Approach to a pale optic disc

A systematic approach with practical tips to diagnose and manage optic disc pallor. Disc pallor is often encountered in the routine clinical practice and remains a diagnostic enigma for most ophthalmologist. I illustrate the relevant practical points to be looked out for to deal with disc pallor.

1. APPROACH TO A PALE OPTIC DISC

2. OVERVIEW INTRODUCTION IMPORTANT POINTS IN HISTORY IMPORTANT POINTS IN EXAMINATION RELEVANT INVESTIGATIONS MANAGEMENT CASE EXAMPLE

3. 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)

4. 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

5. Pale appearance due to Decreased vascularity Capillary dropout Gliosis Increased visibility of scleral laminae

6. AIM OF CLINICAL EVALUATION To determine the possible cause of the disc pallor and whether this is due to A n 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

7. 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

8. Morning glory disc Optic disc drusen Medullated nerve fibres Optic disc pit Optic disc hypoplasia Myopic disc Optic disc coloboma Optic disc pit

9. PATTERNS Ischemic (anterior ischemic optic neuropathy) Inflammatory Toxic/ nutritional Compressive Traumatic Hereditary

10. Main complain is usually a decrease in visual acuity Observant patients will tell about color desaturation and field defects

11. 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

12. 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

13. 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)

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

15. 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

16. 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

17. Margins Neruroretinal rim ( color / thickness) Cupping Lamina cribrosa visibility Nerve fibre layer defects Diffuse Localised Wedge shaped Papillomacular bundle Kestenbaum number

18. 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

19. 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

20. 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

21. 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

22. VISUAL FIELDS Altitudinal field defect Centrocaecal scotoma Bitemporal hemianopia

23. MANAGEMENT Irreversible loss of acuity / field ISCHEMIC : Hypercholesterolemia Low dose aspirin Vascular surgery Pentoxifylline Steroids in acute stage (not recommended)

24. 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

25. 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, 2007 Isabel M. Balderas, MD; Thomas R. Hedges, MD

26. 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

27. MRI BRAIN : normal study NUTRITIONAL INIDCES : normal Suspected LHON 11778 glycine to alanine mutation DISC PALLOR IS NOT TO BE IGNORED

28. THANK YOU