HVOO is rare after hepatectomy and more common after LDLT, with incidence at 0.1% and 5–13%, respectively (Umehara et al., 2012; Shimahara & Yamaoka, 2002). In LDLT, the occlusion usually occurs at the hepatic vein anastomotic site. In the nine reported cases of post-hepatic resection HVOO, there were five right hepatectomies, three right hepatic trisegmentectomy, and one posterior segmentectomy (Sato et al., 2014; Sequeira et al., 1981; Pitre et al., 1992; Paineau et al., 1993; Poon et al., 1998; Benesch et al., 2002; Wang et al., 2010; Di Domenico et al., 2013). Tumor size is considered a risk factor for post-resection HVOO, ranging from 18 to 21 cm. Due to the large tumor size, the vacated spaces were large enough for the remnant liver to migrate and cause torsion of the hepatic venous pedicle and/or IVC. In these cases, treatment consisted of surgical repositioning and fixation in six patients and endovascular stent placement in two patients. One patient had recurrent torsion following surgical fixation and was treated successfully with stenting. In the three cases involving stenting, patients presented with a slowly progressive clinical course, stent placement was successful, and all survived. In two cases, the kinked left hepatic vein was stented and in the other case the compromised IVC was stented. However, in these cases, extensive IVC thrombus was not present as in our patient. Primarily addressing the thrombus is important as it can result in pulmonary emboli, IVC thrombosis, and clot propagation. Given the recent surgery, thrombolysis was contraindicated. Mechnical thrombetomy of the central veins is technically limited by the small caliber of many commercailly available devices. We selected the AngioVac thrombectomy device given the large diameter of the aspiration catheter and the utilization of a venovenous bypass circuit to treat the significant caval clot burden without substantial hemorrhage (Resnick et al., 2016). The underlying IVC narrowing had to be managed by stenting with a large caliber stent with adequate radial force to overcome the torsion caused by the migrated liver remnant. Only after IVC stenting to address the IVC torsion did our patient stabilize. Long-term patency of stenting in the setting of post-resection HVOO is unknown. In our patient, followup imaging demonstrated patency at 24 months on rivaroxaban alone. No secondary interventions were necessary to maintain stent patency.
Some authors believe preservation of the left triangular ligament is inadequate to prevent left liver lobe dislocation after right hepatectomy (Sato et al., 2014). Others suggest surgical fixation of the falciform ligament to the anterior abdominal wall be performed to prevent left lobe migration (Ogata et al., 2005). Early recognition and intervention is key to preventing mortality. Of the nine reported cases, two fatalities resulted from hepatorenal failure from HVOO. Fatalities were attributed to delayed diagnosis and intervention, with surgical intervention performed at seven days and 10 weeks after hepatectomy, respectively.
Elevated liver enzymes are to be expected in patients with HVOO. Sato, et al. reported significant increase in ALT, AST, bilirubin. Serum creatinine was also elevated. These values normalized after corrective surgery (Sato et al., 2014). In our patient, ALT and AST were elevated more signifincantly than the bilirubin level. Serum creatinine was also increased. These normalized after endovascular treatment. Despite its relatively uncommon incidence, HVOO should be consdered in the setting of hepatorenal failure and hemodynamic instability after right hepatectomy and can be successfully treated endovasculalry.