaze
Mean difference, (SD)
Primary position
Upgaze
% Decrease
Primary position
(P value)
Upgaze
(P value)
Decompression
Strabismus
Radiation
21.6 (4.6)
27.9 (6.8)
18.5 (2.8)
24.7 (4.3)
19.4 (4.5)
26.6 (9.3)
17.5 (3.0)
20.1 (4.7)
16.1 (2.8)
16.9 (3.7)
18.4 (5.2)
24.2 (7.1)
⫺4.1 (3.9)
⫺7.8 (5.8)
⫺2.4 (2.9)
⫺7.8 (4.5)
⫺1.0 (5.0)
⫺2.4 (5.8)
18.9%
(P ⬍ 0.001)
27.9%
(P ⬍ 0.001)
13.3%
(P ⬍ 0.01)
31.2%
(P ⬍ 0.01)
5.1%
(P ⫽ 0.35)
9.0%
(P ⫽ 0.17)
IOP ⫽ intraocular pressure; SD ⫽ standard deviation.
Danesh-Meyer et al. 䡠 IOP Changes after Graves’ Orbitopathy
Table 3. Change in Intraocular Pressure After Orbital Decompression Based on Indication for Intervention
Indication for Intervention
Optic neuropathy (n ⫽ 80)
Primary position (SD)
Upgaze position (SD)
Proptosis (n ⫽ 36)
Primary position (SD)
Upgaze position (SD)
Intraocular
Pressure
Before
Intraocular
Pressure
After
Drop in
Intraocular
Pressure
% Decrease in
Intraocular
Pressure
P Value
22.9 (4.1)
30.1 (5.9)
17.9 (3.0)
20.9 (4.8)
5.0 (3.8)
9.2 (5.8)
21.6%
30.7%
⬍0.01
⬍0.01
18.8 (4.7)
23.3 (6.5)
17.1 (2.9)
18.6 (4.5)
1.7 (3.7)
4.7 (4.6)
9.5%
20.1%
⬍0.01
⬍0.01
SD ⫽ standard deviation.
0.01) in upgaze (P ⬍ 0.0001). There was no statistical difference
in IOP in subjects who underwent inferior rectus recession alone
compared with combined inferior and medial rectus recession.
Orbital Radiation
Twenty-eight subjects who underwent orbital radiation had treatment to both eyes. Sixty-eight percent had orbital radiation for
optic neuropathy and 32% for acute orbital inflammation (Table 1).
The mean pretreatment IOP was 19.4 ⫾ 4.5 mmHg in primary
position and 26.6 ⫾ 9.3 mmHg in upgaze. The mean posttreatment
value at 6- to 12-week follow-up was 18.4 ⫾ 5.2 mmHg, in
primary position and 24.2 ⫾ 7.1 mmHg in upgaze, the mean
decrease in IOP being 1 mmHg (5%, P ⫽ 0.35), in primary
position and 2.4 mmHg (9%, P ⫽ 0.17) in upgaze. This difference
was not statistically significant (Table 2). Subjects with pretreatment IOP measurement of less than 21 mmHg had a mean IOP
value of 16.5 mmHg with a posttreatment IOP of 15.8 mmHg, a
decrease of 0.5 mmHg (P ⫽ 0.20). Those subjects in the radiation
group who had a pretreatment value of greater than 21 mmHg
(mean, 23.9 mmHg) had a posttreatment IOP of 22.0 mmHg, a
decrease of 1.9 mmHg (P ⫽ 0.76).
Discussion
This study demonstrates that IOP decreases significantly
after orbital decompression and strabismus surgery in subjects with GO but does not decrease in subjects treated with
orbital radiation.
Orbital Decompression
Orbital decompression resulted in a decrease in IOP postoperatively irrespective of the preoperative IOP. However,
subjects with preoperative IOP values of 21 mmHg or
higher had more than a threefold greater reduction in their
postoperative IOP compared with subjects who started with
an IOP less than 21 mmHg. These findings are supported by
the results of other smaller studies. In a series of 22 eyes (12
subjects) that underwent orbital decompression, Dev et al.11
found a mean postoperative decrease in IOP of 3.0 mmHg.
Seven of eight eyes that had preoperative IOP values greater
than 21 mmHg showed a greater decrease in IOP postoperatively (mean of 5.6 mmHg). Ohtuska12 measured IOP in
six subjects before and after orbital decompression. The
mean IOP decreased from 23.3 to 18.8 mmHg after orbital
surgery. Kalmann and Mourits13 also reported five subjects
who had orbital decompression for GO who had a significant decrease in their postoperative IOP. Another study,14
which used the technique of fat removal orbital decompression, described a mean decrease in IOP of 8.5 mmHg in nine
subjects with preoperative IOP greater than 21 mmHg. Algevere et al.4 reported three of five subjects in whom glaucoma
was “cured” with pterional orbital decompression. However,
the postoperative IOP values were not reported in the study.
Several theories have been invoked in an attempt to
explain the decrease in IOP after orbital decompression.
Increased orbital contents in a confined orbital volume, as
seen in GO, may contribute to elevated IOP by increasing
intraorbital pressure and venous congestion,7,15 subsequently increasing episcleral venous pressure (EVP).16 The
increase in orbital contents is secondary to enlargement of
the extraocular muscles, deposition of glycosaminoglycans,
and lymphocytic infiltration of orbital fat.17 Direct orbital
manometry demonstrated higher orbital tissue tension and
lower orbital compartment compliance (both factors are
thought to be components determining retrobulbar pressure)
Table 4. Change in Intraocular Pressure in Orbital Decompression Group: On and Off Glaucoma Medications
Use of Glaucoma Medications
Using glaucoma medications (n ⫽ 35)
Primary position (SD)
Upgaze position (SD)
Not using glaucoma medications (n ⫽ 81)
Primary position (SD)
Upgaze position (SD)
Intraocular
Pressure
Before
Intraocular
Pressure
After
Drop in
Intraocular
Pressure
% Decrease in
Intraocular
Pressure
25.9 (2.9)
30.5 (3.7)
18.8 (2.7)
21.4 (4.2)
7.1 (3.0)
9.1 (5.1)
27.4%
30.0%
⬍0.001
19.8 (4.0)
26.9 (7.6)
17.0 (3.0)
19.6 (4.9)
2.8 (3.7)
7.3 (6.1)
13.9%
27.2%
⬍0.001
P Value
SD ⫽ standard deviation.
147
Ophthalmology Volume 108, Number 1, January 2001
Table 5. Change in Intraocular Pressure after Treatment
According to Preoperative Intraocular Pressure Range
Preoperative Intraocular
Pressure Categories
Decompression
(n ⴝ 116)
Strabismus
(n ⴝ 32)
Radiation
(n ⴝ 56)
⬍21 mm Hg
Mean preoperative IOP
(SD)
Mean postoperative IOP
(SD)
Mean drop in IOP (SD)
% Decrease
P Value
ⱖ21 mm Hg
Mean preoperative IOP
(SD)
Mean postoperative IOP
(SD)
Mean drop in IOP
(SD)
% Decrease
P value
(n ⫽ 51)
17.3 (2.3)
(n ⫽ 27)
17.8 (2.2)
(n ⫽ 34)
16.5 (2.9)
16.1 (2.8)
15.5 (2.7)
15.8 (2.7)
⫺1.2 (2.8)
6.9
(P ⬍ 0.01)
(n ⫽ 65)
24.9 (3.0)
⫺2.3 (0.71)
12.9
(P ⬍ 0.01)
(n ⫽ 5)
23.0 (0.5)
⫺0.7 (1.4)
4.3
(P ⫽ 0.20)
(n ⫽ 22)
23.9 (2.5)
18.7 (2.5)
19.4 (1.1)
22.0 (4.9)
⫺6.2 (3.5)
⫺3.6 (1.4)
⫺1.9 (4.5)
24.9
(P ⬍ 0.01)
15.7
(P ⫽ 0.11)
7.6
(P ⫽ 0.76)
IOP ⫽ intraocular pressure; SD ⫽ standard deviation.
in the orbits of subjects with GO.18 Other studies have
shown that there is an increased retro-orbital pressure in GO
that is relieved with orbital decompression.15,18,19
An increase in EVP causes a proportional increase in
IOP, according to the Goldmann equation: IOP ⫽ aqueous
inflow/outflow facility ⫹ EVP.
Because decompression surgery decreases orbital pressure and venous congestion, it would be expected to reduce
EVP.4 In fact, orbital decompression has been shown to
allow filling of the ophthalmic vein in subjects who previously had no filling during orbital venography, suggesting a
lowering of EVP.9,20
Thirty-five eyes that underwent orbital decompression
were being treated with at least one topical glaucoma medication. These subjects were referred to the Neuro-ophthalmology Service already on glaucoma medications. The IOP
significantly decreased in this subgroup from 25.9 mmHg
preoperatively to 18.8 mmHg postoperatively, a mean decrease in IOP of 7.1 mmHg or 27%. Hence, most subjects
had their IOP “normalized” to a value less than 21 mmHg as
a result of orbital decompression. This suggests that there
was a significant contribution to the elevated preoperative
IOP from factors that were not being effectively treated by
the glaucoma medication.
Those subjects who underwent orbital decompression
who had optic nerve compression as their indication for
decompression had a greater decrease in their IOP postoperatively than did subjects with proptosis as their indication for surgery. Optic nerve compression is commonly seen
in subjects with little or no proptosis and with a crowded
orbital apex seen on imaging. It would follow that the
smaller decrease in IOP among the subjects who had proptosis as their indication for surgery is because the proptosis
itself has a decompressive effect. By displacing the orbital
contents outside the bony orbit, there is a decrease in the
effective volume of the contents that occupy the bony orbit.
This limited additional space that proptosis offers may
148
allow more room for the congested orbital contents and
subsequently less compression on the globe and subsequent
elevation in IOP.
Strabismus Surgery
To our knowledge (after a literature search of MEDLINE),
our study is the first to statistically evaluate changes in IOP
before and after inferior rectus surgery in GO. Extraocular
muscle surgery decreased IOP in subjects by an average of
2.4 mmHg (12.9%) in primary position and 4.9 mmHg
(22.8%) in upgaze. The mechanism of the increased IOP on
upgaze is thought to be related to inelasticity of the inferior
rectus muscle. The inability to relax when the elevator pulls
the eye upward results in compression of the globe and
subsequent elevation in IOP.21,23
An average rise in IOP of approximately 2 mmHg in
upgaze has been reported to occur in healthy volunteers.24
In many subjects with GO, the average increase of IOP in
upgaze is significantly higher.22,25,32 Fishman and Benes29
demonstrated that there is a direct linear correlation between
the amount of hypotropia as measured in prism diopters and
the increase in IOP in upgaze. High-resolution computed
tomography has demonstrated that an increased IOP in
upgaze may be caused by attempts to rotate the globe
against fibrosed and shortened extraocular muscle.30 This is
usually attributed to restriction specifically of the inferior
rectus muscle. In some subjects the inferior rectus also will
be exerting a tethering effect in primary position. As the
inferior rectus becomes more contracted, it tends to pull the
eye downward. In these subjects, an effort has to be exerted
against the inferior rectus even to bring the eyes into the
primary position. This may increase IOP in the primary
position by the same mechanism.
Orbital Radiation
Orbital radiation is a treatment modality used in the acute,
active phase of GO. Soft tissue signs and optic neuropathy
of GO have been reported to improve after radiation treatment. The effect of orbital radiation on proptosis and extraocular muscle function is less consistent.33,34 Extraocular
muscle size does not change significantly after radiation
therapy.35 In our study, orbital radiation did not result in any
significant change in IOP. In some ways this is surprising
because radiotherapy is known to decrease the inflammatory
component of GO, which should decrease orbital volume.
One possible explanation is that although radiation decreases the inflammatory reaction, the effect on orbital
volume is less significant and therefore does not translate
into a significant reduction in IOP. Longer follow-up time
may have detected a reduction in IOP. Alternatively, it may
be that the number of subjects in our study was too small to
detect a smaller, but potentially significant, reduction in IOP
after radiation.
Our study suggests that in a significant number of subjects with GO, the elevated IOP is related to the underlying
pathophysiology of GO. By relieving these factors the IOP
can be lowered. Our study also highlights the difficulty of
Danesh-Meyer et al. 䡠 IOP Changes after Graves’ Orbitopathy
diagnosing glaucoma in subjects with concomitant GO. It
has been suggested1 that ocular hypertension may be more
common in subjects with GO (24%) compared with the
age-matched general population (5%),36 but a smaller proportion of subjects with GO progress to have glaucomatous
field defects develop. A number of different theories may
explain this presumed lower incidence of glaucoma among
ocular hypertensives, with GO, including less susceptible
optic nerves or elevated IOP for shorter periods of the day
(e.g., on attempted upgaze). Subjects with GO may adopt a
chin-up position that places the globe slightly in downgaze,
relieving the elevated IOP associated with upgaze, attempted upgaze, or even gaze in primary position (the IOP
measured in this position may not reflect the average daily
IOP).
The limitations of this study include that it is a retrospective review of subjects who required intervention for
GO. This represents a small portion of subjects with GO.
Because there was no control group, a comparison could not
be made between change in IOP in subjects undergoing
intervention and those who had no intervention. Subjects in
the orbital decompression group had their IOP measured at
1 to 2 weeks postoperatively. There is no long-term follow-up to determine whether the decline in IOP seen postoperatively is sustained. Subjects who underwent strabismus surgery had significant limitation of upgaze. For these
subjects, it is difficult to assume a standardized technique
for measuring IOP in upgaze. Some subjects had their
eyes fixed in downgaze and had to exert effort to attempt
to bring their globes into the primary position. Finally,
this study did not include the evaluation of optic nerve
appearance, visual acuity, and visual fields in subjects
with elevated IOP. Therefore, a comment cannot be made
on whether there was any change in optic nerve function
after intervention.
Despite these limitations, we believe that the large number of subjects studied that allow statistical evaluation
makes our observations useful. First, our study increases the
body of evidence that suggests that increased intraorbital
pressure and orbital congestion with subsequent venous
obstruction and increased EVP contribute significantly to
elevating IOP in subjects with GO. This is the largest study
of change in IOP in subjects with GO who underwent
orbital or strabismus surgery or radiation. Second, this study
is the first to demonstrate that strabismus surgery results in
an appreciable decrease in IOP in subjects with GO. Third,
our findings suggest that the approach to the patient with
GO and elevated IOP should be modified from ocular hypertension in other settings. Although ocular hypertension
seen in GO subjects may be caused by the coexistence of
two relatively common conditions, the elevated IOP could
be secondary to the underlying pathologic processes that
occur in GO. Finally, subjects diagnosed with glaucoma
who are undergoing orbital decompression or inferior rectus
surgery may have decreased IOP postoperatively. Hence,
GO subjects with a diagnosis of glaucoma should have their
glaucoma status reevaluated after these two surgical procedures.
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