• Am. J. Surg. · Apr 1984

    Case Reports

    Noncardiogenic pulmonary edema after cardiopulmonary bypass. An anaphylactic reaction to fresh frozen plasma.

    • S W Hashim, H R Kay, G L Hammond, G S Kopf, and A S Geha.
    • Am. J. Surg. 1984 Apr 1;147(4):560-4.

    AbstractNine episodes of fulminant noncardiogenic pulmonary edema after cardiopulmonary bypass were observed in eight patients between September 1977 and December 1982. All these catastrophic reactions occurred during administration of fresh frozen plasma 30 minutes to 6 hours after discontinuation of cardiopulmonary bypass. In one patient, two episodes of noncardiogenic pulmonary edema occurred 4 hours apart. In each instance, fresh frozen plasma was being administered. In all patients, pulmonary artery diastolic pressure became elevated during the administration of fresh frozen plasma while left atrial pressure or pulmonary capillary wedge pressure progressively decreased, and cardiac output deteriorated markedly in all but one patient. Corticosteroids, positive end-expiratory pressure, and catecholamines were administered to all patients. All deaths were due to a decrease in cardiac output. Cardiac output did not increase substantially with the use of an intraaortic balloon pump or the administration of catecholamines. The last two patients in the series showed a steady and remarkable improvement in cardiac output when the wedge pressure was increased to a level above 15 mm Hg with the administration of normal saline solution. Our data suggest the following: (1) noncardiogenic pulmonary edema after cardiopulmonary bypass is most probably an anaphylactic reaction to fresh frozen plasma. (2) The syndrome is reversible within hours; in only one patient (who suffered noncardiogenic pulmonary edema twice) did adult respiratory distress syndrome develop. (3) The three deaths were not related to hypoxia but to the deleterious effects of low cardiac output associated with hypovolemia secondary to fluid loss through the lungs and possibly across other capillary beds. Therefore, treatment should include restoration of adequate left-sided filling pressures to achieve satisfactory cardiac output.

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