Acid and Alkali Chemical Eye Burn

Acids

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The severity of the acid burn depends on the concentration of the chemical, the duration of the exposure and the PH of the solution. Inorganic acids include sulphuric acid, nitric acid and hydrochloric acid.

When splashed, these acids may burn the eyelids and face but fortunately the lid closure reflex is so fast that the eyeball is not generally affected. It may, however, suffer subsequently from exposure as a result of scar tissue formation and contraction of the lids.

All solutions are irritating to the eye but rarely serious if their PH is 2.5 or above. Diluted acids produce redness, oedema and small conjunctival hemorrhages. Prolonged exposure causes ulceration and opaqueness of the cornea and conjunctival epithelium. The epithelium normally regenerates to leave a clear cornea. However, if the acid is strong, then stromal opacification and corneal vascularization will occur. The tissues may even be charred by concentrated nitric or sulphuric acids and, in the severest cases, complete destruction of the cornea and anterior structures will result.

The damage caused by acids depends upon the protein affinity of the acid anion and the concentration of the acid. The acids act by combining chemically with the protein of the more superficial tissues to form an insoluble acid proteinate. This acts as a buffer, which limits the penetration of the acid through the tissues, cornea, etc.

Acid burns are generally less severe than alkali burns and they tend to improve with treatment and time. They are common in artificial silk manufacturing, as the viscous process exposes the workers to a fine spray of sulphuric acid. Acid burns are frequently associated with glass injuries resulting from flasks and bottles breaking and there have been reports of exploding car batteries causing sulphuric acid burns to the eyes.

In general, organic acids penetrate the cornea; only slightly and rarely cause dense corneal opacification. This group of acids includes formic, acetic and citric acids.

Alkalis

Alkalis penetrate tissues rapidly. They act by combing with the lipoid cells of the membranes and produce total disruption of cells with softening of the tissues. Once the alkali has gained entry to the corneal stroma, it progresses to Descemet's membrane by the cations combining temporarily with the mucoproteins and collagen. The mucoproteins are then denatured rapidly and the released cations attach themselves to even deeper stromal proteins. The initial appearance of the eye after trauma may be deceiving, showing little apparent damage but it may become worse with time, leaving a totally opaque cornea.

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Salts of weak acids and strong bases, such as sodium carbonate and organic amines have strong alkaline reactions; phenols also act similarly to alkalis.

The ocular effects of alkalis have been studied and noted to progress through three stages:

1. Acute stage: Ischaemic necrosis of the conjunctiva; sloughing of the corneal epithelium; oedema; and opacification of the subconjunctival tissue, the substantia propria and acute iritis.
2. Reparation stage: Epithelium regenerates, vascularization appears and the iritis subsides.
3. Late complications: Symblepharon; an opaque, vascularizated cornea with recurrent ulcerations; uveitis; secondary glaucoma; and cataract.

There is a rapid increase in the intra-ocular pressure after severe chemical burns, especially with alkalis. The mechanisms responsible for the increase in intra-ocular pressure are a temporary shrinkage of the corneal collagen and a breakdown of the blood aqueous barrier due to the lysis of the cells lining and adjacent to, the anterior chamber. This causes intense exudation of cells, etc. into the anterior chamber, which may lead to a severe fibrinous inflammatory reaction in the conjunctiva as well as in the anterior chamber of the eye. This leads to the later complication of symblepharon, an adhesion between the bulber and palpebral conjunctiva and a dry eye.

As the hydroxyl ion concentration increases, the severity of the effects increases; a PH above 11 is exceedingly dangerous. However, as alkalis have different fat solubilities, the penetration ability of the cornea varies. Ammonium hydroxide has the greatest ability to dissolve fats and it penetrates the cornea rapidly, to produce deep injury. Other chemicals frequently involved in burns are the sodium, potassium, ammonium and calcium hydroxides. Lime burns are very serious and commonly occur in building trades.

Calcium oxide is a major ingredient of substances such as cement, lime, mortar, white-washes and numerous other compounds used in industries. When water or tears are added to calcium oxide heat is created, causing a thermal burn. In addition, calcium hydroxide is produced, which increases the damage to the eye. Lime in particular, tends to adhere to the cornea and conjunctiva and causes excessive laceration.

Experiments carried out on rabbits have shown that corneal ulceration after an alkali burn is due to the collagenolytic enzyme produced by the cornea. This had led to the use of collagenase inhibitors, such as L-cysteine in the treatment of alkali burns to reduce the corneal ulceration. Other types of treatment include the use of EDTA, ascorbic acid and citric acid.