Transcript Ophthalmic Emergencies - Emergency Medicine Symposium

Ophthalmic
Emergencies
Swati J. S. Parekh, M.D. F.A.A.O.
Director, Ambulatory Eye Clinic
St. Joseph’s Regional Medical
Center
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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
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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
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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
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Central retinal artery occlusion:
• Hypertension, diabetes, coagulation abnormalities,
trauma, hemoglobinopathies, or cardiac disorders
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Arteritic ischemic optic neuropathy:
• Severe vision loss (no light perception), headache, scalp
tenderness, jaw claudication, fever, and proximal joint
stiffness
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Acute angle-closure glaucoma:
• Pain, diaphoresis, nausea, and vomiting; ascertain
patient's activity at the time
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Retinal detachment:
• Floaters or flashes of light followed by decreases in
visual field or acuity
Ophthalmic Terms
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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
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General
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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
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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
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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
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Extraocular eye movements, and Visual Fields
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Tonometry
• Tonopen or digital
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Slit Lamp
• L/L, SC, K, AC, I, L
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Fundus
CT – image of choice
Labs
• ESR, CRP, CBC/diff
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Path
• Corneal scraping, TA Bx
Traumatic injuries
EPIDEMIOLOGY AND PATHOPHYSIOLOGY
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2,500,000 traumatic eye injuries /yr
USA
• 40,000-60,000 lead to visual loss
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40% of all new cases of monocular
blindness
80% occur in men
average age 30
Chemical Trauma
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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
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Acid exposure
• car battery, bleach, and some refrigerants
• Only penetrate through epithelium
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Corneal Scarring
Copious Irrigation
Immediate, copious
30 minutes – Morgan Lens
lactated Ringer's solution
Normal pH—between 7.3 to 7.6
Blunt trauma
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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
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elevated intraocular and extraocular pressures,
causing permanent damage
Hyphema
• warrants suspicion for penetrating trauma,
orbital fracture, acute glaucoma, or retinal
detachment
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CT for fracture, retrobulbar
hemorrhage, laceration, or
intraocular foreign body
control swelling and pressure
• Cold compresses
• Nasal decongestants
• Lateral canthotomy
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tetanus prophylaxis
Rx Corneal Abrasion
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Cycloplegia
Topical antibiotic
• 4th generation cephalosporin – (Vigamox,Zymar)
• Ointment – (Ciloxan)
• No aminoglycoside – (Tobrex, Gent)
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Topical NSAID
• anesthesia
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NO patch unless 90% involvement
Don’t need strong pain control
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Preseptal Cellulitis
• Warm compress
• Oral Abx
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Orbital Cellulitis
• IV Abx
• CT
• ENT consult for surgical eval
• Beware mucormycosis in
diabetic/immunocompromised pts
Hyphema
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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
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r/o rupture
• If rupture no further exam - EUA
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eye protected – fox shield
CT
systemic antibiotics initiated- NOT
topical
NPO, time of last meal
tetanus prophylaxis
Lid repair
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Avoid retraction of lid margin
• Gray line to gray line
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Check canilicular system
Remove FB
Tetanus prophylaxis
penetrating/lacerating trauma
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damage or destroy anatomic
structures
compromise protective outer layers,
increasing the risk of infection
Sympathetic ophthalmia
• <2%
Inflammatory conditions
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Endophthalmitis
• inflammation in the vitreous chamber
• staphylococci, streptococci, Bacillus cereus, Haemophilus
influenzae, and Candida
• IVDA and pts with indwelling catheters, penetrating
trauma
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Anterior uveitis or iritis
• inflammation in anterior eye structures
• potential for elevated pressures
• Causes: trauma, autoimmune diseases, infection, or
malignancy
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Keratitis
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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
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Bacteria
• Staphylococcus aureus, Pseudomonas aeruginosa,
acanthamoeba
• CL: Extended-wear, wearing while swimming,
homemade saline solution, and inadequate disinfection
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Herpes Virus
• simplex (HSV)- most frequent cause of corneal blindness
in the United States
• zoster (HZV)- not necessarily an emergent problem
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Fungus
• Fusarium, Candida
• trauma to the eye involving plants or soil
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Agricultural workers, persons in warm climates more at risk
• gray-white opacity w/ feathery border, +/- satellite
lesions
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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)
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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
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Very corneal toxic – reserve for confirmed cases
HZV Rx (not always emergency)
• Supportive
• Acyclovir
• Artificial tears, erythro oint (Ilotycin)
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NO Steroids
Inflammatory Conditions
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Symptoms:
• pain, photophobia, or decreased visual
acuity, esp. with consensual stimulus
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Signs:
• SLE - "cell and flare”, adhesions
irregularly shaped pupils
• Lower or Higher IOP
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Bilateral or Recurrent
• Warrents search for systemic cause
Uveitis
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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
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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
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Do Not Patch Possible Infections
Endophthalmitis Rx
• intravitreal Abx
• vitrectomy
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Keratitis Rx
• Cycloplegia
• Corneal scraping
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c & s, stain (gram/geimsa)
• Bacterial
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4th gen cephalosporin/ topical azithromycin (Vigamox/
Azasite, Ciloxan/ Erythro)
• Fungal
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Natamycin
Tectonic PKP
Uveitis/Iritis
• Cycloplegia – pain relief, prevent miotic scarring
• Corticosteroids
• IOP control
Neurovascular conditions
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central retinal artery occlusion
(CRAO), nonarteritic
arteritic anterior ischemic optic
neuropathy (AION)
acute angle closure glaucoma (ACG)
retinal detachment (RD)
CRAO
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thrombus, embolus, or vasculitis
blocks blood flow to the central
retinal artery, resulting in ischemia
and infarction of the retina
CRAO
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Hypertension 2/3 patients
structural cardiac pathology and carotid
atherosclerosis ½ pts
diabetes mellitus ¼ pts
coag abnl, hemoglobinopathies
• esp in younger pts
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trauma
30% to 50% have giant cell or temporal
arteritis
AION
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advanced age, white race, female
gender, family history
• Mean age 70
• Incidence in patients older than 80 is
approx 1%
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Symptoms
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Unilateral severe vision loss
Scalp/forehead tenderness
Jaw claudication
+/- polymyalgia rheumatica
Signs
• APD
• ON edema
• Elevated ESR, CRP
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men, ESR > age/2; women, ESR > (age + 10)/2
ACG
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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
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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
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age > 30 yrs
• Peak age 55-70
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Eskimo or Asian ethnicity
• Eskimo 40x incidence of whites
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hyperopia
female gender
• 3-4x >risk than males
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first-degree relative with ACG
RD
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vitreous separates from the retinal
pigment epithelium
• Flashes
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Separation fibrous aggregates on the
vitreal posterior surface
• prevents light rays from reaching retina
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Separation at retinal vessel may leak
blood into the vitreous body
• Floaters, blurred vision
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Macular involvement can lead to severe,
permanent vision loss
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1 in 15,000 persons each year
50 yrs age
Risk factors: retinal hole,
inflammation, trauma, previous eye
surgery, myopia, and family hx
Treatments
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CRAO
• break up the embolus or move it downstream
to minimize retinal damage
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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
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IV acetazolamide, 500 mg, topical ß-blocker
• rebreathe CO2 from paper bag (carbogen)
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AION
• high-dose corticosteroid if vision loss
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IV methylprednisolone, 250 mg Q 4hr x 3 d
initially, then 60 mg Q 6hr
• TA bx within 2 weeks
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ACG
• Reduce IOP with medication followed by
surgery
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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
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RD
• immediate surgical intervention
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diathermy, cryotherapy, or laser
• patient supine with head turned to the
same side as the detachment
• PX worsens with macular involvement &
duration
Conclusion
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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