[Case of drug-induced angioedema (DIAE) on induction of anesthesia with difficult ventilation due to oropharyngeal edema].

A 69-year-old man with a past history of hypertension on angiotensin II receptor blocker (ARB) for three months presented for radical prostatectomy. Immediately after induction of anesthesia with fentanyl and propofol, mask ventilation became difficult, although no significant hemodynamic changes occurred. Fiberoptic examination revealed severe oropharyngeal edema, but, the trachea was successfully intubated. Afterward, the operation proceeded without complications. He stayed in the ICU for 4 days until the trachea was extubated successfully. He was diagnosed with DIAE because of his history of dyspnea with exclusion of other possible pathophysiological conditions.

A patient with possible TRALI who developed pulmonary hypertensive crisis and acute pulmonary edema during cardiac surgery.

There are very few case reports of transfusion-related acute lung injury (TRALI) under close hemodynamic monitoring. We encountered a case of possible TRALI during on-pump coronary artery bypass grafting (CABG). A 66-year-old man who had undergone on-pump CABG was administered fresh frozen plasma (FFP). One hour after FFP transfusion, pulmonary hypertensive crisis and subsequent hypoxic decompensation occurred. A second cardiopulmonary bypass (CPB) was needed for circulatory and respiratory deterioration. Extracorporeal life support (ECLS), intraaortic balloon pumping (IABP), and nitric oxide therapy were required after the surgery. Despite the severity of the initial state, his recovery was comparatively smooth. ECLS and IABP were removed on postoperative day (POD)1; the patient was extubated and discharged from the ICU on POD7 and POD12, respectively. The diagnosis of TRALI was confirmed by human leukocyte antigen antibody detection in the administered FFP. In addition, lymphocytic immunofluorescence test showed that a cross-match of the plasma from the pooled FFP against the recipient leukocytes was positive. The clinical course of the pulmonary artery hypertension was followed by a decrease in dynamic lung compliance. The mechanism of this phenomenon is unclear. However, it might suggest the possibility of vasoconstriction or obstruction of the peripheral pulmonary artery preceding lung damage, as in the case in animal models reported previously.