1. DISC EDEMA
Prof. Vasudev Anand Rao

2. CAUSES UNILATERAL BILATERAL Papillitis Papilledema
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

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
EARLY PAPILLEDEMA
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 Optic disc pale & elevated (champagne cork
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. ETIOLOGY Endocrine causes Addison’s disease Hypoparathyroidism
Hyperthyroidism
Hypothyroidism
Menopause
Menarche
Pregnancy
Drugs
Vitamin A
Tetracycline
Steroids
OCP
Phenytoin
Indomethacin
Growth hormone
lithium

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

15. DIFFERENTIAL DIAGNOSIS - Ocular
1. PAPILLITIS
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.

16. 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

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 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 Features 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%

29. THANK YOU