Galvis A G
Am J Emerg Med. 1987 Jul;5(4):294-7. doi: 10.1016/0735-6757(87)90354-8.
Treatment by endotracheal intubation or tracheostomy in children with severe and prolonged upper airway obstruction usually results in dramatic improvement; in some rare instances, it is complicated by the development of pulmonary edema. During an eight-year period, the author observed this complication in 20 children. The mechanism of this edema is complex and not yet fully understood. In addition to hypoxia, profound hemodynamic changes occur during the inspiratory phase of the obstruction; highly negative transpulmonary pressure may lead to an increase in pulmonary blood volume and biventricular dysfunction, and possibly disruption of integrity of the pulmonary endothelium. These hemodynamic changes appear to be counterbalanced by the positive pleural and alveolar pressures and decreased venous return during the expiratory component of the obstruction. Nevertheless, when an artificial airway is inserted, this compensation is disrupted abruptly, resulting in an increase in systemic venous return and thus pulmonary edema. Although this type of edema usually is observed in cases of severe obstruction, it may go unrecognized or misdiagnosed.
对患有严重且持续性上呼吸道梗阻的儿童进行气管插管或气管切开治疗通常会带来显著改善；在一些罕见情况下，会并发肺水肿。在八年期间，作者观察到20名儿童出现了这种并发症。这种水肿的机制很复杂，尚未完全明确。除了缺氧外，梗阻吸气期会发生深刻的血流动力学变化；极高的跨肺负压可能导致肺血容量增加和双心室功能障碍，并可能破坏肺内皮的完整性。这些血流动力学变化似乎在梗阻呼气期被胸膜和肺泡正压以及静脉回流减少所抵消。然而，当插入人工气道时，这种代偿会突然被打破，导致体循环静脉回流增加，进而引发肺水肿。虽然这种类型的水肿通常在严重梗阻病例中观察到，但可能未被识别或误诊。
