I refer to the article published in CHEST (June 2007) by Fremont et al1 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.