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 Who is at risk? Older patients with acute or impending PVD Myopic patients Patients with lattice degeneration Patients with history of holes/tears in either eye Patients with history of RD in either eye ACUTE PVD Older patients Myopic patients earlier than hyperopes Pseudophakic earlier than phakic Especially first month post-op Quick succession of flashes for one to two hours Decreasing to single flashes 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 Women>Men; 3:1 ratio Generally starts before 20 years of age Often with a family history of migraine Classic migraine when younger Often turns acephalgic with age (>40) CLASSIC MIGRAINE More common in teens, twenties, thirties Headache is often preceded by an aura Flashing lights in rapid succession for 15-20 minutes; max of 30 minutes then stop Scintillating scotoma Often move across the field of vision 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. ACEPHALGIC MIGRAINE 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 LESS COMMON CAUSES FLASHES OF LIGHT 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 Increased syneresis in myopic patients vs. hyperopic patients Increased syneresis with advancing age Increased syneresis leading up to PVD Immediate cause for dilated fundus exam (DFE) Sudden increase in floater size, quantity, fluidity Small, black floaters appear Flashes of light Curtain of vision PIGMENT IN THE VITREOUS Shafer s sign or Tobacco dust Patient sees as small, black floaters Brown pigment viewed in the anterior vitreous at the slit lamp High predictive value with regards to retinal break More sensitive and specific than symptoms alone Less commonly seen with retinal holes, especially atrophic holes Can also be seen after some types of ocular surgery Remains with previous breaks VITREOUS HEMORRHAGE Sudden increase in small, black floaters and/or large red/black floaters Can result in substantial vision loss if blood fills the vitreous cavity Causes Acute PVD Neovascularization Macroaneurysm Trauma Less common causes SECONDARY TO ACUTE PVD More common in older patients myopic patients following trauma Patient may report flashes before having increased floaters and decreased vision See red blood cells in anterior vitreal exam and vitreal blood on BIO 70% of vitreous hemorrhages due to acute PVD will be associated with a retinal break Refer immediately to vitreoretinal specialist B scan will be performed to rule out tear/detachment if no view of retina possible SECONDARY TO NEOVASCULARIZATION PDR-Proliferative diabetic retinopathy Severe retinopathy OU, possible hx of laser PSR-Proliferative Sickle retinopathy Sea-fan neovascularization OU, Black pt, may be unaware of diagnosis Ischemic CRVO or BRVO Hypertensive, CRVO hx of vision loss in last 6 months, BRVO may be unaware of previous insult, unilateral neovascularization OIS-Ocular ischemic syndrome Unilateral, elderly, hyperlipidemia, other ocular signs of neo Chronic retinal vasculitis Sarcoidosis Eales disease Pars planitis Bilateral OTHER CAUSES OF VITREOUS HEMORRHAGE Macroaneurysm Unilateral Associated with hypertension May see AV nicking, cotton wool spots, NFL hemorrhages Terson s syndrome Following subarachnoid hemorrhage Breakthrough subretinal hemorrhage AMD
VITRITIS White blood cells in the vitreous Patient complains of new onset, small floaters Common in posterior uveitis Toxoplasmosis Pars planitis VKH APMPPE, MEWDS, other white dot syndromes Sarcodosis Lupus Syphilis Others ASTEROID HYALOSIS Large, yellow refractile deposits in the vitreous Calcium laden lipids Usually unilateral If bilateral, usually asymmetric More common in older patients Twice as common in men than women Controversial association with increased risk of diabetes Patients rarely report asteroid hyalosis as floaters, even with dense amounts If new onset symptoms of floaters, look for other cause POST-OPERATIVE FLOATERS Post phacoemulsification Best case Patient had floaters pre-op but can now see them more clearly with cataract removed Next best case Could be a vitreous shift induced PVD Worst case Could be a vitreous shift induced retinal tear Post yag capsulotomy Very common post-yag as fragments of posterior capsule is blown into vitreous Generally subsides by one week post-op CURTAIN OF FIELD LOSS Retinal detachment Branch retinal artery occlusion Branch retinal vein occlusion Ischemic optic neuropathy More commonly NAION Optic neuritis Other visual field defects Stroke, tumor RETINAL DETACHMENT Accompanying flashes/floaters Myopic patient Lattice degeneration/holes/tears Pigment in the vitreous Area of detachment is opposite area of visual field defect Inferior RD produces a superior curtain Superior RD produces an inferior curtain BRVO Sudden sectoral vision loss Usually superior temporal arcade affected Inferior nasal field loss Hemorrhages and CWS along affected arcade 50%-75% associated with HTN Can cause macular edema and neovascularization Will often result in expressed collateral circulation Neovascularization can lead to pre-retinal and/or vitreous hemorrhage
BRAO Sudden sectoral vision loss Whitening of retina, possible emboli at bifurcation Associated with certain systemic conditions Hyperlipidemia Atherosclerosis Carotid artery disease NON-ARTERITIC ISCHEMIC OPTIC NEUROPATHY Sudden, painless loss of vision with APD Visual field defect Often altitudinal Unilateral ONH swelling Often segmental Patients at risk Disk at risk 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