5 - Transient Vision Loss Flashcards
1
Q
Transient Vision Loss
A
- Sudden loss of visual function either partial or complete in 1 or both eyes <24 hours
- Most common cause monocular TVL — retinal ischemia from temporary occlusion of CRAO or its branches
- Most common cause binocular TVL — migraine
2
Q
TVL Examination/History Key Points
A
- Monocular loss implies — prechiasmal vs binocular loss implies — chiasmal or retrochiasmal.
- Rarely — binocular TVL = bilateral ocular disorders
- Transient homonymous hemianopia — may be perceived as monocular TVL in eye with temporal field deficit
- Younger people < 50 = likely migraine causing binocular TVL
- Pregnant women with eclampsia — TVL may be harbinger of more serious and permanent vision loss within days of delivery
- ONH drusen OR papilledema — transient obscurations of vision lasting seconds and precipitated by posture changes
- Sudden TMVL < 15 minutes — suggests retinal ischemia from emboli
- Retinal artery spasm — seconds to hours and diagnosis of exclusion
- Ocular hypoperfusion — TMVL lasting <30 minutes
- Occipital seizures — bilateral visual disturbances lasting a few seconds
- Migraine — 20-30 minutes
3
Q
TVL Examination/History Key Points
A
- Retinal emboli — descending curtain, tunnel-like contraction, sudden complete loss of vision, altitudinal aspect visual loss
- Visual loss exacerbated by exercise — vasospasm, pigment dispersion syndrome, demyelinating disease, ocular hypoperfusion
- Uhthoff phenomenon — transient visual blurring from elevation of body temperature or activity seen in optic neuritis
- Occipital lobe ischemia — whiteout vision both eyes, gradual constriction of peripheral vision without positive phenomena
- Predisposing conditions — CAD, carotid artery stenosis, PAD, DM, HTN, smoking, HLD, arrhythmia, valvulopathy, IVDA, FHx clotting disorder, systemic cancer, Hx connective tissue disease
- Testing — FA to assess for vascular etiology, perimetry to assess for residual visual field deficits
4
Q
TVL Causes
A
- Tear-Film abnormalities
- 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
- Orbital lesions — direct compression of optic nerve + ischemia from positional vasculature obstruction causing TMVL induced by moving eyes
6
Q
TMVL Vascular Causes
A
- Amaurosis — specifically to retinal transient ischemic attack
- Prodromal syndrome of cerebral infarction
- Retinal emboli, optic nerve ischemia from GCA, diffuse ocular hypoperfusion from severe carotid artery disease
- Retinal emboli — painless, acute, resolves over a few minutes.
- Assess for neurological signs
- Emboli — cardiac tumor (myxoma), fat from long bone fractures or pancreatitis, sepsis, talc, silicone, air, corticosteroids
- Atheroma — occurs at bifurcation of internal and external carotid. Emboli may occur on ulcerated atheromatous plaque with any degree of stenosis
- Cardiac emboli — arrhythmia, a-fib, hypokinetic wall segments, endocarditis, valvular heart disease
7
Q
TMVL Vascular Evaluation
A
- Increased risk of stroke, MI, AA
- Bruit — may be absent if total occlusion or may be present if turbulent flow within vessel
- Carotid Duplex, MRA, CTA — looks at carotid arteries, vertebral arteries, aortic arch. Best = MRA/CTA
- Brain imaging to look for associated cerebral ischemia — MRI with DWI
- Echo — TEE more sensitive than TTE
- 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
- Medical treatment — amaurosis = antiplatelet
8
Q
GCA
A
- Malaise, scalp tenderness, jaw claudication, weight loss, proximal joint pain, myalgias, headaches
- Systemic symptoms negative in 20% patients
- ESR, CRP, CBC should be checked in patients >50 with TVL
9
Q
Ocular Hypoperfusion
A
- 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
- Postural TVL — severe stenosis of great vessels or GCA
- 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.
- Light-induced amaurosis — transient blurred vision or TVL on exposure to bright light
- Decreased vision, red eye, painful eye, epsicleral vascular injection, aqueous flare (ischemic uveitis), NVI, NVA, low/normal/high IOP, (low IOP choroidal body ischemia)
- Ocular perfusion — carotid endarterectomy, IOP lowering drugs, PRP, IVA
- Low pre-op IOP may spike after reperfusion
10
Q
Vasospams TVL
A
- Young people
- Vision returns to normal between episodes with good prognosis
- DFE WNL
- Dx of exclusion
- Younger patient consider hyperviscosity syndrome and hypercoagulable states (antiphospholipid, thrombocytosis, thrombophilia disorders, polycythemia)
11
Q
TBVL
A
- Migraine
- Vision returns in 20-30 minutes. Aura lasts 5 minutes and resolves by 1 hour
- Occipital lesions
- AVM, tumor if attacks of headaches occur always on same side
- Occipital ischemia
- Compared to migraines, ischemic hemianopic events sudden in onset and last only a few minutes
- Occipital seizures
- Unformed positive phenomena — swirling lights, bubbles,
- Negative phenomena may occur
- Adults — structural lesiom
- Children — Benign