Das akute Atemnotsyndrom (ARDS) bei Kindern und Jugendlichen

Zusammenfassung

Das akute Atemnotsyndrom (ARDS) tritt jährlich bei 3–6/100 000 Kindern und Jugendlichen auf. Ursächlich sind verschiedenste direkte und indirekte Lungenschäden, wobei Pneumonien und Sepsis, gefolgt von Polytraumata und Ertrinkungsunfällen, die häufigsten sind. Zu 60% sind chronisch kranke Kinder betroffen, darunter 35% mit Störungen der Immunabwehr. Die Sterblichkeit beträgt ca. 25–30%, bei immundefizienten Patienten ca. 50%. Eine Störung der Immunität ist der wichtigste unabhängige Risikofaktor für die Entwicklung und das Überleben eines ARDS. Die dabei auftretende Hypoxämie ist Folge einer Schädigung der alveolokapillären Grenzmembran und des Kollapses der Alveolen bzw. der Ausbildung eines nichtkardiogenen Lungenödems. Durch effektive Beseitigung der auslösenden Ursache, Veränderungen der Beatmungstherapie mit niedrigen Atemzugvolumina und einem endexspiratorischen Druck (PEEP), der ausreicht, den Kollaps eröffneter Alveolarbezirke zu verhindern, und eine differenzierte Kreislauftherapie hat sich die Sterblichkeit durch Hypoxie bei ARDS drastisch vermindert. Aufwändige Therapien wie die Gabe von Surfactant oder die extrakorporale Membranoxygenierung (ECMO) sind selten gerechtfertigt.

Summary

The acute respiratory distress syndrome (ARDS) in children and adolescents occurs with an incidence of 3–6/100 000. The lung injury is caused directly or indirectly, mostly due to pneumonia, sepsis, multiple trauma and near-drowning. Around 60% of patients suffer from underlying chronic disease, 35% are immunodeficient. The mortality improved significantly over the past decade. Total mortality is 25–30%, and 50% in immunocompromised patients. Immunodeficiency is the most important risk factor for development of ARDS and for mortality. Hypoxemia is caused by damage of the alveolo-capillary membrane which leads to alveolar collaps and non-cardiogenic pulmonary oedema. Effective treatment of the causative disease, ventilaton with low tidal volumes and end-exspiratory pressure (PEEP) sufficient to prevent re-collaps of recruited alveolae, prone positioning and appropriate fluid management are the mainstays of treatment. Complex and costly therapies like the application of Surfactant or extracorporeal membrane oxygenation (ECMO) are required rarely.

Schlüsselwörter

Akutes Atemnotsyndrom (ARDS) - nicht-kardiogenes Lungenödem - akutes Lungenversagen

Keywords

Acute respiratory distress syndrome (ARDS) - non-cardiogenic pulmonary oedema - acute lung injury

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