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Unusual severe hypoxemia due to unilateral pulmonary edema after conventional cardiopulmonary bypass salvaged by veno-venous extracorporeal membrane oxygenation: a case report



We report a case in which veno-venous extracorporeal membrane oxygenation (V-V ECMO) saved the life of a patient who developed severe hypoxemia due to unusual unilateral pulmonary edema (UPE) after cardiopulmonary bypass (CPB).

Case presentation

A 69-year-old man underwent aortic valve replacement and coronary artery bypass grafting. Following uneventful weaning off CPB, he developed severe hypoxemia. The ratio of arterial oxygen tension to inspired oxygen fraction (PaO2/FiO2) decreased from 301 mmHg 5 min after CPB to 42 mmHg 90 min after CPB. A chest X-ray revealed right-sided UPE. Immediately established V-V ECMO increased PaO2/FiO2 to 170 mmHg. Re-expansion pulmonary edema (REPE) was likely, as the right lung remained collapsed during CPB following the accidental opening of the right chest cavity during graft harvesting.


V-V ECMO was effective in improving oxygenation and saving the life of a patient who had fallen into unilateral REPE unusually developing after conventional CPB.


Acute pulmonary edema after cardiac surgery develops due to cardiogenic and non-cardiogenic causes and occasionally leads to severe hypoxemia that cannot be managed with mechanical ventilation alone [1, 2]. Unilateral pulmonary edema (UPE) after on-pump minimally invasive cardiac surgeries (MICS) has been increasingly reported [3]. However, reports on UPE after conventional on-pump cardiac surgeries remain very rare [4]. Herein, we report a case in which veno-venous extracorporeal membrane oxygenation (V-V ECMO) saved the life of a patient with severe hypoxemia due to UPE that developed acutely after weaning off conventional cardiopulmonary bypass (CPB).

Case presentation

A 69-year-old man (162 cm, 48.5 kg), with a history of coronary artery disease (CAD) previously treated with percutaneous transluminal coronary angioplasty, hypertension as well as diabetes mellitus under medication, and end-stage diabetic nephropathy on hemodialysis, was scheduled for aortic valve replacement (AVR) and coronary artery bypass grafting (CABG) for newly diagnosed severe aortic stenosis (AS) and recurrent CAD. Preoperative transthoracic echocardiography showed a global left ventricular ejection fraction (in the presence of regional hypokinesis) of 53%, left ventricular diastolic/systolic dimensions of 37/27 mm, and AS due to calcified valve leaflets, with an aortic valve area (AVA) of 0.5 cm2 and indexed AVA of 0.19 cm2/m2. Coronary angiography showed 90% stenotic lesions in the right coronary artery (RCA) and left circumflex artery (LCX).

After the establishment of an arterial line, general anesthesia was induced with midazolam 4 mg and fentanyl 400 µg. Vecuronium bromide 8 mg was given to facilitate tracheal intubation. A central venous catheter and pulmonary artery catheter (PAC) were placed via the right internal jugular vein. Transesophageal echocardiography (TEE) was also used. General anesthesia was maintained with propofol 2 mg/kg/h and remifentanil 0.3 µg/kg/min. Following a median sternotomy, the right internal thoracic artery (RITA) graft and saphenous vein graft (SVG) were harvested. During RITA harvesting, the right chest cavity was accidentally opened but was subsequently left opened until immediately before chest closure. After graft harvesting, CPB was started with the arterial cannula placed in the ascending aorta and venous cannulas placed in the superior and inferior vena cava (IVC). First, on-pump beating CABG was performed, including a RITA-LCX anastomosis and two sequential SVG-RCA anastomoses. Then, the ascending aorta was cross-clamped, and AVR was performed with a Trifecta biological valve. During CPB, the patient received transfusions of 12 units of red cell concentrates and 4 units of irradiated fresh-frozen plasma (FFP).

After completion of the surgical repair, adequate de-airing of the heart was facilitated with a manual lung inflation maneuver and volume loading of the heart. Prior to weaning from CPB, mechanical ventilation was resumed with an inspired oxygen fraction (FiO2) of 1. The patient was successfully weaned off CPB with some inotropic support. His pulmonary artery pressure (PAP) remained normal, and cardiac index (CI) remained at approximately 2.5 L/min/m2. TEE revealed the well-functioning artificial valve, well-preserved left ventricular wall motion, trivial mitral regurgitation (MR), and no enlargement of the left atrium (LA). A significant volume of retained blood was evacuated from the right thoracic cavity. The patient was uneventfully weaned off CPB. The durations of CPB and aortic cross-clamping were 251 min and 127 min, respectively.

After administration of protamine, 4 units of irradiated FFP and 20 units of platelet concentrates were transfused. Shortly after the start of the transfusion, however, he developed progressive hypoxemia. The ratio of arterial oxygen tension to FiO2 (PaO2/FiO2) decreased from 301 mmHg 5 min after CPB to 140 mmHg 45 min after CPB and, further, to 42 mmHg 90 min after CPB (Fig. 1) . As soon as the surgical wound was closed 475 min after the start of surgery, anesthesiologists inserted a return cannula into the right atrium via the left internal jugular vein, while surgeons inserted a drainage cannula into the IVC via the right femoral vein to establish V-V ECMO. A chest X-ray showed diffuse unilateral pulmonary consolidation in the right lung with no increase in a cardiothoracic ratio, indicative of non-cardiogenic UPE (Fig. 2). V-V ECMO with a flow rate of 2 L/min successfully increased PaO2/FiO2 to 170 mmHg (Figs. 2 and 3).

Fig. 1
figure 1

PaO2/FiO2 ratio and SpO2 during and after surgery. PaO2/FiO2, ratio of arterial oxygen tension to inspired oxygen fraction; SpO2, percutaneous arterial oxygen saturation; CPB, cardiopulmonary bypass; ECMO, extracorporeal membrane oxygenation; POD, postoperative day

Fig. 2
figure 2

Chest X-rays A before surgery, B after chest closure, and C on postoperative day 5. The chest X-ray taken immediately after chest closure (B) showed diffuse unilateral pulmonary consolidation in the right lung, with no increase in cardiothoracic ratio, consistent with non-cardiogenic, unilateral pulmonary edema. That taken on POD 5 (C) showed improvement in unilateral pulmonary consolidation. The white arrow depicted in B indicates a return cannula placed via the left internal jugular vein

Fig. 3
figure 3

Hemodynamic changes before, during, and after surgery. Anesthesia starts from 0 on the horizontal axis. BP, blood pressure; HR, heart rate; CI, cardiac index; SpO , percutaneous arterial oxygen saturation; ECMO, extracorporeal membrane oxygenation

The patient was transferred to the intensive care unit. Continuous hemodiafiltration was started via a catheter placed in the left femoral vein. The improvement in oxygenation was maintained with V-V ECMO and pressure-controlled ventilation employing a lung-protective strategy (Fig. 1). The patient was weaned off V-V ECMO on postoperative day (POD) 3 (Fig. 1) and was extubated on POD 7. The patient was, however, re-intubated due to aspiration on POD 7 and re-extubated on POD 13. He returned to the general ward on POD 17 and was subsequently discharged in an ambulatory condition on POD 78. Neither antihuman leukocyte antigen (HLA) antibody nor anti-granulocyte antibody was detected in samples of the transfused blood products.


Acute cardiogenic or non-cardiogenic pulmonary edema sometimes develops in patients undergoing major cardiovascular surgery, although most cases present with bilateral pulmonary edema (BPE) [5]. Reportedly, UPE, which accounts for 2.1% of cardiogenic pulmonary edema (CPE) cases, usually occurs in the right lung [6]. Although there is no specifically established treatment for UPE that differs from BPE, UPE is associated with more severe conditions requiring mechanical ventilation and more intensive inotropic support [6]. The major cause of cardiogenic UPE is MR due to its propensity to flow anatomically into the right superior pulmonary vein [7]. Another underlying mechanism of right-sided UPE is a difference in interstitial flow in the lungs due to the right-sided lymphatic vessels having a smaller aperture and a longer distance to the thoracic duct than left-sided lymphatic vessels [8, 9].

In our patient, UPE occurred in the right lung. However, CPE was unlikely, since TEE did not reveal significant MR or LA enlargement, and instead revealed well-preserved left ventricular wall motion, while the PAC revealed normal PAP and CI, and chest X-ray revealed neither the increased cardiothoracic ratio nor “butterfly pattern” typically seen in CPE.

UPE can develop also due to other pathological conditions, such as acute pulmonary emboli, re-expansion pulmonary edema (REPE), and external compression of the pulmonary vasculatures by a tumor or hematoma, resulting in asymmetrical inflow to the pulmonary arteries or outflow to the pulmonary veins [10]. In our case, the right lung was left collapsed during CPB after discontinuation of mechanical ventilation, since the right chest cavity was opened during RITA graft harvesting. Furthermore, blood retention in the cavity might have aggravated the collapse. Therefore, REPE due to rapid re-expansion of the right lung following its collapse likely caused right-sided UPE. Typically, REPE develops only after the lung collapsed for 72 h or longer is rapidly reinflated [11]. However, since on-pump MICS via right mini-thoracotomies using one-lung ventilation are increasingly being performed, it has become evident that right-sided unilateral REPE can develop much earlier after CPB [12, 13]. Lung collapse is associated with the sequestration of leucocytes, and inflammatory activity is triggered when oxygen is supplied during re-expansion and concomitant reperfusion of the lung [14, 15]. This inflammatory response might be enhanced by multiple factors during cardiac surgery [12]. The inflammatory response to re-expansion and reperfusion can be aggravated by the generalized inflammatory response generated by CPB [12], as suggested by the association between prolonged CPB time and the development of UPE in MICS [13, 14]. The FiO2 set at 1.0 upon resuming ventilation might have worsened the inflammatory reaction during re-expansion, though we reduced the FiO2 to 0.5 immediately after measuring blood gas 5 min after CPB. Furthermore, the restricted bronchial artery blood flow during CPB might worsen lung ischemia [16]. Therefore, the combination of right lung collapse and prolonged CPB time might have resulted in the unilateral REPE in our case, although unilateral REPE has rarely been reported in patients undergoing conventional on-pump cardiac surgery [4], unlike those undergoing on-pump MICS [12, 13].

Since UPE occurred after the start of blood transfusion in our patient, we also considered the possibility of transfusion-related acute lung injury (TRALI) [17,18,19]. However, anti-HLA antibody or anti-granulocyte antibody, which reportedly triggers lung microvascular endothelial damage [19], was not detected in samples of transfused blood products. Additionally, TRALI usually presents with BPE [18]. Therefore, TRALI less likely caused UPE than REPE in our case.

The use of ECMO is indicated when a poor therapeutic response to conventional mechanical ventilation and a high mortality rate are predicted in patients with reversible lung injury [20, 21]. When considering the indication for ECMO, it is recommended to estimate the Murray score, in which a score of 2.5 or more indicates “severe” lung injury [21, 22]. Our patient was indicated for ECMO, since he was highly likely to die from severe hypoxemia without using ECMO, given his Murray score estimated to be 2.75 and PaO2/FiO2 as low as 42 mmHg.

In conclusion, we reported a rare case of UPE with severe hypoxemia that developed after conventional on-pump cardiac surgery. REPE seemed the likely cause of the UPE. V-V ECMO was quite effective in improving oxygenation and saving the patient’s life.

Availability of data and materials

The datasets related to this report are available from the corresponding author upon reasonable request.



Aortic stenosis


Aortic valve area


Aortic valve replacement


Bilateral pulmonary edema


Coronary artery bypass grafting


Coronary artery disease


Cardiac index


Cardiopulmonary bypass


Cardiogenic pulmonary edema


Fresh-frozen plasma

FiO2 :

Inspired oxygen fraction


Inferior vena cava


Left atrium


Left circumflex artery


Minimal invasive cardiac surgery


Mitral regurgitation


Pulmonary artery catheter


Ratio of arterial oxygen tension to fraction of inspired oxygen


Pulmonary artery pressure


Postoperative day


Right coronal artery


Re-expansion pulmonary edema


Right internal thoracic artery


Saphenous vein graft


Transfusion-related acute lung injury


Transesophageal echocardiography


Unilateral pulmonary edema


Veno-venous extracorporeal membrane oxygenation


  1. Bignami E, Frati E, Meroni R, Verzini A, Pozzoli A, Benussi S, Alfieri O. Extracorporeal venovenous membrane oxygenation in the treatment of respiratory insufficiency following cardiac surgery. J Card Surg. 2014;29(2):270–3.

    Article  PubMed  Google Scholar 

  2. Vardas PN, Matthews C, Rosati CM, Beckman DJ. Severe re-expansion pulmonary edema after conventional cardiac surgery: identification and management. J Card Surg. 2019;34(6):525–7.

    Article  PubMed  Google Scholar 

  3. Moss E, Halkos ME, Binongo JN, Murphy DA. Prevention of unilateral pulmonary edema complicating robotic mitral valve operations. Ann Thorac Surg. 2017;103(1):98–104.

    Article  PubMed  Google Scholar 

  4. Toyama M, Nakayama M, Fujita Y, Shimazu S, Sawasaki T. Unilateral pulmonary edema during aortic valve replacement through median sternotomy. Kyobu Geka. 2020;73(6):417–22.

    PubMed  Google Scholar 

  5. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005;353(26):2788–96.

    Article  CAS  PubMed  Google Scholar 

  6. Attias D, Mansencal N, Auvert B, Vieillard-Baron A, Delos A, Lacombe P, N’Guetta R, Jardin F, Dubourg O. Prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema. Circulation. 2010;122(11):1109–15.

    Article  PubMed  Google Scholar 

  7. Bekiaridou A, Kartas A, Moysidis DV, Papazoglou AS, Patsiou V, Baroutidou A, Kamperidis V, Giannakoulas G. Severe mitral regurgitation causing unilateral pulmonary edema: a case report. J Cardiol Cases. 2022;26(2):130–3.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Alarcón JJ, Guembe P, de Miguel E, Gordillo I, Abellás A. Localized right upper lobe edema. Chest. 1995;107(1):274–6.

    Article  PubMed  Google Scholar 

  9. Lesieur O, Lorillard R, Thi HH, Dudeffant P, Ledain L. Unilateral pulmonary oedema complicating mitral regurgitation: diagnosis and demonstration by transoesophageal echocardiography. Intensive Care Med. 2000;26(4):466–70.

    Article  CAS  PubMed  Google Scholar 

  10. Hirata K, Ishimine T, Nakayama I, Yagi N, Wake M, Takahashi T, Taniguchi N, Tengan T. Unilateral left pulmonary edema caused by contained rupture of the ascending aortic dissection. Intern Med. 2021;60(5):751–3.

    Article  PubMed  Google Scholar 

  11. Kasmani R, Irani F, Okoli K, Mahajan V. Re-expansion pulmonary edema following thoracentesis. CMAJ. 2010;182(18):2000–2.

    Article  PubMed  PubMed Central  Google Scholar 

  12. Keyl C, Siepe M. Unilateral lung injury after minimally invasive cardiac surgery: more questions than answers. Eur J Cardiothorac Surg. 2016;49(2):505–6.

    Article  PubMed  Google Scholar 

  13. Irisawa Y, Hiraoka A, Totsugawa T, Chikazawa G, Nakajima K, Tamura K, Yoshitaka H, Sakaguchi T. Re-expansion pulmonary oedema after minimally invasive cardiac surgery with right mini-thoracotomy. Eur J Cardiothorac Surg. 2016;49(2):500–5.

    Article  PubMed  Google Scholar 

  14. Sue RD, Matthay MA, Ware LB. Hydrostatic mechanisms may contribute to the pathogenesis of human re-expansion pulmonary edema. Intensive Care Med. 2004;30(10):1921–6.

    Article  PubMed  Google Scholar 

  15. Boyle EM Jr, Pohlman TH, Cornejo CJ, Verrier ED. Endothelial cell injury in cardiovascular surgery: ischemia-reperfusion. Ann Thorac Surg. 1996;62(6):1868–75.

    Article  PubMed  Google Scholar 

  16. Huffmyer JL, Groves DS. Pulmonary complications of cardiopulmonary bypass. Best Pract Res Clin Anaesthesiol. 2015;29(2):163–75.

    Article  PubMed  PubMed Central  Google Scholar 

  17. Jaworski K, Maślanka K, Kosior DA. Transfusion-related acute lung injury: a dangerous and underdiagnosed noncardiogenic pulmonary edema. Cardiol J. 2013;20(4):337–44.

    Article  PubMed  Google Scholar 

  18. Silliman CC, Ambruso DR, Boshkov LK. Transfusion-related acute lung injury. Blood. 2005;105(6):2266–73.

    Article  CAS  PubMed  Google Scholar 

  19. Peters AL, Van Stein D, Vlaar AP. Antibody-mediated transfusion-related acute lung injury; from discovery to prevention. Br J Haematol. 2015;170(5):597–614.

    Article  CAS  PubMed  Google Scholar 

  20. Tonna JE, Abrams D, Brodie D, Greenwood JC, Rubio Mateo-Sidron JA, Usman A, Fan E. Management of adult patients supported with venovenous extracorporeal membrane oxygenation (VV ECMO): guideline from the extracorporeal life support organization (ELSO). ASAIO J. 2021;67(6):601–10.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Peek GJ, Mugford M, Tiruvoipati R, Wilson A, Allen E, Thalanany MM, Hibbert CL, Truesdale A, Clemens F, Cooper N, Firmin RK, Elbourne D, CESAR trial collaboration. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet. 2009;374(9698):1351–63.

    Article  PubMed  Google Scholar 

  22. Combes A, Schmidt M, Hodgson CL, Fan E, Ferguson ND, Fraser JF, Jaber S, Pesenti A, Ranieri M, Rowan K, Shekar K, Slutsky AS, Brodie D. Extracorporeal life support for adults with acute respiratory distress syndrome. Intensive Care Med. 2020;46(12):2464–76.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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The authors thank and respect the patient and the Juntendo Hospital operating room staff.



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MF, HS, and SS performed the anesthesia and postoperative care. MF, HS, and MH wrote the manuscript. KK and NA collected the data. MH and IK edited the manuscript critically. The authors have read and approved the final manuscript.

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Correspondence to Izumi Kawagoe.

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Fukuda, M., Sakai, H., Koh, K. et al. Unusual severe hypoxemia due to unilateral pulmonary edema after conventional cardiopulmonary bypass salvaged by veno-venous extracorporeal membrane oxygenation: a case report. JA Clin Rep 9, 65 (2023).

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