What are the symptoms of toxic epidermal necrolysis?

What are the symptoms of toxic epidermal necrolysis?

Toxic epidermal necrolysis is actually a more serious condition among drug rashes. If not treated in time, the mortality rate is very high, as high as 10%. Patients with toxic epidermal necrolysis will also have obvious symptoms in their bodies, such as local erythema on the skin and epidermal peeling, and patients will experience obvious tingling and severe pain.

Toxic epidermal necrolysis is a type of drug eruption called epidermolysis bullosa. It is one of the most serious types of drug rash. This disease is rare, but the condition is serious and if not treated in time, the mortality rate can be as high as over 10%. Common allergenic drugs are mainly sulfonamides, antipyretics, analgesics, sedatives, hypnotics or anti-epileptic drugs.

Symptoms and signs

The typical onset of TEN is painful local erythema, which spreads quickly and causes flaccid bullae or epidermal peeling on the erythema. Slight touch or traction may result in large-scale peeling (Nikolsky sign). Exposure of large areas may be accompanied by fatigue, chills, myalgia, and fever. The patient develops extensive erosions within 24 to 72 hours, involving all mucous membranes (eyes, mouth, external genitalia). At this time, the condition is extremely serious and the affected skin is similar to a second-degree burn. Death may result from fluid and electrolyte imbalances and multi-organ complications (eg, pneumonia, gastrointestinal bleeding, glomerulonephritis, hepatitis, infection).

treat

The patient must be hospitalized; the first priority is intensive care and close observation. Suspected drugs should be discontinued immediately. The patient must be isolated to reduce exogenous infection and treated as a severe burn (see Section 276). Protect skin and exposed areas from injury and infection. Replace fluids and lost electrolytes.

Although controversial, systemic corticosteroids can be helpful when started early in the course of the disease. The idea is to stop any more immune damage to the skin. However, systemic corticosteroids will not bring dead keratinocytes back to life or reverse programmed cell death in the skin. Some severe cases require the use of several days of high-dose parenteral corticosteroids. Most scholars recommend 80 to 200 mg/d of methylprednisolone (or its equivalent) intravenously, although some scholars have suggested 500 to 1000 mg/d of intravenously. This type of corticosteroid therapy is often associated with a variety of side effects and therefore needs to be used under very careful management. Corticosteroids often tend to enhance gram-negative or other bacterial sepsis and thus increase mortality. Therefore, if this type of drug is used, a short course of treatment is safer. Bacteremia is the most common cause of death and often occurs in the setting of lung infection, so it must be detected and treated quickly. Because obvious crusting may occur on the conjunctiva, an ophthalmologist consultation is often required. To prevent phimosis, a urologist consultation is also necessary.

Early combined treatment with high-dose immunoglobulin and glucocorticoids. Immunoglobulin G is safe and can feedback inhibit the production of autoantibodies, directly neutralize pathogenic antigens, and fight the production of inflammatory factors. Early application of immunoglobulin treatment is beneficial to promote recovery of skin lesions, shorten the course of the disease and reduce secondary infections.

Glucocorticoids can be used in the form of dexamethasone or methylprednisolone pulse therapy. At the same time, infection should be prevented and supportive treatment should be strengthened. Because the child has a high fever and oral mucosal erosions and cannot eat, attention should be paid to replenishing body fluids to prevent water and electrolyte disorders.

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