APPROACH TO A PALE OPTIC DISC

OVERVIEW

• INTRODUCTION• IMPORTANT POINTS IN HISTORY• IMPORTANT POINTS IN EXAMINATION• RELEVANT INVESTIGATIONS• MANAGEMENT• CASE EXAMPLE

• Rule out the mimics• Clinical diagnosis • Classify– Pattern of optic disc appearance– Etiology

• Investigations to confirm diagnosis• Assess visual prognosis (progressive / static)• Management (if needed)

INTRODUCTION

• End result of a number of pathologic processes leading to loss of axonal fibres and their replacement by glial tissue

• Normal color is salmon pink– Vascularity– Proportional glial and axonal elements

• Pale appearance due to– Decreased vascularity– Capillary dropout– Gliosis– Increased visibility of scleral laminae

AIM OF CLINICAL EVALUATION

• To determine the possible cause of the disc pallor and whether this is due to – An ongoing process which is likely to progress

• Ischemic / compressive

– Result of a previous one time insult• Inflammatory / toxic / traumatic

• Visual prognosis

• Any intervention needed at present

DIFFERENTIAL DIAGNOSIS

•Optic atrophy• Disc coloboma• Optic pit• Morning glory syndrome• Medullated nerve fibres• Myopic disc• Optic disc drusen• Optic disc hypoplasia

Should be kept in mind while looking

at a pale disc

Morning glory disc

Optic disc drusen Medullated nerve fibres

Optic disc pit

Optic disc hypoplasia

Myopic disc

Optic disc coloboma

Optic disc pit

PATTERNS

• Ischemic (anterior ischemic optic neuropathy)• Inflammatory• Toxic/ nutritional• Compressive• Traumatic• Hereditary

• Main complain is usually a decrease in visual acuity

• Observant patients will tell about color desaturation and field defects

IMPORTANT POINTS TO ELICIT IN THE HISTORY

• Unilateral or bilateral

• Children / young adults / elderly population

• Acute sudden loss / gradual diminution

• Precipitating factors (fever / trauma / neurologic symptoms)

• Associated symptoms – Jaw claudication / scalp tenderness / headache– Proptosis – Diplopia

• Exposure to – Drugs (ethambutol / isoniazid / chloroquine / amiodarone) – Toxins (alcohol / methanol /tobacco)– Radiation

• Possibility of malnourishment

• Systemic illness– Atherosclerosis– Hypertension– Diabetes mellitus– Sleep apnea– Thyroid disorder

• Symptoms of B12 deficiency

• Family history

IMPORTANT EXAMINATION POINTS

• GENERAL PHYSICAL– Pallor – Pulse• Rate / rhythm / volume / symmetrical

– Blood pressure (both arms)– Bruit at common carotid (upper border of thyroid

cartilage)– Signs of nutritional deficiency / chronic alcohol

use / chronic smoking– Gait (tunnel vision / ataxia)

• Best corrected visual acuity• Color vision / saturation • Pupillary reaction / RAPD• Squint / ocular movements / nystagmus • Proptosis • Confrontation fields

• Anterior segment– Neovascularisation of iris / angle

• Ocular ischemic syndrome

• IOP• Optic disc appearance– Pallor :

• Diffuse • Sectoral (wedge shaped / temporal / altitudinal/ bow tie)

– Patterns • Primary• Secondary• Consecutive • Glaucomatous

TEMPORAL PALLOR

• Carries papillomacular bundle• Most active fibres with high metabolic activity

• Travel through the centre of the optic nerve– Others report them being scattered throughout

the nerve• Vulnerable to ischemic insult

• Margins

• Neruroretinal rim (color / thickness)• Cupping• Lamina cribrosa visibility• Nerve fibre layer defects – Diffuse– Localised • Wedge shaped • Papillomacular bundle

• Kestenbaum number

• Surrounding retina– Retinitis pigmentosa– DR / hypertensive changes / hemorrhages – Vascular sheathing / attenuation / dilatation– Vascular occlusion– Venous pulsations– Opticociliary shunt vessels– Signs of trauma• Choroidal rupture• Berlin’s edema

Development of Opticociliary shunt vessel

FEATURE PRIMARY SECONDARY CONSECUTIVE

APPEARANCE Chalky white Dirty grey white Waxy pallor

MARGINS Well defined Ill defined Well defined

LAMINA CRIBROSA Well seen Obscured Well seen

VESSELS Normal Peripapillary sheathing

Attenuation

SURROUNDING RETINA

Healthy Hyaline bodies / drusen

Pathology seen

INVESTIGATIONS

• Blood investigations– Hemogram– ESR / CRP– Liver and kidney function– Lipid profile– Blood sugar– Thyroid profile– Nutritional indicators– Hypercoagulale states

• Other investigations– Carotid Doppler– Postural hypotension– Temporal artery biopsy

• SARCOID• COLLAGEN VASCULAR DISEASE• HEAVY METAL screen• LHON mutation screen

• VISUAL FIELD

• IMAGING– MRI BRAIN plus ORBIT

• Suspected chiasmal compression• Suspected compressive neuropathy

– CECT ORBIT• Suspected traumatic neuropathy

– USG ORBIT• Suspected compressive neuropathy

VISUAL FIELDSAltitudinal field defect

Centrocaecal scotoma

Bitemporal hemianopia

MANAGEMENT

• Irreversible loss of acuity / field

• ISCHEMIC :– Hypercholesterolemia– Low dose aspirin– Vascular surgery– Pentoxifylline – Steroids in acute stage (not recommended)

• INFLAMMATORY– Immunosuppressants – Prognosticate for MS

• COMPRESSIVE– According to the lesion– Thyroid

• TRAUMATIC– Pale disc is indicator of irreversible damage

• TOXIC / NUTRITIONAL – Avoid exposure– Vitamin supplementation

CASE• 35-year-old man with diabetes (5 yrs ; on

insulin)• 2 months of blurred vision in his left eye with

near work• No ocular history and never used spectacles• No family history• No history of trauma• Non smoker / alcohol user

Ocular Surgery News U.S. Edition, September 15, 2007Isabel M. Balderas, MD; Thomas R. Hedges, MD

• Vision (best corrected)– Right 6/6 left 6/60– No anisometropia

• Impaired color vision left eye

• Anterior segment normal• Circumpapillary

telangiectatic vessels• No evidence of DR

• MRI BRAIN : normal study• NUTRITIONAL INIDCES : normal

• Suspected LHON

• 11778 glycine to alanine mutation

DISC PALLOR IS NOT TO BE IGNORED

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