SURVEY OF OPHTHALMOLOGY VOLUME 54  NUMBER 4  JULY–AUGUST 2009

MAJOR REVIEW

Orbital Compartment Syndrome: The Ophthalmic

Surgical Emergency
Vanessa Lima, MD,1,2 Benjamin Burt, MBBS,1,2 Igal Leibovitch, MD,3
Venkatesh Prabhakaran, MD,1,2 Robert A Goldberg, MD,4
and Dinesh Selva, FRACS, FRANZCO1,2

1
Oculoplastic and Orbital Division, Department of Ophthalmology and Visual Sciences, University of Adelaide, Adelaide,
Australia; 2South Australian Institute of Ophthalmology, Adelaide, Australia; 3Department of Ophthalmology,
Tel-Aviv Medical Center, University of Tel-Aviv, Tel-Aviv, Israel; and 4Division of Orbital and Ophthalmic Plastic Surgery,
Jules Stein Eye Institute, and the Department of Ophthalmology, David Geffen School of Medicine at UCLA,
Los Angeles, California, USA

Abstract. Orbital compartment syndrome is an uncommon, ophthalmic surgical emergency

characterized by an acute rise in orbital pressure. When intraorbital tension rises, damage to ocular
and other intraorbital structures, including irreversible blindness, may occur if not promptly treated.
The diagnosis of orbital compartment syndrome is completely clinical and early recognition and
emergent orbital decompression (even prior to imaging) is essential in preventing permanent vision
loss. Lateral canthotomy and inferior cantholysis remain the mainstays of management. More extensive
incision of the orbital septum and orbital bony decompression may be necessary in unresponsive cases.
This review discusses the various etiologies and mechanisms resulting in orbital compartment
syndrome, clinical features, imaging findings, treatment, and prognosis. (Surv Ophthalmol 54:441--
449, 2009. Ó 2009 Elsevier Inc. All rights reserved.)

Key words. cantholysis  canthotomy  globe tenting  orbital compartment syndrome 

orbital compression syndrome  orbital decompression  orbital emergency  orbital tension

I. Introduction significant morbidity. In OCS, optic nerve and

Orbital compartment syndrome (OCS) is one of the
few ophthalmic surgical emergencies that both
ophthalmologists and emergency physicians should
be familiar with. The orbit is an enclosed space with
limited ability to expand. Hence, OCS occurs when
an acute rise in volume within confined orbital
spaces results in an acute increase in orbital tension.
The pathophysiology is similar to other compart-
ment syndromes (for instance, limb compartment
syndrome, acute glaucoma) and as a group, com-
partment syndromes are common and result in
retinal compromise may develop rapidly causing
irreversible vision loss. Studies suggest that 60--
100 minutes of raised orbital pressure may cause
permanent visual sequelae.34 Common causes in-
clude acute orbital hemorrhage due to trauma,
surgery, local injections, and preexisting medical
conditions. There are other important etiologies of
OCS such as fulminant orbital cellulitis or intra-
orbital abscess, orbital emphysema, inflammation,
and tumors. Less commonly, prolonged hypoxemia
with capillary leak, foreign material in the orbit,

441
Ó 2009 by Elsevier Inc. 0039-6257/09/$--see front matter
All rights reserved. doi:10.1016/j.survophthal.2009.04.005
442 Surv Ophthalmol 54 (4) July--August 2009
massive fluid resuscitation after burn injury, or
position-dependent edema can result in an acute
rise in orbital pressure. Although there are numer-
ous case reports on OCS from various etiologies, the
diagnostic features and management of this group
of disorders are poorly summarized in the literature.
We review the clinical presentation, radiological
findings, and management of OCS, as early recog-
nition and intervention before visual changes arise
is fundamental.
II. Anatomy
The orbit has a volume of 30 ml, consisting of the
globe, fat, extraocular muscles, vessels, nerves,
lacrimal gland, and lacrimal sac within complex
fascial compartments.10,42 The globe and orbital
contents are bound on three sides by four rigid bony
walls and anteriorly by the orbital septum and
eyelids, which form another fairly inflexible bound-
ary. The medial and lateral canthal tendons attach
the eyelids to the orbital rim and limit the forward
movement of the globe.
The orbit may be divided into several anatomical
spaces including subperiosteal, extraconal, and
intraconal. Different pathologies may typically in-
volve specific anatomical spaces. For example,
orbital cellulitis may be associated with an abscess,
usually occupying the subperiosteal space.
III. Pathophysiology
Visual loss in OCS has been attributed to one or
more of the following causes: central retinal artery
occlusion, direct compressive optic neuropathy,
compression of optic nerve vasculature, and ische-
mic optic neuropathy as the result of stretching of
nutrient vessels.21 Acutely the orbit may compensate
for small increases in orbital volume by forward
movement of the globe and prolapse of fat, then
followed immediately by a rapid rise in orbital
pressure. The orbit, therefore, follows pressure--
volume dynamics with a pathophysiology like other
compartment syndromes in which increased tissue
pressures in an enclosed space are associated with
decreased perfusion.
Normal intraorbital pressure has been measured at
3--6 mm Hg.44,65 When tissue pressure exceeds that
within arteries, flow ceases.6,18 If the vasa nervorum are
affected, optic nerve compromise may occur. Retinal
ischemia results when orbital pressure exceeds central
retinal artery pressure. Because there is no lymphatic
drainage in the orbit, the only outflow pathway is
through major veins such as the superior ophthalmic.
These drainage pathways may be compromised,
LIMA ET AL
further worsening the situation. Besides affecting
perfusion, increased orbital pressure may directly
damage the orbital component of the optic nerve by
compression or stretching.19 In one study, an acute
increase in orbital volume following a 7-ml retrobulbar
injection resulted in significant topographic evidence
of optic disk edema and rim changes which lasted up to
1 month.2
IV. Clinical Presentation and Diagnosis
OCS is essentially a clinical diagnosis. As correct
management depends on a speedy and accurate
diagnosis, it is of great importance to elicit a detailed
history and be familiar with signs of elevated orbital
pressure on examination.
A. HISTORY
Patients may complain of acute onset decreased
vision, double vision, painful periorbital edema, or
proptosis. These symptoms develop rapidly over
a period of minutes to hours, except in cases of an
acute on chronic presentation, such as hemorrhage
within a preexisting lesion. A history of recent
surgery, trauma, chronic sinusitis, or bleeding disor-
der may be elicited. Clinicians should inquire about
the use of anti-platelet, blood-thinning, or thrombo-
lytic medications.1,17 Chronic corticosteroid use may
also increase the tendency for bleeding. Non-pre-
scription drugs (nonsteroidal antiiflammatories, cold
and flu preparations) and herbal supplements (ginko
biloba, ginseng, garlic) should be noted.77
B. EXAMINATION
On examination, there may be decreased visual
acuity with an afferent pupillary defect, and the
intraocular pressure is usually elevated. Orbital signs
often include limited ocular movements and propto-
sis. Periocular edema, tenderness and ecchymosis may
be significant (Fig. 1). Evidence of increased orbital
pressure include ‘‘tense lids’’ and resistance to retro-
pulsion with a minimally ballottable globe: ‘‘a tight
orbit.’’ Fundoscopy may reveal optic disk edema,
retinal venous congestion, central retinal artery
pulsations or occlusion, or retinal edema.16 Significant
ecchymoses or subconjunctival hemorrhage may
occur with orbital hemorrhage. Orbital emphysema
may be suspected if periorbital crepitus is present.41,52
V. Diagnostic Testing
In patients with OCS and rapidly progressing
symptoms and signs, vision loss, or an afferent
papillary defect, emergent orbital decompression
ORBITAL COMPARTMENT SYNDROME 443

Fig. 1. Clinical photograph of a patient with OCS after blunt trauma who had right periocular edema, ecchymosis,
proptosis and limitation in right gaze (left) and left gaze (right).

should not be delayed by further imaging or testing. B. MAGNETIC RESONANCE ANGIOGRAPHY OR

Diagnosis should be made clinically and treatment MAGNETIC RESONANCE VENOGRAPHY
initiated immediately because of the risk of rapid, In cases where underlying vascular anomalies are
irreversible vision loss. If performed in a timely suspected, magnetic resonance angiography (MRA)
manner, however, further testing may confirm the or magnetic resonance venography (MRV) may be
diagnosis or affect management in several ways. The helpful.40 Acute hemorrhage may occur in the
severity of the problem may be demonstrated, setting of venous malformations and lymphangio-
leading to prompt intervention. The initial man- mas of the orbit. These may be characterized and
agement of OCS (canthotomy and cantholysis) is localized with MRA or MRV to better guide
a purely clinical decision and unaffected by imaging; treatment.
however, imaging may reveal the cause of raised
orbital pressure and location of pathology, further
C. ANGIOGRAPHY OR VENOGRAPHY
directing treatment. Emergent imaging is indicated
when initial decompression fails to relieve the OCS, Angiography and venography are the gold stan-
as this may reveal as a treatable cause such as a large dards for visualization of vascular lesions.40 Al-
sub-periosteal hematoma. though they are more invasive and carry a higher
risk of adverse effects, these tests may better
A. COMPUTED TOMOGRAPHY OR MAGNETIC delineate the extent of vascular anomalies.
RESONANCE IMAGING
Computed tomography (CT) is commonly used to D. COAGULATION STUDIES
further evaluate the orbits as it is often immediately For spontaneous orbital hemorrhage, coagulation
available, whereas magnetic resonance imaging (MRI) studies including bleeding time may be useful in
often cannot be obtained in a timely manner. Orbital identifying the underlying cause of coagulopathy.
imaging may reveal posterior globe tenting where the
posterior globe develops a conical shape. A posterior
globe angle of less than 120 in the context of acute
proptosis carries a poorer prognosis with higher risk of
permanent vision loss (Fig. 2).19 It should be noted,
however, that tenting may also be seen in conditions
other than OCS, for example, in association with
severe proptosis or globe subluxation in thyroid
ophthalmopathy.67 Imaging may also identify the
location and source of raised orbital tension, such as
retrobulbar hemorrhage, emphysema, or foreign
material. MRI may be important as different stages of
hemorrhage may be identified. Evidence of acute or
active bleeding may apparent. If a metal foreign body is
Fig. 2. Soft tissue computed tomography of the orbit of
suspected, however, MRI is contraindicated. Imaging a patient with fulminant orbital cellulitis after strabismus
may be particularly helpful in pediatric cases when surgery. Posterior globe tenting of approximately 70 was
subjective responses may be unreliable. revealed, confirming orbital compartment syndrome.
444 Surv Ophthalmol 54 (4) July--August 2009
The severity of the bleeding disorder may be
assessed to guide whether surgical intervention
may be performed safely. Further testing for un-
derlying blood dyscrasias (severe anemia, von
Willebrand disease, hemophilia, leukemia, sickle
cell disease, hepatitis and scurvy) may be required.
E. MANOMETRY
Manometry can be used to measure the orbital
tissue tension directly, but is not commonly em-
ployed. Riemann and coworkers used a 23-G retro-
bulbar needle connected to an infusion pump and
pressure transducer to measure intraobital ten-
sion.65 Although a pressure above 30 mm Hg has
been used to diagnose limb compartment syn-
drome,65 no equivalent data are available for OCS.
Although manometry is technically feasible, it
remains impractical in the urgent clinical setting
due to availability, complicated setup, and
invasiveness.44,56,65
VI. Differential Diagnosis
There are a number of conditions that cause
acute or subacute proptosis and which may also be
associated with lid edema, conjunctival chemosis,
and visual disturbances. These include idiopathic or
specific autoimmune orbital inflammation, thyroid
ophthalmopathy, ruptured dermoid cyst, and pro-
gressively enlarging masses. The clinical courses are
not as rapid as found in OCS. Although orbital
decompression may be required in certain cases,
this is seldom an emergency.
VII. Etiology
A. ORBITAL HEMORRHAGE
Acute hemorrhage within the confined orbital space
may quickly compromise perfusion. In a review of
studies of OCS, orbital hemorrhage from various
causes including trauma, surgery, and other underly-
ing medical conditions accounted for 64% (49/77) of
cases.1,4,11,19,23,26,27,29,31,35,37,41,43,45,46,50--52,54,57,62
1. Trauma
Orbital hemorrhage from facial trauma may result
in OCS,27,31,46,66,74,79,80 and it is often associated
with orbital or facial fractures.72,78 In one study,
orbital hemorrhage was associated with more than
half of all blinding complications in facial trauma,
particularly that with Le Fort II, Le Fort III, and
zygomaticomaxillary fractures.79 Even facial trauma
without evidence of facial fractures may result in
hemorrhage, edema, compression, and vascular
LIMA ET AL
occlusion. Indirect trauma such as uncontrolled
sneezing, coughing, Valsalva, labor, and barotrauma
may result in bleeding into the orbit.77
2. Surgery
Orbital hemorrhage as a postoperative complica-
tion of orbital or periorbital surgery50 is well
described following any surgery in which the orbital
septum in breached. Orbital hemorrhage has been
reported in fracture repair and biopsy of the
orbit.47,53,59 Oculoplastic and lacrimal procedures
at risk for this include blepharoplasty 4,14,20,29,33 and
dacryocystorhinostomy.39
The incidence of orbital hemorrhage associated
with blepharoplasty is 0.055% (1:2,000), and that
with permanent visual loss is 0.04--0.0045% (1:
2,500--1:20,000).20,33 The majority of these cases
occurred within the first 3 hours after surgery, and
the risk significantly decreased after 24 hours.
Bleeding into the orbit is thought to occur when
the septum is breached during preaponeurotic fat
excision. Traction on orbital fat may also occur,
tearing deep orbital vessels. Reflex vasodilatation
after the effects of epinephrine have worn off may
also contribute to postoperative hemorrhage.33
General ophthalmologists should be aware that
OCS may develop from retrobulbar hemorrhage after
routine procedures such as orbital, peribulbar, and
retrobulbar injections.8,11,15,30,57,60,64 Retrobulbar
hemorrhage occurs in less than 2% of retrobulbar
and peribulbar anesthetic injections and may result in
devastating visual loss if not promptly managed.11,57
Orbital hemorrhage may also occur as a result of
non-ophthalmic surgeries. It has been associated
with sinus surgery,8,12,16,22,58,68 facial trauma sur-
gery,24,28,61 orthognathic,50 and neurosurgery in-
volving the anterior or middle cranial fossas. Orbital
hemorrhage is the most common ophthalmic
complication of endoscopic sinus surgery, with an
incidence of 0.12%.16,22,55,58 Arterial bleeding re-
sulting from ethmoidal arteries may lead to OCS.69
In one study, the most frequent cause of visual loss
after repair of facial fractures (18 out of 27
cases—67%) was increased orbital pressure as the
result of hemorrhage.28
3. Hemorrhage into Preexisting Lesions
In addition to trauma and surgery, acute orbital
hemorrhage may occur with underlying disease such
as venous and lymphatic anomalies, ophthalmic
artery aneurysm, orbital myositis, and chronic
sinusitis.77 Orbital venous malformations and lym-
phangiomas may present with acute intralesional
hemorrhage resulting in OCS.71
ORBITAL COMPARTMENT SYNDROME
4. Medical Conditions
Anticoagulant medications, such as aspirin and
other nonsteroidal anti-inflammatory agents, warfa-
rin, and clopidogrel, may play a role in OCS
secondary to hemorrhage, especially following
surgery or trauma. Herbal remedies, such as ginko
biloba, ginseng, and garlic, may have a similar effect.
Bilateral OCS in a patient with retrobulbar hemor-
rhages after thrombolysis for acute myocardial
infarction or pulmonary embolus has been de-
scribed.1,17 Patients with blood dyscrasias, such as
severe anemia, von Willebrand disease, hemophilia,
leukemia, sickle cell disease, hepatitis, and scurvy,
also have an increased propensity for uncontrolled
bleeding.77 In addition, intraorbital hemorrhage in
disseminated intravascular coagulation or antiphos-
pholipid syndrome may lead to OCS.62,73
B. ORBITAL EMPHYSEMA
Traumatic orbital fractures may rarely produce
a ball-valve effect—allowing air to enter, but not leave,
the orbit, producing high orbital pressures.23 Orbital
emphysema resulting in OCS has also been described
in compressed air injuries.13 Orbital emphysema with
OCS has been associated with orbital decompression
and sinus surgery, especially when uncontrolled
coughing and Valsalva occur.16,41
C. ORBITAL CELLULITIS
Orbital cellulitis is an infective process occurring
predominantly in children and young adults com-
monly associated with sinus disease. Fulminant
infection with rapidly progressing orbital inflamma-
tion may lead to OCS. Subperiosteal abscess
formation alone or in combination with orbital
cellulitis may result in an acute rise in orbital
pressure.43,45 OCS may present as an acute de-
terioration in a patient with known orbital cellulitis.
Rare cases of severe orbital cellulitis complicating
strabismus surgery75 or after peribulbar injection
have been reported.36
D. ORBITAL EDEMA
Progressive orbital edema may result in high
orbital tension. This is often associated with trauma
or surgery. In patients with significant thermal
injury, edema results from capillary leakage and
massive fluid resuscitation.70 A contracted eyelid
and septum from the burn injury may further
contribute to increased orbital pressure. Hence
ophthalmologists should be aware of the potential
for OCS in severely burned patients undergoing
extensive fluid resuscitation. OCS may also occur in
traumatic asphyxia syndrome, which is characterized
445
by sudden compressive chest trauma and subse-
quent facial edema, craniocervical cyanosis, and
respiratory failure.63
Patients undergoing prolonged surgery in the
prone position are also at risk of OCS. Hollenhorst
and coworkers reported a series of eight patients
who developed unilateral blindness following prone
positioning while under general anesthesia.38 Ex-
amination revealed a hazy cornea, dilated pupil, and
macular edema in all cases. Five of the cases had
associated proptosis and lid edema. None of these
five patients recovered useful vision, whereas visual
recovery was excellent in the other three cases. Two
further cases of OCS with progressive orbital edema
after spinal surgery in the prone position and
possible direct pressure on periorbital structures
from the headrest device have been reported.48,49
The visual recovery was poor in both cases. The
mechanism of OCS in these cases, as proposed by
Lee, appears to be orbital venous congestion
secondary to mechanical pressure.48 Similarly, a pa-
tient trapped in the prone position after an accident
developed OCS from position-dependent edema.25
E. FOREIGN MATERIAL
OCS has been reported as the result of foreign
materials such as extravasated contrast dye during
catheterization of the middle meningeal artery.26
Hydraulic orbital injection injuries involving hydro-
carbons and other high-pressure liquids have been
associated with OCS.37 During sinus surgery, re-
tained foreign material, such as bacitracin ointment,
may lead to an acute rise in orbital pressure.16 In
addition, two cases of OCS secondary to retention of
oxidized regenerated cellulose in the orbit have
been described.5
F. OTHER CAUSES
Acute orbital inflammation may rarely occur as an
allergic reaction to peribulbar lignocaine injection
for cataract surgery. Progressive inflammation and
OCS may require decompression.76
VIII. Prevention
Patients with orbital trauma or those who have
undergone orbital decompression often have sino-
orbital communications. Advising these patients to
avoid nose-blowing, Valsalva, or coughing may mini-
mize the risk of orbital hemorrhage or emphysema.41
To minimize the development of orbital hemor-
rhage associated with surgery, a careful evaluation of
patient medications is advised. Platelet inhibitors
and blood thinners should be avoided if possible,
including nonprescription medications and herbal
446 Surv Ophthalmol 54 (4) July--August 2009
supplements. Patients with history of hepatitis or
blood dyscrasias should have coagulopathies stabi-
lized prior to surgery.
Intraoperatively, meticulous hemostasis should be
achieved with bipolar cautery and adjuncts such as
gelatin sponge or bone wax. Excision of fat should be
performed under direct visualization and avoidance
of excess traction on deep orbital fat. Blood pressure
should be controlled to avoid high fluctuations.
Gentle awakening from general anesthesia with
adequate pain and nausea control, and suppression
of the cough reflex, may minimize straining and the
risk of orbital hemorrhage or emphysema.50
After surgery, patients at risk for bleeding may be
hospitalized for 24-hour observation when the risk
of hemorrhage is greatest.33,77 Many surgeons will
patch patients postoperatively; however, this has
been discouraged by those who believe that occlu-
sive dressings may delay detection of vision loss and
hemorrhage.33 Patients should be advised to contact
their medical provider immediately if vision loss,
uncontrolled pain, or bleeding occurs.
For cases of orbital cellulitis or inflammation,
prompt treatment with antibiotics or anti-inflamma-
tory agents may minimize orbital pressure. Patients
undergoing extensive procedures requiring prone
positioning may benefit from regular intraoperative
monitoring for signs of increased orbital pressure.
The American Society of Anesthesiologists has
released a practice advisory for perioperative visual
loss associated with spine surgery.3
IX. Management
A. SURGICAL DECOMPRESSION
Emergent decompression may be performed at the
bedside quickly by a lateral canthotomy and inferior
cantholysis.31,68,74 This involves cutting the lateral
canthal tendon along its length to the orbital rim and
disinserting the inferior limb of the tendon from the
bony orbit. Several studies have shown a significant,
immediate decrease in orbital pressure after this
simple procedure.66,79 A study that simulated orbital
hemorrhage by injection of normal saline into sheep
orbits showed that greater reduction in intraocular
pressure was achieved by lateral canthotomy and
cantholysis (30.4 mm Hg) compared with canthotomy
(14.2 mm Hg) or cantholysis (19.2 mm Hg) alone.79
In most cases, the lateral canthus heals spontaneously
thereafter. However, if lower lid ectropion or cosmetic
deformity persists, repair can be performed at a later
date.
In the case of postoperative OCS due to orbital
hemorrhage, we recommend first decompressing
the surgical incision then evacuating the hematoma
LIMA ET AL
and cauterizing bleeding vessels. Physicians should
be readily available for at least the first 24 hours
after surgery to evaluate any warning symptoms and
signs that may arise.33 In a study based on a survey to
members of the American Society of Ophthalmic
Plastic and Reconstructive Surgery, treatment of
OCS following post-blepharoplasty hemorrhage in-
frequently required orbital decompression.33
If lateral canthotomy and inferior cantholysis fail to
relieve orbital tension and restore perfusion to the
optic nerve and retina, further disinsertion of the
superior limb of the lateral canthal tendon may be
performed. Once the canthotomy and cantholysis are
performed, the clinical signs should be rechecked
and, if there is no improvement within a few minutes,
then the orbital septum should be divided from its
attachment to the orbital rims. This release of the
septum can be performed either transconjunctivally
in the lower lid by extending the canthotomy incision
medially or via an anterior approach through the skin
and orbicularis to reach the septum.
When extensive decompression is necessary,
urgent referral to an orbital surgeon for further
management is recommended. The medial, lateral
wall or floor of the orbit may then be removed in the
operating room to provide space for expansion of
orbital contents.
Other forms of decompression have been described
in the literature that may be reserved for patients
requiring urgent surgical treatment with limited access
to an orbital surgeon. Burkat described evacuation of
a hematoma or trapped air in the emergent setting by
means of an inferolateral anterior orbitomy.11 This
involved blunt spreading with scissors into the infero-
lateral quadrant of the orbit through the lateral
canthotomy incision, until the orbital septum is
entered and the hematoma or air may be evacuated.
Direct needle aspiration of hematomas and trapped
intraorbital air to relieve orbital tension has also been
described; however, this carries a risk of globe
perforation.52,54 Liu described fracturing the orbital
floor with a mosquito clamp through an inferior fornix
incision to decompress an orbit with retrobulbar
hemorrhage.53 With this technique, care must be
taken to avoid the infraorbital neurovascular bundle.
Anterior chamber paracentesis has been de-
scribed in reperfusing the central retinal artery.
However, this should be avoided as it may be
associated with significant morbidity in the setting
of increasing orbital tension.33
B. MEDICAL MANAGEMENT
Patients should be advised to avoid coughing or
straining. Cough suppressants, antiemetics, and
stool softeners may be required. The head of the
ORBITAL COMPARTMENT SYNDROME
bed should be elevated at least 45 .14 Ice packs may
reduce blood flow and edema to the orbit. Blood
pressure and coagulopathies should be normalized.
Simultaneous medical treatment of the underlying
cause for OCS should be initiated. For example,
systemic antibiotics should be instituted if infection is
a concern76 and intravenous or oral corticosteroids if
there is inflammation. In addition to limiting post-
traumatic and postoperative edema, high doses of
corticosteroids in acute spinal cord injury have an
antioxidant effect, further protecting neural tissues
from free radical damage that occurs after ischemic
injury.9,32 Many cases of OCS have been treated
adjunctively with corticosteroids, some of which
regained vision, while others did not.28,29,33,49,62,76
The effectiveness of corticosteroids in OCS has not
been assessed in a systematic fashion.
In mild or refractory instances of increased in-
traocular pressure, medical management may in-
clude osmotic agents, carbonic anhydrase inhibitors,
or aqueous suppressants.28,33,50,78 Again, the exact
efficacy of these agents is uncertain. In all cases of
OCS, close monitoring for progression or recurrence
of disease is crucial. Patients should be instructed to
return immediately if there is increased pain,
proptosis, or blurry vision.
X. Prognosis
A. TIME ELAPSED UNTIL TREATMENT
Several studies suggest that delayed treatment of
OCS is more likely to result in permanent vision
loss.7,27,35,43,68 Of six cases of traumatic retrobulbar
hemorrhage with vision loss, Hislop reported that all
four cases with delayed surgical management
sustained complete blindness.35 In contrast, both
cases promptly treated with orbital decompression
and medical management recovered vision fully.
Another study observed that the majority (12/16)
patients with acute orbital hemorrhage and OCS
recovered vision when decompressed within a mean
of 30 hours after symptoms appeared.42
B. GLOBE TENTING
The amount of globe tenting on imaging reflects
the acuteness of proptosis and may predict visual
compromise. A posterior globe angle of less than
120 with acute proptosis carries a poorer prognosis
with higher risk of permanent vision loss requiring
rapid orbital decompression.19
C. AGE
In a series of 10 patients with orbital compartment
syndrome and posterior globe tenting, Dalley found
447
that younger patients recovered more completely.19
Furthermore, older patients presented with more
severe visual loss. In 77 cases of OCS found in the
literature, we found that 81% of cases occurred in
patients more than 20 years old, most commonly
related to trauma (45%) and surgery (32%). Al-
though half of young patients with OCS were found to
have associated trauma or surgery, children with OCS
also presented with a greater proportion of orbital
infection and congenital lesions associated with an
orbital hemorrhage (varix, lymphangioma, multiple
epithelial implantation cysts).
XI. Summary
OCS is a rare but devastating condition whose
incidence may be rising as the result of higher rates of
aspirin, anti-platelet, and thrombolytic use in an aging
population, and increased facial trauma and cosmetic
surgery. Minimizing the risk of OCS after trauma and
surgery is as important as prompt diagnosis and
decompression to save vision. Ophthalmologists and
emergency physicians should be familiar with lateral
canthotomy and inferior cantholysis, as this simple
procedure must be performed rapidly on presentation
to the emergency department. However, if the orbit
remains tense, immediate specialist consultation may
be required for orbital decompression.
XII. Method of Literature Search
Literature search was based on a Medline search
with Pubmed, including the keywords orbital com-
partment syndrome, orbital compression syndrome, orbital
tension, orbital manometry, lateral canthotomy, globe
tenting and orbital decompression. Articles published
between 1965 and 2008 were retrieved. Articles were
restricted to those in English and other-language
publications with English abstracts and references
within these articles were also obtained for review.
References
1. Ahmar W, Mason K, Harley N, Hogan C. An unusual
complication of thrombolysis—bilateral retro-orbital hae-
matomata. Anaesth Intensive Care. 2005;33:271--3
2. Akar Y, Apaydin KC, Ozel A. Acute orbital effects of
retrobulbar injection on optic nerve head topography. Br J
Ophthalmol. 2004;88:1573--6
3. American Society of Anesthesiologists. Practice advisory for
perioperative visual loss associated with spine surgery.
Anesthesiology. 2006;104:1319--28
4. Anderson RL, Edwards JJ. Bilateral visual loss after bleph-
aroplasty. Ann Plast Surg. 1980;5:288--92
5. Arat YO, Dorotheo EU, Tang RA, et al. Compressive optic
neuropathy after use of oxidized regenerated cellulose in
orbital surgery: review of complications, prophylaxis, and
treatment. Ophthalmology. 2006;113:333--7
448 Surv Ophthalmol 54 (4) July--August 2009
6. Ashton H. The effect of increased tissue pressure on blood
flow. Clin Orthop Relat Res. 1975;113:15--26
7. Bailey WK, Paul C, Evans LS. Diagnosis and treatment of
retrobulbar haemorrhage. J Oral Maxillofac Surg. 1993;51:
780--1
8. Bhatti MT, Stankiewicz JA. Ophthalmic complications of
endoscopic sinus surgery. Surv Ophthalmol. 2003;48:389--
402
9. Braughler JM, Hall ED. Effects of multi-dose methylpred-
nisolone sodium succinate administration on injured cat
spinal cord neurofilament degradation and energy metab-
olism. J Neurosurg. 1984;61:290--5
10. Bron AJ, Tripathi RC, Tripathi BJ. Wolff’s Anatomy of the
Eye and Orbit. Oxford, Oxford University Press, 1997. p 752.
11. Burkat CN, Lemke BN. Retrobulbar hemorrhage: infero-
lateral anterior orbitotomy for emergent management. Arch
Ophthalmol. 2005;123:1260--2
12. Buus DR, Tse DT, Farris BK. Ophthalmic complications of
sinus surgery. Ophthalmology. 1990;97:612--9
13. Caesar R, Gajus M, Davies R. Compressed air injury of the
orbit in the absence of external trauma. Eye. 2003;17:661--2
14. Callahan MA. Prevention of blindness after blepharoplasty.
Ophthalmology. 1983;90:1047--51
15. Carroll RP. Blindness following lacrimal nerve block.
Ophthalmic Surg. 1982;13:812--4
16. Castro E, Seeley M, Kosmorsky G, Foster JA. Orbital compart-
ment syndrome caused by intraorbital bacitracin ointment after
endoscopic sinus surgery. Am J Ophthalmol. 2000;130:376--8
17. Chorich LJ, Derick RJ, Chambers RB, et al. Hemorrhagic
ocular complications associated with the use of systemic
thrombolytic agents. Ophthalmology. 1998;105:428--31
18. Dahn I, Lassen NA, Westling H. Blood flow in human
muscles during external pressure or venous stasis. Clin Sci.
1967;32:467--73
19. Dalley RW, Robertson WD, Rootman J. Globe tenting: a sign
of increased orbital tension. AJNR. 1989;10:181--6
20. Demere M, Wood T, Austin W. Eye complications with
blepharoplasty or other eyelid surgery. A national survey.
Plast Reconstr Surg. 1974;53:634--7
21. Dolman PJ, Glazer LC, Harris GJ, et al. Mechanisms of visual
loss in severe proptosis. Ophthal Plast Reconstr Surg. 1991;
7:256--60
22. Dunya IM, Salman SD, Shore JW. Ophthalmic complications
of endoscopic ethmoid surgery and their management. Am J
Otolaryngol. 1996;17:322--31
23. Fleishman JA, Beck RW, Hoffman RO. Orbital emphysema
as an ophthalmologic emergency. Ophthalmology. 1984;91:
1389--91
24. Forrest CR, Khairallah E, Kuzon WM Jr. Intraocular and
intraorbital compartment pressure changes following orbital
bone grafting: a clinical and laboratory study. Plast Reconstr
Surg. 1999;104:48--54
25. Fuller JR, Vote BJT. Upside-down orbitopathy: unilateral
orbital dependent-tissue oedema causing total visual loss.
Clin Exp Ophthalmol. 2001;29:265--7
26. Gerber SL, Duprat G. Orbital compression syndrome after
orbital extravasation of x-ray contrast material. Am J
Ophthalmol. 2000;130:530--1
27. Gerbino G, Ramieri GA, Nasi A. Diagnosis and treatment of
retrobulbar haematomas following blunt orbital trauma:
a description of eight cases. Int J Oral Maxillofac Surg. 2005;
34:127--31
28. Girotto JA, Gamble WB, Robertson B, et al. Blindness after
reduction of facial fractures. Plast Reconstr Surg. 1998;102:
1821--34
29. Goldberg RA, Marmor MF, Shorr N, Christenbury JD.
Blindness following blepharoplasty: two case reports, and
a discussion of management. Ophthalmic Surg. 1990;21:85--9
30. Goldsmith MO. Occlusion of the central retinal artery
following retrobulbar hemorrhage. Ophthalmologica. 1967;
153:191--6
31. Goodall KL, Brahma A, Bates A, Leatherbarrow B. Lateral
canthotomy and inferior cantholysis: an effective method of
urgent orbital decompression for sight threatening acute
LIMA ET AL
retrobulbar haemorrhage. Injury Int J Care Injured. 1999;
30:485--90
32. Hall ED, Braughler JM. Glucocorticoid mechanisms in acute
spinal cord injury: a review and therapeutic rationale. Surg
Neurol. 1982;18:320--7
33. Hass AN, Penne RB, Stefanyszyn MA, Flanagan JC. In-
cidence of postblepharoplasty orbital hemorrhage and
associated visual loss. Ophthal Plast Reconstr Surg. 2004;
20:426--32
34. Hayreh SS, Kolder WE, Weingeist TA. Central retinal artery
occlusion and retinal tolerance time. Ophthalmology. 1980;
87:75--8
35. Hislop WS, Dutton GN. Retrobulbar haemorrhage: can
blindness be prevented? Injury. 1994;25:663--5
36. Hofbauer JD, Gordon LK, Palmer J. Acute orbital cellulitis
after peribulbar injection. Am J Ophthalmol. 2004;118:391--
2
37. Holds JB, Patrinely JR, Zimmerman PL, Anderson RL.
Hydraulic orbital injection injuries. Ophthalmology. 1993;
100:1475--82
38. Hollenhorst RW, Svien HJ, Benoit CF. Unilateral blindness
occurring during anesthesia for neuro-surgical operations.
Arch Ophthalmol. 1954;52:819--30
39. Hurwitz JJ, Eplett CJ, Fliss D, Freeman JL. Orbital hemorrhage
during dacryocystorhinostomy. Can J Ophthalmol. 1992;27:
139--42
40. Kahana A, Lucarelli MJ, Gravey AM, et al. Noninvasive dynamic
magnetic resonance angiography with Time-Resolved Imaging
of Contrast Kinetics (TRICKS) in the evaluation of orbital
vascular lesions. Arch Ophthalmol. 2007;125:1635--42
41. Katz SE, Lubow M, Jacoby J. Suck and spit, don’t blow:
orbital emphysema after decompression surgery. Ophthal-
mology. 1999;106:1303--5
42. Koornneef L. Spatial Aspects of Orbital Musculo-Fibrous
Tissue in Man: A New Anatomical and Histological
Approach. Amsterdam, Swets & Zeitlinger B.V, 1977
43. Korinth MC, Weinzierl MR, Banghard W, Gilsbach JM.
Extended pterional orbital decompression in severe orbital
cellulitis. Acta Neurochir. 2003;145:283--7
44. Kratky V, Hurwitz JJ, Avram DR. Orbital compartment
syndrome. Direct measurement of orbital tissue pressure:
1. Technique. Can J Ophthalmol. 1990;25:293--7
45. Krausen AS, Ogura JH, Burde RM. Emergency orbital
decompression: a reprieve from blindness. Otolaryngol
Head Neck Surg. 1981;89:252--6
46. Larsen M, Wieslander S. Acute orbital compartment
syndrome after lateral blow-out fracture effectively relieved
by lateral cantholysis. Acta Ophthalmol Scand. 1999;77:
232--3
47. Lederman IR. Loss of vision associated with surgical
treatment of zygomatic-orbital floor fractures. Plast Reconstr
Surg. 1981;68:94--9
48. Lee AG. Orbital apex syndrome following cervical spine
surgery. Middle East J Ophthalmol. 2002;10:64--5
49. Leibovitch I, Casson R, Laforest C, Selva D. Ischemic orbital
compartment syndrome as a complication of spinal surgery
in the prone position. Ophthalmology. 2006;113:105--8
50. Li KK, Meara JG, Rubin P. Orbital compartment syndrome
following orthognathic surgery. J Oral Maxillofac Surg.
1995;53:964--8
51. Linberg JV. Orbital emphysema complicated by acute
central retinal artery occlusion: case report and treatment.
Ann Ophthalmol. 1982;14:747--9
52. Linberg JV. Orbital compartment syndromes following
trauma. Adv Ophthalmol Plast Reconstr Surg. 1987;6:51--62
53. Liu D. Complications of fine needle aspiration biopsy of the
orbit. Ophthalmology. 1985;92:1768--71
54. Markovits AS. Evacuation of orbital hematoma by continu-
ous suction. Ann Ophthalmol. 1977;9:1255--8
55. May M, Levine HL, Mester SJ, Schaitkin B. Complications of
endoscopic sinus surgery: analysis of 2108 patients—inci-
dence and prevention. Laryngoscope. 1994;104:1080--3
56. McGowan HD, Hurwitz JJ, Gentles W. Orbitotonography, the
dynamic assessment of orbital tension: 1. Results in subjects
ORBITAL COMPARTMENT SYNDROME 449

without known orbital disease. Can J Ophthalmol. 1984;19:
122--5
57. Mootha VV, Cowden TP, Sires BS, Dortzbach RK. Subper-
iosteal orbital hemorrhage from retrobulbar injection
resulting in blindness. Arch Ophthalmol. 1997;115:123--4
58. Neuhaus RW. Orbital complications secondary to endo-
scopic sinus surgery. Ophthalmology. 1990;97:1512--8
59. Nicholson DH, Guzak SW. Visual loss complicating repair of
orbital floor fractures. Arch Ophthalmol. 1971;86:369--75
60. Olitsky SE, Juneja RG. Orbital hemorrhage after the
administration of sub-tenon’s infusion anesthesia. Ophthal-
mic Surg Lasers. 1997;28:145--6
61. Ord RA. Post-operative retrobulbar haemorrhage and blind-
ness complicating trauma surgery. Br J Oral Surg. 1981;19:202--7
62. Patchett RB, Wilson WB, Ellis PP. Ophthalmic complications
with disseminated intravascular coagulation. Br J Ophthal-
mol. 1988;72:377--9
63. Prodhan P, Noviski NN, Doody DP, et al. Orbital compart-
ment syndrome mimicking cerebral herniation in a 12-yr-old
boy with severe traumatic asphyxia. Pediatr Crit Care Med.
2003;4:367--9
64. Puustjarvi T, Purhonen S. Permanent blindness following
retrobulbar hemorrhage after peribulbar anesthesia for
cataract surgery. Ophthalmic Surg. 1992;23:450--2
65. Riemann CD, Foster JA, Kosmorsky GS. Direct orbital
manometry in patients with thyroid-associated orbitopathy.
Ophthalmology. 1999;106:1296--302
66. Rosdeutscher JD, Stadelmann WK. Diagnosis and treatment
of retrobulbar hematoma resulting from blunt periorbital
trauma. Ann Plast Surg. 1998;41:618--22
67. Rubin PA, Watkins LM, Rumelt S, et al. Orbital computed
tomographic characteristics of globe subluxation in thyroid
orbitopathy. Ophthalmology. 1998;105:2061--4
68. Saussez S, Choufani G, Brutus JP, et al. Lateral canthotomy:
a simple and safe procedure for orbital haemorrhage secondary
to endoscopic sinus surgery. Rhinology. 1998;36:37--9
69. Stankiewicz JA, Chow JM. Two faces of orbital hematoma in
intranasal (endoscopic) sinus surgery. Otolaryngol Head
Neck Surg. 1999;120:841--7
70. Sullivan SR, Ahmadi AJ, Singh CN, et al. Elevated orbital
pressure: another untoward effect of massive resuscitation
after burn injury. J Trauma. 2006;60:72--6
71. Sullivan TJ, Wright JE. Non-traumatic orbital haemorrhage.
Clin Exp Ophthalmol. 2000;28:26--31
72. Thyne GM, Luyk NH. Zygomatic bone fractures complicated
by retrobulbar haemorrhage. NZ Dent J. 1992;88:60--3
73. Vaphiades MS, Brock W, Brown HH, et al. Catastrophic
antiphospholipid antibody syndrome manifesting as an orbital
ischemic syndrome. J Neuroophthalmol. 2001;21:260--3
74. Vassallo S, Hartstein M, Howard D, Stetz J. Traumatic
retrobulbar hemorrhage: emergent decompression by lat-
eral canthotomy and cantholysis. J Emerg Med. 2002;22:
251--6
75. von Noorden GK. Orbital cellulitis following extraocular
muscle surgery. Am J Ophthalmol. 1972;74:627--9
76. Walters G, Georgious T, Hayward JM. Sight-threatening
acute orbital swelling from peribulbar local anesthesia. J
Cataract Refract Surg. 1999;25:444--6
77. Wilcsek GA, Kazim M, Francis IC, et al. Acute orbital
hemorrhage. In Holck DEE, Ng JD (eds): Evaluation and
Treatment of Orbital Fractures. Philadelphia, PA, Elsevier,
2006, pp. 381--9
78. Wood GD. Blindness following fracture of the zygomatic
bone. Br J Oral Maxillofac Surg. 1992;24:12--6
79. Yung C, Moorthy RS, Lindley D, et al. Efficacy of lateral
canthotomy and cantholysis in orbital hemorrhage. Ophthal
Plast Reconstr Surg. 1994;10:137--41
80. Zachariades N, Papavassiliou D, Christopoulos P. Blindness
after facial trauma. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 1996;81:34--7
The authors reported no proprietary or commercial interest in
any product or concept discussed in this article.
Reprint address: Vanessa Lima, MD, Department of Ophthalmol-
ogy and Visual Sciences, Royal Adelaide Hospital, Level 8, North
Terrace, Adelaide, SA 5000, Australia. E-mail: drvanessalima@
gmail.com.

Outline 1. Trauma
2. Surgery
I. Introduction 3. Hemorrhage into preexisting lesions
II. Anatomy 4. Medical conditions
III. Pathophysiology
B. Orbital emphysema
IV. Clinical presentation and diagnosis
C. Orbital cellulitis
A. History D. Orbital edema
B. Examination E. Foreign material
F. Other causes
V. Diagnostic testing
VIII. Prevention
A. Computed tomography or magnetic reso-
IX. Management
nance imaging
B. Magnetic resonance angiography or A. Surgical decompression
magnetic resonance venography B. Medical management
C. Angiography or venography
X. Prognosis
D. Coagulation studies
E. Manometry A. Time elapsed until treatment
B. Globe tenting
VI. Differential diagnosis
C. Age
VII. Etiology
XI. Summary
A. Orbital hemorrhage
XII. Method of literature search