I. Etiology
Herpes simplex keratitis is a type of viral keratitis caused by herpes simplex virus type I, which is a larger DNA virus with a relatively widespread presence. It has an affinity for neural tissue and epithelial cells derived from the ectodermal lobe. Infants over six months of age are not immune to the herpes virus due to the decreasing amount of gammaglobulin received from the mother. The virus can enter the basal cells when the epithelium of the eyes, lips, oral mucosa and skin is damaged.
Two common clinical types are
1, dendritic keratitis: However, about 25% of first-episode cases recur within two years, while the recurrence rate of second-episode cases rises to 50%.
2, chronic superficial herpetic keratitis: all layers of the cornea are occupied by extensive scarring and neovascularization, vision is severely impaired.
3, disciform keratitis: 90% is caused by herpes simplex virus, with a few caused by herpes zoster, cowpox vaccine, mumps or varicella virus. Severe substantial deep damage, can invade the entire corneal parenchyma in diffuse substantial keratitis.
Corneal epithelial edema, can form blisters, and often accompanied by uveitis, called herpetic keratitis uveitis. Corneal vascularization occurs and forms dense scars after healing. The pain is aggravated when secondary glaucoma occurs.
4, chronic herpetic corneal ulcer: a more serious type of deep substantive damage, is a shallow herpes damage after treatment with corticosteroids ulcer deepened and expanded. The ulcer pattern often maintains a much wider dendritic pattern (geoglyph), but is deep and often accompanied by pus accumulation in the anterior chamber. Secondary infection by mycobacteria or bacteria is present in about half of the cases. Deep ulcers can lead to perforation.
III. Diagnosis
1. History questioning: any previous history of herpetic skin damage or monoherpetic keratoconjunctivitis, and any recent precipitating factors (e.g., history of fever). Irritating symptoms such as foreign body sensation, shyness, lacrimation and blurred vision may appear in the eyes (obvious in children, less so in adults).
2, eye examination: primary infection often has herpetic lesions on the eyelids or lid margins, and is often accompanied by painless preauricular lymph node enlargement. The conjunctiva often shows changes of acute follicular conjunctivitis, and the cornea may show typical dendritic or other forms (such as dotted, stellate, map-like, disc-like, etc.) of damage. Corneal hypoesthesia is one of the more characteristic signs to help diagnose this disease.
IV. Treatment
Since primary herpes simplex keratitis is mostly a self-limiting disorder, it generally does not remain cloudy after healing, so only hot compresses, dilated pupils, local bandages or eye pads are needed to prevent secondary infection. If you apply 0.5% herpes ophthalmic ointment locally, five times a day, you can shorten the course of the disease and prevent it from becoming worse.
For secondary herpes simplex keratitis, because of the complexity of the clinical process, the relapse, easy to recur, the damage to eye function, so clinically advocate for more therapies, is briefly described as follows.
1, removal of epithelial cells containing the virus (debridement and cautery method).
2, local application of antiviral drugs; the ideal antiviral drugs should.
(1) act only on the virus without affecting the host cells.
(2) low concentration that can completely inhibit the division and reproduction of the virus.
3. immunotherapy.
4, surgical therapy: for those who do not respond to drug therapy, conjunctival flap plasty or lid margin suture can be used.
For recurrent recurrent herpetic keratitis, despite various treatments still persist, and there is a tendency of perforation, you can consider corneal transplantation, but the results are not very satisfactory. In particular, lamellar keratoplasty is more prone to recurrence than penetrating, probably because the virus latent in the corneal parenchyma has not been completely removed. Discontinuing corticosteroids for several weeks prior to surgery and having no active lesions in the eye is more appropriate for penetrating transplantation.