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Keratitis is the medical term for inflammation of the cornea. The cornea is the dome-shaped window in the front of the eye. When looking at a person's eye, one can see the iris and pupil through the normally clear cornea. The cornea bends light rays as a result of its curved shape and accounts for approximately two-thirds of the eye's total optical power, with the lens of the eye contributing the remaining one-third.. Only the very thin tear film lies between the front of the cornea and our environment. The cornea is about 0.5 millimeter thick. The back of the cornea is bathed in the aqueous fluid that fills the anterior chamber of the eye. The cornea has a diameter of about 13 millimeters ( inch) and, together with the sclera (the white part of the eye) forms the entire outer coat of the eye.
Bacteria most frequently responsible for keratitis include Staphylococci, Hemophilus, Streptococci, and Pseudomonas. If the front surface of the cornea has been damaged
by a small scratch and the surface is not intact, almost any bacteria, including atypical mycobacteria, can invade the cornea and result in keratitis. Ulcerations of the cornea may occur, a condition known as ulcerative keratitis. Before the advent of antibiotics, syphilis was a frequent cause of keratitis. Viruses that infect the cornea include respiratory viruses, including the adenoviruses and others responsible for the common cold. The herpes simplex virus is another common cause of keratitis. There are about 20,000 new cases of ocular herpes in the United States annually, along with more than 28,000 reactivations of the infection. There are about 500,000 people in the U.S. with a history of herpes simplex eye disease. The herpes zoster virus (the virus responsible for chickenpox and shingles) may also cause keratitis if shingles involve the forehead. Fungi such as Candida, Aspergillus, and Nocardia are unusual causes of microbial keratitis, more frequently occurring in people who are immunocompromised because of underlying illnesses or medications. Fusarium keratitis, a type of fungal infection, occurs primarily in contact-lens wearers. Bacterial co-infection can complicate fungal keratitis. Contact-lens wearers are also susceptible to acanthamoeba keratitis caused by an amebic parasite. "River blindness," or onchocercal keratitis, is another parasitic infection of the cornea, rarely seen in developed countries but very common in the Third World.
Physical or chemical trauma is a frequent cause of keratitis. The injury may become secondarily infected or remain noninfectious. Retained corneal foreign bodies are frequent sources of keratitis. Ultraviolet light from sunlight (snow blindness), a tanning light or a welder's arc, contact-lens overwear, and chemical agents, either in liquid form splashed into the eye or in gases in the form of fumes can all result in noninfectious keratitis. Chemical injury or contact lens-related keratitis often causes superficial punctate keratitis, in which the examiner notices myriads of injured surface cells on the affected cornea. Disturbances in the tear film may lead to changes in the corneal surface through drying of the corneal epithelium. This type of keratitis is usually superficial and most commonly is related to dry eyes and is known as keratitis sicca. If the eyes are extremely dry, the surface cells may die and form attached filaments on the corneal surface, a condition known as filamentary keratitis. Inability to close the eyelids properly can also lead to cornea drying, which is a condition termed exposure keratitis. Allergies to airborne pollens or bacterial toxins in the tears may also cause a noninfectious type of keratitis. Autoimmune diseases create a similar appearance, often affecting the periphery of the cornea, termed marginal keratitis or limbic keratitis.
for keratitis?
Major risk factors for the development of keratitis include any break or disruption of the surface layer (epithelium) of the cornea. The use of contact lenses increases the risk for the development of keratitis, especially if when poor hygiene, improper solutions, or overwear are associated with contact-lens use.
A decrease in the quality or quantity of tears predisposes the eye to the development of keratitis. Disturbances of immune function through diseases such as AIDS or the use of medications such as corticosteroids or chemotherapy also increase the risk of developing keratitis.
With proper diagnosis and appropriate treatment including follow-up care, keratitis can usually be managed without causing permanent visual disturbances.
Keratitis At A Glance
Keratitis is the medical term for inflammation of the cornea. Keratitis has many causes, including infection, dry eyes, physical and chemical injury, and underlying medical diseases. The diagnosis of keratitis is made by the use of a slit lamp. If keratitis is treated correctly and promptly, permanent damage to the eye can usually be avoided.
REFERENCES: Acharya, N.R., M. Srinivasan, J. Mascarenhas, et al. "The Steroid Controversy in Bacterial Keratitis." Arch Ophthalmol. 127.9 Sept. 2009: 1231. American Academy of Ophthalmology Cornea/External Disease Panel, Preferred Practice Patterns Committee. "Bacterial Keratitis." San Francisco: American Academy of Ophthalmology (AAO), 2008. Morgan, P.B., N. Efron, N.A. Brennan, et al. "Risk Factors for the Development of Corneal Infiltrative Events Associated With Contact Lens Wear." Invest Ophthalmol Vis Sci. 46.9 Sept. 2005: 3136-3143. Poggio, E.C., R.J. Glynn, and O.D. Schein. "The Incidence of Ulcerative Keratitis Among Users of Daily-Wear and Extended-Wear Soft Contact Lenses." N Engl J Med. 321.12 Sept. 21, 1989: 779-783.
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Medical Care
Many therapies for TSPK have been tried and proven unsuccessful over the years. Antibiotics have been shown to be an ineffective treatment method.[2] Antivirals have had mixed results; mild improvements have been reported with trifluridine, but it has also been reported to cause the disease to disappear more slowly than when treated with corticosteroids alone.[18] In addition, there have been multiple observations that idoxuridine causes persistent subepithelial ghost opacities and scarring in individuals with TSPK; therefore, it is contraindicated.[2, 10, 19]
A few successful therapies for TSPK do exist. Topical lubricants have been shown to be an effective treatment method for relieving clinical symptoms.[20] Topical corticosteroids are now considered to be the mainstream treatment of TSPK, as they have been shown to be very successful in managing both clinical signs and symptoms; however, there is speculation that the natural course of the disease is prolonged secondary to the introduction of these medications.[2, 5] In addition, topical cyclosporine has been reported to be effective when used as a first-line treatment of patients with TSPK, with the advantage of fewer adverse effects compared with corticosteroids.[12, 21, 22] Therapeutic soft contact lenses used on an extended-wear basis also offer an alternative treatment, especially for severe cases, although potential complications (eg, microbial keratitis) may exist.[21, 23] Contact lenses improve symptoms by covering the elevated corneal lesions and nerves, which are constantly in friction with the conjunctiva during blinking.[2, 24] Nagra et al have had overwhelming success with topical corticosteroids, and they suggest an initial management of TSPK with fluorometholone 0.1% (FML 0.1%) or a similar low-dose steroid, followed by the use of stronger steroids, and then extended-wear contact lenses or topical cyclosporine in a stepwise approach.[5] They reinforce an important point that steroids must be tapered gradually over the course of months in many patients, with some patients requiring longer term, infrequent, but regular use (ie, weekly, biweekly). Since therapy is aimed at providing patients with comfort, clinicians should be aware that the minimum strength and dosage of topical anti-inflammatory medications necessary to control symptoms should be prescribed.[17]
Anti-inflammatory agents
Class Summary
These agents decrease inflammation.
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Fluorometholone (FML)
Inhibits edema, fibrin deposition, capillary dilation and phagocytic migration of acute inflammatory response and capillary proliferation, collagen deposition, and scar formation. Decreases inflammation and corneal neovascularization. Suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability. Believed to act by the induction of phospholipase A-2 inhibitory proteins. Used topically, it can elevate IOP and cause steroid-response glaucoma. In clinical studies of documented steroid responders, fluorometholone demonstrated a significantly longer average time to produce a rise in IOP than dexamethasone phosphate. In a small percentage of
individuals, a significant rise in IOP occurred within 1 wk. The ultimate magnitude of the rise was equivalent.
Lubricants, ocular
Class Summary
These agents increase lubrication of the eye.
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Artificial tears (Refresh Tears, Optive, Systane, Celluvisc, Murine, Refresh, Tears Naturale, GenTeal, TheraTears)
Used to increase lubrication of the eye. Contains equivalent of 0.9% NaCl and maintains ocular tonicity. Acts to stabilize and thicken precorneal tear film and prolong tear film breakup time, which occurs with dry eye states. Preparations that have hydroxymethylcellulose or dextran are more viscous and, therefore, can last longer before needing to be reapplied. Preservative-free artificial tears are preferred to avoid preservativeassociated ocular reactions.
Immunomodulators
Class Summary
Cyclosporine ophthalmic drops are thought to act as a partial immunomodulator. The exact mechanism of action is not known.
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Used to relieve dry eyes caused by suppressed tear production secondary to ocular inflammation. Thought to act as partial immunomodulator. Exact mechanism of action is not known.