Background
Acute orbital compartment syndrome (AOCS) is a rare but treatable complication of increased pressure within the confined orbital space. It typically results from facial trauma or a surgical procedure, but many medical conditions have been known to cause AOCS (see Etiology). AOCS must be promptly diagnosed. If left untreated, patients with AOCS may develop retinal ischemia and subsequent irreversible blindness (see Treatment). [1]
Anatomy
The globe and retrobulbar contents are encased in a continuous cone-shaped fascial envelope that is nearly completely bound on all sides by the rigid, bony skull. Fibrous bands known as the tarsal plates form the anterior border, limiting movement. More superficially, the eyelids come together to form the palpebral fissure, which allows the eye to open and close. The lateral and medial aspect of the fissure is formed by the canthi, where the eyelids meet. The volume of an average adult orbit is 30 mL. [1]
Pathophysiology
The variable pathophysiology of acute orbital compartment syndrome has not been fully elucidated. The orbit may compensate for small increases in orbital volume by forward movement of the globe and prolapse of fat, but larger increases result in a rapid rise in orbital tissue pressures.
Therefore, although the orbit is not a fully enclosed space, it follows pressure-volume dynamics with a pathophysiology akin to other compartment syndromes, in which increased tissue pressures in an enclosed space lead to decreased perfusion. In cases of retrobulbar hematoma, the most common cause of AOCS, hemorrhage generally emanates from the infraorbital artery or one of its branches. In acute disease, retrobulbar blood can cause a substantial rise in pressure even with as little of 7 mL of blood. [2]
The optic nerve encases the central retinal artery anatomically, providing some protection. Other vessels within the eye are less protected, which often results in blindness without central artery occlusion in the case of anterior ischemic optic neuropathy. [3] Arterial blood flow has been demonstrated to cease at tissue pressures significantly lower than diastolic blood pressure. [2] Interestingly, why some patients with a retrobulbar hematoma develop orbital compartment syndrome while others do not is unknown. Retrospective analysis has not found fracture mechanism, degree of comminution, blood volume, or dislocation to be predictive of retrobulbar hematoma resulting in AOCS. [4]
This proposed mechanism associated with retrobulbar hematomas usually creates discernible and measurable physical signs of increased orbital pressure, which may prompt sight-saving emergency department therapy. Irreversible visual loss following trauma can also be caused by direct optic neuropathy from nerve impingement, crush, or transection or indirect traumatic optic neuropathy. The exact pathophysiology of indirect traumatic optic neuropathy has not been fully elucidated, but is thought to be a consequence of traumatic transfer of forces through the orbital bones to the intracanicular optic nerve axons and pial microvasculature, causing transient traction on these fragile structures. [5]
Etiology
Retrobulbar hematoma is the most common cause of orbital compartment syndrome. Physical facial assault, motor vehicle collision (MVC), and falls are most frequently implicated in traumatic retrobulbar hematoma. [6] Additional traumatic etiologies include intraocular hematomas, orbital emphysema tracking from a sinus, and subperiosteal hematoma. In one case report, even extension of a subgaleal hematoma resulted in a delayed orbital compartment syndrome (OCS) in a patient with a known bleeding disorder. [7]
Atraumatic causes of AOCS are typically the result of facial surgery. However, AOCS has been reported in large-volume resuscitation, extravasation of contrast material, spontaneous bleeding in the setting of disseminated intravascular coagulation, mass lesions, sclerotherapy, and thyroid-associated orbitopathy. [8]
Risk factors
Patients on antiplatelet or anticoagulation therapy have been found to have a high rate of traumatic retrobulbar hematoma. [9] In addition, case reports have described patients with known bleeding disorders having delayed or atypical presentations. Conversely, orbital blowout fractures have been found to be protective against AOCS, as the "compartment" is disrupted by the displaced facial fracture.
Epidemiology
Acute orbital compartment syndrome is considered a rare complication of facial trauma or surgery. A retrospective review of 727 patients with facial fractures found that 67% sustained some degree of ocular injury. [10] Of these injuries, 18% were categorized as serious and 3% as blinding. All of the latter resulted from optic nerve injury, retinal detachment, or corneal-scleral rupture. Other studies have found AOCS to occur in less than 0.1% of all cases of facial trauma [9] and in 3.6% of patients with diagnosed orbital trauma. [6]
Prognosis
Acute orbital compartment syndrome with visual acuity loss is associated with a poor prognosis. Permanent blindness occurs if effective therapy is not initiated promptly. AOCS due to retrobulbar hematoma is the most common cause of blindness associated with facial trauma. [4]
Emergent decompressive surgery may be sight-saving in patients with severe symptoms. Significant evidence shows that long-term outcomes correlate with time to intervention in patients with severe AOCS. [11] Half of patients presenting with decreased visual acuity due to retrobulbar hematoma experience immediate resolution of symptoms with emergent decompression. Irreversible visual loss can be expected with retinal ischemia that lasts longer than 120 minutes, [12] although some patients may experience partial recovery with decompression outside this window. [6]
Patient Education
For patient education information, see the Eye and Vision Center, as well as Black Eye.
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Lateral canthotomy is performed by incising laterally with sharp scissors.
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Cantholysis is performed by identification and disinsertion of the inferior crus of the lateral canthal tendon, which should allow free mobility of the lower lid margin.
