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Approach to Acute Vision Loss Approach to Acute Vision Loss Acute vision loss is defined by deficit lasting < 24 hours; persistent visual loss is when symptoms persisted > 24 hours. Acute onset vision loss can be generally caused by opacities in cornea or vitreous, retinal abnormalities, optic nerve abnormalities or visual pathway abnormalities or visual cortex defects. The most common causes of acute onset visual loss is due to vascular occlusion of the retina, or cerebrovascular disease, acute angle closure glaucoma. Causes - Vascular cause - Retinal artery occlusion - Retinal vein occlusion - TIA / Stroke - Amaurosis fugax (Giant cell arthritis, GCA) - Ocular cause - Retinal detachment - Vitreous haemorrhage - Optic neuritis / optic neuropathy History - Determine onset of symptoms - Determine monocular or binocular, which area of visual field is involved - Assoc. symptoms - New focal neurology in stroke/TIA Visual pathway lesion. - Floaters, flashing lights, distorted vision more indicative of vitreous or retinal detachment - Eye pain and conjunctival injection should be considered in corneal ulcer, acute angle closure glaucoma, endophthalmitis. Optic neuritis is associated with pain on eye movement. - If < 50 years old, Hx of jaw claudication, headache, polymyalgia rheumatica; you need to rule out GCA. - Hx of trauma - Assess PMHx Examination - Neurological exam if suspect TIA or stroke - Slit lamp - Fundoscopy - Visual acuity + colour vision - Assess pupils for – symmetry, reactivity to light, pupillary reflex - Look for RAPD - indicates a lesion of the eye, or optic nerve anterior to optic chiasm - Eye movement for ophthalmoplegia or pain - Visual fields Management - If you suspect GCA – patient will need high dose steroids to avoid permanent vision loss - Urgent referral to ophthalmology if suspected retinal artery/vein occlusion, acute glaucoma, giant cell arteritis, vitreous haemorrhage, retinal detachment - Consider imaging such as CT, MRI or ultrasound if diagnosis uncertain Approach to the patient with acute monocular visual loss Retinal artery occlusion Central retinal artery occlusion (CRAO) is the blockage of the main blood supply to the retina causing hypoperfusion and ischaemia of the retina and optic nerve. Patients with a history of hypertension, diabetes, atherosclerotic disease or carotid disease are at higher risk of developing CRAO. Causes - Embolus - Cholesterol emboli – seen as Hollenhorsts plaques - Platelet emboli - Calcium emboli – normally from heart valves - Thrombosis - Atherosclerotic disease - Hypercoagulable state such as SLE, antiphospholipid syndrome - Vasculitis CRAO with cherry red spot. Presentation - Painless - Acute monocular vision loss - RAPD present - Fundoscopy - Retinal whitening with macular cherry-red spot Immediate actions - Immediate ophthalmology input - Workup for stroke / TIA - Bloods / ECG - Carotid USS - CT head - Consider Fluorescein angiography Definitive Tx - No optimal treatment - High dose steroid if suspected giant cell arteritis - Ocular massage - Consider anterior chamber paracentesis to reduce IOP Retinal vein occlusion Central retinal vein occlusion (CRVO) is due to compression of atherosclerotic artery on the central retinal vein at the lamina cribrosa causing thrombosis. Tortuous, dilated veins are signs on an impending CRVO. Patients with a history of atherosclerotic disease, hypertension, glaucoma are at a higher risk of developing CRVO. Presentation - Painless monocular vision loss - Presence of RAPD - Fundoscopy - Wide-spread retinal haemorrhage “blood Widespread intra-retinal haemorrhage with cotton wool spots and tortuous veins. and thunder” appearance - Cotton wool spot (ischaemia of retina) - Optic disc oedema Definitive Tx - Treat underlying cause (diabetes, hypertension) - Consider intravitreal injection of anti-VEGT to reduce neovascularisation - Pan-retinal photocoagulation (PRP) if neovascularisation of iris/angle as high risk of developing neovascular glaucoma Retinal Vein Occlusion (RVO) Guidelines Retinal detachment Retinal detachment causes the separation of the inner neurosensory retina from the retinal pigmented epithelium (RPE). The separation leads to progressive loss of vision, and if treated can cause permanent vision loss. Retinal tears or breaks predisposed to retinal detachment. Patients often complain of a curtain moving over visual field. There are 3 main types of retinal detachment: rhegmatogenous, exudative, tractional. Causes Retinal detachment. - Rhegmatogenous (commonest) Accumulation of fluid in subretinal space secondary to retinal tear/breaks - Exudative Inflammatory condition (uveitis) or malignancy ® breakdown of blood-retina-barrier - Tractional Abnormal fibrovascular structure causes contraction of vitreous More common in proliferative diabetic retinopathy Presentation - Floaters, photopsia (flashes of light) – suggest posterior vitreous detachment - Curtain over visual field - Visual loss - Fundoscopy - Vitreous opacity - Detached retinal folds Immediate actions - Immediate referral to ophthalmology if visual field loss, or fundoscopic sign of detachment/haemorrhage Definitive Tx - Laser therapy / Cryotherapy For retinal tears or breaks Creates scar tissue between retina and RPE preventing accumulation of fluid in subretinal - Vitrectomy - Scleral buckling - Pneumatic retinopexy Inject small gas bubble into vitreous cavity CKS - Retinal detachment Diplopia Diplopia (double vision) can generally be classified into monocular vs. binocular. First concern must be possibility of stroke. In monocular diplopia, diplopia persists after covering up one eye, more commonly indicating a refractive problem. In binocular diplopia, diplopia disappears after covering up one eye, indicating ocular misalignment. This can be due to problems in the muscles, nerve or brain. Extensive investigations are needed to establish the cause of misalignment of the visual axes. Causes - Monocular diplopia - Refractive error See Also: - Dry eye Approach to Double Vision in the ED - Corneal opacity Management of diplopia - Cataracts - Macular oedema - Binocular diplopia - Muscle - Nerve – Extraocular nerve palsy - CNS – intracranial haemorrhage, CVA - Neuromuscular junction disorder – Myasthenia gravis - Internuclear ophthalmoplegia Younger patients – suspect MS Older patients, you will need to rule out CVA Assessment - Monocular vs binocular Cover up one eye, assess if diplopia persist - Assess for associated neurological symptoms - Worst headache - Other cranial nerve involvement E.g. cavernous sinus thrombosis – CN V involvement - Hemiparesis or hemiplegia - Cerebellar signs E.g. CN IV palsy with cerebellar sign may indicate compression by posterior fossa tumour - Assess for isolated CN palsy - Examine extraocular movement Which direction makes diplopia worse? Worst in field of action of paralyzed muscle. - Horizontal diplopia – medial/lateral rectus affected by problems with innervation or muscle function. CNVI palsy = most common cause. Assess for internuclear ophthalmoplegia (INO) - impaired horizontal movement due to weak adduction of affected eye and abduction nystagmus of normal eye. - Vertical diplopia – inferior rectus muscle most commonly affected - Orbital floor fracture - Thyroid eye disease - CN IV palsy - Oblique / torsional diplopia – involves superior oblique / inferior oblique muscles - Any pain with eye movement? Immediate actions - If suspect stroke – for immediate CT Brain as potential for thrombolysis Definitive Tx - Consider imaging with CT/ MRI to determine underlying aetiology - Will need ophthalmology/optometrist input for monocular diplopia if suspect refractive error - Will need neurology input especially in binocular diplopia with associated neurology .
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