Herpetic keratitis

Introduction to herpetic keratitis Herpes simplex keratitis is a serious blinding eye disease, and its pathogen is herpes simplex virus. When the patient's body declines, such as a cold, fever, fatigue or severe mental stimulation, it is prone to the disease. 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 seriously affects vision. There has been a tendency to increase gradually in recent times and it is worthy of vigilance. Acyclovir eye drops are preferred for general conditions, and other antiviral eye drops are also available. Supplemented with antibiotic eye drops, interferon, vitamins, etc. Corneal epithelial intact can be supplemented with corticosteroid eye drops, and those with iridocyclitis are used as a mydriatic. basic knowledge The proportion of illness: 0.03% Susceptible people: no special people Mode of infection: non-infectious Complications: corneal ulcer

Causes of herpetic keratitis

Virus infection (75%)

According to different virus-specific antigens, HSV can be divided into two types: type I virus and type II virus type infection sites are head and neck, most eye herpes infections are caused by this type of virus; type II infection The area is genital, occasionally or causing eye infections.

Maternal transmission (15%)

Newborns can be infected through the birth canal. Type II infections in newborns can affect the skin, blood, internal organs and central nervous system, and can be fatal. Monospora virus is highly contagious to humans. The vast majority of the population is infected with it. The positive rate of serum antibody is about 90%. It can be found in 55%~94% of human trigeminal ganglia by molecular biological methods. The lurking of the virus.

Pathogenesis

Among adults over 20 years old, the positive rate of serum antibody is 90%, and only 1 to 10% of clinical clinicians appear. Primary infection refers to the first violation of the human body by the virus. It is only found in children who are not immune to this disease, mostly children from 6 months to 5 years old. After this, the virus is lurking in the sensory neuron of the trigeminal ganglion (TG) for some life, in some non-specific stimuli (cold, fever, malaria, emotional stimuli, menstruation, sun exposure, application of corticosteroids, antispasmodic therapy) And trauma, etc.) induced.

Recent studies have found that herpes simplex virus can be lurking in the sensory neuron of the trigeminal ganglion or lurking in the cornea when the corneal lesion is still. The detailed mechanism of HSK recurrence is unclear. Upon relapse, HSV may be derived from reactivation of the virus that is latent in the ganglion cells, reaching the cornea through axoplasmic transport, or reactivation of the virus that is lurking in the cornea.

The occurrence and recurrence of HSK and the clinical manifestations of the disease are mainly related to the HSV strain of the infected organism, and also have a certain relationship with the immune status of the body. Therefore, the recurrence of HSK is often associated with changes in the immune function of the body.

The superficial type of pathogenesis is that HSV directly infects corneal epithelial cells, which proliferate in cells and cause cell degeneration and necrosis, and fall off to form epithelial defects, forming typical dendritic keratitis. If further enlarged, deeper, corneal cornea can be formed. (geographic keratitis).

The deep type of disease is not the sustained proliferation of the virus, but mainly a host immune response to the monosporin antigen, which is a delayed hypersensitivity reaction mainly based on cellular immunity. After the epithelium or endothelium enters the corneal parenchyma, the inflammatory cells, antigen-antibody complexes or viruses that continuously replicate in the corneal parenchyma cause the collagen plate to dissolve, resulting in different types of deep inflammation, mainly immunological and stromal necrotizing keratitis.

Herpes keratitis prevention

1, strengthen nutrition, eat more foods rich in vitamins A, B, C, such as liver, carrots, fruits, vegetables, etc., enhance the body's resistance.

2. Cultivate the habit of cleaning and loving hygiene. Do not wipe your eyes with dirty hands and dirty handkerchiefs. Wash your face regularly and disinfect it to prevent repeated infections, aggravate the pain and cause adverse consequences.

Herpetic keratitis complications Complications corneal ulcer

It can cause serious complications such as corneal perforation.

Herpetic keratitis symptoms common symptoms visual impairment corneal opacity eye pain corneal ulcer fever photophobia eye foreign body fear of light and tears

1. There is often a history of cold or fever before onset;

2. Photophobia, tearing, foreign body sensation or eye pain, decreased vision;

3. Dendritic keratitis: the ulcer is dendritic or coral-like;

4. Map-like keratitis: enlarged by dendritic ulcers;

5. Discoid keratitis: opacity and edema in the central cornea, the epithelium is almost intact.

Herpes keratitis examination

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 Separation of the virus from the conjunctival sac and the skin blister as necessary. Rabbit corneal vaccination does not cause disease, which 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 distinguished from HSV.

5. Complement binding test The serum anti-VZV antibody titer of patients with varicella increased gradually, and gradually decreased during the recovery period to 6-12 months, which was reduced to only detectable levels. A high titer VZV antibody was detected by the complement binding assay, and the anti-HSV antibody was negative, so it was judged to be caused by VZV infection.

No other special auxiliary checks.

Diagnosis and identification of herpetic keratitis

diagnosis

At present, the diagnosis of HSK relies on the history of the disease and the morphology of corneal lesions for clinical diagnosis. The history of recurrent episodes is an important diagnostic basis. Laboratory diagnosis is not a required clinical diagnostic condition.

Diagnosis basis for primary infection

Most occur in early childhood, and adults are less common. Only about 1% of people have eye symptoms. Mainly manifested as herpes blisters, acute follicular conjunctivitis and punctate keratitis. No scars after the healing, occasionally dendritic keratitis. Its diagnosis relies mainly on serological tests.

Diagnosis basis for recurrent infection

1 typical corneal lesion morphology (branches, maps and discs).

2 history of multiple recurrences.

3 The course of the disease is slow, antibiotic treatment is ineffective, and corticosteroids worsen the condition.

4 The cornea feels dull or disappears.

Skin herpes appeared in the 5 horns, eyelids, and nose.

6 specific recurrence causes.

Differential diagnosis

Dendritic keratitis is a characteristic change in HSK that can be diagnosed once it is discovered. However, the clinical needs to be distinguished from the following pseudodendritic keratitis.

Pseudo-dendritic keratitis caused by varicella-zoster virus

The lesion is small, with no fork or no swelling at the end.

Pseudo-dendritic keratitis caused by Acanthamoeba

Ciliary congestion and eye pain are more dramatic. Radial cell infiltration from the center of the cornea along the nerve to the periphery of the cornea is called radial keratoneuritis.

Recurrent corneal erosion

It has a recurrence tendency, occurs when getting up in the morning, the eye disease is aggravated, and it is relieved in the afternoon and evening. There is no epithelial infiltration edge around the lesion.

Pseudo-dendritic keratitis caused by wearing contact lenses

The occurrence of both eyes, the lesion of the epithelial defect is located in the peripheral part of the cornea at the edge of the lens and the cornea.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.