Postobstructive pulmonary edema after chronic airway obstruction relief: a positive end-expiratory pressure effect.

I refer to the article published in CHEST (June 2007) by Fremont et al 1 describing the hydrostatic mechanism for postobstructive pulmonary edema. This theory only explains the situation in which acute obstruction occurs after extubation (eg, acute laryngospasm), but does not explain conditions with chronic upper airway obstruction. We came across a case of postextubation pulmonary edema that could not be explained solely by hydrostatic mechanism. We report on an elderly man with carcinoma of the larynx, with tumor growth over the vocal cords for 2 years. In preoperative evaluation his cardiovascular system was unremarkable with normal ejection fraction and no diastolic dysfunction. He underwent total laryngectomy with permanent tracheostomy in situ ; the surgery was uneventful. Postoperatively he remained hemodynamically stable and was ventilated with positive pressure ventilation in the recovery room. Once he was conscious and obeying instructions, he was shifted to a T-piece as a weaning protocol. On the T-piece, he developed respiratory distress and went into pulmonary edema, requiring furosemide, nitroglycerin drip, and positive pressure ventilation with a positive end-expiratory pressure (PEEP) of 10. He was symptomatically relieved within a few hours. Repeat echocardiogram did not reveal any cardiac dysfunction, and ECG was also normal. He was gradually tapered off PEEP for the next 24 to 48 h; his intake and output were balanced to the negative side and weaned off by the end of 48 h. If we consider the hydrostatic mechanism described by Fremont et al 1 as the only cause, then the edema should occur when there was an obstruction, but here edema occurred after the relief of o bstruction. We hypothesize the following mechanism, in addi tion to the hydrostatic mechanism. In chronic obstruction of the upper airway, expiration occurs against a resistance, causing a PEEP effect in the bronchial tree. This PEEP is transmitted to alveoli, opposing the perialveolar hydrostatic pressure of heart physiology. 1 While the obstruction is there , there is no infl ux of fl uid into the alveoli and fl uid remains in the interstitium and drains into the peribronchial lymphatics. 2 Surgical relief of this obstruction causes a sudden release of the PEEP effect and as the hydrostatic forces do not come back to normal immediately, 2 it causes alveolar fl ooding and pulmonary edema. The usual measures of decreasing preload and using positive pressure ventilation help in rapid recovery. This hypothesis may help the anesthetist to enable a slow and gradual weaning of patients with chronic upper airway obstruction postoperatively, with a gradual decreasing of the PEEP in the recovery room.