BASICS

DESCRIPTION

• Transient loss of vision in 1 or both eyes

– Transient monocular visual loss (TMVL)

– Transient binocular visual loss (TBVL)

– System(s) affected: Central nervous system, ocular

RISK FACTORS

• Atherosclerosis

• Hypertension

• Diabetes mellitus

• Dyslipidemia

• Cardiac disease

• Obesity

• Hypercoagulable states

• Polymyalgia rheumatica

• Pregnancy

• Medications and drugs

Genetics

Hypercoagulability—Factor V Leiden (AD), antithrombin III deficiency (AD), protein S and C deficiency (AD), dysfibrogenemia (AD), hyperhomocystinemia (AD), and hemoglobin S (AR)

GENERAL PREVENTION

• Smoking cessation

• Control of hypertension

• Achieve and maintain glycemic control

• Treatment of dyslipidemia

• Anticoagulation of atrial fibrillation, high-risk cardioembolic disorders

• Exercise

PATHOPHYSIOLOGY

• TMVL

– Ischemia of retina, optic nerve, choroid

– Ocular—surface disease, angle-closure glaucoma, and hyphema

• TBVL

– Transient ischemic attack–ischemia of occipital cortex

– Migraine–cortical spreading depression

– Seizure–neuronal hyperexcitability and hypersynchrony

ETIOLOGY

• TMVL

– Ischemia

– Atherosclerotic large-vessel disease–carotid or ophthalmic artery, aortic arch stenosis with decreased ocular perfusion or thromboembolism. Coincident hypotension may elicit symptoms

– Cardioembolic–arrhythmia, valvular disease, thrombus, tumor with embolization to eye, etc.

– Vasculitis–giant cell arteritis causing retinal artery occlusion or arteritic anterior ischemic optic neuropathy

– Hypercoagulable states– retinal arteriolar or venous thrombosis. Cardiac thrombi

– Carotid artery dissection–traumatic or spontaneous with occlusion or thromboembolism

– Retinal artery vasospasm– retinal migraine. Especially in young adults. Associated headache or periorbital pain

– Papilledema and optic disc drusen–edema causes decreased retinal perfusion

– Central retinal vein occlusion–decreased venous outflow

– Ocular disease

Angle-closure glaucoma, hyphema, surface disease

• TBVL

– Ischemia: Vertebrobasilar insufficiency (VBI) secondary to atherosclerotic disease, cardioembolic source, or vertebrobasilar dissection. Hypotension often elicits symptoms.

– Migraine

– Seizure

COMMONLY ASSOCIATED CONDITIONS

• Atrial fibrillation

• Trauma–head and neck. Carotid and vertebrobasilar dissection

• Polymyalgia rheumatica–giant cell arteritis

• Hypotension

DIAGNOSIS

HISTORY

• TMVL versus TBVL- monocular or binocular visual loss. Patients with binocular hemianopic visual field loss will often incorrectly assign it to the eye with the temporal field loss and report monocular visual loss.

• Duration and frequency of visual loss–sudden or abrupt onset. Much overlap of duration

– Seconds: Transient visual obscurations of papilledema or optic disc drusen. Ocular surface disease which improves with blinking or eye rubbing

– Seconds to minutes: (30 sec to 30 min) Ischemic

– Minutes: (10–60 min) migraine

– Minutes–days: Seizures

– Frequency of events–isolated or recurrent

• Description of visual loss

– Positive visual phenomena

– Photopsias (e.g., flashes, sparkles)–ischemia more likely to have negative visual phenomena

– Scintillating fortification scotoma (migratory, bright, zigzag light)–migraine

– Flickering, bright-colored shapes, geometric forms—seizures

– Negative visual phenomena

Curtain, shade, altitudinal, or complete loss–ischemic TMVL

Blurry, foggy, hazy, patchy, dim–nonspecific, often ischemic TMVL

Dim, blurred, and complete–ischemic TBVL

• Precipitating factors

– Orthostasis–-hypotension produces symptoms in critical arterial stenosis.

– Light-induced–severe carotid stenosis or giant cell arteritis

– Head or neck trauma, chiropractic manipulation–carotid or vertebral dissection

• Associated symptoms

– TMVL

– Contralateral hemisensory or motor symptoms, lightheadedness, aphasia–carotid stenosis

– Neck pain, headache, ipsilateral Horner’s syndrome, contralateral sensory or motor symptoms–carotid dissection

– Headache, scalp tenderness, jaw claudication, myalgias, diplopia–giant cell arteritis

– Eye pain–retinal vasospasm in young adults with a prior history of migraine, angle-closure glaucoma

– TBVL

Vertigo, diplopia, dysarthria, facial numbness–VBI

Severe headache or posterior neck pain with VBI symptoms–vertebrobasilar dissection

Headache following visual loss, nausea, vomiting, photophobia–migraine

Headache, altered consciousness, nausea, vomiting, blinking, nystagmus—seizure

• Drugs and medications

– Prescription, over the counter, illicit, oral contraceptives, cocaine

• Family history

– Cerebrovascular and cardiac disease

– Migraine

– Clotting disorders

PHYSICAL EXAM

• Vital signs

• Carotid auscultation–bruit in carotid stenosis

• Palpate superficial temporal artery–decreased pulse, cords, and tenderness in giant cell arteritis

• Visual acuity–may be reduced if permanent retinal or optic nerve ischemia

• Pupils—may have afferent papillary defect with permanent retinal or optic nerve ischemia

• Extraocular motility—may have cranial nerve palsy in giant cell arteritis

• Slit-lamp examination

– Corneal dryness, keratitis

– Narrow angles—angle-closure glaucoma

– Hyphema

– Neovascularization of iris or angle, flare in anterior chamber–ocular ischemic syndrome

• Tonometry–low intraocular pressure: ocular ischemic syndrome or high intraocular pressure: Angle-closure glaucoma

• Funduscopic exam

– Optic nerve-disc edema, drusen

– Retina

Cotton wool spots, retinal edema or hemorrhage, arteriolar narrowing, boxcarring or sheathing, venous dilation

Cholesterol emboli–yellowish orange, refractile, rectangular, often at vessel bifurcation. Source: Carotid or great vessels

Platelet—fibrin emboli–dull, grayish white, long. Source: Carotid, heart valves, coagulopathy

Calcific-chalk white, large, and round. Source: Heart valves, great vessels

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Automated visual field defect present if permanent retinal or optic nerve ischemia

• Elevated erythrocyte sedimentation rate and C-reactive protein. CBC: thrombocytosis in giant cell arteritis

• EKG–atrial fibrillation or sick sinus syndrome

• CBC, SPEP, PT, PTT, factor V Leiden, protein S and C, antithrombin III, homocystine, fibrinogen, antiphospholipid antibodies may identify hypercoagulable state, especially in young patients without risk factors for vascular disease.

• Lipid profile–elevated in atherosclerotic disease

Imaging

Initial approach

• TMVL

– Carotid duplex ultrasonography–identifies degree of carotid stenosis and plaque morphology. May identify carotid dissection

– Transthoracic echocardiography—detects mural thrombi, valvular and wall motion pathology, and tumors.

– MRI brain–identifies parenchymal ischemic disease. May identify carotid dissection

– CTA or MRA of brain and neck–mural thickening and luminal narrowing of carotid dissection. Can demonstrate carotid stenosis and plaque.

• TBVL

– MRI brain–may demonstrate ischemic areas in posterior circulation distribution. Reserve for atypical presentation of migraine. See Migraine chapter.

– CTA or MRA brain and neck: Stenosis or occlusion of vertebrobasilar system in patients with dissection

– Transthoracic echocardiography–See TMVL above.

Follow-up & special considerations

• Transesophageal echocardiography–reserve for patients with high degree of suspicion of valvular disease, septal defects, and aortic arch disease

• Carotid angiography—differentiates 99% stenosis from complete occlusion

• Holter monitor–may identify intermittent arrhythmia

Diagnostic Procedures/Other

• Intravenous fluorescein angiogram–retinal, optic nerve, or choroidal ischemia

• Temporal artery biopsy—giant cell arteritis

• EEG–epileptiform activity in seizures

Pathological Findings

Temporal artery biopsy: inflammatory mononuclear cell infiltrate with destruction of internal elastic lamina; giant cells may be present

DIFFERENTIAL DIAGNOSIS

See Etiology

TREATMENT

MEDICATION

First Line

• Giant cell arteritis–See Giant cell arteritis chapter.

• Carotid stenosis >70%—ASA 325 mg/day, clopidogrel 75 mg/day, or ASA 25 mg plus dipyridamole 200 mg b.i.d.

• Carotid or vertebral dissection—anticoagulation with i.v. heparin followed by warfarin

• Cardiac disease—treatment of arrhythmia, valvular disease, CHF. Anticoagulation (target INR 2.5)

• Seizures–anticonvulsant therapy

• Vasospasm in young patients–calcium channel blockers

Second Line

Carotid or vertebral dissection–anti-platelet therapy if anticoagulation is contraindicated

SURGERY/OTHER PROCEDURES

Carotid stenosis 70–99% and good surgical candidate–carotid endarterectomy

IN-PATIENT CONSIDERATIONS

Admission Criteria

• Giant cell arteritis with visual loss

• Carotid or vertebral dissection

• Unstable cardiac arrhythmia

Nursing

Instruct patient to report any change in vision or neurologic status

Discharge Criteria

• TMVL (non-cardioembolic): Long-term antiplatelet therapy (1)

• Atrial fibrillation, cardioembolic source, some hypercoagulable states: Long-term anticoagulation

• Giant cell arteritis: Oral prednisone taper over 1–2 years dictated by symptoms, sedimentation rate, and C-reactive protein.

• Discontinue cigarette smoking

• Blood pressure reduction

• Fasting blood glucose <126 mg/dL

• Treatment of hyperlipidemia

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• Follow-up with neuro-ophthalmology in 1 week

• Follow-up with neurology and/or cardiology as dictated by underlying disease

DIET

Avoid excessive alcohol use.

PROGNOSIS

• In most young patients (<45 years of age) with TMVL, no etiology will be found. Their risk of stroke is low (2)[C].

• In TMVL with 50–99% carotid stenosis who were treated medically the 3-year risk of ipsilateral stroke is 10% (3)[A].

COMPLICATIONS

• Cerebrovascular accident

• Myocardial infarction

• Death

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