Fugax

Lov Sarin


BASICS


DESCRIPTION


Amaurosis fugax is defined as transient monocular visual loss secondary to ischemia or vascular insufficiency.


EPIDEMIOLOGY


Incidence


50,000 new cases a year in the United States (2)[C]


RISK FACTORS


• Hypertension


• Hypercholesterolemia


• Smoking


• Diabetes


GENERAL PREVENTION


Lifestyle choices such as diet, exercise, and smoking cessation can help mitigate risk factors.


PATHOPHYSIOLOGY


• Transient ischemia to the retina or optic nerve results in visual field loss for seconds to minutes.


– Field loss generally begins in upper field and sometimes in the lower field and periphery.


– Patchy or sectorial field loss may occur.


– Recurrent events tend to follow the same pattern.


– Full visual recovery often occurs.


ETIOLOGY


• Thromboembolic:


– Transient disruption in the ophthalmic circulation due to atherosclerotic emboli from ipsilateral common carotid artery and its branches.


– Cardiac embolism may result from valvular disease secondary to rheumatic heart disease, mitral valve prolapse, marantic or infectious endocarditis, and calcific valve disease.


• Hemodynamic:


– Change in posture, exercise, exposure to bright light in the setting of extensive atherosclerotic arterial occlusive disease especially involving aortic arch branches


– Hypoperfusion secondary to low cardiac output or acute hypovolemia


– Alteration of blood flow from systemic disturbance of blood viscosity, cellularity, or coagulability


– Vasospasm or retinal arterial system leading to retinal migraine


• Ocular vascular disease:


– Anterior ischemic optic neuropathy due to giant cell arteritis, atherosclerosis, or thrombosis secondary to acute occlusion or severe narrowing of the posterior ciliary arteries leading to acute optic nerve head ischemia


– Central retinal vein occlusion can begin with amaurotic episodes due to slowing of retinal arterial circulation as the central retinal vein is occluded.


– Malignant arterial hypertension can cause optic nerve head ischemia.


COMMONLY ASSOCIATED CONDITIONS


• Carotid occlusive disease


• Valvular heart disease


DIAGNOSIS


HISTORY


• Determine if the visual symptoms are consistent with amaurosis.


• Patients describe decreased vision progressing over seconds and lasting for seconds to minutes.


– Monocular vision loss generally occurs for seconds to minutes and recovers completely.


– Visual loss may occur like a “curtain.”


– Upper field affected>lower field>periphery.


• Ask for symptoms concerning giant cell arteritis (in patients over 55).


– Scalp tenderness


– Fever


– Weight loss


– Jaw claudication


– Proximal muscle weakness


PHYSICAL EXAM


• Measure blood pressure, heart rate, and rhythm


• Auscultation of heart and carotid arteries


• Palpation of temporal arteries


• Complete ophthalmic exam with dilated fundus exam by an ophthalmologist or neuro-ophthalmologist


– Assess pupillary reactions, and look for afferent pupillary defect


– Ocular signs of ischemia:


Retinal pallor


Hemorrhages


Distended veins


Microaneurysms


Cotton wool spots


Hollenhorst plaques


DIAGNOSTIC TESTS & INTERPRETATION


Lab


Initial lab tests

• Workup for amaurosis should commence without delay and rule out giant cell arteritis and to evaluate for occult cardiac disease


– Complete blood count


– Erythrocyte sedimentation rate


– C-reactive protein


– Lipid panel


– Diabetes workup


– Consider workup for hypercoagulable state: Factor V Leiden, lupus anticoagulant, deficiency of protein C/protein S/antithrombin III.


Imaging


Initial approach

• Duplex ultrasound of carotid arteries:


– Identify occlusion, stenosis, and ulceration at carotid bifurcation.


– Consider cerebral CT or MR angiography to evaluate for embolic disease.


– Fluorescein angiography can document retinal ischemia if results of initial imaging are negative.


– Carotid angiography is indicated when duplex reveals stenosis but not when the study is normal (4)[A].


– Echocardiogram is indicated to identify cardiac embolic sources.


Follow-up & special considerations

Patient should follow up with their primary care physician for a thorough systemic evaluation.


Diagnostic Procedures/Other


Further cardiac workup should include EKG and possible Holter monitor.


Pathological Findings


Atheromatous carotid plaques are generally composed of platelet-fibrin thrombi, cholesterol crystals, calcification, and lipid deposition.


DIFFERENTIAL DIAGNOSIS


• Embolic:


– Carotid bifurcation thromboembolism


– Great vessel or distal internal carotid artery atheroembolism


– Cardiac emboli (valve, mural thrombi, intracardiac tumor)


– Drug abuse-related intravascular emboli


• Hemodynamic:


– Extensive atheromatous occlusive disease


– Inflammatory arteritis (Takayasu’s disease)


– Hypoperfusion (cardiac failure, acute hypovolemia, disturbance of blood viscosity, coagulability, or content)


• Ocular:


– Anterior ischemic optic neuropathy


– Central or branch retinal artery occlusion


– Central retinal vein occlusion


– Nonvascular (vitreous floaters, hemorrhage, angle closure glaucoma, tumor, congenital anomalies of optic disc such as drusen and staphyloma)


• Neurologic:


– Brainstem, vestibular, oculomotor lesions


– Optic neuritis, optic nerve, or chiasm compression


– Papilledema


– Multiple sclerosis


– Migraine


– Psychogenic


• Idiopathic


TREATMENT


MEDICATION


• Aspirin 300–325 mg/day reduces stroke prevalence and further transient ischemic attack (TIA) in patients with TIA (4)[A].


– Address modifiable risk factors such as hypertension, hypercholesterolemia, and smoking


– Carotid stenosis <50%


– Aspirin and risk factor treatment (4)[A]


– Cardio embolism requires appropriate management such as anticoagulation for mural thrombus, aspirin for mitral valve prolapse, etc.


– Patients with clinical and laboratory evidence of giant cell arteritis (elevated ESR/CRP/platelets) should be placed on high-dose corticosteroids and referred to vascular surgery or oculoplastics for temporal artery biopsy.


ADDITIONAL TREATMENT


General Measures


• It is of upmost importance to recognize ocular vascular diseases that can present with amaurosis.


– Arteritic anterior ischemic optic neuropathy (giant cell arteritis)


– Glaucoma (especially angle closure)


SURGERY/OTHER PROCEDURES


• Carotid stenosis 50–70%:


– Treatment is controversial. Aspirin and risk factor treatment. Carotid endarterectomy is indicated in patients with associated TIA or minor stroke, cerebral infarction on MR or CT, retinal emboli, carotid bulb ulceration, and failure of aspirin therapy (4)[A].


• Carotid stenosis >70%:


– Carotid endarterectomy is indicated (3)[A].


ONGOING CARE


PROGNOSIS


• Annual incidence of stroke in patients with amaurosis is 2% (3).


• 95% of endarterectomy patients are free of ipsilateral stroke for 8 years (1).


COMPLICATIONS


The rate of stroke and death associated with carotid endarterectomy is 6.5% (4).



REFERENCES


1. Berstein EF, Dilley RB. Late results following carotid endarterectomy for amaurosis fugax. J Vasc Surg 1987;6:333–340.


2. Brown RD, Petty GW, O’Fallon WM, et al. Incidence of transient ischemic attack in Rochester, Minnesota, 1985–1989. Stroke 1998;29:2109–2113.


3. Ferguson GG. The North American Symptomatic Carotid Endarterectomy Trial: Surgical results in 1415 patients. Stroke 1999;30:1751–1758.


4. Poole CJM, Ross Russell RW. Mortality and stoke after amaurosis fugax. J Neurol Neurosurg Psychiatry 1985;48:902–905.

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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Fugax
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