Trauma may damage the optic nerve at any point between the optic nerve head and the optic chiasm. Traumatic optic neuropathy occurs via three principal mechanisms:
- Compression by fractured bone, hemorrhage or edema (potentially reversible).
- Laceration by bone or foreign body, such as a bullet or knife (irreversible).
- Shearing injury as a result of blunt trauma (variable prognosis). External force produces movement of the optic nerve and its vascular supply within a relatively inelastic framework of bone and connective tissue. Occasionally, the force is sufficient to cause avulsion of the optic nerve head. Avulsion refers to a tearing away of a part of the body, in this instance the optic nerve from the globe.
The principal symptom is decreased vision after traumatic injury to the eye or periocular area. The patient may, however, fail to notice monocular loss of vision in the presence of distracting injuries. The object(s) responsible for the trauma, the amount of force applied and the point of impact affect the severity of nerve damage. The onset of visual loss following the incident varies: immediate visual loss suggests avulsion or laceration, whereas delayed loss of vision is more compatible with potentially reversible compression (e.g., a secondary bleed around the optic nerve).
As in any case of ocular trauma, visual acuity must be recorded; and penetrating ocular injury, ruptured globe and hyphema must be excluded before proceeding with the ocular examination. Signs of optic neuropathy include decreased visual acuity, relative afferent papillary defect, decreased color vision and visual field defects. When the optic nerve head is damaged, fundoscopy often reveals peripapillary hemorrhages or edema. If the damage is in the optic canal, the disc usually appears normal; optic disc pallor does not develop for several weeks following the injury. Disc pallor observed immediately following trauma suggests preexisting optic neuropathy.
Traumatic optic neuropathy has been reported in approximately 4 percent of patients with midfacial, supraorbital or frontal sinus fractures.
Reduced visual acuity following trauma is a medical emergency. Prompt treatment of a potentially reversible condition may prevent permanent loss of vision. In susceptible individuals, apparently minor trauma may cause severe damage to the optic nerve.
Exclude other traumatic ocular conditions, e.g. Vitreous Hemorrhage, Retinal Detachment.
Patients with suspected acute traumatic optic neuropathy are admitted to hospital.
Imaging investigations identify the mechanism and nature of optic nerve damage. Orbital computed tomography (CT), with thin sections through optic canal, is particularly useful in delineating fractures and hematomas within the optic canal. Magnetic resonance imaging (MRI) provides additional definition of soft tissues, including the optic nerve. B-scan ultrasound occasionally detects foreign bodies that elude other imaging modalities. Formal visual field testing supplies an accurate baseline measurement for subsequent review.
Although management is controversial, a common initial treatment is high-dose intravenous corticosteroid therapy (e.g., methylprednisolone), often for several days. The rationale is to minimize acute inflammation and soft tissue swelling around the optic nerve. Antibiotics are also indicated for sinus wall fractures or penetrating injuries.
Surgical decompression of the optic canal may also be considered, particularly in the setting of an enlarging optic nerve sheath hematoma and/or edema.
Review and prognosis
The prognosis of traumatic optic neuropathy is variable. Vision may spontaneously improve in approximately one-third of patients. Visual acuity, color vision and pupillary responses are recorded daily. Should vision deteriorate when steroids are ceased, treatment is recommenced. Upon completion of inpatient treatment, patients are often reviewed monthly initially, with decreasing frequency thereafter.
Severe contusion injury resulting in avulsion of the optic nerve head & damage to surrounding choroid, with consequence of total blindness to the eye.