Volume 26, Issue 1 , Pages 178-179, February 2012
Noncardiogenic Pulmonary Edema in a Cardiac Surgery Patient: Never a Welcome Sight for the Anesthesiologist
Article Outline
- Diagnosis: Noncardiogenic Pulmonary Edema Resulting From a Severe Protamine Reaction
- Supplementary data
- References
- Copyright
Key words: anesthesiology , protamine reaction , pulmonary edema , adverse effects , drug effects , blood transfusion , cardiopulmonary bypass
A 78-YEAR-OLD woman presented for redo aortic and mitral valve replacement and primary tricuspid valve repair. Aside from New York Heart Association Class IV congestive heart failure on the basis of a ruptured bioprosthetic mitral valve, her past medical history was relatively noncontributory. Anesthesia was induced in a hemodynamically neutral fashion, and anticoagulation was achieved with 30,000 IU of heparin and supplemented to maintain an activated coagulation time of greater than 500 seconds. The patient received a 4-g bolus of tranexamic acid followed by an infusion of 1 g/h. Intravenous hydrocortisone (100 mg) was administered because of the anticipated duration of cardiopulmonary bypass (CPB) time.
Replacement of the valves was performed successfully, and the patient was weaned from CPB with the support of milrinone, epinephrine, norepinephrine, and vasopressin infusions. Intravenous protamine sulfate (450 mg) was administered through a peripheral intravenous catheter over 15 minutes. Two units of fresh frozen plasma (FFP) were infused slowly for the treatment of coagulopathy after bypass. Approximately 15 minutes after completion of the protamine infusion and 20 minutes after initiation of the FFP, peak inspiratory pressures suddenly increased from 20 to 50 cmH2O, tidal volumes dropped dramatically, and the patient became difficult to ventilate. Examination of the patient's endotracheal tube yielded a profuse amount of frank serosanguinous fluid originating from the tube. The attached Hygrobac S Filter (Mallinckrodt Inc, Mirandola, Italy) became occluded from the copious amount of fluid if a suction catheter was not passed down the endotracheal tube every five minutes (Fig 1 and Video 1 [supplementary video is available online]). What is the diagnosis?
Fig 1.
A profuse amount of serosanguinous fluid originating from the endotracheal tube of a patient after the administration of protamine; the accompanying Hygrobac S Filter (bottom right) is fully saturated with fluid.
Diagnosis: Noncardiogenic Pulmonary Edema Resulting From a Severe Protamine Reaction
The differential diagnosis of serosanguinous fluid appearing in an endotracheal tube is limited, but each possibility represents a potentially critical event that requires immediate intervention. Given the clinical context, the possibility of a protamine reaction was recognized immediately, and the patient was promptly given 50 mg of diphenhydramine. Fortunately, the patient had been given hydrocortisone earlier, and an epinephrine infusion was already running. Positive end-expiratory pressure of 10 cmH2O was applied, and aggressive volume resuscitation and uptitration of the norepinephrine and vasopressin infusions were needed to maintain an adequate blood pressure. Transfusion-related acute lung injury (TRALI) was considered, but the decision was made to continue the transfusion of FFP because similar supportive measures already were underway. Transesophageal echocardiographic (TEE) findings and pulmonary artery occlusion pressures both suggested that this pulmonary edema was noncardiogenic in origin; the TEE also showed normal right ventricular function, decreasing the likelihood of a significant pulmonary embolism. The absence of frank blood made pulmonary artery rupture less likely, but the surgeon was asked to inspect the chest, and the possibility continued to be considered as the situation evolved. Interestingly, pulmonary artery pressures did not increase relative to baseline. This finding has been described in a previous report of a similar reaction.1 The patient's systemic hypotension soon stabilized; however, with the multitude of simultaneous interventions it was difficult to determine which were most responsible. Minimal consideration was given to returning to CPB. A remarkable volume of frothy fluid continued to be produced; the total volume of fluid was measured at 600 mL, but it was estimated that at least an equivalent volume was lost to the surrounding environment.
The patient was transferred to the cardiac surgery intensive care unit without incident. A chest radiograph (Fig 2) was consistent with diffuse pulmonary edema, which was increased markedly in comparison to her preoperative films. After some initial hemodynamic lability, inotropic and ventilatory support were weaned gradually, and the patient was extubated on postoperative day 4. At the last follow-up 1 month later, the patient was stable on the ward awaiting return to her local hospital.
Fig 2.
A postoperative chest radiograph showing diffuse pulmonary edema.
Pulmonary edema in the context of cardiac surgery and CPB can present an interesting diagnostic challenge given the relative complexity of the patient, the procedure, and the anesthetic. Fortunately, once the diagnosis of noncardiogenic pulmonary edema has been established, the supportive treatment for all forms is largely the same, consisting of volume resuscitation, hemodynamic support, and positive pressure ventilation.1 A common finding in case reports describing protamine reactions is the concomitant transfusion of FFP or other blood products and the recognition that TRALI may have contributed to the clinical picture.2 Although the authors certainly acknowledge that this case of noncardiogenic pulmonary edema could potentially be explained by TRALI, it was believed that a protamine reaction was more likely for several reasons. First, the relative immediacy of the reaction was more suggestive of a relationship to protamine, given that TRALI often develops within several hours.3, 4, 5, 6, 7 A review by Horrow8 showed that noncardiogenic pulmonary edema attributed to protamine typically occurred between 20 and 60 minutes. Two recent case reports described protamine reactions that occurred 5 and 10 minutes after completion of the protamine infusion, respectively.1, 9 The authors realize that occasional TRALI reactions have been reported to occur within minutes, but a survey of the literature seems to indicate that a more delayed presentation is considered normal.5, 6, 7 The relatively slow transfusion of blood products also made TRALI less likely, given that TRALI is typically reported after the rapid transfusion of plasma-rich components.7 Finally, the improvement of the noncardiogenic pulmonary edema, despite the continued delivery of blood products, suggested that TRALI was less likely. However, in the absence of further immunologic testing, which was not pursued with this patient, it is impossible to definitively exclude TRALI.
Supplementary data
Video 1. Removal of the Hygrobac S Filter from the endotracheal tube shows the rapid flow of serosanguinous fluid from the patient's endotracheal tube.
References
- Noncardiogenic pulmonary edema associated with protamine administration during coronary artery bypass graft surgery . J Clin Anesth . 1999;11:675–681
- . Protamine and protamine reactions . Int Anesthesiol Clin . 2004;42:135–145
- . Transfusion-related acute lung injury: A change of perspective . Neth J Med . 2009;67:320–326
- Transfusion-related acute lung injury (TRALI): Current concepts and misconceptions . Blood Rev . 2009;23:245–255
- . Transfusion-related acute lung injury: Current concepts for the clinician . Anesth Analg . 2009;108:770–776
- . Transfusion-related acute lung injury (TRALI): Clinical presentation, treatment, and prognosis . Crit Care Med . 2006;34:S114–S117
- . Transfusion-related acute lung injury (TRALI): Presentation, epidemiology and treatment . Intensive Care Med . 2007;33:S12–S16
- . Protamine allergy . J Cardiothorac Anesth . 1988;2:225–242
- Dramatic post-cardiotomy outcome, due to severe anaphylactic reaction to protamine . Eur J Cardiothorac Surg . 2003;24:325–327
PII: S1053-0770(10)00422-2
doi:10.1053/j.jvca.2010.09.026
© 2012 Elsevier Inc. All rights reserved.
Volume 26, Issue 1 , Pages 178-179, February 2012
