Contents
Potentially blinding ocular injuries and constitute a true ocular emergency requiring immediate assessment and initiation of treatment
Classification
Roper-Hall (Ballen) classification system:
Based on the degree of corneal haze and the amount of perilimbal blanching/ischemia
Pathophysiology
Acid burns:
Acids precipitate tissue protein, creating a barrier to further ocular penetration. Due to this fact acid injuries tend to be less severe than alkali injuries.
Alkali burns:
Alkali burns cause corneal damage by pH change, ulceration, proteolysis and collagen synthesis defects. Alkali substances are lipophilic and penetrate the eye more rapidly than acids. The basic substance can quickly deposit within the tissues of the ocular surface causing saponification reaction within those cells. The damaged tissue secrete proteolytic enzymes as part of an inflammatory response which leads to further damage.
- Alkali substances can penetrate into the anterior chamber causing cataract formation, damage to the ciliary body and damage to the trabecular meshwork.
Clinical features
Chemical injuries of the eye produce extensive damage to the ocular surface epithelium, cornea, anterior segment and limbal stem cells resulting in permanent unilateral or bilateral visual impairment.
Immediate phase:
The immediate phase begins the moment a chemical agent comes in contact with the ocular surface
Acute phase of recovery (first 7 days):
Tissues rid themselves of contaminants while re-establishing the superficial protective layer of corneal epithelium.
Early reparative phase (8-20 days)
Transition period of ocular healing, in which the immediate regeneration of ocular surface epithelium and acute inflammatory events give way to chronic inflammation, stromal repair and scarring.
- Corneal ulceration tends to occur
Late reparative phase and sequelae (3 weeks):
Characterized by completion of healing with good visual prognosis (Grade I and II) and complications in those with guarded visual prognosis (Grade III and IV)
- Late complications of chemical burns:
- Poor vision
- Corneal scarring
- Xerophthalmia
- Dry eyes
- Symblepharon
- Ankyloblepharon
- Glaucoma
- Uveitis
- Cataract
- Adenexal abnormalities: Lagophthalmos, entropion, ectropion and trichiasis.
Management
Modalities to promote reepithelization are:
- Preservative free tear substitutes (ameliorate persistent epitheliopathy, reduce the risk of recurrent erosions and accelerate visual rehabilitation)
- Bandage soft contact lens (promote epithelial migration, helps in the basement membrane regeneration and enhances epithelial stromal adhesion)
- Investigational drugs:
- Retinoic acid (treatment of ocular surface disorders associated with goblet cell dysfunction)
- Epidermal growth factor and fibronectin – Has a favorable effect on promoting epitheliazation.
Support repair and minimizing ulceration:
- Ascorbate (reduces corneal thinning and ulceration)
- Collagenase inhibitors (promote wound healing by inhibiting collagenolytic activity and thus preventing stromal ulceration)
- Cysteine, acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine and citrate
Control inflammation:
- Corticosteroids (reduce inflammatory cell infiltration and stabilize neutrophilic cytoplasmic and lysosomal membranes)
Surgical management:
Late reparative phase treatment
- Conjunctival/tenons advancement
- Tissue adhesives
- Therapeutic penetrating keratoplasty
- Amniotic membrane transplantation
Limbal stem cell transplantation
Rehabilitating ocular chemical injuries that have resisted treatment.