ophthalmic emergencies l.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Ophthalmic Emergencies PowerPoint Presentation
Download Presentation
Ophthalmic Emergencies

Loading in 2 Seconds...

play fullscreen
1 / 58

Ophthalmic Emergencies - PowerPoint PPT Presentation


  • 597 Views
  • Uploaded on

Ophthalmic Emergencies. Swati J. S. Parekh, M.D. F.A.A.O. Director, Ambulatory Eye Clinic St. Joseph’s Regional Medical Center. By definition, an ophthalmic emergency requires immediate medical attention to avert permanent visual impairment.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Ophthalmic Emergencies' - niveditha


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
ophthalmic emergencies

Ophthalmic Emergencies

Swati J. S. Parekh, M.D. F.A.A.O.

Director, Ambulatory Eye Clinic

St. Joseph’s Regional Medical Center

slide2
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.
top 10
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

trauma
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
inflammatory conditions
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
neurovascular conditions sudden onset of vision changes
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
ophthalmic terms
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.
facts to elicit from the history
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)
history physical exam and laboratory studies
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
slide10
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
traumatic injuries epidemiology and pathophysiology
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
chemical trauma
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
copious irrigation
Copious Irrigation

Immediate, copious

30 minutes – Morgan Lens

lactated Ringer's solution

Normal pH—between 7.3 to 7.6

blunt trauma
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
slide16
CT for fracture, retrobulbar hemorrhage, laceration, or intraocular foreign body
  • control swelling and pressure
    • Cold compresses
    • Nasal decongestants
    • Lateral canthotomy
  • tetanus prophylaxis
rx corneal abrasion
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
slide21
Preseptal Cellulitis
    • Warm compress
    • Oral Abx
  • Orbital Cellulitis
    • IV Abx
    • CT
    • ENT consult for surgical eval
    • Beware mucormycosis in diabetic/immunocompromised pts
hyphema
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
penetrating injury
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
lid repair
Lid repair
  • Avoid retraction of lid margin
    • Gray line to gray line
  • Check canilicular system
  • Remove FB
  • Tetanus prophylaxis
penetrating lacerating trauma
penetrating/lacerating trauma
  • damage or destroy anatomic structures
  • compromise protective outer layers, increasing the risk of infection
  • Sympathetic ophthalmia
    • <2%
inflammatory conditions33
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

common corneal pathogens
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
slide35
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)
slide37
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
inflammatory conditions40
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
slide42
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
slide43
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
neurovascular conditions
Neurovascular conditions
  • central retinal artery occlusion (CRAO), nonarteritic
  • arteritic anterior ischemic optic neuropathy (AION)
  • acute angle closure glaucoma (ACG)
  • retinal detachment (RD)
slide45
CRAO
  • thrombus, embolus, or vasculitis blocks blood flow to the central retinal artery, resulting in ischemia and infarction of the retina
slide46
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
slide47
AION
  • advanced age, white race, female gender, family history
    • Mean age 70
    • Incidence in patients older than 80 is approx 1%
slide48
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
slide49
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
slide50
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
slide52
RD
  • vitreous separates from the retinal pigment epithelium
    • Flashes
  • Separation fibrous aggregates on the vitreal posterior surface
    • prevents light rays from reaching retina
  • Separation at retinal vessel may leak blood into the vitreous body
    • Floaters, blurred vision
  • Macular involvement can lead to severe, permanent vision loss
slide53
1 in 15,000 persons each year
  • 50 yrs age
  • Risk factors: retinal hole, inflammation, trauma, previous eye surgery, myopia, and family hx
treatments
Treatments
  • CRAO
    • break up the embolus or move it downstream to minimize retinal damage
      • More likely if begun within 8 hours of onset of symptoms
    • digital pressure applied to the globe several times for a few seconds, repeated every few minutes
    • decrease intraocular pressure
      • IV acetazolamide, 500 mg, topical ß-blocker
    • rebreathe CO2 from paper bag (carbogen)
slide55
AION
    • high-dose corticosteroid if vision loss
      • IV methylprednisolone, 250 mg Q 4hr x 3 d initially, then 60 mg Q 6hr
    • TA bx within 2 weeks
slide56
ACG
    • Reduce IOP with medication followed by surgery
      • topical pilocarpine 2% Q 5 min x 3, timolol 0.5% x 1, acetazolamide 500 mg orally or IV
      • laser iridectomy
    • Control Pain and vomiting
    • Prophylactic iridectomy of fellow eye
slide57
RD
    • immediate surgical intervention
      • diathermy, cryotherapy, or laser
    • patient supine with head turned to the same side as the detachment
    • PX worsens with macular involvement & duration
conclusion
Conclusion
  • History and physical exam can help make a prompt and accurate diagnosis of ophthalmic emergencies
  • Important to administer appropriate therapies until the ophthalmologist can assess the patient