Staphylococcal scalded skin syndrome

Introduction to staphylococcal scalded skin syndrome Staphylococcal Scalded Skin Syndrome (SSSS) has been described as neonatal exfoliation-like dermatitis, Staphylococcus aureus toxic epidermal lysis, bacterial toxic epidermal necrolysis, Ritter's disease, neonatal keratin Separation. The disease is a severe acute generalized exfoliative pustulosis in the newborn. It is characterized by loose scald-like bullae and large epidermal exfoliation on the systemic erythema. Occasionally in adults, in 1966, Toxic Epidermal Necrolysis (TEN) was also caused by Staphylococcus, and Ritter's disease and TEN were also caused by Staphylococcus, and Ritter's disease was identical to the clinical and pathological pathology of TEN. . In 1967, Lyell divided TEN into gold and grape type, drug type, other types and special hairstyles according to different causes. It is considered that Ritter's disease is a gold-and-glucose type. SSSS was identified as an independent disease in 1977, separate from toxic epidermal necrolysis. basic knowledge The proportion of sickness: 0.01% - 0.03% Susceptible people: good for newborns Mode of infection: non-infectious Complications: bronchial pneumonia sepsis abscess

The cause of staphylococcal scalded skin syndrome

The disease is mainly caused by coagulase-positive phage group II 71 type Staphylococcus aureus, a serious skin infection, this type of staphylococcus can produce epidermal toxins, causing skin damage, and now found group I or III Some staphylococci can also produce epidermal lysis toxins. Tests have shown that epidermal lysis toxins are mainly excreted by the kidneys. Infants and young children excrete very slowly. This toxin is increased in serum and causes skin damage and exfoliation. Coccidial skin scald-like syndrome is more common in people with nephritis, uremia, physical weakness, impaired immune function or severe staphylococcal septicemia, which may be associated with renal excretory function and low immune function.

Staphylococcal scalded skin syndrome prevention

1. Pay attention to the cleanliness of the baby, the diaper should be clean, and the medical staff or family members with purulent skin disease can not be in contact with the newborn.

2. Strengthen care and keep warm. Pay attention to oral and eye care.

3. In the early stage, a sufficient amount of effective antibiotics should be used to remove the S. aureus infection in the body and stop the production of bacterial toxins. And antibiotic susceptibility test, in order to choose the appropriate antibiotics. Methicillin can be given, 1 to 1.5 g for adults, 1 to 6 hours for intramuscular injection, and 150 to 250 mg per kilogram of body weight per day for children, divided into 4 intramuscular injections. Or give erythromycin at a dose of 80mg / (kg · d) intravenous drip. For the penicillin-resistant strain, the cephalosporin V number, o-chloropenicillin, etc. may be used, and other second or third generation cephalosporins may also be used.

4. Pay attention to water, electrolyte balance, supplement nutrition, and strengthen supportive therapy, such as blood transfusion.

5. There are different opinions on the application of hormones. It is forbidden to use hormones alone. Because hormones can cause immunosuppression, it is not only useless, but harmful. However, some people advocate the use of antibiotics in the early stage and the combination of hormones to reduce the toxins of bacteria. For patients who are difficult to determine the cause and diagnosis at one time, antibiotics and hormones may be combined. Once it is clear that it is a Staphylococcus aureus type TEN, the treatment of hormones should be stopped immediately.

6. Local use of non-irritating fungicides, such as 0.5% to 1% neomycin emulsion for external use. The blisters are preferably removed, and then wetted with 1:5000 ~ 1:10000 potassium permanganate solution or 1:2000 berberine solution, cleaned and medicated 1% gentian violet solution rubbed and so on.

Staphylococcal scalded skin syndrome complications Complications bronchopneumonia sepsis abscess

Can be secondary to bronchial pneumonia, sepsis, abscess or gangrene and other deaths, mostly in infants and young children, after a sharp, high mortality.

Staphylococcal scalded skin syndrome symptoms Common symptoms Slight skin trauma is... Pustular skin tenderness irritating, peeling, sore throat, facial edema, fatigue, erythema (clear boundary

Patients often have prodromal symptoms, including fatigue, fever, irritability, sore throat, and obvious tenderness of the skin. The erythema usually starts from the head and spreads within 48 hours, eventually giving the skin a wrinkled paper appearance due to the appearance of loose blisters in the superficial epidermis. The patient's Nikolsky sign was positive, and after 1 to 2 days, the bullae began to peel off, leaving a moist surface of the base and a thin lacquer-like suede. Usually, the site of exfoliation occurs first in the flexion site, and the patient presents with sad face, perioral scarring, radial cracks, and mild facial edema. After 3 to 5 days, the skin lesions began to desquamate and crusted. After 10 to 14 days, the epithelium regenerated and no scar was left after the skin lesions healed. The palmar and mucous membranes are not tired.

Examination of staphylococcal scalded skin syndrome

SSSS is a toxin-mediated disease and, therefore, pathogens cannot be obtained from lesions. It can be cultured from the external site of the lesion to the Staphylococcus aureus which is excreted toxin. The most common sites include the conjunctiva, nasopharynx, umbilicus, rectum and blood. Blood culture is often negative in children but positive in adults. Histologically damaged skin is a superficial subcortical blister with no epidermal necrosis. The white blood cell count can be increased or normal. At the same time, blood urea nitrogen, serum creatinine, electrolytes, etc. are checked. Screening for carriers of Staphylococcus aureus.

Diagnosis and identification of staphylococcal scalded skin syndrome

diagnosis

According to the onset of illness, extensive erythema of the skin, loose bullae, exfoliation of the epidermis, positive Nie's sign, and more common in infants and young children can be diagnosed.

The histopathology of this disease is parakeratosis, the stratum corneum can be reticular, the stomata of the spinous cell layer, the vacuole and nucleus of the spine cells, the gap between the stratum corneum and the spinous layer, the dermis with edema and congestion, blood vessels There is a moderately high inflammatory infiltration around.

Differential diagnosis

1. Fallic erythroderma: The lesion is diffuse flushing, with a lot of squamous scales on the surface, no pustules and erosions, scalp, eyebrows, and limbs with seborrheic dermatitis. Chronic course, using adequate antibiotics. invalid.

2. Neonatal impetigo: Some clinical manifestations are similar to this disease. Some people think that it may be the same type of disease, but the new impetigo is mainly pustule, does not form systemic erythroderma, Nissl's sign is negative, no The epidermis is loosened and often occurs within half a month of birth.

3. Non-gold grape type toxic epidermal necrolysis: It is important to distinguish between gold and Portuguese and non-Golden and Portuguese. Because the treatment is different, the prognosis is different. Most non-S. aureus type is caused by drugs. This part of the patient is actually a type of drug eruption, mainly found in adults, lesions pleomorphic, like polymorphic erythema, Nie's sign is only positive for lesions; and gold-and-glucose type is not damaged skin Nie's sign Also positive, pathological changes are not the same, non-S. aureus type epidermis full layer necrosis, subepidermal blister; and gold and Portuguese type is epidermal superficial necrosis, epidermis blister.

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