eMedicine Specialties > Emergency Medicine > Ophthalmology

Acute Orbital Compartment Syndrome

Author: David A Peak, MD, Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
Contributor Information and Disclosures

Updated: Nov 3, 2009

Introduction

Background

Orbital injuries commonly accompany facial trauma, necessitating knowledge of the spectrum of potential ocular injuries. Acute orbital compartment syndrome is a rare but treatable complication of increased pressure within the confined orbital space. The condition presents with recognizable physical findings and progressive visual deficit. Recognition and prompt treatment may prevent blindness.¹

Pathophysiology

The variable pathophysiology of acute orbital compartment syndrome has not been elucidated fully. 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 The orbit may compensate for small increases in orbital volume by forward movement of the globe and prolapse of fat, followed immediately by a rapid rise in orbital tissue pressures. The orbit, therefore, follows pressure-volume dynamics with a pathophysiology akin to other compartment syndromes, in which increased tissue pressures in an enclosed space are associated with 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 initially may produce similar compressive features that rapidly 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 Graves orbitopathy.

All of the above conditions may create discernible and measurable physical signs of increased orbital pressure, which may prompt sight-saving ED 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 but is thought to be related to traumatic transfer of forces through the orbital bones to the intracanicular optic nerve axons and pial microvascular resulting in nerve ischemia and edema with a localized compartment syndrome but 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.

Frequency

United States

Acute orbital compartment syndrome is considered a rare complication of facial trauma or surgery. A retrospective review of 727 patients with facial fractures found 67% sustained some degree of ocular injury.³ Eighteen percent of these injuries were categorized as serious and 3% as blinding. All of the latter resulted from optic nerve injury, retinal detachment, or corneal-scleral rupture.

Mortality/Morbidity

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.

Clinical

History

• Eye pain
• Diplopia
• Visual loss
• Reduction of ocular motility
• Proptosis

Physical

• Proptosis (best visualized in coronal/superior view while the patient is in a semi-reclined position)
• Increased intraocular pressure
• Ecchymosis of eyelids
• Chemosis - Often severe and may be bloody
• Ophthalmoplegia
• Afferent pupillary defect
• Decreased visual fields
• Papilledema
• Decreased visual acuity - Acuity may be measured in the patient with acute trauma via handheld eye chart or even counting fingers at a distance. Acuity should be rechecked at periodic intervals, and any decrease is cause for concern.
• Central retinal artery pulsation
• Pale optic disc (late)
• Cherry-red macula (rare)

Causes

• Retrobulbar hematoma is the most common etiology usually secondary to trauma or as a consequence of 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 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 additionally been reported as an etiology.

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