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Intraoperative Pulmonary Tumor Embolism from Renal Cell Carcinoma and a Patent Foramen Ovale Detected by Transesophageal Echocardiography
Intraoperative Pulmonary Tumor Embolism from Renal Cell Carcinoma and a Patent Foramen Ovale Detected by Transesophageal Echocardiography Nils Schallner, MD, Norbert Wittau, MD, Vadim Kehm, MD, Frank Humburger, MD, Rene Schmidt, MD, and Daniel Steinmann, MD
P
ULMONARY TUMOR EMBOLIZATION from renal cell carcinoma is a fatal complication during nephrectomy since it is associated with high perioperative mortality and cardiopulmonary morbidity. A persistent patent foramen ovale (PFO) is a heart defect that can be found in approximately one-fourth of the population and increases the risk for ischemic stroke and arterial embolization. A unique case of intraoperative pulmonary tumor embolism is described in a patient with a previously undiagnosed PFO, in whom intraoperative transesophageal echocardiography (TEE) led to fast diagnosis, successful surgical embolus removal and closure of the PFO.
IAS
LA
PFO
RA
CASE REPORT A 58-year-old man with right renal cell carcinoma was scheduled for radical nephrectomy. The patient’s past medical history was significant for fatigue, flank pain, and hematuria. The patient presented without any relevant comorbidities or medication upon admission. Computer tomography (CT) scan for staging revealed a right-sided renal tumor with suprahepatic inferior vena cava (IVC) invasion (level III according to Neves and Zincke).1 The patient was scheduled for surgery under general anesthesia without cardiopulmonary bypass (CPB). Premedication consisted of oral midazolam, 7.5 mg, and general anesthesia was induced with 200 mg of propofol, 150 g of fentanyl, and 8 mg of cisatracurium. Anesthesia was maintained with isoflurane (0.8% end-tidal concentration) and supplemented with fentanyl and cisatracurium. Hemodynamics and central venous pressure (CVP) were normal during induction and the initial period of the operation (mean arterial pressure 70-80 mmHg, heart rate 60-80 beats per minute, CVP 10-15 mmHg). During preparation and mobilization of the IVC tumor thrombus, the patient suddenly presented with broad complex tachycardia (120-130 beats per minute), severe hypotension (systolic blood pressure below 70 mmHg), a drop in oxygen saturation to below 90%, a decrease of
IAS LA RA RV
Fig 1. Intraoperative transesophageal echocardiographic modified midesophageal four-chamber view showed a massively dilated right atrium and ventricle with bowing of the intra-atrial septum to the left. IAS, intra-atrial septum; LA, left atrium; RA, right atrium; RV, right ventricle. (Color version of figure is available online.)
Fig 2. Intraoperative transesophageal echocardiographic midesophageal bicaval view showed a patent foramen ovale. IAS, intraatrial septum; PFO, patent foramen ovale; RA, right atrium; LA, left atrium. (Color version of figure is available online.)
PetCO2 values to 15 mmHg, and an increase of CVP to above 25 mmHg. Additionally, the patient showed clinical signs of superior vena cava obstruction. Blood gas analysis showed profound hypoxemia (PaO2 53 mmHg and oxygen saturation 73%; FIO2 1.0) and hypercarbia (PaCO2 60 mmHg). The patient required resuscitation with repetitive boluses of 100 g of epinephrine and a subsequent continuous infusion of epinephrine (0.1 g/kg/min) to re-establish a systolic blood pressure above 90 mmHg. Tumor embolization was postulated as the reason for the hemodynamic instability and TEE was initiated. TEE showed a massively dilated right atrium and ventricle with a right-to-left shift of the atrial septum (Fig 1). A large tumor embolus was detected, with complete obstruction of the right pulmonary artery (PA) (Video 1). In addition, numerous air bubbles were detected in the ascending aorta, and a PFO with a significant right-left shunt also was observed (Fig 2 and Video 2). An emergency sternotomy and subsequent CPB were accomplished within 15 min. Once CPB was established, epinephrine dosing could be reduced (0.05 g/kg/min) and later replaced by dobutamine (10 g/ kg/min). However, the patient needed additional infusion of norepinephrine at low doses (0.01 g/kg/min) to establish a mean arterial pressure above 75 mmHg. The cardiac surgical procedure was performed as follows: After thoracotomy, the aorta and both the superior and inferior vena cava were cannulated to establish CPB. Fibrillation was initiated to have good operating conditions for closure of the PFO. Subsequently, after re-establishing sinus rhythm, the tumor embolus
From the Department of Anesthesia and Critical Care Medicine, University Medical Center Freiburg, Freiburg, Germany. Address reprint requests to Nils Schallner, MD, Department of Anesthesia and Critical Care Medicine, University Medical Center Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany. E-mail: [email protected] © 2011 Elsevier Inc. All rights reserved. 1053-0770/2501-0025$36.00/0 doi:10.1053/j.jvca.2009.10.027 Key words: pulmonary tumor embolism, patent foramen ovale, renal cell carcinoma, nephrectomy, transesophageal echocardiography
Journal of Cardiothoracic and Vascular Anesthesia, Vol 25, No 1 (February), 2011: pp 145-147
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SCHALLNER ET AL
Fig 3. Surgical specimen of the tumor embolus retrieved from the right PA. The tumor embolus broke apart during removal and measured 10 ⴛ 3 ⴛ 2.5 cm in total. (Color version of figure is available online.)
(Fig 3) was removed from the right PA via open pulmonary embolectomy. After successful embolectomy, right tumor nephrectomy was completed. TEE showed a patent right PA and closed foramen ovale. The right atrium and ventricle remained distended with partially restored function. For emergence from CPB, continuous infusion of epinephrine (0.1 g/kg/min) was restarted and the patient was transferred to the intensive care unit (ICU) under stable conditions. During initial treatment in the ICU, the patient required continuous infusion of epinephrine, norepinephrine and milrinone. During the following days, the patient was weaned from catecholamine therapy and was discharged from the ICU on day 11. TEE showed good recovery of right heart function. The patient made an uneventful recovery and was discharged home on day 20. DISCUSSION
Renal cell carcinomas typically invade the vascular system and form tumor thrombus.2 Up to 10% of the cases present with a tumor thrombus in the venous system. Tumor embolization is a fatal complication with an approximate incidence of 1.5% overall and 3.5% in tumors invading the IVC.3 If tumor embolization occurs, mortality is high. Thus, prompt diagnosis and removal are crucial for survival. In contrast to other diagnostic tools such as CT scan or angiography, TEE can facilitate diagnosis directly in the operating room without interfering with resuscitation efforts.4-7 TEE imaging may facilitate successful embolectomy and subsequently aid the perioperative treatment of persistent right ventricular dysfunction.4,7 In this case, the authors were able to diagnose a PFO with right-to-left shunting with TEE during the episode of acute right-sided heart failure. The PFO might not have been patent prior to the event. With normal cardiac pressure ratios, a PFO leads to left-to-right shunting with pulmonary recirculation without hypoxemia. In this patient, shunt reversal was due to elevated pressure in the pulmonary circulation. Right-to-left
shunting dilutes arterial oxygen content by admixture of mixed venous blood and compromises pulmonary gas exchange, producing profound hypoxemia. Furthermore, patients with a PFO are at high risk for paradoxical embolism, resulting in ischemic stroke or peripheral artery occlusion. It has been described that a PFO in patients with pulmonary embolism increases mortality and morbidity.8 The authors cannot exclude that paradoxical embolism occurred in this case, especially because air bubbles were detected in the ascending aorta by TEE. However, the patient did not suffer any kind of stroke or peripheral artery obstruction. In this case of pulmonary artery obstruction by tumor embolism, right-to-left shunting also demonstrated a “therapeutic” effect. The PFO possibly served as a “pressurerelief” valve into the left heart and into the systemic circulation, thereby attenuating the degree of right-heart decompensation.9 In this acute situation, the PFO may have prevented complete hemodynamic collapse by maintaining a marginal systemic blood pressure until CPB was initiated. These assumptions are supported by the fact that the patient remained relatively stable with catecholamine support during the initial resuscitation period and made an uneventful recovery without permanent rightheart insufficiency. Therefore, the patent PFO might have been life-saving for this patient. TEE enabled the authors to detect the PFO and diagnose the tumor pulmonary embolism that subsequently led to embolectomy and closure of the PFO. Even though not recommended for routine use, in the authors’ opinion intraoperative TEE should be done routinely in all patients during resection of renal cell carcinomas invading the IVC for two reasons. Primarily, TEE allows direct observation of tumor embolization. Observation of such an event can lead to the surgeon’s decision to clamp the IVC above the tumor to prevent further embolization. Secondarily, TEE provides immediate diagnosis of a significant embolic event. In support of this argument, recent guidelines state, that TEE is indicated in procedures in which sudden deterioration of cardiac function might occur.10 In summary, TEE served as a valuable tool for the diagnosis and management of intraoperative pulmonary tumor embolism. TEE views, such as the midesophageal fourchamber view, midesophageal ascending aortic short-axis view, and midesophageal bicaval view should be considered of particular importance in such circumstances. The clinical course implies that right-to-left shunting into the systemic circulation through the PFO observed by TEE potentially facilitated successful resuscitation by attenuating right heart decompensation and preventing cardiovascular collapse. However, it remains to be investigated whether the beneficial effects observed in this case outweigh the potential drawbacks, such as hypoxemia or paradoxical embolization, and translate into a substantial improvement of clinical outcome in similar cases.
REFERENCES 1. Neves RJ, Zincke H: Surgical treatment of renal cancer with vena cava extension. Br J Urol 59:390-395, 1987 2. Wotkowicz C, Wszolek MF, Libertino JA: Resection of renal tumors invading the vena cava. Urol Clin North Am 35:657-671, 2008
3. Shuch B, Larochelle JC, Onyia T, et al: Intraoperative thrombus embolization during nephrectomy and tumor thrombectomy: Critical analysis of the University of California-Los Angeles experience. J Urol 181:492-498, 2009
INTRAOPERATIVE PULMONARY TUMOR EMBOLISM
4. Sasaoka N, Kawaguchi M, Sha K, et al: Intraoperative immediate diagnosis of acute obstruction of tricuspid valve and pulmonary embolism due to renal cell carcinoma with transesophageal echocardiography. Anesthesiology 87:998-1001, 1997 5. de Waal EE, Bruins P, Lahpor JR, et al: Chasing the tumor thrombus. Anesth Analg 101:332, 2005 6. Komanapalli CB, Tripathy U, Sokoloff M, et al: Intraoperative renal cell carcinoma tumor embolization to the right atrium: Incidental diagnosis by transesophageal echocardiography. Anesth Analg 102:378-379, 2006 7. Larney V, Charles R, Brown AS, et al: Value of transoesophageal echocardiography for diagnosis of intraoperative tumour embolization. Anaesth Intensive Care 34:797-800, 2006
147
8. Konstantinides S, Geibel A, Kasper W, et al: Patent foramen ovale is an important predictor of adverse outcome in patients with major pulmonary embolism. Circulation 97:1946-1951, 1998 9. Moua T, Wood KE, Atwater BD, et al: Major pulmonary embolism and hemodynamic stability from shunting through a patent foramen ovale. South Med J 101:955-958, 2008 10. Practice guidelines for perioperative transesophageal echocardiography. A report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology 84: 986-1006, 1996
P
ULMONARY TUMOR EMBOLIZATION from renal cell carcinoma is a fatal complication during nephrectomy since it is associated with high perioperative mortality and cardiopulmonary morbidity. A persistent patent foramen ovale (PFO) is a heart defect that can be found in approximately one-fourth of the population and increases the risk for ischemic stroke and arterial embolization. A unique case of intraoperative pulmonary tumor embolism is described in a patient with a previously undiagnosed PFO, in whom intraoperative transesophageal echocardiography (TEE) led to fast diagnosis, successful surgical embolus removal and closure of the PFO.
IAS
LA
PFO
RA
CASE REPORT A 58-year-old man with right renal cell carcinoma was scheduled for radical nephrectomy. The patient’s past medical history was significant for fatigue, flank pain, and hematuria. The patient presented without any relevant comorbidities or medication upon admission. Computer tomography (CT) scan for staging revealed a right-sided renal tumor with suprahepatic inferior vena cava (IVC) invasion (level III according to Neves and Zincke).1 The patient was scheduled for surgery under general anesthesia without cardiopulmonary bypass (CPB). Premedication consisted of oral midazolam, 7.5 mg, and general anesthesia was induced with 200 mg of propofol, 150 g of fentanyl, and 8 mg of cisatracurium. Anesthesia was maintained with isoflurane (0.8% end-tidal concentration) and supplemented with fentanyl and cisatracurium. Hemodynamics and central venous pressure (CVP) were normal during induction and the initial period of the operation (mean arterial pressure 70-80 mmHg, heart rate 60-80 beats per minute, CVP 10-15 mmHg). During preparation and mobilization of the IVC tumor thrombus, the patient suddenly presented with broad complex tachycardia (120-130 beats per minute), severe hypotension (systolic blood pressure below 70 mmHg), a drop in oxygen saturation to below 90%, a decrease of
IAS LA RA RV
Fig 1. Intraoperative transesophageal echocardiographic modified midesophageal four-chamber view showed a massively dilated right atrium and ventricle with bowing of the intra-atrial septum to the left. IAS, intra-atrial septum; LA, left atrium; RA, right atrium; RV, right ventricle. (Color version of figure is available online.)
Fig 2. Intraoperative transesophageal echocardiographic midesophageal bicaval view showed a patent foramen ovale. IAS, intraatrial septum; PFO, patent foramen ovale; RA, right atrium; LA, left atrium. (Color version of figure is available online.)
PetCO2 values to 15 mmHg, and an increase of CVP to above 25 mmHg. Additionally, the patient showed clinical signs of superior vena cava obstruction. Blood gas analysis showed profound hypoxemia (PaO2 53 mmHg and oxygen saturation 73%; FIO2 1.0) and hypercarbia (PaCO2 60 mmHg). The patient required resuscitation with repetitive boluses of 100 g of epinephrine and a subsequent continuous infusion of epinephrine (0.1 g/kg/min) to re-establish a systolic blood pressure above 90 mmHg. Tumor embolization was postulated as the reason for the hemodynamic instability and TEE was initiated. TEE showed a massively dilated right atrium and ventricle with a right-to-left shift of the atrial septum (Fig 1). A large tumor embolus was detected, with complete obstruction of the right pulmonary artery (PA) (Video 1). In addition, numerous air bubbles were detected in the ascending aorta, and a PFO with a significant right-left shunt also was observed (Fig 2 and Video 2). An emergency sternotomy and subsequent CPB were accomplished within 15 min. Once CPB was established, epinephrine dosing could be reduced (0.05 g/kg/min) and later replaced by dobutamine (10 g/ kg/min). However, the patient needed additional infusion of norepinephrine at low doses (0.01 g/kg/min) to establish a mean arterial pressure above 75 mmHg. The cardiac surgical procedure was performed as follows: After thoracotomy, the aorta and both the superior and inferior vena cava were cannulated to establish CPB. Fibrillation was initiated to have good operating conditions for closure of the PFO. Subsequently, after re-establishing sinus rhythm, the tumor embolus
From the Department of Anesthesia and Critical Care Medicine, University Medical Center Freiburg, Freiburg, Germany. Address reprint requests to Nils Schallner, MD, Department of Anesthesia and Critical Care Medicine, University Medical Center Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany. E-mail: [email protected] © 2011 Elsevier Inc. All rights reserved. 1053-0770/2501-0025$36.00/0 doi:10.1053/j.jvca.2009.10.027 Key words: pulmonary tumor embolism, patent foramen ovale, renal cell carcinoma, nephrectomy, transesophageal echocardiography
Journal of Cardiothoracic and Vascular Anesthesia, Vol 25, No 1 (February), 2011: pp 145-147
145
146
SCHALLNER ET AL
Fig 3. Surgical specimen of the tumor embolus retrieved from the right PA. The tumor embolus broke apart during removal and measured 10 ⴛ 3 ⴛ 2.5 cm in total. (Color version of figure is available online.)
(Fig 3) was removed from the right PA via open pulmonary embolectomy. After successful embolectomy, right tumor nephrectomy was completed. TEE showed a patent right PA and closed foramen ovale. The right atrium and ventricle remained distended with partially restored function. For emergence from CPB, continuous infusion of epinephrine (0.1 g/kg/min) was restarted and the patient was transferred to the intensive care unit (ICU) under stable conditions. During initial treatment in the ICU, the patient required continuous infusion of epinephrine, norepinephrine and milrinone. During the following days, the patient was weaned from catecholamine therapy and was discharged from the ICU on day 11. TEE showed good recovery of right heart function. The patient made an uneventful recovery and was discharged home on day 20. DISCUSSION
Renal cell carcinomas typically invade the vascular system and form tumor thrombus.2 Up to 10% of the cases present with a tumor thrombus in the venous system. Tumor embolization is a fatal complication with an approximate incidence of 1.5% overall and 3.5% in tumors invading the IVC.3 If tumor embolization occurs, mortality is high. Thus, prompt diagnosis and removal are crucial for survival. In contrast to other diagnostic tools such as CT scan or angiography, TEE can facilitate diagnosis directly in the operating room without interfering with resuscitation efforts.4-7 TEE imaging may facilitate successful embolectomy and subsequently aid the perioperative treatment of persistent right ventricular dysfunction.4,7 In this case, the authors were able to diagnose a PFO with right-to-left shunting with TEE during the episode of acute right-sided heart failure. The PFO might not have been patent prior to the event. With normal cardiac pressure ratios, a PFO leads to left-to-right shunting with pulmonary recirculation without hypoxemia. In this patient, shunt reversal was due to elevated pressure in the pulmonary circulation. Right-to-left
shunting dilutes arterial oxygen content by admixture of mixed venous blood and compromises pulmonary gas exchange, producing profound hypoxemia. Furthermore, patients with a PFO are at high risk for paradoxical embolism, resulting in ischemic stroke or peripheral artery occlusion. It has been described that a PFO in patients with pulmonary embolism increases mortality and morbidity.8 The authors cannot exclude that paradoxical embolism occurred in this case, especially because air bubbles were detected in the ascending aorta by TEE. However, the patient did not suffer any kind of stroke or peripheral artery obstruction. In this case of pulmonary artery obstruction by tumor embolism, right-to-left shunting also demonstrated a “therapeutic” effect. The PFO possibly served as a “pressurerelief” valve into the left heart and into the systemic circulation, thereby attenuating the degree of right-heart decompensation.9 In this acute situation, the PFO may have prevented complete hemodynamic collapse by maintaining a marginal systemic blood pressure until CPB was initiated. These assumptions are supported by the fact that the patient remained relatively stable with catecholamine support during the initial resuscitation period and made an uneventful recovery without permanent rightheart insufficiency. Therefore, the patent PFO might have been life-saving for this patient. TEE enabled the authors to detect the PFO and diagnose the tumor pulmonary embolism that subsequently led to embolectomy and closure of the PFO. Even though not recommended for routine use, in the authors’ opinion intraoperative TEE should be done routinely in all patients during resection of renal cell carcinomas invading the IVC for two reasons. Primarily, TEE allows direct observation of tumor embolization. Observation of such an event can lead to the surgeon’s decision to clamp the IVC above the tumor to prevent further embolization. Secondarily, TEE provides immediate diagnosis of a significant embolic event. In support of this argument, recent guidelines state, that TEE is indicated in procedures in which sudden deterioration of cardiac function might occur.10 In summary, TEE served as a valuable tool for the diagnosis and management of intraoperative pulmonary tumor embolism. TEE views, such as the midesophageal fourchamber view, midesophageal ascending aortic short-axis view, and midesophageal bicaval view should be considered of particular importance in such circumstances. The clinical course implies that right-to-left shunting into the systemic circulation through the PFO observed by TEE potentially facilitated successful resuscitation by attenuating right heart decompensation and preventing cardiovascular collapse. However, it remains to be investigated whether the beneficial effects observed in this case outweigh the potential drawbacks, such as hypoxemia or paradoxical embolization, and translate into a substantial improvement of clinical outcome in similar cases.
REFERENCES 1. Neves RJ, Zincke H: Surgical treatment of renal cancer with vena cava extension. Br J Urol 59:390-395, 1987 2. Wotkowicz C, Wszolek MF, Libertino JA: Resection of renal tumors invading the vena cava. Urol Clin North Am 35:657-671, 2008
3. Shuch B, Larochelle JC, Onyia T, et al: Intraoperative thrombus embolization during nephrectomy and tumor thrombectomy: Critical analysis of the University of California-Los Angeles experience. J Urol 181:492-498, 2009
INTRAOPERATIVE PULMONARY TUMOR EMBOLISM
4. Sasaoka N, Kawaguchi M, Sha K, et al: Intraoperative immediate diagnosis of acute obstruction of tricuspid valve and pulmonary embolism due to renal cell carcinoma with transesophageal echocardiography. Anesthesiology 87:998-1001, 1997 5. de Waal EE, Bruins P, Lahpor JR, et al: Chasing the tumor thrombus. Anesth Analg 101:332, 2005 6. Komanapalli CB, Tripathy U, Sokoloff M, et al: Intraoperative renal cell carcinoma tumor embolization to the right atrium: Incidental diagnosis by transesophageal echocardiography. Anesth Analg 102:378-379, 2006 7. Larney V, Charles R, Brown AS, et al: Value of transoesophageal echocardiography for diagnosis of intraoperative tumour embolization. Anaesth Intensive Care 34:797-800, 2006
147
8. Konstantinides S, Geibel A, Kasper W, et al: Patent foramen ovale is an important predictor of adverse outcome in patients with major pulmonary embolism. Circulation 97:1946-1951, 1998 9. Moua T, Wood KE, Atwater BD, et al: Major pulmonary embolism and hemodynamic stability from shunting through a patent foramen ovale. South Med J 101:955-958, 2008 10. Practice guidelines for perioperative transesophageal echocardiography. A report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology 84: 986-1006, 1996