Transcript Chemical Burn

Chemical Burn
F.Fesharaki MD
1387
Chemical Injuries of the eye
Common
The offending chemical may be in
the form of a solid , liquid ,
powder , mist or vapor.
Home , Industry, Assault
Acidic or Alkali agents are the
most toxic agents.`
Acid Burns
Acidic chemicals produce
H+
The more powerful acid is
more toxic
The anionic component is
also important in toxicity.
• HF is a weak acid but fluorid
anion penetrates like Alkalis
into the eye
• Nitric acid produces yellowish
epithelial opacity of the cornea
• Chromic acid produces brown
discoloration of cornea and
chronic conjuctivtis
• Sulfuric acid : in car battery
•Acid denature and
precipitate
proteins
Alkali Burns
Raise the PH of tissues and
saponification of fatty acid in cell
membrane
Cellular disruption
Penetrating corneal stroma
Destroying proteoglycan ground
substance and collagen fibers
Peneterating into the anterior
chamber
Clinical Findings
Epithelial defect:
Flouresceine staining of
the cornea and
conjunctiva.
Clinical Findings
Stromal opacity :
Ranging from clear conea
to severe stromal opacity.
Better observed after
24-36 h.
Clinical Findings
Perilimbal ischaemia:
Limbal blanching.
The limbus contains
corneal stem cells
Clinical Findings
Ocular adnexa
Skin burns
Eyelid function
Blinking reflex
exposure
Grading of Severity
Grade I: clear cornea, no limbal ischemia
(excellent prognosis)
Grade II: Hazy cornea but visible iris
details, less than one third of limbal
ischemia(Good prognosis)
Grade III: Hazy cornea(iris details not
visible) , between one-third and half of
limbal ischemia (Gaurded prognosis)
Grade IV: opaque cornea and more than
half of limbal ischemia (very poor
prognosis)
Management of Chemical
injuries
The most important step:
Immediate and copious irrigation of
ocular surface with water or normal
saline solution
1-2 litre
1-2 hours
Checking conjunctival PH
• Removal of particulate
material from ocular
surface
• Double eversion of upper
eyelid
• Paracentesis of anterior
chamber
Antibiotic Drops
Infection
prophylaxy
corticosteroids
Excellent inhibitors of
PMN(polymorphonuclear
leakocyte) function
Intensive topical corticosteroid
administration is recommended
for the acute phase (first 2weeks)
The dosage should be markedly
reduced after 2weeks, because
steroids can inhibit wound healing
and increase the risk of infection
Oral Tetracycine
Potent chelator of calcium
Inhibits degranulation of
PMNs
Inhibiting PMN-induced
collengenolysis
• Topical 1%
medroxyprogesterone
• Effective in
suppressing collagen
. Break down
Vitamin C
2grams of oral ascorbic acid per
day
Promoting collagen synthesis
Vitamin C is a cofactor for
collagen synthesis
Severe alkali burns reduce
aqueous humour ascorbic acid
Potentially toxic to kidneys
Topical Cycloplegics
Significant ant.chamber
reaction
Atropine may delay
corneal epithelial and
stromal wound healing
Controlling IOP
Oral carbonic anhydrase
inhibitors
If corneal epithelium is
healing normally, topical
therapies can be used.
Promoting Epithelial Healing
Intensive nonpreserved
lubricants
Removal of necrotic
epithelium
Bandage contact lense
Tarsorrhaphy
Impending Corneal
Perforation
Glue
Pach gralt
Penetrating keratoplasty
Conj. Flap is not recommended
Nonhealing epithelial Defects
Dry eye and exposure therapies
Bandage contact lense.
PTK: phototherapeutic keratectomy
Topical drug toxicity:
Benzalkalonium- chloride
Lanoline in ointments
Amniotic membrane transplantation
Limbal stem cell transplantation
Amniotic Membrane
Transplantation
May be helpful in
suppressing inflammation
and promoting
reepithelialization and
prevention of symblepharon
formation
Limbalstem Cell
Transplantation
May be performed as soon as
2weeks after chemical injury if
no signs of corneal
epithelialization have appeared
Prognosis of limbal grofts is
better when the eye is not very
inflamed
Corneal Transplantion
1-2 years later .
after ocular surface
reconstruction
NO inflammation
No Glaucoma
Only in binocular cases
keratoprosthesis
THE END