herpetic keratitis
Introduction
Introduction to herpes zoster keratitis Herpes zosterophthalmicus may be associated with orbital inflammation, conjunctivitis, keratitis, scleritis, uveitis, retinopathy (acute retinal necrosis), optic neuritis, ophthalmoplegia, and the like. 60% of them can develop herpeszosterkeratitis, which causes corneal scarring and severely affects vision. There has been a tendency to increase gradually in recent times and it is worthy of vigilance. basic knowledge Sickness ratio: 0.5% Susceptible people: no specific people Mode of infection: contact spread Complications: optic neuritis scleritis
Cause
The cause of herpes zoster keratitis
Primary infection (45%):
Varicella and herpes zoster virus (VZV) are the same virus. Different immune status can lead to chickenpox or herpes zoster. After the initial infection of VZV, the virus is lurking in one or more viruses. In the nerve cells of the spinal ganglia or in the cells of the sensory ganglia of the brain, when the body's immunity declines, the virus is reactivated, descending along the sensory nerve fibers to the skin, proliferating in a certain sensory nerve and the area of the eye, and herpes zoster occurs. It is most common in the first branch of the trigeminal nerve.
Secondary infection (45%):
The virus is caused by recurrent infection of varicella zoster virus (VZV). The virus is latent in the trigeminal ganglion. When the cellular immune function is decreased or induced by other external stimuli, the virus is activated and multiplies. Patients with immunodeficiency, such as AIDS patients, cell transplant patients, and patients with a history of cancer, recent surgery, and history of trauma, are also prone to recurrent infection of VZV lurking in the body.
Pathogenesis
Is the result of one of the following factors or a combination:
1. Direct invasion of the cornea by the virus.
2. The host develops an inflammatory response to the intact virus or viral antigen in the cornea.
3. The body undergoes an autoimmune response to the altered tissue.
4. Secondary changes occur due to corneal sensation loss, eyelid abnormalities, and tear film changes on the corneal surface.
Prevention
Herpes zoster keratitis prevention
Pay attention to rest, work and rest, life in an orderly manner, and maintaining an optimistic, positive and upward attitude towards life can be of great help in preventing diseases.
Complication
Herpes zoster keratitis complications Complications optic neuritis scleritis
Corneal ulcer, anterior chamber empyema and iris atrophy.
Symptom
Herpes zoster keratitis symptoms Common symptoms Droplet corneal keratitis sensation disorders Nasal tip or nose appears... Corneal ulcer herpes zoster-like appearance
1. Pre-existing symptoms of herpes zoster in the whole body include general malaise, fever, chills and pain along the distribution of nerve skin, small blisters lined up in the skin; accompanied by neuralgia, extremely persistent pain from tingling, rash lasting for several months Neuralgia can last for several years. Herpes zoster is different from HSV and can invade the dermis. After the blisters are cured, permanent scars remain.
2. Corneal expression: About 60% of eye herpes zoster can cause corneal lesions. VZV is extremely vulnerable to the first branch of the trigeminal nerve. The occurrence of keratitis occurs after the appearance of rash, especially the herpes on the tip or nose. For the signs of invasion of the nasal ciliary nerve, keratitis and iritis must occur, and the manifestations of keratitis are various, mainly in the following types:
(1) superficial punctate keratitis: the earliest manifestation of herpes zoster keratitis, which occurs within a few days after the appearance of the rash, the surface of the cornea is coarse, slightly higher than the turbidity of the corneal surface, mostly occurring around the cornea Department, the surface often attached with sticky secretions, irregular coloration of fluorescein, tiger red staining is more obvious, no ulceration after shedding, these irregular turbidity points are turbid epithelial cells aggregated, may be a virus The result of the invasion may also be the result of the virus multiplying in the epithelial cells, and in some cases, the virus inclusion bodies can be found in the nucleus.
(2) subepithelial infiltration and numb keratitis: surface punctate keratitis can resolve itself within a few days, and some soon combine to form subepithelial infiltration, and further form nummular keratitis, It is considered to be a typical lesion of herpes zoster keratitis.
(3) pseudo-dendritic keratitis: dendritic keratitis associated with herpes zoster, because its morphology and HSV-like dendritic keratitis are very similar, the main difference is: its corneal lesions are slightly, slightly higher than the cornea Surface, light, moderate fluorescein staining, unlike HSK grooved depression, staining obvious; its dendritic lesions do not have the same terminnal bulb as HSK, so called pseudodendritic keratitis (pseudodendritic Keratitis) and distinguish.
(4) Mucous plaque keratitis: is a special type of chronic keratitis. About 5% of patients with herpes zoster will develop such corneal lesions. The onset time varies greatly from rash. It can occur from 7 days to 3 years, but most of them appear in 2 to 7 months. The typical change is a spotted lesion composed of mucus material on the surface of the cornea. Sometimes there are linear or dendritic lesions with clear edges. Usually multiple, can occur in any part of the corneal surface, its size and shape can be changed every day, acetylcysteine can dissolve it, fluorescein is medium coloration, tiger red staining is bright, the pathogenesis is not very clear It may be related to factors such as abnormal tear film, corneal sensory nerve palsy and eyelid regurgitation.
(5) Neuroparalytic keratitis: In the case of severe trigeminal neuralgia, the corneal sensation disappears completely. After the illness, it can last for several months to one year, and even does not recover for a long time. The long-term sensory disorder is about 9% of patients can cause neurotrophic keratitis, severe cases can lead to corneal ulcers, secondary bacterial infections, corneal abscess or anterior chamber empyema.
(6) discoid keratitis: after several months, subepithelial infiltration can develop deep into the stromal to form neovascularized corneal stroma or discoid keratitis, slit lamp microscopy for post-corneal elastic membrane folds, light section The infiltrative edema is thickened, and the lipid-like deposits are often left in the posterior wall of the cornea in the turbid area. It may not be absorbed for a long time. It may be an abnormal metabolite of corneal stromal cells (Keratocyte), which can be combined with the discoid cornea caused by HSK and vaccinia virus. Differentiation of stromal inflammation, sometimes corneal uveitis or corneal endotheliitis (examined by specular reflex, corneal endothelium can be found).
When there are specific signs of skin, eye and cornea, it is generally not difficult to diagnose, the atypical signs are rare, and the cases with less rash are often misdiagnosed as HSK. The author believes that when keratitis or other eye signs appear, and the following characteristics are present Should be suspected of VZV.
Examine
Examination of herpes zoster keratitis
1. Epithelial scraping in the acute phase of conjunctival and corneal epithelial scraping to examine macrophages and intranuclear eosinophilic inclusions, but can not be distinguished from HSV.
2. Virus isolation If necessary, the virus is separated from the conjunctival sac and the skin blister, and the corneal vaccination does not cause disease. This point can be differentiated from HSV.
3. Determination of serum neutralizing antibodies can be measured 4 days after the disease, reaching a peak at 2 weeks, and dropping to an undetectable level after 1 year.
4. Fluorescein-labeled antibody staining technique Take the corneal epithelial smear and directly stain with fluorescein-labeled antibody to prove that there is a virus infection in the infected cells. Because of the specificity of the labeled fluorescein-labeled antibody, it can be associated with HSV. the difference.
5. Complement binding test The serum anti-VZV antibody titer of patients with varicella increased gradually, and gradually decreased in the recovery period to 6-12 months, and it was reduced to only detectable level. High titer VZV antibody was detected by complement fixation test. The anti-HSV antibody is negative, so it can be judged to be caused by VZV infection.
Diagnosis
Diagnosis and differentiation of herpes zoster keratitis
1. A history of unilateral facial rash.
2. Skin scars or brownish precipitates in this area.
3. The iris shrinks.
4. The anterior chamber is calm (more concentrated than other uveitis pigments).
The identification with HSK is mainly based on the diagnosis of pathogenicity. Morphologically, the pseudo-dendritic keratitis caused by varicella-zoster virus has small corneal lesions, no bifurcation or nodular enlargement at the end.
