Brun-Buisson C J, Bonnet F, Bergeret S, Lemaire F, Rapin M
Crit Care Med. 1985 Jan;13(1):55-6. doi: 10.1097/00003246-198501000-00015.
Delayed-onset pulmonary edema complicating severe diabetic ketoacidosis was observed twice in one patient. Hemodynamic measurements during the second episode showed normal transmural pulmonary capillary wedge pressure, suggesting an alteration in alveolocapillary permeability. Hyperventilation and acidosis may underlie this alteration. Vigorous fluid therapy, while decreasing oncotic pressure, may also contribute to the pulmonary edema. The two episodes in one patient suggest that pulmonary microvascular diabetic angiopathy may predispose some diabetics with severe ketoacidosis to increased-permeability pulmonary edema.
一名患者曾两次出现严重糖尿病酮症酸中毒并发迟发性肺水肿。第二次发作期间的血流动力学测量显示跨壁肺毛细血管楔压正常，提示肺泡毛细血管通透性改变。过度通气和酸中毒可能是这种改变的基础。积极的液体治疗在降低胶体渗透压的同时，也可能促使肺水肿的发生。同一患者的两次发作提示，肺微血管糖尿病性血管病变可能使一些严重酮症酸中毒的糖尿病患者易患通透性增加性肺水肿。
