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Acute orbital compartment syndrome is defined as an acute elevation of intraorbital pressure with resultant rapid ocular dysfunction. Patients typically present with ocular pain, proptosis, and blurry vision. Clinical signs of an acute orbital compartment syndrome include decreased visual acuity, elevated intraocular pressure (>40 mmHg), an afferent papillary defect, chemosis, mydriasis, diminished retropulsion of the affected globe to direct manual pressure, ophthalmoplegia, and fundoscopic signs of retinal ischemia (rare).1–28
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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 posttraumatic retrobulbar hemorrhage leading to an orbital compartment syndrome, with subsequent rapid loss of vision.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 (e.g., neoplasms, infections, and inflammations).10
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Acute orbital compartment syndromes demand prompt recognition because irreversible loss of vision and even permanent blindness occurs without rapid treatment.11 Once the diagnosis of an acute orbital compartment syndrome is made, emergent surgical intervention is indicated. An immediate lateral canthotomy and cantholysis are indicated within 1 hour of injury and ocular dysfunction. 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 within the bony orbit.
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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 162-1). The LCT originates from the superior and inferior lateral tarsal plates (Figure 162-1) and attaches to the lateral orbital tubercle of the zygoma (Figures 162-1 & 162-2). The LCT consists of a superior crus from the superior tarsal plate and a inferior crus from the inferior tarsal plate. 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.12 Immediately anterior to the LCT is Eisler's pocket, a ...