Chapter 6:
Cornea
Author:
PHYSIOLOGY
The cornea functions as a protective membrane and a "window" through which light rays pass to the retina. Its transparency is due to its uniform structure, avascularity, and deturgescence. Deturgescence, or the state of relative dehydration of the corneal tissue, is maintained by the active bicarbonate "pump" of 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 chemical or physical 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. On the other hand, damage to the epithelium causes only transient, localized edema of the corneal stroma that clears when the epithelial cells regenerate. Evaporation of water from the precorneal tear film produces hypertonicity of the film; that process and direct evaporation are factors that draw 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. To pass through the cornea, drugs must therefore have both a lipid-soluble and a water-soluble phase.
CORNEAL RESISTANCE TO INFECTION
The epithelium is an efficient barrier to the entrance of microorganisms into the cornea. Once the epithelium is traumatized, however, the avascular stroma and Bowman's layer become susceptible to infection with a variety of organisms, including bacteria, amebas, and fungi. Streptococcus pneumoniae (the pneumococcus) is a true bacterial corneal pathogen; other pathogens require a heavy inoculum or a compromised host (eg, 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 and fungi.
Local or systemic corticosteroids modify the host immune reaction in several ways and may allow opportunistic organisms to invade and flourish.
PHYSIOLOGY OF SYMPTOMS
Since the cornea has many pain fibers, most corneal lesions, superficial or deep (corneal foreign body, corneal abrasion, phlyctenule, interstitial keratitis), cause pain and photophobia. The pain 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 somewhat, 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 minimal in herpetic keratitis because of the hypesthesia associated with the disease, which is also a valuable diagnostic sign.
Although tearing and photophobia commonly accompany corneal disease, there is usually no discharge except in purulent bacterial ulcers.
INVESTIGATION OF CORNEAL DISEASE
Symptoms & Signs
The physician examines the cornea by inspecting it under adequate illumination. Examination is often facilitated by instillation of a local anesthetic. Fluorescein staining can outline a superficial epithelial lesion that might otherwise be impossible to see. The biomicroscope (slitlamp) is essential in proper examination of the cornea; in its absence, a loupe and bright illumination can be used. One should follow the course of the light reflection while moving the light carefully over the entire cornea. Rough areas indicative of epithelial defects are demonstrated in this way.
The patient's history is important in corneal disease. A history of trauma can often be elicited-in fact, foreign bodies and abrasions are the two most common corneal lesions. A history of corneal disease may also be of value. The keratitis of herpes simplex infection is often recurrent, but since recurrent erosion is extremely painful and herpetic keratitis is not, these disorders can be differentiated by their symptoms. The patient's use of local medications should be investigated, since corticosteroids may have been used and may have predisposed to bacterial, fungal, or viral disease, especially herpes simplex keratitis. Immunosuppression also occurs with systemic diseases, such as diabetes, acquired immume deficiency syndrome (AIDS), and malignant disease, as well as with specific immunosuppressive therapy.
Laboratory Studies
To select the proper therapy for corneal infections, especially suppurating ulceration, laboratory aid is essential. Bacterial and fungal ulcers, for example, require completely different medications. Since a delay in identifying the organism may severely compromise the ultimate visual result, scrapings from the ulcer should be stained by both Gram's and Giemsa's stains and the infecting organism identified if possible while the patient waits. Cultures for bacteria and fungi must be done at the same time, since identification of the organism is critical. Appropriate therapy can then be instituted immediately. Therapy should not be withheld if an organism cannot be identified by smear and staining.
Morphologic Diagnosis of Corneal Lesions
A. Epithelial Keratitis:
The corneal epithelium is involved in most types of conjunctivitis and keratitis and in rare cases may be the only tissue involved (eg, in superficial punctate keratitis). The epithelial changes vary widely from simple edema and vacuolation to minute erosions, filament formation, partial keratinization, etc. The lesions vary also in their location on the cornea. All of these variations have important diagnostic significance (Table 6-1), and biomicroscopic examination with and without fluorescein staining should be a part of every external eye examination.
B. Subepithelial Keratitis:
There are a number of important types of discrete subepithelial lesions. These are often secondary to epithelial keratitis (eg, the subepithelial infiltrates of epidemic keratoconjunctivitis, caused by adenoviruses 8 and 19). They can usually be observed grossly but may also be recognized in the course of biomicroscopic examination of epithelial keratitis
C. Stromal Keratitis:
The responses of the corneal stroma to disease include infiltration, representing accumulation of inflammatory cells; edema manifested as corneal thickening, opacification, or scarring; thinning or melting, which may lead to perforation; and vascularization. The patterns of these responses are less specific for disease entities than those seen in epithelial keratitis, and the clinician often must rely on other clinical information and laboratory studies for clear identification of causes
D. Endothelial Keratitis:
Dysfunction of the corneal endothelium results in corneal edema, initially involving the stroma and later the epithelium. This contrasts with corneal edema due to raised intraocular pressure, in which the epithelium is affected before the stroma. As long as the cornea is not too edematous, it is often possible to visualize morphologic abnormalities of the corneal endothelium with the slitlamp. Inflammatory cells on the endothelium [keratic precipitates (KPs)] are not always an indication of endothelial disease because they are also a manifestation of anterior uveitis, which may or may not accompany stromal keratitis.
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10.1036/1535-8860.ch6