Liver resection provides a substantial survival benefit to patients with primary or secondary liver tumors.1 However, the postresection mortality rate remains an important concern in these patients, with reported rates ranging from 2% to 10%.2,3 Insufficient future liver remnant (FLR) volume is a well-recognized contraindication to major hepatectomy because of the risk of posthepatectomy liver failure (PHLF).4 A recent study found that 70% of patients who died after liver resection had PHLF, with approximately 50% of those deaths directly attributed to PHLF.5, 6 Although the etiology of PHLF is multifactorial, the functionality and volume of the FLR are strong independent predictors of the occurrence of PHLF.7,8 This has fueled the search for a safe and effective method to improve the functionality and volume of the FLR before liver resection.

For decades, portal vein embolization (PVE) has been the standard preoperative strategy to induce FLR hypertrophy. By redirecting portal inflow from the diseased lobe to the contralateral lobe, PVE triggers adaptive hypertrophy of the FLR.9 PVE is effective in many cases; however, its drawbacks include relatively modest hypertrophy (often requiring 4–8 weeks to achieve ∼10%–20% FLR volume increase) and a substantial dropout rate due to tumor progression during the waiting period.10, 11, 12 Indeed, only approximately 60% to 80% of patients who undergo PVE ultimately proceed to resection, with cancellations commonly attributed to insufficient FLR growth or disease advancement.5 These limitations have driven interest in strategies to accelerate and amplify liver regeneration.

Associating liver partition and portal vein ligation for staged hepatectomy (ALPPS) was introduced in 2007 to overcome the slow kinetics of PVE.13 In the ALPPS approach, an in-situ liver split and portal ligation are performed in the first stage, followed by a second-stage completion hepatectomy after 1 to 2 weeks. ALPPS achieves strikingly rapid hypertrophy; the initial series reported ∼74% FLR volume increase in 9 days, corresponding to a kinetic growth rate (KGR) of approximately 7% per day (far exceeding PVE’s typical KGE of ∼0.5%–1% per day).14 ALPPS can convert most patients into candidates for resection, with reported resection rates of ∼90%+.13,15 However, this comes at the cost of high surgical morbidity and complexity. Early studies of ALPPS noted unacceptable perioperative mortality and morbidity, with initial mortality rates approaching 8% to 12% and severe complications seen in 30% to 40% of patients.13,16 Refinements in patient selection have improved ALPPS outcomes, but its invasive two-stage nature and physiological stress remain as limitations of this procedure.16,17

Liver venous deprivation (LVD) has emerged as a minimally invasive alternative designed to combine the strengths of PVE and ALPPS. First described by Guiu et al in 2016,18 LVD involves concomitant embolization of the ipsilateral hepatic vein(s) alongside portal embolization. The rationale is that by depriving the tumor-bearing lobe of both its inflow (portal) and outflow (hepatic venous drainage), a more intense atrophy of the treated lobe and a more robust hypertrophic response in the FLR can be achieved.18 The physiological mechanism underlying LVD is twofold. The first part of the mechanism involves augmented regenerative stimulus, in that the combined inflow and outflow occlusion causes greater hepatocyte apoptosis and necrosis in the embolized lobe, releasing growth factors that drive contralateral lobe hyperplasia. The second part of the mechanism involves prevention of collaterals. After PVE alone, venous collaterals may form between segments (e.g., through the open hepatic veins), partially decompressing the congested lobe and attenuating hypertrophy signals.19,20 The hepatic vein embolization component of LVD effectively “seals off” the embolized lobe, preventing trans lobar shunting of blood or growth factors. In essence, LVD creates an environment akin to an in-situ split (complete ischemic segregation of lobes) without actual parenchymal transection. This novel approach promised to accelerate FLR growth beyond what PVE alone could achieve while avoiding the surgical morbidity of ALPPS.

Early clinical results supported this concept. Guiu et al18 reported that simultaneous portal and hepatic vein embolization was feasible and well-tolerated, inducing “fast and important hypertrophy” of the FLR. A subsequent pilot study termed the technique “radiologically assisted simultaneous porto-hepatic embolization” (RASPE).21 These small series noted that LVD could be helpful in patients at high risk of PVE failure (eg, those with small baseline FLRs or aggressive tumors) by achieving adequate liver growth in a shorter timeframe.19 For example, Le Roy et al22 observed in a preliminary report that combined portal and hepatic vein embolization led to successful FLR hypertrophy and resection in patients who might otherwise require ALPPS. Such findings laid the groundwork for larger studies and have catalyzed international interest (eg, the DRAGON and HYPER-LIV trials) to rigorously compare LVD versus PVE.

In short, LVD is useful as an innovative solution to an ongoing clinical challenge: how to maximize FLR regeneration safely and quickly. By leveraging the physiologic synergy of dual-vein embolization, LVD aims to bridge the gap between PVE’s safety and ALPPS’s efficacy. The technique was conceived to address PVE’s shortcomings (insufficient or slow hypertrophy in some patients) while mitigating ALPPS’s drawbacks (operative risk and complexity). The rationale for LVD is strongly supported by experimental and early clinical data showing that depriving a lobe of both portal inflow and hepatic outflow creates a potent stimulus for liver regeneration.21,23 Thus, LVD has rapidly gained momentum as a promising strategy to reduce dropouts and improve resectability in patients with marginal FLR, all through a single-stage percutaneous intervention.

The first part of the LVD procedure involves right portal vein embolization. Via trans-splenic or transhepatic access, an Amplatzer vascular plug is used concurrently with n-butyl cyanoacrylate (NBCA) to prevent reflux and facilitate distal penetration of the embolic. At our institution, trans-splenic access is preferred, as it allows easy cannulation of the portal venous branches and safe embolization with NBCA as it flows away from the catheter tip (Fig. 1). The second part of LVD involves right hepatic vein embolization. Via transjugular access, plug-assisted NBCA embolization is performed (Fig. 1). Additional accessory right hepatic veins are also embolized.

The Amplatzer plug–assisted NBCA embolization technique allows the interventionalist to embolize both the portal and hepatic veins safely in one session.24 Key technical points include planning for variant anatomy, using dual access (transhepatic and transvenous) for optimal control, and ensuring complete occlusion of targeted vessels (with plugs securing proximal inflow/outflow and glue filling the distal branches). When executed properly, LVD leads to effective deprivation of the selected lobe’s blood supply and venous drainage, setting the stage for a dramatic hypertrophic response in the remnant liver. LVD technique is discussed in detail by Knott et al.24