AUTHOR AND EDITOR INFORMATION

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• Clinical
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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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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.

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. 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.¹ 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

Section 3 of 11  

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• Multimedia
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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.

DIFFERENTIALS

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Other Problems to be Considered

Direct optic neuropathy from nerve impingement, crush, or transection
Graves orbitopathy
Orbital neoplasm
Direct injury from surgical dissection
Lens dislocation

WORKUP

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Lab Studies

• No laboratory studies are absolutely indicated. Baseline routine laboratory evaluation may be requested for a patient who requires urgent medical treatment or urgent surgical decompression. Consider blood dyscrasia and pharmacologic anticoagulation and platelet inhibitors, which may prolong bleeding time.

Imaging Studies

• CT scan or MRI of the orbit may help to identify the etiology of compression, to exclude alternative diagnoses, and to establish the diagnosis. Finding of a retrobulbar hematoma on CT scan for a patient with clinical findings suggestive of acute ocular compartment syndrome confirms the diagnosis.
• In patients with severe symptoms (eg, change in visual acuity) or rapidly evolving symptoms and signs consistent with increased intraocular pressure (IOP), imaging may delay sight-saving therapy and result in permanent vision loss. In these cases, initiate therapy before imaging studies.

Procedures

• Perform direct funduscopy on all patients and repeat serially if symptoms evolve.
• IOP determination: Record IOP as an integral component of examination.

TREATMENT

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Prehospital Care

• Trauma evaluation should proceed as per standards for patients with head trauma/multiple trauma, with assessment for life-threatening injuries and stabilization for transport.
• Field treatment of pain, agitation, and emesis may be appropriate to avoid further increase in IOP. If intubation is necessary, pretreat with agents that protect intracranial/intraocular pressures.
• Use protective eye shields during transport when the differential diagnosis includes penetrating eye injury or scleral rupture.
• Check visual acuity early and often. Loss of visual acuity, in contradiction to other symptoms and signs, requires immediate emergent attempts at orbital decompression.

Emergency Department Care

• Assessment for concomitant life-threatening injuries takes priority over all other considerations.
• Immediately employ medical therapy. Osmotic agents and carbonic anhydrase inhibitors are part of established protocols at many centers. Most experts also recommend high-dose steroid therapy as a standard of care. Less agreement exists for use of topical beta-blockers and multiple osmotic agents.
• Irreversible optic-nerve pathology may occur with as little as 2 hours of ischemia. Rapid employment of medical therapy and ophthalmologic consultation should proceed promptly with diagnosis.
• Lateral canthotomy/inferior cantholysis
• • Emergent decompressive surgery for severe symptoms (eg, decreased visual acuity) may save sight.
  • ED physicians should be familiar with this procedure if emergent ophthalmologic consultation is unavailable (see Emergency Department Care).
• The emergency procedure of choice for acute visual acuity loss associated with acute orbital compartment syndrome is dissection of the lateral canthus and disinsertion of at least the inferior crus of the lateral canthal tendon, which allows complete mobility of the lower lid. Visual loss without clear signs consistent with increased IOP is not an indication for this procedure. Other primary indications for lateral canthotomy and cantholysis include an IOP greater than 40 mm Hg and proptosis, which may be used as a criterion for unconscious patients whose visual acuity cannot be determined. Secondary criteria include afferent pupillary defect, ophthalmoplegia, cherry-red macula, optic nerve head pallor, and severe pain, but these are all considered less sensitive or very late signs. Contraindication for this procedure would be a suspected ruptured globe.
• Perform lateral canthotomy, as follows (see Media file 1):
• 1. Clean the area with sterile saline.
  2. Inject approximately 1 mL of lidocaine 1-2% with or without epinephrine into the lateral canthus.
  3. Apply a hemostat/clamp with one side anterior and one side posterior to the lateral canthus and advance until the rim of the bony orbit is felt.
  4. Clamp for 30-60 seconds.
  5. Perform the lateral canthotomy by carefully cutting through the crushed, demarcated line to the orbital rim/lateral fornix to avoid traumatizing the orbit.
• Perform inferior catholysis by using one of the following methods (see Media file 2):
• • Traditional approach: Grasp lower eyelid with forceps and pull out/downward away from eye. Identify the canthal ligament by either inspection or palpation. Incise the inferior crus of the lateral canthal ligament with scissors to avoid traumatizing the orbit
  • The Sweep technique: Grasp the lower eyelid with forceps and pull out/downward away from eye. Carefully place the lateral side of an opened pair of curved scissors against the palpebral conjunctiva of the lateral eyelid. Slowly sweep laterally toward the canthotomy incision. When the inferior crus of the lateral canthal ligament is encountered impeding continued lateral sweeping, carefully move the other scissor blade into position and incise to avoid traumatizing the orbit. The sweep technique may be particularly useful in cases when massive edema makes canthal ligament identification difficult.
• Recheck the IOP, and dissect the superior crus in a similar fashion if an adequate decrease has not been achieved. Special care should be taken to avoid any trauma to the lacrimal gland.
• • In an experimental model, lateral canthotomy produced a mean IOP reduction of 14.2 mm Hg; isolated disinsertion, 19.2 mm Hg; and combined, 30.4 mm Hg.
  • Other methods to reduce IOP, including anterior chamber paracentesis and insertion of a mosquito clip inferiorly to break through the inferior orbital floor, are beyond the scope of this discussion.
• Immediately test visual acuity postprocedure. If vision fails to improve, as possibly expected in cases of confined subperiosteal hematoma, operative orbital decompression or hematoma evacuation should be considered.

Consultations

• Emergent ophthalmologic consultation is required in all cases.
• Emergent oromaxillary facial surgery consultation is required if the etiology is postsurgical and in all cases in which hemorrhage is suspected within the optic canal or optic nerve sheath.

MEDICATION

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The goal of pharmacotherapy is to reduce morbidity and to prevent complications.

Drug Category: Hyperosmotic agents

These agents decrease IOP by direct osmosis of water.

Drug Category: Carbonic anhydrase inhibitors

These agents decrease IOP by decreasing production of aqueous humor in anterior chamber. Additionally, they reduce systolic BP, which may help control hemorrhage.

Drug Category: Corticosteroids

These agents exert an anti-inflammatory effect and an antioxidant effect that decreases production of free-radical metabolites.

Drug Category: Beta-blockers

These agents decrease IOP by decreasing production of aqueous humor.

Drug Category: Antiarrhythmic Agent, Class I-b

Anesthetics that inhibit depolarization of type C sensory neurons used.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• Cosmetic repair of lateral canthotomy may be performed in the hospital and usually affords a good outcome. Repair of canthal tendons can be performed at the discretion of the specialist. Repair can be delayed for several days if necessary.
• Compartment syndrome is one of the accepted indications for hyperbaric oxygen therapy. Case reports of improvement in vision using hyperbaric oxygen as adjunct therapy in acute orbital compartment syndrome exist.

Transfer

• Transfer for specialty consultation and/or further workup (including CT scan or MRI) is indicated when an acute orbital compartment syndrome diagnosis is entertained.
• Initiate treatment prior to transfer in patients with visual acuity loss or rapidly evolving symptoms with signs of increased IOP.

Deterrence/Prevention

• Prevention of morbidity (visual loss) depends on early diagnosis and treatment.

Complications

• Irreversible visual loss can be expected with retinal ischemia that lasts longer than 120 minutes.

Patient Education

• For excellent patient education resources, visit eMedicine's Eye and Vision Center. Also, see eMedicine's patient education article Black Eye.

MISCELLANEOUS

Section 9 of 11  

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• Miscellaneous
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Medical/Legal Pitfalls

• Failure to make the diagnosis
• Failure to initiate prompt therapy
• Ordering time-consuming diagnostic tests in patients with visual acuity loss or rapidly advancing symptoms prior to initiation of therapy
• Failure to initiate therapy in patients with visual acuity loss or rapidly advancing symptoms or signs prior to transfer
• Failure to obtain emergent specialty consultation

MULTIMEDIA

Section 10 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Lateral canthotomy is performed by incising laterally with sharp scissors.
	View Full Size Image
Media type:  Image

Media file 2:  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.
	View Full Size Image
Media type:  Image

REFERENCES

Section 11 of 11

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1. Holt GR, Holt JE. Incidence of eye injuries in facial fractures: an analysis of 727 cases. Otolaryngol Head Neck Surg. Jun 1983;91(3):276-9. [Medline].
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3. Goodall KL, Brahma A, Bates A, Leatherbarrow B. Lateral canthotomy and inferior cantholysis: an effective method of urgent orbital decompression for sight threatening acute retrobulbar haemorrhage. Injury. Sep 1999;30(7):485-90. [Medline].
4. Hayreh SS, Kolder HE, Weingeist TA. Central retinal artery occlusion and retinal tolerance time. Ophthalmology. Jan 1980;87(1):75-8. [Medline].
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6. Larsen M, Wieslander S. Acute orbital compartment syndrome after lateral blow-out fracture effectively relieved by lateral cantholysis. Acta Ophthalmol Scand. Apr 1999;77(2):232-3. [Medline].
7. Leibovitch I, Casson R, Laforest C, Selva D. Ischemic orbital compartment syndrome as a complication of spinal surgery in the prone position. Ophthalmology. Jan 2006;113(1):105-8. [Medline].
8. Li KK, Meara JG, Joseph MP. Reversal of blindness after facial fracture repair by prompt optic nerve decompression. J Oral Maxillofac Surg. Jun 1997;55(6):648-50. [Medline].
9. Li KK, Meara JG, Rubin PA. Orbital compartment syndrome following orthognathic surgery. J Oral Maxillofac Surg. Aug 1995;53(8):964-8. [Medline].
10. McInnes G, Howes DW. Lateral canthotomy and cantholysis: a simple, vision-saving procedure. CJEM. Jan 2002;4(1):49-52. [Medline].
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13. Patchett RB, Wilson WB, Ellis PP. Ophthalmic complications with disseminated intravascular coagulation. Br J Ophthalmol. May 1988;72(5):377-9. [Medline].
14. Prodhan P, Noviski NN, Butler WE, Eskandar E, Ellen Grant P, Whalen MJ, et al. Orbital compartment syndrome mimicking cerebral herniation in a 12-yr-old boy with severe traumatic asphyxia. Pediatr Crit Care Med. Jul 2003;4(3):367-9. [Medline].
15. Rosdeutscher JD, Stadelmann WK. Diagnosis and treatment of retrobulbar hematoma resulting from blunt periorbital trauma. Ann Plast Surg. Dec 1998;41(6):618-22. [Medline].
16. Sacks SH, Lawson W, Edelstein D, Green RP. Surgical treatment of blindness secondary to intraorbital hemorrhage. Arch Otolaryngol Head Neck Surg. Jul 1988;114(7):801-3. [Medline].
17. Samples JR, Hedges JR. Ophthalmologic procedures. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency Medicine. 3^rd ed. Philadelphia: WB Saunders Co; 1998:1089-119.
18. Simeone FA, Vinall P. Mechanisms of contractile response of cerebral artery to externally-applied fresh blood. J Neurosurg. Jul 1975;43(1):37-47. [Medline].
19. Sullivan SR, Ahmadi AJ, Singh CN, Sires BS, Engrav LH, Gibran NS. Elevated orbital pressure: another untoward effect of massive resuscitation after burn injury. J Trauma. Jan 2006;60(1):72-6. [Medline].
20. Wood CM. The medical management of retrobulbar haemorrhage complicating facial fractures: a case report. Br J Oral Maxillofac Surg. Aug 1989;27(4):291-5. [Medline].
21. Yung CW, Moorthy RS, Lindley D, Ringle M, Nunery WR. Efficacy of lateral canthotomy and cantholysis in orbital hemorrhage. Ophthal Plast Reconstr Surg. Jun 1994;10(2):137-41. [Medline].

Article Last Updated: Dec 18, 2007