herpes simplex keratitis
Introduction
Brief introduction of herpes simplex keratitis Corneal inflammation caused by herpes simplex virus infection is called Herpessimplex keratitis (HSK). HSV-1 keratitis is a common and serious corneal disease, which is the first cause of corneal disease incidence and blindness. Herpes simplex keratitis is the most common common keratitis. It has increased and increased in recent years. Due to the widespread use of antibiotics and corticosteroids, the incidence rate is increasing. It is often caused by recurrent episodes that seriously impair visual function. There is no effective drug for controlling recurrence in the clinic, which has become a worldwide important cause of blindness. basic knowledge The proportion of the disease: the probability of the population is 0.13% Susceptible people: no specific people Mode of infection: non-infectious Complications: iridocyclitis glaucoma
Cause
Causes of herpes simplex keratitis
Viral infection (88%):
HSV is highly contagious to humans. Among adults over 20 years old, the positive rate of serum antibody is 90%, and the clinical clinical patients only account for 1 to 10%. The primary infection is only found in children who are not immune to the virus. Most children from 6 months to 5 years old, the virus is lurking in the body after the primary infection, and secondary infections are more common in children and adults over 5 years old, some non-specific stimuli such as cold, fever, malaria, emotional stimulation, Menstruation, sun exposure, application of corticosteroids, withdrawal and trauma may all be the cause of recurrence. According to the opinions of Nesbarn and Green, the incidence of this disease is as follows:
1. Dominant or latent infection HSV spreads from tears to the cornea, conjunctiva, deep tissue and appendages.
2. The nerve latent infection HSV migrates from the trigeminal nerve ending along the nerve cord to the nucleus of the trigeminal ganglion, and lurks here, and the virus disappears from the surrounding tissue.
3. The activation of HSV in neurons under the action of various provocative drivers destroys the patient's systemic stable state, and the virus in the latent infection process is activated and returns to the surrounding tissue along the nerve axis.
4. The surrounding tissue reproduction virus propagates in the surrounding tissues and spreads into the tears.
5. Recurrence of keratitis.
6, lurking in neurons again.
After the primary infection, the virus lurks in the body for a lifetime, and the secondary infection is more common in children and adults over 5 years old. Some non-specific stimuli such as cold, fever, malaria, emotional stimulation, menstruation, sun exposure, application of corticosteroids, trauma, etc. Both may be the cause of recurrence.
Pathogenesis
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. Most of them are children from 6 months to 5 years old. After that, the virus is permanently lurking in the trigeminal ganglion (TG). The sensory neuron is induced in some non-specific stimuli (cold, fever, malaria, emotional stimuli, menstruation, sun exposure, corticosteroids, expectoration and trauma).
Recent studies have found that when the corneal lesions are still, herpes simplex virus can be lurking in the sensory neuron of the trigeminal ganglion or in the cornea. The detailed mechanism of HSK recurrence is still unclear. When recurring, HSV may be derived. The virus lurking in the ganglion cells reactivates, reaches the cornea through axoplasmic transport, or reactivates the virus that is lurking in the cornea.
The occurrence, recurrence and clinical manifestations of HSK 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 continuous proliferation of the virus, but mainly a host immune response to the monosporin antigen. It is a delayed hypersensitivity reaction mainly based on cellular immunity. After the HSV enters the corneal parenchyma from the epithelium or endothelium, inflammation Cells, antigen-antibody complexes or viruses that are constantly replicating within the corneal parenchyma cause the collagen plate to dissolve, producing different types of deep inflammation, mainly immunological and stromal necrotizing keratitis.
Incidence factor
The mechanism of recurrence is not well understood. In addition to the factors (types and strains) of HSV itself and latent infections, the host is at least related to the following factors.
1. Cellular immunity: Recently, more data indicate that humoral immunity does not seem to play a role in the recurrence of stromal patients, because the whole body droplets IgM, IgG have no significant changes; while cellular immunity is lower than normal, Easty The lymphocyte transformation test in patients with stromal type was reported to be significantly lower than that in epithelial patients and normal population. Centifan reported that the leukocyte migration inhibition test in relapsed patients was also lower than in the normal population. Kato Fujiko (1979) used five non-specific antigens for subcutaneous injection. Delayed intradermal reactions to determine cellular immune status, resulting in more than three antigen-positive patients, 98% of the normal population, 71% of the stromal patients, the two have significant differences, in addition, clinically common long-term application of corticosteroids Patients with immunosuppressive agents or lymphocytic leukemia, multiple myeloma patients are prone to severe HSV keratitis, and the other side proves that cellular immune function is low, which is a major factor leading to the recurrence of this disease.
2. Histocompatibility antigen (HLA): Recent studies have shown that this disease has a certain relationship with the presence of HLA antigen. Zimmermann et al found that the frequency of HLA-B4 in relapsed patients was significantly higher than that of normal people. The seminar pointed out that the incidence of DRW3 in the matrix-type group was 48%, while that in the control group was 24%. There were significant differences between the two. Foster reported that HLA-A3 was significantly increased in patients with frequency recurrence, and B8 and B27 were slightly increased. 80% of non-recurrent patients are HLA-A2, so A3, B8, and B27 may be considered as a factor for recurrence of a disease, and A2 is a factor that resists recurrence. In short, research on this aspect is only the beginning, and there are still few cases to be treated. further demostrate.
3. Atopy: Atopy is an allergic reaction related to family lineage and responsiveness (mainly IgE). Statistics by Blndi, Michel, Denis, etc. indicate that 37% of patients have atopy, while normal people only 10 to 15% have atopy, and there are significant differences between the two. The patients use desalination and other extracts for desensitization therapy. After 1 to 5 years of observation, the clinical symptoms and recurrence are all reduced.
Prevention
Herpes simplex keratitis prevention
Strictly grasp the indications, develop good hygiene habits, and strictly abide by the lens removal and disinfection treatment.
At present, viral infection in keratitis has exceeded bacterial infection. Herpes simplex keratitis has a long course of disease and is prone to recurrence. Attention should be paid to increase physical fitness. Once sick, antiviral eye drops should be frequently used, and antibiotic eye drops should be used to prevent bacteria. Infection, corticosteroid eye drops cannot be abused in order to relieve symptoms during the active period of ulcers, so as to avoid serious complications such as exacerbations and even corneal perforation.
Complication
Herpes simplex keratitis complications Complications, iridocyclitis, glaucoma
Often complicated by limited macrofocal keratopathy, iridocyclitis, anterior chamber empyema, secondary glaucoma, and permanent residual corneal scar.
Symptom
Herpes simplex virus keratitis symptoms common symptoms herpes keratitis ciliary congestion and tearing corneal ulcer scarring
1, the primary infection:
The primary infection only occurs in patients with negative serum antibody, which is more common in children. Infants within 6 months can obtain anti-herpes virus antibodies from the mother through the placenta. The factors are rare, and gradually disappear with the antibody, 1 to 3 years old. The most susceptible to infection, 60% of infections by the age of 5, more than 90% of infections at the age of 15.
The primary infection mainly manifests as systemic fever and swollen lymph nodes in the ear. Eye damage is extremely rare. The main ones are:
(1) herpetic eyelid inflammation: the eyelid rash of the family after a week of blistering, sputum sputum does not leave pain.
(2) acute follicular conjunctivitis: conjunctival hyperemia, swelling, follicular hyperplasia, and even pseudomembrane.
(3) punctate or dendritic keratitis: about two-thirds of patients with these two symptoms may have keratitis or dendritic keratitis changes.
2, recurrent infection:
In the past, there was herpes virus infection, and there were antibodies in the serum. Under the action of the provocative factors, the first cases of recurrence or recurrence were recurrent infections, and the source of infection was mostly endogenous (ie, the virus was present in the cornea, lacrimal gland, and conjunctiva. Within the ganglion, a few may also be exogenous.
(1) Shallow type
The lesions affect the epithelial and superficial stromal layers and are the most basic type of the disease. They are also the most common and most easily diagnosed types in the clinic, including dendritic keratitis and map-like corneal ulcers.
1 dendritic keratitis
This type is the result of direct infection of epithelial cells by HSV. After the virus invades epithelial cells, it causes cell proliferation and degeneration, and then necrosis and shedding to form epithelial defects. Epithelial cells at the edge of the lesion area show active virus proliferation (ie, epithelial cell infiltration). Therefore, the virus isolation rate can reach 90% to 100%, point, dendritic and map keratitis: within a few days after the cause, the eye has irritation symptoms, depending on the location of the lesion can affect vision or less impact on vision, The corneal epithelial layer appears grayish white, almost transparent, slightly bulging needle-like vesicles, which can be expressed as dots or arranged in rows or clusters. It is a corneal herpes. This period is very short, usually only hours to tens of hours. Therefore, it is often overlooked. Some patients have changed at the time of treatment. Sometimes they are misdiagnosed as "conjunctivitis". If they are found and treated in time, there will be almost no traces after healing. The herpes will be arranged in a row, and soon the fusion will be expanded and the central epithelium will fall off and form. Strips of ulcers, with branches extending, each with a bifurcation at the end, forming a typical dendritic ulcer, in the edema of the corneal epithelial cells at the edge of the ulcer Living virus exists, inflammation continues to develop, and it can form a tortuous map-like or star-shaped ulcer. Sometimes there may be multiple ulcers arranged in an island shape, but regardless of the shape, it is generally only extended as a face. In the superficial layer, fluorescein staining clearly shows that the corneal ulcer epithelial defect is stained dark green, while the surrounding is surrounded by the pale green infiltration edge, indicating that there is edema and looseness in this part of the epithelium, which is the characteristic of the disease, the cornea Sensory loss is a typical sign of herpetic keratitis. The distribution of sensory sensation depends on the extent, duration and severity of corneal lesions. The corneal sensation of the lesion often decreases or disappears, but the sensitivity of the surrounding cornea is relatively increased. Therefore, there are significant pain, friction and tearing in the main sense. Most cases of superficial ulcers can heal within 1-2 weeks after active treatment, but the infiltration of superficial parenchyma takes several weeks and several months to absorb. , leaving a very thin cloud, generally affecting less vision.
After the dendritic or map-like ulcers heal, sometimes the opaque epithelial cells are lined up or branched. The pseudo-branches are in the process of healing. More epithelial cells extend from different directions to the lesion and eventually As a result of the confluence, the corneal epithelium here is slightly elevated, but the fluorescein staining is generally negative. Over time, the pseudo-branches can be smoothed and disappeared. Do not mistake the infection and continue to apply antiviral drugs because the toxicity of the drug can be To make it worse, in fact, the application of long-term antiviral drugs can produce pseudo-branches and keratitis.
In a few uncontrolled cases, the lesions can continue to develop deeper, resulting in opacity of the corneal parenchyma. The turbidity is mainly the edema and infiltration of the corneal parenchyma, generally starting from the bottom of the ulcer and gradually spreading to the deep, until the posterior elastic layer, its grayish white , translucent, sometimes slightly grayish yellow, due to edema and cell infiltration, the cornea can be significantly thickened, the posterior elastic layer and the endothelial layer can be swollen or rough or strip wrinkles, often accompanied by iritis reaction, due to the cornea, aqueous humor Turbidity and KP, often can not be observed satisfactorily, a few cases are still accompanied by anterior chamber empyema, at this time the pupil must be fully dispersed to prevent post-adhesion, ulcers spread to deep cases, although active treatment, ulcer healing still needs 2 to 4 Week time, as for the absorption of parenchymal edema and infiltration, can last for several months, the cornea is in an inflammatory state for a long time, can be gradually thinned, even ulcer perforation, in the ulcer stage, very few cases can still be secondary to bacterial or fungal infection, should cause note.
The ulcerated foci of marginal epithelial keratitis caused by HSV infection is similar to dendritic corneal ulcer, except that the lesion is located at the edge of the cornea, which is characterized by conjunctival hyperemia, corneal stroma infiltration, and neovascularization. The patient's symptoms are heavier and the response to treatment is not ideal.
The shape is dendritic, the lesions vary in size, and can be single or multiple branches. The ends or branches are nodular, the lesions are 1 mm wide, the central micro-depression, and the margins are gray-white proliferative bulges, after the slit lamp According to the partial examination method, the ridge is composed of fine gray-white particles, and the fluorescein staining is positive in the lesion area, and can be gradually diffused to the surrounding epithelium. The initial or atypical change of the operation dendritic keratitis has vesicularity. Keratitis, punctate keratitis, stellate keratitis and filamentous keratitis.
Clinically similar to this type is dendritic keratitis caused by herpes zoster virus.
2 map corneal ulcer
The dendritic keratitis was further enlarged and deepened, and the epithelial cells at the edge of the ulcer showed active virus proliferation, and the positive rate of virus isolation was second only to keratitis.
Expanded branches or irregular maps, irregular edges, jagged, surrounded by obvious gray-white bulging edges, turbid edema of the stromal layer at the bottom of the ulcer, often combined with post-elastic film wrinkles and anterior chamber flash.
The need to distinguish from the corneal ulcer of the map is epithelial erosive disease caused by epidemic conjunctival keratitis and other eye diseases. The posterior reflex examination of the slit lamp shows the infiltration of the marginal part of the former (+), and the latter is (-).
After the cure, most of the remains of the spotted sputum, if continued to develop deep, can become a deep ulcer; epithelial healing, disease progression can develop into disc keratitis; improper treatment can develop into dystrophic ulcers.
(2) Deep type
The lesions affect the deep layers of the stromal and endothelial layers and are a complex type of the disease, including discoid keratitis, stromal necrotizing keratitis, deep ulcers, and corneal uveitis.
1 disc keratitis
After the superficial lesions are healed, the stromal layer still has chronic edema and infiltration, which can develop into discoid keratitis. A few can also directly develop disease after onset. The exact pathogenesis is still not very clear. The direct sensory theory of viruses, the theory of antigen-antibody reaction and the theory of endothelial damage, the current tendency of antigen-antibody reaction theory, the matrix and endothelial cells are mesoderm, and the susceptibility to herpes simplex virus is not like that of the epithelial cells, so the pathological changes caused are not cells. Proliferation and degeneration, but the result of delayed hypersensitivity to viral antigens. Discoid keratitis is characterized by more edema than infiltration of the stromal layer, and stromal necrosis is activated by the deposition of immune complexes in the stromal layer. Complement, attracting a large number of neutrophils, causing matrix infiltration more than edema, leading to tissue damage and dissolution, the separation of the above two types of viruses is difficult to succeed, but electron microscopy, the presence of virus particles can be found in stromal cells.
Due to the characteristics of the corneal circulation, there is an approximately disc-shaped gray-white turbid area in the center or in the center of the cornea. The spring contour is blurred due to edema of the stromal layer, and there is an incompletely transparent area around. There are fewer new blood vessels in the turbid area. And obviously thickened, almost all cases are accompanied by posterior elastic layer wrinkles, fluorescein staining is negative, active period may be accompanied by cutaneous edema and epithelial keratitis, in addition to discoid opacity, can also be expressed in a variety of The form is diffuse, limited, ring-shaped, horseshoe-shaped, etc.
In discoid keratitis, 90% is caused by herpes simplex virus. This long-term 10% may occur before the banding, and corneal changes caused by viruses such as vaccinia and mumps must be distinguished according to medical history and virus isolation.
Discoid keratitis has a good prognosis. In a few cases, after the matrix edema subsides, the ring can be horseshoe-shaped opacity. Chronic or long-term topical corticosteroids can cause degenerative herpes.
2 stromal necrotizing keratitis
It is rare in clinical practice. In the stromal layer of turbid edema, dense gray-white plaques and agglomerated turbidity appear. Later, they gradually expand and fuse with each other, and tissue dissolution occurs. The clinical and pathological changes and corneal transplantation The rejection is very similar.
Although corneal stromaitis accounts for only 2% of the initial cases of HSK, it accounts for 20% to 48% of recurrent cases. The corneal stroma can be affected by many factors. The corneal epithelium and endothelial virus infection can affect the corneal stroma and cause the cornea. The edema of the matrix, the corneal stroma caused by corneal epithelium and endothelium, the treatment is mainly for corneal epithelium and endothelium. There are two main types of corneal stroma inflammation in clinical manifestation. One is the matrix caused by direct infection of the virus. Necrotic keratitis (necrotizing interstitial keratitis), another type of immune stromal keratitis caused by an immune response in the stroma (some patients may have the effect of a virus).
Matrix necrotizing keratitis is common in dendritic keratitis that has previously recurred many times, as well as discoid keratitis that is being treated with topical corticosteroids. The cornea is characterized by severe stromal inflammation with inflammatory cell infiltration, necrosis, and neovascularization. Scars, occasionally thinning and perforation, accompanied by iridocyclitis, occasionally secondary glaucoma, its natural course is 2 to 12 months, the condition is heavy, there is no effective treatment, the prognosis is very poor.
The clinical manifestations of immune keratitis are various, mainly manifested by infiltration and edema of the corneal stroma. Generally, the corneal epithelium is intact, and may be accompanied by an immune ring. The immune ring is a deposition of antigen-antibody complexes, and new cases may occur in repeated recurrence cases. Blood vessels, because some cases of corneal stroma lesions appear disc-shaped, so many authors call this type of disc keratitis (disciform keratitis), according to its pathophysiological mechanism, discoid keratitis is mainly caused by corneal endothelium lesions Corneal stroma edema.
Matrix necrotizing keratitis is one of the most serious types of this disease, the prognosis is very poor, often can cause post-elastic membrane bulging, perforation and iris prolapse.
3 deep ulcers
In the case of improper treatment of superficial lesions, the deterioration of exacerbation, especially the abuse of corticosteroids, has made the already low level of cellular immunity lower, while inhibiting the synthesis of fibroblasts, collagen and mucopolysaccharides, resulting in deep ulcers. Forming, although there are active lesions (infiltration of epithelial cells) in the edge of this type of ulcer, the positive rate of virus isolation is generally low, and the examination of immune function mostly shows that the cellular immune function is low.
The ulcer is located in the center or the center of the cornea. After the 1/2 matrix is deep, the ciliary congestion is obvious. The formation has lost the dendritic or map-like typical appearance, but it is almost circular or elliptical, and there are radial wrinkles around the ulcer. There are gray-white necrotic tissue at the bottom of the ulcer. In severe cases, the elastic membrane bulges, the anterior chamber is empy, perforation and even mixed infection.
This type of clinically easy to be confused with bacterial causal corneal ulcer and fungal anterior chamber pyogenic corneal ulcer (especially mixed infection) must be distinguished according to medical history, smear and culture examination.
The prognosis of this type is very poor. If you let it go naturally, there are often widespread pre-adhesion, secondary glaucoma, endophthalmitis, etc., and even the risk of losing the eyeball. Even if the scar is healed, it will become blind.
4 corneal uveitis
These two types are often associated with the occurrence of iridocyclitis, so it is called keratitis, which can have shallow damage first, and then involves deep tissue, which can also begin in deep (iritis or endotheliitis), and then spread Throughout the cornea, it has been confirmed that in some cases, the presence of virus can be detected in the aqueous humor. Long-term local application of corticosteroids may be a cause of this type of increase.
In addition to the corresponding corneal changes, slit lamp examination, corneal or massive pigmented KP may appear in the posterior wall of the cornea, anterior chamber empyema (occasion of blood) and elevated intraocular pressure, iris and pupil margin often have knots The knot is formed, and the gray-white depigmentation spot remains after the regression.
Whether there is a simple herpes iritis is still controversial. This type is more common when the influenza is in epidemic.
Same disc keratitis or deep ulcer.
(3) Hereditary herpes type
Although the lesion can affect the whole layer, it is mainly in the shallow layer, including chronic surface keratitis and dystrophic ulcer.
From the development of superficial lesions and simple discoid keratitis, it is a chronic process, which may be related to the loss of corneal sensation, abnormal lacrimal gland, damage of anterior elastic membrane, inflammation of stromal layer, and recent emphasis on epithelial basal cell regeneration. Unstable, the toxicity of antiviral drugs and the disorder of endothelial function are more directly related. Therefore, local long-term abuse of corticosteroids and anti-monomethylene drugs and repeated use of corrosive and antispasmodic therapy are the direct causes of this type. Separation is difficult to achieve, and immune function tests are mostly in the normal range.
1 chronic surface keratitis
Morphological changes, manifested as multiple epithelial erosion, filamentous keratitis and small vesicular keratitis.
2 dystrophic corneal ulcer
The epithelial erosion is unhealed for a long time, and the hair is repeatedly peeled off to form a dystrophic corneal ulcer. The ulcer has a sharp edge and has no rounded or elliptical edge of the epithelial infiltration. The irritation is mild, so there is an inert ulcer (indolent ulcer). ) is called.
Neurotrophic keratitis: Neurotrophic keratitis may be caused by an infection or immune response. This type of patient is often accompanied by corneal neurological dysfunction or tear film abnormalities, which are generally not active during viral infection, and some patients show no Indolent ulcer, the lesion can be limited to the surface of the corneal epithelium and the shallow layer of the matrix, but also can be developed to the deep layer of the matrix. The ulcer is generally round, with smooth curling, which is not changed for a long time. Causes corneal perforation, its formation is multi-factor, including basement membrane damage, active inflammation in the matrix, tear dysfunction and neurotrophic effects. The toxic effects of antiviral drugs are often the cause of the persistence of such ulcers, sterilized Sexual ulcers are difficult to heal. Its treatment is first to protect the corneal epithelium. The easiest way is to dress up the affected eye (or use a therapeutic soft microscope) and stop all medications, including various artificial tears containing toxic preservatives. Surgical treatment.
In the past, this type was called late degenerative herpes. In fact, this type is not the final result of the development of this disease. As long as the diagnosis is clear, local stimulation should be reduced as much as possible (including various drugs), and epithelial repair should be promoted. Many cases are still expected. Get a better outcome.
Examine
Herpes simplex keratitis examination
Laboratory diagnosis
(1) Fluorescent antibody staining technique: Take infected cells or aqueous humor cells in the lesion area, directly stain with fluorescent antibody, and find specific particle fluorescence staining in the infected cytoplasm or nucleus, which can make rapid diagnosis in 1-2 hours. Due to the specificity of the labeled fluorescent antibody, the type I or type II virus can be distinguished under a fluorescence microscope.
(2) Virus isolation: It is the most reliable cause diagnosis of this disease. The methods used are:
1 mouse inoculation in the brain, the most commonly used, most sensitive, mice died of herpetic encephalitis within 2 to 3 days;
2 chicken embryo chorioallantoic membrane inoculation, Hela, VERO, FL, Hepz and other passage cell culture, are suitable for herpes virus reproduction, 24- to 48 hours of cytopathic, obvious swelling of the round cell foci.
(3) Scraping the rabbit cornea, it has a certain diagnostic value, but the economic cost is high.
(4) cytological examination: taking the cornea, conjunctiva or eyelid blisters scraping for HE staining can be found in multinucleated giant cells, nuclear inclusion bodies and wind-like epithelial cells, this method can only confirm the virus infection, but can not distinguish whether HSV infection.
(5) Electron microscopy: Virus particles can be found in infected cells. This method is quick and easy, but it cannot be distinguished from herpes zoster virus.
(6) Serological examination: taking the serum of the acute phase and the recovery period for the determination of the titer of the neutralizing antibody, if the increase is more than 4 times, the diagnosis can be confirmed. This method is only applicable to the primary infected person, and the secondary infected person is in the blood before the onset. There are already high neutralizing antibodies, so the clinical application value is not great.
(7) Examination of immune function status: including examination of humoral immune serum (immunoglobulin) and cellular immunity, especially the latter is paid more and more attention. The methods used are: rosette test, lymphocyte transformation test and leukocyte migration inhibition In experiments, some people also used non-specific antigens such as phytohemagglutinin (PHA), purified protein derivatives (PPD), streptokinase-chain enzyme (SK-SD), nystatin, parotid gland, etc. for intradermal injection. Its delayed skin allergic reaction, although not specific, is simple and has a certain value.
(8) Other methods: The number of fluorescein permeation system is a new diagnostic method. After fluorescein ion is introduced into the eye for 18 hours, the content of aqueous humor is measured by a fluorometer, which has certain value for understanding the function of corneal epithelium and endothelium. Especially for hereditary herpes.
The clinical manifestations of this disease are complex. In addition to the typical branches, maps and discoid corneal lesions, there are some atypical clinical changes, which bring great difficulties to diagnosis and treatment. Each type not only has unique clinical features, but The pathogenesis and treatment principles are also different. The staining types can be transformed with each other. The factors that determine this transformation are very complicated, except for the type of HSV and the immune function of the strain and host (mainly cellular immunity). In addition, it is also related to treatment methods (especially the application of corticosteroids).
Diagnosis
Diagnosis and identification of herpes simplex keratitis
clinical diagnosis:
(1) Diagnostic basis of primary infection: more occurs in early childhood, adults are less common, and only 1% of patients with ocular symptoms, mainly herpes blisters, acute follicular conjunctivitis and punctate keratitis After leaving no scars, occasionally dendritic keratitis, the diagnosis depends mainly on serological examination.
(2) Diagnostic basis for recurrent infection:
1 typical corneal lesion morphology (branches, maps and discs);
2 multiple medical history of recurrence;
3 The course of disease is slow, antibiotic treatment is ineffective, and corticosteroids make the condition worse;
4 the cornea feels dull or disappears;
5 mouth horns, eyelids, and skin herpes on the nose;
6 specific recurrence causes.
Differential diagnosis
Dendritic keratitis is a characteristic change in HSK that can be diagnosed once it is discovered, but clinically differentiated from the following pseudodendritic keratitis.
1. False dendritic keratitis caused by varicella-zoster virus: the lesion is small, with no bifurcation or nodules at the end.
2. Pseudo-dendritic palliditis caused by Acanthamoeba: Ciliary congestion and eye pain are more dramatic. Radial cell infiltration from the central cornea along the nerve to the periphery of the cornea is called radial keratoneuritis.
3. Recurrent corneal erosion: has a tendency to relapse, occurs when getting up in the morning, the eye disease is aggravated, relieved in the afternoon and evening, and there is no epithelial infiltration edge around the lesion.
4. Pseudo-dendritic keratitis caused by contact lens contact: the occurrence of both eyes, the lesion of the epithelial defect is located at the edge of the corneal peripheral lens and the cornea.
5. It should also be differentiated from discoid keratitis caused by other causes such as vaccinia and mumps.
