scleral vesicles
Introduction
Introduction Herpes zoster viral scleral inflammation is often accompanied by conjunctival and superficial scleral vesicles or corneal dendritic changes. Herpes zoster is caused by reactivation of varicella-zoster virus (VZV). VZV morphology is indistinguishable from HSV and belongs to the same DNA virus, but its antigenicity is different. This enveloped 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. May cause skin papules, herpes or blisters, conjunctivitis or superficial scleral edema and corneal dendritic ulcers.
Cause
Cause
(1) Causes of the disease
Herpes zoster is caused by reactivation of varicella-zoster virus (VZV). VZV morphology is indistinguishable from HSV and belongs to the same DNA virus, but its antigenicity is different. This enveloped 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 an unimmunized person (usually a child) is chickenpox. More than 90% of adults in the United States have had VZV infection. The infection persists without clinical symptoms and the virus is present in the trigeminal ganglion in a latent form. The body's immune system cannot effectively destroy the virus and only produces immunological mechanisms. Usually 10 years after the initial infection with VZV, 20% of people cause recurrent infections to produce herpes zoster. Herpes zoster mostly invades the thoracic nerve, and 9% to 16% of patients invade the trigeminal nerve, and the most common one is the ocular nerve involvement. The forehead branch, lacrimal gland branch and nasal eye branch of the ocular nerve are susceptible to VZV invasion, and the direct invasion of the herpes simplex virus causes skin papules, herpes or blisters, conjunctivitis or superficial scleral edema and corneal dendritic ulcer; the immune response to the virus can be Causes scleritis, scleral inflammation, keratitis, trabecular inflammation, and anterior uveitis.
Examine
an examination
Related inspection
Herpes simplex virus (HSV) fundus examination
Herpes zoster is characterized by severe pain, unilateral, no more than the midline of the body to the other side, single or multiple sensory nerve distribution areas of the skin or mucosal herpes. Although the incubation period of the intrinsic virus is not clear, the incubation period for exposure to an exogenous virus usually ranges from a few days to a few weeks. 4 to 5 days before herpes, the patient developed headache, discomfort, chills, fever and local lymphadenopathy. There was neuralgia 2 to 3 days before the rash. The rash began to appear as a cluster of miliary to soy-sized papules and herpes, which quickly became blisters. The blister fluid was clear, the wall was tight and the base was red, distributed along the nerve, and banded. The skin between the vesicles was normal, and the blisters subsided 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 the first herpes zoster skin lesion. About 50% of patients over the age of 60 develop postherpetic neuralgia.
It has been reported that scleritis accounts for 0.68% to 8% of herpes zoster viral eye diseases. Scleritis can occur in the acute phase (10 to 15 days after the onset of skin lesions), most of which occurs months or years after herpes zoster virus eye disease and is often associated with eye surgery. Herpes viral scleritis is mostly diffuse or nodular anterior scleritis, and can also develop into necrotizing anterior scleritis.
Conscious symptoms include redness, eye pain, conjunctival sac secretion, and decreased vision. The severity of eye pain is parallel to the degree of inflammation, which is exacerbated at night and can be radiated to the eyebrow and the periorbital. The conjunctival sac secretion is mucoid, and those with keratitis have photophobia and tearing.
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 it can be seen. Nodular anterior scleritis forms a persistent, surrounded nodule with a purplish red color and painful rejection. The nodule is single or multiple, the center is transparent, and it is completely inactive. The junction between the nodule and the surface organization is clear. The conjunctival and scleral superficial blood vessels are jacked up by the nodules. The anterior sclera is dark purple.
If the lesion continues to progress, it can cause necrotizing anterior scleritis. The sclera in front of the equator shows yellow-gray spots. In severe cases, the sclera is partially carrion-like necrosis, which may have one or more sites. If the tissue falls off, it eventually causes the sclera to perforate and form a grape swollen. The sclera needs to be repaired for several months, leaving a permanent scleral thinning and scarring. Frequent recurrence occurs in different parts of the first scleritis, even for many years. Herpes zoster viral scleritis with stromal keratitis, whether it is immunological discoid keratitis or white necrotic stromal keratitis, can develop into corneal sclerosis and even marginal ulcerative keratitis. It can also be associated with anterior uveitis, which forms fan-shaped iris atrophy and/or trabecular inflammation, and further develops into secondary glaucoma. Corneal sensation of damage and fan-shaped iris atrophy contribute to the diagnosis of herpes zoster viral scleritis.
Scleral laminitis can occur before the rash, often accompanied by conjunctival and superficial sclera vesicles or corneal dendritic changes. The scleral outer inflammation is simple or nodular, and the lesions are all located in the superficial sclera. The former can be seen in the superficial sclera congestion, the radial expansion of the blood vessels is distorted, the color is red, and the lesion range is limited. The latter forms a nodule that is located in the superficial sclera and is surrounded by blood. More nodules, single hair, 1 ~ 2mm size. The sclera deep in the nodule is clearly visible and the vascular plexus remains normal. Scleral laminitis caused by direct invasion of the virus, lasts for 3 to 4 weeks, no sequelae. Immune-mediated episcleritis occurs within 10 to 15 days after lesions.
According to the medical history and characteristic clinical manifestations, it is not difficult to diagnose. Patients with scleritis, previously with herpes zoster ophthalmicus, especially with corneal sensation and iris atrophy, should be highly suspected of HZS.
Diagnosis
Differential diagnosis
Differential diagnosis of scleral vesicles:
Transparent blisters with different corneal sizes: diseases caused by bullous keratopathy, which are characterized by tarnishing of the corneal epithelium, transparent blisters of varying sizes, and recurrence after rupture. The state in which blisters are formed in the corneal epithelial layer is called bllous keratopathy. It used to be called macrobubble keratitis. In fact, it is not an inflammation, but a denaturation, which is the result of the abnormality of the layer, especially the endothelium, and the storage of water in the epithelial layer. Caused by abnormal or disrupted corneal endothelial cells. The number of normal corneal endothelial cells is about 3,000/mm2, which may occur when it is reduced to 500-1000/mm2. After cataract surgery, ocular trauma, advanced glaucoma, severe uveitis, Fuch's corneal dystrophy, corneal transplantation failure, etc. may cause corneal endothelial cell destruction and reduction, leading to macrofocal keratopathy.
Herpes zoster is characterized by severe pain, unilateral, no more than the midline of the body to the other side, single or multiple sensory nerve distribution areas of the skin or mucosal herpes. Although the incubation period of the intrinsic virus is not clear, the incubation period for exposure to an exogenous virus usually ranges from a few days to a few weeks. 4 to 5 days before herpes, the patient developed headache, discomfort, chills, fever and local lymphadenopathy. There was neuralgia 2 to 3 days before the rash. The rash began to appear as a cluster of miliary to soy-sized papules and herpes, which quickly became blisters. The blister fluid was clear, the wall was tight and the base was red, distributed along the nerve, and banded. The skin between the vesicles was normal, and the blisters subsided within 2 weeks, often leaving permanent scars, varying degrees of sensation and severe banding neuralgia.
