Scarbrough F E, Wittenberg J M, Smith B R, Adcock D K
Medical College of Georgia, Augusta, USA.
Anesth Prog. 1997 Summer;44(3):110-6.
Pulmonary edema that follows upper airway obstruction may occur in a variety of clinical situations. The predominant mechanism is forced inspiration against a closed or occluded glottis, inducing large intrapleural and transpulmonary pressure gradients favoring the transudation of fluid from the pulmonary capillaries into the interstitium. Postanesthetic laryngospasm has been implicated as the most frequent cause of this syndrome in adults. Risk factors for development of postlaryngospasm pulmonary edema include difficult intubation; nasal, oral, or pharyngeal surgical site; and obesity with obstructive apnea. The syndrome is recognized by development of hypoxia shortly (1-90 min) after a laryngospasm. A chest radiograph will reveal a symmetric bilateral infiltrate with normal heart size. Cardiogenic pulmonary edema and aspiration must be ruled out. Treatment is directed at correction of hypoxia with supplemental oxygen and use of diuretics (furosemide). Occasionally patients may require intubation.
上气道梗阻后发生的肺水肿可能出现在多种临床情况中。主要机制是在声门关闭或阻塞的情况下用力吸气,导致胸膜腔内和跨肺压力梯度增大,促使液体从肺毛细血管渗入间质。麻醉后喉痉挛被认为是成人该综合征最常见的原因。喉痉挛后肺水肿发生的危险因素包括插管困难;鼻、口或咽部手术部位;以及伴有阻塞性呼吸暂停的肥胖。该综合征在喉痉挛后不久(1 - 90分钟)出现缺氧时被识别。胸部X线片将显示双侧对称浸润,心脏大小正常。必须排除心源性肺水肿和误吸。治疗旨在通过补充氧气纠正缺氧并使用利尿剂(呋塞米)。偶尔患者可能需要插管。