neuropathy Traumatic optic

Traumatic Optic Neuropathy

이연희 충남의대 안과

Traumatic optic neuropathy

충남대 이연희

Introduction

• Traumatic optic nerve injury

• Causes: motor vehicle & bicycle accidents, head trauma from falls and falling debris, stab and gunshot wounds, endoscopic sinus surgery, seemingly trivial injuries

• Part of the spectrum of head trauma : seen in 0.5% to 2%

• Incidence of loss of consciousness : 20% - 75%

• Prognosis for visual recovery is poor

Classification

• Direct injury

• Directly by a projectile, knife, or other object that penetrates the orbit to damage the optic nerve

• Indirect injury

• Broad definition

: Injury from the non-penetrating effects of trauma, including hemorrhage, edema, and concussion

• Narrow definition

: Injury from forces transmitted to the optic nerve via the orbital apex and optic canal

Optic nerve avulsions

• A type of TON

• Traumatic separation of the optic nerve from the globe at the level of the lamina cribrosa without rupture of the optic nerve sheath or the adjacent sclera

• May be caused by sudden, forceful rotations of the eye

• Typically produce a partial or complete ring of hemorrhage at optic nerve head

Pathophysiology of indirect injury

1. Blow to the malar and frontal areas -> Shock wave -> Transmitted to optic foramen 2. Coup-Contrecoup

3. Violent rotation

1. Shock wave

Some studies suggest that compression of the superior orbital rim is transferred and concentrated in the orbital roof and optic canal.

Holographic interferometry

• Very sensitive method of demonstrating surface perturbations

• More concentrated the fringes, the more surface is deformed

A static lodging study

Deformation of the orbital roof 5 - 8 mm from optic foramen

A static lodging study

2. Coup-contrecoup

• Optic nerve is fixed within the optic canal

• Coup-contrecoup forces whip mobile portions of optic nerve against fixed Structures

3. Violent rotation

• Relatively minor non-penetrating injury from pointed objects such as fingers, poles,

• Sudden rotation of the globe in the direction of the object

Concept of primary and 2ndary injury

• Primary injury

• Mechanical shearing of the optic nerve axons

• Necrosis owing to immediate ischemia from damage to the microcirculation

• Subsequent RGC degeneration

• Secondary injury

• Vascular ischemia and/or trauma induce swelling within optic canal

• Further ischemia

• Visual dysfunction may delayed in up to 10%

Clinical assessment

• Often unavoidable delays

• When patients have life-threatening injuries

• Concomitant decreased level of consciousness

• Cinical findings

• Typical of most optic neuropathies : decreased acuity, color and visual field

• Commonly visual acuity : 20/400 or less

• Normal fundus, disc avulsion, retinal whitening

• Definite RAPD in unilateral case

Clinical assessment

• Neuroimaging : CT

• May reveal specific pathology compromising the optic nerve a

• Critical for surgical planning if optic canal decompression is considered

• Normal in many cases

• Optic canal fractures

: No consistent correlation between visual loss

Treatment

• No evidence-based guidelines

• Four main treatments

• Steroids

• Surgery

• Combination of steroids and surgery

• Conservative management

High-dose corticosteroids

• Range of methyl-PD regimens -Levin et al

• Mega dose( > 5400 mg/d)

• Very-high-dose (2000 - 5400 mg/d)

• High-dose (500 - 1999 mg/d)

• Moderate-dose (100 - 499 mg/d)

• Low dose (<100 mg/d)

High-dose corticosteroids

• National Acute Spinal Cord Injury Study II

• randomized, double-blind, placebo-controlled study

• The use of High-dose steroids( methyl-PD : 5.4 mg/kg per hour for 24 or 48 hours within 8 hours of injury

• Significantly improved both motor and sensory function

High-dose corticosteroids

• Since 1990, there have been many studies

• But, No robust data that steroids provide any additional benefit over conservative management

High-dose corticosteroids

• Corticosteroid Randomization After Significant Head Injury (CRASH) trial –Lancet 2005

• International double-masked randomized placebo-controlled trial

• infusion of a corticosteroid on the risk of death and disability after head injury

• Conclusion: higher risk of mortality in patients with head injury treated with high-dose corticosteroids

Might be harmful in TON patients who have coexisting head injuries!

Surgical decompression of optic canal

• Rationale: Swelling of nerve within optic canal could further compromise blood supply

• Limitations in study

• small retrospective case series

• variety of injury mechanisms

• tendency to operate severe patients

• concomitant steroid treatment

• inherent difficulty defining improvement

• Results

• visual improvement :0 -72% VS 0 - 67% in simple observation

• Can be considered in conscious patients with delayed visual loss or optic nerve sheath hematoma

Conservative management

• No robust data that steroids provide any additional benefit over conservative management

• Spontaneous recovery in 30% of adults, 40% of children

• TON presenting more than 8 h after the initial injury should not be treated with steroids; treatment initiation within the 8 h window remains controversial - Yu and Griffiths Coch Collab 2009

International Optic Nerve Trauma Study(IONTS)-

• 133 patients from 16 countries

• 3 arms : observational, steroid, surgical + steroids,

• Only 7% of the cohort observational arm

• Visual acuity improvement

Surgery: 32% VS corticosteroids: 52% VS untreated :57%

• Conclusion

“Sufficient evidence to conclude that neither corticosteroids nor optic canal

Treatment outline

• Frank discussion of the basis for visual loss & current understanding

• Corticosteroids

• No general consensus

• methyl-PD 250mg intravenously every 6 h for 24–48 h in 8h of injury is a reasonable option

• In the absence of new information, corticosteroids should not be used

• Decompression of optic canal

• Can be considered in conscious patients with delayed visual loss or optic nerve sheath hematoma