CLINICAL SCIENCES

Orbital Arteriovenous Malformations

Sunil Warrier, MBBS; Venkatesh C. Prabhakaran, MS, MRCOphth; Alejandra Valenzuela, MD;
Tim J. Sullivan, FRANZCO; Garry Davis, FRANZCO; Dinesh Selva, FRANZCO

Objective: To present the clinical features, manage-
ment, and outcomes in a series of patients with orbital
arteriovenous malformations (AVMs).
Methods: Clinical records of patients with orbital AVMs
confirmed using angiography were reviewed as a retro-
spective, noncomparative, interventional case series.
Results: Eight patients (3 women and 5 men) with uni-
lateral AVMs and a mean age of 39 years (median, 36.5
years; range, 26-70 years) were reviewed. Findings ex-
isted for an average of 11.2 years before diagnosis and
included periocular mass (7 patients, 88%); periocular
edema, pulsation/bruit, proptosis, episcleral conges-
tion, and previous trauma (4 patients each, 50%); el-
evated intraocular pressure (3 patients, 38%); pain and
reduced visual acuity (2 patients each, 25%); and restric-
tion of extraocular movements, and diplopia (1 patient
each, 12%). All of the patients except 1 underwent sur-
gical resection, with 3 (38%) receiving preoperative em-
bolization of feeder vessels; all of the patients had initial
resolution of manifestations after treatment.
Conclusions: Angiography is essential for diagnosis and
for planning the management of orbital AVMs. Treat-
ment depends on patient-specific features and includes
observation, embolization, and surgical excision or com-
bined preoperative embolization/excision. Given their vas-
cular nature, the main cause of poor management out-
comes is perioperative hemorrhage. Outcomes after a
multidisciplinary approach are good, with few recur-
rences reported at follow-up.
Arch Ophthalmol. 2008;126(12):1669-1675

Author Affiliations: South
Australian Institute of
Ophthalmology and Discipline
of Ophthalmology and Visual
Sciences, University of
Adelaide, Adelaide, South
Australia (Drs Warrier,
Prabhakaran, Davis, and Selva);
and Department of
Ophthalmology, Royal Brisbane
Hospital, Brisbane, Queensland
(Drs Valenzuela and Sullivan),
Australia.
I
NTRAORBITAL ARTERIOVENOUS
malformations (AVMs) are rare
lesions that are thought to be con-
genital in origin.1 They are de-
rived embryologically from the
arterial system, the venous system, or both.
They are high-flow, progressively enlarg-
ing communications between arteries and
veins that bypass normal capillary beds,
usually with multiple feeder arteries, a cen-
tral nidus, and numerous dilated drain-
ing veins.2 The diagnosis of an orbital AVM
is based on angiographic and histologic
findings. Findings on selective angiogra-
phy include an engorged, rapidly filling,
proximal arterial system; the malforma-
tion; and the distal venous outflow. His-
tologic analysis reveals thick-walled, ir-
regular arterial and venous channels with
and without stromal hemorrhage.3
Appearance on initial examination is
variable, as although the lesions are often
congenital, they may not cause symptoms
in childhood. Stimuli for growth include
menarche, pregnancy, and trauma.2 Com-
mon findings include periocular pain, di-
lated corkscrew vessels on the globe ex-
tending to the limbus, proptosis, pulsation,
bruit, and raised intraocular pressure.4 We
report the largest case series, to our knowl-
edge, of symptomatic orbital AVMs, with an-
giographic evidence and outcomes after in-
tervention. A review of the literature to
better define the features and management
of orbital AVMs was also undertaken.
METHODS
This is a multicenter, retrospective study of all
patients with orbital AVMs who were seen in
2 orbital units: South Australian Institute of
Ophthalmology, January 1, 2004, to January
1, 2007 (2 patients), and Royal Brisbane Hos-
pital, January 1, 2001, to January 1, 2006 (6
patients). The inclusion criterion was an an-
giographically proved AVM involving the or-
bit. Medical records were reviewed for the fol-
lowing data: age; sex; ethnicity; duration of
signs and symptoms; clinical presentation; site
involved; imaging findings on angiography,
computed tomography, or magnetic reso-
nance imaging angiography; treatment modali-
ties; and outcomes. Response to treatment was
evaluated by resolution of the signs and symp-
toms noted at the initial examination and pa-
tient satisfaction.
RESULTS
CASE SERIES
This study included 8 patients (3
women and 5 men) with a mean age of

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Table 1. Initial Clinical Signs and Symptoms in 8 Patients
With Orbital Arteriovenous Malformations
Patients,
No. (%)
Periocular mass
Periocular swelling a
Pulsation/bruit
Proptosis
Previous trauma
Edema/congestion of episclera/conjunctiva
Elevated intraocular pressure
Pain
Reduced visual acuity
Restriction of extraocular movement
Diplopia
a Intermittent swelling was described in 1 patient.
39 years (median, 36.5 years; range, 26-70 years).
Seven patients were white and 1 was Malay. All of the
cases were unilateral. The mean duration from initial
clinical signs and symptoms to diagnosis and treat-
ment was 11.2 years (median, 8 years; range, 3
months to 30 years). The presenting signs and symp-
toms are summarized in Table 1. The most common
finding was a periocular mass in 7 patients (88%),
with periocular swelling and edema, pulsation/bruit,
proptosis, previous trauma, and episcleral congestion
in 4 patients each (50%).
Computed tomography or magnetic resonance imaging
localized the AVM to the superomedial quadrant of the
orbit in 3 patients, the superolateral quadrant in 2, the
inferolateral quadrant in 2, and the entire medial orbit
in 1. The latter patient had a giant facial AVM that had a
significant orbital component. Aside from this giant le-
sion, all of the AVMs were located in the anterior orbit.
Angiography was available for all 8 patients. Feeder ar-
teries were noted from the internal carotid artery in 5 pa-
tients (63%), of which 4 were from the ophthalmic ar-
tery, and from the external carotid artery in 3 patients
(38%).
Preoperative embolization of feeder vessels was per-
formed in 3 patients (38%). Polyvinyl alcohol particles5
were used in 2 patients and platinum microcoils (Beren-
stein Liquid Coils; Boston Scientific, Natick, Massachu-
setts)6 in 1. Incisions appropriate to location were used
in the 7 patients (88%) who underwent surgical man-
agement. Feeder vessels were identified using angiogra-
phy and were ligated, with careful excision of the mal-
formations ensuring hemostasis. In the case of the giant
facial AVM, reconstruction after excision of the facial com-
ponent was accomplished using a radial forearm free flap.
Histologic analysis in all cases revealed lesions with thick-
ened arterial and venous components, consistent with
AVMs.
After surgical debulking, substantial symptomatic
improvement was noted regarding proptosis, raised
intraocular pressure, reduced visual acuity, and peri-
ocular swelling in all of the patients. Pain was persistent
in 2 patients (25%), with 1 requiring further surgical
intervention. Diplopia was reported in 2 patients (25%)
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postoperatively, of which 1 required strabismus surgery
to attain binocular vision. Mean follow-up was 27
months (range, 3-48 months), during which 6 patients
remained symptom free and 1 each (as described previ-
ously herein) required further procedures. Patient
demographics and management are outlined in
7 (88)
Table 2.
4 (50)
4 (50)
4 (50) ILLUSTRATIVE CASE
4 (50)
4 (50) A 47-year-old woman complained of persistent pain,
3 (38)
2 (25)
discomfort, and increasing redness and size of a right
2 (25) periorbital lesion, which was present since childhood
1 (12) and had been debulked at least 20 times before review.
1 (12) She had episodes of severe pain associated with recur-
rent intralesional hemorrhages. Her best-corrected vi-
sual acuity was 6/6 in both eyes. She had 2.5 mm of
nonaxial proptosis of the right eye. Dilated, abnormal
vessels were noted on the right temporal conjunctiva
and sclera together with enlargement of the palpebral
lobe of the lacrimal gland (Figure 1). Ocular move-
ments were not restricted, and no distensibility was
noted when using the Valsalva maneuver. The remain-
der of the ocular examination, including the fundus,
was unremarkable. Magnetic resonance imaging of the
orbits revealed a vascular malformation in the supero-
temporal orbit (Figure 2). Angiography showed an
AVM in the right orbit with feeder vessels from the oph-
thalmic artery and multiple branches arising from the
superficial temporal and maxillary branches of the ex-
ternal carotid artery. After discussion with the patient,
it was decided that preoperative embolization of the
malformation would not include the feeder vessels from
the ophthalmic artery because of the risk of blindness.
Hence, preoperative embolization using polyvinyl alco-
hol particles occluded the external carotid artery feeder
vessels, but residual flow was evident from the ophthal-
mic artery branches (Figure 3). The lesion was de-
bulked via a lateral orbitotomy after the largest feeder
vessel from the lacrimal artery was exposed and clipped
(Figure 4). Histopathologic examination confirmed
an AVM (Figure 5). The patient was asymptomatic for
8 months before developing recurrent symptoms of per-
sistent pain and discomfort. Further debulking surgery
was performed, with initial symptom resolution, but
the patient remains symptomatic at this stage. She is
considering superselective catheterization of the oph-
thalmic artery preoperatively.
COMMENT
We describe herein a series of 8 patients with angio-
graphically and histologically proved orbital AVMs, which,
to our knowledge, is the largest series in the literature.
All of the patients except 1 underwent surgery, with
or without previous embolization, generally with good
results.
Vascular malformations of the orbit are complex and
varied lesions. Rootman3 used hemodynamic concepts
to classify them into subtypes. Type 1 encompasses lymph-
angiomas and combined venous–lymphatic system mal-
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 Table 2. Patient Demographics and Diagnosis and Management of Orbital AVMs

Duration
Patient No./ of
Sex/Age, y Symptoms Symptoms
1/M/27 6y Periocular mass, slowly
increasing size,
pulsation positive
2/M/26 4y Periocular mass,
intermittent eyelid
swelling, pulsation
positive
3/F/41 3y Pain, eyelid lesion, and
bulbar conjunctival
hyperemia
4/M/43 20 y Periocular mass and
swelling, diplopia,
6-mm proptosis,
pulsation positive
5/M/28 16 y Periocular mass, 4-mm
proptosis, reduced VA
6/F/70 3 mo Periocular mass,
pulsation positive
7/M/32 10 y Periocular mass and
swelling, 5-mm
proptosis, decreased
VA, increased IOP,
edema, and congestion
of episclera
8/F/46 30 y Periocular mass and
swelling, pain,
increased IOP, 2.5-mm
proptosis, edema, and
congestion of episclera
Side Angiography Treatment Progress Comments
L AVM anterior Refused treatment Lost to follow-up after Boxing trauma to
superolateral orbit; 3 mo left side
multiple ICA feeder
vessels
L AVM anterior Surgical excision Mild and regressing Trauma causing left
superolateral orbit; without swelling orbital fracture
feeder vessels from embolization owing postoperatively;
STA, facial artery, to numerous feeder follow-up, 11 mo
ophthalmic artery vessels
R AVM anterior Surgical excision Decreased pain only Encephalocele
superomedial orbit; without on bending; surgically
feeder vessels from embolization follow-up, 37 mo managed in past
ophthalmic artery and
ethmoidal artery
L AVM anterior Preoperative Horizontal diplopia that Trauma to left orbit
superomedial orbit; embolization using required strabismic 20 y before initial
feeder vessels from platinum correction; other examination
ophthalmic artery microcoils6; surgical symptoms resolved;
excision follow-up, 48 mo
L Giant AVM filling entire Surgical excision Resolution of None
medial orbit; feeder symptoms; mild
vessels identified from diplopia in extreme
ethmoidal artery up and down gaze;
follow-up, 10 mo
R AVM anterior Surgical excision Resolution of None
superomedial orbit; symptoms;
multiple feeder temporary
vessels from supraorbital nerve
supraorbital vessels hypoesthesia;
follow-up, 48 mo
R AVM anterior Preoperative Resolution of signs None
inferolateral orbit; embolization using and symptoms;
feeder vessels from PVA particles5; follow-up, 12 mo
maxillary, facial, surgical excision
lingual, and
ophthalmic arteries
R AVM anterior Preoperative Resolution of Considering
superotemporal orbit; embolization of ECA symptoms for 8 mo preoperative
feeder vessels from feeder vessels using before recurrence; embolization of
STA and maxillary and PVA particles5; follow-up, 12 mo ophthalmic artery
ophthalmic arteries surgical debulking feeder vessels

Abbreviations: AVM, arteriovenous malformation; ECA, external carotid artery; ICA, internal carotid artery; IOP, intraocular pressure; L, left; PVA, polyvinyl alcohol;
R, right; STA, superficial temporal artery; VA, visual acuity.

formations with essentially no flow. Type 2 encom-

passes low-flow lesions, including distensible, directly
communicating venous malformations and nondisten-
sible lesions with little venous communication. Both
AVMs and cavernous hemangiomas are included in type
3, with antegrade flow from the arterial through to the
venous side.
As described at the beginning of this article, AVMs
are high-flow communications between arteries and
veins, bypassing normal capillary beds. Orbital AVMs
are rare lesions, and Wright,7 in a series of 627 patients
with proptosis, found only 3 AVMs. A review of the lit-
erature disclosed only 361,2,8-34 reported cases of orbital
AVMs. A selection of these cases is summarized, high-
lighting various management options and outcomes
(Table 3). The most common presenting feature was
proptosis, followed by a periocular lesion and pain.
Figure 1. Clinical photograph highlighting dilated, abnormal vessels on the
Most lesions were located in the superior orbit. Sponta- right temporal conjunctiva and sclera together with enlargement of the
neous hemorrhage is uncommon, with only 1 case palpebral lobe of the lacrimal gland.

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 A B

Figure 2. Magnetic resonance images (T1, contrast enhanced) of the orbits. A, Axial image showing a vascular malformation in the right superotemporal orbit
with a characteristic flow void (arrow). B, Coronal image highlighting a right superotemporal vascular malformation with vessels evident in the muscle cone.

Figure 4. Intraoperative photograph of the excision of an orbital

arteriovenous malformation with identification of a lacrimal artery feeder
vessel via lateral orbitotomy.
Figure 3. Preoperative angiogram after embolization revealing residual flow
via the ophthalmic artery feeding vessels to a right orbital arteriovenous
malformation.

being reported.25 This is in contrast to histologically
similar cerebral AVMs, which manifest most commonly
with hemorrhage (approximately 50%)35 and are re-
sponsible for 1% of all strokes.36 There is a tendency for
orbital AVMs to expand slowly, with factors such as
menarche, pregnancy, and trauma implicated in their
growth. Trauma was a feature in 50% of the patients
in this series but was previously reported in only 5
patients.2,13,15,29
Orbital AVMs are best considered to be congenital ham-
artomas, with trauma possibly precipitating hemody-
namic changes, leading to symptoms. Based on loca-
tion, they may be classified into 3 types: purely orbital,
orbital and periorbital, and orbital with retinal or cere-
bral AVMs (Wyburn-Mason syndrome). The first 2 groups
are more common (33 of 36 reviewed cases [92%]: 26
[72%] purely orbital and 7 [19%] orbital and perior-
bital). Wyburn-Mason syndrome can include any com-
bination of cutaneous angiomas and retinal, orbital, and
cerebral AVMs, with cutaneous manifestations being the
least common.37 Three of 36 orbital AVMs (8%) re-
viewed for this article could be classified into this cat-
egory. It is unclear whether the Wyburn-Mason syn-
drome is a separate disorder or simply a multifocal
manifestation of AVM. Note that cerebral AVMs may cause
secondary orbital congestion because of atypical venous
drainage into the orbital veins.38 Garrity et al39 use the
term secondary type of orbital AVM to describe this phe-
nomenon, although no AVM of the orbit exists in this
condition.
Diagnosis of orbital AVMs is based on angiographic
findings highlighting an engorged, rapidly filling proxi-
mal arterial system, a malformation, and distal venous
outflow.3 Histologic analysis of these lesions includes ir-
regularity in the thickness of the muscularis layer in the
affected arteries and veins and the presence of a partial

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 elastica in some vessels.40 A nidus of cellular stroma is
found between the vessels.
The diagnosis can be aided by clinical history and non-
invasive tests, such as flow Doppler studies, and by com-
puted tomography and magnetic resonance imaging to
highlight the extent of the lesions. Because these lesions
are rare, they must be considered in the differential di-
agnosis of orbital vascular lesions with similar clinical
features, such as carotid-cavernous fistulas, dural-
cavernous sinus fistulas, orbital arteriovenous fistulas
(AVFs), and cerebral AVMs with drainage into orbital
veins. Orbital AVF is the only condition that may be con-
fused with orbital AVM on radiology and angiography.
Orbital AVFs may be traumatic or spontaneous and are
limited to the orbit, with no connection to the cavern-
ous sinus.41 These lesions can be differentiated from or-
bital AVMs on angiography: AVFs demonstrate a direct
arteriovenous connection without the intervening ni-
dus that is characteristic of AVMs. Orbital AVFs are rare,
with only 10 reported cases; the subject is well reviewed
by Yazici and coworkers.41
The management of orbital AVMs is based on a mul-
tidisciplinary approach. As described earlier, the slow
growth and the low incidence of hemorrhage permit ob-
servation in many cases. Regression is well documented
in cerebral AVMs but has not been reported in orbital
lesions.42 Indications for intervention include visual com-
promise, patient discomfort related to symptoms, and aes-
thetic concerns when the lesions extend outside the or-
bit. The primary treatment for orbital AVMs is surgical
excision with or without preoperative embolization. Ra-
diotherapy using newer techniques to focus radiation onto
the lesion (linear accelerator, proton beam, or gamma
knife) has been used for cerebral AVMs and works by in-
ducing thrombosis42; however, this method has not been
used for orbital lesions.
Surgery seems to be a safe and effective treatment for
orbital lesions, and the predominantly excellent results
from this and other case series2,15 highlight the impor-
tance and effectiveness of preoperative embolization.
Goldberg et al15 in 1993 reported 3 cases of orbital AVM
that were successfully managed with combined emboli-
zation and surgical resection. One patient complained of
persistent supraorbital swelling on bending that, on an-
giography, was found to represent a varix. Another se-
ries2 consisted of 3 patients with orbital AVMs managed
with combined embolization and surgical resection, with
little morbidity. Exposure keratopathy developed in 1 pa-
tient owing to vertical shortening of the lower eyelid,
which was subsequently surgically corrected. Since the
advent of superselective angiography32 and small cath-
eters, it has become possible to locally restrict flow to the
lesions, thus reducing their bulk before resection. It also
changes the flow property from a dynamic to a static pro-
cess, thus reducing the risk of hemorrhage periopera-
tively. In small lesions, with high surgical risk, emboli-
zation alone has been successful.32 This is possible in only
a few cases given the propensity of AVMs to form col-
lateral circulation. This form of catheterization is also use-
ful in the diagnosis of small AVMs of the posterior orbit,
such as those involving the dura of the optic nerve.22 Cur-
rently, these lesions have few therapeutic options.
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Figure 5. Histologic section with adjacent medium-sized arteries, veins, and
arterialized veins, consistent with an arteriovenous malformation
(hematoxylin-eosin original magnification ⫻20).
Positioning of a catheter when embolizing ophthal-
mic artery feeder vessels must be distal to the posterior
ciliary and central retinal vessels, or larger emboliza-
tion particles aimed at greater-caliber vessels should
be used. This should be accompanied by provocative
testing with lidocaine to ensure ocular blood flow. The
technique involves the injection of enough lidocaine
to replace blood flow for at least 2 seconds so that
there is sufficient time for perfusion through the tissue
and, hence, provocation. The detection of a scotoma
on testing localizes ocular blood flow.43 Surgical resec-
tion should be via an approach specific to the location
of the AVM. Rootman et al 29 advocated the use of
microvascular clips as opposed to bipolar cautery
whenever possible to ensure a more precise effect
around delicate tissue.
Review of the literature shows that recurrences were
reported when incomplete excision or partial emboliza-
tion alone was performed,10,21,22,31 highlighting the ten-
dency of these lesions to recruit new feeder vessels when
their supply is partially reduced. This tendency to recur-
rence was also demonstrated in the illustrative case in
this series, in which preoperative embolization of the ex-
ternal carotid feeder vessels but not the internal carotid
feeder vessels was performed.
The risk-benefit ratio must be evaluated on a case-by-
case basis before interventional management is under-
taken in orbital AVMs. Their natural history must be un-
derstood and considered, alongside the risks of
neuroradiologic and surgical interventions. Visual com-
promise and persistent or progressive patient discom-
fort are the main indicators for intervention. We found,
in this series of 8 patients and in the literature, that a mul-
tidisciplinary approach, when successful, is often cura-
tive in these rare lesions.
Orbital AVMs are rare lesions that usually manifest
in a chronic manner. They are an important differen-
tial diagnosis in any suspected orbital vascular abnor-
mality. Angiography is essential for diagnosis and for
planning management. Their management depends on
patient-specific features and includes observation,
embolization, and surgical excision or combined pre-
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 Table 3. Selected Reported Cases of Orbital AVMs: Management and Outcomes

Patient Duration
Sex/ of
Source Age, y Symptoms Symptoms Side Angiography Treatment Progress Comments
27
Murali et al, M/53 1y Proptosis, bruit, R Feeder vessels from No treatment Spontaneous Disappearance
1981 visual loss ophthalmic artery thrombosis of of bruit
and IMA superior ophthalmic
vein; disappearance
of AVM
Howard et al,21 M/19 2y Proptosis, upper R AVM superotemporal Initial biopsy and Immediate None
1983 eyelid edema orbit; feeder embolization of IMA; disappearance of
vessels from IMA, surgery via lateral proptosis;
STA, and MMA orbitotomy for recurrence recurrence 4 y later;
asymptomatic
immediately after
surgery
Gross and F/60 1y Headache, L AVM superior orbit Heifetz clamp incorporating Asymptomatic at 5-y None
Hornblass,18 proptosis, anterior to orbital major proximal and distal review
1989 episcleral rim ends and left in situ
venous
congestion,
thrill, raised
IOP
Tsai et al,32 M/30 8y Decreasing VA, R AVM fed only by Superselective catheterization Proptosis and pain Previous
1990 proptosis, ophthalmic artery and embolization using settled; vision stable radiotherapy
increasing PVA at 2-y review for AVM
pain, bruit
Rootman M/31 20 y Proptosis, bruit, L AVM superolateral Preoperative embolization Postoperative History of
et al,29 1992 pain orbit; feeder and surgical resection angiography at 1 mo trauma
vessels from showed small
ophthalmic artery residual nidus;
and MMA self-resolving
hemorrhage at 8
mo; asymptomatic
at 18 mo
Chakrabortty M/27 23 y Proptosis, R AVM fed by Initially clipped; postoperative Unknown None
et al,11 1993 chemosis, ophthalmic artery angiography showed
visual loss recruitment of new feeder
vessels, which were
embolized; surgical
removal followed by
exenteration for cosmetic
reasons
Goldberg et F/22 18 y Upper eyelid R AVM superior orbit Initial excision abandoned Normal ocular Initial
al,15 1993 mass, owing to hemorrhage; examination complaint
proptosis radiotherapy and findings at 3 mo during
reexcision; embolization pregnancy;
with ophthalmic artery periods of
spasm and visual growth
compromise; second during
embolization and surgical menarche
excision
Hieu et al,20 F/39 1 mo Proptosis, raised R AVM retrobulbar, Surgical excision via No recurrence, None
1997 IOP, visual intraconal space; fronto-orbital craniectomy resolution of signs
loss feeder vessels and symptoms
from dilated
ophthalmic artery
and ECA
Yasuhara F/7 1y Visual loss L AVM: submaxillary, Embolization ⫻ 6 and Disappearance of None
et al,33 1999 retinal, orbital, and radiotherapy to submaxillary lesion;
middle subdural submaxillary AVM; gamma other lesions stable
knife treatment to orbital at 1 y
AVM
Moin et al,25 F/75 Several Proptosis, R AVM in retrobulbar Lateral orbitotomy and Unknown First report of
2000 days diplopia, space; fed from debulking, aborted owing spontaneous
conjunctival ophthalmic artery to hemorrhage; attempted hemorrhage
chemosis embolization; exenteration
Pathak-Ray F/7 Unknown Reduction in L Retinal and orbital Observation No change at 3 y Wyburn-
et al,28 2001 vision AVM Mason
syndrome
Trombly et al,31 F/11 Unknown Upper and lower R AVM in orbit and Surgical excision complicated BCVA 20/80 with None
2006 eyelid lesion, forehead; feeder by hemorrhage; serial ptosis and
thrill vessels from right incomplete embolizations; exotropia; lesion
ophthalmic artery, planned for exenteration prominent and
R and L ECAs disfiguring at 2 y

Abbreviations: AVM, arteriovenous malformation; BCVA, best-corrected visual acuity; ECA, external carotid artery; IMA, internal maxillary artery; IOP, intraocular
pressure; L, left; MMA, middle meningeal artery; PVA, polyvinyl alcohol; R, right; STA, superficial temporal artery; VA, visual acuity.

operative embolization and surgical excision. Given rhage. Outcomes after a multidisciplinary approach
the vascular nature of orbital AVMs, the main cause of are generally good, with few recurrences reported at
poor management outcomes is perioperative hemor- follow-up.

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 Submitted for Publication: May 9, 2008; final revision
received July 2, 2008; accepted July 4, 2008.
Correspondence: Sunil Warrier, MBBS, Department of
Ophthalmology and Visual Sciences, Royal Adelaide Hos-
pital, North Terrace, Adelaide, South Australia, Austra-
lia 5000 (drskwarrier@gmail.com).
Financial Disclosure: None.
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