traumatic optic neuropathy

Clinical case presentation

Dr. Samten Dorji

Chief complaint

• A 28 year old male who was admitted in emergency ward after motor vehicle accident complained of loss of vision in his right eye.

Personal details• He is from Korphu, Trongsa and currently living in Thimphu working as tourist guide.

History of chief complaint

• On 09/08/2015 around midnight he was involved in a road traffic accident

• After the accident he only remembers waking up in the emergency ward with no vision in the right eye with no associated pain.

• He had alcohol prior to that incident.

History cont.

• Systemic review• Past ocular history/ocular

medications/systemic medications/comorbidities/allergies/family history

Differential diagnosis

Examination Right eye Left eye

Visual acuity NPL 6/6With pinholeColor vision Normal

Extraocular movements Normal Normal Lids and adnexa Severe lid ecchymosis

with oedemaNormal

Conjunctiva and sclera normal normalCornea clear clearAnterior chamber Normal depth and quiet Normal depth and quietIris and lens Normal NormalPupil RAPD +ve Round regular and

reactive

Examination cont.Right eye Left eye

IOP by I care 14 mmhg 13mmhg

Dilated funduscopy

Disc pink, oval and margins clearCDR 0.3: 1Macula normalAV ratio 2:3Periphery NAD

Disc pink oval and margins clearCDR 0.3:1Macula normalAV ratio 2:3Periphery NAD

Systemic examination

• General appearance= conscious and rational

• CVS: PR=86bpm BP=110/70mmhg, heart sounds normal

• RS: 16/min chest clear• Abdomen: unremarkable• Nervous system: no neurological

weakness

Case summary

• A 28 year old male with no previous ocular history complained loss of vision in his right eye after a motor vehicle accident with episode of loss of consciousness.

• On eye examination he had NPL visual acuity in the right eye with positive RAPD. He had severe right eyelid ecchymosis but anterior segment and posterior segment appeared normal.

Differential diagnosis• Eyelid swelling• Corneal injury• Hyphema• Traumatic cataract• Lens dislocation• Commotio retinae• Retinal detachment• Retinal or vitreous haemorrhage• Traumatic optic neuropathy• Cortical blindness

Traumatic optic neuropathySupporting points

• Loss of vision associated with trauma

• Episode of loss of consciousness• Positive RAPD• Normal anterior segment and

posterior segment

Traumatic optic neuropathy(TON)

Optic nerve avulsion

Indirect TON

Direct TON

Cortical blindnessSupporting points

• Loss of vision associated with trauma • Episode of loss of consciousness• Normal anterior segment and posterior

segment

Non supporting points

• Loss of vision in one eye• APD present

Investigation

Problems

• Loss of vision in right eye with NPL visual acuity with positive RAPD

• Acute cerebral haematoma in right temporal lobe and acute sub arachnoid haemorrhage in the right fronto-parieto-temporal region

• Communited fracture seen in right maxilla and bleed in right maxillary sinus

Management

• Conservative managementArtificial tears and chloramphenicol

ointment• Neurosurgical management• ENT management

Subject review

Traumatic optic neuropathy

Outline

• Introduction • Epidemiology • Pathophysiology• Work up• Management• Prognosis

Introduction

• Whenever there is a head trauma the optic nerves are by far the most common site of visual pathway trauma.

Optic nerve avulsion Direct injury TON Indirect injury TON

Epidemiology

• Incidence: TON occurs in approximately 1.6% of cases of head trauma and 2.5% of cases of midface and maxillofacial trauma.

• Age: 1–89 years (mean: 29).• Sex: the male-female ratio is 4:1.

Work/industrial 11%Farm 2%Home 33%School 1%Recreation/sport 12%Street/highway 23%Public building 3%Unknown 12%Other 3%

Place of optic nerve injury

USEIR DATA based on 427 cases

Causes of injuryPublished studies

Number of cases

MVA Bicycle Fall Assault Other

8 164 74(45%) 7(4%) 44(27%) 21(13%) 18(11%)

Pathophysiology Optic nerve avulsion• Rapid increase in intraocular pressure can

disinsert optic nerve.• Sudden rise in the intraorbital pressure

stretches the optic nerve until it is avulsed from its scleral insertion.

• Extreme rotation and displacement of the globe within the orbit disrupt the laminar region of the optic disc.

Direct TONPenetrating impact

displaced fracture or spicule of bone in the region of the optic

canal.

Indirect TON

Anterior indirect TON

• Involvement of the optic disc and the segment of the retrobulbar optic nerve containing the central retinal artery

Posterior indirect TON

Evaluation Optic nerve avulsion

• Reduced vision to NPL• Fundus Immediately after injury disc is

obscured by overlying vitreous haemorrhage

Afterwards the scleral canal is seen devoid of disc

• Ultrasound or CT scanning are useful in confirming the presence of optic nerve avulsion

Indirect TON• Visual loss may range from a

minimal decline to NPL• APD• Impaired color vision• Fundus appear normal in

posterior indirect TON• Visual field defects Central scotomas Nerve fiber bundle defects

• Electrophysiology: The visual evoked potential(VEP) may be used to document conduction delays in comatose patients. Initial VEP may correlate well with the final visual acuity

• High-resolution CT in both the coronal and axial planes should be performed to detect facial and optic canal fractures.

• MRI is occasionally a valuable adjunct to CT in imaging the intracanalicular and intracranial segments of the optic nerve for disruption or hematoma.

• Orbital ultrasonography should be performed in patients with anterior indirect optic neuropathy.

Direct optic nerve injury• External inspection: evaluation of the

depth, direction, and extent of orbital and eyelid wounds from sharp objects is important no matter how minimal the external injury.

• Imaging studies: MRI and CT• Complete neurologic assessment is

required as many of these patients have associated brain injuries

Management Optic nerve avulsion

• The visual prognosis is generally poor• No effective treatment

Indirect TON

Medical treatment: megadose corticosteroids• Methylprednisolone 30 mg/kg is

administered intravenously over 30 minutes, followed by 15 mg/kg 2 hours later. This compensates for the rapid serum half-life of methylprednisolone. Treatment is continued with 15 mg/kg every 6 hours for 24–48 hours.

• Histamine type 2 receptor antagonist

• Surgical management: optic canal decompression

• Extremely limited• Observation • If within 8 hours and with no concomitant traumatic brain injury with no medical

comorbidities megadose steroids can be considered

Direct TON

Same as in indirect TON

Prognosis optic evulsion Indirect TON Direct TONPoor • If complete loss of vision occurs

at the moment of impact, the damage is usually permanent

• Mild to moderate posterior indirect TON may show significant spontaneous improvement over 3-6 months

• If immediate blindness follows a direct injury, it is usually permanent

• The prognosis of direct TON is worse than that of indirect TON

Recap

• Introduction • Epidemiology • Pathphysiology• Work up• Management• Prognosis

Thank you

References • Kuhn, Ference and Pieramici, Dante J. OCULAR

TRAUMA principles and practice. First edition. New York: Thieme, 2002

• Gerstenblith Adam T. and Rabinowitz Michael P. (eds.). The WILLS EYE MANUAL. Sixth edition. Philadelphia: LIPPINCOTT WILLIAMS AND WILKINS, 2012

• Kanski Jack J. and Bowling Brad. Clinical Ophthalmology A SYSTEMATIC APPROACH. Seventh edition. Elsevier limited, 2011

• Yanoff Myron and Duker Jays. OPHTHALMOLOGY. Third edition. Elsevier Inc. , 2009