RESUMO
Aunque la varicela suele ser una enfermedad benigna, algunas complicaciones pueden ser mortales, como la púrpura fulminante posvaricelosa. Su mecanismo fisiopatogénico se explica por la producción de anticuerpos para las proteínas C y S de la cascada de la coagulación, lo que puede tener consecuencias funestas con la producción de coagulopatía de consumo en personas con déficits parciales de estas proteínas. El tratamiento es sintomático y consiste básicamente en la administración de plasma fresco congelado (para suplir las proteínas que se consumen), de antitrombina III y heparinización (para tratar la producción de trombos) y de antiinflamatorios, como los corticoides; sin embargo, se están introduciendo tratamientos nuevos, como la prostaglandina E1 intravenosa y la prostaciclina (AU)
Although varicella is usually a benign disease, some of its complications, such as post-varicella purpura fulminans, can be fatal. Its pathophysiological mechanism is caused by the production of antibodies to protein C and protein S in the coagulation cascade. This could have fatal consequences for those patients with partial deficiency of these proteins that develop disseminated intravascular coagulation. Treatment is symptomatic: fresh frozen plasma to treat protein depletion, antithrombin III and heparinization against thrombus formation, and anti-inflammatory drugs (steroids). However, new therapies, such as prostaglandin E1 IV and prostacyclin, are being introduced (AU)
Assuntos
Humanos , Feminino , Pré-Escolar , Varicela/complicações , Varicela/tratamento farmacológico , Varicela/patologia , Proteína C/imunologia , Proteína S/imunologia , Antitrombina III/farmacologia , Antitrombina III/uso terapêutico , Heparina/uso terapêutico , Alprostadil/uso terapêutico , Gangrena/patologia , Equimose/enfermagem , Púrpura/embriologia , Plasma/fisiologia , Síndromes Compartimentais/complicaçõesRESUMO
Although varicella is usually a benign disease, some of its complications, such as post-varicella purpura fulminans, can be fatal. Its pathophysiological mechanism is caused by the production of antibodies to protein C and protein S in the coagulation cascade. This could have fatal consequences for those patients with partial deficiency of these proteins that develop disseminated intravascular coagulation. Treatment is symptomatic: fresh frozen plasma to treat protein depletion, antithrombin III and heparinization against thrombus formation, and anti-inflammatory drugs (steroids). However, new therapies, such as prostaglandin E1 IV and prostacyclin, are being introduced.
