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SURESH NAIDU
2009
Ocular Emergencies
Anatomy of the Eye
Anatomy
 The outermost layer is composed of the cornea
and sclera.
 The middle layer consists of the choroid, ciliary
body, and iris.
 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
Anterior Segment
 Conjunctiva
 Cornea
 Anterior sclera
 Aqueous humor
 Iris
 Lens
 Anterior and posterior
chambers
Posterior Segment
 Vitreous
 Retina
 Choroid
 Posterior sclera
 Optic nerve
Eye Exam
 External examination - asymmetry, proptosis,
enophthalmos, orbital rim,lids,ducts
 Visual acuity - Snellen eye chart, Counting fingers, light
perception
 CN II - VII - pupils, visual fields, EOMs, facial droop
 Pupillary reaction
 Tonometery
 Slit lamp – anterior segment
 Fundoscopy – posterior segment
OCULAR EMERGENCIES SEEN IN
ED
TRAUMA
-PENETRATING
-BLUNT
-BURNS(CHEMICAL,THERMAL)
NON TRAUMA
-INFECTIOUS- eg orbital cellutis,orbital
abcess,preseptal cellulitis
-NON INFECTIOUS –acute close angle glaucoma,
CRVO, CRAO, retinal detachment
?
Stye/ hordeolum
 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)
 Treatment
-erythromycin ointment bd
for 7-10 days
?
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.
ACUTE RED EYE
ACUTE RED EYE
 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.
ACUTE RED EYE- Q 2 ask
 DO YOU HAVE PAIN?
Biggest distinguishing
factor between emergent
and non-emergent
 Do you wear contacts?
(increased risk of keratitis-
corneal infection)
 Do you have any
associated symptoms?
Nausea/vomiting/abdomin
al pain + red eye often
can signal acute
glaucoma.
 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.
Acute Painless Visual Loss
 Differential includes: cerebral vascular accident,
central retinal artery occlusion, central retinal vein
occlusion, wet macular degeneration, vitreous
hemorrhage.
 Important history and physical findings:
 DETERMINE IF MONOCULAR OR BINOCULAR
 Determine temporal sequence of visual loss, ie
intermittent v constant and stable v. worsening.
Ocular Emergencies to be
discussed…
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
Closed-angle glaucoma
 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.
Closed angle glaucoma
-clinical findings
 Red eye with fixed, mid-dilated pupil, hazy cornea.
 Extreme eye pain
 IOP very elevated (>40 often)
 Nausea/vomiting and abdominal pain
 Reduced visual acuity
 Often shallow anterior chamber or narrow or closed
angle on slit lamp examination(in our set up we don’t
do slit lamp examination or tonometry….)
1. Angle closure glaucoma - Treatment
and ED management
 Treatment: Lower IOP:
 Acetazolamide 500 mg orally once
 Timolol and pilocarpine drops three times over
fifteen minutes
 Immediate referral to an ophthalmologist ….(in
our ed we refer just based on clinical
suspicions….no slit lamp,no tonometry)
Retinal detachment
 Pathophysiology: separation
of neurosensory layer of
retina from underlying
choroid and retinal pigment
epithelium.
 Risk factors- increasing age,
history of posterior vitreous
detachment, myopia
(nearsightedness), trauma,
diabetic retinopathy, family
history of RD
Retinal detachment
 Signs and symptoms- “black curtain coming
down over visual field”, bright flashes of light,
especially in patient with risk factors.
 KEY ED MGMT POINT- know “classic”
presentation so you can refer to an
ophthalmologist quickly.
 Treatment is surgical…..
Foreign body eye
Foreign body
 Signs and symptoms: foreign body sensation,
tearing, red, or painful eye. Pain often
relieved with the instillation of anesthetic
drops.
 Stain with flourescein stain and illuminate
under blue fluorescent light (Wood’s lamp) is
effective to see corneal epithelial defects.
 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.
Orbital blowout fracture
 Consider when inferior orbital
rim has palpable bony
defect, patient has diplopia,
especially on upward gaze,
decreased vision, and history
of trauma.
 Mechanism of upward
diplopia: broken bone
causes direct entrapment of
inferior rectus or edema and
inflammation leads to
functional entrapment of
inferior rectus.
 Diagnosis: tear drop sign on
blow out # in OMV
Orbital blowout fracture
 Disposition - If no diplopia, minimal displacement, and no muscle
entrapment, discharge with ophthalmology follow up within a
week.
 When does the patient need surgery? For enophthalmos, muscle
entrapment, or visual loss.
 ED management:
 Ice packs beginning in ED and for 48 hrs will help decrease
swelling associated with injury.
 Elevate head of bed (decrease swelling).
 If sinuses have been injured, give prophylactic antibiotics and
instruct patient not to blow nose.
 Treat nausea/vomiting with antiemetics.
Foreign body - ED management
 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.
 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.
?
CORNEAL INJURY
Corneal injuries
 Abrasions and lacerations
 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.
 Diagnosis: flourescein staining
to see epithelial defect. Also
Seidel’s test for aqueous leakage
to diagnose laceration.
Corneal injuries
 Seidel’s 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.
 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.
CORNEAL ABRASION
MILD ABRASION SEVERE ABRASION
CORNEAL LACERATION
?
Chemical burns
 A TRUE OCULAR EMERGENCY!!!
 ONLY ophthalmic presentation in which treatment should
not be delayed to check visual acuity.
 ED Treatment: IRRIGATE, IRRIGATE, IRRIGATE!
 If possible, irrigate for 30 minutes using IV bag with NS
or LR’s 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.
Chemical burns
 Clinical Pearls
 Studies have shown that up to 10 L of irrigation can be
necessary to achieve normal pH.
 Irrigation with tap water immediately has been shown to
improve outcome and reduce healing time.
 Do not attempt to neutralize acid with base or vice versa.
 Before irrigation, give anesthetic drop to improve efficacy of
irrigation. Also can sweep fornices to remove any remaining
chemical debris.
 After irrigation, give broad spectrum antibiotics (tobramycin,
ciprofloxacin), topical anesthetics, tetanus prophylaxis.
 If conjunctiva and cornea appears white, sign of very severe
burn.
Chemical burns
 Acid v. Alkali
 Alkali- cause coagulation necrosis. Will denature
collagen and destroy vessels
 More common and worse than acid burns. Require
immediate ophthalmologic consultation.
 Found in: household cleaners, fertilizers
 Acid- cause coagulation necrosis
 Found in: automobile batteries (sulfuric acid), industrial
cleaners.
 Common common ED presentation is automobile battery
explosion.
Ruptured globe
 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)
?
Ruptured globe
Diagnosis:
 Signs and symptoms: pain, decreased vision,
hyphema, loss of anterior chamber depth, “tear-
drop” pupil which points toward laceration, severe
subconjunctival hemorrhage completely encircling
the cornea.
 Diagnosis: positive Seidel’s test, clinical exam.
Ruptured globe - ED
management
 If ruptured globe is suspected, immediately place an
eye shield to protect eye from further manipulation.
 Do not perform tonometry.
 CT head and orbit to evaluate for concomitant
facial/orbital injury.
 IV antibiotics within 6 hrs of injury. Cefazolin +
ciprofloxacin provides good coverage.
 Tetanus prophylaxis.
 Antiemetics and analgesics decrease risk of Valsalva
or movement which could increase IOP.
 Refer to ophthalmology for surgical management.
Central Retinal Artery Occlusion
 Pathophysiology:
emboli to central retinal
artery leads to “ocular
stroke.”
 Classic presentation:
extremely sudden,
acute unilateral non-
painful visual loss.
Often prior history of
amarousis fugax.
 Ocular exam: cherry red
spot on fundoscopic
examination.
Central retinal artery occlusion
 Risk factors: vasculopathic risks: hypertension,
age>70, hyperlipidemia, diabetes,
hypercoagulable states, sickle cell disease,
collagen vascular diseases.
 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.
Central Retinal Artery Occlusion -
ED Managment
 Must have VERY high index of suspicion, especially in
patients with appropriate risk factors.
 Immediate referral to an ophthalmologist. Retina can
become irreversibly damaged in 100 min.
 Mannitol 0.25-2.0 g/kg IV or acetazolamide 500 mg
PO once to reduce IOP. Topical timolol also helpful.
 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.
 Ophthalmologist may perform paracentesis of
aqueous humor to reduce IOP.
?
Retrobulbar hematoma
 Pathophysiology: Trauma, surgery, rarely spontaneous, can all
lead to compartment syndrome of orbit.
 Suspect if:
 trauma and pain,
 proptosis
 decreased visual acuity
  IOP
 ED treatment: Limited role for ED
Referal to OPTHAL….
?
ORBITAL INFECTIONS
Smith and Spencer and modified by Chandler
 Group I - Preseptal cellulitis
 Group II - Orbital cellulitis
 Group III - Subperiosteal abscess
 Group IV - Orbital abscess
 Group V - Cavernous sinus thrombosis
Orbital cellulitis
 sudden onset of fever,
 proptosis,
 restricted eye movement,
 swelling
 redness of the eye lids
ORBITAL INFECTIONS
Orbital infections develop via
 direct inoculation
 extension from adjacent structures
 hematogenous spread.
60% of infections develop from the direct spread of
sinusitis, most commonly ethmoidal.
 preseptal space, particularly from preseptal (or
periorbital) cellulitis in children
 from the pharynx, middle ear, facial skin, nose,
lacrimal gland (dacryocystitis), or dentition.
ORBITAL INFECTIONS
Mortality/Morbidity
Cavernous sinus
thrombosis
Brain abscess or
meningitis
Permanent vision loss
ED disposition
Preseptal cellulitis-if no sign of
orbital involvement,adults can
be discharged,but children has
to be admitrd for parentral
antibiotics.
Orbital cellulitis- need
admission,iv antibiotics
Orbital abcess-need surgery
References
www.emedicine.com/emergency
Tintannali’s emergency medicine –ocular
emergencies
www.vetmed.wisc.edu/Data/CourseMaterial/Miller/Emer
gencies.pdf
OCULAR EMERGENCIES -Patrick Lenaghan, MSIV
www.aafp.org/afp/20070915/829.

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Ocular emergencies

  • 3. Anatomy  The outermost layer is composed of the cornea and sclera.  The middle layer consists of the choroid, ciliary body, and iris.  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
  • 4. Anterior Segment  Conjunctiva  Cornea  Anterior sclera  Aqueous humor  Iris  Lens  Anterior and posterior chambers
  • 5. Posterior Segment  Vitreous  Retina  Choroid  Posterior sclera  Optic nerve
  • 6. Eye Exam  External examination - asymmetry, proptosis, enophthalmos, orbital rim,lids,ducts  Visual acuity - Snellen eye chart, Counting fingers, light perception  CN II - VII - pupils, visual fields, EOMs, facial droop  Pupillary reaction  Tonometery  Slit lamp – anterior segment  Fundoscopy – posterior segment
  • 7. OCULAR EMERGENCIES SEEN IN ED TRAUMA -PENETRATING -BLUNT -BURNS(CHEMICAL,THERMAL) NON TRAUMA -INFECTIOUS- eg orbital cellutis,orbital abcess,preseptal cellulitis -NON INFECTIOUS –acute close angle glaucoma, CRVO, CRAO, retinal detachment
  • 8. ?
  • 9. Stye/ hordeolum  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)  Treatment -erythromycin ointment bd for 7-10 days
  • 10. ?
  • 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  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  DO YOU HAVE PAIN? Biggest distinguishing factor between emergent and non-emergent  Do you wear contacts? (increased risk of keratitis- corneal infection)  Do you have any associated symptoms? Nausea/vomiting/abdomin al pain + red eye often can signal acute glaucoma.  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  Differential includes: cerebral vascular accident, central retinal artery occlusion, central retinal vein occlusion, wet macular degeneration, vitreous hemorrhage.  Important history and physical findings:  DETERMINE IF MONOCULAR OR BINOCULAR  Determine temporal sequence of visual loss, ie intermittent v constant and stable v. worsening.
  • 16. Ocular Emergencies to be discussed… 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  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  Red eye with fixed, mid-dilated pupil, hazy cornea.  Extreme eye pain  IOP very elevated (>40 often)  Nausea/vomiting and abdominal pain  Reduced visual acuity  Often shallow anterior chamber or narrow or closed angle on slit lamp examination(in our set up we don’t do slit lamp examination or tonometry….)
  • 19. 1. Angle closure glaucoma - Treatment and ED management  Treatment: Lower IOP:  Acetazolamide 500 mg orally once  Timolol and pilocarpine drops three times over fifteen minutes  Immediate referral to an ophthalmologist ….(in our ed we refer just based on clinical suspicions….no slit lamp,no tonometry)
  • 20. Retinal detachment  Pathophysiology: separation of neurosensory layer of retina from underlying choroid and retinal pigment epithelium.  Risk factors- increasing age, history of posterior vitreous detachment, myopia (nearsightedness), trauma, diabetic retinopathy, family history of RD
  • 21. Retinal detachment  Signs and symptoms- “black curtain coming down over visual field”, bright flashes of light, especially in patient with risk factors.  KEY ED MGMT POINT- know “classic” presentation so you can refer to an ophthalmologist quickly.  Treatment is surgical…..
  • 23. Foreign body  Signs and symptoms: foreign body sensation, tearing, red, or painful eye. Pain often relieved with the instillation of anesthetic drops.  Stain with flourescein stain and illuminate under blue fluorescent light (Wood’s lamp) is effective to see corneal epithelial defects.  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  Consider when inferior orbital rim has palpable bony defect, patient has diplopia, especially on upward gaze, decreased vision, and history of trauma.  Mechanism of upward diplopia: broken bone causes direct entrapment of inferior rectus or edema and inflammation leads to functional entrapment of inferior rectus.  Diagnosis: tear drop sign on blow out # in OMV
  • 25. Orbital blowout fracture  Disposition - If no diplopia, minimal displacement, and no muscle entrapment, discharge with ophthalmology follow up within a week.  When does the patient need surgery? For enophthalmos, muscle entrapment, or visual loss.  ED management:  Ice packs beginning in ED and for 48 hrs will help decrease swelling associated with injury.  Elevate head of bed (decrease swelling).  If sinuses have been injured, give prophylactic antibiotics and instruct patient not to blow nose.  Treat nausea/vomiting with antiemetics.
  • 26. Foreign body - ED management  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.  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.
  • 27. ?
  • 29. Corneal injuries  Abrasions and lacerations  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.  Diagnosis: flourescein staining to see epithelial defect. Also Seidel’s test for aqueous leakage to diagnose laceration.
  • 30. Corneal injuries  Seidel’s 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.  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.
  • 33. ?
  • 34. Chemical burns  A TRUE OCULAR EMERGENCY!!!  ONLY ophthalmic presentation in which treatment should not be delayed to check visual acuity.  ED Treatment: IRRIGATE, IRRIGATE, IRRIGATE!  If possible, irrigate for 30 minutes using IV bag with NS or LR’s 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  Clinical Pearls  Studies have shown that up to 10 L of irrigation can be necessary to achieve normal pH.  Irrigation with tap water immediately has been shown to improve outcome and reduce healing time.  Do not attempt to neutralize acid with base or vice versa.  Before irrigation, give anesthetic drop to improve efficacy of irrigation. Also can sweep fornices to remove any remaining chemical debris.  After irrigation, give broad spectrum antibiotics (tobramycin, ciprofloxacin), topical anesthetics, tetanus prophylaxis.  If conjunctiva and cornea appears white, sign of very severe burn.
  • 36. Chemical burns  Acid v. Alkali  Alkali- cause coagulation necrosis. Will denature collagen and destroy vessels  More common and worse than acid burns. Require immediate ophthalmologic consultation.  Found in: household cleaners, fertilizers  Acid- cause coagulation necrosis  Found in: automobile batteries (sulfuric acid), industrial cleaners.  Common common ED presentation is automobile battery explosion.
  • 37. Ruptured globe  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)
  • 38. ?
  • 39. Ruptured globe Diagnosis:  Signs and symptoms: pain, decreased vision, hyphema, loss of anterior chamber depth, “tear- drop” pupil which points toward laceration, severe subconjunctival hemorrhage completely encircling the cornea.  Diagnosis: positive Seidel’s test, clinical exam.
  • 40.
  • 41. Ruptured globe - ED management  If ruptured globe is suspected, immediately place an eye shield to protect eye from further manipulation.  Do not perform tonometry.  CT head and orbit to evaluate for concomitant facial/orbital injury.  IV antibiotics within 6 hrs of injury. Cefazolin + ciprofloxacin provides good coverage.  Tetanus prophylaxis.  Antiemetics and analgesics decrease risk of Valsalva or movement which could increase IOP.  Refer to ophthalmology for surgical management.
  • 42. Central Retinal Artery Occlusion  Pathophysiology: emboli to central retinal artery leads to “ocular stroke.”  Classic presentation: extremely sudden, acute unilateral non- painful visual loss. Often prior history of amarousis fugax.  Ocular exam: cherry red spot on fundoscopic examination.
  • 43. Central retinal artery occlusion  Risk factors: vasculopathic risks: hypertension, age>70, hyperlipidemia, diabetes, hypercoagulable states, sickle cell disease, collagen vascular diseases.  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  Must have VERY high index of suspicion, especially in patients with appropriate risk factors.  Immediate referral to an ophthalmologist. Retina can become irreversibly damaged in 100 min.  Mannitol 0.25-2.0 g/kg IV or acetazolamide 500 mg PO once to reduce IOP. Topical timolol also helpful.  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.  Ophthalmologist may perform paracentesis of aqueous humor to reduce IOP.
  • 45. ?
  • 46. Retrobulbar hematoma  Pathophysiology: Trauma, surgery, rarely spontaneous, can all lead to compartment syndrome of orbit.  Suspect if:  trauma and pain,  proptosis  decreased visual acuity   IOP  ED treatment: Limited role for ED Referal to OPTHAL….
  • 47. ?
  • 48. ORBITAL INFECTIONS Smith and Spencer and modified by Chandler  Group I - Preseptal cellulitis  Group II - Orbital cellulitis  Group III - Subperiosteal abscess  Group IV - Orbital abscess  Group V - Cavernous sinus thrombosis
  • 49. Orbital cellulitis  sudden onset of fever,  proptosis,  restricted eye movement,  swelling  redness of the eye lids
  • 50. ORBITAL INFECTIONS Orbital infections develop via  direct inoculation  extension from adjacent structures  hematogenous spread. 60% of infections develop from the direct spread of sinusitis, most commonly ethmoidal.  preseptal space, particularly from preseptal (or periorbital) cellulitis in children  from the pharynx, middle ear, facial skin, nose, lacrimal gland (dacryocystitis), or dentition.
  • 52. ED disposition Preseptal cellulitis-if no sign of orbital involvement,adults can be discharged,but children has to be admitrd for parentral antibiotics. Orbital cellulitis- need admission,iv antibiotics Orbital abcess-need surgery
  • 53. References www.emedicine.com/emergency Tintannali’s emergency medicine –ocular emergencies www.vetmed.wisc.edu/Data/CourseMaterial/Miller/Emer gencies.pdf OCULAR EMERGENCIES -Patrick Lenaghan, MSIV www.aafp.org/afp/20070915/829.