Apex Orbital Fracture Clinical Presentation

Updated: May 20, 2016
  • Author: Bhupendra C K Patel, MD, FRCS; Chief Editor: Hampton Roy, Sr, MD  more...
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Presentation

History

Most patients present with a history of blunt orbital trauma. Penetrating trauma is less common. Demand for the facial trauma surgeon continues, being largely the result of motor vehicle accidents, industrial accidents, sports-related facial trauma, and assault.

Past ophthalmic history is required, with emphasis on antecedent spectacles, decreased vision, amblyopia, strabismus, and previous ocular surgery.

A history of visual loss must be sought. This may be difficult in patients with head injuries. If vision is decreased, it is important to assess if vision was lost at the time of injury or subsequently. Progressive decrease in vision suggests an optic neuropathy due to hemorrhage into the optic nerve sheath, retrobulbar hematoma, compression by a bony fragment, or possibly arachnoiditis at the site of fracture.

Diplopia confirms binocular misalignment. Diplopia will be worse in the field of gaze of the paretic muscle. Diplopia may not be present with significant ptosis or monocular loss of vision.

Sensory disturbances in the distribution of V1 and V2 may be present but is frequently a feature not volunteered until specifically asked about.

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Physical

Initial management of the patient with facial injuries should be aimed at assessing the airway security, hemodynamic stability, and cervical spine integrity. An assessment of neurologic status must be made, and head injuries must be excluded. Additional soft tissue and bony injuries of the head and neck must be sought.

In patients with suspected orbital apex fractures, the examination should focus on an assessment for the presence of an optic neuropathy, an evolving orbital compartment syndrome, or a ruptured globe, because these 3 things may demand acute intervention.

Assessment of vision is as follows:

  • Visual acuity: Each eye must be recorded. Spectacles may break at the time of injury, and pinhole vision may need to be recorded.

  • Color vision: In the acute setting, formal color testing charts (eg, Ishihara plates) may not be available, but subjective assessment of red desaturation may be made at the bedside.

  • Visual fields: Confrontation fields may be performed at the bedside prior to more formal perimetric assessment.

Assessment of pupil responses: The direct and consensual light responses reveal information about the afferent and efferent arms of the light reflex. An absolute or relative afferent pupil defect or an efferent pupil defect (as seen in third nerve palsy, ciliary ganglion injury, and traumatic mydriasis) is recorded.

Assessment of ocular motility: An assessment of the field of binocular single vision is made and recorded. Volitional movements are examined at the bedside, while forced ductions and force generation examinations are undertaken with appropriate topical anesthesia and patient cooperation. These assessments help differentiate between ocular motility disturbance caused by entrapped muscles, intramuscular hematoma, and nerve damage.

Assessment of integrity of cranial nerve V: Sensory disturbances should be sought in the territories of branches of V1 and V2.

Orbital inspection, palpation, and assessment of globe position, as follows:

  • Periocular ecchymosis, edema, and proptosis are common features of blunt trauma.

  • Orbital hematoma, intraorbital emphysema, and orbital volume changes with orbital wall fractures all alter the globe position.

  • Axial displacement of the globe should be assessed by exophthalmometry.

  • Increased resistance to globe retropulsion is seen with orbital hemorrhage.

  • Disruption of the mucosal integrity of the maxillary or ethmoidal sinus may result in subcutaneous or intraorbital emphysema.

  • Orbital rim fractures are suspected in the presence of an orbital rim step-off.

  • Traumatic telecanthus is seen in naso-orbito-ethmoid (NOE) fractures and lateral canthal dystopia is seen in displaced zygomaxillary complex (ZMC) fractures.

An ocular assessment is required to exclude a coexistent globe rupture or injury. The intraocular pressure is recorded. Anterior segment trauma including corneal injury, hyphema, iridodialysis, lens dislocation, and posterior segment trauma including retinal commotio, retinal detachment, choroidal rupture, and scleral rupture, is sought.

Pharmacologic pupil dilation for the purposes of an adequate fundus examination may need to be delayed to allow neurologic pupil observations in the trauma patient. However, even in the undilated pupil, an examination of the optic disc usually may be obtained with a direct ophthalmoscope to assess optic nerve head perfusion, disc swelling, and peripapillary hemorrhages. In patients with head injuries, pharmacological pupil dilation should only be undertaken after neurosurgical consultation.

Various syndromes have been described to define clinical presentations with traumatic (and nontraumatic) lesions of the orbital apex, as follows:

  • Traumatic optic neuropathy (involvement of cranial nerve II): The intracanalicular optic nerve may be damaged by sphenoid fractures; however, optic canal fractures are seen in the minority of cases of traumatic optic neuropathy, and they do not correlate with the severity of the injury. The firm attachment of the dural sheath to the optic nerve may make the intracanalicular nerve particularly susceptible to acceleration or deceleration injuries.

  • SOF syndrome (involvement of cranial nerves III, IV, V1, and VI): The SOF syndrome is characterized by dysfunction of cranial nerves III, IV, V1, and VI. Features include ophthalmoplegia, upper eyelid ptosis, a nonreactive dilated pupil, anesthesia over the ipsilateral forehead, loss of corneal sensation (and hence loss of corneal reflex), and occasionally, orbital pain and proptosis. A neurotrophic keratopathy may develop. The mechanism of injury is generally an extension of a fracture into the SOF. [11]

  • Orbital apex syndrome (involvement of cranial nerves II, III, IV, V1, and VI): The orbital apex syndrome is a SOF syndrome with loss of vision. [12]

  • Cavernous sinus syndrome (involvement of cranial nerves III, IV, V1, V2, VI, and periarterial sympathetic plexus): The addition of sensory deficits in the maxillary branch of the trigeminal nerve and involvement of the orbital sympathetic innervation is seen.

Traumatic carotid-cavernous fistula may be present. Fractures in the posterior orbit may extend into the foramen lacerum, causing disruption of the internal carotid artery within the cavernous sinus. Orbital signs are present with vascular congestion, proptosis, chemosis, ophthalmoplegia, elevated intraocular pressure (IOP), and a vascular bruit.

Cerebrospinal fluid (CSF) rhinorrhea may present if there is an associated fracture involving the sphenoid sinus, fovea ethmoidalis, or cribriform plate.

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Causes

Orbital apex fractures may be the result of nonpenetrating blunt trauma, such as seen with motor vehicle accidents or assaults, or penetrating trauma such as with orbital foreign bodies.

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