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Ophthalmology Back to Basic Maryam Abtahi March, 2015 Red Eye and Emergencies Chemical burn In chemical burn, what is your first action: Irrigate the eye with, water, normal saline,… Next steps: Check PH of the conjunctival fornix Check vision, pupil, continue the exam ….. Chemical burn Acid , coagulate proteins and inhibit further corneal penetration Alkali, worse prognosis Opaque cornea has poor prognosis Never try to neutralize Rx: Topical cycloplegic Topical antibiotics Topical steroid Ruptured globe If a ruptured globe is suspected, the first action to take is to: First ABC, R/O head trauma Don’t press on the eye ball Don’t check the IOP Check Vision Shield the eye NPO Tetanus IV antibiotics Ruptured globe R/o intraocular foreign body with orbital CT scan, specially in metal on metal hammering Blunt Trauma Need to be referred, Decreased vision Shallow anterior chamber Hyphema Abnormal pupil Ocular misalignment Retinal damage Intraocular foreign body The best study to evaluate a patient with intraocular foreign body is CT scan of the orbits Orbital Floor Fracture • Medical management : no nose blowing Systemic antibiotic only if sinusitis • Surgical repair : Fracture of more than 50% of the floor, Diplopia not improving, Enophthalmos more than 2 mm Blow-Out Fracture Blow out fracture, white eye In children , might cause muscle entrapment and ischemia, Risk of bradycardia . One of the ophthalmology emergency, Hyphema It is the result of a tear in an iris vessel. It can be associated with other ocular injuries. It should be referred to ophthalmologist. There is risk of re-bleeding in 2-5 days after trauma In management , no aspirin , no valsalva Risk of re-bleed highest on days 2-5 , resulting in Increased IOP, corneal staining, iris necrosis, Corneal Abrasion Corneal abrasion in contact lens wearer Never patch the eye Topical antibiotic Refer to an ophthalmologist The risk of ulceration is significantly higher than in not –contact Lens wearer, specially pseudomonas infection Corneal abrasion Never prescribe topical anesthetics, No topical steroid In case of linear abrasions examine under the lid Corneal ulcer Local necrosis of the cornea due to infection (white vs. clear in abrasion) Lesion extend to the stroma, associated with thinning, Urgent referral to ophthalmologist Culture Topical antibiotic every hour Herpes simplex HSV type 1 90%, With fluorescein and cobalt blue, dendritic ulcer Referral to an ophthalmologist Antiviral topical or oral Steroid risk of geographic ulcer Herpes zoster ophthalmicus Herpes zoster involving the ophthalmic division of cranial nerve V (V1) is more likely to have ocular involvements if the tip of the nose is involved: Hutchinson sign Complications : Keratitis, corneal perforation, scar Iritsis, secondary glaucoma, cataract, Cranial nerve palsy …. Herpes Zoster Ophthalmicus Management Oral antiviral In cases of conjunctival involvement erythromycin Refer to ophthalmologist Steroid should be prescribed by ophthalmologist, if needed. Cornea Tips Keratoconus Kayser-Fleischer ring Bilateral thinning and Wilson disease bulging of the cornea Associated with down’s syndrome, atopy, irregular astigmatism , scar, stromal edema Rx: spectacle, CL, cross linking, penetrating keratoplasty, Arcus senile Hypercholesterolemia if under 40 yrs. Conjunctivitis Conjunctival injection with discharge, Should be treated with a topical antibiotic if discharge is purulent,( bacterial ) Should be treated with parenteral antibiotic if gonococcal.(fig.) Prominent itching symptoms is in allergic conjunctivitis Lymphatic Drainage Temporal conjunctiva to preauricular nodes Nasal conjunctiva to Submandibular nodes Conjunctivitis Papillae Allergic conjunctivitis Bacterial conjunctivitis Follicles Viral conjunctivitis Chlamydial conjunctivitis Pterygium It is a benign growth of fibro-vascular triangular tissue over the cornea Sun exposure More common on the nasal side of the conjunctiva In an early stage into maybe managed with use of artificial tears and topical vasoconstrictors Excision in chronic inflammation, cosmesis, threat to visual axis, 5% recurrence rate if with conjunctival autograft. Subconjunctival hemorrhage Asymptomatic Can be associated with HTN, or vasculopathy , or anticoagulant therapy, specially in recurrent one Resolve spontaneously in 2-3 weeks No need for stopping NSAID or Systemic anticoagulant for resolution. . Episcleritis Usually complain of mild pain. Have engorged superficial vessels overlying the sclera below the conjunctiva. 1/3 associated with systemic connective tissue disease 1/3 bilateral 1/3 M/F Scleritis vs. episcleritis To differentiate, Place a drop of Phenylephrine 2.5% , re-examine after 10-15 min , epi-scleral vessel should blanch. Scleritis , severe pain, more likely associated with systemic disease like : Collagen vascular disease, Granulomatous disease Infections Metabolic, gout, Chemical Idiopathic Cellulitis Pre-septal : trauma, skin infection Orbital : secondary to sinus infection, facial, tooth, or trauma Differentiating signs , in orbital cellulitis: Proptosis Limited ocular motility Decreased vision RAPD Marked Conjuctival chemosis Pain on eye movement Marked leukocytosis, Cellulitis Treatment of pre-septal cellulitis Warm compress Systemic antibiotic If severe or under 1 year old treat as orbital Orbital Cellulitis Complication : Vision loss, Meningitis Brain abscess Cavernous sinus thrombosis, Death Management Patient admission Blood culture 2 Intravenous AB Ophthalmologic consultation Chalazion Presents with acute, tender swelling of the lid Management includes warm compresses and lid hygiene for 2 Weeks Chronic case after 2-3 month might need incision and drainage Chalazion Mucoromycosis Request stat ophthalmology and ENT consultations to rule out a life–threatening fungal infection (mucoromycosis) Diabetic patient with ketoacidosi, Frozen globe, + RAPD Acute angel closure glaucoma Characteristic of acute angel closure glaucoma Sever eye pain, N&V, Decreased vision High IOP Shallow angle A fixed and dilated pupil Corneal edema Acute angel closure glaucoma risk factors Hyperopia Asian, Inuit people Age>70 Mature cataract Female Shallow anterior chamber Family history Pupil dilation Acute angel closure glaucoma What is your next plan: Refer to ophthalmologist for laser iridotomy What would be the next plan Laser iridotomy Aqueous suppression with BACH Beta-blocker. adrenergic., cholinergic, hyperosmolar Miotics to reverse the pupillary block Temporal Arteritis or Giant Cell Arteritis F > 60 y/o Abrupt monocular loss of vision, pain over temporal artery , jaw claudication, diplopia, PMR, constitutional scalp tenderness, temporal artery beading Diagnosis : temporal artery biopsy Treatment high dose steroid, start immediately , before the biopsy Temporal Arteritis Immediately ESR, CRP, A low or normal sedimentation rate does not exclude the diagnoses The most common cranial nerve paralysis that occur involves the third cranial nerve. CRAO Sudden unilateral vision loss and cherry red spot in the macula, Cause Emboli from carotid artery , heart( arrhythmia, valvular, endocarditis) Thrombosis Temporal arteritis Management, within 2 hour Digital massage of the globe to dislodge an embolus Topical beta blockers AC paracenthesis by an ophthalmologist Lid laceration repair should include a) b) c) d) Assessment of possible canalicular injury Foreign body removal Tetanus prophylaxis All of the above Ophthalmia Neonatarum Toxic conjunctivitis occurs in day one secondary to instillation of silver nitrate or erythromycin ointment that used as conjunctivitis prophylaxis , no treatment needed Gonococcal day 5-7 , is the most serious one Chlamydial , need systemic treatment Herpes simplex after 2-3 weeks Ophthalmia Neonatarum Chlamydia Occurs usually after 21 days of age, between 2-3 weeks Requires two weeks of systemic erythromycin for effective treatment If not treated can cause pneumonitis, arthritis, and other systemic infection Uveitis Anterior, pain photophobia blurred ciliary flush, miotic pupil, KP, Etiologies :HLA B27 , idiopathic , infection like lyme, syphilis, TB, herpes, sarcoid, trauma, Rx: steroid, cycloplegic Intermediate, foater , blurred vision Causes: sarcoidosis, lyme, MS Posterior , blurred vision, floaters, Etiologies: infections, inflammations, autoimmune, malignancies, Vision Loss Acute vision loss Trauma / foreign body Retinal detachment CRAO/CRVO Chronic Vision loss Cataract Refractive error Corneal dystrophy Irreversible VL ARMD(macular degeneration) Glaucoma Diabetic retinopathy Medication Prolonged use of topical ophthalmic anesthetics can cause Corneal damage, Any corneal damage Topical steroid side effects Worsening of corneal fungal ulcers Worsening of bacterial keratatis Worsening of herpetic dendritic keratitis Cataracts Open-angle glaucoma What mechanism of action do cycloplegic use to relieve pain? Paralysis of ciliary spasm Glaucoma Glaucoma POAG PACG Common 95% Rare 5% Chronic Acute onset Painless Painful red eye Moderate IOP Normal cornea , pupil No symptom Extremely IOP Haze cornea, middilated pupil , N/V, halo around light Glaucoma Risk factor for open-angel glaucoma include Elevated intraocular pressure African racial heritage Age Positive family history for glaucoma Corneal thickness Secondary glaucoma caused by Uveitis Chronic steroid use Trauma Remember IOP is a risk factor for open angle glaucoma , its not part of its definition An optic nerve with glaucomatous damage Increased C:D ratio Significant C:D asymmetry Flamed shape disc hemorrhage 360 prepapillary atrophy Nasal displacement large vessels Thinning and notching of the neuroretinal rim Beta blockers Decrease production Beta blockers can worsen congestive heart failure, Myasthenia Gravis, Betaxolol is relatively selective beta 1 blockers Topical beta blockers decrease the production of the aqueous humor Can masked symptoms of hypoglycemia Prostaglandin analogue Latanoprost (xalatan) : Increased outflow Side effects, Conjunctival hyperemia Increased iris pigmentation Lengthening of the eyelashes Macular edema Sunken eye Retinal disease Retina has 10 layers CRVO Central retinal vein occlusion Blood and thunder fundus Second most common vascular retinopathy after DM, Risk factor HTN, DM, glaucoma, arteriosclerotic vascular disease, hyperviscosity, (PV, OCP, sickle cell, lymphoma, leukemia, Treatment of underlying disease and complications Macular edema, neovascularization of retina and iris, vitreous hemorrhage RD , Retinal Detachment Rhegmatogeneous (most common) caused by tear or hole, Treatment with scleral buckle, or pneumatic retinopexy,… Tractional In diabetic retinopathy, CRVO, sickle cell, ROP, trauma, Treatment surgery Exudative posterior uveitis, central serous retinopathy tumor Treatment of the underlying disease Retinal tear Supratemporal retina , most common site for horseshoe tears Caused by PVD posterior vitreous detachment or trauma, Posterior vitreous detachment Normal aging of vitreous liquefaction Sign and symptom Floater , flashes Weiss ring : glial tissue around the optic disc Complication: Tear, RD, more in high myopia Refer to ophthalmologist, dilated exam , F/U No specific treatment Age-related macular degeneration Leading cause of blindness, cause metamorphosia, Risk factors F, older age, family hx, smoking, Caucasian, blue eye Dry (nonexudative) 90%: Drusen in dry (hyaline material) medical. Monitor, antioxidants Wet (exudative) 10%: laser, PDT, intravitreous injection of anti-VEGF Diabetic retinopathy In diabetic retinopathy, most common cause of vision loss in young people, may be caused by Macular edema , Most common cause of vision loss in BDR Macular ischemia Vitreous hemorrhage BDR: background DR, non-prolifrative Non-proliferative Diabetic Retinopathy Signs of nonproliferative diabetic retinopathy Microaneurysm Dot and blot hemorrhages Hard exudates Intraretinal hemorrhages Cotton wool spot Screening Patient with type 2 diabetes should be evaluated by an ophthalmologist, at the time of diagnoses. Type 1 diabetes should be evaluated five years after diagnoses but not before puberty Proliferative Diabetic Retinopathy Proliferative diabetic retinopathy, optic disc neovascularization Retinitis pigmentosa Dx? Triad? APO Arteriolar narrowing Perivascular bony-spicule Optic disc pallor Pediatrics Strabismus Crania nerves palsy 3th nerve palsy : Exotropia and hypotropia , ptosis, 6th: Esotropia, Remember : need imaging if young or associated with neurological signs, th 4 4th :hypertropia and head tilt nerve palsy Amblyopia Reduction of best corrected visual acuity due to cortical suppression of sensory input, Or more than 2 lines difference in acuity between two eyes. Etiologies Strabismus , Refractive, Deprivation Treatment Occlusion or atropine cycloplegic of the good eye ? Horner syndrome Ptosis Miosis Anhydrosis Heterochromia ? DDx Leukocoria DDx Retinoblastoma Cataract Retinal coloboma ROP Toxocariasis Retinal detachment ? ? Kawasaki Kawasaki disease No to steroid Yes Aspirin ? conjunctivits ? Conjunctivitis Oral mucosal rash Measles Manifestation of systemic diseases Ocular malignancies The most common site of metastasis to the eye is the Choroid Ocular malignancies Metastasis , most common intraocular malignancy in adult Breast in F, lung in M , Neuroblastoma in children Malignant melanoma , most common primary intraocular tumor in adult BCC of lid most common lid malignany Intracranial hypertension The most common ocular manifestation is bilateral optic disc edema, papilledeam The most common visual symptoms are transient visual obscurations. Idiopathic intracranial hypertension can be associated with vitamin A or D toxicity tetracycline , steroid withdrawal. Intracranial hypertension Other symptoms Nausea/Vomiting/Headache Pulsatile tinnitus Normal neuro-imaging High ICP , in LP, lumbar puncture Connective tissue disorders Sjogren syndrome Is associated with dry eye and antibodies such as anti SS-A antibodies, Migraine Not always accompanied by headache Visual symptoms vary from scintillations to total bilateral loss of vision, which is usually temporary. Hypertension Optic disc swelling in the malignant hypertension Indicates that the patient is at increased risk for developing heart failure and hypertensive encephalopathy. Retinopathy the most common ocular manifestation of HTN. Key features of chronic HTN: AV nicking, blot hemorrhages, cotton wool spots, microaneurysm Thyroid eye disease Thyroid eye disease Might occurs even when the patient has normal serum thyroid hormone level. Can result in severe visual loss from optic nerve compression or corneal damage. Thyroid eye disease NO SPECS No sign Only sign lid retraction, lag Soft tissue swelling periorbital edema Proptosis Extra-ocular muscle weakness (diplopia) Corneal exposure Sight loss HIV, AIDS Cotton-wool Patches in AIDS patients a) Indicate obstruction of the pre-capillary arterioles with infarction of the superficial retina DDx of CWS Diabetic retinopathy HTN retinopathy HIV MS and Optic neuritis Young female Blurred vision , decreased color vision, 2º to optic neuritis, eye pain specially in ocular movement Diplopia 2º to internuclear ophthalmoplegia RAPD, ptosis, uveitis, optic atrophy, nystagmus, optic neuritis In optic neuritis, treatment with oral steroid will increase the risk of MS Randoms Snellen acuity :Testing distnace, 20 feet /smallest line patient can see ,20/40: what the patient can see at 20 feet(numerator), a normal person can see at 40 feet (denominator) Near reflex: Eye convergence, pupil constriction,lens accomodation LR6 SO4 AE3 Thick cornea overstimate IOP , thin cornea understiamte it Structure responsible for refractive power 1.cornea 2/3 2.lens 1/3 Thank you! 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