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Ocular Emergencies for the Primary Care Optometrist

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Ocular Emergencies for the Primary Care Optometrist Ocular Emergencies Ocular Emergencies for the Disclosure Statement Primary Care Optometrist . Honorarium, Speaker, Consultant, Research Grant: Aerie, Alcon, Allergan, B+L, Carl Zeiss, Glaukos, Heidelberg, Novartis, Topcon, Michael Chaglasian, OD, FAAO Associate Professor Illinois Eye Institute Illinois College of Optometry [email protected] What is a “True” Emergency? “True” Emergency . Pain (vs. discomfort) . History is key to differentiating emergency versus urgency . Current or potential for: Phone or in person Vision loss Proper triage is essential Structural damage After hours protocol Needs immediate (same day) attention Your office and your specialists Medico-legal implications History Emergency Exam Vision Recent ocular disease or One or both eyes? surgery . Acuity . External examination Visual field Other diseases . Visual fields . SLE Sudden or gradual cardiac, vascular, or . Pupils Blurred or lost? autoimmune . IOP Diplopia? viruses . Ocular Motility . Fundus exam Mono or Bino Medications or recent Pain changes to medications Redness Nausea/vomiting Onset Trauma Contact lenses M. Chaglasian, OD 1 Ocular Emergencies Emergency Kit “True” Emergency . Chemical Burns . Eye shield . pH paper Alkaline . Pressure patch . Bandage CL’s . Sterile eye wash . Diamox . Central Retinal Artery Occlusion . Alger brush . Topical drops . Forceps Antibiotics NSAID’s . Golf spud . Both have extremely high risk of severe and permanent Steroids vision loss which can be prevented via immediate Cycloplegics intervention and treatment Chemical Trauma Chemical Burns . Copious irrigation anesthetic . Acid exposure speculum Only penetrate through epithelium sterile saline v tap water car battery, vinegar, and some refrigerants . Contacts can be removed after irrigation . Sweep fornices – repeatedly . Alkaline exposure Penetrates tissues more easily and . Examination after irrigation and neutralization of pH have a prolonged effect . Debride necrotic tissue lime, (plaster, cement) lye, ammonia found in household . Want neutral pH of 7.0 – cleaners, fertilizers, and pesticides check q15min with pH paper . Have patient bring agent if possible Chemical Burns Roper Hall Classification of Ocular Burns . Determine area of involvement Assessed by extent of FL staining Grade Prognosis Limbal Ischemia Corneal Damage Assess depth of conjunctival penetration 1 Good None Epithelial Damage Vascular ischemia, necrosis of limbal and bulbar conjunctiva 2 Good Less than 1/3 Haze but iris detail Loss of limbal vascular plexus is key indicator to severity of visible permanent vision loss 3 Guarded 1/3‐1/2 Total haze that obscures iris . Check IOP 4 Poor >1/2 Opaque cornea Tonopen IOP meds M. Chaglasian, OD 2 Ocular Emergencies Alkali Chemical Burn Alkali Chemical Burn . 50 yo CM bricklayer . Needs more irrigation and debridement . Mortar splashed in eyes 1 day prior . Emergency amniotic membrane transplant (AMT) . Went to ER, eyes rinsed, given drops and Augmentin . c/o FBS, OD; OS feels fine . VA: OD HM; OS 20/20-2 . pH: 10 OD, 7.4 OS Chemical Burn Management Chemical Burn - Ocular Sequelae . Cycloplegic . Tarsorraphy . Advanced glaucoma . Chronic Dry Eye . AB or AB/steroid combo ung Glue/permanent . Eyelid destruction . Persistent epithelial defects/ RCE . Pain control . Symblepharon . Infectious keratitis Cyclo, steroids, NSAIDs . AMT . Cicatricial Entropion - months . Stromalysis . Artificial tears . Limbal stem cell transplant . Pressure patch Uninjured eye - autograft . Trichiasis . Perforation . Ectropion . Irreversible intraocular damage BCL not tolerated Close relative – allograft . Oral narcotics/NSAID . Ankyloblepharon . Phthisis bulbi . Topical sodium ascorbate 10% . Corneal transplant . Descemet membrane . Hypopyon and Citrate Oral . Artificial corneas . Doxycycline detachment . Diamox . Retinal detachments Amniotic Membrane Transplant (not Bandage) AMT . Used as a surgical graft, where the tissue is integrated into the host. Amniotic membrane provides the scaffold for re-epithelialization. When used as a graft, AM is typically glued or sutured in place, and epithelium is expected to grow over it. Amniotic membrane is the innermost layer of the placenta, with 3 layers: . AMT has an low immune response, so few rejections Epithelium . Shown to: thick basement membrane: supports epi call migration and inhibits apoptosis 1. epithelialization Avascular stromal matrix: rich in growth factors & protease inhibitors 2. fibrosis, inflammation, scarring 3. provides an anti-inflammatory and anti-scarring effect that AM applied with epithelial-basement minimizes the buildup of scar tissue side facing UP, stroma DOWN . Other uses: Acts as basement membrane for corneal epithelium to grow over Stevens-Johnson syndrome Bullous /band keratopathy, pterygia Prevent post-op adhesion of conj/sclera in trabeculectomy 16. Sippel KC, et al. Amniotic membrane surgery. Curr Opin Ophthalmol 2001;12:269-281 M. Chaglasian, OD 3 Ocular Emergencies CRAO CRAO . Sudden, painless, unilateral loss of vision . 47yoCF with 3 day h/o blur, OS, with severe loss . (+) APD yesterday . Swollen, pale posterior pole . Had been seen twice in previous week . “Cherry red” spot 1 MD, 1 OD • Vascular attenuation &/or boxcarring of flow Dx: Dry eyes in arteries & veins Tx: Artificial tears Spoke to tech yesterday • May see an embolus in vessel on optic nerve . Casual about coming in Patient findings CRAO OD OS . In office AC paracentesis & digital massage ASA 20/20 Distance Acuity CF 1’ . To Cardiologist (+) APD Echocardiogram 12 TA 12 . To ER BP 128/79 Blood work ESR: rule out Temporal Arteritis WNL SLE WNL . To PCP Hematology workup . To Retina Brimonidine Vision Never Improved CRAO CRAO Causes . Echocardiogram Dilated aortic root . Emboli . In patients of 70 years of associated with connective tissue dx 74% cholesterol age and older, . Blood work: 10.5% calcific giant cell arteritis is more ESR: minimally elevated 15.5% platelet-fibrin likely to be the cause than Elevated homocysteine level . Thrombosis in younger patients. amino acid in blood derived from the digestion of . Vasculitis protein-rich foods GCA Elevated PTT (Partial thromboplastin test) . Post-trauma Other hypercoagulability factors negative Negative CT, MRI, MRA M. Chaglasian, OD 4 Ocular Emergencies CRAO CRAO Testing ESR & CRP . Incidence . Risk Factors Carotid Doppler – r/o GCA r/o emboli from 3.5/10,000 in general Age >40 population CBC/lipid profile carotid Systemic conditions Cardiology referral Auto-immune . 92% of patients have HTN, DM, CV dx, prior MI, </= CF acuity stroke, hypercholesterol, risk of MI Inflammatory Only ~ 8% will experience hypercoagulable state Hematology VA improvement Social/Medication history workup . Two thirds of patients experience Smoking Coagulopathies 20/400 vision while only one in six will experience 20/40 vision Younger pts or better. CRAO CRAO & Mortality . Retina suffers no detectable damage up to 97 . Patients with emboli have a 56% mortality rate over 9 years, minutes compared to 27% for an age-matched population without emboli . BUT sustains massive, irreversible damage after 4 hours . Life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-matched population without CRAO Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723‐36. CRAO – Acute treatment CRAO – Acute treatment • Lower IOP • Anterior chamber paracentesis • remove 0.1 to 0.4 ml of aqueous fluid within the first 24 hours. Move occlusion • Digital ocular massage Carbon/carbogen inhalation • Some use 3‐Mirror Lens CO dilates arterioles & increases O delivery to ischemic • IOP lowering agents 2 2 tissues Paper bag – dilate retinal vessel Remove embolus Local intraarterial fibrinolysis (LIF) was associated with similar visual outcomes but increased rate of adverse reactions when compared to observation in the EAGLE study. The study did not recommend LIF for acute CRAO. M. Chaglasian, OD 5 Ocular Emergencies CRAO Urgencies . Risk of neovascularization . Giant Cell Arteritis . Penetrating injury NVD, NVI, NVG . Endophthalmitis . Ruptured globe Reports from 2.5-35% . CRVO . Lacerations 18.2% @ an average of 8.5 weeks post CRAO . Papilledema . Corneal foreign body . Optic neuritis . Retinal detachment . Corneal abrasion . Orbital cellulitis . Iritis Ocular neovascularization following central retinal artery occlusion: prevalence and timing of onset. Eur J Ophthalmol. 2010 . Corneal ulcer Nov‐Dec;20(6):1042‐6. Giant Cell Arteritis / Temporal Arteritis Background on GCA . Giant cell arteritis (GCA) is the most common primary vasculitis in adults. Histopathologically, GCA is marked by generalized granulomatous inflammation of medium- to large-sized vessels that occurs in the elderly. Patients commonly note associated symptoms such as headache, jaw claudication, diplopia, myalgias, and constitutional symptoms. The most commonly feared sequela of GCA is permanent visual loss secondary to arteritic anterior ischemic optic neuropathy (AAION). Since the vision loss from AAION can progress rapidly, and can involve the fellow eye within a matter of days, GCA is considered an ophthalmologic emergency. Giant Cell Arteritis / Temporal Arteritis GCA Exam Findings . Inflammation of medium & large sized arteries of the . CRAO body, restricting blood flow & causing pain . VA loss usually unilateral, but risk of loss in other eye if . AION not
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