Transcript disc odema - M.M.Joshi Eye Institute

DISC EDEMA
Prof. Vasudev Anand Rao
CAUSES
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UNILATERAL
Papillitis
Anterior Ischemic optic
neuropathy
Neuroretinitis
Papillophlebitis
Ischemic CRVO
Anterior compressive optic
neuropathies (orbital
tumors)
Infiltrative optic
neuropathies
Ocular hypotony
Foster-Kennedy syndrome
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BILATERAL
Papilledema
Hypertension
Diabetic papillopathy
Advanced Graves disease
Cavernous sinus
thrombosis
Carotid cavernous fistula
Leber hereditary optic
neuropathy
PAPILLEDEMA: “optic disc swelling”
• Conventionally the term refers to
hydrostatic non-inflammatory optic disc
swelling that results from raised intracranial
tension.
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
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 FEATURES
SIGNS
1. PUPILLARY REACTION -normal until optic atrophy sets in
2. FUNDOSCOPY
EARLY PAPILLEDEMA
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Hyperemia/elevation of disc
Blurred margins
Loss of SVP
Superficial hemorrhage
CLINICAL FEATURES
ESTABLISHED/FULLY DEVELOPED PAPILLEDEMA:
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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:
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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
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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 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
PSEUDOTUMOR CEREBRI
Or Benign Intracranial hypertension
Defined by 4 criteria
1. Increased intracranial pressure
2. Normal or small ventricles
3. No evidence of intracranial mass lesion
4. Normal CSF composition
Usually idiopathic seen in young obese women
ETIOLOGY
Endocrine causes
• Addison’s disease
• Hypoparathyroidism
• Hyperthyroidism
• Hypothyroidism
• Menopause
• Menarche
• Pregnancy
Drugs
• Vitamin A
• Tetracycline
• Steroids
• OCP
• Phenytoin
• Indomethacin
• Growth hormone
• lithium
TREATMENT
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Weight loss
Acetazolamide
Lumbar puncture
Surgical decompression (ventriculo-peritomeal shunt)
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.
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
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”
ETIOPATHOGENESIS
1.
2.
3.
IDIOPATHIC
DEMYELINATING (Always Retrobulbar)
Isolated
– a/w multiple sclerosis
– neuromyelitis optica
– schilder’s disease
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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,cystice
rcosis
– VACCINES:BCG,DPT,TT,HepB,variola and influenza
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.
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)
CINICAL FEATURES
SIGNS
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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
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VEP-Delayed latency and decreased amplitude
FAG to differentiate from other causes-dilated and telangiectatic
vs with leak from capillaries
CINICAL FEATURES
Field defects in optic neuritis
Papillitis
Neuroretinitis
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
MRI scan showing demyelinating
optic neuritis
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
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 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%
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