This is the first case of sequential portal vein embolization and combined left and middle hepatic vein embolization reported in the literature. Currently, the mortality associated with liver resection ranges from 0 to 5% with a morbidity ranging from 10 to 20% [4, 5]. The morbidity and mortality of extended left hepatectomy is higher than that of major resections with a reported mortality of 0% to 11.9 % and morbidity of 53% . The most common cause of mortality is abdominal sepsis and postresectional liver failure secondary to insufficient FLR. Consequently, different techniques have been used to increase FLR. In addition to ensuring an adequate FLR, the risk of postoperative hepatic congestion in our patient was significant given the patient’s right-dominant middle hepatic vein.
Portal vein embolization (PVE) has been shown to increase FLR between 7% to 27% of the total liver volume (TLV) or 20 to 46% beyond pre-PVE FLR two to eight weeks after PVE, and is therefore used to increase FLR in patients deemed to have a small remnant liver [1, 4, 7]. PVE has been shown to increase resectability rate in up to 7% of patients with a benefit in postoperative outcomes. The sufficient FLR required in a normal liver is > 20% of the total liver volume; in patients with impaired liver function this is believed to be > 40% .
Chemotherapy has been associated with increased risk of liver injury: fluorouracil (5-FU) has been associated with steatosis; oxaliplatin-based regimens have been associated with vascular injuries; and irinotecan-based regimens have been associated with steatosis and steatohepatitis. The exact consequence of these histopathological lesions is unclear but patients with steatohepatitis have been shown to have higher incidences of posthepatectomy complications . The regenerative ability of chemotherapy injured livers has been shown to be unimpaired following portal vein embolization .
PVE has been utilized in extended right hepatectomies, has been found to be safe and can increase the remnant liver . In this case, the patient’s liver appeared to be grossly steatotic and the ideal FLR required for a safe resection was unclear. In this case, on volumetric analyses the posterior section appeared to be < 25% of total liver volume and the left portal vein was embolized with an increase in FLR to 30%.
PVE is not without risks; the greatest concern is for rapid tumor growth due to the increased production of growth stimulants, presumably in response to PVE. Animal models and one human study in humans have produced inconclusive data . After PVE, careful monitoring of tumor response is warranted, and some have recommended concurrent chemotherapy after PVE to control for the deleterious effects PVE may have on tumor growth [8, 12].
The role of hepatic vein embolization in improving resectability rates and the safety of extended resections of patients with FLR < 20% after PVE is unclear. Hwang et al. recently showed, in a study of 12 patients who underwent hepatic resection for hepatobiliary malignancy, that sequential right hepatic vein embolization after right PVE had an incremental effect on the FLR. Immunohistochemistry showed increased apopotosis after hepatic vein embolization following PVE, suggesting that hepatic vein embolization induced a more severe injury. Hepatic vein embolization was shown to be safe and did not appear to increase blood liver enzymes any more than did portal vein embolization . The study only included patients who underwent right-sided resections and therefore, only patients who underwent right hepatic vein embolization .
This report is the first to document the use of left and middle vein embolization in an attempt to increase FLR. In this case, after PVE, the FLR increased to > 30%, but after hepatic vein embolization no additional increase was documented on volumetric analysis. There was a transient increase in liver enzymes after portal vein and hepatic vein embolization which normalized prior to the curative resection, and no complications were associated with either procedure.
Venous congestion associated with sacrificing the middle hepatic vein has been associated with physiological impairment, functional small-for-size syndrome, loss of the graft and death of living liver transplant donors [13–18]. Management of the middle hepatic vein remains a controversial topic, especially for right graft living donor liver transplants. Using CT volumetric analysis, many centers have devised algorithms that attempt to predict the risk of congestion associated with middle hepatic vein harvest [13, 18, 19]. Some centers have advocated the utilization of vein reconstruction to prevent congestion . Congestion leads to necrosis of the marginal zones of the remnant liver and may lead to increased biliary complications and potentially infection. Scatton et al. showed that hepatic congestion was associated with impaired liver function and volumetric regeneration. Even though the clinical consequences of congestion were moderate in the healthy donor population, this effect may be severe in patients after extended resection with small remnants and diseased livers .
The role of hepatic congestion in decreasing the remnant liver and increasing morbidity and mortality after extended resections has been documented in a number of studies [21–24]. Lang et al. found that, when using computer-assisted risk analysis to plan for major hepatectomies, the amount of devascularized liver tissue was greater than 20% and up to 43% of that anticipated by 2D CT. Most of the reduction in vascularized liver tissue resulted from hepatic congestion. In particular, for patients who were to undergo extended left hepatectomies, a large portion of segment six drained into the middle hepatic vein. Based on their preoperative findings, the surgical team involved planned vein reconstructions for these patients after intraoperative confirmation of hepatic congestion.
Multiple studies have reported on their experience of venous reconstruction to prevent hepatic congestion, with good outcomes. Venous reconstruction increases the complexity of the operation and is associated with complications . We hypothesize that an alternative to venous reconstruction could be preoperative hepatic vein embolization to increase collateralization gradually so as to decrease early hepatic congestion. Our patient appeared to be at high risk of congestion given his large accessory vein draining from his right liver into the middle hepatic vein. Using an animal model, Ku et al. showed that preoperative hepatic vein embolization resulted in increased collateralization of interlobar and interlobular collaterals in two weeks. In the only published case report to document an increase in venous drainage after hepatic vein embolization, a right hepatic vein embolization was done to enable an inferior right hepatic vein-preserving left hepatic trisectionectomy with combined resection of the distal right hepatic vein without reconstruction. Preoperative hepatic vein embolization increased drainage via the inferior right hepatic vein, allowing a safe resection without congestion .
Preoperative studies can now identify patients with middle hepatic vein-dominant right livers, and a study to evaluate the benefits of preoperative hepatic embolization prior to resection in these groups of patients is warranted because it may decrease postoperative hepatic congestion, and may preclude the need for venous reconstruction. Hepatic vein embolization is associated with the risk of dislodgement of the embolic material because the hepatic vein is retrograde and the vein is larger distally than proximally.