Refers to a technique used before hepatic resection to increase the size of liver segments that will remain after surgery.
The process redirects portal blood to segments of the future liver remnant, resulting in hypertrophy.
Indicated when the future liver remnant, is either too small to support essential function or marginal in size and associated with a complicated postoperative course.
Shown to reduce postoperative morbidity and increase the number of patients eligible for curative intent resection.
Can be combined with other therapies in novel ways to improve surgical outcomes.
Large-volume resections place patients at risk for complications of liver insufficiency, particularly in the perioperative period before the remnant has increased in volume.
The percentage of liver that remains after surgery, termed the future liver remnant (FLR), is a strong independent predictor of postsurgical hepatic dysfunction and complications.
Preoperative portal vein embolization is a safe image-guided procedure that causes hypertrophy of the FLR by redirecting portal blood to the non-tumor-bearing liver.
Reduces postoperative morbidity and increases the number of patients eligible for curative intent resection.
The atrophy to hypertrophy complex refers to liver regeneration that occurs after hepatocyte injury due to toxicity, vascular occlusion, or trauma.
Regeneration occurs mainly from hyperplasia, or an increase in cell number, rather than simply an increase in cell size.
The adult liver is relatively quiescent with a tiny fraction of cells (<0.01%) undergoing mitosis.
After injury, the noninjured liver rapidly undergoes regeneration, with degree of hyperplasia is proportional to the degree of injury.
With injury involving greater than ~10% of liver volume leads to a more generalized response in the remaining liver, with up to 95% of cells undergoing mitosis.
Following resection of a two-thirds hepatectomy, the liver can regenerate lost volume within 2 weeks.
Regeneration is stimulated by growth factors released by the liver, as well as extrahepatic growth factors transported by the portal vein.
The crucial role of the portal vein is evidenced by the fact that the greatest hypertrophy occurs in the periportal zone.
Doppler studies demonstrate that the degree and timing of liver regeneration correlates with the transient increase in portal flow following PVE.
Hepatocyte growth factor (HGF) plays a central role in liver regeneration.
HGF also stimulates the release of cytokines such as interleukin-6 and TNF-α, which also promote regeneration.
There is diminished or delayed liver regeneration observed in people with diabetes with insulin resistance and patients with cirrhosis.
Insulin acts synergistically with HGF and other growth factors to repair the liver.
Decreased regenerative capacity occurs with cirrhotic livers due to a poor response to growth factors and diminished portal flow rates.
Regeneration after PVE occurs slower than after hepatic resection, possibly due to apoptosis, as opposed to frank necrosis, which occurs after PVE.
PVE could improve surgical outcomes by mitigating the rise in portal pressure that occurs during surgery, as well as prevent perioperative liver dysfunction by increasing future liver remnant mass.
Increased FLR volume is associated with improved biliary excretion, albumin uptake, and postoperative liver function testing.
A safe procedure that causes few adverse effects and can be performed on an outpatient basis, with no procedure-related mortality.
After PVE, half of the patients experience no significant change in liver function tests, and the other half demonstrate small fluctuations that return to baseline after 3 days.
After PVE, white blood cell count changes minimally, if at all, and albumin levels or prothrombin time are typically unaffected.
Unlike the postembolization syndrome that occurs after arterial embolization, patients rarely experience nausea, fever, or significant pain, as PVE primarily causes apoptosis rather than ischemic necrosis, thus limiting the release of inflammatory signalers.
Before major hepatectomy, multiphase contrast-enhanced computed tomography (CT) is obtained for preoperative planning and FLR evaluation, with vascular landmarks for hepatic resection identified, and FLR volume is assessed by CT measurements.
The absolute size of the FLR, however, is not sufficient to predict which patients will benefit from PVE.
Larger patients require a larger liver mass to support essential functions compared with smaller patients.
FLR must be standardized relative to patient size as a ratio of FLR to total functional liver volume.
Factors are taken into account in deciding which patients would benefit from PVE: extent of liver resection, baseline liver function, and complexity of the planned surgery.
PVE is indicated in cases where the FLR is either too small to support essential function or is borderline and associated with a complicated postoperative course.
The indocyanine green (ICG) clearance test can quantify liver function.
ICG is a tricarbocyanine dye that binds albumin and distributes in the blood pool shortly after injection, and is cleared from the body exclusively via biliary excretion.
In patients with normal liver function, an FLR as low as 10% can support essential hepatic function.
Postoperative complications and length of stay are significantly reduced among patients with sFLR >20%, and for patients with normal livers, PVE is advocated for sFLR <20%.
Patients with hepatic steatosis had significantly higher rates of postoperative hepatic dysfunction, blood transfusions, and stays in the intensive care unit.
There is a correlation between hepatotoxic chemotherapy regimens and postoperative complications.
Consider PVE for patients with sFLR <30% and either hepatic steatosis or significant exposure to hepatotoxic chemotherapy.
Many patients with cirrhosis are not considered candidates for major hepatic resection owing to an unacceptable risk of perioperative death.
Some patients with Childs-Pugh class A cirrhosis and preserved liver function are considered for resection if their sFLR is >40%, below which PVE is indicated.
Additional factors are considered in determining whether any individual patient should undergo PVE include: age, comorbidities, and complexity of the planned resection.
The two absolute contraindications to PVE are extensive ipsilateral tumor thrombus and clinically evident portal hypertension.
With ipsilateral tumor thrombus, PVE is contraindicated because most of the portal flow has already been diverted, and delivery of embolic agent is difficult.
Clinically evident portal hypertension is a contraindication to hepatectomy, and therefore PVE is not indicated.
PVE in the setting of mild portal hypertension or advanced fibrosis is possible but considered relatively contraindicated owing to the increased risk of nontarget embolization and complications such as bleeding esophageal varices.
Other relative contraindications include uncorrectable coagulopathy and renal insufficiency.
The goal of PVE is to achieve complete portal occlusion of targeted segments.
Embolizing the entire portal tree including distal branches is important to prevent portoportal shunts.
All diseased segments are targeted to maximize hypertrophy of the FLR and prevent hypertrophy of segments planned for resection.
A variety of embolic agents have been utilized and for PVE should be well tolerated by the patient, cause complete occlusion without subsequent recanalization, and be easy to administer.
The majority of procedures target the right lobe before right hepatectomy (RPVE) or the right lobe plus segment 4 prior to extended right hepatectomy.
Left lobe PVE is rarely indicated because the right lobe is asymmetrically larger than the left and typically sufficient in size to support function.
Volumetric studies have shown that even with extended left hepatectomy involving segments 2, 3, and 4 with extension to the caudate, the sFLR is typically >33%.
An extended right hepatectomy typically leaves an sFLR <20%.
Can be performed by transileocolic, ipsilateral, or contralateral approaches.
The transileocolic portal vein embolization, is a surgical procedure performed under general anesthesia.
With the transileocolic portal vein embolization a right lower quadrant incision is made and a vascular sheath introduced directly into an ileocolic venous branch.
Subsequently a catheter is then advanced under fluoroscopic guidance into the portal vein for subsequent embolization.
Today most centers with dedicated interventional radiology services prefer transhepatic approaches.
Percutaneous portal vein embolization can be achieved via an ipsilateral approach, through the tumor-bearing liver, or contralateral approach through the FLR.
For either, a distal portal branch is accessed under ultrasound guidance, a vascular sheath is secured, flush portography is performed to assess for variations in portovenous anatomy.
Portal pressures are measured because significant portal hypertension is a contraindication to hepatic resection.
Anterior branches of the right portal vein are typically targeted because these have been associated with a lower complication rate.
Complications of percutaneous PVE are: sub scapular hematoma, hemobilia, hemoperitoneum, vascular injuries, pneumothorax, and cholangitis, nontarget embolization, recanalization of embolized segments, and complete portal vein thrombosis.
An acceptable minor complication rate is up to 25% and major complication rate no greater than 5%.
The overall morbidity is 2.2%, with 0% procedure-related mortality.
Complication rates after PVE appear to be higher in patients with chronic liver disease owing to an increased risk of thrombosis of the nonembolized portal vein.
The degree of hypertrophy expected after PVE differs depending on the degree of underlying liver disease.
Patients with otherwise normal livers regenerate at 2 weeks postprocedure at a rate of 12 to 21 cm3/day, compared with 9 cm3/day in cirrhotic patients.36
In normal livers, sufficient hypertrophy typically occurs within 2 to 4 weeks, whereas regeneration in patients with cirrhosis can take ≥4 weeks.
Most patients with cirrhosis do not meet resection criteria, those who are considered for resection require a relatively robust sFLR (>40%) to lower their acceptable risk of postoperative liver insufficiency and mortality.
PVE successfully in increases the number of cirrhotic patients eligible for surgery and concomitantly improving perioperative outcome.
In patients with normal liver function, PVE is indicated when sFLR is <20%.
Transcatheter arterial chemoembolization commonly used to provide locoregional control of unresectable HCC, and interest has developed in applying this therapy in sequence with PVE prior to hepatectomy for HCC.
Cirrhotic livers demonstrate a decreased propensity to regenerate and often require longer time intervals to achieve satisfactory hypertrophy.
After TACE necrosis occurs and leads to increased rates of liver regeneration.
HCC derives it blood supply preferentially from the hepatic artery.
After PVE, hepatic arterial flow within the embolized segment increases which can lead to an accelerated growth of tumors.
TACE may therefore provide local control of tumors during the interval between PVE and resection.
HCC is associated with the formation of arterioportal shunts that can attenuate the effects of PVE, which is typically performed upstream from the shunts.
Arterioportal shunts are also targeted during TACE.
Two-stage hepatectomy was developed as a means of providing potentially curative therapy to patients with colorectal metastases confined to both lobes of the liver.
A two-stage surgical approach, often using hypertrophy following PVE, can provide a curative option to carefully selected patients.
During the first stage of hepatectomy, tumor within the FLR is resected or, in some cases, ablated.
When the FLR is devoid of tumor, PVE can be performed to increase its mass. PVE is often necessary because these patients typically receive hepatotoxic neoadjuvant chemotherapy, and therefore a FLR >30% is pref2242ed.
After PVE, a right or extended right hepatectomy can be safely performed.