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ocular disease 3 > optic neuropathy 2 > Flashcards

optic neuropathy 2 Flashcards

1
Q

 Ischemic, non-inflammatory condition
 Vascular insult to pre-laminar and retro-laminar optic
nerve
 Clinical presentation
 Acute painless vision loss: mild to severe
 Typically older patient with cardiovascular risk
factors
 Disc at risk

A

optic neuropathy (naion)

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2
Q

Opticnerveappearance
 Hyperemicedema
 Flamehemorrhages
 +/-macularstar

A

NAOIN CHARACTERISTICS

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3
Q

naion vf defects

A

Altitudinal:62%
 Inferior:47%
 Centralscotoma:21%


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4
Q 
 HTN
 DM
 Age>55years
 Atheroscleroticdisease
 Glaucoma
 Smallopticnerves:mechanical 
 Viagra?
 M>F
 Bilateral (sequential)
A

risk factors for naion

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5
Q

 Some visual recovery possible

 May have mild improvement/deterioration

A

naion prognosis

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6
Q

va outcomes of naion

A

 50%: VA > 20/60

 40%: VA

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7
Q

 Chronic HTN causes alteration in autoregulatory response
 Vasodilation fails to occur in decreased BP
 Nocturnal hypotension occurs in morning hours
 Ischemia to PCA results decreased optic nerve perfusion

A

naion pathogenesis

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8
Q

 Age:40+
 1+vasculopathicriskfactors:HTN,DM,elevated
cholesterol, smoking
 Oneeyeinvolved
 VerysuddenVA/VFloss,typicallyuponwaking
 Noeyepain,diplopia,orneurologicsymptoms
 NormalEOMs
 +RAPD
 Mild-severehyperemicONHswelling
 FellowONH:“discatrisk”

A

naion clinical diagonistic criteria

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9
Q 
 Monitor in 2-4 weeks
 If VA or VF still worsening, diagnosis is suspect and
patient needs workup
 If stable, re-examine in 3-4 months
 Prognosis
 Sameeyerecurrence:3-5%
 Felloweyeinvolvement:25%
 40%recoversomeVA,butVFremainspoor
A

naion follow up

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10
Q

pathogenesis of AION

A

inflammationofelastictissueinarterial walls results in vessel occlusion

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11
Q

epidemiology of aion

A

 Age: 65+
 F>M
 75% bilateral: fellow eye involved in 1-2 days
 Decreased likelihood of fellow eye involvement after 6-8 weeks of initial insult
 50% have polymyalgia rheumatica: pain and stiffness of shoulders, pelvic girdle, and torso

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12
Q 
 Severe VA loss preceded by episodes of transient vision loss
 Scalp tenderness
 Jaw claudication
 Mild fever
 Weight loss
 Arthralgias/myalgias
A

symptoms of aion

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13
Q

opthalmic emergency pathy

A

aion

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14
Q

 Pallid optic nerve swelling
 No hemorrhages
 Extensive cotton wool spots
 Preceded by episodes of TIA

A

signs of aion

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15
Q

 Management
 STAT hospital admission and IV steroids for 3-5 days, then
oral taper (on final day of IV treatment) x 1+ year
 Temporal artery biopsy
 Laboratory: ESR, CRP
 GCA: systemic vasculitis of medium and large arteries
 Self limiting, but may persist for years
 Oral steroids protect surviving ON as disease burns itself out
 Steroids may be discontinued after 12-18 months unless symptoms or blood inflammatory markers persist
 Use ESR and CRP levels to guide steroid taper

A

management of aion

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16
Q

 Rule out early onset DM, HTN, and hyperlipidemia
 r/o elevated homocysteine
 r/o vasculitides: SLE, Wegener’s
 r/o coagulopathy
 Bloodwork: ESC, CRP, ACE, ANA, RPR-VDRL, RBC Folate, B12, Bartonella, Lyme

A

naion in pts

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17
Q

 Cardiac
 Spinal
 Thoracic
 Abdominal

A

POSTSURGICAL pion

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18
Q

 Vasculitis(GCA)

 Atherosclerosis  Radiation

A

spontaneous pion

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19
Q

PatientrecoversconsciousnesstodiscoverpoorVA

in one/both eyes

A

symptom of pion

20
Q

 Initiallyopticdiscisnormal
 Pallordevelopsin4-6weeks  RAPD
 IfRAPDabsentandbothpupilsbrisklyreactive
 Suspectbilateralposteriorcerebralarteryinfarction  Akacorticalblindness

A

signs of pion

21
Q 
 Diagnosis of exclusion
 Unilateral or bilateral
 Vision typically unaffected
 May be a mild form of NAION
 Diabetic retinopathy usually present
 Hyperemic disc swelling with dilated pre-laminar vessels
 VF: enlarged blind spot
 Disc swelling resolves within
2-10 months
 May have mild residual pallor
A

diabetic papillopathy

22
Q

papillopathy vs. papilitis

A

papilitis: swelling of nerve
papillopathy: disease of optic nerve

23
Q

Optic nerve edema caused by raised intracranial pressure

A

PAPILLEDEMA

24
Q

 Clear fluid that surrounds the CNS
 Gives support, protection, and nourishment
 Present in ventricles, central canal of spinal cord, and subarachnoid space
 Produced in choroid plexus of third, fourth, and lateral ventricles
 Enters into dural venous sinuses via arachnoid granulations
 Drains via internal jugular veins

A

CSF

25
Q

HOW DO WE GRADE PAPILLEDMA

A 
FRISEN SCALE
 Stage 0: normal optic nerve 
 Stage 1: very early
 Blurring of superior, inferior, and nasal aspects
 No elevation
 Normal temporal disc
 Incomplete peripapillary halo
 Stage 2: early
 Blurring of all borders
 Elevation of nasal border
 Complete peripapillary halo
 Stage 3: moderate
 Increased diameter of ONH
 Partial obscuration of vessel at disc margin
 Peripapillary halo with finger-like extensions

 Stage 4: marked
 Elevation of entire nerve head
 Near total obscuration of major blood vessels on the disc
 Stage 5: severe
 Dome-shaped protrusion of disc
 Obliteration of cup
 Total obscuration of blood vessels on the disc

26
Q

stage 1 frisen scale

A 
very early
 Blurring of superior, inferior, and nasal aspects
 No elevation
 Normal temporal disc
 Incomplete peripapillary halo
27
Q

stage 2 frisen scale

A

early
 Blurring of all borders
 Elevation of nasal border
 Complete peripapillary halo

28
Q

stage 3 frisen scale

A

moderate
 Increased diameter of ONH
 Partial obscuration of vessel at disc margin
 Peripapillary halo with finger-like extensions

29
Q

stage 4 frisen scale

A

marked
 Elevation of entire nerve head
 Near total obscuration of major blood vessels on the disc

30
Q

stage 5 frisen scale

A

severe􏰁
Dome-shaped protrusion of disc
􏰁 Obliteration of cup
􏰁 Total obscuration of blood vessels on the disc

31
Q

Medical emergency

 Immediate neuro-imaging to r/o intracranial mass

A

papilledema

32
Q

 Bilateral
 Optic nerve function preserved early in its course
 VA can be compromised from macular edema
 Visual fields: typically enlarged blind spots
 Absent spontaneous venous pulsation
 20%ofnormalsdonothaveSVP

A

clinical features of papillee

33
Q 
 Headache
 Nonspecific characteristics
 Worsens with valsalva manouver
 Transient visual obscurations
 Mild blurring to complete blindness
 Lasts for few seconds
 Precipitated by postural changes
 Pulsatile tinnitus: whooshing sound in ear(s) in time with pulse
 Diplopia
 Abducens palsy
A

symptoms of papilledema

34
Q

 MRI to r/o structural lesion
 Lumbar puncture to confirm increased ICP and
analyze CSF constituents
 MRV to r/o venous sinus thrombosis
 Laboratory: r/o inflammatory/infectious etiology

A

diagnostic workup for papilledema

35
Q

4 mechanisms of increased icp

A

 Increased brain volume: common
 Space-occupying lesion: tumor, hemorrhage, abscess
 Cerebral edema: trauma, metabolic disease
 Decreased CSF drainage: common
 Hydrocephalus
 Meningitis
 Subarachnoid hemorrhage
 Venous sinus thrombosis
 Extracranial venous outflow obstruction
 Increased CSF production: rare
 Decreased skull volume: rare

36
Q

 COPD
 Malignant HTN
 Sleep apnea
 Renal failure

A

medical disorders causing pseudotumor cerebri

37
Q

medications causing pseudotumor cerebri

A

 Tetracycline antibiotics
 Excessive vitamin A
 Steroids
 Birth control pills

38
Q

venous obstruction causing pseudotumor cerebri

A

 Cerebral venous sinus thrombosis

 Jugular venous thrombosis

39
Q

 Aka idiopathic intracranial hypertension
 Modified Dandy Criteria
 Signs and symptoms of increased ICP
 No localizing neurological signs (except VI palsy)
 Patient is awake and alert
 No evidence of intracranial mass on MRI/CT
 Normal MRV
 LP opening pressure of >25 cmH2O with normal CSF composition

A

pseudotumor cerebri: unknown causes

40
Q

 MRI of brain and orbits with contrast
 MRV: r/o venous sinus thrombosis
 CSF microbiology, biochemistry, and cytology
 Blood pressure, temperature, chest x-ray
 CBC, electrolytes, glucose, liver function, ESR, CRP, ACE, ANA, RPR-VDRL

A

 All of the following must be performed and found to be negative: IIH investigations

41
Q 
 Weight loss: 6% reduction results in papilledema resolution
 Acetazolamide (Diamox)
 Oral diuretics
 Steroids
 Surgical intervention
 Lumbo-peritoneal shunt
 Optic nerve sheath fenestration
 Repeated LP
A

IIH treatment

42
Q 
 Papillophlebitis
 Diabetic papillopathy  CRVO
 NAION
 AION
 Infiltrative
 Infectious
A

unilateral optic nerve edema aka papillitis

43
Q

 Leukemia
 Lymphoma
 Breast, lung, bowel metastases
 Sarcoid granuloma

A

infiltration of one or both optic nerves

44
Q

symptoms of infiltrative optic neuropathy

A

 Patients usually have known malignancy

 Acute, subacute, or slowly progressive VA and VF loss

45
Q

 Normal, swollen, or pale ONH
 MRI: enlargement of optic nerve
 LP: increased protein, malignant cells

A

signs of infiltrative optic neuropathy

46
Q

treatment for infiltrative optic neuropathy

A

urgent referral to oncology

ocular disease 3 (10 decks)

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