DISC EDEMADISC EDEMA

Prof. Vasudev Anand Rao Prof. Vasudev Anand Rao

CAUSESCAUSESUNILATERAL

• Papillitis• Anterior Ischemic optic

neuropathy • Neuroretinitis • Papillophlebitis• Ischemic CRVO• Anterior compressive optic

neuropathies (orbital tumors)• Infiltrative optic neuropathies• Ocular hypotony• Foster-Kennedy syndrome

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

BILATERAL• Papilledema• Hypertension• Diabetic papillopathy• Advanced Graves disease• Cavernous sinus

thrombosis• Carotid cavernous fistula• Leber hereditary optic

neuropathy

PAPILLEDEMA: “optic disc swelling”PAPILLEDEMA: “optic disc swelling”

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

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

ETIOLOGY1. 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 system3. Cerebral edema4. Impaired CSF absorption by arachnoid villi:

Meningitis Raised venous pressure SAH/trauma Communicating hydrocephalus

5. Severe systemic hypertension6. Idiopathic (pseudo tumor cerebri):7. Decreased size of cranial vault:

Craniosynostosis Thickening of skull

8. Hypersecretion of choroids plexus tumor

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

CLINICAL FEATURESSIGNS

1.PUPILLARY REACTION -normal until optic atrophy sets in

2. FUNDOSCOPY

EARLY PAPILLEDEMA

Hyperemia/elevation of disc Blurred margins Loss of SVP Superficial hemorrhage

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

CLINICAL FEATURES

CHRONIC/VINTAGE PAPILLEDEMA:

Optic disc pale & elevated (champagne cork appearance) Disc obliterated Opticociliary shunts

CLINICAL FEATURES

ATROPHIC PAPILLEDEMA:

Pale grey disc with reactive gliosis Narrow and sheathed vessels Retina shows pigmentary changes and choroidal folds

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.

UNILATERAL PAPILLEDEMAUNILATERAL 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

– 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

PSEUDOTUMOR CEREBRIPSEUDOTUMOR CEREBRI

Or Benign Intracranial hypertension

Defined by 4 criteria1. Increased intracranial pressure2. Normal or small ventricles3. No evidence of intracranial mass lesion4. Normal CSF compositionUsually idiopathic seen in young obese women

Or Benign Intracranial hypertension

Defined by 4 criteria1. Increased intracranial pressure2. Normal or small ventricles3. No evidence of intracranial mass lesion4. Normal CSF compositionUsually idiopathic seen in young obese women

ETIOLOGYETIOLOGY

Endocrine causes• Addison’s disease• Hypoparathyroidism• Hyperthyroidism• Hypothyroidism• Menopause • Menarche• Pregnancy

Endocrine causes• Addison’s disease• Hypoparathyroidism• Hyperthyroidism• Hypothyroidism• Menopause • Menarche• Pregnancy

Drugs• Vitamin A• Tetracycline• Steroids• OCP• Phenytoin• Indomethacin• Growth hormone• lithium

Drugs• Vitamin A• Tetracycline• Steroids• OCP• Phenytoin• Indomethacin• Growth hormone• lithium

TREATMENTTREATMENT

• Weight loss• Acetazolamide• Lumbar puncture• Surgical decompression (ventriculo-peritomeal

shunt)

• Weight loss• Acetazolamide• Lumbar puncture• Surgical decompression (ventriculo-peritomeal

shunt)

DIFFERENTIAL DIAGNOSIS - Ocular

Papillitis Papilledema

1.Presentation U/L B/L

2.Vision Sudden loss Unimpaired initially

3.Pupil RAPD present RAPD absent

4.Media Hazy near posterior vitreous Media clear

5.Pain/tendeness of eyeball Present Absent

6.Hemorrhages/exudates Less More(in established)

7.Disc swelling +2 to +3D >+3D

8.Field defects central/centrocaecal scotoma Enlargement of blind spot, later peripheral constriction.

9.X-ray skull Normal Silver beaten appearance, erosion of dorsum sellae,post clinoid

10.CT/MRI Demyleinating ICSOL etc.

1. PAPILLITIS

DIFFERENTIAL DIAGNOSIS - Ocular 2. PSUEDOPAPILLEDEMA

• 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

• 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

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

OPTIC NEURITIS : “Inflammation of the optic nerve”

OPTIC NEURITIS : “Inflammation of the optic nerve”

1. IDIOPATHIC

2. DEMYELINATING (Always Retrobulbar)

3. Isolated

– a/w multiple sclerosis

– neuromyelitis optica

– schilder’s disease

1. IDIOPATHIC

2. DEMYELINATING (Always Retrobulbar)

3. Isolated

– a/w multiple sclerosis

– neuromyelitis optica

– schilder’s disease

ETIOPATHOGENESISETIOPATHOGENESIS

ETIOPATHOGENESISETIOPATHOGENESIS• 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

• 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

ETIOPATHOGENESISETIOPATHOGENESIS

4.IMMUNE RELATED LOCAL

Uveitis, sympathetic ophthalmitis. SYSTEMIC

sarcoidosis, Wegener’s polyarteritis nodosa, SLE etc.

5.METABOLIC AnemiaDiabetesStarvation

6.DRUGS AND TOXINS INH, ethambutol, etanercept, INFa, tobacco, alcohol,

quinine.

CINICAL FEATURESCINICAL FEATURES

Commonly unilateral, more in females and mean age is 30-35 yrs.

SYMPTOMS

Triad of

Loss of central visionEye painDecreased colour vision

Other

Altered perception of moving objectsWorsening of symptoms with elevation of body

temperature(uhthoff sign)

CINICAL FEATURESCINICAL FEATURESSIGNS

• 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 haze2. Retrobulbar neuritis: normal3. 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

CINICAL FEATURESCINICAL FEATURES

Field defects in optic neuritis

Papillitis

Neuroretinitis

INVESTIGATIONSINVESTIGATIONSTo determine cause for optic neuritis

1.Complete Hemogram2. CRP, ESR, Mantoux3. VDRL4. Serology-ANA, Toxoplasma, Lymes5. PNS X-ray, chest x ray(sarcoidosis)6. X ray skull, CT7. MRI(demyleinating plaques-2 or more

predictive of deveplopment of MS)8. Lumbar puncture-CSF pleocytosis and

oligoclonal bands

MRI scan showing demyelinating optic neuritis

MRI scan showing demyelinating optic neuritis

TREATMENTTREATMENT

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

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

Clinical FeaturesClinical FeaturesFeatures Arteritic AION Non Arteritic AION

Age >60yrs 40-60yrs

Sex Ratio F>M F=M

Vision loss Severe Moderate (>6/60)

Laterality Fellow eye affected in 95% within days to wks

Fellow eye affected in <30% in months or yrs

Optic disc Pale edema, may be sectoral

Hyperemic or pale edema

Assoc. Signs Scalp tenderness, palpable tender, non-pulsatile temporal artery

Assoc. HT – 40%, DM – 24%

Shock, nocturnal hypotension

ESR >40 mm in 1st hr 20-40mm in 1st hr

FAG Disc and choroidal filling delay

Disc filling delay

Treatment IV methylprednisolone ? Levadopa-carbidopa

Prognosis Poor Improvement in upto 43%

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