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Sudden Painless Vision Loss - Coggle Diagram
Sudden Painless Vision Loss
Vitreous Hemorrhage
Characteristics
Clouding of normally transparent eye structures
Common Causes of Vitreous Hemorrhage
Proliferative retinopathy
Retinopathy that may lead to sufficient retinal ischemia to drive upregulation of vascular endothelial growth facotr and subsequent retinal neovascularization (bleed and cause retinal hemorrhage)
Posterior vitreous detachment
Sites of Vitreous Attachment
Vitreous base, Macula, Retinal blood vessels, optic nerve
Pathophysiology
Vitreous hemorrhage may occur if blood vessel is broken as vitreous separates
Symptoms
Sudden onset of new flashes and floaters, normal vision typically, and vitreous hemorrahge can blur vision
Treatment
None, patient should obtain a dilated retinal exam, warn patients of symptoms of retinal detachment
Retinal tear
Full thickness break in retina
Symptoms
Sudden onset flashes and floaters typically more than with PVD
More likely to be associated with vitreous hemorrhage causing moderate to severely blurred vision
Treatment
Laser Retinopexy
Retinal Artery Occlusion
Central
Symptoms
Sudden, severe painless los of vision +/- amarosis fugax
Clinical Exam
Reduced visual acuity, relative afferent pupillary defect, fundus may initially be normal but cherry-red spot may appear, recanilizes over 4-6 weeks and retinal opacification resolves
Etiology
Embolic
Cholesterol from carotid artery atherosclerosis, fibrin platelet from large vessel atherosclerosis, calcium from cardiac valvular disease
Non-Embolic
Vasculitis, Thrombosis, Other rarer causes
Work Up
Vascular risk factors, embolic sources, arteritic investigations, Screen from thrombophillia, and vasculitis
Treatment
Goals
Restore ocular perfusion, prevent ischemic events
Tolerance time
1.5 hrs - No Damage, 4 hrs - Massive irreversible retinal damage
Branch
Symptoms
Sectoral visual field with or without reduced visual acuity
Clinical Exam
Embolus typically visible proximal to localized retinal opacification, resolves leaving atrophic inner retina
Etiology
Simialr to Central
Work Up/Traetment
Same are central
Visual Prognosis
80% improve to >20/40, residual visual field defects common
Retinal Vision Occlusion
Symptoms
Sudden painless loss of vision (metamorphosia)
Clinical Exam
Intraretinal hemorrhages, nerve fiber layer infarcts, retinal edema, dilated and tortuous retinal veins
Pathophysiology
Compression of vein by thickened atherosclerotic artery, turbulent flow -> Thrombus formation
Macular Edema
Treatment
Observation (if no macular edema and visual acuity intact)
Intravitreal injectinos
Standard of Care, ANti VEGF, Steroid
Lase photocoagulation
Sector or pan-retinal photocoagulation
Macular Hemorrhage
Characteristics
Choroidal neovascularization, treated with intravitreal injections of anti-VEGF
Retinal Detachment
Types
Traction
Caused by abnomrla membranes on surface of the retina
Exudative
Caused by exudation of fluid from choroid into subrentinal space
Rhegmatogenous
Caused by 1+ retinal tears
Pathogenesis
Posterior vitreous Detachment -> Retinal Tears + Vitreous traction -> liquified vitreous -> RRD
Symptoms
New onset flashes and floateres followed by loss of portion of visual field
Treatment
In Office: Pneumatic Retinopexy
Intravitreal gas injection + Cryopexy or laser retinopexy
Operating Room
Scleral Buckel
Utilize scleral indentation to externally relieve traction on retinal tears
Vitrectomy
Intraocular surgerry to remove vitreous and internally relieve traction on retinal tears
Combined scleral bucle and vitrectomy
Prognosis
high success rate for re-attachemnt
Macula status is primary pre-op determinant of visual outcome (macula ON - will end up 20/50 or better, macula OFF - 75% better than 20/70 if less than a week, 50% if loonger)
Anterior ishcemic optic neuropathy
Types
Arteritic (giant cell arteririts) - Infalmmatory
Non-arteritic (NAION) - Vascular