Herpes zoster virus scleritis

Introduction to herpes zoster viral scleritis The initial infection of the virus is often manifested as chickenpox. The virus is latently lurking in the body and activated by certain factors, and then manifested as banded sores, both of which are acute infectious diseases, which are very clinically and epidemiologically The difference is generally self-limiting, rarely due to serious complications, and scleritis caused by the virus is rare, and occurs several months after the initial infection of the virus. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific people Mode of infection: non-infectious Complications: glaucoma

The cause of herpes zoster viral scleritis

(1) Causes of the disease

Herpes zoster is caused by reactivation of varicella-zoster virus (VZV). VZV morphology is indistinguishable from HSV. It belongs to DNA virus but has different antigenicity. VZV contains at least five glycoproteins with a DNA molecular weight of approximately 80 million. Humans are the only known natural host of the virus.

(two) pathogenesis

Varicella and herpes zoster are two independent clinical manifestations of this disease in different immune populations. The primary infection caused by non-immune people (usually referred to as children) is chickenpox, more than 90% in the United States. Adults have had VZV infection, and the infection persists without clinical symptoms. The virus exists in a latent form in the trigeminal ganglion. The body's immune system cannot effectively eliminate the virus, and only produces immunological mechanisms. Usually it is infected with VZV 10 for the first time. After the year, 20% of people cause recurrent infection to produce herpes zoster, herpes zoster mostly invades the thoracic nerve, 9% to 16% of patients invade the trigeminal nerve, and the first branch of the eye, the most involved in the ocular nerve, the ocular nerve The forehead, lacrimal gland and nasal ciliary are all susceptible to VZV invasion, and the direct invasion of herpes zoster virus causes skin papules, herpes or blisters, conjunctivitis or superficial scleral edema and corneal dendritic ulcer; immune response to the virus can cause sclera Inflammation, scleral inflammation, keratitis, trabecular inflammation and anterior uveitis.

Herpes zoster viral scleritis prevention

Chickenpox is highly contagious. The source of infection should be isolated according to the respiratory tract. It should be 6 days after the rash has started, or all the rashes are dry and scarred. Patients with herpes zoster do not need to be isolated. Those who are in close contact should be observed for 21 to 28 days.

1. Passive immunization: high-priced human anti-VZV immunoglobulin, the dosage is 100mg in 1 year old, 250mg in 1~5 years old, 500mg in 6~10 years old, 750mg in 11~14 years old, 1000mg in 15 years old, intramuscular injection.

2. Active immunization: The vaccine is mainly attenuated and vaccinated by the attenuated vaccine of Oka in Japan in 1974 and the human diploid lung cell W138 in the United States.

Herpes zoster viral scleritis complications Complications glaucoma ptosis

In addition to skin damage, VZV-infected eye lesions include conjunctivitis, scleral inflammation, scleritis, uveitis, glaucoma, scarring eye contracture, paralytic ptosis, retinitis, acute retinal necrosis, optic disc edema, Pupil abnormalities and ocular nerve paralysis.

Herpes zoster virus scleritis symptoms common symptoms scleral vesicle skin lightning pain herpes scleral perforation corneal dendritic changes sclera congestion scleral outer inflammation herpes neuralgia tears herpes zoster-like appearance

Herpes zoster is characterized by severe pain, unilateral, does not exceed the midline of the body to the other side, single or multiple sensory nerve distribution areas of skin or mucosal herpes, although the incubation period of the intrinsic virus is not clear, contact with foreign sources The incubation period of sexual viruses usually ranges from a few days to a few weeks. Patients with headaches, discomfort, chills, fever and local lymph nodes are 4 to 5 days before herpes. Neuropathic pain occurs 2 to 3 days before rash, and rashes begin to appear as clusters. The fusion of miliary to soy-sized papules, herpes, quickly became blister, the blister fluid is clear, the wall is tight and shiny, the base is blushing, distributed along the nerve, banded, the skin between the blisters is normal, and the blisters subsides within 2 weeks. , often leaving permanent scars, varying degrees of sensation and severe banding neuralgia.

Post-herpetic neuralgia caused by herpes zoster viral vasculitis and neuritis can last for more than 2 months after initial herpes zoster skin lesions, and about 50% of patients over 60 years of age develop post-herpetic neuralgia.

It has been reported that scleritis accounts for 0.68% to 8% of herpes zoster viral eye disease, and scleritis can occur in the acute phase (10 to 15 days after the onset of skin lesions), most of which appear months or years after herpes zoster virus eye disease And often associated with eye surgery, herpes viral scleritis is mostly diffuse or nodular anterior scleritis, can also develop into necrotizing anterior scleritis.

Conscious symptoms include red eyes, eye pain, conjunctival sac secretions, decreased vision, etc. The severity of eye pain is parallel to the degree of inflammation. It is exacerbated at night, and can be radiated to the eyebrow and periorbital, and the conjunctival sac secretion is mucinous. People with keratitis develop photophobia and tears.

Signs: diffuse anterior scleritis, systemic complication is less and less, mainly characterized by diffuse hyperemia and swelling of the superficial sclera, accompanied by high edema of the conjunctiva, can not see the deep vascular and scleral tissue of the sclera, need to drop 1 : 1000 adrenaline in the conjunctival sac, so that the superficial congestion disappears before the nodular anterior scleritis forms a persistent wrap nodule, color purple, pain refused to press, nodules single or multiple, center transparent, It is completely inactive, the junction between the nodule and the superficial tissue is clear, the conjunctival and scleral superficial blood vessels are topped by the nodules, and the anterior sclera is dark purple. If the lesion continues to progress, it can cause necrotizing anterior scleritis, and the sclera in front of the equator shows yellow-gray spots. In severe cases, the sclera is partially carrion-like necrosis. It may have one or more sites. If the tissue falls off, it will eventually lead to perforation of the sclera and form a grape swollen. The sclera will be repaired for several months. The permanent sclera will be thinned, scars and recurrence will occur frequently. Different parts of the first scleritis, even for many years, herpes zoster viral scleritis with stromal keratitis, whether it is immune discoid keratitis or white Necrotic stromal keratitis can develop into corneal sclerosis, and even marginal ulcerative keratitis, may also be associated with anterior uveitis, the formation of fan-shaped iris atrophy and / or trabecular inflammation, further developed into secondary glaucoma, Corneal sensation of damage and fan-shaped iris atrophy contribute to the diagnosis of herpes zoster viral scleritis.

Scleral outer layer inflammation can occur before the rash, often accompanied by conjunctival and superficial sclera vesicles or corneal dendritic changes, scleral outer inflammation is simple or nodular, lesions are all located in the superficial sclera, the former can be seen superficial scleral congestion, blood vessels Radial dilation, distorted, reddish color, limited range of lesions, the latter formed in the superficial sclera, surrounded by hyperemia, can move nodules, nodules more than a single, 1 ~ 2mm size, deep sclera clear It can be seen that the vascular plexus remains in a normal state, and the sclera outer inflammation is caused by direct invasion of the virus. It lasts for 3 to 4 weeks without sequelae, and the immune-mediated episcleritis occurs within 10 to 15 days after the lesion.

Examination of herpes zoster viral scleritis

Laboratory tests are important for diagnosis and differential diagnosis. Tzanck smears are frequently used laboratory diagnostic methods to detect viral particles 3 days after skin, conjunctival herpes or dendritic corneal ulcers, suggesting that skin damage is caused by a Caused by herpes virus, it is not specific for the diagnosis of herpes zoster, alkaline Giemsa, hematoxylineosin, Wrights or methylene blue stains can show the cytoplasm and Inclusion within the nucleus, but can not distinguish between VZV and HSV, direct or indirect immunofluorscence technique (IFT), immunoperoxidase (IPD), radioimmunoassay (RIA), convective immunity ( Countercurrent immunoelectrophoresis (CIEP), agar gel immunodiffusion (AID) and enzyme-linked immunosorbent assay (ELISA) can find VZV in damaged tissues and contribute to diagnosis.

The first VZV infection produces cellular immunity and IgG, IgM, IgA anti-VZV antibodies, high levels of IgG anti-VZV antibodies throughout childhood, recurrent infection of VZV, can produce rapidly increasing antibodies, and enzyme immunoassay by immobilized cells (enzyme Immunoassay, EIA) or membrane antigen fluorescein-labeled antibody test (FAMA) for the detection of 2 samples, one in the infection process, and the other in the pre-infection or post-infection sampling, comparing 2 samples increased Or a reduction of 4 times or more can confirm the diagnosis, and the herpes zoster anti-VZV IgG single titer >1:640 can also be diagnosed.

Since HZS can be mediated by viral immunity, Giemsa staining, IFT, electron microscopy, and scleral tissue culture VZV may be negative, but the diagnosis of HZS cannot be ruled out.

Scleral pathology revealed chronic inflammatory granuloma with multinucleated giant cells, epithelial cells, and inflammatory microangiopathy, which may be difficult to detect with immunohistochemistry.

Diagnosis and identification of herpes zoster viral scleritis

According to the medical history and characteristic clinical manifestations, it is not difficult to diagnose. Patients with scleritis have herpes zoster ophthalmicus, especially corneal sensation and iris atrophy. HZS should be highly suspected.

Need to identify with herpes zoster, the latter often relapse, the distribution is not regular, occurs at the junction of the skin and mucous membranes, blister is small, easy to break, systemic symptoms are mild, other insect bites, the body of immunosuppressed patients Sexual rash, contact dermatitis, small pustules and allergic reactions may be similar to shingles and must be noted.

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