Ophthalmic Emergencies

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Ophthalmic Emergencies Powered By Docstoc
					      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.
   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
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
   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

   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
   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
   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

   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
   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
   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
   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
   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
  Immediate, copious
  30 minutes – Morgan Lens
  lactated Ringer's solution
  Normal pH—between 7.3 to 7.6
                     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
   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
   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
   Preseptal Cellulitis
    • Warm compress
    • Oral Abx
   Orbital Cellulitis
    • IV Abx
    • CT
    • ENT consult for surgical eval
    • Beware mucormycosis in
      diabetic/immunocompromised pts
                 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
   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
   Avoid retraction of lid margin
    • Gray line to gray line
   Check canilicular system
   Remove FB
   Tetanus prophylaxis
    penetrating/lacerating trauma
   damage or destroy anatomic
    structures
   compromise protective outer layers,
    increasing the risk of infection
   Sympathetic ophthalmia
    • <2%
          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
   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
   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)
   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 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
Uveitis
   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
   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
   central retinal artery occlusion
    (CRAO), nonarteritic
   arteritic anterior ischemic optic
    neuropathy (AION)
   acute angle closure glaucoma (ACG)
   retinal detachment (RD)
                  CRAO
   thrombus, embolus, or vasculitis
    blocks blood flow to the central
    retinal artery, resulting in ischemia
    and infarction of the retina
                     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
                    AION
   advanced age, white race, female
    gender, family history
    • Mean age 70
    • Incidence in patients older than 80 is
      approx 1%
   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
                       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
   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
                         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
   1 in 15,000 persons each year
   50 yrs age
   Risk factors: retinal hole,
    inflammation, trauma, previous eye
    surgery, myopia, and family hx
                      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)
   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
   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
   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
   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

				
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