BASICS

DESCRIPTION

Traumatic optic neuropathy (TON) is an optic neuropathy which occurs after head or ocular trauma. 2 mechanistic etiologies are recognized.

• Direct TON

Trauma resulting from penetrating foreign body which damages optic nerve

• Indirect TON

Trauma transmits concussive force to optic nerve. No foreign body or penetration.

• Anterior indirect TON

– Due to sudden anterior displacement or torsion of globe

– Often has funduscopic signs (e.g., optic nerve avulsion, optic nerve edema, retinal edema, or central retinal artery and vein occlusion)

• Posterior indirect TON

– Most common cause of TON

– Due to frontal, orbital, or midfacial trauma

– Almost always has normal optic nerve appearance

System(s) affected: Central nervous system

EPIDEMIOLOGY

• Predominant age: 20–40 years

• Predominant sex: Male

• Occurs in 1–5% of closed head injuries

PATHOPHYSIOLOGY

• Direct TON

Penetrating foreign body damages nerve or causes hemorrhage. Hemorrhage compresses surrounding structures causing ischemia, axonal block, and axonal death.

– Optic nerve transection

– Optic nerve contusion or foreign body impingement

– Compressive optic neuropathy secondary to orbital or intrasheath hemorrhage

• Indirect TON

– Anterior indirect TON

– Sudden anterior displacement of globe

– Optic nerve avulsion, central retinal artery or vein occlusion

– Posterior indirect TON

Trauma transmits concussive force to nerve.

Shearing, stretching, compression, or transection of optic nerve

Focal block of axonal conduction

Contusion necrosis

Ischemic necrosis

Late demyelination

ETIOLOGY

• Direct TON

– Penetration foreign body (e.g., knife, bullet, BB)

– Postoperative complication

Endoscopic sinus surgery

Maxillofacial surgery

Ocular surgery (e.g., retrobulbar anesthesia, orbital surgery, blepharoplasty)

• Indirect TON

– Closed head injury

Motor vehicle accident

Bike accident

Falls

Assaults

COMMONLY ASSOCIATED CONDITIONS

• Loss of consciousness

• Intraorbital or intracranial foreign bodies

• Orbital hemorrhage

• Orbital, maxillofacial, or basilar skull fracture

• Optic canal fracture

• Intracranial hemorrhage

DIAGNOSIS

HISTORY

• Location of trauma

– Frontal, orbital, or midfacial

• Mechanism of trauma

– Direct TON

– Foreign body

– Indirect TON

Sudden deceleration injury

Trauma occasionally may seem insignificant

• Onset of visual loss

– Immediately after injury or reported when patient regains consciousness

– If delayed: Suspect expanding nerve sheath or orbital hemorrhage

• Associated symptoms:

– Loss of consciousness

– Anosmia, diabetes insipidus, other neurologic deficits imply skull base fracture

PHYSICAL EXAM

• Vital signs

• External Ocular Exam

– Orbital findings:

Ecchymoses, edema, and emphysema

Proptosis

Penetrating wound or foreign body

• Ocular motility

Ophthalmoplegia may be due to:

– Muscle trauma

– Orbital hemorrhage

– Cranial nerve palsy (basilar skull fracture)

• Visual acuity

– May range from 20/20 to no light perception

• Pupil exam

– Critical for diagnosis, especially in an unconscious patient

– Afferent papillary defect: present in unilateral TON. May be absent if there is bilateral TON

• Funduscopic exam

– Optic nerve appears normal in posterior indirect TON

• Optic nerve avulsion, edema (unusual), central retinal artery and vein occlusion—anterior indirect TON

DIAGNOSTIC TESTS & INTERPRETATION

Lab

Initial lab tests

• Slit-lamp examination—exclude ruptured globe

• Tonometry-–intraocular pressure may be elevated in orbital compartment syndrome or decreased in occult ruptured globe

• Visual fields

– Automated or confrontation—a variety of defects (e.g., altitudinal, arcuate, paracentral, or central scotoma) may be present

• Color vision

– Ishihara color plates-–dyschromatopsia

– Red desaturation-–present

• Flash VEP-–abnormal or absent in affected eye. Useful in unconscious patient.

Follow-Up & Special Considerations

• Low vision specialist for patients with poor visual outcome

• Occupational therapy for patients with poor visual outcome

Imaging

• CT scan

– Imaging Recommendations

– Axial and coronal planes

– Thin sections and reconstructions

– Attention to optic canal

– Spiral CT-–short scan time helpful in children

– Orbital CT findings

– Periorbital soft-tissue edema

– Orbital hematoma

– Optic nerve sheath hemorrhage

– Optic nerve transection

– Foreign body

– Orbital, facial, or optic canal fracture

– Head CT findings

Basilar skull fracture

Optic canal fracture

Epidural, subdural, subarachnoid, or cerebral hemorrhage

• MRI: Not always necessary. Better identifies soft-tissue findings

– Imaging recommendations

– First exclude metallic foreign body with CT or plain film

– Gadolinium enhanced

– Thin sections

– Orbital MRI findings:

– Optic nerve sheath hemorrhage

– See orbital CT findings

– Brain MRI findings:

Chiasmal edema and hemorrhage

See head CT findings

DIFFERENTIAL DIAGNOSIS

• Nonorganic visual loss

• Ruptured globe

• Retinal detachment

TREATMENT

MEDICATION

If patient seen within 8 h of injury

• Corticosteroids

– High-dose steroids may be offered although there is no proven clinical benefit (1)[A]

– Thorough discussion with patient and family

– Methylprednisolone 30 mg/kg i.v. bolus followed by 5.4 mg/kg/h for 48 h (2)[A]

– Histamine 2 blocker to protect gastric mucosa

– Side effects: Peptic ulcer disease, gastrointestinal bleed, hyperglycemia, hypertension, weight gain, osteoporosis, and psychosis

ADDITIONAL TREATMENT

General Measures

• Cardiovascular and respiratory stabilization of patient

• Multidisciplinary approach: Consult otolaryngology, neurology, and/or neurosurgery if indicated

Issues for Referral

Neuro-ophthalmology in 2–3 days

COMPLEMENTARY & ALTERNATIVE THERAPIES

Observation alone of TON is a valid treatment option.

SURGERY/OTHER PROCEDURES

• Optic canal decompression

– May be offered to patient although there is no proven clinical benefit (3)[A]

– Consider if fracture fragment impinging on optic nerve.

– Consider if no improvement in visual acuity after 48 h of i.v. steroids

– Only at institutions with experienced surgeons

– Avoid in the comatose patient

• Removal of foreign body or fracture fragment if optic nerve impingement

• Optic nerve sheath fenestration if optic nerve sheath hemorrhage is demonstrated on MRI

• Canthotomy/cantholysis if orbital compartment syndrome and optic nerve compression

IN-PATIENT CONSIDERATIONS

Initial Stabilization

Address cardiovascular or respiratory compromise

Admission Criteria

• Floor or ICU status determined by general neurologic status and severity of associated injuries

• Treatment with i.v. steroids

• Operative cases

Nursing

• Check visual acuity every 2 h for first 24 h, and thereafter daily.

• Instruct patient to report any decrease in vision.

Discharge Criteria

• Untreated TON

• Visually stable TON treated with i.v. steroids or operatively

• Neurologically stable

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Neuro-ophthalmology in 2–3 days

PATIENT EDUCATION

• Report any decrease in vision or increase in swelling, proptosis, or pain to neuro-ophthalmologist

• If any change in mental status: Call 911

PROGNOSIS

• Variable: 32–57% of patients have improvement in vision.

• Better in patients with indirect TON than direct TON

• Poor if initial visual acuity is no light perception

COMPLICATIONS

• Decreased visual acuity, decreased color vision, and visual field defects

• Periorbital scarring

• Post-concussive syndrome

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