Acute Orbital Compartment Syndrome

Updated: Nov 04, 2015
  • Author: David A Peak, MD; Chief Editor: Robert E O'Connor, MD, MPH  more...
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Overview

Background

Acute orbital compartment syndrome is a rare but treatable complication of increased pressure within the confined orbital space. It is typically secondary to facial trauma or a surgical procedure (see Etiology). Patients present with recognizable physical findings and a progressive visual deficit (see Clinical). Recognition and prompt treatment may prevent blindness (see Treatment). [1]

For patient education information, see the Eye and Vision Center, as well as Black Eye.

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Anatomy

The globe and retrobulbar contents are encased in a continuous cone-shaped fascial envelope that is bound on all sides by 7 rigid bony walls, except anteriorly, where the orbital septum and eyelids form another fairly inflexible boundary. The medial and lateral canthal tendons attach the eyelids to the orbit rim and limit the forward movement of the globe. [2, 3]

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Pathophysiology

The variable pathophysiology of acute orbital compartment syndrome has not been elucidated fully. 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. When the pressure within the orbit exceeds central retinal artery, pressure ischemia results.

In cases of retrobulbar hematoma, hemorrhage generally emanates from the infraorbital artery or one of its branches. In acute disease, retrobulbar blood can cause a substantial rise in pressure unless decompressive drainage occurs through concomitant orbital wall fractures into paranasal sinuses. Presumably, the central retinal artery is afforded some protection from direct compression by its anatomic position within the optic nerve and from increasing tissue pressures by its higher systolic pressure.

Lower pressure prelaminar capillaries and peripapillary choroid and postciliary arteries, which lie within muscle cones and enter the eye around the optic nerve to supply the uveal tract and anterior optic nerve, are afforded no such protection. Resulting blindness without irreversible central artery occlusion has been documented and termed anterior ischemic optic neuropathy. Retrobulbar hematoma is most likely to occur as an ophthalmologic or maxillofacial postoperative complication.

Subperiosteal hematoma caused by trauma or surgery may initially produce similar compressive features that are followed by compartment syndrome tissue-pressure dynamics as volume increases. Traumatic or postoperative orbital emphysema from a sinus communication that produces a 1-way valve may produce confined pressure increases that can compromise vascular perfusion as well.

Finally, increased intraocular (globe) pressure from traumatic intraocular hematomas may cause pressure-related decreased ocular perfusion similar to that caused by mass lesions or thyroid-associated orbitopathy.

All of the above conditions usually create 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. Indirect traumatic optic neuropathy is more common than direct traumatic optic neuropathy, but the exact pathophysiology has not been fully elucidated.

Indirect traumatic optic neuropathy is thought to be related to traumatic transfer of forces through the orbital bones to the intracanicular optic nerve axons and pial microvasculature, resulting in nerve ischemia and edema with a localized compartment syndrome without a measurable increase in orbital pressures. This form of vision-threatening ischemia should be evaluated by a specialist to consider prompt operative decompression/hematoma.

Vasospasm associated with blood product decomposition, as seen in cerebral vessels, has been proposed as another means of optic nerve pathology.

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Etiology

Retrobulbar hematoma is the most common cause of orbital compartment syndrome and is usually secondary to trauma or a surgical procedure. Other potential etiologies of an increase in orbital compartment pressures include infection, intraocular emphysema, tumor, and inflammation.

Acute orbital compartment syndrome has been reported following large-volume resuscitation (including in burn patients), traumatic asphyxia syndrome, extravasated contrast material, and as a complication of spinal surgery in the prone position. Spontaneous bleeding from vascular anomalies or complications related to sclerotherapy for such disorders have been reported to cause acute orbital compartment syndrome. Disseminated intravascular coagulation has been reported as an etiology.

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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. [4] 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.

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Prognosis

Acute orbital compartment syndrome with visual acuity loss is associated with a poor prognosis. Permanent blindness occurs if effective therapy is not initiated in a timely manner. Emergent decompressive surgery (ie, lateral canthotomy and inferior cantholysis) may save sight in patients with severe symptoms. However, irreversible visual loss can be expected with retinal ischemia that lasts longer than 120 minutes.

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