The orbital apex is the most posterior portion of the pyramidal-shaped orbit, positioned at the craniofacial junction. The anatomy of the orbital apex is significant for the complex association between bony, neural, and vascular elements.[1] Fractures of the apex rarely are isolated because they occur in the association with or as extension of fractures of the facial skeleton, base of skull, or other more anterior orbital fractures. See the image below.
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Axial CT scan exhibiting a left apex fracture through the optic canal. Note associated lateral wall and medial wall fractures. This patient also requi....
The anatomy of the orbital apex should be reviewed briefly, with emphasis on the neurovascular structures traversing the optic canal, superior orbital fissure (SOF), and inferior orbital fissure.
Two bony roots that connect the lesser wing of the sphenoid with the body of the sphenoid form the optic canal. The inferior root separates the optic canal from the superior orbital fissure and also is referred to as the optic strut. The superior root forms the roof of the optic canal and separates it from the anterior cranial fossa. The body of the sphenoid forms the medial wall of the canal. From an anterior view, the entrance to the optic canal is the most superior and medial structure in the apex. Each optic canal passes posteromedially at an angle of approximately 35° to the sagittal and opens posteriorly into the chiasmatic groove (which terminates posteriorly at the tuberculum sellae). The canal has an intimate relationship to the sphenoid sinus, and with extensive sinus pneumatization, the optic canal may become completely surrounded by a posterior ethmoidal Onodi air cell, the sphenoid sinus, or an aerated anterior clinoid process.
In adults, the canal is 6.5 mm in diameter and about 8-12 mm in length. The canal transmits the optic nerve and the ophthalmic artery. Throughout its intraorbital and intracanalicular course, the optic nerve is surrounded by pia mater, arachnoid, and dura mater, giving the nerve a sheath. Therefore, optic nerve is a white matter tract of the brain and carries with it meningeal coverings. Within the orbit, the optic nerve is quite mobile; however, within the canal, the optic nerve sheath remains adherent to the sphenoid periosteum and thus is fixed.
The SOF is situated between the greater and lesser sphenoid wings, with the optic strut at its superomedial margin. It lies between the roof and lateral wall of the orbit. The SOF is divided at the spina recti lateralis by the annulus of Zinn, the common tendinous origin of the recti muscles. Lateral to the annulus of Zinn, the SOF transmits the lacrimal nerve, frontal nerve, trochlear nerve, the superior ophthalmic vein, and it may transmit a recurrent branch of the lacrimal artery. Within the annulus pass the superior division of III, nasociliary nerve, inferior division of III, abducent nerve, and fibers from the internal carotid sympathetic plexus.
The inferior orbital fissure lies between the orbital floor and lateral wall and communicates with the pterygopalatine and infratemporal fossae. It transmits the maxillary nerve (which continues to give the infraorbital nerve), the zygomatic nerve, the infraorbital artery, venous communications between the inferior ophthalmic vein and the pterygoid plexus, and an orbital branch of the pterygopalatine ganglion.
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.[2, 3, 4, 5]
Radiographically, orbital apex fractures consist of the following 3 basic types: linear, without dislocation of fragments; comminuted, usually with fragment dislocation; and apex avulsion, with an intact optic foramen. In a series of 23 apex fractures by Unger in 1984, 20 were comminuted, 1 was linear, and 2 consisted of avulsion of the extreme apex with an intact optic foramen within the avulsed fragment.[6] Clinically, fractures into a sinus are technically open fractures, and a risk of contamination from the sinus microbiological flora exists.
Orbital apex fractures present with different symptoms and signs depending on the degree of injury to important neural and vascular structures.[7] Various syndromes have been defined to describe these clinical presentations. However, in view of the complex anatomy and response to injury of the apex, the clinical findings in any single patient may be unreliable in defining the exact site and extent of any fractures seen on neuroimaging. It is apparent that significant injury to the neurovascular structures of the orbital apex may be present without a fracture.[8] Optic canal fractures may be seen in about 50% of patients with posterior traumatic optic neuropathy.[9, 10]
The frequency of recognized orbital apex fractures has increased with the improvement of imaging techniques. Several series reviewed the incidence of fractures with trauma. Unger et al examined 490 patients admitted with nonpenetrating blunt head trauma and found orbital apex fractures in 6 patients, sphenoid bone fractures in 78 patients (of which 8 involved the lesser wing), and 30 involved the body of the sphenoid bone. Ghobrial et al reviewed 112 consecutive patients with base of skull fractures, 15% had sphenoid fractures.
Mortality/Morbidity
Mortality associated with orbital apex fractures are due to associated intracranial trauma or associated with injury to the adjacent internal carotid artery. Morbidity is common due to injury to neurovascular structures.
Injury to the optic nerve leads to visual loss, being most commonly from an indirect posterior traumatic optic neuropathy. The visual loss from traumatic optic neuropathy may vary from partial to complete, and the degree of recovery may vary. Also reported is visual loss from optic nerve sheath hematoma, optic nerve transection, and optic nerve impingement from a penetrating foreign body or bony fracture. Vision loss from optic nerve compression associated with retrobulbar hemorrhage also has been reported.
Injury to cranial nerves III, IV, and VI presents as extraocular muscle nerve palsy, with manifest diplopia.
Injury to cranial nerve V presents as sensory disturbance to areas supplied by branches of the trigeminal (V) nerve.
Sex
A review of 490 traumatic blunt head injury patients resulted in a male-to-female ratio of approximately 1.5:1, reported by Unger et al.
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.
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.
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.
In the context of facial trauma and suspected fractures, noncontrast CT scans are the most appropriate initial imaging technique.[13, 14, 15, 9, 6]
Associated intracranial injury, associated facial fractures, and intraorbital hematoma may be assessed.
Axial and coronal views 3-mm cuts review the orbit, and 1-mm axial cuts may be used to assess the optic canal. Coexistent cervical injury may preclude direct coronal projections. Reconstructed coronal views may be needed in patients with neck injury. See the images below.
View Image
Axial CT scan exhibiting a left apex fracture through the optic canal. Note associated lateral wall and medial wall fractures. This patient also requi....
View Image
Coronal reconstruction of CT scan of left orbital apex fracture through the optic canal. This patient presented with an orbital apex syndrome. Note th....
Plain radiography
The orbital apex may be visualized with 2 radiographic projections, the angled anteroposterior (AP) view for the superior orbital fissure and the oblique view for the optic foramen.
MRI
The poor resolution of bone on MRI significantly limits its role in general orbital trauma. However, in the context of orbital apex trauma and traumatic optic neuropathy, better soft tissue differentiation may be obtained. In particular, MRI reveals the abnormal signal indicative of recent hemorrhage in optic nerve sheath hematoma.[16, 17, 18]
Angiography
Angiography may be considered in patients with orbital apex fractures and with clinical features consistent with a carotid artery injury, revealing carotid artery dissection, carotid artery spasm, or carotid-cavernous fistula.
Visual field assessment: Automated static threshold perimetry (eg, Humphrey Visual Field analysis) or kinetic perimetry (eg, Goldmann perimetry) may be used in patients with adequate cooperation and fixation to document visual field disturbance with optic neuropathy. No specific visual field loss pattern is pathognomonic for traumatic optic neuropathy.
Formal color testing: Dyschromatopsia is expected in optic neuropathy, and it may be formally documented with use of the Farnsworth-Munsell 100 hue test or the Farnsworth panel D-15. These tests require patient cooperation and may not be appropriate in the acute setting.
Documentation of oculomotility disturbance: Serial documentation of a field of binocular single vision allows assessment of progression of diplopia. In patients with normal retinal correspondence, other methods of serial documentation include the Hess screen.
Beta-2 transferrin is a definitive test for CSF rhinorrhea.
Electrophysiology: Visual-evoked potentials (VEP) may assess the integrity of the visual pathway and are able to compare pathways from each eye. They are a consideration in patients with altered level of consciousness or in whom bilateral optic neuropathy is suspected.
The management of orbital apex fractures is determined by the patient's specific functional deficits and overall status. Associated neurosurgical emergencies take precedence. Associated craniofacial skeletal and ocular injuries may require treatment. The initial radiographic trauma series may not fully elucidate the details of apex fractures, and dedicated fine-cut CT scans or an MRI may be required.
In cases where vision is decreased and optic nerve injury is suspected, consideration must be given to medical and/or surgical nerve decompression. Indirect traumatic optic neuropathy is considered the result of forces transmitted to the orbital apex and optic canal at the time of injury. Axon shearing occurring at the time of injury, contusion of the intracanalicular optic nerve axons, ischemia and microinfarction of axons due to damage to pial microvasculature, direct bony impingement with a canal fracture, and continued edema and hemorrhage within the closed space of the optic canal all have been proposed to play a role in the pathophysiology of traumatic optic neuropathy. Theoretically, reduction in optic nerve compression and edema may salvage those axons with reversible damage. However, treatment remains controversial. Currently, 3 treatment options exist, as follows: observation alone, high-dose corticosteroids, and surgical optic canal decompression.[19]
Numerous case reports and case series have described the use of steroids and optic nerve decompression surgery and the outcomes in traumatic optic neuropathy.[20]
The International Optic Nerve Trauma Study attempted to compare the visual outcome of traumatic optic neuropathy treated with corticosteroids, optic canal decompression surgery, or observation.[21] The presence of an orbital apex fracture was not discussed, although patients with orbital penetrating injuries were excluded. It was a comparative nonrandomized interventional study with concurrent treatment groups; 127 patients with unilateral optic nerve were included. Results showed that visual acuity increased by 3 or more lines in 32% of the surgery group (n = 33), 52% of the corticosteroid group (n = 85), and 57% of the untreated group. After adjustment for baseline visual acuity, there was no significant difference between any of the groups. No clear benefit was found for either steroid therapy or optic canal decompression surgery.
The management of oculomotility disturbance generally falls under the care of a strabismus specialist. In many cases of a traumatic SOF syndrome, significant recovery of extraocular muscle occurs.[11] If strabismus surgery is contemplated, a period of more than 6 months is allowed to achieve maximal spontaneous recovery.
Several methods are available for surgical decompression of the optic canal. These include a medial approach via an external ethmoidectomy; an inferomedial approach via a transantral, transethmoidal approach; a sublabial transsphenoidal approach; a supraorbital-subfrontal approach; and endoscopic transethmoidal approach.[22] The details of these surgical approaches are beyond the scope of this article.
Minimally invasive transcaruncular optic canal decompression was found to be successful in one case of traumatic optic neuropathy; however, visualization using this approach may be limited, and an adequate decompression is more difficult working down a long narrow optical cavity.[23]
Surgical decompression may have an increased role in the management of an optic neuropathy associated with optic nerve impingement from a penetrating foreign body or displaced bony fragment, and also in the presence of a MRI-confirmed subdural sheath hematoma, where an optic nerve sheath fenestration has been advocated. However, there is no definitive proof that moving bony fragments in the optic canal improves the chance of visual recovery. Indeed, it has been argued that further trauma, which is inherent in a surgical approach to the optic canal, may further risk visual integrity.
Orbital apex fractures may involve the posterior portion of the medial orbital wall, near the apex. In such cases, repair using a superomedial orbital approach or a transcaruncular approach may be successful .[24]
Nasal endoscopic approaches to traumatic orbital apex syndrome are still the most popular when decompression of the superior and medial walls of the orbital apex and optic canal are necessary.[25]
A multidisciplinary approach to the orbital apex injury may be warranted.
Review by the neurosurgical service is indicated to assess associated intracranial injury.
Review by an ophthalmology service is indicated to help follow indices of vision (visual acuity, color vision, visual fields), follow any globe injury, and aid in long-term management of strabismus.
Radiology should be consulted to help interpret the radiographic findings in the context of the clinical presentation. The possibility of associated carotid artery injury may require interventional radiologic review and angiographic procedures.
Long-term follow-up care is required in those with optic neuropathy, continued diplopia, and disturbance of trigeminal nerve.
Visual recovery with traumatic optic neuropathy may take several months. More formal visual assessment may be undertaken in the outpatient setting (eg, perimetry, electrophysiology).
Diplopia, with extraocular muscle paresis, also may take many months to improve maximally. Having stable strabismus for several months prior to strabismus surgery is advocated.
The presence of an anesthetic cornea may lead to a neurotrophic keratopathy, especially if associated with a dry eye (in elderly patients and with lacrimal gland trauma or deinnervation), and/or facial nerve palsy (eg, skull base fractures of the temporal bone).
Continued neurologic observations and serial visual acuity assessments are appropriate with an orbital apex fracture. Progressive loss of vision may be seen with a compressive neuropathy of optic nerve sheath hematoma, bony impingement, or orbital hemorrhage.
Associated complications of trauma include CSF leak and carotid-cavernous fistula may not present early in the course of care and should be watched for. Diabetes insipidus presented in one series.
In Unger's 1984 review of 23 orbital apex fractures (in 17 patients), documented complications included optic nerve damage (n = 3), SOF syndrome (n = 6), orbital apex syndrome (n = 2); in this series, it was not possible to satisfactorily examine 13 orbits because of soft tissue injury, globe rupture, or altered level of consciousness.[6]
In Unger's 1990 review of 78 patients with sphenoid fractures, 21 patients had documented complications of the fracture. These included optic nerve injury with decrease in vision (n = 5), extraocular muscle palsy (n = 3), internal carotid artery injury (n = 5), CSF leak (n = 7), and diabetes insipidus (n = 1).[3]
In Ghobrial's 1986 series of 17 sphenoid fractures, 3 patients had traumatic optic neuropathy, and 3 had a SOF syndrome.[2]
Complications of surgical decompression of the optic canal include direct or collateral damage to the optic nerve axons and vascular supply. When orbital apex surgery is contemplated, the potential for iatrogenic damage to other apex structures and intracranial structures must be balanced against the potential for a functional improvement in any individual patient.
Complications of medical treatment are those of high-dose steroids, including hyperglycemia, hypokalemia, osteonecrosis, gastric ulceration, acute pancreatitis, and opportunistic infections. See Medication.
With improved imaging of trauma patients, it is apparent that many patients with orbital apex fractures do not present with neurovascular complications. However, many patients do have significant associated craniofacial trauma, with resultant mortality and morbidity.
In nonpenetrating trauma, significant improvement in extraocular muscle paresis may occur, because the injury is presumably a neuropraxia to some degree. The prognosis in indirect traumatic optic neuropathy is reported in the International Optic Nerve Trauma Study, where many patients improved.[21] The initial visual acuity was a strong predictor of the final visual acuity.
For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center. Also, see eMedicineHealth's patient education article Black Eye.
Bhupendra C K Patel, MD, FRCS, Professor of Ophthalmic Plastic and Facial Cosmetic Surgery, Department of Ophthalmology and Visual Sciences, John A Moran Eye Center, University of Utah School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Disclosure: Nothing to disclose.
Additional Contributors
Ron W Pelton, MD, PhD, Private Practice, Colorado Springs, Colorado
Disclosure: Nothing to disclose.
Simon F Taylor, MBBS, FRACS, FRANZCO, Clinical Senior Lecturer, Oculoplastic Surgery, Save Sight Institute, University of Sydney, Australia
Axial CT scan exhibiting a left apex fracture through the optic canal. Note associated lateral wall and medial wall fractures. This patient also required a craniotomy for a subdural hematoma.
Axial CT scan exhibiting a left apex fracture through the optic canal. Note associated lateral wall and medial wall fractures. This patient also required a craniotomy for a subdural hematoma.
Coronal reconstruction of CT scan of left orbital apex fracture through the optic canal. This patient presented with an orbital apex syndrome. Note the displaced bone fragment from the lateral wall of the sphenoid sinus.
Axial CT scan exhibiting a left apex fracture through the optic canal. Note associated lateral wall and medial wall fractures. This patient also required a craniotomy for a subdural hematoma.
Coronal reconstruction of CT scan of left orbital apex fracture through the optic canal. This patient presented with an orbital apex syndrome. Note the displaced bone fragment from the lateral wall of the sphenoid sinus.
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