Patients with the tumor thrombus in the inferior vena cava (IVC) have a great risk of pulmonary embolism [1,2] and obstruction of tricuspid valve  during operative management. There has been several reports about intraoperative cardiac arrest and death due to such situations. [1,4] Therefore, immediate diagnosis and the subsequent management is an important challenge for anesthesiologists.
This case report describes a patient with renal cell carcinoma that extended into the IVC and caused acute obstruction of tricuspid valve and pulmonary tumor embolism intraoperatively, which were immediately diagnosed by transesophageal echocardiography (TEE) and were successfully managed by the rapid institution of cardiopulmonary bypass (CPB).
A 35-yr-old woman, weighing 53 kg, was admitted to our hospital with appetite loss and left abdominal pain. Physical examination revealed a palpable mass in the left upper quadrant. Laboratory results showed a hematocrit of 30% and the elevation of leukocyte count (11,500), alkaline phosphatase (378 U/l), and lactic acid dehydrogenase (2,786 U/l). Radiologic examinations, including computed tomography, inferior venocavograms (Figure 1), and transthoracic echocardiography revealed a left renal mass with a tumor thrombus extending upward to near the right atrium. The chest radiograph revealed the metastatic lesions in the left lower lung area. This patient was scheduled for left nephrectomy, dissection of lymph nodes, and removal of the tumor thrombus using cardiopulmonary bypass (CPB).
Anesthesia was induced with intravenous fentanyl (0.2 mg), midazolam (5 mg), and thiopental (100 mg) after previous placement of an epidural catheter. Anesthesia was maintained with 66% nitrous oxide in oxygen, fentanyl, and isoflurane. Monitoring included electrocardiography, arterial and central venous pressure, pulse oximetry, end-tidal carbon dioxide monitor, and rectal temperature measurement. Two-dimensional transesophageal echocardiography (TEE; SDD870, Aloka, Tokyo, Japan) probe was placed to monitor the tumor thrombus. Tumor thrombus floating freely in the IVC near the right atrium, but no mass were observed in the four-chamber view of the heart.
With the patient in the supine position, the left nephrectomy was started by urologists. Operation and anesthesia proceeded uneventfully. About 5 h after abdominal incision, the left kidney and renal artery were isolated. At this time, blood gas analysis showed the pHa was 7.36; PaO2, 169 mmHg; PaCO2, 40 mmHg; base excess, -2.4 (FiO2, 0.3). While the surgeons were dissecting lymph nodes around the renal artery, arterial blood pressure suddenly decreased from 94/61(70) mmHg to 49/39(42) mmHg. Concurrently end-tidal carbon dioxide decreased from 31 to 26 mmHg. An increase in the central venous pressure from 5 to 13 mmHg immediately followed. Immediately the inspired oxygen concentration was increased to 100%, and ephedrine (8 mg) was administrated, but there was no reaction. At this time, the embolization of tumor thrombus was suspected, and TEE was performed to search for the embolization. The tumor thrombus was discovered in the four-chamber view of the heart. The thrombus occluded the tricuspid valve and was moving between right atrium and ventricle (Figure 2). Although the tricuspid valve was moving, it could not prevent regurgitation. Gradually it appeared that thrombus separated into parts and moved into pulmonary artery (Figure 3). At this time, ephedrine (5 mg), methoxamine (2 mg), dopamine (10 micro gram [center dot] kg sup -1 [center dot] min sup -1), and dobutamine (10 micro gram [center dot] kg sup -1 [center dot] min sup -1) were administered, but failed to restore the blood pressure. Blood gas analysis showed that the pHa was 7.46; PaO2, 374 mmHg; PaCO2, 27 mmHg; and base excess, -3.6. Eight minutes later, cardiac arrest developed, and external cardiac massage was commenced. While the right femoral artery and vein were exposed, sternotomy was performed, and subsequently open cardiac massage was commenced. After heparinization (250 U/kg) and cannulation of the right femoral artery and vein, CPB was instituted. A second venous cannula in the superior vena cava was added. The time from the beginning of hypotension to commencement of CPB was 28 min. A pulmonary arteriotomy was performed, and the tumor thrombus was removed from the left, right, and the main pulmonary artery. Next, the right atrium was opened, and the tumor thrombus was removed. Residual tumor in the IVC was removed by using a Fogarty catheter. At this time, no residual tumor was observed by TEE. Finally, the left nephrectomy was completed. After insertion of a Swan-Ganz catheter, CPB was discontinued uneventfully. The operation was completed without additional complication.
The patient was transferred to the intensive care unit where she recovered without myocardial injury and neurologic complication. She initially did well, but subsequently died of metastatic disease.
Although massive pulmonary tumor embolism from renal cell carcinoma occurs relatively rarely, [5,6] tiny emboli appear to occur more commonly. Winterbauer et al.  and Arkless  reported pulmonary tumor emboli in 31% and 26% of patients with renal cell carcinoma, respectively. The possibility of pulmonary embolism from renal cell carcinoma is considerably enhanced when tumor extends into the renal vein or IVC.  Therefore, it is considered that the risk of pulmonary embolism is high during surgical treatment in patients with renal cell carcinoma extending into the IVC because the hemodynamics are unstable and because the IVC is manipulated intraoperatively.  Wilkinson et al.  reported a patient with renal cell carcinoma extending above the diaphragm who developed massive pulmonary embolism during a radical nephrectomy. Milne et al  also reported a case of massive intraoperative pulmonary tumor embolus from renal cell carcinoma invading the IVC, who developed cardiac arrest and required open cardiac massage and institution of CPB.
Intraoperative symptoms associated with pulmonary embolism include hemodynamic changes such as a decrease in arterial pressure and increase in central venous pressure, hypoxemia, and a reduction in end-tidal carbon dioxide tension with a large increase of the arterial to end-tidal carbon dioxide tension gradient. However, diagnosis of pulmonary embolism may be difficult in the operating room because diagnostic procedures such as pulmonary scintigraphy, transthoracic echocardiography, or angiography cannot be performed usually. Therefore, TEE has become the procedure of choice in the evaluation of the patient with embolic events. [9,10] Langeron et al.  reported a case in which the thromboembolus migrating from the right atrium to the right ventricle was observed with TEE, and pulmonary embolism was intraoperatively diagnosed. However, as the limitation of TEE, there is the possibility of missing small emboli or those that have already passed into the pulmonary vascular bed.  Nevertheless, Kasper et al.  reported that there is a close correlation between size of the right pulmonary artery and mean pulmonary artery pressure in patients with pulmonary embolism and changes in the right-to-left ventricular end-diastolic area ratio correlate with severity of pulmonary obstruction.
Obstruction of tricuspid valve is another possible intraoperative fatal complication in patients with renal cell carcinoma. Utley et al.  reported a patient with Wilms' tumor extending into the IVC, in which acute obstruction of the tricuspid valve occurred, and circulation was arrested. However, diagnosis of obstruction of the tricuspid valve was made only after the immediate sternotomy and institution of CPB. Wilson et al.  reported a patient undergoing pelvic surgery for bleeding fibroids, in which obstruction of tricuspid valve caused by massive thrombus was diagnosed by using TEE intraoperatively. To our best knowledge, we believe that this is the first report in which acute obstruction of tricuspid valve from renal cell carcinoma invading the IVC was intraoperatively diagnosed by using TEE. Diagnosing intraoperative tumor events in the IVC, atrium, ventricle, and pulmonary artery without any delay can allow us immediate treatment of patients including interruption of the vena cava and embolectomy under the CPB.
Once the fatal complication such as massive pulmonary embolism and obstruction of tricuspid valve occurred, institution of CPB may be mandatory to save the patient. Milne et al.  reported a patient with renal cell carcinoma invading the IVC, in which cardiac arrest occurred during a radical nephrectomy with CPB available on standby, and the time from the beginning of hypotension to commencement of CPB was approximately 10 min. Wilkinson et al.  also reported that emergency institution of CPB was required for salvage of a patient with intraoperative massive pulmonary embolism, and the time to commencement of CPB was within 20 min, with CPB on standby. However, in this case it took approximately 30 min to commence CPB from the beginning of hypotension. With more delay, the patient might have been in jeopardy. Therefore, we believe that it is important to prepare for CPB with it on standby.
In conclusion, we present a case in which massive pulmonary embolism and obstruction of tricuspid valve from renal cell carcinoma invading the IVC were intraoperatively diagnosed by TEE. TEE is inevitably necessary for intraoperative monitoring of tumor events in the IVC, atrium, ventricle, and pulmonary artery in such patients.