Endoscopic optic nerve decompression for traumatic optic neuropathy

ENDOSCOPIC OPTIC NERVE DECOMPRESSION FOR TRAUMATIC OPTIC NEUROPATHY ERICA R. THALER, MD, DONALD C. LANZA, MD, DAVID W. KENNEDY, MD

This article reviews a new operative technique in treating traumatic optic neuropathy (TON): endoscopic optic nerve decompression. The definitions and diagnosis of TON are discussed, and a review of the currently practiced therapeutic options for TON is undertaken. The relevant surgical anatomy and endoscopic technique are described in detail, including possible potential complications from the procedure. Our experience suggests this is a viable alternative to other surgical approaches for optic nerve decompression.

Surgical decompression of the optic nerve for the treatment of loss of visual acuity is described for fibro-osseous lesions of the optic canal, orbital pseudotumor, and Graves' orbitopathy. 1 Perhaps the most common indication for this surgical procedure is for treatment of traumatic optic neuropathy (TON). Although much has been written on this subject, varying definitions, small study groups, and widely divergent treatment protocols have made it difficult for the practitioner to find guidance in management of optic nerve decompression for TON. Thus, the precise surgical technique and indications for this procedure remain controversial. Although reviewing the diagnosis of TON, the treatment options, and surgical anatomy, this article focuses on the operative technique for endoscopic decompression of the optic nerve. DEFINITION

Traumatic optic neuropathy (TON) is perhaps best defined as posttraumatic visual loss without visible injury to the eye, and without direct injury to the optic nerve. Direct injury to the optic nerve classically has been described as an injury from a penetrating foreign body. TON, which is considered an indirect injury, results from damage secondary to contusion or fracture in the optic canal. 2 Mechanisms of optic nerve injury include those that are irreversible and those that are reversible. Irreversible mechanisms include tearing of nutrient vessels leading to infarction and atrophy, and direct avulsion. Reversible mechanisms include compression from hemorrhage; compression from edema; vascular thrombosis; and vascular spasm. The location of optic nerve injury is most commonly in the intracanalicular segment, because here the optic nerve sheath is attached to the bony optic canal. 3,4 A fracture in this location or shearing forces from deceleration impact in this area would more likely result in injury to the optic nerve. Moreover, the bony canal is a closed space, less forgiving of

edema. Estimates of the incidence of TON in closed-head trauma range from 2% to 15°/o.5,6 DIAGNOSIS

TON is diagnosed by a thorough ophthalmologic examination. This may be difficult because patients are often obtunded or unconscious, and loss of visual acuity or even light perception may be rapidly progressive after the traumatic event. The most reliable indicator of optic nerve injury is an afferent pupillary defect (Marcus-Gunn pupil phenomenon) in the absence of any other sign of ocular injury. The ocular fundus has a normal appearance early on in the course of injury. At 3 to 6 weeks after injury, the optic disk will appear pale, a sign of optic atrophy. Appropriate evaluation and treatment of associated maxillofacial and head injuries are performed. A computed tomographic (CT) scan is obtained (soft tissue and bony windows with 1- to 2-mm cuts both axial and coronal through the orbit) to evaluate the bony anatomy of the orbital apex and the adjacent structures, particularly the ethmoid and sphenoid sinuses. This will help to localize the injury and may identify a displaced fracture impinging on the optic nerve. Any suspicion of concurrent carotid injury is assessed and followed for the development of a carotid-cavernous sinus fistula. A magnetic resonance imaging or angiographic (MRI/MRA) scan may be essential in these circumstances. If this condition is not suspected by history, physical or CT imaging, then awaiting MRI can result in unnecessary loss of valuable time if decompression is planned. Visual field checks, red color saturation, and visual-evoked responses are valuable in the patient with non-emergent visual deterioration. Thus, these tests are not typically obtained in the trauma victim with sudden visual compromise. SURGICAL ANATOMY

From the Division of Rhinology, Department of OtorhinolaryngologyHead and Neck Surgery, University of Pennsylvania, Philadelphia, PA. Address reprint requests to Donald C. Lanza, MD, Associate Professor, Director, Division of Rhinology, Department of Otorhinolaryngology-Head and Neck Surgery, University of Pennsylvania, 5 Silverstein Pavilion, 3400 Spruce St, Philadelphia, PA 19104. Copyright © 1996 by W.B. Saunders Company 1043-1810/96/0703-0011 $05.00/0

An understanding of the anatomy of the optic nerve and surrounding structures is critical in undertaking care of patients with TON, particularly if surgery is contemplated. The optic nerve is surrounded by all three meningeal layers as it courses through the optic canal to the optic chiasm, which sits above the pituitary gland. Lying with it, but typically inferolateral, is the ophthalmic artery, which will give off the central retinal artery approximately 10 mm behind the globe. The precise course of ophthalmic artery

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varies among individuals and occasionally may be positioned medially along the optic nerve at four o'clock. The central retinal artery enters the optic nerve medially. The optic canal, which is part of the lesser sphenoid wing, is just superolateral to the sphenoid sinus. In 78% of patients, the nerve is covered by 0.5 mm of bone, which is the lateral wall of the sphenoid, and in 4% this bone is dehiscent. 7 The canal is wide with thin walls proximally toward the optic chiasm and narrow with thick walls distally at the optic tubercle. The optic tubercle is the thick bulge of the medial aspect of the bone surrounding the optic foramen. 8 Depending on the degree of pneumatization or the presence of sphenoethmoid (Onodi) cells, the optic tubercle can be seen within the sphenoid sinus or at the junction of the sphenoid and posterior ethmoid sinuses. 8 Important to note is the variable degree to which the sphenoid sinus pneumatizes. Three levels of pneumatization are recognized: conchal, presellar, and post-sellar. In a coronal plane, the optic nerve traverses roughly at the same vertical height as the roof of the ethmoid sinuses and the anterior and posterior ethmoidal arteries. The distance of the posterior ethmoidal artery to the optic nerve during an external ethmoidectomy is variable, but is generally positioned only millimeters anteriorly. The mnemonic for the locations of the foramina along the medial orbital wall is the number series 24-12-6, which are the average distances in millimeters from the anterior lacrimal crest to the anterior ethmoidal foramina, from the anterior to posterior ethmoidal artery, and from the posterior ethmoidal artery to the optic nerve, respectively. 9 It should be recalled that the very presence or absence of the vasculature structures is variable and that unilateral absence of the anterior ethmoidal artery has been estimated to be as high as 14%. 1° The carotid artery runs inferolateral to the optic nerve as the vessel heads toward the cavernous sinus. The carotid canal is considered "clinically dehiscent" in the sphenoid sinus in as many as 23% of patients u (see Fig 1). The fusion of the pia mater and arachnoid surrounding the optic

nerve at the orbital apex emerges as the anulus of Zinn as the optic nerve exits the optic canal. Subarachnoid space is maintained patent in the optic canal. The anulus of Zinn is the fibrous anulus to which extraocular muscles fuse in the orbital apex. OVERVIEW

OF THERAPEUTIC

Treatment of TON remains controversial because, as the rarity of the condition dictates, large prospective trials have been difficult. It is generally accepted that once the diagnosis of TON is made, treatment is indicated. There are three treatment options widely practiced: (1) high dose corticosteroid therapy, (2) surgical optic nerve decompression, or (3) a combination of surgery and steroids. Although controlled studies are lacking, high dose corticosteroids have been used to treat TON with apparent success. The rationale for such treatment comes from successful use of high dose steroids in other central nervous system trauma. 12,13 The mechanism of action is thought to be reduction of tissue edema with resultant prevention of cell death. Blood supply is also increased to the injured area. A bolus of methyl prednisolone of 30 m g / k g is administered and continued at 15 m g / k g every 6 hours for 48 hours. Several series have reported significant restoration of vision with steroid use in TON (62% to 86%).14,15 Surgical decompression of the optic nerve has been described as early as 1916, via a craniotomy approach. Decompression of the nerve medially through the lateral wall of the sphenoid and ethmoid sinuses was begun in the 1960s, and has been reported with widely varying success rates (12% to 79%). 16,17 The therapeutic mechanism is, rather than to prevent edema, to allow more room for expansion of the traumatized nerve, thus limiting secondary compression-induced trauma. A variety of external approaches have been described, including transantraltransethmoidal, sublabial, and transnasal. Combination therapy is practiced by many. One such treatment algorithm is to begin treatment with high dose steroids every 6-hour intervals for 48 hours. Patients whose vision improves are gradually tapered off steroids. Patients with vision worse than 20/200 or who show deterioration on steroids may be candidates for optic nerve decompression. TM Decision to proceed with surgery is often difficult. A meta-analysis reviewing the literature comparing these different treatment options found no statistically significant difference among the varying regimens. 19 TECHNIQUE OF ENDOSCOPIC DECOMPRESSION

FIGURE 1. Photograph of a right infraoptic recess in the sphenoid sinus (large arrow). The optic nerve lies superior to this and the carotid artery bulge lies inferior.

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OPTIONS

NERVE

Endoscopic optic nerve decompression offers several advantages over other surgical approaches. It requires no external incision. There is no orbital retraction during the procedure. The endoscopes provide excellent visualization of the dissection. The major caveat to its use is that it should only be undertaken by an experienced endoscopic surgeon. Before deciding to proceed with endoscopic optic nerve decompression, the patient's CT scan is carefully reviewed. Inspection of the optic canal and sinus anatomy includes evaluation for signs of fracture, integrity of skull base, type and extent of sphenoid pneumatization including whether or not a sphenoethmoid (Onodi) cell is present (see Fig 2), the location of the intersinus septum and its relationship to the optic nerve and carotid artery, the location and relationENDOSCOPIC OPTIC NERVE DECOMPRESSION

FIGURE 2. Coronal CT scan of sphenoid sinuses shows a left-sided Onodi cell (large arrow). Confirmation that this is a sphenoethmoid cell is made on axial CT scan. Access to the left optic nerve (small arrow) requires opening of this cell.

ship of the optic nerve and carotid artery to one another, and possible dehiscence of the carotid artery. 8 Again, carotid cavernous fistulization should be considered in association with this evaluation. The surgery is performed under general anesthesia. This work is typically performed with a 0° nasal endoscope. Occasionally, a 30 ° endoscope is of value. The nasal mucosa is decongested with oxymetazoline, followed by lateral nasal wall injection of lidocaine with epinephrine. A transoral, sphenopalatine block via the greater palatine foramen is also performed. A complete endoscopic sphenoethmoidectomy is performed while carefully skeletonizing the medial orbital wall. Concurrent endoscopic septoplasty

may be indicated depending on surgical access. 2° Care is used to avoid unnecessary trauma or stripping of surrounding mucosa, because this will facilitate postoperative healing. A large middle meatal antrostomy that includes the natural ostium secures the anterior and inferior limits of the dissection, but is only necessary when the orbital apex is difficult to distinguish as it tapers toward the sphenoid sinus. The attachments of the middle turbinate are maintained superiorly and inferolaterally. Occasionally, partial middle turbinate resection may be required. The natural opening of the sphenoid sinus is identified adjacent to the superior turbinate and widely opened with a Hijak rotating sphenoid punch. Complete removal of the anterior face of the involved sphenoid sinus will often result in near total removal of the superior turbinate. Within the sphenoid sinus, the optic nerve is often readily identified in the superolateral aspect of the sphenoid sinus. Lamina papyracea in the posterior ethmoid is elevated away from the periorbita with a Freer or Cottle elevator. Care is used to avoid violation of the periorbita and injury to the adjacent medical rectus. Orbital fat herniating through periorbita can be obstructive, and cautery in this region may result in inadvertent injury to the medial rectus muscle. Occasionally, a very prominent optic tubercle requires drilling with a cutting bur, because the bone is very thick in this location (see Fig 3). Simultaneous irrigation via a ureteral stent placed alongside the drill inside the nose is essential to prevent burning of bone and the underlying structures. Endoscopically guided drilling with a diamond bur is then performed for the remainder of the dissection. The optic canal is gradually drilled from anterior to posterior. Once the canal is significantly thinned down, small curets and otologic instruments can be used to remove the remaining layers. Occasionally, depending on the degree of sphenoid pneumatization, longer neurosurgical instruments are required. The goal of decompression is to expose nerve nearly 180% on its medial half from orbital apex to optic chiasm (see Fig 4). Once the bone has been removed, the optic nerve sheath may be opened with a disposable arachnoid knife. How-

FIGURE 3. Illustration shows a complete left sphenoethmoidectomy, with the drill being used to remove the left optic tubercle. THALER ET AL

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t r o u b l e s o m e bleeding is e n c o u n t e r e d in the course of dissection, p l a c e m e n t of an o x y m e t a z o l i n e - i m p r e g n a t e d neurosurgical pledget m a y be sufficient for bleeding to subside. If bleeding is m o r e significant, microfibrillar collagen a d m i x e d w i t h t h r o m b i n a n d s u b s e q u e n t Gelf o a m ® (Upjohn, Kalamazoo, MI) m a y be gently placed within the s p h e n o i d sinus. Bipolar cautery is m u c h preferred to suction unipolar cautery. Complications of orbital h e m a t o m a or carotid or cavernous sinus bleeding should be anticipated, a n d the surgeon p r e p a r e d to act swiftly in these instances. A careful review of the patient's nasal anatomy with endoscopy and CT scan preoperatively is the best means of preventing these devastating complications.

ACKNOWLEDGMENT We a c k n o w l e d g e Jill Foster, MD, Oculoplastic Surgeon, at the Cleveland Clinic for assistance w i t h Figure 3. We a c k n o w l e d g e P e g g y Agolino a n d Lili H o u c k for their assistance in p r e p a r a t i o n of the manuscript.

REFERENCES FIGURE 4. Photograph of decompressed left optic nerve in a 10-year-old boy (large arrow) as it appears after endoscopic procedure. Key: y, orbital fat; x, left maxillary sinus mucosa.

ever, the n e e d to p e r f o r m this m a n e u v e r is s o m e w h a t controversial a n d can lead to a cerebrospinal fluid leak. H e m o s t a s i s t h r o u g h o u t the p r o c e d u r e is meticulously sought. Residual bleeding in the e t h m o i d cavity m a y be p a c k e d w i t h a Merocel ® K e n n e d y sinus p a c k (Merocel Surgical Products, Mystic, CT) coated with m u p i r o c i n ointment. The patient is m a i n t a i n e d p o s t o p e r a t i v e l y on antibiotics and steroids, w h i c h are g r a d u a l l y tapered off.

COMPLICATIONS Despite the d r e a d complication of blindness, this is an elective p r o c e d u r e and, as in all surgical procedures, the patient should be fully i n f o r m e d of the risks, benefits, and alternatives to this procedure. In the head-injured patient, it can be impossible to obtain consent on an i m m e d i a t e basis. Given that vision remains in one eye a n d the other concurrent injuries m a y require m o r e e m e r g e n t attention, family m e m b e r s are reluctant to expose the patients to the risk of the procedure. Patients are i n f o r m e d of the potential need for turbinate resection. If extensive turbinate resection is required, then an u n c o m f o r t a b l e sense of nasal obstruction d u r i n g quiet breathing or nasal crusting m a y occur. Potential decrease in sense of smell, p o s t o p e r a t i v e sinus or orbital infection, CSF leak, direct brain injury, further c o m p r o m i s e of the optic n e r v e w i t h loss of light perception (if not already lost), diplopia, and carotid injury are other possible complications. If s e p t o p l a s t y is required for access, the patient is i n f o r m e d of its a t t e n d a n t risks. If a cerebrospinal fluid leak occurs either f r o m the t r a u m a itself or f r o m the surgical dissection, repair is r e c o m m e n d e d as described elsewhere. 21 A l u m b a r drain for 3 d a y s m a y also be a p p r o p r i a t e in this situation. Problems w i t h hemostasis m a y render the endoscopic a p p r o a c h difficult, particularly in the individual w h o has associated sinus a n d nasal cavity injuries with attendant posttraumatic e d e m a and irregular bleeding surfaces. Careful hemostasis t h r o u g h o u t this p r o c e d u r e is p a r a m o u n t . If

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