Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke · 2002
[Lung edema follows inspiratory stridor--another pitfall for the anesthesiologist].
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Lindenskov Paal H H, Hanem Sigrid, Sponheim Sjur
Аннотация
BACKGROUND: Patients with heart failure or elevated intracranial pressure are at risk of developing lung oedema when anaesthesized. Lung oedema may develop in patients with airway obstructions as well.
MATERIAL AND RESULTS: We refer to a four-year-old boy anaesthesized for elective adenotomia and paracentesis. After being extubated, he developed a moderate inspiratory stridor lasting for hours. Clinically he normalized in two hours on a therapy with oxygen in a mask with continuous positive airway pressure (CPAP) and finally bronchodilator therapy with epinephrine and salbutamol. Successive lung X-rays showed lung oedema almost normalizing in 48 hours.
INTERPRETATION: The triggering mechanism of lung oedema in airway obstruction is the negative intrathoracal pressure generated because of forced inspiratory effort. This pressure is transformed to a negative interstitial hydrostatic pressure that according to Starling's hypothesis on capillary filtration may generate a lung oedema. We conclude that our patient with nasal polyps had a lowered threshold for developing lung oedema faced with postextubatory complications causing inspiratory stridor. Pathogenic mechanisms are discussed.
MATERIAL AND RESULTS: We refer to a four-year-old boy anaesthesized for elective adenotomia and paracentesis. After being extubated, he developed a moderate inspiratory stridor lasting for hours. Clinically he normalized in two hours on a therapy with oxygen in a mask with continuous positive airway pressure (CPAP) and finally bronchodilator therapy with epinephrine and salbutamol. Successive lung X-rays showed lung oedema almost normalizing in 48 hours.
INTERPRETATION: The triggering mechanism of lung oedema in airway obstruction is the negative intrathoracal pressure generated because of forced inspiratory effort. This pressure is transformed to a negative interstitial hydrostatic pressure that according to Starling's hypothesis on capillary filtration may generate a lung oedema. We conclude that our patient with nasal polyps had a lowered threshold for developing lung oedema faced with postextubatory complications causing inspiratory stridor. Pathogenic mechanisms are discussed.