Chemical eye burns

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

The degree of chemical burn depends on the properties of chemical agents, the area of action on the surface of the eye, the duration of exposure (chemical retention on the surface of the eyeball), and the concomitant effects of the type of thermal exposure. Alkalides tend to penetrate deeper than acids, which coagulate surface proteins forming a protective barrier. Ammonia and sodium hydroxide cause serious damage due to rapid penetration. The hydrofluoric acid used in engraving and cleaning glass also has the property of rapidly penetrating the eye tissues, while the effect of sulfuric acid can be complicated by thermal and high-energy impact after explosions of automobile batteries.

[1], [2], [3], [4], [5], [6], [7]

Pathophysiology of chemical eye burn

Eye damage in severe chemical influences has the following mechanism:

• Necrosis of conjunctival and corneal epithelium with destruction and occlusion of limbal vascularization. The loss of limbal stem cells can subsequently lead to an increase in the conjunctiva and vascularization of the cornea or the formation of epithelial defects with ulceration and perforation. Other long-term effects include impaired wetting of the ocular surface, the formation of the symphobaron and cicatricial curvature.
• Deeper penetration causes the release and precipitation of glycosaminoglycans, the opacity of the stroma of the cornea.
• 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 the synthesis of collagen and the regeneration of the cornea.
• Hypotension and phthisis of the eyeball may develop.

Coronary epithelium and stroma healing:

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

Assessment of the severity of chemical eye burns

Acute chemical burns are divided by severity for the planning of appropriate treatment and final prognosis. Assessment of severity is made on the basis of the integrity of the transparency of the cornea and the severity of limbal ischemia. Later, the filling of the deep and superficial vessels of the limbus is assessed.

1. I degree: clear cornea and absence of limbal ischemia (excellent prognosis).
2. II degree: opacity of the cornea, but with visible details of the iris, ischemia less than 1/3 (120) limbs (good prognosis).
3. Ill degree: complete loss of corneal epithelium, turbidity of the stroma, masking the details of the iris, ischemia from 1/3 to half (from 120 to 180) limbs (cautious prognosis).
4. IV degree: Totally turbid cornea and ischemia more than half (> 180)) limb (very poor prognosis).

Other changes that should be considered in the initial evaluation: the length of epithelial loss of the cornea and conjunctiva, changes in the iris, lens condition and intraocular pressure.

[8], [9], [10], [11], [12]

Emergency help with chemical eye burn

Chemical burn is the only eye injury that requires immediate treatment without studying history and doing thorough research. Emergency care includes the following.

1. Abundant irrigation is necessary to minimize contact time with the chemical agent and as soon as possible to normalize the pH in the conjunctival cavity. Physiological saline (or its equivalent) is used to irrigate the eye for 15-30 minutes or until the pH normalizes completely.
2. Double eyelid reversal should be performed in such a way that each fragment of material remaining in the conjunctival vault, such as lime or cement, could be removed.
3. Surgical treatment of necrotic sections of the corneal epithelium should be performed taking into account subsequent re-epithelialization.

[13], [14], [15], [16]

Medical treatment of chemical eye burn

Moderate damage (I-II degrees) is treated with a short course of local steroids, cycloplegia and a prophylactic course of antibiotics for about 7 days. The main goal of treating more severe burns is to reduce inflammation, provide epithelial regeneration and prevent corneal ulceration.

1. Steroids reduce inflammation and neutrophilic infiltration, but they slow down stromal healing by reducing collagen synthesis and inhibiting the migration of fibroblasts. For this reason, topical application of steroids can be beneficial at the beginning of treatment and should be reversed through 7-10 in the afternoon, when the formation of the corneal ulcer is most likely. They can be replaced with non-steroidal anti-inflammatory drugs that do not affect the function of keratocytes.
2. Ascorbic acid alters the condition of the affected tissues and improves wound healing, providing the synthesis of mature collagen due to 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 potent inhibitor of neutrophil activity and reduces the intensity of the inflammatory reaction. The formation of extracellular calcium complex with citrates (chelacine) also inhibits collagenase. Local sodium citrate 10% is installed 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 inhibitors of collagenase and also inhibit neutrophil activity, reducing the ulceration reaction. Apply both topically and systemically (for example, doxycycline 100 mg 2 times a day).

Surgical treatment of chemical eye burn

Surgical treatment at an early stage may be necessary for revascularization of the limbus, restoration of the population of limbal cells and arches. One or more of the following interventions can be performed:

• Mobilization of the tenon capsule and hemming it to the limb in order to restore limbal vascularization, which prevents corneal ulceration.
• Transplantation of limbal stem cells from another patient's eye (autograft) or from a donor (allograft) to restore normal corneal epithelialization.
• Adding an amniotic membrane to ensure epithelialization and reduce fibrosis.

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

• Elimination of conjunctival and symphobaron.
• Transplant flaps of the conjunctiva or mucosa.
• Correction of eyelid deformities.
• Keratoplasty should be delayed for at least 6 months and later to ensure maximum resolution of the inflammatory response.
• Keratoprosthesis can be performed on the eyes with the greatest damage, as the results of the traditional transplantation are unsatisfactory.