Optic Nerve Decompression for Traumatic Optic Neuropathy Treatment & Management

The most widely accepted contemporary treatments for traumatic optic neuropathy have included observation, steroids, and surgical decompression, but concerns about the use of corticosteroids in patients with acute brain trauma have led to recommendations to not treat traumatic optic neuropathy with steroids. ^[21] Lack of a prospective large-scale clinical trial perpetuates controversy as to the optimal treatment for traumatic optic neuropathy. ^[16] The timing and type of decompression procedure and selected use and optimal dosing of perioperative corticosteroids have also been widely reported but have not been validated by controlled outcome trials. ^[22]

A revision of the Cochrane review on this topic found only a single double-masked, randomized, controlled trial comparing placebo to high-dose intravenous steroids for traumatic optic neuropathy but concluded that no convincing evidence suggests steroids provided any additional benefit to vision. ^[23]

Nonetheless, a survey of members of the American Society of Ophthalmic Plastic and Reconstructive Surgery and the North American Neuro-Ophthalmology Society found that out of 165 respondents, 60% treated traumatic optic neuropathy with corticosteroids. This included 67% of oculoplastic surgeons and 47% of neuro-ophthalmologists. Twenty-three percent of respondents managed traumatic optic neuropathy with surgery. ^[24]

A more in-depth discussion of steroid therapy for traumatic optic neuropathy can be found in the Medscape Drugs & Diseases article Traumatic Optic Neuropathy.

Surgical optic nerve decompression (OND) is a reasonable and reported treatment for traumatic optic neuropathy. Evidence suggests that initial visual acuity (IVA) of no light perception is the most significant determinant of outcome in traumatic optic neuropathy. Patients with IVA of no light perception treated surgically within 7 days of injury had a better improvement degree than patients managed medically.

Various surgical approaches for decompression of the optic canal include transfrontal craniotomy, extranasal transethmoidal, transnasal ethmoidal, lateral facial, and endoscopic procedures. ^[4] An intranasal endoscopic approach is favored because of the proximity of the optic nerve to the sphenoid sinus and Onodi cell. Advantages of this approach include lack of external scars, preservation of olfaction, decreased morbidity, and faster recovery time. ^{[5, 6, 7]}

Chen et al reported that endoscopic optic nerve decompression can be safely and effectively achieved via a direct sphenoidotomy performed through the sphenoid ostium, in patients with high sphenoidal pneumatization and no supersphenoethmoidal air cells. The study involved five cases of traumatic optic neuropathy, with a 45°-angled endoscope used to reach the optic nerve canal. ^[25]

Emanuelli et al reported a relatively good risk-benefit ratio in patients with posttraumatic optic neuropathy when a protocol was followed in which patients received endovenous steroid therapy no more than 8 hours after injury, with endoscopic endonasal decompression of the intracanalicular segment of the optic nerve performed within 12-24 hours after the start of medical treatment. The study involved 26 patients, with a maximum 41-month follow-up period. ^[26]

Obtain imaging studies to delineate the exact anatomical relationship of the optic nerve and carotid artery to the posterior ethmoid cells and sphenoid sinus. If receiving megadose systemic corticosteroids, the patient may continue these drugs at a tapered dosage. If the patient has completed a preoperative corticosteroid trial, administer a loading dose of dexamethasone 1.5 mg/kg (or equivalent) a few hours preoperatively. The steroid's anti-inflammatory effect reduces the inflammation induced by surgery. Preoperative systemic antibiotics may be initiated once surgery is scheduled to suppress any preexisting chronic rhinosinusitis.

The authors have been successfully using endoscopic optic nerve decompression for the past decade. Although the use of a computerized surgical navigation system is not mandatory, the systems offer anatomical assistance. The operation is performed entirely with a zero-degree endoscope.

Begin the procedure with a total sphenoethmoidectomy using a modified Messerklinger/Stammberger/Christmas technique. At the beginning of the operation, slowly inject 1% Xylocaine with 1:100,000 units epinephrine near the pterygopalatine and anterior ethmoid areas to facilitate intraoperative hemostasis. Injections within the posterior septum are made later when operative exposure is available. To take advantage of this hemostatic window of opportunity, complete the operation within 2 hours. Do not use intraoperative electrocautery because of its potential to damage the optic nerve and major vessels. To prevent inadvertent use of cautery, no electrocautery is connected within the operating room during the procedure.

The powered microdebrider (shaver) is used extensively for all parts of this operation, including bone removal. For thin bone and soft tissue, use a 12° angled shaver blade. Totally remove the uncinate process in its inferior two thirds and leave the maxillary antrostomy untouched. After a standard ethmoidectomy, insert the microdebrider through the natural ostium of the sphenoid and shave laterally to remove the sphenoid face.

After the sphenoid sinus is opened and the lamina papyracea is clearly delineated, make a hole through the thin lamina bone with a small curette, 1 cm anterior to the sphenoid face and immediately anterior to the bulge in the lateral sphenoid/posterior ethmoid wall caused by the optic nerve. Use care to avoid damage to the periorbita. (Opening the periorbita at this stage would hinder subsequent intraoperative visualization because of the prolapse of orbital fat into the ethmoid cells.) Remove the lamina bone posterior to the opening with the use of curettes and Blakesley forceps. As the bone removal moves posteriorly, the bone becomes thicker.

Expose the optic nerve and its sheath for a distance of approximately 10-15 mm. Thin the thick bone of the medial wall of the optic canal with the powered microdebrider fitted with a 3- or 4-mm straight, spherical, or angled router burr. Curettes may be used to complete the bony removal. The bony opening should expose at least 120° of the circumference of the nerve. Longitudinal opening of the Zinn rings and optic nerve sheath may now be performed. Clinical indications for opening these structures have not been elucidated clearly. The authors perform this fenestration only when preoperative visual acuity is at light perception level or worse. If the procedure is performed, longitudinally incise the optic nerve sheath with a very sharp sickle-shaped blade. The importance of a sharp blade cannot be overemphasized, since tractional force—even that induced by the cutting motion of the blade—on the optic nerve and sheath must be minimized.

Once the bony canal has been removed and the sheath has been incised, the procedure is concluded. No intranasal packing is placed.

Continue the systemic steroid therapy started preoperatively every 8 hours for 24 hours. If the patient had preexistent nasal or sinus mucosa inflammation, the steroids may be converted to oral prednisone and continued at a tapered dosage for 1-2 weeks. Postoperative antibiotic therapy has no known role, except perhaps in patients with preoperative chronic rhinosinusitis.

On the first postoperative day, start the patient on bulb-syringe saline nasal irrigations 3 times per day. Continue these irrigations for at least 1-2 weeks, until normal mucociliary function again is active.

Objectively define recovery of visual function based on serial assessment of multiple visual function parameters (eg, visual acuity, visual field, quantitation of afferent papillary defect, assessment of abnormal color vision). Perform daily follow-up evaluations immediately after trauma, during megadose methylprednisolone therapy, and immediately after surgical therapy. Less frequent examinations (q4-7d) are warranted during the intermediate period following surgery. Long-term follow-up is appropriate at a point 3 months or longer from the date of injury to document the final level of visual function.

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

Injury to the globe, optic nerve, and extraocular muscles can result if the periorbita is breached during the removal of the lamina papyracea. A study of optic canal decompression on cadaveric specimens found microscopic evidence of injury to the optic nerve, pia, and an extraocular muscle, and dural fraying in the specimens. ^[27]

Injury to the anterior ethmoidal artery can produce an orbital hematoma and further aggravate the optic nerve status.

CSF leaks, meningitis, pneumocephalus, and death may occur after trauma to the cranial floor and dura.

Massive intracranial bleeding and stroke may follow injury to the intracranial internal carotid artery.

Numerous published reports are available that detail the clinical outcome of treatment modalities for traumatic optic neuropathy. Unfortunately, many of these reports are retrospective, have a limited number of patients, or suffer from one or more biases or deficiencies.

In 1999, Levin and the International Optic Nerve Trauma Study published the results of a multicenter, comparative, nonrandomized study of 133 patients with traumatic optic neuropathy. ^[28] To date, this is the largest series on steroid treatment available. The purpose of this study was to compare the visual outcome of traumatic optic neuropathy treated with corticosteroids, optic canal decompression surgery, or observation without treatment. Treatment, when undertaken, was initiated within 7 days of the injury. Seventy-six investigators in 16 countries collected the data between 1994 and 1997. Treatment decisions followed the investigators' customary practice, and no specific protocols for corticosteroid treatment or surgical technique were followed.

The study showed that visual acuity improved by 3 lines or better in 32% of patients treated with surgery, 52% of patients treated with corticosteroids, and 57% of patients in the untreated group. No clear benefit was found for either corticosteroid therapy or optic canal decompression. The study also found that the dosage or timing of corticosteroid treatment or the timing of optic canal decompression was not associated with an increased probability of improved visual acuity. Within the limitations of the study design, the authors concluded that neither corticosteroid therapy nor optic canal decompression should be considered the standard of care for patients with traumatic optic neuropathy. The authors suggested that whether to initiate treatment on an individual patient basis is reasonable for clinicians to decide.

In 1996, Cook et al performed a retrospective metaanalysis of all published English-language cases and selected non–English-language cases of traumatic optic neuropathy. ^[29] The authors found that vision recovery in treated patients was significantly better than in nontreated patients, but the authors found no difference in vision improvement among patients treated with steroids alone, surgical decompression alone, or combined steroid and surgical decompression.

Contrary to the findings of the International Optic Nerve Trauma Study, Kountakis et al (in a retrospective study of traumatic optic neuropathy patients treated from 1994-1998) showed that patients treated with surgical decompression following failed megadose steroid therapy fared significantly better than patients treated with megadose steroids alone. ^[19]

The role of delayed optic nerve decompression (OND), (defined as surgical decompression undertaken 2 weeks to several months after injury) in traumatic optic neuropathy remains unclear. However, the limited studies point to some benefit when this treatment is used as salvage therapy on patients who are not completely blind after steroid therapy failed.

Although the need for a large-scale, prospective, randomized, controlled treatment trial is evident, many individuals believe such a trial is unlikely, given the low incidence of traumatic optic neuropathy and difficulties that exist in the randomization of patients. To date, little evidence exists to guide the management of traumatic optic neuropathy. The only basis for medical treatment for traumatic optic neuropathy has been extrapolated from the randomized trials for treatment of spinal cord injury. Newer studies, however, point to increased complications in patients who received high-dose corticosteroid treatment after spinal cord injury or acute head injury, as reviewed by Steinsapir in 2006. ^[21] The risks associated with the use of high-dose corticosteroids and the risks of surgery along with a lack of evidence of clear benefit of either treatment must be considered in the management of traumatic optic neuropathy.

A better understanding of the cellular and biochemical mechanisms that involve normal and traumatized axons, glia, and myelin sheaths may eventually lead to better interventions for traumatic optic neuropathy. A better delineation of surgical indications and the standardization of operative technique will be welcomed advances. The role of adjuvant neuroprotective agents will probably be advanced. Although corticosteroids are but one type of neuroprotective agent, the recent expansion in basic science research regarding other neuroprotective agents may lead to a redirection in future therapy for this condition.

Researchers have been examining the role of A2A adenosine receptor as a potential therapeutic target for halting further retinal glial cell degeneration. ^[30] A recent murine study using transcorneal electrical stimulation in traumatic optic neuropathy found that this treatment may provide some delay in and protection from neuronal death in select responder groups of mice. ^[31] Further studies need to be done to define responders and nonresponders, but this article presents an interesting development on traumatic optic neuropathy treatment. Thus far, these and similar studies have been conducted in animal models but there is great hope that such endeavors will lead to improved treatment of traumatic optic neuropathy.