DISC EDEMA
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Transcript of DISC EDEMA
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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