Emergency Physicians must be able to promptly recognize and manage
an acute orbital compartment syndrome, which is defined as an acute
elevation of intraorbital pressure with resultant ocular dysfunction.
The diagnosis of an orbital compartment syndrome is based on clinical
signs and symptoms. Patients typically present with ocular pain,
proptosis, afferent pupillary defects, and diminished visual acuity.
Clinical signs of an acute orbital compartment syndrome include chemosis,
elevated intraocular pressure, mydriasis, diminished retropulsion
of the affected globe to direct manual pressure, ophthalmoplegia,
and fundoscopic signs of retinal ischemia (rare).
Orbital compartment syndromes have been described in multiple
clinical settings. The presentation that Emergency Physicians will
most likely encounter is an acute post-traumatic retrobulbar hemorrhage
leading to an orbital compartment syndrome.1,2 Orbital
compartment syndromes have been documented following blepharoplasty,
retrobulbar anesthesia, orbital and sinus surgery, orbital fractures
with intraorbital emphysema, spontaneous subperiosteal hemorrhages,
and spontaneous retrobulbar hemorrhages.3–9 Orbital
compartment syndromes may also occur as the result of chronic and
progressive disease processes.10
Acute orbital compartment syndromes
demand prompt recognition because irreversible loss of vision occurs
without rapid treatment.11 The exact etiology of vision
loss in orbital compartment syndromes remains speculative. Possible
causes include optic nerve ischemia, direct optic nerve damage,
and retinal artery occlusion.12,13 Once the diagnosis of
an acute orbital compartment syndrome is made, emergent surgical
intervention is indicated. Immediate lateral canthotomy and cantholysis
are indicated within 1 hour of injury and ocular dysfunction. The primary therapy for an acute orbital
compartment syndrome is surgical intervention. Medical interventions
aimed at reducing intraocular pressure (e.g., mannitol, acetazolamide,
topical beta-blockers, etc.) should be considered adjunctive therapy
and not a substitute for surgical intervention.
The orbit of the eye is a closed space posterior to the orbital
septum and contained within the bony orbit. The lateral wall of
the orbit is formed by the zygomatic bone. The posterior wall is
formed by the sphenoid bone. The medial wall is formed by the ethmoid
bone. The roof is formed by the frontal bone. The floor
is formed by the maxillary bone. The globe is enclosed
in a fascial envelope.
The medial and lateral canthal tendons provide structural fixation
of the eyelids to the orbital rim. The lateral canthal tendon (LCT)
is located posterior and inferior to the lateral canthal fold (Figure
139-1). The LCT originates from the lateral tarsal plates (Figure
139-1) and attaches to the lateral orbital tubercle of the zygoma
(Figure 139-2). The LCT measures 10.6 mm (SD +/− 0.9 mm)
in length from its attachment site to the lateral canthal angle.
It is 10.2 mm (SD +/− 0.8
mm) in width at its origin at the lateral ends of the tarsal plates.
It attaches 1.5 mm (SD +/− 0.3
mm) behind the orbital margin and approximately 9.7 mm (SD +/− 0.8
mm) below the frontozygomatic suture at the lateral orbital tubercle....