Small blisters that line the skin with pain

Introduction 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 the cells of one or more spinal ganglia or in the cells of the sensory ganglia. When the body's immunity declines, the virus is reactivated, descending along the sensory nerve fibers to the skin, proliferating in a region of sensory nerves and eyes, and herpes zoster occurs, with the third branch of the trigeminal nerve being the most common.

Cause

(1) Causes of the disease

The disease is caused by recurrent infection of varicella zoster virus (VZV), which is lurking in the trigeminal ganglion. When the body's cellular immune function declines or is induced by other external stimuli, the virus is activated and multiplied. Patients with immunodeficiency, such as AIDS patients, cell transplant patients, and patients with a history of cancer, recent surgery, and traumatic history, are also prone to recurrent infection of VZV lurking in the body.

(two) 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.

an examination

Related inspection

Herpes simplex virus (HSV)

Whole body performance

Prodromal symptoms of herpes zoster include general malaise, fever, chills and pain along the distribution of the nerve skin, small blisters in the skin lined up; accompanied by neuralgia, and extremely persistent pain from tingling. The rash lasts for several months and the neuralgia can last for several years. Unlike HSV, herpes zoster can invade the dermis, and permanent scars remain after the blisters are cured.

2. Corneal performance

About 60% of herpes zoster can cause corneal lesions. VZV is very easy to invade 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. Symptoms of invasion of the nerves, followed by keratitis and iritis. The performance of keratitis is diverse, mainly in the following types:

(1) Superficial punctate keratitis: the earliest manifestation of herpetic keratitis, which occurs within a few days after the appearance of the rash. The surface of the cornea presents a coarse, slightly higher turbidity point on the surface of the cornea, which occurs mostly in the peripheral part of the cornea. The surface often has sticky secretions, which are irregularly colored on fluorescein. The tiger red staining is more obvious, and it does not form after shedding. ulcer. These irregular turbidity points are caused by the accumulation of turbid epithelial cells, which may be the result of virus invasion or the result of virus propagation in epithelial cells. In some cases, virus inclusion bodies can be found in their nucleus.

(2) subepithelial infiltration and numb keratitis: surface punctate keratitis can resolve itself within a few days, and some soon combine with each other to form subepithelial infiltration, and further form nummular keratitis. The latter is considered to be a typical lesion of herpes zoster keratitis.

(3) False dendritic keratitis: dendritic keratitis associated with herpes zoster, which is very similar in morphology to HSV dendritic keratitis. The main difference is that the corneal lesions are slight, slightly higher than the corneal surface, light and moderate fluorescein staining, unlike the HSK grooved depression, the staining is obvious; the end of the dendritic lesion does not have the spherical enlargement like HSK (terminnal bulb), so called pseudodendritic keratitis (pseudodendritic keratitis) and differentiated.

(4) Mucous plaque keratitis: is a special type of chronic keratitis, which occurs in about 5% of patients with herpes zoster. The onset time varies widely, from 7 days to 3 years after the rash, but most occur in 2 to 7 months. It is typically a spotted lesion of the mucous material on the surface of the cornea that is micro-embossed, sometimes with linear or dendritic lesions, with clear edges, usually multiple, that can occur anywhere on the surface of the cornea, its size and shape. It can be changed every day. Acetylcysteine dissolves it. The pathogenesis is not very clear and may be related to factors such as tear film abnormalities, corneal sensory nerve palsy and eyelid regurgitation.

(5) Neuroparalytic keratitis: In the case of severe trigeminal neuralgia, the corneal sensation disappears completely, and it can last for several months to one year after recovery, and even does not recover for a long time. About 9% of patients with long-term sensory disturbances 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 examination of post-corneal elastic membrane wrinkles, light-spotted infiltrates edema thickening, leucorrhea corneal deposits often remain in the posterior wall of the cornea, long-term non-absorption, may be abnormal metabolites of corneal stromal cells (Keratocyte), this The point can be distinguished from the discoid keratitis caused by HSK and vaccinia virus. Corneal uveitis or corneal endotheliitis can sometimes occur (inspected by specular reflectometry, which can be found in the corneal endothelium with a drip cornea). When there are unique signs of skin, eyes and cornea, it is generally not difficult to diagnose. Cases with atypical signs and fewer rashes are often misdiagnosed as HSK. The authors believe that VZV should be suspected when keratitis or other ocular signs are present with the following characteristics.

Differential diagnosis

Skin Lightning Pain: If there is "lightning pain" on the surface of the skin and a similar situation occurs for several days, it may be asymptomatic herpes zoster. The skin of the diseased part has the size of mung bean, the papules with large tension, and the blisters. The light can have a normal skin interval in each cluster. In severe cases, the large pieces can be fused and distributed in a strip shape. After a few days, the clear and transparent blisters become turbid pus. The blister can be partially broken to form a smash, and this type of syndrome is easier to distinguish. However, in a few cases, there is only neuralgia and no skin damage. This asymptomatic herpes zoster is easily misdiagnosed. If the lesion occurs on the face, it is easy to be misdiagnosed as trigeminal neuralgia; it occurs at the edge of the rib and is easily mistaken for intercostal neuralgia. Other misdiagnosis is angina pectoris, ulcer disease, biliary or renal colic, appendicitis, or early glaucoma.

After the yellow skin of the toe skin, purple black: purple black after the yellow skin of the toe skin is one of the symptoms of dislocation.

1. The vast majority occur in men, mostly between the ages of 25 and 40.

2. Occurs at the end of the extremities, the lower extremities are more common.

3. Before the onset, there were smoking, cold, and history of calf trauma.

4. The initial limbs are heavy, cold, numb, acupuncture-like pain in the toes, twitching pain in the calf muscles, and intermittent claudication. After the cold of the hands and feet, the pain increased, and the dorsal artery pulsation weakened. Or accompanied by superficial vein migration thrombophlebitis, and some have this performance before the onset.

Recurrent herpes zoster: Herpes zoster is an acute skin disease caused by varicella-zoster virus, herpes simplex virus type 1 and type 2, but patients are most concerned about herpes zoster Will it be repeated? In response to this problem, experts believe that herpes zoster and varicella are the same virus, in which the primary infection is varicella, and then the virus may enter the spinal ganglia or the sensory ganglia of the cranial nerve and lurk in the spinal cord, but The latent virus can no longer cause symptoms or be reactivated several years later to cause herpes zoster. In addition, when the immune system is reduced due to some other diseases, or when an immunosuppressive product is used, it may cause the virus to recur.

Epidermal full-thickness necrosis and subepidermal bullae: Toxic necrotizing epidermolysis type drug eruption The skin manifests as full-thickness of the epidermis and formation of subepidermal bullae. Clinical manifestations, acute onset, accompanied by high fever, irritability, lethargy, convulsions, coma and other obvious symptoms of systemic poisoning. The skin manifests as full-thickness of the epidermis and formation of subepidermal bullae. At the beginning, it was a large piece of bright red patches, followed by purple-brown. In 1 to 2 days, bullae appeared on the spots and expanded, and the sub-synthesis was several tens of centimeters in size, showing most parallel strips of crepe. The bullae are easily rubbed and there is a large smash, similar to a second degree burn. Nilolsky sign (10), at the same time, mouth, eye, nose, upper respiratory tract, genital area, esophageal mucosa, can be widely affected. A large erosion surface appears after the mucosa falls off. The pain is extreme. The body temperature often lasts at 40 ° C, and does not retreat for 2 to 3 weeks. Heart, kidney, liver, and brain are also often affected. The prognosis is serious, and the mortality rate is 25% to 50%. More often due to secondary infection, liver and kidney dysfunction, water and electrolyte disorders and death.

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