Stromal Keratitis


Stromal keratitis

Description, Causes and Risk Factors:

Stromal keratitis is a viral infection of the eye caused by the herpes simplex virus (HSV). There are two major types of the virus. Type I is the most common and primarily infects the face, causing the familiar "cold sore" or "fever blister." Type II is the sexually transmitted form of herpes, infecting the genitals.

While both Type I and Type II herpes can spread to the eye and cause infection, Type I is by far the most frequent cause of stromal keratitis. Infection can be transferred to the eye by touching an active lesion (a cold sore or blister) and then your eye.

Type I herpes is very contagious and is commonly transmitted by skin contact with someone who has the virus. Almost everyone — about 90 percent of the population — is exposed to Type I herpes, usually during childhood. After the original infection, the virus lies in a dormant state, living in nerve cells of the skin or eye. Reactivation can be triggered in a number of ways, including:

    Stress.

  • Sun exposure.

  • Fever.

  • Trauma to the body (such as injury or surgery).

  • Menstruation.

  • Certain medications.

Once herpes simplex is present in the eye, it typically infects the eyelids, conjunctiva and cornea. It may also infect the inside of the eye; however, this is much less common.

Other conditions causing stromal keratitis include Epstein Barr virus, mumps, measles, Lyme disease, Acanthamoeba infection, tuberculosis, syphilis, sarcoidosis and onchocerciasis. However, the most common cause of active stromal keratitis is the herpes simplex virus, accounting for over 70% of unilateral active cases. Syphilis is the cause of approximately 50% of bilateral inactive cases. Although syphilis is the leading cause of inactive, bilateral stromal keratitis, it is actually responsible for less than 20% of total cases.

There are two types of stromal keratitis that may occur during herpes simplex infections: necrotizing and non-necrotizing. Necrotizing stromal keratitis is a more severe form of herpetic stromal keratitis and manifests as a dense, cheesy, yellow-white stromal infiltration often following recurrent herpetic disease. There will be epithelial ulceration, stromal edema, dense vascularization, profound corneal thinning, and possible perforation. Non-necrotizing stromal keratitis does not have the same propensity to move toward ulceration, thinning, and perforation. Untreated, non-necrotizing stromal keratitis runs an indolent, self-limiting course over several months. Fortunately, the majority of stromal keratitis cases are non-necrotizing.

Of the estimated 50,000 cases reported annually in the U.S., about 50% are estimated to be recurrent cases. Recurrent infections are more likely to invade the corneal stroma and cause scarring and loss of vision. Stromal manifestations appear in approximately 25% of recurrences. Whereas the epithelial form of the disease is a direct result of the viral infection itself, stromal keratitis appears to be a largely immune-mediated disease.

Symptoms:

Patients with stromal keratitis will present with pain, photophobia, lacrimation, and blepharospasm. Vision is typically reduced in the acute, active phase. The presentation may be either unilateral or bilateral. There will often be a history of ocular infection or systemic disease.

Diagnosis:

The disease is often diagnosed with a slit lamp examination. Tinted eye drops that highlight the affected areas of the cornea may be instilled to help the doctor evaluate the extent of the infection.

Treatment:

Stromal keratitis are often treated with combined corticosteroid and antiviral therapy. Frequent topical steroid therapy is initially prescribed. The dose is subsequently titrated, based on clinical response, to the lowest dosage necessary to control inflammation. Concurrent antiviral medication is used to prevent or limit lytic epithelial keratitis. The optimal dose and the route of administration have not been determined. One common recommendation is to use a topical antiviral agent and a corticosteroid with equal frequency until the steroid dosage can be reduced to a once-daily or less regimen. Alternatively, oral acyclovir in moderate doses (1-2 g/d) achieves therapeutic concentrations in the aqueous humor and may be more effective than topical agents in treating HSV keratouveitis. In necrotizing stromal keratitis, systemic antiviral is also preferred because of corneal toxicity concerns.

Irregular astigmatism resulting from chronic stromal keratitis may be correctable with rigid gas-permeable contact lenses. Patients with visually significant corneal opacities or corneal perforations may require penetrating keratoplasty for visual rehabilitation. If possible, a small descemetocele or perforation in an inflamed eye may initially be managed with tissue adhesive, bandage contact lens, and/or amniotic membrane transplantation. Corneal transplantation should ideally be deferred until the eye is less inflamed.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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