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Ocular Trauma
Mohamad Abdelzaher
MSc
Epidemiology
 40% of monocular blindness is related to trauma
The leading cause of monocular blindness
 70-80% injured are males
 Age: more in children and young age group
 Incidence of penetrating eye injuries: 3.6/100000
 Occupation : construction, industry
 Sports : boxing , racket sports
 Motor vehicle accidents
Classification
Ocular Injuries
Mechanical
Blunt
Perforating
Chemical
Thermal
Physical
Assessment
Rule out life threatening injuries
Rule out globe threatening injuries
Examine both eyes
Image
Plan for treatment
Blunt ocular trauma
Direct force
“coop”
Shock waves
“counter-coop”
Antero-posterior compression
& equatorial expansion
Orbital blow-out fractures
Fracture Floor
Signs of orbital floor blow-out fracture
•Periocular ecchymosis
and oedema
• Infraorbital nerve
anaesthesia
• Ophthalmoplegia typically in up and
down gaze (double
diplopia)
Enophthalmos - if
severe
Lid
Black “raccoon” eye
Traumatic ptosis
Lid laceration
Surgical emphysema
Conjunctiva
Subconjunctival hemorrhage
Conjunctival laceration
Cornea
Corneal abrasion
Corneal FB
Corneal rupture with iris prolapse
Sclera
Scleral rupture
Anterior Chamber
Hyphema
Iris
Iridodialysis
Aniridia
Ciliary Body
Angle recession
CB shut down
“Hypotony”
Iridocyclitis
Lens
Dislocation
Cataract
Vitreous
Vitreous hemorrhage
Choroid
Choroidal rupture
Choroidal detachment
Retina
Commotio retinae
Retinal detachment
Penetrating injuries
• Without FB retention:
- Cut wound: lid, conjunctiva, cornea, …
- Infection: corneal, endo, panophthalmitis
- Sympathetic ophthalmitis
• With Intraocular FB:
Mechanical
Cut wound:
lid,
conjunctiva,
cornea, …
Infection
FB reaction
corneal,
endo,
panophthal
mitis
-Non specific
-Siderosis
bulbi “Fe”
-Chalcosis
bulbi “Cu”
Chalcosis bulbi
Kayser Fleischer’s ring
Sunflower cataract
Cemical Ocular Injuries
 Most chemical substances that come in contact with the
conjunctiva or cornea cause little harm.
 The chief danger comes from alkali-containing compounds
found in household cleaning fluids, fertilizers and pesticides.
They erode and opacify the cornea.
 Acid-containing compounds (battery fluid, chemistry labs) are
somewhat less dangerous.
 There are no antidotes to these chemicals. The best you can
do is to dilute them immediately with plain water.
 The resultant reaction of the tissue causes the damage.
Treatment should be instituted
immediately, even before testing
vision.
Emergency treatment:
1-copious irrigation of the eyes,
preferably with saline or ringer
lactate.
Don’t use acidic solutions to neutralize
alkalis or vice versa.
Pull down the lower eyelid and evert
the upper eyelid to irrigate the
fornices
2-irrigation should be continued until
neutral PH is reached.
Except lime
For mild to moderate burns (during and after
irrigation):
•
•
•
•
cycloplegic
topical antibiotic
oral pain medication
if increase IOP use drugs to reduce it (acetazolamide,
methazolamide add b blocker if additional IOP
control is required)
• frequent use of preservative free artificial tear
For severe burns (Treatment after irrigation):
• Admission to the hospital
• Lysis of conjunctival adhesion
• Debride necrotic tissue
• Topical antibiotic
• Topical steroid
• Antiglaucoma medication if the IOP is increased or cant be
determined
• Frequent use of preservative free artificial tear
• Other consideration:
Therapeutic contact lenses, collagen, amniotic membrane
transplant
IV ascorbate and citrate for alkali burns
If any melting of the cornea occurs, collagenase inhibitors
may be used
If the melting progresses an emergency patch graft or corneal
transplat may be necessary.
A hazy cornea following an alkali burn
Physical Injuries
Glass blower
Iron melter
Arc flash
Infra Red
UVR
Cataract
Photophthalmia
• Punctate epithelial erosions “photophthalmia”