A vast number of retroperitoneal tumors can cause a thrombus in the venous drainage of the kidney: extending from the renal vein to the inferior vena cava (IVC) and including cephalad migration to the right atrium. In children, potential sources of IVC thrombi include Wilms tumor, clear cell sarcoma of the kidney, adrenocortical carcinoma, and neuroblastoma; in adults, urothelial carcinoma of the renal pelvis, lymphoma, retroperitoneal sarcoma, adrenocortical carcinoma, pheochromocytoma, and angiomyolipoma are all potential causes of an IVC thrombus. However renal cell carcinoma (RCC) is by far the most common cause, with 18% of RCC cases having venous thrombi (of these, 36% have IVC thrombus involving the origin of the renal vein to the level of the right atrium).
IVC thrombi have two components: tumor thrombus (tumor cells contained within a blood coagulum) and bland thrombus (blood coagulum without tumor cells). Tumor thrombus encourages the formation of bland thrombus because it alters venous drainage hemodynamics. The distinction between these two components is critical and forms the basis of the operative management of IVC thrombi.
Management of IVC thrombi is complicated by the handling of the underlying tumor. This is an important consideration since tumors associated with IVC thrombi are typically aggressive. In the case of RCC with venous thrombus, 10% have associated positive regional lymph nodes, 25% have associated metastases, and 50% show perirenal fat invasion. Radical nephrectomy with regional lymph node dissection should accompany thrombectomy in nearly all cases.
Pulmonary Embolism, Anticoagulation, and IVC Filters
Patients with renal tumors are at increased risk of pulmonary embolism because of malignancy-associated hypercoagulability and potential venous thrombus embolization. Anticoagulation with heparin or low-molecular-weight heparin (not coumadin) is recommended as soon as a tumor thrombus is detected. Although evidence supporting this recommendation is limited, we have noted several important benefits to perioperative anticoagulation, including (1) a reduced risk of pulmonary embolism, (2) tumor thrombus shrinkage, and (3) bland thrombus shrinkage and/or prevention. Temporary suprarenal IVC filters are another option but not recommended because of the risk of contralateral renal and hepatic vein thrombosis, the risk of provoking embolization, and the impediment that these devices can pose to future IVC thrombectomy. The risk of intraoperative thrombus detachment and the possibility of interval thrombus growth in the period immediately preceding surgery compels us to recommend transesophageal echography (TEE) for level II to IV thrombi.
In about one third of cases, tumor thrombi have an independent blood supply arising from the renal artery or the aorta itself. Angiographic infarction of the blood supply to the tumor thrombus can help shrink a large thrombus to a more reasonable size, sometimes allowing bypass and/or hepatic mobilization to be avoided. Angioembolization can be considered for caval thrombi when (1) the thrombus appears to invade the IVC, (2) the thrombus is intrahepatic or suprahepatic and cannot be immediately excised, (3) the thrombus is associated with a bleeding kidney, and (4) when deep hypothermic arrest is planned since the status of the coronary arteries can be evaluated simultaneously. The optimal timing between thrombus angioembolization and operative vena caval thrombectomy is unknown. There is a theoretical risk of causing an iatrogenic pulmonary embolization of the tumor thrombus when angiography is done, but this appears to be minimal. Also, severe ischemia-related flank pain and tumor lysis syndrome can result from angioembolization.
Urologists that do not routinely handle the IVC and aorta should consult a vascular surgeon for level II–III thrombi to aid in vena cava control and reconstruction. A cardiothoracic surgeon must be consulted preoperatively for level III and IV thrombi because access to the mediastinal compartment for vascular bypass and thrombus removal may be required. A cardiologist or cardiac anesthetist should also be consulted for level II–IV thrombi to allow for intraoperative TEE.
Tumor Thrombus Level
Traditionally, IVC thrombi have been defined and managed according to the cranial extent of the tumor thrombus ( Table 11.1 , Fig. 11.1 ). Magnetic resonance imaging (MRI) is probably the best overall method of imaging a suspected tumor thrombus because it is noninvasive and avoids the risk of thrombus embolization associated with percutaneous venocavography. However, modern three-dimensional reconstructed computed tomography (CT) angiograms can also produce excellent results. Though classification by thrombus level is clinically useful in most cases, it does not consider the presence of bland thrombus in the infrarenal IVC, a factor that can dramatically complicate patient management.
|Incidence Rate in RCC
|Proportion of Thrombi
|Cranial Extent of Thrombus
|Management of Tumor Thrombus
|Confined to renal vein
|Within 2 cm of renal vein ostium
|IVC milking, partial IVC occlusion, ostial cavotomy
|Below hepatic veins
|Complete IVC mobilization/control, infrahepatic cavotomy
|Between hepatic veins and diaphragm
|Complete occlusion: suprahepatic IVC clamping, infrahepatic cavotomy
|Partial occlusion: veno-venous bypass, infrahepatic cavotomy
|Deep hypothermic arrest, infrahepatic cavotomy, right atriotomy
Bland Thrombus Group
A grouping system that complements tumor thrombus levels and helps with intraoperative decision making has been devised at the Mayo Clinic ( Table 11.2 , Fig. 11.2 ). The key addition of this grouping system is the consideration of the location and extent of bland thrombus and its impact on IVC management.
|Mayo Thrombus Group
|Incidence Rate in RCC
|Proportion of Thrombi
|Associated Bland Thrombus
|Additional IVC Management
|At or below common iliac veins
|Infrarenal IVC filter (e.g., Greenfield)
|Infrarenal IVC, separate from tumor thrombus
|Infrarenal IVC interruption with vena cava clip
|Infrarenal IVC, mixed with tumor thrombus
|Infrarenal IVC resection
Level I Vena Caval Thrombectomy
Level I caval thrombi are partially occlusive, nonadherent, and do not require extensive IVC dissection or any form of bypass. As they extend minimally into the IVC, they can routinely be treated in a similar fashion to level 0 thrombi: reduced into the renal vein, encompassed with an appropriately shaped vascular clamp, and removed in continuity with the kidney and renal vein, after oversuturing the caval defect with a running 4-0 Prolene suture. Of note, kidney mobilization can occur before or after thrombectomy according to surgeon preference and the concern for tumor embolization.
Proceed with a midline or anterior subcostal incision, position a self-retaining retractor, reflect the colon, Kocherize the duodenum (right-sided tumor), develop the anterior pararenal space, and expose the great vessels. Using care not to mobilize the renal vein or IVC too much, find the renal artery in the interaortocaval region and secure it with a 2-0 silk ligature or a large clip. This is an important first step toward reducing blood loss and complications.
Gently mobilize the kidney outside the renal fascia, divide the ureter, and dissect the IVC above and below the renal vein ( Fig. 11.3 ). Identify the contralateral renal vein and place a vessel loop around it. Repeat this maneuver around the suprarenal and infrarenal IVC. These vessel loops can then be passed through a short (3–6-inch) 18F red rubber catheter and used as Rummel tourniquets. We prefer Rummel tourniquets over vascular clamps as they are more easily adjustable and less likely to pinch and fracture the tumor thrombus. Again, this degree of vascular control is not necessary for most level I thrombi but is prudent if there is doubt about the thrombus level or if imaging studies are not fairly recent. Starting as cranially as possible, place a hand on the IVC, gently pinch it closed, and then apply the Rummel tourniquets so that the infrarenal IVC, contralateral renal vein, and suprarenal IVC are closed (in that order). Milk the IVC toward the ostium of the renal vein. Place a C-shaped Satinsky vascular clamp around the ostium of the renal vein, approaching from lateral to medial and partially occluding the IVC. Ensure that the thrombus is located entirely within jaws of the clamp before closing it. Palpate the IVC for evidence of any other thrombus. Ready the suction and two sponge sticks (to compress the IVC if needed) and place laparotomy sponges around the renal vein to catch any malignant cells that may drip from the open renal vein. Circumferentially incise the renal ostium using a scalpel, fine-tip Metzenbaum, or Potts scissors. Be careful not to cut away too much IVC or to cut into tumor thrombus.
Extract the thrombus intact by gentle downward traction on the renal vein ( Fig. 11.4 ). Wrap a gauze around the renal vein stump and thrombus and secure it with a silk ligature. This helps prevents tumor spillage. Dissect the medial attachments of the kidney, ligating the renal artery again before division.
Inspect the IVC for evidence of residual tumor thrombus, irrigating its lumen with heparinized saline solution (100 U/mL) for improved visualization. Close the IVC defect with a running closure using a 4-0 Prolene on a BB vascular needle ( Fig. 11.5 ). Prior to tying the knot, ask Anesthesia to apply positive airway pressure, pinch the infrarenal IVC closed, and then release the Satinsky clamp. Allow 5–10 mL of blood to escape from the caval defect to flush out any residual thrombus fragments and debris before pulling the suture tight and tying the closure down. Proceed with a regional lymphadenectomy if indicated. Irrigate the wound copiously with sterile water. Leave a closed suction drain to monitor for postoperative bleeding.
Level II Vena Caval Thrombectomy
Level II vena caval thrombi often require extensive IVC mobilization, including in some instances ligation and division of lumbar veins in order to obtain control proximal and distal to the thrombus. In most cases, vascular bypass is not necessary. Exposure for a left-sided tumor thrombus is more difficult because the IVC is best accessed from the right retroperitoneum while the tumor is best accessed from the left. In this setting, the midline and chevron incisions provide the best access, as the right and left colons must be mobilized to get adequate exposure.
Proceed with a subcostal chevron incision, mobilize the colon, develop the anterior pararenal space, and identify and ligate the renal artery. If handling a left-sided tumor, ligate and divide the adrenal, lumbar, and gonadal branches of the renal vein as needed. These branches are often dilated and friable, occasionally containing bland thrombus that can also be malignant (perform frozen section if suspicious). Mobilize the kidney outside of the renal fascia and divide the ureter. If not performed before, mobilize the right colon and small bowel, perform a Kocher maneuver, develop the right anterior pararenal space, and expose the great vessels. Carefully dissect the IVC from the liver to its bifurcation, ligating the right gonadal vein on its anterior surface. (Note: While dissecting the IVC, the surgeon has essentially started the regional lymphadenectomy. Taking a few extra moments to fully dissect the IVC of its fatty lymphatics can save time later in the case.) Obtain vascular control sequentially in the following order: (1) ligate the ipsilateral renal artery, (2) clamp the infrarenal IVC, (3) clamp the contralateral renal vein, (4) clamp the suprarenal IVC, and (5) ligate accessory hepatic veins to the caudate lobe (optional maneuver to gain 2–3 cm of additional infrahepatic IVC exposure) ( Fig. 11.6 ). Optionally, the contralateral renal artery can be clamped to prevent renal engorgement while the venous outflow is temporarily clamped. This is more of an issue for left-sided tumors since the right kidney does not have significant venous collateralization to shunt blood when the right renal vein is clamped. While obtaining vascular control, be very gentle to avoid dislodging the thrombus. Prior to clamping, some surgeons give 0.5 mg/kg of intravenous heparin to prevent clamp-related thrombotic complications.