DISC EDEMA

1. DISC EDEMA Prof. Vasudev Anand Rao

2. UNILATERAL Papillitis Anterior Ischemic optic neuropathy Neuroretinitis Papillophlebitis Ischemic CRVO Anterior compressive optic neuropathies (orbital tumors) Infiltrative optic neuropathies Ocular hypotony Foster-Kennedy syndrome BILATERAL Papilledema Hypertension Diabetic papillopathy Advanced Graves disease Cavernous sinus thrombosis Carotid cavernous fistula Leber hereditary optic neuropathy CAUSES

3. PAPILLEDEMA: “optic disc swelling” • Conventionally the term refers to hydrostatic non-inflammatory optic disc swelling that results from raised intracranial tension.

4. ETIOLOGY • 1. Intracranial space occupying lesion • neoplasm (location of the tumor is more important than size) • abscess/inflammatory mass • hemorrhage/infarct • A-V malformation • 2. Obstruction of ventricular system • 3. Cerebral edema • 4. Impaired CSF absorption by arachnoid villi: • Meningitis • Raised venous pressure • SAH/trauma • Communicating hydrocephalus • 5. Severe systemic hypertension • 6. Idiopathic (pseudo tumor cerebri): • 7. Decreased size of cranial vault: • Craniosynostosis • Thickening of skull • 8. Hypersecretion of choroids plexus tumor

5. CLINICAL FEATURES • SYMPTOMS • Ocular: • Visual acuity-normal in early ,decreased when established and grossly affected when atrophic • Amaurosis fugax(spasm of arteries) • Central vision affected late(selective loss of peripheral neurons) • Diplopia(assoc. 6th cranial nerve palsy in raised ICT) • General: • Headache (bifrontal/occipital) more in the morning, • aggravated by coughing straining • Projectile vomiting • Loss of consciousness/ focal neurological deficits

6. CLINICAL FEATURES • SIGNS • PUPILLARY REACTION -normal until optic atrophy sets in • 2.FUNDOSCOPY • EARLYPAPILLEDEMA • Hyperemia/elevation of disc • Blurred margins • Loss of SVP • Superficial hemorrhage

7. CLINICAL FEATURES • ESTABLISHED/FULLY DEVELOPED PAPILLEDEMA: • Engorged & tortuous veins • Numerous flame shaped hemorrhages • Cotton wool spots, hard exudates • Peripapillary edema (paton’s lines) • Retinal folds/macular star

8. CLINICAL FEATURES • CHRONIC/VINTAGE PAPILLEDEMA: • Optic disc pale & elevated (champagne cork appearance) • Disc obliterated • Opticociliary shunts

9. CLINICAL FEATURES • ATROPHIC PAPILLEDEMA: • Pale grey disc with reactive gliosis • Narrow and sheathed vessels • Retina shows pigmentary changes and • choroidal folds

10. CLINICAL FEATURES • 3. FIELD CHANGES • Early-normal • Established-enlargement of blind spot • Chronic-peripheral constriction • End stage-total loss • 4. FLUORESCEIN ANGIOGRAPHY • To differentiate true and pseudopapilledema • Dilatation of surface capillaries and leakage of dye • in the late phase • 5. NEUROIMAGING • Features of raised ICT-silver beaten appearance with erosion of posterior clinoid process and dorsum sellae • Cause of raised ICT may be identified.

11. UNILATERAL PAPILLEDEMA • Asymmetric • Foster Kennedy syndrome Seen in patients with frontal lobe/olfactory lobe tumors, meningiomas of olfactory groove/sphenoidal wing, characterized by optic atrophy on the side of the tumor caused by direct pressure on the nerve and papilledema on the opposite side because of raised ICT. • Prior optic atrophy, congenital abnormality in disc, high myopia

12. PSEUDOTUMOR CEREBRI Or Benign Intracranial hypertension Defined by 4 criteria • Increased intracranial pressure • Normal or small ventricles • No evidence of intracranial mass lesion • Normal CSF composition Usually idiopathic seen in young obese women

13. Endocrine causes Addison’s disease Hypoparathyroidism Hyperthyroidism Hypothyroidism Menopause Menarche Pregnancy Drugs Vitamin A Tetracycline Steroids OCP Phenytoin Indomethacin Growth hormone lithium ETIOLOGY

14. TREATMENT • Weight loss • Acetazolamide • Lumbar puncture • Surgical decompression (ventriculo-peritomeal shunt)

15. DIFFERENTIAL DIAGNOSIS - Ocular 1. PAPILLITIS

16. Hypermetropia: Crowded nerve fibers at disc. More in children, no enlargement of blind spot Astigmatism Optic nerve head drusen: Calcium containing refractile bodies within substance of optic nerve head. Seen in USG. Autofluorescence Hazy media DIFFERENTIAL DIAGNOSIS - Ocular 2. PSUEDOPAPILLEDEMA

17. DIFFERENTIAL DIAGNOSIS - Ocular 3.AION/LHON/TOXIC AMBLYOPIAS 4.OCULAR HYPOTONY Effusion from choroidal vessels 5.RAISED INTRAOCULAR PRESSURE: Obliteration of peripapillary vessels by raised IOP 6.CRVO

18. OPTIC NEURITIS : “Inflammation of the optic nerve” ETIOPATHOGENESIS • IDIOPATHIC • DEMYELINATING (Always Retrobulbar) • Isolated • a/w multiple sclerosis • neuromyelitis optica • schilder’s disease

19. ETIOPATHOGENESIS • INFECTIOUS AND PARAINFECTIOUS • LOCAL: • Orbital cellulites • Sinusitis • Teeth, tonsil • Meninges, brain or base of skull. • SYSTEMIC: • VIRAL-measles, mumps, rubella, chickenpox, herpes, CMV and EBV. • BACTERIAL-T.B,syphilis,cat scratch disease,lyme’s • FUNGAL-cryptococcosis,histoplasmosis • PARASITImalaria,pneumocystis,toxoplasma,toxocara,cysticercosis • VACCINES:BCG,DPT,TT,HepB,variola and influenza

20. ETIOPATHOGENESIS • 4.IMMUNE RELATED • LOCAL • Uveitis, sympathetic ophthalmitis. • SYSTEMIC • sarcoidosis, Wegener’s polyarteritis nodosa, SLE etc. • 5.METABOLIC • Anemia • Diabetes • Starvation • 6.DRUGS AND TOXINS • INH, ethambutol, etanercept, INFa, tobacco, alcohol, quinine.

21. CINICAL FEATURES • Commonly unilateral, more in females and mean age is 30-35 yrs. • SYMPTOMS • Triad of • Loss of central vision • Eye pain • Decreased colour vision • Other • Altered perception of moving objects • Worsening of symptoms with elevation of body temperature(uhthoff sign)

22. CINICAL FEATURES • SIGNS • Decreased visual acuity • Tenderness • Marcus gunn pupil (RAPD) • Decreased colour vision and contrast sensitivity • Visual field defects: classically central/centrocaecal scotoma • but other defects can also occur • Fundus changes • 1. Papillitis: edema, hyperemia, blurred margins, dilated • tortuous vs, few exudates and vitreous haze • 2. Retrobulbar neuritis: normal • 3. Neuroretinitis: macular star with exudates • VEP-Delayed latency and decreased amplitude • FAG to differentiate from other causes-dilated and telangiectatic vs with leak from capillaries

23. CINICAL FEATURES Field defects in optic neuritis Papillitis Neuroretinitis

24. INVESTIGATIONS To determine cause for optic neuritis 1.Complete Hemogram 2. CRP, ESR, Mantoux 3. VDRL 4. Serology-ANA, Toxoplasma, Lymes 5. PNS X-ray, chest x ray(sarcoidosis) 6. X ray skull, CT 7. MRI(demyleinating plaques-2 or more predictive of deveplopment of MS) 8. Lumbar puncture-CSF pleocytosis and oligoclonal bands

25. MRI scan showing demyelinating optic neuritis

26. TREATMENT • 1. ONTT Regimen - Intravenous methylprednisolone 250mg q 6 h for 3 days followed by • Oral prednisolone 1 mg/kg/day for 11 days, • tapered with 20mg on 15th day and 10mg on 16th and 18th day • 2. Posterior sub-tenon injection of triamcinolone • 3. Vitamin B12 • 4. Treatment of identifiable cause

27. Ischemic optic neuropathy • Infarction of prelaminar or laminar portions of optic nerve caused by occlusion of posterior ciliary artery. • Seen in >50 yrs. • H/s/o giant cell arteritis or predisposing factors like DM/HT • Pale swollen disc with splinter hemorrhages • Altitudinal scotoma Classified as Arteritic & Non-Arteritic

28. Clinical Features

29. THANK YOU