Central retinal artery occlusion: Difference between revisions
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== | == Differential Diagnosis == | ||
{{Acute vision loss noninflamed DDX}} | {{Acute vision loss noninflamed DDX}} | ||
*Amaurosis fugax | |||
*[[Temporal Arteritis]] | |||
*[[Acute_Angle-Closure_Glaucoma|Acute glaucoma]] | |||
== Treatment == | == Treatment == | ||
Revision as of 13:37, 14 October 2014
Background
The first branch of internal carotid artery is the ophthalmic artery. Visual loss from CRAO is usually painless and is more common in the elderly with carotid artery disease
- Cherry red spot (fundoscopy)
- Macula is thinnest portion of retina
- Intact underlying choroidal circulation remains visible through this section
- Macular area maintains normal color (red) versus surrounding ischemic, pale retina due to differing blood supplies
- Restoration of blood flow within 100min may lead to complete recovery
- Occlusion >240min leads to irreversible damage
Etiology
- Embolism
- Thrombosis
- Temporal Arteritis
- Vasculitis
- Sickle Cell Disease
- Trauma
- Vasospasm (migraine)
- Glaucoma
- Low retinal blood flow (carotid stenosis or hypotension)
Clinical Features
- Sudden, painless, monocular vision loss
- Often preceded by episodes of amaurosis fugax
Diagnosis
- APD
- Fundoscopy
- Pale retina, cherry red macula
- Boxcar segmentation of blood column
Differential Diagnosis
Acute Vision Loss (Noninflamed)
- Painful
- Arteritic anterior ischemic optic neuropathy
- Optic neuritis
- Temporal arteritis†
- Painless
- Amaurosis fugax
- Central retinal artery occlusion (CRAO)†
- Central retinal vein occlusion (CRVO)†
- High altitude retinopathy
- Open-angle glaucoma
- Posterior reversible encephalopathy syndrome (PRES)
- Retinal detachment†
- Stroke†
- Vitreous hemorrhage
- Traumatic optic neuropathy (although may have pain from the trauma)
†Emergent Diagnosis
- Amaurosis fugax
- Temporal Arteritis
- Acute glaucoma
Treatment
- Consult ophtho with goals for reducing itraocular pressure, dislodging the embolus or increasing arterial flow
No evidence supporting or refuting the following treatments: [1]
- Ocular massage
- Intermittent direct digital pressure applied through closed eyelid x 10-15 sec w/ rapid release to create pressure gradient to dislodge embolism
- Timolol ophthalmic 0.5% to decrease IOP
- Increase PCO2 leading to retinal artery vasodilation/increased retinal blood flow
- Rebreathe into paper bag x10 min q hr
- Inhale 95% O2 and 5% CO2 (Carbogen)[2]
- Anterior chamber paracentesis
- Causes acute drop in IOP to dislodge embolism
- Intraarterial fibrinolysis or low dose systemic thrombolytics[3][4]
- Acetazolamide, 500 mg IV or PO
- Mannitol
Disposition
- D/c w/ ophtho f/u in 1-4wk
See Also
Source
- ↑ Rudkin A et al. Clinical characteristics and outcome of current standard management of central retinal artery occlusion. Clin Experiment Ophthalmol 2010; 38:496-501
- ↑ Atebara N. Efficacy of anterior chamber paracentesis and carbogen in treating nonarteritic central retinal artery occlusion. Ophthalmology 1995; 102:2029-2038
- ↑ Schumacher M, et al: Central retinal artery occlusion: Local intraarterial fibrinolysis versus conservative treatment, a multicenter randomized trial. Ophthalmology 2010; 117:1367-1375
- ↑ Chen C et al: Efficacy of intravenous tissue-type plasminogen activator in central retinal artery occlusion: Report from a randomized, controlled trial. Stroke 2011; 42:2229-2234.