Visual Loss

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



REFERENCES


1. Albers GW, Hart RG, Lutsep HL, et al. AHA Scientific statement: Supplement to the guidelines for the management of transient ischemic attacks: A statement from the Ad Hoc Committee On Guidelines for the Management of Transient Ischemic Attacks, Stroke Council, American Heart Association. Stroke 1999;30:2502–2511.


2. Tippin J, Corbett JJ, Kerber RE, et al. Amaurosis fugax and ocular infarction in adolescents and young adults. Ann Neurol 1989;26:69–77.


3. Benavente O, Eliasziw M, Streifler JY, et al., for the North American Symptomatic Carotid Endarterectomy Trial Collaborators. Prognosis after transient monocular blindness associated with carotid artery stenosis. N Engl J Med 2001;345:1084–1090.

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