TRAUMATIC OPTIC NEUROPATHY

DR ARPITA

“Trauma-induced injury to the optic nerve occurring anywhere along the nerve’s intraorbital to intracranial length”.

ANATOMY OF OPTIC NERVE

EPIDEMIOLOGY Traumatic optic neuropathy occurs in 0.5-5 % of patients presenting with

closed head trauma and in 2.5 % of patients presenting with midfacial fracture

Young > Old Males > Females

Steinsapir KD, Goldberg RA. Traumatic optic neuropathy:a

critical update. Compr Ophthalmol Update. 2005;6(1):11-21.

ETIOLOGY

CLASSIFICATION

DIRECT INJURIES Result from objects that penetrate the orbit

and impinge on the optic nerve causing optic neuropathy by partial or complete transection of the optic nerve sheath. Hemorrhages within and around the nerve may also occur

Lead to immediate changes in the fundus which can be detected on ophthalmoscopic examination

INDIRECT INJURIES Indirect TON is caused by the

transmission of forces to the optic nerve from a distant site without disruption of normal tissue structures. The deformative stress transmitted to the skull from blunt trauma is concentrated in the region of the optic canal.

INDIRECT INJURIES 1. Anterior : the central retinal artery

enters and the central retinal vein exits the optic nerve 8-12 mm posterior to the insertion of the nerve into the globe. Injuries anterior to this site are termed anterior.

2. Posterior: the injury is posterior to site of entry of the central retinal artery and exit of central retinal vein

PATHOGENESIS PRIMARY MECHANISM Shearing injury – localised ischemia and

optic nerve edema – further ischemia due to compartment syndrome

Permanent damage

SECONDARY MECHANISMS

1. Ischemia and reperfusion injury 2. Bradykinin 3. Calcium ions 4. Cell mediated mechanisms

CLINICAL FEATURES TON is a clinical diagnosis which is made

when there is evidence of optic neuropathy following a history of a blunt or a penetrating trauma

May be associated with multi-system trauma which needs attention first and respiratory and cardiovascular resuscitation and stabilization are priority.

History: Mechanism of injury Loss of consciousness, nausea and/or vomiting, headache, clear nasal discharge

Visual acuity –testing may be difficult depending on the patient's mental status, use of sedatives, narcotics

Pupillary evaluation - Relative afferent papillary defect (RAPD) is the sine qua non in cases of unilateral TON.

In the absence of RAPD either there is no TON or there is bilateral TON

Globe rupture , IOFB, fracture EOM motility Color vision - Checking red

desaturation is a useful alternative if color plates are not available.

Visual fields – Any type of field defects may be seen in optic nerve trauma e.g.

altitudinal, central, paracentral, hemianopic,etc.

Fundus examination

INVESTIGATIONS Neuroimaging VEP ERG

D/D Ischemic optic neuropathy Optic neuritis Tumor / aneurysm compressing on

nerve

MANAGEMENT Essentially by a multi-disciplinary

approach involving the ophthalmologist, physician, neuro-surgeon, and an otorhinolaryngologist

The optimum management protocol is yet to be elucidated as there is paucity of prospective large-scale clinical trials

Observation Steroids Surgery

Primary injury to the optic nerve fibers by

transection or infarction at the time of injury results

in permanent damage.

Neural dysfunction secondary to compression

within the optic canal, as a result of edema and

hemorrhage, may respond to medical or surgical

intervention.

MEDICAL The use of high-dose corticosteroids

after optic nerve injury began in the 1980 s following the report of Anderson et al

Anderson RL, Panje WR, Gross CE. Optic nerve blindness following

blunt forehead trauma. Ophthalmology 1982; 89:445–455.

National Acute Spinal Cord Injury Study 2 [NASCIS II], a multicenter clinical trial that evaluated patients with acute spinal cord injury

In this study, patients were treated with placebo,

methylprednisolone [MP], or naloxone

The study showed that Methylprednisolone (30 mg/kg loading dose, followed by 5.4 mg/kg/h for 24 h) started within 8 hours of injury was associated with a significant improvement in both motor and sensory function compared to patients treated with a placebo

CRASH COCHRANE REVIEW

SURGERY Fukado et al in the largest series of 400 cases had

suggested good results in optic canal decompressive surgery

Various surgical approaches for decompression of the optic canal include trans-frontal craniotomy, extra-nasal trans-ethmoidal, trans-nasal trans-ethmoidal, lateral facial, sublabial and endoscopic approaches

Fukado Y. Results in 400 cases of surgical decompression of the optic nerve. Mod ProblOphthalmol 1975;14:474–481

INDICATIONS Radiologically evident bony fracture fragment

impinging on optic nerve in the intracanalicular portion , or an optic nerve sheath hemamtoma in a TON pt with vision of < 6/60 on presentation

Failure to improve or deterioration of vision after 48 hrs of megadose steroid therapy in a TON pt with , < 6/60 vision at presentation and with no radiological evidence of fracture / hematoma in intracanalicular region of optic nerve

However, this option should be approached with extreme caution because of the proximity to the cavernous sinus and carotid siphon and possible bony instability of the skull base

The International Optic Nerve Trauma Study

A total of 133 patients who were initially assessed within 3 days of the optic nerve injury were treated with

corticosteroids, optic canal decompression surgery, or observed without treatment

Visual acuity increased by 3 or more lines in

32% of the surgery group, 57% of the untreated group, 52% of the steroid group

The study failed to find benefit for either corticosteroid therapy or optic canal decompression

SUMMARY Optic nerve laceration: No effective

treatment. Optic nerve head avulsion: No

effective treatment. Optic nerve sheath hematoma: Optic

nerve sheath fenestration may be helpful in the acute stage if optic neuropathy is progressing and no other cause is evident.

Deceleration injury : Effective treatment of posterior indirect TON is, at best, extremely limited.

In the vast majority of cases, observation alone is recommended

High-dose corticosteroids should never be offered by ophthalmologists to patients with concomitant traumatic brain injury (TBI) or if the TON is older than 8 hours.

If steroids are considered (no evidence of TBI, injury within 8-hour window, no medical comorbidities), the lack of definitive therapeutic evidence and significant side effects must be discussed with the patient and/or family and the primary team.

Bone impingement of the optic canal: Endoscopic optic canal and orbital apex decompression may be offered in select cases, especially if the optic neuropathy is progressive.

However, this option should be approached with extreme caution because of the proximity to the cavernous sinus and carotid siphon and possible bony instability of the skull base.

The procedure should only be performed by an otolaryngologist experienced in stereotactic endoscopic sinus and skull base surgery.

The patient and/or family should also be informed that there is no definitive data that proves efficacy of this procedure in TON and that optic canal decompression may result in additional damage to the intracanalicular optic nerve

FOLLOW UP Daily follow up - acute phase following

trauma, immediately after surgical therapy, and during the period of mega-dose corticosteroid therapy.

Weekly follow up - intermediate period following trauma, surgery, or discontinuation of steroid therapy

Long term - to document the final level of visual function

Prognosis Poor prognostic factors:

1. Presence of blood within the posterior ethmoidal cells

2. Age over 40 years 3. Loss of consciousness associated

with traumatic optic neuropathy, and 4. Absence of recovery after 48 hours

of steroid treatment

CURRENT RESEARCH Neurotrophic growth factors –

Monosialogliosides Gene transfer of anti inflammatory

cytokines New family of corticosteroids - lazaroids