The cornea functions both as a protective barrier and as a “window” through which light rays pass to the retina. Its transparency is due to its uniform structure, avascularity, and deturgescence (see Chapter 1). Deturgescence, or the state of relative dehydration of the corneal tissue, is maintained by the bicarbonate “pump” provided by the endothelium and the barrier function of the epithelium and endothelium. The endothelium is more important than the epithelium in the mechanism of dehydration, and damage to the endothelium is far more serious than damage to the epithelium. Destruction of the endothelial cells causes edema of the cornea and loss of transparency, which is more likely to persist because of the limited potential for recovery of endothelial function. Damage to the epithelium usually causes only transient, localized edema of the corneal stroma that clears with the rapid regeneration of epithelial cells. Evaporation of water from the precorneal tear film produces hypertonicity of the film. Together with direct evaporation, this draws water from the superficial corneal stroma in order to maintain the state of dehydration.
Penetration of the intact cornea by drugs is biphasic. Fat-soluble substances can pass through intact epithelium, and water-soluble substances can pass through intact stroma. Therefore, to pass through the cornea, drugs must be soluble in both lipids and water.
Corneal Resistance to Infection
The epithelium is an efficient barrier to the entrance of microorganisms into the cornea. If the epithelium is defective, the avascular stroma and Bowman's layer become susceptible to infection with a variety of organisms, including bacteria, Acanthamoeba, and fungi. Streptococcus pneumoniae (the pneumococcus) is a true bacterial corneal pathogen; other pathogens require a heavy inoculum, compromised barrier function, or a relative immune deficiency to produce infection.
Moraxella liquefaciens, which occurs mainly in alcoholics (as a result of pyridoxine depletion), is a classic example of the bacterial opportunist, and in recent years a number of new corneal opportunists have been identified. Among them are Serratia marcescens, Mycobacterium fortuitum-chelonei complex, viridans streptococci, Staphylococcus epidermidis, and various coliform and proteus organisms, along with viruses, Acanthamoeba, and fungi.
Local or systemic corticosteroids modify the host immune reaction in several ways and may allow opportunistic organisms to invade and flourish.
Since the cornea has many pain fibers, most superficial or deep corneal lesions cause pain and photophobia. The pain of epithelial disease is worsened by movement of the lids (particularly the upper lid) over the cornea and usually persists until healing occurs. Since the cornea serves as the “window” of the eye and refracts light rays, corneal lesions usually blur vision, especially if centrally located.
Photophobia in corneal disease is the result of painful contraction of an inflamed iris. Dilation of iris vessels is a reflex phenomenon caused by irritation of the corneal nerve endings. Photophobia, severe in most corneal disease, is ...