Course # 132 Flashes and Floaters and Curtains, Oh My!
FLASHES and FLOATERS and CURTAINS, OH MY!!! FLASHES OF LIGHT Vitreous is the villain Retinal traction Retinal hole Retinal tear Migraine Classic migraine Acephalgic migraine Other less common causes Jill Autry, OD, RPh Eye Center of Texas Houston VITREOUS IS THE VILLAIN ACUTE PVD Who is at risk? Older patients Myopic patients earlier than hyperopes Older patients with acute or impending PVD Pseudophakic earlier than phakic Myopic patients Especially first month post-op Patients with lattice degeneration Quick succession of flashes for one to two hours Patients with history of holes/tears in either eye Decreasing to single flashes Patients with history of RD in either eye Especially in a particular gaze Noticed more in the dark Increased floaters often with one central floater Happens in the other eye within 1-2 years WHAT TO DO? Dilate patient OU, this is not a case for OPTOS!!! Look for pigment in vitreous Careful exam of the retina If no holes/tears/pigment/blood but having flashes See in one week If no holes/tears/pigment/blood and flashes have stopped See in three-four weeks Discuss signs/symptoms of RD, document, give patient after hours contact info WHEN TO REFER? Unsure of your ability to carefully examine retina Pigment in the vitreous found Patients reporting small black floaters as well as larger floaters Patient reports curtain of vision Retinal hole, tear, retinal bleeding, or RD found Vitreous hemorrhage 75% of patients with a PVD vitreous hemorrhage have a tear
MIGRAINE CLASSIC MIGRAINE Women>Men; 3:1 ratio More common in teens, twenties, thirties Headache is often preceded by an aura Generally starts before 20 years of age Flashing lights in rapid succession for 15-20 minutes; max of 30 Often with a family history of migraine minutes then stop Classic migraine when younger Scintillating scotoma Often move across the field of vision Often turns acephalgic with age (>40) Heat waves, jagged lines, tunnel vision, colored spots, positive and negative scotomata, etc. have been reported Onset of headache Headache is often debilitating with nausea, vomiting, photophobia, etc. LESS COMMON CAUSES ACEPHALGIC MIGRAINE FLASHES OF LIGHT Visual symptoms only without onset of HA More typical as patient ages Common in patient with history of classic migraines when younger Flashes of light, scotoma, etc. still last 10-15 minutes with abrupt cessation No headache Retinal inflammation Retinal vascular occlusion Choroidal tumor Optic neuropathy Compressive or ischemic Occipital lobe cerebral vascular accident (CVA) VITREOUS FLOATERS Vitreous syneresis Pigment in the vitreous Red blood cells in the vitreous White blood cells in the vitreous Asteroid hyalosis Post-operative Post-op phacoemulsification Post-op yag capsulotomy VITREOUS SYNERESIS Clear, jelly-like, branching strands suspended in the vitreous humor Described as floaters as they cast an image on the retina More frequent following rapid movements of the eye More noticeable when looking at a blank surface or monochromatic background
VITREOUS SYNERESIS PIGMENT IN THE VITREOUS Increased syneresis in myopic patients vs. hyperopic Shafer s sign or Tobacco dust patients Patient sees as small, black floaters Increased syneresis with advancing age Brown pigment viewed in the anterior vitreous at the slit lamp Increased syneresis leading up to PVD High predictive value with regards to retinal break Immediate cause for dilated fundus exam (DFE) More sensitive and specific than symptoms alone Sudden increase in floater size, quantity, fluidity Less commonly seen with retinal holes, especially atrophic Small, black floaters appear holes Flashes of light Can also be seen after some types of ocular surgery Curtain of vision Remains with previous breaks VITREOUS HEMORRHAGE SECONDARY TO ACUTE PVD More common in Sudden increase in small, black floaters and/or large older patients red/black floaters myopic patients Can result in substantial vision loss if blood fills the following trauma vitreous cavity Patient may report flashes before having increased Causes floaters and decreased vision Acute PVD See red blood cells in anterior vitreal exam and vitreal Neovascularization blood on BIO Macroaneurysm 70% of vitreous hemorrhages due to acute PVD will be associated with a retinal break Trauma Refer immediately to vitreoretinal specialist Less common causes B scan will be performed to rule out tear/detachment if no view of retina possible SECONDARY TO NEOVASCULARIZATION OTHER CAUSES OF VITREOUS HEMORRHAGE PDR-Proliferative diabetic retinopathy Severe retinopathy OU, possible hx of laser Macroaneurysm PSR-Proliferative Sickle retinopathy Unilateral Sea-fan neovascularization OU, Black pt, may be unaware of diagnosis Associated with hypertension Ischemic CRVO or BRVO Hypertensive, CRVO hx of vision loss in last 6 months, BRVO may be unaware May see AV nicking, cotton wool spots, NFL hemorrhages of previous insult, unilateral neovascularization OIS-Ocular ischemic syndrome Terson s syndrome Unilateral, elderly, hyperlipidemia, other ocular signs of neo Following subarachnoid hemorrhage Chronic retinal vasculitis Breakthrough subretinal hemorrhage Sarcoidosis Eales disease AMD Pars planitis Bilateral
VITRITIS ASTEROID HYALOSIS White blood cells in the vitreous Large, yellow refractile deposits in the vitreous Patient complains of new onset, small floaters Calcium laden lipids Common in posterior uveitis Usually unilateral Toxoplasmosis If bilateral, usually asymmetric Pars planitis More common in older patients VKH Twice as common in men than women APMPPE, MEWDS, other white dot syndromes Controversial association with increased risk of diabetes Sarcodosis Patients rarely report asteroid hyalosis as floaters, even Lupus with dense amounts Syphilis If new onset symptoms of floaters, look for other cause Others POST-OPERATIVE FLOATERS CURTAIN OF FIELD LOSS Post phacoemulsification Retinal detachment Best case Branch retinal artery occlusion Patient had floaters pre-op but can now see them more clearly with cataract removed Branch retinal vein occlusion Next best case Ischemic optic neuropathy Could be a vitreous shift induced PVD More commonly NAION Worst case Optic neuritis Could be a vitreous shift induced retinal tear Other visual field defects Post yag capsulotomy Stroke, tumor Very common post-yag as fragments of posterior capsule is blown into vitreous Generally subsides by one week post-op RETINAL DETACHMENT BRVO Accompanying flashes/floaters Sudden sectoral vision loss Myopic patient Usually superior temporal arcade affected Lattice degeneration/holes/tears Inferior nasal field loss Pigment in the vitreous Hemorrhages and CWS along affected arcade Area of detachment is opposite area of visual field defect 50%-75% associated with HTN Inferior RD produces a superior curtain Can cause macular edema and neovascularization Superior RD produces an inferior curtain Will often result in expressed collateral circulation Neovascularization can lead to pre-retinal and/or vitreous hemorrhage
BRAO NON-ARTERITIC ISCHEMIC OPTIC NEUROPATHY Sudden sectoral vision loss Sudden, painless loss of vision with APD Whitening of retina, possible emboli at Visual field defect bifurcation Often altitudinal Associated with certain systemic conditions Unilateral ONH swelling Often segmental Hyperlipidemia Patients at risk Atherosclerosis Disk at risk Carotid artery disease Small, crowded optic nerve head at highest risk Patients often have vasculopathic conditions Diabetes, hypertension, hyperlipidemia Amiodarone-induced optic neuropathy can mimic NAION OPTIC NEURITIS Decreased vision over days Unilateral Pain on eye movements Decreased color vision (red cap test) + RAPD Visual field defects vary Swollen disc or retrobulbar MRI of Brain and Orbits with Flair sequencing VISUAL FIELD DEFECTS Bilateral Homonymous hemianopsia Stroke and trauma Superior quadranopsia Temporal lobe- Pie in the sky Tumor more common; also stroke Inferior quadranopsia Parietal lobe- Pie on the floor Stroke more common; tumor less likely Macular sparing Occipital lobe