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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