TRAUMATIC OPTIC NEUROPATHY

Signs and Symptoms

Disc pallor from trauma.

Patients with traumatic optic neuropathy typically experience sudden, severe, unilateral vision loss following blunt injury to the head or face. The condition may manifest immediately or within hours or days following the trauma. Occasionally, the vision loss may be insidious, and in some cases the patient may be unaware of any visual deficit until it is detected by routine examination.

Most commonly, patients are male and in their teens or twenties. The history often includes a blow to the head severe enough to induce loss of consciousness or high-speed penetration of the globe by foreign material.

Examination of these patients reveals variably reduced acuity and/or visual field defects, which may be central, paracentral, arcuate or altitudinal in nature. An afferent pupillary defect is characteristic, and dyschromatopsia may be noted in accordance with the severity of the vision loss.

Ophthalmoscopic evaluation varies greatly. Initially, practitioners may note a completely normal fundus without any signs of disc edema, ischemia or other abnormalities. In other cases, a grossly edematous optic nerve head, vitreous hemorrhage, venous congestion or retinal edema may be seen. In the vast majority of cases, however, optic disc pallor ensues within several weeks of the injury.

Pathophysiology

Traumatic optic neuropathy results from injury sustained during trauma to the orbital rim or frontal area. In adults, the etiology is typically a bicycle or motor vehicle accident, but may also include physical assault, falls, sports-related injuries, or (rarely) orbital surgery. There are a variety of ways in which the optic nerve can be damaged, and in some cases the pathophysiology may be multifactorial. Mechanisms include transection or avulsion of the nerve, hematoma of the nerve sheath, optic nerve compression secondary to bony fracture of the orbital apex, or penetrating orbital foreign body. Most commonly, however, concussive shock waves are implicated; transmission of these forces to the bones and meninges of the orbit results in contusion of the intracanalicular optic nerve. Subsequently, the axons and microvasculature are compromised by ischemia and reactive edema, as well as generalized compressive forces. In rare instances, the neuropathy may develop months after the initial trauma, a consequence of scarring within the optic canal that leads to secondary nerve compression.

Management

Temporal pallor and nerve fiber layer atrophy from trauma.

High-resolution imaging of the head is critical in any case of blunt trauma to ensure that no additional or life-threatening intracranial damage has been sustained. Particular attention should be given to the orbital apex, optic canal, and cavernous sinus if vision is compromised. A complete neurological assessment is also indicated in these cases, especially if there was loss of consciousness. Fortunately, most patients with traumatic optic neuropathy will have been seen in the emergency department of their local hospital prior to optometric or ophthalmologic consultation, so these tests will likely have already been ordered by the ER physician.

With regard to treatment, there are presently three options: (1) careful observation; (2) systemic corticosteroid therapy or; (3) optic nerve decompression surgery. While a fair number of patients with traumatic optic neuropathy experience some spontaneous improvement of vision, there is great variability in outcome. Negative prognostic factors include blood in the posterior ethmoid cells, loss of consciousness, older age (i.e., >40), and complete loss of vision at the initial presentation.^1,2 In the 1990s, researchers quoting the Second National Acute Spinal Cord Injury Study recommended megadose systemic corticosteroid therapy on all patients with traumatic optic neuropathy within eight hours of injury.^3,4 Those patients not responding to such therapy after several days, or those with poorer visual acuity (i.e., finger counting or worse) at initial presentation were considered candidates for optic canal decompression surgery.

Recent studies have concluded that medical and/or surgical intervention might be of questionable value in many cases. It has been suggested that patients without negative prognostic indicators may be effectively managed with careful monitoring of their resolution.^1,5 Furthermore, research has shown that there is no significant difference in final visual acuity relating to dose (low vs. high vs. mega) or timing of corticosteroid therapy, nor is there a significantly different outcome between patients treated with steroids or surgical decompression of the optic canal.^5,6 Patients with traumatic optic neuropathy should, therefore, be addressed and managed via one or more of the above outlined options on an individual basis, following proper assessment and consultation.

Clinical Pearls

• There is no classic presentation to traumatic optic neuropathy. The involved optic nerve may be edematous, hemorrhagic or pale at the time of examination. Visual acuity and fields may likewise be minimally affected or severely compromised. The key to diagnosis lies in a thorough history and meticulous ocular evaluation.
• In evaluating for possible bony fractures of the orbit or skull, computed tomography (CT) is the vastly preferable technique. In addition to being far less expensive than MRI, CT offers much better resolution of bone, and also can demonstrate orbital hemorrhage in the early stages following trauma.
• In those cases that involve penetrating orbital injury or fracture of the sinus walls, systemic antibiotic therapy is mandatory to prevent secondary cellulitis.