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

Ocular adnexa Skin burns Eyelid function Blinking reflex exposure 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

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