Chemical eye burns

Chemical eye burns range from minor to blinding. Most are accidents, less often the result of assault. 2/1 of accidental burns occur at work, the rest at home. Alkaline burns are twice as common as acid burns, as alkali is more widely used both at home and in industry. The most common alkalis are ammonia, sodium hydroxide, and lime. The most common acids are sulfuric, sulfurous, hydrofluoric, acetic, chromic, and hydrochloric.

The severity of a chemical burn depends on the nature of the chemical agents, the area of action on the ocular surface, the duration of action (retention of the chemical on the ocular surface), and accompanying effects such as thermal action. Alkalis tend to penetrate deeper than acids, which coagulate the surface proteins that form the protective barrier. Ammonia and sodium hydroxide cause severe damage due to rapid penetration. Hydrofluoric acid, used in engraving and glass cleaning, also tends to penetrate the ocular tissue rapidly, while sulfuric acid effects can be complicated by thermal and high-energy effects from car battery explosions.

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Pathophysiology of chemical burns of the eye

Eye damage from severe chemical exposure has the following mechanism:

• Necrosis of the conjunctival and corneal epithelium with destruction and occlusion of limbal vascularization. Loss of limbal stem cells may subsequently lead to conjunctival enlargement and corneal vascularization or to the formation of epithelial defects with ulceration and perforation. Other late sequelae include impaired ocular surface wetting, symblepharon formation, and cicatricial entropion.
• Deeper penetration causes the release and deposition of glycosaminoglycans, clouding of the corneal stroma.
• Penetration of the chemical agent into the anterior chamber causes damage to the iris and lens.
• Damage to the ciliary epithelium disrupts the production of ascorbate, which is necessary for collagen synthesis and corneal regeneration.
• Hypotony and phthisis of the eyeball may develop.

Healing of corneal epithelium and stroma:

• The epithelium heals through the migration of epithelial cells, which are formed from limbal stem cells.
• Phagocytosis of damaged collagen by keratocytes and synthesis of new collagen occurs.

Evaluation of the severity of chemical eye burns

Acute chemical burns are classified by severity to plan appropriate treatment and final prognosis. Severity is assessed based on the preservation of corneal transparency and the severity of limbal ischemia. Later, the filling of deep and superficial limbal vessels is assessed.

1. Grade I: transparent cornea and absence of limbal ischemia (excellent prognosis).
2. Grade II: corneal opacity, but with visible details of the iris, ischemia of less than 1/3 (120) of the limbus (good prognosis).
3. Grade III: complete loss of corneal epithelium, stromal opacity obscuring details of the iris, ischemia of 1/3 to half (120 to 180) of the limbus (guarded prognosis).
4. Grade IV: totally cloudy cornea and ischemia of more than half (>180) of the limbus (very poor prognosis).

Other changes to look for during the initial evaluation include the extent of corneal and conjunctival epithelial loss, iris changes, lens status, and intraocular pressure.

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First aid for chemical eye burns

A chemical burn is the only eye injury that requires immediate treatment without taking a history and performing a thorough examination. Emergency care includes the following steps.

1. Copious irrigation is necessary to minimize contact time with the chemical agent and to normalize the pH in the conjunctival cavity as quickly as possible. Saline (or its equivalent) is used to irrigate the eye for 15-30 minutes or until the pH is completely normalized.
2. Double eversion of the eyelids must be performed so that any fragment of matter remaining in the conjunctival fornix, such as lime or cement, can be removed.
3. Surgical treatment of necrotic areas of corneal epithelium should be performed taking into account subsequent re-epithelialization.

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Drug treatment for chemical eye burns

Moderate injuries (grades I-II) are treated with a short course of topical steroids, cycloplegia, and prophylactic antibiotics for approximately 7 days. The main goals of treatment for more severe burns are to reduce inflammation, promote epithelial regeneration, and prevent corneal ulceration.

1. Steroids reduce inflammation and neutrophil infiltration, but they slow stromal healing by reducing collagen synthesis and inhibiting fibroblast migration. For this reason, topical steroids may be useful at the beginning of treatment and should be discontinued after 7-10 days, when corneal ulceration is most likely to occur. They can be replaced by nonsteroidal anti-inflammatory drugs that do not affect keratocyte function.
2. Ascorbic acid changes the state of damaged tissues and improves wound healing by providing synthesis of mature collagen by corneal fibroblasts. Locally, sodium ascorbate 10% is instilled every 2 hours in addition to the systemic dose of 2 g 4 times a day.
3. Citric acid is a powerful inhibitor of neutrophil activity and reduces the intensity of the inflammatory reaction. Formation of an extracellular calcium complex with citrates (chelacin) also inhibits collagenase. Locally, 10% sodium citrate is instilled every 2 hours for 14 days. The goal of this treatment is to eliminate the second wave of phagocytes, which usually occurs 7 days after the burn.
4. Tetracyclines are collagenase inhibitors and also inhibit neutrophil activity, reducing the ulceration reaction. They are used both locally and systemically (eg, doxycycline 100 mg 2 times a day).

Surgical treatment of chemical eye burns

Early surgical treatment may be necessary to revascularize the limbus and restore the limbal cell population and fornices. One or more of the following procedures may be performed:

• Mobilization of Tenon's capsule and its suturing to the limbus in order to restore limbal vascularization, which prevents corneal ulceration.
• Transplantation of limbal stem cells from the patient's other eye (autograft) or from a donor (allograft) to restore normal corneal epithelialization.
• Amniotic membrane grafting to ensure epithelialization and reduce fibrosis.

Surgical treatment in the long term may include the following interventions:

• Elimination of conjunctival adhesions and symblepharon.
• Transplantation of conjunctival or mucous flaps.
• Correction of eyelid deformities.
• Keratoplasty should be delayed for at least 6 months or longer to ensure maximum resolution of the inflammatory reaction.
• Keratoprosthesis can be performed on eyes with the most damage, since the results of traditional transplantation are unsatisfactory.