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Early perioperative death associated with reexpansion pulmonary edema during liver transplantation

Early Perioperative Death Associated With Reexpansion Pulmonary Edema During Liver Transplantation Wagner C. Marujo, Flavio Takaoka, Rita M. A. Moura, Fernando L. Pandullo, Andre R. Morrone, Marcelo M. Linhares, Alexandre Teruya, and Isaac Altikes Hydrothorax is a frequent finding in patients with end-
REPE during a LT that rapidly led to the patient’s stage liver disease. During the hepatectomy phase of liver
demise and speculate if this condition has not been transplantation, it is often needed to evacuate large pleu-
ral effusions. The acute expansion of the collapsed lung
can cause reexpansion pulmonary edema with variable
clinical significance. However, this complication has
rarely been reported after liver transplantation. In conclu-

Case Report
sion, we report on an overwhelming reexpansion pulmo-
nary edema during a liver transplantation that rapidly led

A 47-year-old male farmer with Child-Turcotte-Pugh C cir- to the patient’s demise and speculate if this condition has
rhosis secondary to recurrent hepatitis B underwent hepatic not been under recognized in the transplantation setting.
retransplantation. Preoperative cardiovascular and respiratory (Liver Transpl 2005;11:1439-1443.)
work-up showed only moderate right pleural effusion.
After induction of the anesthesia, the ventilator was set to conventional parameters (fraction of inspired oxygen: 40%; Noncardiogenicacutepulmonaryedema(PE)may positiveend-expiratorypressure,5cmH O)and2large-bore complicate the perioperative course of patients central catheters were placed into the right internal jugular undergoing liver transplantation (LT).1,2 Using radiog- vein. Arterial blood gases and hemodynamic measurements raphy and partial pressure of oxygen, arterial/fraction of were within the normal range. Induction of immunosuppres- inspired oxygen ratio Ͻ300 as diagnostic criteria, sion consisted of 1 g bolus of methylprednisolone that was Aduen et al. found PE in 52% of the patients undergo- administered immediately before portal reperfusion. Cal- ing LT.3 Immediate PE occurred in 25% of the patients, 9% had late PE (developing de novo in the During the operation, in the process of taking down dense first 16 to 24 hours), and 18% had persistent PE (devel- adhesions, the right diaphragm was inadvertently severed and oping immediately and persisting for at least 16 hours).
the pleural space entered. Two and a half liters of icteric Immediate PE had little clinical consequence, resolving pleural effusion were rapidly drained out. We inserted a chesttube, but negative pressure was not applied. Table 1 depicts within 24 hours, but persistent permeability-type PE relevant respiratory and hemodynamic findings throughout portended a worse outcome. This diffuse edema has the procedure. No major hemodynamic changes occurred been attributed to multiple etiologies: fluid overload, after clamping the inferior vena cava and portal vein. Veno- transfusion-related acute lung injury (TRALI), acute venous bypass was not used. Immediately after portal revas- respiratory distress syndrome (ARDS), and PE associ- cularization, there was a short period (less than 2 minutes) of ated with fulminant hepatic failure.2 The underlying systemic hypotension (mean arterial pressure, 32 mm Hg), pathophysiologic disturbances involve either an imbal- accompanied by mild bradycardia (heart rate, 62 beats/min).
ance in the transcapillary hydrostatic forces (hydro- Vasopressors were not used, and the patient recovered spon- static-type PE) or a disruption of the permeability bar- taneously. Only a few minutes following the revascularization A rare cause of noncardiogenic PE is a form of a Abbreviations: PE, pulmonary edema; LT, liver transplantation;
nondiffuse type of pulmonary endothelial injury that TRALI, transfusion-related acute lung injury syndrome; ARDS, occurs following rapid air expansion of a collapsed lung, acute respiratory distress syndrome; REPE, reexpansion pulmonary the so-called reexpansion pulmonary edema (REPE).4 In the LT setting, large pleural effusions are a common From the Transplantation Program, Hospital Alema˜o Oswaldo finding and are frequently evacuated during the proce- Received March 9, 2005; accepted August 22, 2005. dure. It is well recognized that the rapid evacuation of Address reprint requests to: Wagner C. Marujo, MD, Liver Trans- large volumes of air or fluid from the pleural space can plantation Program, Hospital Alema˜o Oswaldo Cruz, Rua Prof. Arthur cause REPE with variable clinical significance. How- Ramos, 96, cj. 111; Sa˜o Paulo—SP, 01454-905, Brazil. Telephone: 55-11- ever, this complication after LT was only reported by 3816.6655; FAX: 55-11-3816.7130; E-mail: Copyright 2005 by the American Association for the Study of Jabber et al., who described a single case with a benign Published online in Wiley InterScience ( Herein, we report an overwhelming perioperative Liver Transplantation, Vol 11, No 11 (November), 2005: pp 1439 - 1443 Table 1. Perioperative Variations of Hemodynamic and Ventilatory/Respiratory Parameters
Abbreviations: ICU, intensive care unit; HR, heart rate; MAP, mean arterial pressure; CVP, central venous pressure; PAWP, pulmonaryartery wedge pressure; MPAP, mean pulmonary artery pressure; CI, cardiac index; PVRI, pulmonary vascular resistance index; FiO2,fraction of inspired oxygen; PEEP, positive end-expiratory pressure; Sat O2, arterial saturation of oxygen.
*Clinical onset of pulmonary edema.
†Values between parentheses represent significant transient variations in the parameter during that period of time.
‡Evolution of the variables within that period of time.
of the portal vein, the oxygenation deteriorated (arterial oxy- coagulopathy (international normalized ratio, 3.2), hypergly- gen saturation, 85-90%) and a large volume of icteric plasma- cemia (234 mg/dL), only mild metabolic acidosis (arterial like fluid started pouring out from the endotracheal cannula.
blood – pH, 7.31; PCO , 38 torr; base excess, Ϫ6.4 mEq/L) Pulmonary pressures and vascular resistance indexes increased and normal serum potassium. The calculated partial pressure 20%, but left heart filling pressures remained within the nor- of oxygen, arterial/fraction of inspired oxygen at the arrival at mal range. Over the following 4 hours, an extra volume of the intensive care unit was 236 (normal Ͼ300). The chest 3.0 L of the same fluid was suctioned from the endotracheal tube was apparently functioning properly. Chest auscultation cannula. Throughout the rest of the procedure, frequent but revealed almost no breath sounds in the lower right chest and short episodes of oxygen desaturation (arterial oxygen satura- crackles in the mid portion of the same side. Auscultation on tion, 80-86%) occurred, requiring transient increases of frac- the left side was jugged to be normal. Electrocardiography was tion of inspired oxygen (up to 60%) and vigorous endotra- unremarkable. The mean pulmonary artery pressure and pul- cheal suction. Positive end-expiratory pressure level remained monary vascular resistance index increased. The chest radiog- raphy (Fig. 1) showed a homogenous condensation in the The operation was technically demanding but uneventful.
lower and middle lobes of the right lung. Intraoperative Cold ischemia time was 19.5 hours. The anhepatic phase lasted 58 minutes. Upon arterial reperfusion, the macroscopic Over the following 5 hours, 2.7 L of a fluid similar to the appearance of the liver was unremarkable. One hour later, pleural and ascitic fluids were aspirated from the trachea. The there were objective signs that the graft was working properly: aspirate was slightly frothy, non – blood stained, and had total production of good-looking bile, satisfactory urinary output, protein and bilirubin ratios of 0.8, compared to plasma. Dur- recovery of normothermia, and no overt clinical coagulopa- ing the same period, the peritoneal and chest drains collected thy. Throughout the procedure, 10 units of packed blood 830 mL and 470 mL, respectively. A chest film taken 4.5 cells, 22 units of fresh frozen plasma, and 10 units of platelets hours after the patient’s arrival at the intensive care unit showed the same radiographic pattern depicted earlier (Fig.
Upon arrival at the intensive care unit, the patient was 2). Hemodynamic monitoring continued to show unremark- awakening from anesthesia and needed to be sedated. The able left heart filling pressures. We increased the positive urinary output was adequate and the ascitic fluid was not end-expiratory pressure level to 10 cm H O and placed the frankly hemorrhagic. Despite relatively high serum levels of patient in a slightly right lateral decubitus. We then managed aminotransferase (aspartate aminotransferase, 3,400 IU/L; to correct the patient’s fluid balance but we were not able to alanine aminotransferase, 2,500 IU/L), other laboratory tests improve his cardiac output using inotropic drugs. The pul- suggested good allograft function: moderate laboratory monary artery wedge pressure mildly increased (18 mm Hg) but the cardiac index fell (2.7 L/min per m2). Despite aggres-sive ventilatory and hemodynamic support, severe hypoxemiaand a sustained increase in pulmonary vascular resistanceindex (872 dynes.s.cmϪ5) and mean pulmonary artery pres-sure (47 mm Hg) were followed by refractory hemodynamicinstability. The patient died 6 hours after arriving at the unit.
The autopsy determined the cause of death as bi-lobar (lower and middle right lung lobes) reexpansion pulmonaryedema associated with circulatory collapse secondary to rightheart failure and sustained hypoxemia. In the affected pulmo-nary lobes, the alveolar spaces were filled with edema fluid.
Large macrophages with the cytoplasm full of acidophilicfluid and scattered neutrophils and mononuclear cells werealso seen in the alveolar space. The pulmonary epithelium wasintact. The alveolar interstitium was moderately expanded byedema. There was a mild septal pulmonary capillaritis pro-duced by a mixed infiltration of neutrophils, macrophages,and mononuclear cells. The nonaffected lung depicted onlymild interstitial edema. The liver pathology showed mild tomoderate harvesting injury.
Figure 2. Chest film taken 4.5 hours after the patient’s
arrival at the intensive care unit showing the same radio-
graphic pattern depicted earlier.

Noncardiogenic diffuse PE is a frequent finding imme-diately following LT and may significantly contribute terfly wing” signal) is a mild enlargement of the heart to the perioperative morbidity and mortality.1,2 A very and major pulmonary vessels and a heterogeneous lung common perioperative scenario is the occurrence of infiltrate, especially in central and dependent areas, usu- hydrostatic PE caused by water and sodium retention ally accompanied by pleural effusions. However, iso- and low oncotic pressure observed in end-stage liver lated overhydration is particularly difficult to recog- disease. This picture can be aggravated by the almost nize.6 In any case, the interstitial PE begins to be inevitable fluid overloading and overhydration associ- mobilized in the first 24 to 72 hours, in a process that ated with transfusion of multiple blood products, sig- can be expedited with forced diuresis and adequate nificant crystalloid infusion, and marked intraoperative postoperative fluid management. However, in severe fluid shifts. The typical radiographic appearance (“but- cases, hypoxemia may delay the weaning process fromthe ventilatory support.
The occurrence of permeability-type, diffuse PE in the LT setting is apparently less common. The inci-dence of clinically relevant events is less than 1%.2 Themost likely reason is TRALI. It has been postulated thatTRALI is induced by granulocytes that aggregate in thepulmonary microvasculature after activation by trans-fusion-derived antibodies, biologically active lipids, orother yet unidentified agents.7 Its true incidence isunknown and the attendant morbidity and mortalitymay be underappreciated. TRALI is characterized bythe rapid onset of respiratory distress, hypoxia, andnoncardiogenic PE during or soon after transfusion ofblood products. Most cases last only 2 to 6 hours. How-ever, mortality rates as high as 25% have been re-ported.8 Radiographic examination reveals diffuse and Figure 1. Chest film immediately after the patient’s
fluffy infiltrates. Treatment is based only on aggressive arrival at the intensive care unit showing condensation in
respiratory support.9 ARDS is another form of PE that the lower and middle right lung lobes, signs of mild fluid
overload and no significant pleural effusions. The chest

can occur following LT. Infection accounts for approx- tube and central catheters were properly located.
imately half of the cases and its occurrence in the LT setting has been considered an ominous sign. A diffuse alveolar reexpansion, triggering endothelial activation damage involves both the endothelial and epithelial and neutrophil sequestration (priming event). This surfaces and disrupts the lung barrier. Cardinal clinical event would be followed by local enhancement of the features of ARDS are the insidious onset of refractory inflammatory cascade by attracting and activating cir- hypoxemia and bilateral pulmonary infiltrates, but no culating proinflammatory cytokines, antibodies and primed cells generated upon reperfusion, hepatic fail- REPE is a form of non-diffuse, permeability-type PE ure, or TRALI, resulting in endothelial damage and that occasionally occurs following acute evacuation of capillary leak (second-hit).2 In addition, the release of air or fluid from the pleural space, allowing rapid expan- inflammatory mediators into the systemic circulation sion of a long period collapsed lung. The underlying that occurs following gut-liver reperfusion can cause mechanism of REPE is not well defined. It is likely significant systemic endothelial injury.14,15 Likewise, a caused by an inflammatory response secondary to severe harvesting injury might provide the milieu to the expansion-related mechanical stress and reperfusion release of inflammatory mediators into the systemic injury to the alveolar-capillary membrana.11 Its inci- circulation.14 Despite relatively good allograft function dence varies from 14% in clinical observations, up to in the immediate postoperative period, the presence of 27% in animal models.4 Following the precipitating very early and high elevations of aminotransferase seems event, the condition has been observed within the first to support that the graft suffered a significant preserva- hour in 64% of the patients or within 24 hours in the tion injury. In this complex scenario, a significant har- remainder.12,13 The process usually resolves in less than vesting injury might have indirectly contributed to the 72 hours, but mortality rates as high as 20% have been distinctive clinical course. Moreover, a systemic endo- thelial injury, with a high incidence of pulmonary During LT, evacuation of large volumes of pleural edema, is frequently observed in patients with fulmi- effusion is not rare, and REPE might have been under- recognized. REPE may be a contributing factor for the Despite the fact that REPE is 1 of the causes of PE respiratory distress that frequently occurs in the early and its main clinical manifestation (acute respiratory postoperative period. Because of its ordinarily benign distress) is indistinctive of other etiologies of PE, some and transient clinical course, associated with nonspe- clinical and radiological features clearly distinguish cific radiographic signs, REPE findings may be over- REPE from the other etiological entities, as follows: (1) lapped by other perioperative pulmonary complications absence of either clinical, hemodynamic or laboratorial following LT, such as pleural effusions, atelectasis, data to support cardiogenic PE etiology—normal/low TRALI, and hydrostatic PE. REPE usually occurs in the pulmonary artery wedge pressure; (2) REPE is not a lung that was collapsed, but it can oddly happen in the diffuse injury of the lung and is always related to rapid evacuation of air or fluid from the ipsi- or contralateral In the only other reported case of REPE during LT, pleural space; (3) characteristic radiological features of despite significant hypoxemia, the clinical course was REPE are patchy or homogenous consolidation cir- benign.5 In ordinary cases, less than 20 mL of frothy cumscribed to segments or lobes of the affected lung; sputum is usually eliminated over the first 30 minutes (4) the characteristic radiological picture of TRALI or of the acute phase. Up to our patient’s demise, an aston- ARDS is a bilateral “white-out” infiltrate; and (5) REPE ishing volume of almost 6 L flooded into his pulmonary does not respond to forced diuresis and is not accom- alveoli in 8 hours. Factors occasionally present in the panied by elevated heart filling pressures.
LT setting, such as fluid overloading and TRALI, might The diagnosis of REPE is based on clinical grounds, have also contributed to this overwhelming flood.
indistinctive ipsi- or contralateral lobar consolidation However, except for ARDS and its causative factors, on radiography, and hemodynamic parameters incom- diffuse-type PE usually resolves within 24-48 hours patible with volume overload. The clinical features of after LT and has little clinical consequences, irrespec- REPE vary from asymptomatic radiographic findings tive of etiology and physiopathogenesis. In fact, TRALI alone to severe cardiopulmonary manifestation. Treat- might be associated with a worse outcome.3 ment exclusively relies on ventilatory and hemody- We speculate that a second-hit phenomenon might namic support. Alternative forms of ventilatory sup- explain the overwhelming magnitude of the pulmonary port, such as high-frequency or independent lung leak in this particular case. The alveolar-arterial mem- ventilation may be able to provide better ventilation/ brane in the collapsed lung would be initially hit by perfusion match.17 One should be aware that REPE shear-stress and/or free-radical injury that occur upon might occur in the rather complex and intricate LT scenario with a dramatic clinical manifestation, eventu- 7. Silliman CC, Ambruso DR, Boshkov LK. Transfusion-related ally leading to circulatory collapse.
acute lung injury. Blood 2005;105:2266-2273.
8. Toy P, Popovsky MA, Abraham E, Ambruso DR, Holness LG, Kopko PM, et al. Transfusion-related acute lung injury: Defini- Acknowledgement
tion and review. Crit Care Med 2005;33:721-726.
9. Sevransky JE, Levy MM, Marini JJ. Mechanical ventilation in The authors thank the attendant surgeons of Pro-Figado for sepsis-induced acute lung injury/acute respiratory distress syn- their invaluable assistance in the operative procedure.
drome: An evidence-based review. Crit Care Med 2004;32(Suppl):S548 - S553.
10. Piantadosi CA, Schwartz DA. The acute respiratory distress syn- References
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11. Sherman SC. Reexpansion pulmonary edema: A case report and 1. Afessa B, Gay PC, Plevak DJ, Swensen SJ, Hemantkumar GP, review of the current literature. J Emerg Med 2003;24:23-27.
Krowka MJ. Pulmonary complications of orthotopic liver trans- 12. Jackson RM, Veal CM, Alexander B, Brannen AL, Fulmer JD.
plantation. Mayo Clin Proc 1993;68:427-434.
Re-expansion pulmonary edema. Am Rev Respir Dis 1988;137: 2. Yost CS, Matthay MA, Gropper MA. Etiology of acute pulmo- nary edema during liver transplantation: A series of cases with 13. Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Re-ex- analysis of the edema fluid. Chest 2001;119:219-223.
pansion pulmonary edema. Ann Thorac Surg 1988;45:340-345.
3. Aduen JF, Stapelfeldt WH, Johnson MM, Jolles HI, Grinton SF, 14. Matuschak GM, Henry KA, Johanns CA, Lechner AJ. Liver- Divertie GD, Burger CD. Clinical relevance of time of onset, lung interaction following Escherichia coli bacteremic sepsis and duration, and type of pulmonary edema after liver transplanta- secondary hepatic ischemia/reperfusion injury. Am J Respir Crit 4. Matsuura Y, Nomimura T, Murakami H, Matsushima T, Kake- 15. Olthoff KM. Molecular pathways of regeneration and repair hashi M, Kajihara H. Clinical analysis of reexpansion pulmonary after liver transplantation. World J Surg 2002;26:831-837.
16. Trewby PN, Warren R, Contini S, Crosbie WA, Wilkinson SP, 5. Jaber S, Perrigault P-F, Souche B, Pouzeratte Y. Re-expansion Laws JW, Williams R. Incidence and pathophysiology of pulmo- pulmonary edema with normal pulmonary artery occlusion pres- nary edema in fulminant hepatic failure. Gastroenterology 1978; sure during liver transplantation. Intensive Care Med 2002;28: 17. Cinella G, Dambrosio M, Brienza N, Ranieri VM. Reexpansion 6. Groeneveld AB, Polderman KH. Acute lung injury, overhydra- pulmonary edema with acute hypovolemia. Intensive Care Med tion or both? Crit Care 2005;9:136-137.


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