Transient corneal stromal edema induced by cold has been reported in a variety of settings, including individuals with Raynaud disease and those with cranial nerve V (trigeminal) dysfunction. Research suggests that sensory denervation of the eye influences ocular temperature regulation and alters the morphologic characteristics and the function of corneal cells, including the endothelium.
Ultraviolet Radiation
The corneal epithelium is highly susceptible to injury from ultraviolet (UV) radiation. Initially, the patient is asymptomatic; painful foreign-body sensation and photophobia typically begin a few hours after exposure, when the injured epithelial cells are shed. The condition is generally self-limited, and the epithelium heals within 24 hours.
The most common causes of ocular UV injuries are unprotected exposure to sunlamps, arc welding, and prolonged outdoor exposure to reflected sunlight. Snow blindness, which occurs in skiers and mountain climbers, is caused by UV light reflected from snow. Appropriate protection with UV-filtering eyewear can prevent such injuries. Treatment consists of patching to minimize discomfort from eyelid movement, topical antibiotic ointment, and cycloplegia. If discomfort is severe, patients may require oral analgesics.
Ionizing Radiation
Exposure to ionizing radiation may be associated with nuclear explosions, x-rays, and radioisotopes. The amount of exposure is related to the amount of energy, the type of rays emitted, and the patient’s proximity to the ionizing source. Tissue destruction may be the result of direct killing of cells; cellular DNA changes that produce lethal or other mutations; or radiation damage to blood vessels, with secondary ischemic necrosis. Longer wavelengths penetrate less deeply, causing a more intense reaction in superficial layers. Shorter wavelengths penetrate to deeper tissues and may not cause extensive damage to superficial tissues.
Most cases of ocular exposure to ionizing radiation involve the conjunctiva, cornea, and possibly the lacrimal glands. Conjunctival edema occurs acutely, often followed by scarring, shrinkage, loss of tear production, and alterations in conjunctival blood vessels with telangiectasia. Necrosis of the conjunctiva and underlying sclera can occur if radioactive material (or a radiomimetic agent such as mitomycin C) is embedded in the conjunctiva. Punctate corneal epithelial erosions are seen acutely. Explosions involving ionizing radiation may lead to perforation of ocular tissues with immediate radiation necrosis.
Management of acute problems includes removal of all foreign bodies. Poor wound healing is a hallmark of ionizing radiation injuries. Late complications are related to lack of tears, loss of corneal sensation, loss of corneal epithelium and its failure to heal, secondary microbial keratitis, vascularization, and keratitis. Depending on the severity of the injury, artificial tears, a bandage soft contact lens, tissue adhesive, or tarsorrhaphy may be necessary to stabilize the ocular surface. If there is recurrent epithelial breakdown despite these measures, significant conjunctival scarring typically precludes the use of a conjunctival flap. If the fellow eye has not been injured, a contralateral autologous conjunctival flap may be helpful. Alternatively, an amniotic membrane transplant, limbal stem cell transplant, or mucous membrane graft may be employed. The prognosis for penetrating keratoplasty in these situations is poor due to the severely compromised ocular surface.
Chemical Injuries
Chemical trauma to the external eye is a common problem that can range in severity from mild irritation to complete destruction of the ocular surface epithelium, corneal opacification, loss of vision, and even loss of the eye. The offending chemical may be in the form of a solid, liquid, powder, mist, or vapor. Chemical injuries can occur in the home, most commonly from detergents, disinfectants, solvents, cosmetics, drain cleaners, oven cleaners, ammonia, bleach, and other common household alkaline agents. Fertilizers and pesticides are common offending agents in agricultural chemical injuries. In the workplace, plaster and cement products are frequent causes of alkali burns due to calcium hydroxide. Chemical injuries occurring in industry are usually caused by caustic chemicals and solvents. Some of the worst ocular chemical injuries result when strong alkalis (eg, lye) or acids are used for assault.
Whenever possible, the offending chemical agent should be identified, because the severity of a chemical injury depends on the pH, the volume and duration of contact, and the inherent toxicity of the chemical. The most severe chemical injuries are caused by strong alkalis and, to a lesser extent, acids. These solutions cause damage by drastically altering the concentration of highly reactive hydrogen and hydroxyl ions in affected tissues.
Alkali Burns
Strong alkalis raise the pH of tissues and cause saponification of fatty acids in cell membranes and ultimately cellular disruption. Once the surface epithelium is damaged, alkaline solutions readily penetrate the corneal stroma, where they rapidly destroy the proteoglycan ground substance and collagen fibers of the stromal matrix. Strong alkaline substances may also penetrate the anterior chamber, producing severe tissue damage and intense inflammation.
The visual prognosis is often determined by the extent of ocular surface injury (Table 13-1) and the presence and degree of skin burns and their effect on eyelid function. The most unfavorable visual prognosis is associated with extensive limbal epithelial damage and intraocular chemical penetration. The limbus contains corneal epithelial stem cells; hence, damage to this area can lead to a disruption in the normal repopulation of the corneal epithelium. Severe damage to the limbal area can be appreciated as limbal “blanching”—as the vascular supply to this critical area is disrupted via death of vascular endothelial cells. Resultant ischemia to the limbus and anterior segment can have dire consequences for eyes thus affected (Figs 13-1, 13-2, 13-3). Repopulation of the corneal surface epithelium with cells that do not have the proper degree of differentiation leads to “conjunctivalization” of the cornea, which is associated with vascularization, poor epithelial adhesion and recurrent breakdown, and possibly chronic inflammation if the original trauma is severe. Intraocular chemical penetration is often accompanied by cataract formation and secondary glaucoma; the latter is thought to result from damage to the outflow tract and conjunctival cicatrization, which can affect outflow facility. In the most severe cases, phthisis of the globe may occur.
Colby KA. Chemical injuries of the eye. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2010, module 1.
Table 13-1
Figure 13-1 Mild, grade II alkali burn. Note inferior scleral ischemia. (Courtesy of James J. Reidy, MD.)
Figure 13-2 Moderate, grade III alkali burn with corneal edema and haze.