(Radiographics. 2002;22:1063-1076.)
© RSNA, 2002
Transhepatic Portal Vein Embolization: Anatomy, Indications, and Technical Considerations1
David C. Madoff, MD,
Marshall E. Hicks, MD,
Jean-Nicolas Vauthey, MD,
Chusilp Charnsangavej, MD,
Frank A. Morello, Jr, MD,
Kamran Ahrar, MD,
Michael J. Wallace, MD and
Sanjay Gupta, MD
1 From the Departments of Diagnostic Imaging (D.C.M., M.E.H., C.C., F.A.M., K.A., M.J.W., S.G.) and Surgical Oncology (J.N.V.), University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Box 57, Houston, TX 77030-4009. Recipient of a Cum Laude award for an education exhibit at the 2001 RSNA scientific assembly. Received February 14, 2002; revision requested March 12 and received March 22; accepted March 22. Address correspondence to D.C.M. (e-mail: dmadoff@di.mdacc.tmc.edu).
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Abstract
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Portal vein embolization (PVE) is increasingly being accepted as a useful procedure in the preoperative treatment of patients selected for major hepatic resection. PVE is performed via either the percutaneous transhepatic or the transileocolic route and is usually reserved for patients whose future liver remnants are too small to allow resection. It is a safe and effective method for inducing selective hepatic hypertrophy of the nondiseased portion of the liver and may thereby reduce complications and shorten hospital stays after resection. A thorough knowledge of hepatic segmentation and portal venous anatomy is essential before performing PVE. In addition, the indications and contraindications for PVE, the methods for assessing hepatic lobar hypertrophy, the means of determining optimal timing of resection, and the possible complications of PVE need to be fully understood before undertaking the procedure. Technique may vary among operators, and further research is necessary to determine the best embolic agents available and the expected rates of liver regeneration for PVE. Nevertheless, as hepatobiliary surgeons become more experienced at performing extended hepatic resections, PVE may be requested more frequently.
© RSNA, 2002
Index Terms: Liver, anatomy, 761.92 • Liver, blood supply, 761.92 • Liver, regeneration • Liver, surgery, 761.451 • Portal vein, anatomy, 957.92 • Portal vein, therapeutic embolization, 957.1264
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Discuss portal venous anatomy and normal variants as they pertain to PVE.
- Recognize the indications for PVE and describe methods for evaluating FLR hypertrophy.
- Discuss the technical considerations related to and possible complications of PVE.
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Introduction
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In recent years, major advances in hepatobiliary surgical techniques have led to improved perioperative outcomes in patients who undergo hepatic resection. In particular, fatal liver failure following resection has become exceedingly rare. However, complications associated with cholestasis, fluid retention, and impaired synthetic function still contribute to prolonged recovery time and extended hospitalization (1).
Transhepatic percutaneous portal vein embolization (PVE) is one approach that is gaining increasing acceptance in the preoperative treatment of selected patients prior to major hepatic resection. Induction of selective hypertrophy of the nondiseased portion of the liver with PVE in patients with either primary or secondary hepatobiliary malignancy with small estimated future liver remnants (FLR) may result in fewer complications and shorter hospital stays following resection (2,3). Additionally, PVE performed in patients initially considered unsuitable for resection due to lack of sufficient remaining normal parenchyma may add to the pool of candidates for surgical treatment.
As regional cancer therapy techniques become more widespread, many clinicians may request PVE as an adjunct for treatment.
In this article, we discuss and illustrate normal portal venous anatomy and anatomic variants, indications and contraindications for PVE, technical considerations and periprocedural issues related to percutaneous transhepatic PVE, and potential complications of the procedure.
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Anatomic Considerations
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Couinaud and Anglo-Saxon Classification Systems of Liver Segments
A comprehensive knowledge of functional liver anatomy is imperative for performing PVE. The most widely used classification system was proposed in 1957 by Couinaud (4) and is shown in Figure 1. The liver is divided into two hemilivers (left and right, separated by the main portal fissure) and eight segments. Hepatic segmentation is based on the distribution of the portal pedicles and the location of the hepatic veins. The Couinaud classification system and the corresponding Anglo-Saxon classification system are shown in Table 1.
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Figure 1. Schematic illustrates Couinaud segmental liver anatomy and the normal portal venous structures. The possible hepatic resection procedures are also shown. IVC = inferior vena cava, PV = portal vein.
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Normal Portal Venous Anatomy
The portal vein is formed in the retroperitoneum by the confluence of the superior mesenteric vein and the splenic vein behind the neck of the pancreas and courses behind the duodenal bulb. The main portal vein and the right and left portal veins are in the hilar fissure. The portal bifurcation may be extrahepatic (48% of cases), intrahepatic (26%), or located right at the entrance of the liver (26%) (5,6). Figures 1 and 2 illustrate the most common portal venous anatomy. On the right, there are usually two sectoral portal branches (anterior and posterior); on the left, there are two parts to the (main) left portal vein: the extrahepatic portion (pars horizontalis, ie, the horizontal part) and the intrahepatic portion (pars umbilicalis, ie, the umbilical [vertical] part).
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Figure 2a. (a, b) Schematics illustrate the normal portal vein (PV) branches from anterior (a) and inferior (b) perspectives. hp = horizontal part, LPV = left portal vein, RPV = right portal vein, up = umbilical (vertical) part. (c) Three-dimensional computed tomographic (CT) reformatted image (anterior view) demonstrates normal portal venous anatomy. LPV = left portal vein, PV = portal vein, RPV = right portal vein.
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Figure 2b. (a, b) Schematics illustrate the normal portal vein (PV) branches from anterior (a) and inferior (b) perspectives. hp = horizontal part, LPV = left portal vein, RPV = right portal vein, up = umbilical (vertical) part. (c) Three-dimensional computed tomographic (CT) reformatted image (anterior view) demonstrates normal portal venous anatomy. LPV = left portal vein, PV = portal vein, RPV = right portal vein.
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Figure 2c. (a, b) Schematics illustrate the normal portal vein (PV) branches from anterior (a) and inferior (b) perspectives. hp = horizontal part, LPV = left portal vein, RPV = right portal vein, up = umbilical (vertical) part. (c) Three-dimensional computed tomographic (CT) reformatted image (anterior view) demonstrates normal portal venous anatomy. LPV = left portal vein, PV = portal vein, RPV = right portal vein.
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In general, the sectoral branch divides into several segmental portal branches, which in turn supply the various segments. One segmental branch usually supplies segments II, VI, and VII and, more rarely, segment III. Segments IV, V, and VIII are commonly supplied by more than one segmental branch. Segmental veins then divide into subsegmental branches, which further divide into small veins leading to the portal venule of the liver acinus.
Portal Venous Variants
Anatomic variants of the portal vein are uncommon (10%–15% of cases) (Figs 3, 4) (7). However, when present, they are important to recognize because they may have profound implications for whether PVE or subsequent resection can be performed successfully. In a small portion (11%) of the population, the portal vein divides into one left and two right portal branches. This variant, known as portal trifurcation, is present if three branches stem from the main portal trunk: the posterior branch, the anterior branch, and the left main branch (Figs 3b, 4b). In addition, the right anterior segment portal vein may branch from the left main portal vein (4% of cases), or the left main portal vein may branch from the right anterior portal vein. Alternatively, the right posterior branch may stem from the main portal trunk, with the anterior branch forming a bifurcation with the left portal vein (5% of cases). Quadrifurcation of the portal vein can also occur, consisting of a branch for segment VII, a branch for segment VI, an anterior branch, and a left main portal branch (left portal vein) (Fig 3c). In exceptional cases, a branch for subsegment IVb or an additional branch for segments VI, VII, or even VIII may stem from the portal bifurcation. Only very rarely (1% of cases) is bifurcation of the portal vein completely absent (ie, no right portal vein) (Fig 3e) (8,9). When this occurs, the solitary portal vein in the hilum passes through the entire liver, either from right to left or from left to right. Failure to recognize this variation in the setting of hilar portal ligation leads to hepatic failure and death. Resection or liver transplantation may require portal vein resection and reconstruction, which greatly increases the complexity of these procedures (8,9).
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Figure 3a. Schematics illustrate selected variants of the portal venous system. hp = horizontal part, LPV = left portal vein, PV = portal vein, up = umbilical (vertical) part. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch. (b) Portal trifurcation. (c) Portal quadrifurcation. (d) Bifurcation of the right portal vein (RPV) into anterior (Ant.) and posterior (Post.) branches, which supply segments V/VIII and VI/VII, respectively. (e) Complete absence of the right portal vein. All hepatic segments are supplied by the left portal vein.
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Figure 3b. Schematics illustrate selected variants of the portal venous system. hp = horizontal part, LPV = left portal vein, PV = portal vein, up = umbilical (vertical) part. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch. (b) Portal trifurcation. (c) Portal quadrifurcation. (d) Bifurcation of the right portal vein (RPV) into anterior (Ant.) and posterior (Post.) branches, which supply segments V/VIII and VI/VII, respectively. (e) Complete absence of the right portal vein. All hepatic segments are supplied by the left portal vein.
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Figure 3c. Schematics illustrate selected variants of the portal venous system. hp = horizontal part, LPV = left portal vein, PV = portal vein, up = umbilical (vertical) part. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch. (b) Portal trifurcation. (c) Portal quadrifurcation. (d) Bifurcation of the right portal vein (RPV) into anterior (Ant.) and posterior (Post.) branches, which supply segments V/VIII and VI/VII, respectively. (e) Complete absence of the right portal vein. All hepatic segments are supplied by the left portal vein.
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Figure 3d. Schematics illustrate selected variants of the portal venous system. hp = horizontal part, LPV = left portal vein, PV = portal vein, up = umbilical (vertical) part. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch. (b) Portal trifurcation. (c) Portal quadrifurcation. (d) Bifurcation of the right portal vein (RPV) into anterior (Ant.) and posterior (Post.) branches, which supply segments V/VIII and VI/VII, respectively. (e) Complete absence of the right portal vein. All hepatic segments are supplied by the left portal vein.
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Figure 3e. Schematics illustrate selected variants of the portal venous system. hp = horizontal part, LPV = left portal vein, PV = portal vein, up = umbilical (vertical) part. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch. (b) Portal trifurcation. (c) Portal quadrifurcation. (d) Bifurcation of the right portal vein (RPV) into anterior (Ant.) and posterior (Post.) branches, which supply segments V/VIII and VI/VII, respectively. (e) Complete absence of the right portal vein. All hepatic segments are supplied by the left portal vein.
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Figure 4a. Three-dimensional CT reformatted images demonstrate selected portal venous system variants. Ant. RPV = anterior right portal vein, LPV = left portal vein, Post. RPV = posterior right portal vein, PV = (main) portal vein. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch (cf Fig 3a). (b) Portal trifurcation (cf Fig 3b).
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Figure 4b. Three-dimensional CT reformatted images demonstrate selected portal venous system variants. Ant. RPV = anterior right portal vein, LPV = left portal vein, Post. RPV = posterior right portal vein, PV = (main) portal vein. (a) Bifurcation of the right posterior sectoral branch from the left main portal branch, with the right anterior sectoral branch arising from the left main portal branch (cf Fig 3a). (b) Portal trifurcation (cf Fig 3b).
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Additional variations can occur in both the right and left portal systems. It is extremely important to be aware of portal anomalies because failure to do so can lead to nontarget embolization with potential risk to the FLR.
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Justification for and Pathophysiologic Features of PVE
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PVE was developed because the liver has the ability to regenerate. This phenomenon was first described in 1920 by Rous and Larimore (10) after they ligated portal vein branches in rabbits and noted that the ligated (ipsilateral) lobe became atrophic and the nonligated (contralateral) lobe became hypertrophic. Other authors have reported that portal vein occlusion secondary to tumor invasion or ligation leads to atrophy of the ipsilateral lobe and hypertrophy of the contralateral lobe (11–13). Consequently, major hepatic resections involving up to 75% of the liver can be performed, provided that the FLR is not functionally compromised (eg, by cirrhosis) (14–16).
The liver regenerates following extended right or left hepatectomy or some other major atypical resection provided two or three adjacent segments remain (17,18). Liver regeneration is a fundamental parameter of the liver’s response to injury, and the underlying mechanisms are twofold. First, hepatocytes have the ability to dedifferentiate and clonally expand, leading to increases in hepatic cell mass and number (3). Second, intrahepatic and extrahepatic factors (the most potent intrahepatic factor being hepatocyte growth factor [HGF]) contribute to induction and control of hepatocyte growth. These factors represent a response to hepatocellular injury. Other mitogenic factors (eg, epidermal growth factor, transforming growth factor [TGF]-
) and cytokines (eg, tumor necrosis factor-, interleukin-6) also lead to rapid gene induction and regeneration. Importantly, insulin works synergistically (ie, is comitogenic) with HGF, which contributes to the slower rates of hypertrophy seen in diabetic patients (19,20). Extrahepatic factors are carried primarily by the portal vein and not by the hepatic artery (3,21–23).
Liver regeneration usually peaks within the first 2 weeks after PVE. Studies in swine have shown that regeneration peaks within 7 days of PVE, with 14% of hepatocytes undergoing replication (24). Regeneration rates reported for humans are comparable to those found in animals. Noncirrhotic livers demonstrate the fastest regeneration: 12–21 cm3/d at 2 weeks after PVE, approximately 11 cm3/d at 4 weeks, and 6 cm3/d at 32 days (3,15,25,26). Livers in patients with cirrhosis or diabetes regenerate more slowly (approximately 9 cm3/d at 2 weeks) (3,25,26).
Transcatheter PVE was first performed in 1984 (27), but its use for the induction of selective hepatic hypertrophy prior to extended hepatic resection was first reported by Makuuchi et al (14) in 1990. The rationale for using PVE in this setting is that PVE minimizes the sudden elevation in portal pressure at resection that can result in hepatocellular damage in the residual liver. This change in portal pressure, in combination with surgical manipulation, may result in hepatic congestion and postresection dysfunction (27–29). Metabolic changes are also minimized after resection following PVE because a lesser relative decrease in hepatocyte cell mass may improve overall tolerance for major resection (14). Finally, portal blood flow to the unembolized liver as measured with Doppler ultrasonography (US) increased significantly, then decreased toward baseline (without reaching the baseline value) after 11 days (3,30). The resulting rate of hypertrophy correlated well with the flow rate measurements (3,30).
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What to Expect Clinically after PVE
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Changes in liver function following PVE are usually minor and transient (50% of patients have no appreciable change) (3). When transaminase levels rise, they usually peak at a level less than three times baseline 1–3 days after embolization and return to baseline by 7–10 days, regardless of the embolic material used. Slight changes in total bilirubin value and white blood cell count may be seen. Synthetic function (eg, prothrombin time) is almost never affected.
Because PVE is considerably less toxic than arterial embolization, side effects are minimal (3). Signs and symptoms of postembolization syndrome, such as nausea and vomiting, are rare. Fever and pain are infrequent. This is because PVE produces no distortion of anatomy, minimal inflammation (except immediately around the embolized vein), and little or no parenchymal or tumor necrosis (14,31). Animal studies have shown that hepatocytes undergo apoptosis but not necrosis following portal vein occlusion (24,32).
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Indications and Contraindications for PVE
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Indications
At present, four factors are important to consider when deciding whether to perform PVE. First, the ratio of FLR to total estimated liver volume (TELV) should be calculated. Second, cases need to be categorized into those with and those without underlying liver disease because this factor will determine how much FLR is needed to reduce postoperative morbidity and mortality. The minimum absolute liver volume necessary to support postresection hepatic function has not been clearly defined. However, a FLR/TELV ratio of at least 25% is recommended in patients with otherwise normal livers, with a ratio of at least 40% in patients in whom the liver is considered compromised (eg, from chronic liver disease or high-dose chemotherapy) (2,3,25,26,33,34). When FLR/TELV ratios are below these levels, PVE may be performed in an attempt to increase FLR volume. Third, the presence of systemic disease such as diabetes mellitus may limit hepatic hypertrophy. As mentioned earlier, insulin is a comitogenic factor with HGF that often leads to slower rates of regeneration (19,20). Fourth, planning for the type and extent of the anticipated surgical procedure (eg, right hepatectomy and pancreaticoduodenectomy) is important because more functional hepatic reserve may be required to reduce postoperative morbidity.
Contraindications
Thus far, we have found no absolute contraindications for PVE; however, there are a number of relative contraindications. Patients with metastatic disease such as distant metastases or periportal lymphadenopathy cannot undergo resection and therefore are not candidates for PVE. Patients with widespread intrahepatic disease involving the entire right lobe and segment I, II, or III or involving the entire left lobe and segment VI or VII are not candidates for right or left trisegmentectomy, respectively and would not benefit from PVE. Other relative contraindications for PVE include an uncorrectable coagulopathy, tumor invasion of the portal vein, tumor precluding safe transhepatic access, biliary dilatation (in cases of biliary tree obstruction, drainage is recommended), portal hypertension, and renal failure, which requires dialysis. PVE in cases of tumor invasion of the portal vein may not be warranted because there may be no significant benefit from the procedure. Although we always try to avoid portal venous access through tumor, it may not be possible if the tumor burden is great. However, there is no realistic concern for exacerbating tumor spread or injuring the diseased segments. In our study of 26 patients who underwent PVE (35), we reported a complication (ie, subcapsular hematoma) that occurred when portal venous access through tumor was gained inadvertently. If concern does exist, the contralateral approach (ie, access through the FLR) may be used. However, this option must be weighed against the possibility of causing injury to the FLR or the portal veins that supply it.
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Methods for Calculating FLR Volumes
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CT with volumetrics is the cornerstone for planning surgical resection (3). There are different methods of calculating liver volumes, making comparison of results obtained at different institutions difficult. One method measures the resected and total liver volumes and estimates the size of the "normal" (nondiseased) liver by subtracting tumor volume (33,36):
This method can be complicated in cases involving multiple tumors and does not account for the actual functional liver volume when there is biliary dilatation or vascular obstruction. In addition, this method does not directly measure the FLR volume (2,33,36).
At our institution, we directly measure the FLR and estimate the TELV with a formula based on the patient’s body weight and body surface area that was previously described (37) so that the FLR/TELV ratio can be calculated. This method allows uniform comparison of FLR volume prior to extended resection with or without preoperative PVE (2,3,37). With this calculation, a correlation between FLR and surgical outcome can be established (2). CT is performed immediately prior to PVE and approximately 2–4 weeks after PVE to determine the degree of FLR hypertrophy.
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Technical Considerations and Periprocedural Issues
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Preprocedure Work-up
Prior to PVE, a complete patient history is taken and a thorough physical examination performed. We also perform necessary laboratory studies including complete blood count, prothrombin time, total bilirubin value, liver function tests, blood urea nitrogen/creatinine levels prior to PVE. If the patient has an elevated total bilirubin value (>3.0 mg/dL), percutaneous or endoscopic biliary drainage is performed. Cross-sectional imaging for procedural planning is performed immediately prior to PVE to document the extent of disease (ie, extrahepatic disease or involvement of the planned FLR), FLR size, and portal venous anatomy.
PVE Technique
On the day of the procedure, prophylactic broad-spectrum antibiotics (eg, cefazolin, ceftriaxone sodium) are administered intravenously for prevention of biliary sepsis. Although general anesthetic may be requested, the procedure is most often performed with local anesthetic (1% lidocaine hydrochloride; Astra USA, Westborough, Mass) and intravenously administered sedatives (midazolam hydrochloride; ESI Lederle, Philadelphia, Pa; fentanyl citrate; Abbott Laboratories, North Chicago, Ill) that allow the patient to remain conscious. US of the liver is performed to determine the best access route into the portal venous system. Under sterile conditions, access into the portal venous system is gained with US or fluoroscopic guidance or both. The procedure is performed with fluoroscopy. The ipsilateral approach (access through the portion of the liver to be resected) is recommended so as not to injure the FLR.
Technique will vary depending on the institution and the surgical resection planned (eg, left versus right, hepatectomy versus trisegmentectomy). In addition, either the percutaneous transhepatic or transileocolic venous approach is used depending on whether an interventional radiology suite is available. The latter approach is used by surgeons and is performed at open laparotomy with direct cannulation of the ileocolic vein.
Although trisectoral left PVE can be performed with similar techniques, we have had no reason to perform this procedure at our institution. Nagino et al (18) reported on the percentage of liver removed during various hepatic resections and found that a left trisegmentectomy with caudate lobectomy is equivalent to a 67% resection. This resection results in a 33% FLR/TELV ratio, a level well above the lowest ratio that is considered safe (25%). Therefore, in this article we offer guidelines for trisectional PVE performed prior to right trisegmentectomy (Fig 5) (35). Right PVE is performed using a similar technique without embolization of the segment IV portal veins. The needle system chosen is at the operator’s discretion. We often use a 22-gauge Chiba needle (Neff Percutaneous Access Set; Cook, Bloomington, Ind), which is placed into a branch of the ipsilateral portal venous system. The Seldinger technique is used to place a 6-F vascular sheath (Boston Scientific, Natick, Mass) into the main right portal vein or a main portal branch. Flush portography is performed with a 5-F angiographic pigtail catheter (Cook) in the main portal vein. Anteroposterior, right and left anterior oblique, and craniocaudal projections are obtained to best delineate the portal venous anatomy. Selective left portal vein injections are performed. Left portal vein segments (IVa and IVb) are embolized with a Tracker microcatheter (Target Therapeutics, Freemont, Calif) placed coaxially through a 5-F selective angiographic catheter. Polyvinyl alcohol (PVA) particles (Contour; Boston Scientific/Target Vascular, Freemont, Calif) ranging from 300 to 500 µm and microcoils (Platinum Microcoils; Target Therapeutics) are used to embolize segments IVa and IVb. The particle size was chosen so as not to occlude the microcatheter. For right portal vein embolization (segments V–VIII), we use a 5-F reversed curve catheter (Cook) to deliver PVA particles ranging from 300 to 1,000 µm and 0.035- or 0.038-inch coils (Gianturco; Cook). The 5-F catheter was chosen for ease of manipulation into the right portal branches, given the severe angulation of the right portal tree with the ipsilateral approach. The smaller PVA particles are used first to occlude the smaller distal portal branches. The larger PVA particles (up to 1,000 µm) are used later to help occlude the larger, more proximal tertiary branches. Coils are then used to occlude second-order branches.
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Figure 5a. Right PVE. (a) Portal venogram shows a 5-F pigtail flush catheter (black arrow) placed through a 6-F vascular sheath (white arrows). (b) Selective left portogram shows the veins that supply segment IV (arrows). (c) Selective right portogram demonstrates normal subsegmental portal branches. (d) Final portogram reveals that the left lateral segment portal branches (large arrows) and segment IV veins (small arrows) continue to have blood flow.
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Figure 5b. Right PVE. (a) Portal venogram shows a 5-F pigtail flush catheter (black arrow) placed through a 6-F vascular sheath (white arrows). (b) Selective left portogram shows the veins that supply segment IV (arrows). (c) Selective right portogram demonstrates normal subsegmental portal branches. (d) Final portogram reveals that the left lateral segment portal branches (large arrows) and segment IV veins (small arrows) continue to have blood flow.
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Figure 5c. Right PVE. (a) Portal venogram shows a 5-F pigtail flush catheter (black arrow) placed through a 6-F vascular sheath (white arrows). (b) Selective left portogram shows the veins that supply segment IV (arrows). (c) Selective right portogram demonstrates normal subsegmental portal branches. (d) Final portogram reveals that the left lateral segment portal branches (large arrows) and segment IV veins (small arrows) continue to have blood flow.
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Figure 5d. Right PVE. (a) Portal venogram shows a 5-F pigtail flush catheter (black arrow) placed through a 6-F vascular sheath (white arrows). (b) Selective left portogram shows the veins that supply segment IV (arrows). (c) Selective right portogram demonstrates normal subsegmental portal branches. (d) Final portogram reveals that the left lateral segment portal branches (large arrows) and segment IV veins (small arrows) continue to have blood flow.
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Embolization is performed until stasis or near stasis is achieved. Right PVE often requires 4–6 bottles (400–600 mg) of PVA. Right trisectional PVE often requires 5–7 bottles (500–700 mg) of PVA. More PVA may be required depending on whether vascular shunts are present. Repeat portography is performed to evaluate embolization. The access tract is embolized with 3-mm coils on completion of the procedure.
Postembolization Monitoring and Deciding When to Operate
Evaluation for signs of postembolization syndrome or liver insufficiency includes review of patient symptoms, clinical signs, and laboratory data (such as elevated white blood cell count, increasing transaminase levels, or prothrombin time). Patients are discharged when they are clinically stable and without complaints, usually the next day.
Repeat CT is performed after 2–4 weeks to assess FLR hypertrophy and disease spread. If liver regeneration occurs and there is no spread of disease that would contraindicate the procedure, resection is performed. Otherwise, follow-up CT is performed at monthly intervals. Because the minimum safe FLR volume that would contraindicate resection has not yet been determined, we still perform resection in all patients who demonstrate regeneration (35). Although studies in animals show that most regeneration occurs within the first 2 weeks, this has not yet been proved in humans.
Selective hepatic lobar hypertrophy is illustrated in Figures 6 and 7.
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Figure 6a. Selective hepatic lobar hypertrophy in a 63-year-old man with hepatocellular carcinoma and a pancreatic mass. (a) CT scan obtained prior to PVE shows a 5-cm necrotic mass (arrow) in segments VI and VII. Arrowheads indicate the FLR (segments I-IV). The FLR/TELV ratio was 22.3%. (b) CT scan obtained following PVE shows substantial FLR hypertrophy. The FLR/TELV ratio was 37.9%, representing an increase of 15.6%. The patient subsequently underwent successful right hepatectomy and pancreaticoduodenectomy.
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Figure 6b. Selective hepatic lobar hypertrophy in a 63-year-old man with hepatocellular carcinoma and a pancreatic mass. (a) CT scan obtained prior to PVE shows a 5-cm necrotic mass (arrow) in segments VI and VII. Arrowheads indicate the FLR (segments I-IV). The FLR/TELV ratio was 22.3%. (b) CT scan obtained following PVE shows substantial FLR hypertrophy. The FLR/TELV ratio was 37.9%, representing an increase of 15.6%. The patient subsequently underwent successful right hepatectomy and pancreaticoduodenectomy.
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Figure 7a. Selective hepatic lobar hypertrophy in a 55-year-old man with cholangiocarcinoma. (a, b) CT scans obtained prior to (a) and following (b) PVE show the FLR (segments I-III) (arrowheads). The FLR/TELV ratio was 17.0% before PVE and 25.1% after PVE, representing an increase of 8.1%. The patient subsequently underwent successful right trisegmentectomy. (c) CT scan obtained following resection demonstrates a massive liver remnant.
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Figure 7b. Selective hepatic lobar hypertrophy in a 55-year-old man with cholangiocarcinoma. (a, b) CT scans obtained prior to (a) and following (b) PVE show the FLR (segments I-III) (arrowheads). The FLR/TELV ratio was 17.0% before PVE and 25.1% after PVE, representing an increase of 8.1%. The patient subsequently underwent successful right trisegmentectomy. (c) CT scan obtained following resection demonstrates a massive liver remnant.
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Figure 7c. Selective hepatic lobar hypertrophy in a 55-year-old man with cholangiocarcinoma. (a, b) CT scans obtained prior to (a) and following (b) PVE show the FLR (segments I-III) (arrowheads). The FLR/TELV ratio was 17.0% before PVE and 25.1% after PVE, representing an increase of 8.1%. The patient subsequently underwent successful right trisegmentectomy. (c) CT scan obtained following resection demonstrates a massive liver remnant.
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Important Unresolved Issues Regarding PVE
In PVE performed prior to an extended right hepatectomy, increasing attention has been given to embolization of segment IV. This embolization is performed for two reasons: (a) all tumor-bearing liver is embolized because accelerated tumor growth has been reported with incomplete embolization (38), and (b) segment IV embolization may contribute to better hypertrophy of segments I, II, and III before extended right hepatectomy (18). In addition, it is important to avoid reflux of the embolic material into the veins that will supply the FLR because bilateral or main portal vein occlusion remains a risk.
Results of PVE at multiple institutions are shown in Table 2. In addition to PVA and coils, many other embolic agents have been used depending on operator preference, with similar results. These agents include cyanoacrylate, ethiodized oil, an absorbable gelatin sponge (Gelfoam; Upjohn, Kalamazoo, Mich), thrombin, microspheres, and absolute alcohol. Table 3 shows a partial comparison of the results of using different agents as reported in the literature. In addition, it is currently unclear how much embolic material is necessary to achieve a specific degree or rate of hypertrophy. As mentioned earlier, we perform embolization until stasis or near stasis is achieved. In the use of particulate agents, it is unclear what size particles will lead to better regeneration.
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Potential Complications of PVE
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Complications secondary to PVE are uncommon. However, when they do occur, they are similar to those associated with any other percutaneous transhepatic procedure and include transient hemobilia, bleeding (eg, subcapsular hematoma [Fig 8]), and infection. Complications more specific to PVE include the need for reembolization, portal vein thrombosis (Fig 9), and portal hypertension resulting in esophageal variceal hemorrhage. A complication specific to the transileocolic approach is small bowel obstruction. The complications reported in our study (Table 2) did not preclude successful resection.
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Figure 8. Subcapsular hematoma in a 73-year-old man with liver metastases secondary to colon carcinoma. CT scan shows a large subcapsular hematoma (arrowheads) that developed following PVE. The patient subsequently underwent successful hepatic resection.
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Figure 9a. Portal vein thrombosis in a 50-year-old man with cholangiocarcinoma who had undergone successful PVE. Three weeks later, the patient developed severe abdominal pain. (a) CT scan reveals portal vein thrombosis of the main and left portal veins (arrows) and the expected thrombosis of the right portal vein and segment IV portal veins. (b) CT reformatted image shows an aberrant left gastric vein (arrow) that supplies the segment II portal veins. (c) Portogram shows thrombosis in the main (arrow) and left (arrowhead) portal veins. (d) Portogram obtained after treatment with a 30-hour infusion of recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, Calif) (infusion rate = 0.4 mg/h and 0.6 mg/h in the left and main portal veins, respectively) and mechanical thrombolysis (Angiojet; Possis, Minneapolis, Minn) shows patency of the portal venous tree. Although narrowing of the left portal vein from residual thrombus or stenosis was seen (arrow), no intervention was performed to avoid triggering further thrombotic events. (e) Left portal venogram shows patency of the veins that supply segments II and III. The patient subsequently underwent successful extended right trisegmentectomy.
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Figure 9b. Portal vein thrombosis in a 50-year-old man with cholangiocarcinoma who had undergone successful PVE. Three weeks later, the patient developed severe abdominal pain. (a) CT scan reveals portal vein thrombosis of the main and left portal veins (arrows) and the expected thrombosis of the right portal vein and segment IV portal veins. (b) CT reformatted image shows an aberrant left gastric vein (arrow) that supplies the segment II portal veins. (c) Portogram shows thrombosis in the main (arrow) and left (arrowhead) portal veins. (d) Portogram obtained after treatment with a 30-hour infusion of recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, Calif) (infusion rate = 0.4 mg/h and 0.6 mg/h in the left and main portal veins, respectively) and mechanical thrombolysis (Angiojet; Possis, Minneapolis, Minn) shows patency of the portal venous tree. Although narrowing of the left portal vein from residual thrombus or stenosis was seen (arrow), no intervention was performed to avoid triggering further thrombotic events. (e) Left portal venogram shows patency of the veins that supply segments II and III. The patient subsequently underwent successful extended right trisegmentectomy.
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Figure 9c. Portal vein thrombosis in a 50-year-old man with cholangiocarcinoma who had undergone successful PVE. Three weeks later, the patient developed severe abdominal pain. (a) CT scan reveals portal vein thrombosis of the main and left portal veins (arrows) and the expected thrombosis of the right portal vein and segment IV portal veins. (b) CT reformatted image shows an aberrant left gastric vein (arrow) that supplies the segment II portal veins. (c) Portogram shows thrombosis in the main (arrow) and left (arrowhead) portal veins. (d) Portogram obtained after treatment with a 30-hour infusion of recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, Calif) (infusion rate = 0.4 mg/h and 0.6 mg/h in the left and main portal veins, respectively) and mechanical thrombolysis (Angiojet; Possis, Minneapolis, Minn) shows patency of the portal venous tree. Although narrowing of the left portal vein from residual thrombus or stenosis was seen (arrow), no intervention was performed to avoid triggering further thrombotic events. (e) Left portal venogram shows patency of the veins that supply segments II and III. The patient subsequently underwent successful extended right trisegmentectomy.
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Figure 9d. Portal vein thrombosis in a 50-year-old man with cholangiocarcinoma who had undergone successful PVE. Three weeks later, the patient developed severe abdominal pain. (a) CT scan reveals portal vein thrombosis of the main and left portal veins (arrows) and the expected thrombosis of the right portal vein and segment IV portal veins. (b) CT reformatted image shows an aberrant left gastric vein (arrow) that supplies the segment II portal veins. (c) Portogram shows thrombosis in the main (arrow) and left (arrowhead) portal veins. (d) Portogram obtained after treatment with a 30-hour infusion of recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, Calif) (infusion rate = 0.4 mg/h and 0.6 mg/h in the left and main portal veins, respectively) and mechanical thrombolysis (Angiojet; Possis, Minneapolis, Minn) shows patency of the portal venous tree. Although narrowing of the left portal vein from residual thrombus or stenosis was seen (arrow), no intervention was performed to avoid triggering further thrombotic events. (e) Left portal venogram shows patency of the veins that supply segments II and III. The patient subsequently underwent successful extended right trisegmentectomy.
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Figure 9e. Portal vein thrombosis in a 50-year-old man with cholangiocarcinoma who had undergone successful PVE. Three weeks later, the patient developed severe abdominal pain. (a) CT scan reveals portal vein thrombosis of the main and left portal veins (arrows) and the expected thrombosis of the right portal vein and segment IV portal veins. (b) CT reformatted image shows an aberrant left gastric vein (arrow) that supplies the segment II portal veins. (c) Portogram shows thrombosis in the main (arrow) and left (arrowhead) portal veins. (d) Portogram obtained after treatment with a 30-hour infusion of recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, Calif) (infusion rate = 0.4 mg/h and 0.6 mg/h in the left and main portal veins, respectively) and mechanical thrombolysis (Angiojet; Possis, Minneapolis, Minn) shows patency of the portal venous tree. Although narrowing of the left portal vein from residual thrombus or stenosis was seen (arrow), no intervention was performed to avoid triggering further thrombotic events. (e) Left portal venogram shows patency of the veins that supply segments II and III. The patient subsequently underwent successful extended right trisegmentectomy.
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Conclusions
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PVE is a safe and effective method for inducing selective hepatic hypertrophy in the appropriate clinical setting. This technique, usually reserved for those patients whose FLR is too small to allow safe resection, may reduce complications and shorten hospital stays after resection. A thorough knowledge of hepatic segmentation and portal venous anatomy is essential. In addition, the indications, contraindications, methods for evaluating for hepatic lobar hypertrophy, timing of surgery, and possible complications need to be fully understood before performing PVE. Technique may vary among operators, and further research is necessary to determine the best embolic agents available and the expected rates of liver regeneration for PVE.
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Footnotes
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Abbreviations: FLR = future liver remnant,
HGF = hepatocyte growth factor,
PVA = polyvinyl alcohol,
PVE = portal vein embolization,
TELV = total estimated liver volume
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References
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- Tsao JI, Loftus JP, Nagorney DM, Adson MA, Ilstrup DM. Trends in morbidity and mortality of hepatic resection for malignancy: a matched comparative analysis. Ann Surg 1994; 220:199-205.[Medline]
- Vauthey JN, Chaoui A, Do KA, et al. Standardized measurement of the future liver remnant prior to extended liver resection: methodology and clinical associations. Surgery 2000; 127:512-519.[CrossRef][Medline]
- Abdalla EK, Hicks ME, Vauthey JN. Portal vein embolization: rationale, technique and future prospects. Br J Surg 2001; 88:165-175.[CrossRef][Medline]
- Couinaud C. Le foie: études anatomiques et chirurgicales Paris, France: Masson, 1957; 75.
- Schultz SR, LaBerge JM, Gordon RL, et al. Anatomy of the portal vein bifurcation: intra- versus extrahepatic location: implications for transjugular intrahepat
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Abstract
LEARNING OBJECTIVES
