Chemical Injuries

Chemical injury is one of the true ophthalmic emergencies. It is the trauma due to chemical exposure to the external eye. This trauma ranges from mild irritation to severe damage of the ocular surface and anterior segment with permanent loss of vision.

1. Alkalis
   • Most dangerous, with rapid penetration.
   • Examples include ammonia, lime, potassium hydroxide.
2. Acid
   • Less severe than alkali and do not penetrate into the eye as readily as alkaline substances.
   • Examples include acetic acid, sulfuric acid, sulfurous acid.
3. Other Irritants (e.g., pepper spray)
   • They have neutral pH and cause more discomfort to the eye than actual damage.

• Chemical burns constitute 7.7% to 18% of all ocular trauma.
• 2/3rd of the incidents are in young males.
• 2/3rd are caused by alkali.
• 60% occur in workplace accidents, 30% occur at home, and about 10% are as a result of an assault.
• 20% of the chemical injuries result in significant visual and cosmetic disability.
• Only 15% of patients with severe chemical injuries achieve functional visual rehabilitation.

The severity of the injury is related to the type, volume, concentration, duration of exposure, and degree of penetration of the chemical. The mechanism of injury also differs slightly between acids and alkali.

Acids

• Acids dissociate into hydrogen ions and anions in the cornea i.e. HCL ➔ H+ + Cl-
• The hydrogen molecule damages the ocular surface by altering the pH while the anion causes protein denaturation, precipitation, and coagulation.
• Protein coagulation generally prevents deeper penetration of acids.
• An exception to this is hydrofluoric acid, which behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption.

Alkali

• Alkaline substances dissociate into hydroxyl ion and a cation in the ocular surface e.g., NaOH ➔ Na+ + OH-
• The hydroxyl ion saponifies cell membrane fatty acids, while the cation interacts with the stromal collagen and glycosaminoglycans.
• This interaction facilitates deeper penetration into and through the cornea and into the anterior segment.

Clinical Symptoms

• Pain
• Lacrimation
• Photophobia
• Diminution of vision
• Blepharospasm

Signs

1. Lid
   • Edema, trichiasis, corneal ulcer, lagophthalmos, etc.
2. Ocular Surface
   • Dry eye, corneal scarring, opacity, corneal melt, conjunctival ulcer, injection, chemosis, etc.
3. Elevated Intraocular Pressure (Secondary Glaucoma)

• Roper Hall Classification
• Duas Classification

• Immediate
• Acute Stage: day 0 to 7
• Early Repair: day 7 to 21
• Late Repair: after day 21

Immediate

• The cornea can be clear, hazy, opaque, and accompanied by total epithelial loss, depending on which grade.

Acute Stage: Day 0 to 7

• There is bimodal intraocular pressure elevation. The initial peak is due to compression of the globe due to shortening of collagen fibers, while the second peak is a result of increased episcleral venous pressure, tympanic membrane damage, and tympanic membrane obstruction by inflammatory cells.
• There is corneal clouding due to stromal edema and changes in proteoglycans.
• There is also infiltration of ocular structures by polymorphonuclear leukocytes, monocytes, etc.

Early Repair: Day 7 to 21

• There is inflammation that parallels the epithelial regeneration.
• Conjunctival and corneal epithelium begins to regenerate.
• Corneal opacities begin to clear. They clear completely during this phase in mild to moderate injuries.
• Invasion of fibroblasts and synthesis of new collagen, glycosaminoglycan reach a peak by 14 days after injury.
• It is during this stage that corneal ulceration tends to occur.

Late Repair: After Day 21

• There is corneal vascularization in more severe corneal injuries.
• Tear film abnormality is seen here: aqueous deficiency due to damage to accessory lacrimal glands and scarring of ductule opening of the major lacrimal gland; and mucin deficiency due to damage to the goblet cells.
• Increased intraocular pressure.
• Hypotony due to severe damage to the ciliary body.
• Permanent loss of corneal innervation resulting in neurotrophic keratitis.
• Glaucoma due to damage to outflow channels.

• Emergency Treatment
• Medical Therapy
• Surgical Therapy

Emergency Treatment

• Immediate irrigation with any non-toxic fluid (e.g., normal saline, water, lactated ringers, diphoterine - new irrigate, effective, polyvalent, amphoteric, and chelating). The speed of irrigation is more important than the irrigate.
• Double eversion of the upper eyelid should be performed so that any retained particulate matter trapped in the fornices is identified and removed.
• Debridement of the necrotic area of corneal epithelium should be performed at the slit lamp to promote re-epithelialization and remove associated chemicals.
• Admission to the hospital is required if the injury is severe to ensure adequate eye drop instillation in the early stage.

Medical Therapy

This alone is enough to successfully treat patients with mild to moderate injuries (grades I and II). It includes:

• Antibiotics (e.g., topical erythromycin ointment, topical fluoroquinolones)
• Cycloplegic agents (e.g., atropine, cyclopentolate)
• Steroid drops (e.g., prednisolone)
• Artificial tears and other lubricating drops
• Ascorbic acids
• Citric acids

Surgical Therapy

Early surgeries to promote revascularization of the limbus, restore the limbal cell population, and reestablish the fornices. Examples are:

• Limbal stem cell transplantation
• Amniotic membrane grafting
• Gluing or keratoplasty

Late surgeries may involve:

• Division of conjunctival bands and symblepharon
• Conjunctival or other mucous membrane grafting
• Correction of eyelid deformities such as cicatricial entropion
• Keratoplasty for corneal scarring should be delayed for at least 6 months and preferably longer to allow maximal resolution of inflammation
• A keratoprosthesis may be required in a very severely damaged eye

• Symblepharon
• Secondary glaucoma
• Lagophthalmos
• Corneal opacity
• Corneal abrasion
• Conjunctival inflammation
• Secondary cataract
• Conjunctival scarring
• Corneal scarring and vascularization
• Complete globe atrophy
• Corneal ulceration
• Corneal thinning and perforation
• Pseudo pterygium