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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).

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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

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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.

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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.

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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....

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