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Ophthalmic Emergencies

Ophthalmic Emergencies. By : O. Ahmadi, MD. Professor Assistant of Esfahan Medical School, Emergency Department of Al-Zahra Hospital. By definition, an ophthalmic emergency requires immediate medical attention to avert permanent visual impairment.

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Ophthalmic Emergencies

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  1. Ophthalmic Emergencies By : O. Ahmadi, MD. Professor Assistant of Esfahan Medical School, Emergency Department of Al-Zahra Hospital

  2. By definition, an ophthalmic emergency requires immediate medical attention to avert permanent visual impairment. • Recognize the signs and symptoms of these emergencies, obtain an ophthalmic consult, and manage the patient until the patient is seen by an ophthalmologist.

  3. Top 10 1. Trauma – blunt 2. Trauma – penetrating 3. Trauma – burn 4. Infection – contact lens 5. Infection – viral, HSV/HZV, bacterial 6. Neurovascular – CRAO, CRVO 7. Neurovascular – Diabetes 8. Neurovascular – AACG 9. Neurovascular – TA 10. Neurovascular - RD

  4. Trauma • If chemical exposure, to what chemicals? • If blunt or penetrating trauma, what was the object and where did it strike? • Loss of consciousness • Use of power tools

  5. Inflammatory conditions • Recent illness, surgery, trauma, or infection • Contact lens wearer/Agriculture worker • Autoimmune diseases (rheumatoid arthritis, sarcoidosis, ankylosing spondylitis, or Reiter's syndrome) • Infection (herpes simplex, herpes zoster, Lyme disease, or tuberculosis) • Malignancy

  6. Neurovascular conditions Sudden onset of vision changes • Central retinal artery occlusion: • Hypertension, diabetes, coagulation abnormalities, trauma, hemoglobinopathies, or cardiac disorders • Arteritic ischemic optic neuropathy: • Severe vision loss (no light perception), headache, scalp tenderness, jaw claudication, fever, and proximal joint stiffness • Acute angle-closure glaucoma: • Pain, diaphoresis, nausea, and vomiting; ascertain patient's activity at the time • Retinal detachment: • Floaters or flashes of light followed by decreases in visual field or acuity

  7. Ophthalmic Terms • Amaurosis fugax Transient blindness. • Boxcarring The segmented appearance of the arteries or veins with a severe embolus. • Cells and flare WBCs (cells) in the anterior chamber and the reflection of light (flare) on protein shed from the inflamed iris or ciliary body. • Chemosis Edema of the bulbar conjunctiva, causing swelling around the cornea. • Ciliary flush Circumcorneal conjunctival injection. • Hollenhorst plaques Cholesterol emboli that appear as glistening yellow deposits occluding the retinal vasculature. • Hyphema Blood in the anterior chamber of the eye. • Hypopyon The layering of WBCs inferiorly in the anterior chamber of the eye. • Metamorphopsia Distortion of the visual image resulting in cloudy, foggy, or wavy vision. • Oblique flashlight test The shining of a flashlight tangentially from the lateral canthus toward the medial canthus so as to reveal a shadow on the medial aspect of the iris. Assesses anterior chamber depth. • Relative afferent pupillary defect The absence of direct pupillary response to light but intact consensual response to light. Assesses optic nerve function.

  8. Facts to elicit from the history • General • Are both eyes affected or only one? • Time of onset • Recurrence • Events preceding the current state • Recent history of ocular disease or surgery • Other diseases, specifically cardiac, vascular, or autoimmune • Family history for ocular problems • Current medications or recent changes to medications • Changes in vision (lost, blurred, or decreased vision; diplopia, sudden or gradual) • Visual acuity before the current event • Other symptoms (pain, nausea, vomiting)

  9. History, physical exam, and laboratory studies • Focused H & P • In case of chemical burn, irrigate first talk/look later • Visual acuity— the vital sign of the eyes • External anatomy • trauma, neuromuscular compromise, skin rash/vesicles, foreign bodies, or deviations from normal anatomy • both eyes • Pupillary response • damage to the optic nerve may not be seen for weeks • relative afferent pupillary defect - early sign often develops within seconds of ischemia or optic nerve damage • Extraocular eye movements, and Visual Fields

  10. Tonometry • Tonopen or digital • Slit Lamp • L/L, SC, K, AC, I, L • Fundus • CT – image of choice • Labs • ESR, CRP, CBC/diff • Path • Corneal scraping, TA Bx

  11. Traumatic injuries EPIDEMIOLOGY AND PATHOPHYSIOLOGY • 2,500,000 traumatic eye injuries /yr USA • 40,000-60,000 lead to visual loss • 40% of all new cases of monocular blindness • 80% occur in men • average age 30

  12. Chemical Trauma • alkaline exposure • lye, ammonia found in household cleaners, fertilizers, and pesticides • destroys cell structure • more dangerous than an acid exposure because penetrate and have a prolonged effect • Acid exposure • car battery, bleach, and some refrigerants • Only penetrate through epithelium • Corneal Scarring

  13. Copious Irrigation Immediate, copious 30 minutes – Morgan Lens lactated Ringer's solution Normal pH—between 7.3 to 7.6

  14. Blunt trauma • Superficial FB – flourescein stain • fractures, hemorrhage, or damage to the globe or adnexa • Fx sharp edges that can cause entrapment or damage to the muscle or globe • Retrobulbar hemorrhage - analogous to compartment syndrome • elevated intraocular and extraocular pressures, causing permanent damage • Hyphema • warrants suspicion for penetrating trauma, orbital fracture, acute glaucoma, or retinal detachment

  15. CT for fracture, retrobulbar hemorrhage, laceration, or intraocular foreign body • control swelling and pressure • Cold compresses • Nasal decongestants • Lateral canthotomy • tetanus prophylaxis

  16. Rx Corneal Abrasion • Cycloplegia • Topical antibiotic • 4th generation cephalosporin – (Vigamox,Zymar) • Ointment – (Ciloxan) • No aminoglycoside – (Tobrex, Gent) • Topical NSAID • anesthesia • NO patch unless 90% involvement • Don’t need strong pain control

  17. Preseptal Cellulitis • Warm compress • Oral Abx • Orbital Cellulitis • IV Abx • CT • ENT consult for surgical eval • Beware mucormycosis in diabetic/immunocompromised pts

  18. Hyphema • r/o rupture • Fox shield all times • Restrict activity (BRP only) • Cycloplegia, corticosteroids • Control intraocular pressure • r/o sickle/sickle trait • 10-20% rebleed rate cx • corneal staining, glaucoma

  19. Penetrating Injury • r/o rupture • If rupture no further exam - EUA • eye protected – fox shield • CT • systemic antibiotics initiated- NOT topical • NPO, time of last meal • tetanus prophylaxis

  20. Lid repair • Avoid retraction of lid margin • Gray line to gray line • Check canilicular system • Remove FB • Tetanus prophylaxis

  21. penetrating/lacerating trauma • damage or destroy anatomic structures • compromise protective outer layers, increasing the risk of infection • Sympathetic ophthalmia • <2%

  22. Inflammatory conditions • Endophthalmitis • inflammation in the vitreous chamber • staphylococci, streptococci, Bacillus cereus, Haemophilus influenzae, and Candida • IVDA and pts with indwelling catheters, penetrating trauma • Anterior uveitis or iritis • inflammation in anterior eye structures • potential for elevated pressures • Causes: trauma, autoimmune diseases, infection, or malignancy • Keratitis • Inflammation of the cornea • Causes: bacterial, viral, or fungal infection • Can rapidly cause blindness or perforation • immune complexes inflammatory cpd. corneal scar

  23. Common Corneal Pathogens • Bacteria • Staphylococcus aureus, Pseudomonas aeruginosa, acanthamoeba • CL: Extended-wear, wearing while swimming, homemade saline solution, and inadequate disinfection • Herpes Virus • simplex (HSV)- most frequent cause of corneal blindness in the United States • zoster (HZV)- not necessarily an emergent problem • Fungus • Fusarium, Candida • trauma to the eye involving plants or soil • Agricultural workers, persons in warm climates more at risk • gray-white opacity w/ feathery border, +/- satellite lesions

  24. HSV = Emergency • usually unilateral clear vesicles on an erythematous base that progress to crusting (can be bilateral), does have to follow dermatome • Prior hx of sores • Dendrite has true terminal bulbs that stain well (HZV terminal bulbs adhere to the epithelium and do not stain well)

  25. HSV Rx • Self limiting – leaves scar • Systemic acyclovir • trifluorothymidine 1% drops (Viroptic) 9/day or vidarabine 3% ointment (Vira-A), 5/day x 14 days • Very corneal toxic – reserve for confirmed cases • HZV Rx (not always emergency) • Supportive • Acyclovir • Artificial tears, erythro oint (Ilotycin) • NO Steroids

  26. Inflammatory Conditions • Symptoms: • pain, photophobia, or decreased visual acuity, esp. with consensual stimulus • Signs: • SLE - "cell and flare”, adhesions irregularly shaped pupils • Lower or Higher IOP • Bilateral or Recurrent • Warrents search for systemic cause

  27. Uveitis

  28. Endophthalmitis • worsening pain, redness, and decreased vision esp in setting of recent sx • floaters, purulent discharge, or fever • eyelid edema, decreased red reflex, hypopyon, or corneal abscess • Leukocytosis, diagnostic vitrectomy with cultures and smear • culture contact lenses or case • Keratitis • red eye, photophobia, decreased vision, or discharge • Foreign body sensation and inability to open the eye • Fluorescein- dendrites or ulcerations • SLE: corneal opacification, ciliary flush

  29. Do Not Patch Possible Infections • Endophthalmitis Rx • intravitreal Abx • vitrectomy • Keratitis Rx • Cycloplegia • Corneal scraping • c & s, stain (gram/geimsa) • Bacterial • 4th gen cephalosporin/ topical azithromycin (Vigamox/ Azasite, Ciloxan/ Erythro) • Fungal • Natamycin • Tectonic PKP • Uveitis/Iritis • Cycloplegia – pain relief, prevent miotic scarring • Corticosteroids • IOP control

  30. Neurovascular conditions • central retinal artery occlusion (CRAO), nonarteritic • arteritic anterior ischemic optic neuropathy (AION) • acute angle closure glaucoma (ACG) • retinal detachment (RD)

  31. CRAO • thrombus, embolus, or vasculitis blocks blood flow to the central retinal artery, resulting in ischemia and infarction of the retina

  32. CRAO • Hypertension 2/3 patients • structural cardiac pathology and carotid atherosclerosis ½ pts • diabetes mellitus ¼ pts • coag abnl, hemoglobinopathies • esp in younger pts • trauma • 30% to 50% have giant cell or temporal arteritis

  33. AION • advanced age, white race, female gender, family history • Mean age 70 • Incidence in patients older than 80 is approx 1%

  34. Symptoms • Unilateral severe vision loss • Scalp/forehead tenderness • Jaw claudication • +/- polymyalgia rheumatica • Signs • APD • ON edema • Elevated ESR, CRP • men, ESR > age/2; women, ESR > (age + 10)/2

  35. ACG • anterolateral portion of the iris occludes the canal of Schlemm • retinal ganglion cell death and irreversible vision loss • Stimulates strong vasovagal response • Nausea/vomitting can lead to met acidosis • Etiology - pupillary block 90% • aqueous flow from the posterior chamber is occluded where the lens meets the iris • posterior chamber pressure builds, bowing the iris and narrowing the angle until the outflow pathway is obstructed

  36. age > 30 yrs • Peak age 55-70 • Eskimo or Asian ethnicity • Eskimo 40x incidence of whites • hyperopia • female gender • 3-4x >risk than males • first-degree relative with ACG

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