Alkalis

More than 25,000 chemical products with the potential to cause chemical eye injuries have been identified, many of which may be classified as acids or bases, oxidizing or reducing agents, or corrosives. The most frequently implicated chemical agents are acids and bases. The severity of the injury is related to the nature, concentration, quantity and pH of the chemical involved, and the duration and surface area of exposure.³ In particular, a history of a high-velocity (explosive) chemical or thermal injury should always raise suspicion of an associated intraocular foreign body.

Wet and dry cement, ammonia, lye, potassium hydroxide, magnesium hydroxide, and lime, constitute the most common causes of alkali injury to the eye.2,5,8 The severity of an alkali injury is governed by the pH, rather than the properties of the cation.² Therefore, the most severe injuries are typically caused by ammonia and lye⁸ which are both capable of rapid penetration into the eye. The damage inflicted by lime injuries is reduced by the formation of calcium soaps that precipitate and hinder further penetration.² Firework injuries deserve special mention as the presence of magnesium hydroxide results in a combined chemical and thermal injury. The most important agents causing alkali and acid injuries to the eye are summarized in Table 29.1.

Acids

The most common causes of acid burns are sulphuric, sulphurous, hydrofluoric, acetic, chromic, and hydrochloric acids.² The strength of an acid depends on its ability to lose a proton; strong acids ionize completely in an aqueous solution. However, the most severe acid injuries are caused by hydrofluoric acid, as a result of its unique properties. In addition to the action of the dissociated proton, which is the primary mechanism of damage by other acids, hydrofluoric acid has a unique dissolving action which allows it to quickly penetrate into deeper tissues.² Moreover, hydrofluoric acid chelates all calcium and magnesium from cells, thereby halting cellular biochemical activity.

Although alkalis typically cause the most serious chemical injuries, the presence of an acid injury does not preclude an equally devastating ocular injury as very strong acids penetrate just as rapidly as alkalis. Indeed, studies have shown no clinically significant differences in clinical course and prognosis between severe acid and alkali burns.⁹

Structural and Biochemical Alterations

The severity of an ocular chemical injury is influenced by the ability of the chemical to penetrate the eye. Alkalis characteristically penetrate the eye more rapidly than acids.2,3,10 The hydroxyl ion (OH) saponifies plasma membranes, resulting in cell disruption and death, while the cation is responsible for the penetration of the specific alkali.^2,3,10 Stronger alkalis are associated with more rapid penetration and the penetration rate increases in ascending order from calcium hydroxide, potassium hydroxide, sodium hydroxide to ammonium hydroxide.¹⁰ Changes in aqueous humor pH are observed within a few seconds of contact with ammonium hydroxide, and within 3–5 minutes after sodium hydroxide injury.^10,11 Ultimately, irreversible tissue damage occurs when the pH rises above 11.5.^2,10

In alkali injuries, cations react with the carboxyl (COOH) groups of stromal collagen and glycosaminoglycans.2,10 Hydration of glycosaminoglycans results in loss of clarity of the stroma, whereas, hydration of collagen fibrils causes distortion of the trabecular meshwork and the release of prostaglandins, these sequelae combine to produce elevations in intraocular pressure.¹⁰

In general, as previously noted, acids penetrate the corneal stroma much less readily than alkalis.2,3,10,12 The hydrogen ion mediates damage due to pH alteration, while the anion causes precipitation and denaturation of proteins in the corneal epithelium and anterior stroma.¹⁰ Precipitation of the epithelial proteins affords a degree of protection by providing a physical barrier against further ingress.^2,3,10,12 However, in the event that an acid succeeds in penetrating the stroma, the damage to ocular structures is similar to that observed in alkali injury.² Alterations include precipitation of extracellular glycosaminoglycans and corneal opacification, distortion of the trabecular meshwork, changes in anterior chamber pH, damage to anterior chamber structures, and reduced aqueous ascorbate levels.^2,10 Vascular damage results in ischemic injury.

Both acids and bases may mediate osmolar damage to the delicate physiology of the cornea.² Chemical insults to the eye may initiate large changes in osmolarity, and the resultant osmolar stress gives rise to cellular dysfunction and destruction. The limited buffering capacity of the cornea affords little protection against a variety of chemical and toxic insults. In the event that the buffering capacity is overwhelmed, there is an immediate cessation of biochemical activity, such as protein synthesis.¹³

Injury, Repair and Differentiation

Inflammation

Chemical injury to the eye is associated with a dramatic release of pro-inflammatory mediators and the infiltration of inflammatory cells into injured tissue. Regulation of this inflammatory response is crucial, as a robust and prolonged inflammatory response may have a detrimental effect on wound healing.

Severe chemical injuries are characterized by two waves of inflammation; the first wave occurs in the first 24 hours and the second wave begins at approximately 7 days and peaks 2 to 3 weeks post injury. The intensity of the first wave may be critical for the recruitment of the second wave.² The second wave of inflammation coincides with the period of maximal corneal degradation and repair, and may facilitate the sterile enzymatic digestion of the corneal stroma. Sterile ulceration is associated with the infiltration of polymorphonuclear leukocytes, and conversely, the exclusion of inflammatory cells from the corneal stroma is associated with cessation of sterile ulceration.²

Sequelae

A summary of potential ophthalmic sequelae of chemical burns is provided in Table 29.2. Figure 29.1 highlights some of the complications of chemical burns.

Irrigation

Emergency management is oriented towards prompt irrigation and the removal of residual chemical debris from the eye. The objectives are to minimize the ingress of the chemical agent into the anterior chamber, and to remove a potential reservoir for ongoing injury. The most important intervention is immediate copious irrigation at the scene of the incident.17,18 Irrigation should be continued until pH neutralization is achieved. Animal models have demonstrated that external irrigation for 90 minutes reduces the pH by 1.5 units.¹¹ In a non-controlled human study involving 66 eyes, immediate copious irrigation resulted in less severe injury, compared with eyes which were not irrigated.¹⁷ Although there may be an advantage in the use of amphoteric buffering solutions,¹⁰ urgency may necessitate the use of any available neutral irrigation fluid.

Where possible, topical anesthetic drops should be applied to reduce pain and blepharospasm, thereby enhancing irrigation. Care should be taken to remove all particulate matter, and this mandates eyelid eversion (double eversion may be necessary) and cleaning of the fornices. In some severe cases, a general anesthetic or sedation may be necessary to effectively remove particulate matter.

Aqueous Humor Replacement

External irrigation is of limited value in eliminating chemicals once they have reached the intraocular chambers. Animal models of alkali injuries have shown that paracentesis lowers the aqueous humor pH by 1.5 pH units. Subsequent anterior chamber reformation, with buffered phosphate solution, lowers the aqueous humor pH by a further 1.5 pH units.¹¹ However, the value of paracentesis and irrigation of the anterior chamber following a severe chemical injury remains controversial.² Nonetheless, it may be reasonable to consider aqueous humor replacement in patients with severe injuries presenting within the first 2 hours post exposure.