Radiologic hepatobiliary interventions

Portal vein

The majority of the nutrient blood flow to the liver is via the portal vein, which drains the splanchnic circulation and spleen. The most common abnormality involving the portal vein is portal hypertension, typically as a sequela of cirrhosis (see Chapters 74 , 79 , 81 , and 85 ). Clinical manifestations of portal hypertension include splenomegaly, thrombocytopenia, varices, ascites, and liver failure. In 1969 Rosch and colleagues reported the first case of transjugular intrahepatic portosystemic shunt (TIPSS) in dogs (see Chapter 85 ). Thirteen year later, Colapinto and colleagues (1982) reported the first human application of TIPSS. In this procedure, a path is created from the hepatic vein to the portal vein through the liver parenchyma, thereby decreasing portal pressure and relieving patients from intractable ascites or acute variceal bleeding. Initially the tract was formed with serial dilators or balloon dilation, with limited success. When the Palmaz metallic balloon expandable stents became available in the mid-1980s, procedural success improved, and the technique gained widespread acceptance. Further refinement using covered self-expanding stents has improved long-term patency, making this a viable option not only for patients with life-threatening hemorrhage but also as a means to control intractable ascites. ^,

The most significant complication of TIPSS is hepatic encephalopathy because of the volume of blood shunted past the liver parenchyma (see Chapter 77 ). As a result, the presence of hepatic encephalopathy is a relative contraindication to the procedure. Other contraindications include right heart failure, hepatic vein occlusion, and sepsis. The risk of cardiac decompensation after TIPSS can be predicted noninvasively.

In patients with hepatic encephalopathy and portal hypertension or patients with “left-sided (sinistral) portal hypertension” (gastric varices because of splenic vein occlusion), balloon-occluded retrograde transvenous obliteration (BRTO) or balloon-occluded antegrade transvenous obliteration (BATO) may be preferable to TIPSS. BRTO and BATO refer to procedures in which a high-risk or bleeding gastric varix is catheterized and sclerosed, typically with a mixture of Ethiodol, Sotradechol, and air agitated through a three-way stopcock. In patients with isolated sinistral portal hypertension because of occlusion of the splenic vein, recanalization of the occluded splenic vein or embolization of the splenic artery may be considered.

In some cases, portal vein narrowing or occlusion because of extrinsic compression by tumor may cause symptoms similar to those seen in cirrhotic portal hypertension. In such cases, placement of a self-expanding stent can relieve varices and ascites. This is most commonly seen in patients with locally advanced pancreaticobiliary cancer, where portal vein stenting may also improve thrombocytopenia, broadening chemotherapy options.

Another procedure that has gained widespread acceptance is portal vein embolization (PVE) as an adjunctive procedure before hepatic resection (see Chapter 102C ). Patients with a suboptimal future liver remnant (FLR), which can be assessed volumetrically (i.e., with computed tomography [CT] or magnetic resonance imaging [MRI]) or functionally (e.g., indocyanine green clearance), may undergo contralateral PVE to induce preoperative hypertrophy of the FLR (see Chapter 102C ). In patients with cirrhosis, most surgeons believe that a FLR of greater than 40% of the total liver volume (TLV) is optimal. For patients without underlying liver disease, a FLR of greater than 25% is thought to be acceptable. Other risk factors for impaired liver function include diabetes, prior chemotherapy, and steatosis, and therefore the desired volume of the FLR is best assessed on a case-by-case basis.

PVE to improve the safety of hepatic resection was first proposed by Makuuchi and colleagues in 1990. Initially, this procedure was performed via a transileocolic approach that required laparotomy and general anesthesia. Although ligation of a portal vein branch can be carried out during a laparotomy, today this procedure is most commonly performed percutaneously, typically as an outpatient procedure. A wide range of agents have been used to perform the procedure, including ethanol, Gelfoam, thrombin, polyvinyl alcohol, glue, spherical embolic agents, coils, and sclerosing agents. No agent has proven superior; each is expected to increase the absolute FLR/TLV in the range of 8% to 10%. Complications are uncommon, the most significant being nontarget embolization to the main portal vein or portal vein supplying the FLR, which could preclude operation. This occurs in less than 1% of patients.

Liver hepatic venous deprivation is another technique to improve contralateral hepatic hypertrophy before major hepatic resection. In this procedure, both the portal and hepatic veins in the hemiliver to be resected are embolized to maximize growth of the FLR and allow major hepatic resection.

Hepatic artery

Unlike portal vein interventions, which are most commonly undertaken to treat the sequela of portal hypertension or, in the case of PVE, as adjunct to hepatic resection, most transarterial interventions in the liver are done to effect treatment of unresectable malignancy or for control of bleeding in the setting of trauma (see Chapters 21 , 94 , 113 , 115 , and 116 ).

Both primary and metastatic liver tumors derive the majority of trophic blood supply from the hepatic artery, unlike the non–tumor-bearing parenchyma, which receives the majority of nutrient flow from the portal vein (see chapter 5 ). Therefore administering a treatment to the artery can affect tumor regression while minimizing collateral damage to the underlying parenchyma.

In the mid-1970s, it was recognized that the unusual dual vascular supply to the liver might allow effective transarterial treatment for hypervascular metastases from neuroendocrine tumors, as well as primary hepatocellular carcinoma (HCC). Subsequently, transarterial treatments have been applied to a wide variety of hypervascular tumors, including sarcoma and breast cancers, as well as some tumors that are not particularly hypervascular by imaging, such as colon cancer or cholangiocarcinoma (see Chapter 94 ).

Different forms of treatment have been administered via the hepatic artery to treat such tumors, including chemotherapy infusion, bland (particle) embolization (transcatheter arterial embolization [TAE]), transarterial chemoembolization with lipiodol (TACE), embolization with drug-eluting beads (DEB-TACE), and radioembolization (RAE; see Chapter 94 ). Two randomized trials have demonstrated improvement in overall survival in patients with HCC treated with TACE compared with patients who received best supportive care. ^, To date, there has been no study demonstrating a significant difference in overall survival among any method of embolization, including TACE, DEB-TACE, TAE, or RAE. ^,

Indications for arterially directed therapy include control of symptoms (e.g., pain or hormonal-related symptoms because of neuroendocrine liver metastases; see Chapter 91 ), control of tumor in the liver to prolong survival, progression of disease after systemic treatment, and local tumor control to maintain eligibility for liver transplant in select patients with HCC (see Chapter 89 ). Transarterial therapies are rarely, if ever, curative and instead are intended to be repeated upon disease progression. In cases of minimal disease burden, ablation may be performed in conjunction with embolization as a potentially curative therapy (see Chapter 96 ). In this instance, performing the embolization immediately before ablation has the advantage of depositing contrast-laden particles within the tumor to assist in targeting with the ablation device and also decreasing the “heat sink” effect, whereby flowing blood continues to “cool” the tumor margin, potentially increasing the risk of local recurrence. Occluding arterial blood flow may increase the zone of ablation. In some cases, the angiogram may identify additional sites of disease undetected on preprocedure imaging, changing the treatment plan.

Selection criteria differ slightly with each treatment option. Broadly speaking, patients with unresectable disease involving less than 50% of the liver without underlying liver disease or with well-compensated (Childs-Pugh score A–B7) cirrhosis may be candidates. In the past, portal vein occlusion was considered an absolute contraindication because of the reported higher complication rate and risk of death. More recently, series of patients with portal vein occlusion treated with TAE, TACE, and RAE have been shown to respond to treatment without a significant increase in complications, thus supporting its use in this group of patients with limited treatment options.

The complication profiles differ slightly between the various transarterial therapies. TACE is infrequently associated with bone marrow suppression and alopecia. Radiation-induced liver failure occurs in 1% to 2% of patients who undergo RAE; however, radiologic findings of cirrhosis and portal hypertension are seen in greater than 50% of patients with neuroendocrine tumor treated with whole liver RAE at a mean of 4.1 years after treatment. With varying frequency, intra-arterial therapy is associated with arterial sclerosis and arterial occlusion, which can make future intervention more difficult. This is more commonly seen with TACE and DEB-TACE than with TAE. ^, The clinical relevance of this angiographic finding is that over time tumors can derive arterial supply from nonhepatic collateral vessels, making treatment more challenging and creating a higher risk of nontarget embolization. Branches that commonly give rise to extrahepatic tumor supply include the right phrenic, internal mammary, gastroduodenal, intercostal, and renal capsular arteries.

Complications include nontarget embolization, liver failure, vessel injury, and postembolization syndrome. Postembolization syndrome occurs in the majority of patients, other than those treated with RAE, and consists of some degree of pain, fever, and/or nausea that can last for several days. Prolonged pain may suggest nontarget embolization to the pancreas, resulting in pancreatitis, or to the gallbladder or upper gastrointestinal (GI) tract, resulting in cholecystitis or gastric or duodenal ulceration.

The hepatic artery is also a vessel that may require intervention after liver transplant. After primary graft malfunction, hepatic artery thrombosis (HAT) is the second leading cause of graft failure after liver transplant and is a major cause of transplant-related mortality (see Chapter 111 ). This complication can result from technical issues with the anastomosis, including disparate diameters of donor and recipient vessels, and tension on, or kinking of, the anastomosis. In most cases, HAT occurs within the first 100 days and manifests as fulminant hepatic necrosis and/or biliary tract ischemia and necrosis, resulting in sepsis. Because these patients are immunosuppressed to prevent graft rejection, the gram-negative sepsis resulting from biliary necrosis can be very difficult to treat (see Chapter 111 ).

Early posttransplant screening Doppler ultrasound (US) can be used to detect abnormal flow in the hepatic artery. If this test is abnormal, a contrast study (US, CT, or angiography) should be considered. To salvage the organ, a precious resource, revascularization is often attempted after documentation of abnormal flow, even in asymptomatic patients.

Other hepatic artery complications may develop post-transplant, including stenosis and pseudoaneurysm. As with occlusion, revascularization with catheter-directed thrombolysis, angioplasty, and/or stent placement is effective in the majority of cases with hepatic artery stenosis. Pseudoaneurysm is a rare but potentially fatal complication that may be treated with a covered stent graft (see Chapters 111 and 115 ).

After blunt abdominal trauma, the liver is the second most commonly injured abdominal organ after the spleen (see Chapter 113 ). The American Association for the Surgery of Trauma Injury Scoring Scale was developed to help guide management of these patients. Injuries to the hepatic artery include pseudoaneurysms, which can be unifocal or multiple, resulting in a “starry sky” appearance of multiple sites of extravasation/injury on angiography. Focal extravasation or pseudoaneurysm is usually treated with coil embolization of the affected vessel distal and proximal to the injury, or with a covered stent. In the case of multifocal injury, particle embolization of the hepatic artery may be performed. Because of the dual blood supply to the liver discussed earlier, embolization of the hepatic artery in the presence of a patent portal vein is rarely of clinical consequence. Hepatic artery injury may occur after iatrogenic hepatic interventions, either surgical or percutaneous, such as biliary drainage or TIPSS, and is treated similarly with coil embolization or covered stent placement.

Hepatic vein

The least common vascular target of endovascular intervention in the liver is the hepatic vein. Budd-Chiari is a potentially life-threatening disease of heterogeneous etiology, resulting in obstruction of hepatic venous outflow that occurs in less than one per million persons (see Chapter 86 ). Acutely, patients are symptomatic with abdominal pain and ascites, and over time, centrilobular fibrosis and cirrhosis may develop. Initial therapy includes systemic anticoagulation, but the benefit of anticoagulation alone is debatable. Patients with ongoing symptoms may benefit from thrombolysis, venoplasty, and/or stent placement and, in some cases, TIPSS (see Chapter 85 ).

Stenosis of the intrahepatic or suprahepatic inferior vena cava may occur as a complication after orthotopic liver transplantation, and symptomatology mimicking Budd-Chiari may ensue. Elevated velocities by Doppler US suggest the diagnosis, and a pressure gradient of greater than 6 mm Hg across the stenosis at venography is diagnostic. Venoplasty or, in select cases, stent placement can alleviate symptoms and preserve graft function.