Lindenskov Paal H H, Hanem Sigrid, Sponheim Sjur
Anestesiavdelingen Rikshospitalet 0027 Oslo.
Tidsskr Nor Laegeforen. 2002 Sep 20;122(22):2184-6.
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.
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.
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.
心力衰竭或颅内压升高的患者在麻醉时易发生肺水肿。气道阻塞患者也可能发生肺水肿。
我们提到一名4岁男孩,因择期腺样体切除术和腹腔穿刺术接受麻醉。拔管后,他出现了持续数小时的中度吸气性喘鸣。临床上,在面罩吸氧并持续气道正压通气(CPAP)治疗以及最终使用肾上腺素和沙丁胺醇进行支气管扩张剂治疗两小时后,他恢复正常。后续的肺部X光片显示肺水肿在48小时内几乎恢复正常。
气道阻塞时肺水肿的触发机制是由于用力吸气努力产生的胸腔内负压。根据斯塔林关于毛细血管滤过的假说,这种压力会转化为负的间质静水压,从而可能导致肺水肿。我们得出结论,我们这位患有鼻息肉的患者在面对拔管后导致吸气性喘鸣的并发症时,发生肺水肿的阈值较低。文中讨论了致病机制。