ERISIPELA PEDIATRIA PDF

como uma infecção mais superficial de partes moles, como celulite ou erisipela, e com outras semelhanças quanto à eti- ologia e aos fatores predisponentes. pediatría cuidados del recién nacido normal nota: bibliografía en las diapositivas “recién nacido normal”. en el manual amir de pediatría ed., página. Mecanismos de infecção. Celulite Derme Tratamento Erisipela Celulite clínica – Cirurgia pediát Copy of Sessão clínica – Cirurgia pediátrica.

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Pyodermitis are primary skin infections mainly caused by pyogenic bacteria of erisi;ela Staphylococcus and Streptococcus genera. They are relatively common diseases that affect adults and children.

There have been frequent reports of bacterial resistance to the recommended antibiotics over the last few years; however, new substances are in use or under development, and this represents an evolution in the treatment erispela pyodermitis. This peiatria aims at describing clinical, diagnostic and therapeutical features of major pyodermitis: Bacterial infections; Review; Staphylococcus; Streptococcus; Skin infections staphylococcal.

The skin has resident bacteria, which live as commensal bacteria, and transient bacteria, which can occasionally colonize the skin. The resident flora consists mainly of Gram-positive cocci Staphylococcus epidermidisdiphtheroids Corynebacterium and Brevibacterium and anaerobic rods Propioni bacterium.

The organisms of the resident flora contribute to resistance against colonization with pathogenic bacteria pediatira hydrolyzing lipids and producing free fatty acids, which are toxic to many prdiatria. The transient flora is mainly represented by Staphylococcus aureus coagulase- positive and by Streptococcus pyogenes.

These bacteria, originating from the environment, show pathogenicity usually in the presence of a disturbance of skin integrity. Pyodermitis are defined as primary skin infections caused mainly by pyogenic bacteria of the Staphylococcus and Streptococcus genera. Among staphylococci, Staphylococcus aureus S. The skin is the natural habitat of many species of staphylococci.

There is permanent colonization with S. The main defense against staphylococci is neutrophil phagocytosis. Conditions that predispose to skin colonization due to low resistance to the agent include atopic dermatitis, diabetes mellitus, dialysis, intravenous drug use, liver dysfunction and HIV infection. Direct invasion occurring at small breaks in the mucous membranes, skin and its appendages results in a variety of superficial infections.

Streptococci almost always participate in the microbiota of the oral or gastrointestinal tract, and they are among the most common agents of human diseases. The most virulent streptococci belong to group A and have the M protein on their surface, which protects against phagocytosis and increases adherence to epithelial tissues. This is due to the fact that successive infections, symptomatic or unapparent, with prevalent serotypes in the community confer lasting and specific immunity against this pathogen.

The summer season favors skin infections, as it facilitates the installation and maintenance of the microclimate, heat and moisture necessary for the development of infectious agents. In the pathogenesis of pyodermitis we must consider host factors: With regard to the microorganism, the degree of pathogenicity and virulence is considered, which basically derives from the invasive potential determined by the presence of antiphagocytic elements on the bacterial surface and the ability to produce toxins.

Although the etiology of pyodermitis is basically the same, there are several distinct clinical forms with regard to morphology, evolution, pathogenesis, complications and therapy. Impetigo is a superficial skin infection caused mainly by staphylococci and, less often, streptococci or a combination of both bacteria. The disease is common and more prevalent in children.

There are two variants of the disease: Staphylococci have been the cause of bullous impetigo and group A streptococci are most frequently the causative organisms in nonbullous impetigo.

The purulent exudate dries and forms the classic thick yellowbrown crust meliceric. When removed, the crust quickly reappears. Although exposed areas of skin are affected more often in adults, in children any site can be affected.

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In staphylococcal bullous impetigo, small breaks in the skin allow the onset of infection with the formation of blisters caused by staphylococcal exfoliative toxins produced on site. The disease affects children, most often in the face and legs; however, it can also involve other areas. Nikolsky’s sign is not present. The lesions are small, multiple and in various stages of development.

Staphylococcal bullous impetigo does not jeopardize the general health of the individual, and fever is only present when there are multiple lesions.

Locally, there is minor discomfort and itching may occur. In the two variants, after the vesiculobulla ruptures and there is crust formation, central clearing and peripheral extension can lead to a circinate lesion, mimicking superficial fungal infection.

Lesions are usually asymptomatic and may sometimes show mild itching or burning. There is rapid development of satellite lesions by contamination of other areas, by scratching, or where there was contact with the exudate. The appearance of lesions of impetigo, which usually follows bruising, abrasions, minor trauma or insect bites, occurs in people whose skin surface was already colonized with group A streptococci, and lack of hygiene is an important predisposing factor. The bacterium can also implant on pre-existing skin lesions caused by eczema or scabies, a condition called impetiginization.

The diagnosis is achieved through clinical examination. The smear of the aspirated vesicle fluid subjected to direct microscopy and Gram-stained reveals the presence of Gram-positive cocci, and culture of the exudate beneath the crusts can reveal group A streptococci or staphylococci. The differential diagnosis of nonbullous impetigo should include herpes simplex, herpes zoster and scabies.

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The presence of atopic dermatitis, seborrheic dermatitis, chickenpox and scabies should also be considered. It is important to differentiate bullous impetigo from bullous drug eruption, bullous tinea, chickenpox, herpes simplex, staphylococcal scalded skin syndrome, as well as other less correlated conditions – dermatitis herpetiformis, erythema multiforme, bullous pemphigoid and pemphigus vulgaris. Invasive infection can complicate untreated impetigo caused by S.

It may cause cellulitis, lymphangitis and bacteremia, resulting in osteomyelitis, septic arthritis, pneumonitis and even sepsemia. Glomerulonephritis, caused by nephritogenic strains of S. Generally, the patient develops nephritic syndrome 3 to 6 weeks after skin infection.

The severity of renal involvement ranges from asymptomatic microscopic hematuria with normal renal function to acute renal failure. The acute phase usually resolves between 6 to 8 weeks. The treatment of impetigo involves cleaning and removing the crusts with warm water and soap, which should be done two to three times daily.

An antibiotic ointment or cream should be then applied, preferably one that is exclusively topical and with a low sensitizing power, such as mupirocin or fusidic acid. This approach is sufficient to clear mild to moderate cases, since the infection is often self-limited.

Recently, efisipela has been revealed as a new topical pediatroa to treat cases of impetigo. Retapamulin is the first member of a new class of antibiotics called pleuromutilins. It was approved by the FDA in April for the treatment of impetigo, when the disease is caused by S. It can be used in children nine months old or older. When there are widespread or bullous lesions, systemic administration of antibiotics is recommended, such as common or penicillinase-resistant semisynthetic penicillin, e.

Oral azithromycin, mg on the first day followed by mg over the next four days, in adults, has similar efficacy to that of oxacycline in treating skin infections. In patients allergic to penicillin, macrolides, such as erythromycin, are effective at the same dosage as penicillin for 5 to 7 days. Ecthyma is a pyogenic infection of the skin caused primarily by Streptococcus; however, Staphylococcus can also be found. The basic lesion consists of an erythematous plaque, often slightly swollen, measuring 2 to 3 cm in diameter.

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A vesicle or vesiculopustule soon develops and rapidly ruptures, forming a superficial ulcer covered by hard, thick and adherent honey-colored crusts. The border of the ulcer is indurated and erisi;ela and the granular tissue extends deep into the dermis. As it progresses, it may affect the subcutaneous cell tissue.

Ersiipela form of the disease manifests mainly in environments with poor hygiene. Factors such as low socio-economic status, malnutrition and immunodeficiency considerably influence its evolution.

It may result from impetigo that has not been properly treated. There are often multiple lesions and they are frequently found eriipela the feet, legs, thighs and buttocks.

Differential diagnosis should be done with stasis ulcers and cutaneous leishmaniasis. Several weeks of pediatrria therapy are needed for clearing. Treatment should be administered for 10 days with oral antibiotics such as dicloxacillin or a pediateia such as cephalexin. Possible complications are the same as those erisipella impetigo, especially glomerulonephritis. Staphylococcus aureus can be isolated more rarely. It primarily affects adults between 40 and 60 years of age, predominantly women.

The condition is characterized by redness, swelling, heat and pain, accompanied by fever, chills, malaise and oftentimes nausea or vomiting. The diagnosis of erysipelas is basically achieved through clinical examination. Venous insufficiency, fungal skin infections, lymphedema, diabetes mellitus, obesity, immunosuppression, respiratory tract infection and alcoholism are risk factors for erysipelas.

It is recommended that the treatment of erysipelas act not only on the infection, but also on lymphatic aspects. Long-term therapy for lymphedema is essential to prevent recurrence of erysipelas and aggravation of lymphatic disorder.

The therapeutic management of erysipelas consists in the introduction of antibiotics together with general measures, such as rest and elevation of the affected limb. Patients without signs of local or general severity can be treated orally with amoxicillin, The criteria for assessing the peditaria for hospitalization include age over 60 years, location in the face, signs of local severity such as blisters and necrosis or general severity such as confusion and hypotension, as well as co-morbidity factors such as immunosuppression, heart or kidney failure.

In a nosocomial environment and when there is strong suspicion of pediatrka with methicillin-resistant Staphylococcus aureus MRSAvancomycin and, erisipea recently, linezolid are recommended alternatives.

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Although relatively new, it shows great promise in treating a variety of gram-positive organisms, including MRSA. Taking into account the low risk of deep vein thrombosis 4. Only the existence of a clinical context that establishes a moderate to high thromboembolic risk can justify their use.

Measures to reduce recurrences include the treatment of predisposing factors. Staphylococcal scalded skin syndrome. Staphylococcal scalded skin syndrome SSSSalso known as Ritter’s disease, is caused by exfoliative toxins produced by some strains of S.

The toxin is antigenic and, when produced, triggers an immune response Figure 4. Two antigenically distinct forms of enterotoxins have been identified: In adults SSSS is associated with underlying diseases related to immunosuppression, altered immunity and renal insufficiency. In general, the infection is not in the skin, but pediiatria, in the form of otitis, conjunctivitis and other infections.

A few days after the pddiatria of staphylococcal infection, fever and diffuse erythema appear, over which large flaccid blisters develop and rapidly rupture, resulting in large areas of erosion surrounded by epidermal patches, corresponding to the detached skin. Nikolsky’s sign is present.