5 - Transient Vision Loss Flashcards

1
Q

Transient Vision Loss

A
  1. Sudden loss of visual function either partial or complete in 1 or both eyes <24 hours
  2. Most common cause monocular TVL — retinal ischemia from temporary occlusion of CRAO or its branches
  3. Most common cause binocular TVL — migraine
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2
Q

TVL Examination/History Key Points

A
  1. Monocular loss implies — prechiasmal vs binocular loss implies — chiasmal or retrochiasmal.
    1. Rarely — binocular TVL = bilateral ocular disorders
  2. Transient homonymous hemianopia — may be perceived as monocular TVL in eye with temporal field deficit
  3. Younger people < 50 = likely migraine causing binocular TVL
  4. Pregnant women with eclampsia — TVL may be harbinger of more serious and permanent vision loss within days of delivery
  5. ONH drusen OR papilledema — transient obscurations of vision lasting seconds and precipitated by posture changes
  6. Sudden TMVL < 15 minutes — suggests retinal ischemia from emboli
  7. Retinal artery spasm — seconds to hours and diagnosis of exclusion
  8. Ocular hypoperfusion — TMVL lasting <30 minutes
  9. Occipital seizures — bilateral visual disturbances lasting a few seconds
  10. Migraine — 20-30 minutes
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3
Q

TVL Examination/History Key Points

A
  1. Retinal emboli — descending curtain, tunnel-like contraction, sudden complete loss of vision, altitudinal aspect visual loss
  2. Visual loss exacerbated by exercise — vasospasm, pigment dispersion syndrome, demyelinating disease, ocular hypoperfusion
  3. Uhthoff phenomenon — transient visual blurring from elevation of body temperature or activity seen in optic neuritis
  4. Occipital lobe ischemia — whiteout vision both eyes, gradual constriction of peripheral vision without positive phenomena
  5. Predisposing conditions — CAD, carotid artery stenosis, PAD, DM, HTN, smoking, HLD, arrhythmia, valvulopathy, IVDA, FHx clotting disorder, systemic cancer, Hx connective tissue disease
  6. Testing — FA to assess for vascular etiology, perimetry to assess for residual visual field deficits
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4
Q

TVL Causes

A
  1. Tear-Film abnormalities
  2. Intermittent angle-closure — transient visual obscurations + halos and pain should prompt gonioscopy for angle assessment. May see glaukomflecken = small anterior subcapsular opacities secondary to lens epithelial necrosis resulting from acute angle closure glaucoma.
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5
Q

TVL Orbital Causes

A
  1. Orbital lesions — direct compression of optic nerve + ischemia from positional vasculature obstruction causing TMVL induced by moving eyes
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6
Q

TMVL Vascular Causes

A
  1. Amaurosis — specifically to retinal transient ischemic attack
  2. Prodromal syndrome of cerebral infarction
  3. Retinal emboli, optic nerve ischemia from GCA, diffuse ocular hypoperfusion from severe carotid artery disease
  4. Retinal emboli — painless, acute, resolves over a few minutes.
  5. Assess for neurological signs
  6. Emboli — cardiac tumor (myxoma), fat from long bone fractures or pancreatitis, sepsis, talc, silicone, air, corticosteroids
  7. Atheroma — occurs at bifurcation of internal and external carotid. Emboli may occur on ulcerated atheromatous plaque with any degree of stenosis
  8. Cardiac emboli — arrhythmia, a-fib, hypokinetic wall segments, endocarditis, valvular heart disease
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7
Q

TMVL Vascular Evaluation

A
  1. Increased risk of stroke, MI, AA
  2. Bruit — may be absent if total occlusion or may be present if turbulent flow within vessel
  3. Carotid Duplex, MRA, CTA — looks at carotid arteries, vertebral arteries, aortic arch. Best = MRA/CTA
  4. Brain imaging to look for associated cerebral ischemia — MRI with DWI
  5. Echo — TEE more sensitive than TTE
  6. If no cardiac or carotid source of embolism — systemic processes that contribute to stroke should be considered including age, HTN, DMT2, ischemic heart disease, HLD, smoking, sleep apnea. If suspicious look for hypercoagulable states + collagen vascular diseases + syphilis depending on presenting signs and symptoms
  7. Medical treatment — amaurosis = antiplatelet
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8
Q

GCA

A
  1. Malaise, scalp tenderness, jaw claudication, weight loss, proximal joint pain, myalgias, headaches
  2. Systemic symptoms negative in 20% patients
  3. ESR, CRP, CBC should be checked in patients >50 with TVL
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9
Q

Ocular Hypoperfusion

A
  1. CRVO — may report TVL for seconds to minutes with full recovery to normal vision afterwards. Symptoms may predate visual loss for a few days or weeks or symptoms may cease when collaterals develop
  2. Postural TVL — severe stenosis of great vessels or GCA
  3. Ocular Ischemic Syndrome — hypotensive, ischemic retinopathy. Low retinal artery pressure, poor perfusion, midperipheral dot-and-blot hemorrhages, dilated veins, MAs, narrowed arteries, macular edema, recurrent orbital pain improving when patient lies down suggestive of carotid occlusive disease.
    1. Light-induced amaurosis — transient blurred vision or TVL on exposure to bright light
    2. Decreased vision, red eye, painful eye, epsicleral vascular injection, aqueous flare (ischemic uveitis), NVI, NVA, low/normal/high IOP, (low IOP choroidal body ischemia)
    3. Ocular perfusion — carotid endarterectomy, IOP lowering drugs, PRP, IVA
      1. Low pre-op IOP may spike after reperfusion
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10
Q

Vasospams TVL

A
  1. Young people
  2. Vision returns to normal between episodes with good prognosis
  3. DFE WNL
  4. Dx of exclusion
  5. Younger patient consider hyperviscosity syndrome and hypercoagulable states (antiphospholipid, thrombocytosis, thrombophilia disorders, polycythemia)
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11
Q

TBVL

A
  1. Migraine
    1. Vision returns in 20-30 minutes. Aura lasts 5 minutes and resolves by 1 hour
  2. Occipital lesions
    1. AVM, tumor if attacks of headaches occur always on same side
  3. Occipital ischemia
    1. Compared to migraines, ischemic hemianopic events sudden in onset and last only a few minutes
  4. Occipital seizures
    1. Unformed positive phenomena — swirling lights, bubbles,
    2. Negative phenomena may occur
    3. Adults — structural lesiom
    4. Children — Benign
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