This document provides an overview of ocular anatomy and various ocular emergencies commonly seen in the emergency department. It describes the anatomy of the eye in three layers - outer, middle, and innermost. Various ocular emergencies are then discussed in more detail, including acute angle closure glaucoma, retinal detachment, foreign bodies, corneal abrasions and lacerations, chemical burns, ruptured globe, central retinal artery occlusion, and orbital infections. For each condition, the pathophysiology, clinical findings, diagnosis and emergency department management are summarized. The goal is to equip emergency physicians with the essential knowledge to identify and treat potentially sight-threatening ocular emergencies.
3. Anatomy
ď The outermost layer is composed of the cornea
and sclera.
ď The middle layer consists of the choroid, ciliary
body, and iris.
ď The innermost is the retina, which gets its
circulation from the vessels of the choroid as well
as the retinal vessels, which can be seen in an
opthalmoscope
7. OCULAR EMERGENCIES SEEN IN
ED
TRAUMA
-PENETRATING
-BLUNT
-BURNS(CHEMICAL,THERMAL)
NON TRAUMA
-INFECTIOUS- eg orbital cellutis,orbital
abcess,preseptal cellulitis
-NON INFECTIOUS âacute close angle glaucoma,
CRVO, CRAO, retinal detachment
9. Stye/ hordeolum
ď Stye is a localized
infection or
inflammation of the
eyelid margin involving
hair follicles of the
eyelashes (ie, external
hordeolum) or
meibomian glands (ie,
internal hordeolum)
ď Treatment
-erythromycin ointment bd
for 7-10 days
11. Chalazion
slowly enlarging nodule on
the eyelid that is formed
by inflammation and
obstruction of a
sebaceous gland.
Chalazia can further be
categorized into
superficial(inflammation of
Zeis sebaceous glands) or
deep (Inflammation of the
meibomian glands ),
depending on which
glands are blocked.
Treated as stye.
13. ACUTE RED EYE
ď Key worrisome clinical findings (ophthal referral needed):
Pain: Pain in eye often indicates more serious
intraocular pathology (iritis, glaucoma).
Discharge: if purulent, think about bacterial
conjunctivitis.
Visual acuity: if decreased, usually more serious
cause.
Pupil: if sluggish, worry about acute glaucoma
Pattern of redness: CILIARY FLUSH: Redness
worst near cornea, usually serious intraocular
cause: iritis or glaucoma.
14. ACUTE RED EYE- Q 2 ask
ď DO YOU HAVE PAIN?
Biggest distinguishing
factor between emergent
and non-emergent
ď Do you wear contacts?
(increased risk of keratitis-
corneal infection)
ď Do you have any
associated symptoms?
Nausea/vomiting/abdomin
al pain + red eye often
can signal acute
glaucoma.
ď DD - Viral/bacterial conjunctivitis
(viral most common and least
serious), foreign body (check
cornea), subconjunctival
hemorrhage (hx of straining
common), angle closure
glaucoma, iritis, keratitis.
15. Acute Painless Visual Loss
ď§ Differential includes: cerebral vascular accident,
central retinal artery occlusion, central retinal vein
occlusion, wet macular degeneration, vitreous
hemorrhage.
ď§ Important history and physical findings:
ď DETERMINE IF MONOCULAR OR BINOCULAR
ď Determine temporal sequence of visual loss, ie
intermittent v constant and stable v. worsening.
16. Ocular Emergencies to be
discussedâŚ
1. Closed-angle glaucoma
2. Retinal detachment
3. Foreign body
4. Orbital fractures
5. Corneal abrasions
/lacerations
6. Chemical burns
7. Ruptured globe
8. CRAO
9. Retrobulbar hematoma
10. Orbital infections
17. Closed-angle glaucoma
ď Pathophysiology:
Ciliary body normally
produces aqueous humor
which travels around iris
to be drained by canal of
schlemm. When iris
blocks the canal of
Schlemm, an acute
increase in eye pressure
results, leading to rapid
damage to optic nerve
and irreversible visual
loss.
18. Closed angle glaucoma
-clinical findings
ď Red eye with fixed, mid-dilated pupil, hazy cornea.
ď Extreme eye pain
ď IOP very elevated (>40 often)
ď Nausea/vomiting and abdominal pain
ď Reduced visual acuity
ď Often shallow anterior chamber or narrow or closed
angle on slit lamp examination(in our set up we donât
do slit lamp examination or tonometryâŚ.)
19. 1. Angle closure glaucoma - Treatment
and ED management
ď Treatment: Lower IOP:
ď Acetazolamide 500 mg orally once
ď Timolol and pilocarpine drops three times over
fifteen minutes
ď Immediate referral to an ophthalmologist âŚ.(in
our ed we refer just based on clinical
suspicionsâŚ.no slit lamp,no tonometry)
20. Retinal detachment
ď Pathophysiology: separation
of neurosensory layer of
retina from underlying
choroid and retinal pigment
epithelium.
ď Risk factors- increasing age,
history of posterior vitreous
detachment, myopia
(nearsightedness), trauma,
diabetic retinopathy, family
history of RD
21. Retinal detachment
ď Signs and symptoms- âblack curtain coming
down over visual fieldâ, bright flashes of light,
especially in patient with risk factors.
ď KEY ED MGMT POINT- know âclassicâ
presentation so you can refer to an
ophthalmologist quickly.
ď Treatment is surgicalâŚ..
23. Foreign body
ď Signs and symptoms: foreign body sensation,
tearing, red, or painful eye. Pain often
relieved with the instillation of anesthetic
drops.
ď Stain with flourescein stain and illuminate
under blue fluorescent light (Woodâs lamp) is
effective to see corneal epithelial defects.
ď KEY ED MANAGEMENT: irrigation with NS
flush out FB.If unable to flush by irrigation,it is
probably embedded,referal to opthalmo
required.If patient history worrisome for
foreign body, but nothing is visualized on
initial exam, EVERT the eyelids. It can be
removed using small needle.
24. Orbital blowout fracture
ď Consider when inferior orbital
rim has palpable bony
defect, patient has diplopia,
especially on upward gaze,
decreased vision, and history
of trauma.
ď Mechanism of upward
diplopia: broken bone
causes direct entrapment of
inferior rectus or edema and
inflammation leads to
functional entrapment of
inferior rectus.
ď Diagnosis: tear drop sign on
blow out # in OMV
25. Orbital blowout fracture
ď Disposition - If no diplopia, minimal displacement, and no muscle
entrapment, discharge with ophthalmology follow up within a
week.
ď When does the patient need surgery? For enophthalmos, muscle
entrapment, or visual loss.
ď ED management:
ď Ice packs beginning in ED and for 48 hrs will help decrease
swelling associated with injury.
ď Elevate head of bed (decrease swelling).
ď If sinuses have been injured, give prophylactic antibiotics and
instruct patient not to blow nose.
ď Treat nausea/vomiting with antiemetics.
26. Foreign body - ED management
ď In ED, can attempt to remove it from cornea or
conjunctiva with a small needle. First place topical
anesthetic, and place topical antibiotic before and
after removal. Only attempt if <25% of corneal
thickness is involved.
ď KEY ED MANAGEMENT: If patient history
worrisome for foreign body, but nothing is
visualized on initial exam, EVERT the eyelids.
Many foreign bodies become lodged in upper lid
and are not visible on initial exam.
29. Corneal injuries
ď Abrasions and lacerations
ď Symptoms: extreme eye pain, relieved with
lidocaine drops. Visual acuity usually decreased,
depending on location of injury in relation to visual
axis. Also, inflammation leading to corneal edema
can decrease VA.
ď Diagnosis: flourescein staining
to see epithelial defect. Also
Seidelâs test for aqueous leakage
to diagnose laceration.
30. Corneal injuries
ď Seidelâs test: Under blue light, place damp
flourescein strip over site of injury. If full thickness
laceration is present, you will see dark stream of fluid
within green flourescein dye. This is indicative of
aqueous leakage which is diluting the green dye.
ď ED management: for abrasions, topical antibiotics
and follow up with ophthalmologist. For lacerations,
<1 cm, topical antibiotics and discharge with follow
up. If >1 cm, refer to ophthalmologist to rule out globe
rupture and for possible suture placement.
34. Chemical burns
ď A TRUE OCULAR EMERGENCY!!!
ď ONLY ophthalmic presentation in which treatment should
not be delayed to check visual acuity.
ď ED Treatment: IRRIGATE, IRRIGATE, IRRIGATE!
ď If possible, irrigate for 30 minutes using IV bag with NS
or LRâs connected to irrigating lens placed on eye. Then,
close eye, and after five minutes, check pH with litmus
paper in inferior conjunctival fornix. Irrigate until neutral
pH (7.0) is maintained for thirty minutes.
35. Chemical burns
ď Clinical Pearls
ď Studies have shown that up to 10 L of irrigation can be
necessary to achieve normal pH.
ď Irrigation with tap water immediately has been shown to
improve outcome and reduce healing time.
ď Do not attempt to neutralize acid with base or vice versa.
ď Before irrigation, give anesthetic drop to improve efficacy of
irrigation. Also can sweep fornices to remove any remaining
chemical debris.
ď After irrigation, give broad spectrum antibiotics (tobramycin,
ciprofloxacin), topical anesthetics, tetanus prophylaxis.
ď If conjunctiva and cornea appears white, sign of very severe
burn.
36. Chemical burns
ď Acid v. Alkali
ď Alkali- cause coagulation necrosis. Will denature
collagen and destroy vessels
ď More common and worse than acid burns. Require
immediate ophthalmologic consultation.
ď Found in: household cleaners, fertilizers
ď Acid- cause coagulation necrosis
ď Found in: automobile batteries (sulfuric acid), industrial
cleaners.
ď Common common ED presentation is automobile battery
explosion.
37. Ruptured globe
ď Penetrating trauma leads to corneal or scleral
disruption and extravasation of intraocular contents.
Can lead to:
- Irreversible visual loss
- Endophthalmitis -
inflammation of the intraocular
cavities (image)
39. Ruptured globe
Diagnosis:
ď Signs and symptoms: pain, decreased vision,
hyphema, loss of anterior chamber depth, âtear-
dropâ pupil which points toward laceration, severe
subconjunctival hemorrhage completely encircling
the cornea.
ď Diagnosis: positive Seidelâs test, clinical exam.
40.
41. Ruptured globe - ED
management
ď If ruptured globe is suspected, immediately place an
eye shield to protect eye from further manipulation.
ď Do not perform tonometry.
ď CT head and orbit to evaluate for concomitant
facial/orbital injury.
ď IV antibiotics within 6 hrs of injury. Cefazolin +
ciprofloxacin provides good coverage.
ď Tetanus prophylaxis.
ď Antiemetics and analgesics decrease risk of Valsalva
or movement which could increase IOP.
ď Refer to ophthalmology for surgical management.
42. Central Retinal Artery Occlusion
ď Pathophysiology:
emboli to central retinal
artery leads to âocular
stroke.â
ď Classic presentation:
extremely sudden,
acute unilateral non-
painful visual loss.
Often prior history of
amarousis fugax.
ď Ocular exam: cherry red
spot on fundoscopic
examination.
43. Central retinal artery occlusion
ď Risk factors: vasculopathic risks: hypertension,
age>70, hyperlipidemia, diabetes,
hypercoagulable states, sickle cell disease,
collagen vascular diseases.
ď What is a cherry red spot? cilioretinal artery will
maintain perfusion of macula, so macula appears
pink and healthy against pale background of
ishcemic retina.
44. Central Retinal Artery Occlusion -
ED Managment
ď Must have VERY high index of suspicion, especially in
patients with appropriate risk factors.
ď Immediate referral to an ophthalmologist. Retina can
become irreversibly damaged in 100 min.
ď Mannitol 0.25-2.0 g/kg IV or acetazolamide 500 mg
PO once to reduce IOP. Topical timolol also helpful.
ď Massage orbit with finger. This is thought to help
dislodge the clot from a larger to smaller retinal artery
branch, minimizing area of visual loss.
ď Ophthalmologist may perform paracentesis of
aqueous humor to reduce IOP.
46. Retrobulbar hematoma
ď Pathophysiology: Trauma, surgery, rarely spontaneous, can all
lead to compartment syndrome of orbit.
ď Suspect if:
ď trauma and pain,
ď proptosis
ď decreased visual acuity
ď ď IOP
ď ED treatment: Limited role for ED
Referal to OPTHALâŚ.
48. ORBITAL INFECTIONS
Smith and Spencer and modified by Chandler
ď Group I - Preseptal cellulitis
ď Group II - Orbital cellulitis
ď Group III - Subperiosteal abscess
ď Group IV - Orbital abscess
ď Group V - Cavernous sinus thrombosis
49. Orbital cellulitis
ď sudden onset of fever,
ď proptosis,
ď restricted eye movement,
ď swelling
ď redness of the eye lids
50. ORBITAL INFECTIONS
Orbital infections develop via
ď direct inoculation
ď extension from adjacent structures
ď hematogenous spread.
60% of infections develop from the direct spread of
sinusitis, most commonly ethmoidal.
ď preseptal space, particularly from preseptal (or
periorbital) cellulitis in children
ď from the pharynx, middle ear, facial skin, nose,
lacrimal gland (dacryocystitis), or dentition.
52. ED disposition
ďPreseptal cellulitis-if no sign of
orbital involvement,adults can
be discharged,but children has
to be admitrd for parentral
antibiotics.
ďOrbital cellulitis- need
admission,iv antibiotics
ďOrbital abcess-need surgery