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Hepatobiliary System and Vascular-Interventional Procedures

A.J. Hicks

Vascular-Interventional radiology (VIR) plays an important part in the diagnosis, management,


and treatment of hepatobiliary pathologies that many Americans suffer from. This article
discusses the normal anatomy and function of the liver, gallbladder, pancreas, and bile ducts.
This article will also overview the subspecialty of VIR, as well as the specific procedures that are
performed by the VIR team.

After completing this article, readers should be able to:


Describe the anatomy and functions of the hepatobiliary system
Overview vascular interventional radiology
Describe procedures for hepatobiliary pathologies through vascular-interventional
radiology

While the hepatobiliary system is termed an accessory to the digestive system, its
function in digesting and metabolizing the food we consume is more than auxiliary. The stomach
chemically denatures nutrients from food to only a certain degree, but it is the only primary
organ in the digestive system that performs this function without assistance from other organs.
Proper function of the hepatobiliary system helps complete digestion, and it also plays a role in
metabolism, transportation, storage, and hormone secretion. When compromised, this system
greatly affects quality of life; however, VIR plays a helping hand in diagnosing and alleviating
some of the pathologies experienced.

Hepatobiliary Anatomy and Function


The purposes of the hepatobiliary system include: regulating composition of blood;
processing nutrients absorbed by the intestines; removing toxins from the blood; produce, store,
and transport bile; and produce cholesterol and other important proteins and hormones.1 The
hepatobiliary system consists of the liver, gallbladder, pancreas, and biliary ducts.

Liver

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Anatomy
Other than skin, the liver is the largest organ in the human body weighing on average 3
pounds (~1.5 kg). This soft, rubbery organ is wedge or prism shaped, reddish-brown, and is
covered by a fibrous, connective tissue capsule called the Glissons Capsule.2 The liver is further
protected and held in place by the serous layer of the peritoneum; folds of the peritoneum form
ligaments that adhere the liver to the diaphragm and anterior abdominal wall. The liver is divided
into four lobes; the right lobe is five to six times larger than the tapered left lobe and are
separated by the falciform ligament which runs down the anterior surface of the liver to the
inferior border. This ligament attaches the liver to the rectus sheath, the inner layer of anterior
abdominal wall. The superior aspect of the liver is connected to the diaphragm by the wide
coronary ligament which is divided into anterior and posterior segments. In between these
segments is the bare area of the liver, a portion not covered by the peritoneum, which directly
relates with the diaphragm. The anterior and posterior segments of the coronary ligament fuse in
triangular fashion on the lateral borders of the right and left lobes, and these conjunctions are
called the right and left triangular ligaments.3
On the inferior, concave surface of the liver lies the smaller caudate and quadrate lobes.
The caudate lobe is positioned on the postero-superior portion of the right lobe bounded by the
inferior vena cava (IVC) and fissure of the ligamentum venosum, a remnant of the ductus
venosus from fetal circulation, on the right and left respectively. The quadrate lobe lies on the
antero-inferior portion of the right lobe bounded by the gallbladder on the right and round
ligament, remnant of the umbilical vein, on the left. The round ligament joins the inferior
falciform ligament and connects to the umbilicus, also known as the navel or belly button.3 Also,
the inferior surface of the right lobe has a short, deep fissure known as the porta hepatis. This
hilum separates the caudate and quadrate lobes, and it serves as the entry and exit point for
neurovascular structures and hepatic bile ducts (See Figure 1).4

Being the largest organ within the human body, the liver receives ~25% of cardiac output
(1500 mL/min); uniquely the liver receives both oxygenated and deoxygenated blood.5 The
common hepatic artery, a branch of the celiac artery stemming from the abdominal aorta,
supplies blood to the liver via the proper hepatic artery which runs alongside the portal vein and

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common bile duct forming the portal triad. The proper hepatic artery bifurcates into right and left
hepatic arteries that supply the liver with one-third of its blood supply (500 mL/min), but this
blood is fully oxygenated so it supplies one-half of the livers oxygen.5 The other two-thirds
(1000 mL/min) come from the portal vein that transports deoxygenated blood from the intestines,
stomach, spleen, and pancreas to the liver. This blood is filled with nutrients from digestion as
well as metabolites, medications, and toxins consumed by the body. Blood then drains out of the
liver into the IVC through the hepatic veins in which there are two groups. The primary group is
the right, left, and median hepatic vein with the right being much larger than the rest. The
secondary groups of vessels are called the short veins; the left anterior group consists of two to
three veins that drain out of the caudate lobe into the IVC, and the right anterior group which
comes out of the posterior lobe and extrude into the anterior IVC.6
The structural units of the liver are hepatic lobules, roughly hexagonal structures made of
plates of hepatocytes that radiate from a central vein.7 Between adjacent plates of hepatocytes,
which account for 80% of liver mass, are bile canaliculi which are ducts that collect bile created
by hepatocytes. This bile then flows through bile ductules and bile ducts before they merge
together to form the right and left bile ducts, which come together and exit the liver to form the
common hepatic duct. Also within lobules are hepatic sinusoids which are porous blood spaces
formed by fenestrated capillaries from hepatic portal veins and hepatic arteries. The sinusoids
give hepatocytes access to oxygen, nutrients, toxins, and waste materials in the blood. This blood
flows centrally in the lobule towards a central vein which sends blood to hepatic veins then into
the IVC. Additionally, star-shaped phagocytes called reticuloendothelial cells (Kupffer cells)
reside in sinusoids which remove dead red and white blood cells.8 Similar to the portal triad
observed in the porta hepatis, the corners of lobules consist of a bile duct, a hepatic artery
branch, and a hepatic portal vein branch (See figure 2).

Functions
The livers large presence within the body physically also correlates with its great
importance within the body as it assists with many facets of digestion, storage, and blood
filtration that are necessary to sustain life. As the largest organ within the body, it also takes in
and filters a great amount of blood from both the hepatic artery and the portal vein. Around 25%

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(1500mL) of the resting cardiac output goes through the liver at a time. Not only is this amount
of blood pumped to the liver to be filtered, but the liver also acts as a blood reservoir holding
about 10% of the bodys blood. When necessary during complications in other body systems, it
can hold up to 1L of blood. As the blood comes in through the hepatic artery and portal vein, the
blood will be detoxified, and excessive drug and hormones such as thyroxine and steroid
hormones will be filtered out of the blood. The blood from the portal vein will also come into
contact with the Kupffer cells, and as the blood flows by these cells the bacteria will be
entrapped into these large phagocytic macrophages. Fewer than 1% of the bacteria will
successfully pass by these cells.9
For the metabolizing of fats, the liver acts indirectly by producing bile and directly by
further breaking down fatty acids within itself. As long as there are bile acids returning to the
liver through the portal vein, bile will be constantly secreted from the liver. Bile consists of bile
acids, cholesterol, phospholipids, and bilirubin. Each day around 800-1000 mL of dilute bile is
secreted from the liver through the common hepatic duct that will either be channeled down the
cystic duct to be stored in the gallbladder or to continue down the common bile duct to be used
in the duodenum to assist in the emulsification of fats.9 The amount of bile stored will vary
depending on fasting and digestive stages. Even throughout the fasting stage, there are small
fluctuations in the amount of bile that will be sent to the duodenum based on the cyclical nature
of the Migrating Motor Complex and the amount of bile acids available. Often there will be an
increase of bile secreted after a bolus makes it to the small bowel and the bile acids are returned
back to the liver to be used again. On average about 10% of the bile secreted will make it to the
duodenum during the fasting stage, and the remaining will be sent to the gallbladder to be stored
and concentrated. Directly the liver also helps to desaturate fatty acids with dehydrogenase in
order for other cells to have unsaturated fats.
A persons life is also dependent on the livers ability to metabolize proteins. Along with
other organs, it assists in the deamination of proteins. This process creates a large amount of
ammonia that would become toxic to the body if the liver was not able to filter it out with the
byproduct being urea. The liver breaks down proteins, but it also forms plasma proteins and
synthesizes certain amino acids.
Another key role that the liver fulfills is buffering glucose. When there are excess
amounts of glucose present in the blood that the muscles do not use at that time, the liver will

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serve as a storage facility. Glucokinase along with other enzymes convert glucose and other
monosaccharides that are capable of being reduced to glucose into glycogen through
glycogenesis. Once transformed into glycogen it can be stored in the liver for later use, and
when it will be needed the process of glycogenolysis will converted it back to glucose.
Glycogenolysis occurs when epinephrine and glucagon are secreted and received by hepatocytes
which activate phosphorylase and cause this conversion to take place. Once the the glycogen is
broken down the glucose will become available to bring blood glucose levels back to normal
levels or to prepare for a quick, expected expenditure of a large amount of energy.

Gallbladder
Anatomy
This 8-10 cm long, muscular, thin-walled sac resides on the shallow area of the posterior
aspect of the livers right lobe. The gallbladder is responsible for storing, concentrating, and
propelling bile created by the liver into the duodenum.8 Similar to the stomach, the gallbladders
mucosa is composed of simple columnar epithelium that forms ruggae. The organs middle wall
is composed of smooth muscle similar to the muscularis mucosa of the GI tract which contracts
to secret bile into the cystic duct. The epithelial layer is responsible for concentrating gallbladder
bile 10-fold because it absorbs water and electrolytes from the bile that contains hydrophobic
bile salts.10 The gallbladder is held in place against the liver by a fold of visceral peritoneum that
extends from the liver capsule, this fold forms the outer layer of the gallbladder. The gallbladder
is organized into three regions. The fundus is the widest section that tapers into the body, which
tapers more to former the narrower neck. As the neck of the gallbladder approaches the common
hepatic duct, it angles superiorly to form the cystic duct which then angles inferiorly towards the
common bile duct.8 The cystic duct is about 7 mm in diameter, has a mucosa that contains spiral
valves, called valves of Heister, and has no sphincter between it and the common bile duct (See
Figure 3).10

Function
As the liver secretes bile, some will be stored in the gallbladder. While it remains in the
gallbladder, the bile will become concentrated to around 10% of its original volume as the
electrolytes and water will be absorbed.10 With the changing amounts of bile needed in the

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duodenum, the gallbladder and the adjoining common bile duct, controlled greatly by the
sphincter of Oddi, are affected by neurohormonal mechanisms. During the fasting or
interdigestive phase, bile will accumulate in the gallbladder. Small amounts will pass through to
the duodenum during the relaxation phases of the sphincter of Oddi. Both the gallbladder and
the sphincter of Oddi are continually contracting rhythmically during this phase. The gallbladder
has equal propulsive and non-propulsive contractions to prevent settling of materials that could
form issues such as gallstones. The sphincter of Oddi must maintain enough pressure with
simultaneous contractions with the duodenum in order to prevent bacteria and enzymes from
refluxing into the ampulla of Vater.
Once digestion begins with the cephalic stage in response to visual, olfactory, and taste
stimuli, the amount of bile secreted to the duodenum increases to 30-40%.10 The amount
secreted will increase gradually until it reaches its maximum around 30-60 minutes into
digestion. During this time the increased amount of bile reaching the duodenum is due to a
combination of the gallbladder contracting and the sphincter of Oddi relaxing. The vagus nerve
causes the gallbladder to contract and with the ingestion of fatty foods, the hormone
cholecystokinin (CCK) is also secreted to further contract the gallbladder to release the optimal
amount of bile. After digestion, the gallbladder will need to fill again, and for this process to
occur the vagus nerve must be antagonized by the ganglionic blocker hexamethonium and
atropine. The splanchnic nerve must then stimulate relaxation in the gallbladder, and the amount
of CCK must decrease.
With the release of CCK during the intestinal phase of digestion, the sphincter of Oddi is
relaxed. In order for the bile to be pushed out of the gallbladder to pass through the common bile
duct into the duodenum with little resistance, the vagus nerve works in conjunction with CCK to
further relax the sphincter.10

Pancreas
Anatomy

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The pancreas is an intriguing gland because it has both exocrine and endocrine properties,
meaning that it secretes chemical substances through ducts into the gastrointestinal tract and
releases hormones directly into the bloodstream, respectively.11 The pancreas is a soft, J-shaped,
slender gland that resides transversely in the retroperitoneum behind the stomach. It weighs
about 100 grams and is about 15 cm (6 in) long with the head of the pancreas resting in the c-
shaped curve of the duodenum and in front of the IVC and left renal vein. The uncinate process
is the lower half of the head and wraps behind the superior mesenteric vein and artery and is in
front of the aorta.12 The body of the pancreas rests behind the lower half of the stomach the tail
ends in the hilum of the spleen (See Figure 4).8
The major pancreatic duct, or the duct of Wirsung, runs from the tail through the body to
the head of the pancreas where it descends inferiorly through the head. The common bile duct
runs through the head of the pancreas and joins the duct of Wirsung to form a common channel
called the hepatopancreatic ampulla, which secretes bile and pancreatic juices into the medial
surface of the duodenum through the major duodenal papilla (ampulla of Vater)12. Inflow into the
duodenum is controlled by a smooth muscle sphincter (of Oddi) which is located at the terminal
end of the hepatopancreatic ampulla. It also prevents backflow of duodenal contents into the
common bile duct and major pancreatic duct. Additional sphincters are located at the terminal
ends of the duct of Wirsung and the common bile duct to prevent backflow of bile and pancreatic
juices, respectively.13 An accessory pancreatic duct runs anterosuperior to the major pancreatic
duct and enters the duodenum through the minor duodenal papilla (See Figure 5).
The body and tail of the pancreas are vascularized by pancreatic branches of the splenic
artery, a branch of the celiac trunk. The head of the pancreas is vascularized by the superior and
inferior pancreaticoduodenal arteries which are branches of the gastroduodenal and superior
mesenteric arteries (SMA).14 Vasculature of the pancreas provides important collateral blood
flow of the celiac trunk and SMA. The superior and inferior pancreaticoduodenal veins drain into
the portal vein and superior mesenteric vein respectively while the rest of the pancreas drains
into the splenic vein which then drains into the portal vein.13
Function
Pancreatic acini produce pancreatic juices that consist of digestive enzymes and a large
amount of sodium bicarbonate that are sent to the duodenum to assist with digestion via the duct
of Wirsung as it joins with the common bile duct before entering the duodenum. The presence of

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sodium bicarbonate serves to buffer to the acidic gastric chime, inactivate pepsin, and create an
environment for pH sensitive digestive enzymes.8 This response is due to the presence of chyme
in the upper section of the small intestine which secretes the hormone secretin. The makeup of
the pancreatic juices is also partially determined by the type of food that is being digested.
The other two important chemical substances produced in the pancreas are insulin and
glucagon that are produced the islets of Langerhans. There are 1-2 million islets present in the
pancreas that surround small capillaries to release insulin and glucagon directly into the blood
stream. Insulin is produced by the beta cells that make up around 60% of the cells in the islets.
Insulin is released upon the consumption of a meal high in carbohydrates that will increase the
blood glucose levels. When insulin is released it will allow for the glucose in the blood to enter
into muscle cells for use and lower blood glucose levels. The alpha cells make up around 25% of
the islets.15 These cells produce glucagon that will stimulate the liver to convert glycogen back
to glucose when blood glucose levels become too low.

VIR Overview
Vascular-Interventional Radiology (VIR) is the sub-specialty of radiology that utilizes
minimally invasive procedures to treat numerous diseases in almost every organ system in the
body.16 The use of sterile techniques and state-of-the-art fluoroscopy equipment and surgical
supplies allows the VIR team to diagnose and treat various pathologies with improved health
outcomes and minimal risk of adverse effects. Compared to open surgery, interventional
procedures require less recovery time, decreased risks, and a decreased amount of pain patients
experience. Each VIR team includes Interventional Radiologists, Interventional Technologists,
and a nursing team.
Interventional Radiologists are board-certified and fellowship-trained physicians who
specialize in interventional procedures. In order to become an interventional radiologist, one
must graduate from an accredited medical school, pass a licensing examination, and complete at
least 5 years of residency or graduate medical education. One must also complete at least one
year of an American Board of Medical Specialties (ABMS) certified fellowship program that
emphasizes minimally-invasive, image-guided procedures at an accredited teaching institution.
After these steps Certification by the American Board of Radiology (ABR) is granted.17
Interventional radiologists will have: extensive training and show expertise in radiation safety,

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radiation physics, and the biological effects of radiation; the skills to diagnose diseases through
the use of other imaging modalities; and the ability to use X-ray and fluoroscopy to navigate
small instruments through blood vessels and organs to treat diseases.
Interventional Radiology Technologists are technically, radiologically, and clinically trained
individuals who use complex imaging practices to assist in the performance of interventional
procedures. These technologists assist interventional radiologists in the execution of intricate
procedures through their knowledge of anatomy, patient positioning, procedure protocol,
technological factors, radiation safety and protection, as well as patient care. In order to be an
interventional technologist, one must demonstrate two years of formal education through an
accredited hospital based program or a 2- or 4-year educational program at an academic
institution and obtain certification through the American Registry of Radiologic Technologists
(ARRT) in diagnostic radiography and vascular-interventional (VI) radiography.18 The VI
technologist will: obtain all equipment necessary for your procedure; sterilely prep tools for
interventional radiologist and patient for procedure; operate and troubleshoot X-ray equipment;
and demonstrate knowledge of human anatomy, vascular-interventional procedures, and
patient/radiation safety.
Interventional Radiology Nurses work closely with radiologists and technologists to ensure
the highest level of patient care throughout the entire interventional process. Pre-procedure,
nurses are responsible for informing the patient about the procedure and answering any questions
the patient may have. Close examination of the patients medical history, including allergies, lab
results, and prior diagnoses, allows the nurse to properly administer the proper amount of
moderate sedation and needed medications. Doing so along with monitoring patient vital signs
will alert the nurse to any adverse events that may occur. The nursing team will meet
jurisdictional regulatory requirements set by the Joint Commission (JCO) regarding moderate
sedation and basic and advanced life-support.19 Certified Registered Nurse Anesthetists (CRNA)
will handle any procedures that require general anesthesia. Post-procedure, nurses are in charge
of monitoring the patients recovery from the procedure as well as discharge the patient with
pertinent information and supplies. Additionally, these nurses will have a spectrum of knowledge
in VIR procedures, meaning they will know indications/contraindications for procedures and
have basic knowledge of radiation safety.

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VIR Procedures
Vascular-Interventional radiology has shown increased use in diagnosing and treating
hepatobiliary pathologies. The following procedures are performed regularly in VIR units.

Transjugular Liver Biopsy (TJLB)


This procedure is indicated with patients who have suspected hepatocellular disease, such
as cirrhosis, accompanied with the presence of ascites, coagulopathy, or the need for a wedged
portal pressure; contraindicated if the patient has an INR above 1.5 or a platelet count below
50,000.20 Chronic inflammation of the liver due to causes such as alcohol abuse, viral Hepatitis B
or C, or fatty liver disease can tested by performing this biopsy. Compared to the percutaneous
method, sampling liver tissue via jugular access can be done in a safer manner because the liver
capsule is not being punctured with a biopsy needle reducing the risk of intraperitoneal bleeding.
The only downside is that this method does not allow for the sampling of discrete liver masses
unless they are adjacent to the hepatic vein being accessed.20
The patient will be laid supine with either the left or right internal jugular vein (IJ)
sterilely prepped and draped. The IJ will be accessed using ultrasound guidance and a
micropuncture kit equipped with a 21-Gauge needle, 5-French outer catheter, and 40 cm wire
guide. Once access is achieved a suitable guidewire, usually a Rosen or Amplatz Super Stiff
guidewire, replaces the microwire and the outer catheter is exchanged for a 9-French 35-40cm
vascular sheath. The guidewire is advanced through the SVC-right atrium-IVC and into the right
hepatic vein which is located just caudal to the inferior cave-atrial junction.21 A 5-French
multipurpose catheter is then used to perform a hepatic venogram to confirm the identity and
patency of the vein. The middle or left hepatic vein can be accessed as well but that changes the
orientation of the biopsy needle. Once access into the hepatic vein is achieved, the multipurpose
catheter is replaced with an occlusion balloon catheter and placed in the mid-portion of the
hepatic vein. Wedged and free hepatic vein pressures are taken to assess the hepatic pressure
gradient, optimally less than 5 mmHg, which allows the changes in intraportal pressure to be
assessed after drug treatment, the risk of bleeding by rupture of esophageal varices to be
evaluated, and the survival or the risk of hepatic encephalopathy to be predicted.22 Afterwards,
the end of the sheath is placed just inside the right hepatic vein and the guidewire and catheter
are replaced with a cutting-type TJLB kit consisting of a rigged cannula and spring-loaded

10
needle system (See Figure 6). The cannula is advanced 3-4 cm in the vein from the IVC and
rotated anteriorly and caudally to avoid piercing the liver capsule. The biopsy needle is then
advanced through the cannula and inserted a few millimeters into the hepatic parenchyma and
the spring-loaded mechanism is fired, deploying the needle and obtaining the liver sample; three
samples are taken to provide an adequate amount of tissue for sampling.20 These samples are then
stored and transported to a lab for testing. A technical success rate of this procedure is 87-97%
with the main technical error being the inability to find a suitable hepatic vein for access.

Transjugular Intrahepatic Portosystemic Shunt (TIPS)


Stent grafts can be placed to create a low resistance channel between the hepatic vein and
the intrahepatic portion of the portal vein. This method was created by Josef Rosch in 1969 to
relieve portal hypertension and its accompanying symptoms such as variceal bleeding and
ascites. 20,23 By creating an alternative pathway for portal blood to drain into systemic
circulation, vascular resistance of the liver lessens backflow of blood to the intestines, stomach,
and esophagus. Some of the contraindications for this procedure are if the patient has severe
hepatic failure, biliary/systemic sepsis, biliary obstruction, or severe left- or right-sided heart
failure.20 Ultrasound examination with Doppler interrogation, or a contrast-enhanced CT or MRI
needs to be performed before the TIPS procedure to verify patency of the hepatic and portal vein.
Also, if there is tense ascites present, a large-volume paracentesis needs to be performed before
the TIPS to allow for the liver to return to its normal anatomical location.20
Similar to the set up of a TJLB, the patient is laid supine and the right internal external
jugular is sterilely prepped; the left side can be accessed but many patients complain of chest
pain due to rigged devices being used. The IJ is accessed with a micropuncture kit and the right
hepatic vein is accessed with an angled guidewire and angled Berenstein catheter that is rotated
posterolaterally. It is important that right or middle hepatic vein access is confirmed because
accidental selection of an accessory hepatic vein can lead to procedure failure and serious
complications. Once hepatic vein access is confirmed, a wedged hepatic venogram is performed
with CO2 gas to help identify the location and patency of the main portal vein as well as the left
and right branches. Using the venogram as a guide, the radiologist will then commence to bridge
the gap across the hepatic parenchyma using a TIPS placement kit such as the Rosch-Uchida
transjugular liver access kit that includes a 0.038-inch flexible trocar and 5-French catheter

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assembly. The target location for the shunt on the portal side is just to the left or right of the main
portal vein bifurcation, the location of entry through the hepatic vein is based on patient anatomy
as well as parenchymal thickness. Intravascular ultrasound (IVUS) is a good alternative to a
venogram, which when inserted femorally, provides real-time imaging during the process of
crossing liver tissue with a needle.20
Once the liver parenchyma is crossed, the inner Trocar stylet is removed from the 5-
French catheter while aspirated. Once portal blood is aspirated freely, contrast is injected through
the catheter to confirm the entry into the portal vein, and when this is confirmed a guidewire and
catheter are inserted into the portal vein to perform venography. The pressure gradient between
the portal vein and right atrium are taken to confirm the placement of the TIPS stent. A gradient
of >12 mmHg is an indication for the stent and anything lower hints at the presence of a
competitive shunt.24 The intrahepatic parenchymal tract is then dilated using a 8- or 10-mm high
pressure angioplasty balloon to make space for the self-expanding stent graft. The nitinol-base,
polytetrafluoroethylene-covered Viatorr stent-graft is 8-12 mm in diameter, variable in length,
and has 2 cm of bare stent at the portal end of the device (See Figure 7).20 Covered stents have
replaced bare metal stents because they exhibit lower rates of stent insufficiency (8% vs. 54%),
variceal bleeding (6% vs. 11%), and hepatic encephalopathy (22% vs. 32%).24

Transarterial Embolization
Hepatomas, or primary liver tumors, are the 9th most common cause of cancer death in
the US.25 Some major risk factors for hepatomas, also known as hepatocellular carcinomas
(HCCs), are chronic liver disease and alcohol cirrhosis. These malignant lesions usually go
unnoticed until they become large enough to start causing pain, a palpable mass, or obstructive
jaundice. Up until 20 mm in diameter, these tumors have varying vasculature that can be imaged
and need to be biopsied for diagnosis; in contrast, large hepatomas are highly vascularized
making them easily noticeable in contrast-enhanced imaging studies.
While liver transplantation is the best treatment for hepatomas, different methods of
transcatheter embolization provides physicians the ability to control local liver tumors. Bland
embolizations that usually consist of small polyvinyl alcohol particles (50-150 micrometers) can
be used to stop the bleeding of ruptured hepatomas and infarct malignant tissue, but other
methods are preferred. Transarterial chemoembolization (TACE) is widely used treatment that

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involves the injection of an emulsion of chemotherapy drugs and iodized oil (Lipiodol) through
the hepatic artery feeding into the hepatoma.25 Lipiodol is radiopaque making visualization of the
drug administration through the hepatic artery possible allowing radiologists to track their
progress. Another method causes for the use of drug-eluting microspheres containing
chemotherapeutic agents. This method allows for better control of the drug delivery because the
use of these small microspheres is thought to improve penetration into the tumor and prevent
premature halting of the procedure prematurely due to early stasis through the artery.25 Different
than TACE, radioembolization utilizes radioactive microspheres to treat primary and metastatic
tumors. These microspheres are composed of either glass (Theraspheres) or resin (Sirspheres)
and contain the radioisotope yttrium90 (Y-90) which has a half-life of 64.2 hours.26 Due to the
radioactive nature of the substance, the dosing and transportation of the isotope is solely in the
hands of the hospitals nuclear medicine team who specializes in the handling and management
of such substances. Also these microspheres are not radiopaque so injection of these radioactive
spheres is difficult due to decreased visualization.
Patients are laid supine on the examination and the femoral artery is accessed because
hepatomas receive most of their blood from the hepatic artery. Once access is gained, a vascular
sheath inserted and a guidewire and a Mickelson or Cobra catheter is directed up the aorta
seeking the origin of the celiac artery. From there the hepatic artery feeding the hepatoma is
navigated, and microwires and microcatheters need to be used because the chemotherapy agents
and radioactive isotopes need to be administered as close to the hepatoma as possible to avoid
shunting toxic and radioactive substance through the tumor into healthy tissue.

Percutaneous Biliary Drainage (PBD)


Biliary obstruction is the blockage of any duct in the hepatobiliary system that carries bile
to the duodenum. There are two types of biliary obstructions: intrahepatic and extrahepatic.
Intrahepatic obstructions are caused at the cellular level by hepatitis, cirrhosis, or drugs that
cause hepatocellular necrosis. One of the predominant causes of extrahepatic obstruction is
cholelithiasis, or gallstones, with 20% of the US population above 65 years old developing them
and 1 million new cases being reported each year.27 Gallstones are a result of high cholesterol
concentration in the bile and low amounts of bile salts. When these stones migrate from the
gallbladder into the bile ducts, it is termed choledocholithiasis and is a mechanism that prevents

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the down flow of bile. Another common cause are neoplasms along the biliary tract:
cholangiocarcinomas, ampullary carcinomas, and gallbladder carcinomas. These malignancies,
along with metastatic lesions and pancreatic tumors all create strictures around bile ducts
preventing the flow of bile. Common symptoms of biliary obstruction are right upper quadrant
pain, fever, and obstructive jaundice. If untreated, biliary obstruction could lead to acute
cholangitis, a bacterial infection of the bile tract that can lead to severe bacteremia and sepsis.
The arrival of endoscopic retrograde cholangiopancreatography (ERCP) has diminished
the use of percutaneous transhepatic cholangiography (PTC) and percutaneous biliary drainage
(PBD) as diagnostic and therapeutic procedure, but they are still offered in many VIR
departments. PTC and PBD work in conjunction with each other because in order to place a PBD
catheter, the biliary tree obstruction must be opacified. The placement of a PBD catheter
decompresses the biliary tract that is experiencing increased pressure due to bile accumulation.
This bile now has the ability to flow out of the body or into the duodenum via the PBD catheter.
For a PTC, the patient is laid supine and the right flank is prepared for access using sterile
practices and local anesthesia. Under fluoroscopic guidance a 22-Gauge 15 inch Chiba needle is
advanced through an intercostal space 1-2 cm below the lowest lung position during inhalation.
The needle is advance towards the 12th vertebral body in one motion parallel to the table. The
stylet of the needle is removed and the needle is slowly withdrawn as diluted contrast is injected
with the goal of illuminating the biliary tract. If there is no sign of a bile duct opacification, the
same act is repeated a couple degrees lower but the needle should not be fully removed so only
one hole in the liver capsule exists. Once the bile duct tract is accessed, more contrast is injected
to outline the biliary system.28
Once a favorable duct is entered, a 0.018-inch guidewire is inserted through the needle
towards the hilum and common hepatic duct. If the patient has a hilar obstruction or is a
candidate for a stent, a peripheral duct will be accessed. Once the guidewire reaches the hilum of
the hepatic bile duct, it is replaced with a 5-French sheath assembly, and once situated the 4-
French inner plastic cannula and 0.018-inch guidewire are exchanged for a 0.035 or 0.038-inch
J-guidewire. The 5-French sheath is replaced by a hockey stick shaped catheter and the J wire is
replaced with a straight tip hydrophilic guidewire; these two instruments are then advanced
towards the biliary obstruction. Contrast is injected above the stricture to find the point were the
catheter and wire will bridge past it and gain access to the rest of the bile duct. The wire is

14
advanced past the stricture and the catheter soon follows until it reaches the proximal jejunum.
The hydrophilic wire is replaced with an 0.035 superstiff guidewire, giving solid purchase for the
percutaneous tract to be dilated with a 7-French dilator and 9-French peel-away to make room
for the 8.3-French biliary drainage catheter. A 32-side hole catheter is used for lower tract
obstructions and a 42-side hole is used for hilar obstructions. This catheter is inserted over the
superstiff guidewire all the down to the duodenum, and its location is verified with a contrast
injection.28

15
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9, 2017.

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25. Kaufman JA, Lee MJ. Visceral Arteries. In: Vascular and Interventional Radiology: The
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metastatic disease to the liver. Semin Intervent Radiol 2006;23(1):64-72. doi:10.1055/s-
2006-939842.

27. Bonheur JL. Biliary Obstruction. Medscape 2016. Available at:


http://emedicine.medscape.com/article/187001-overview#a4. Accessed April 10, 2017.

28. Lee MJ. Biliary Intervention. In: Vascular and Interventional Radiology: The Requisites.
2nd ed. Philadelphia, PA: Elsevier; 2014:451-473.

A.J. Hicks is in the process of earning his B.S. in Radiologic Science from the School of Allied
Health at the University of North Carolina at Chapel Hill. He has previously earned a B.A. in
Exercise and Sport Science from the same university.

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Figure 1: Liver anatomy. From Netter FH. Abdomen. In: Atlas of Human Anatomy. 6th ed.
Philadelphia, PA: Elsevier; 2014:261-353.

19
Figure 2: Hepatic lobule. From OpenStax. Accessory Organs in Digestion: The Liver, Pancreas,
and Gallbladder. In: Anatomy and Physiology. OpenStax; 2013. Available at:
http://cnx.org/contents/FPtK1zmh@6.27:esgfrPlv@3/Accessory-Organs-in-Digestion-.

Figure 3: Gallbladder anatomy. From OpenStax. Accessory Organs in Digestion: The Liver,
Pancreas, and Gallbladder. In: Anatomy and Physiology. OpenStax; 2013. Available at:
http://cnx.org/contents/FPtK1zmh@6.27:esgfrPlv@3/Accessory-Organs-in-Digestion-.

20
Figure 4: Pancreas anatomy. From Netter FH. Abdomen. In: Atlas of Human Anatomy. 6th ed.
Philadelphia, PA: Elsevier; 2014:261-353.

21
Figure 5: Biliary Tract. From Netter FH. Abdomen. In: Atlas of Human Anatomy. 6th ed.
Philadelphia, PA: Elsevier; 2014:261-353.

22
Figure 6: TJLB Quick-Core Biopsy Needle. From Dohan A, Guerrache Y, Boudiaf M, Gavini JP,
Kaci R, Soyer P. Transjugular liver biopsy: indications, technique and results. Diagn Interv
Imaging 2014;95(1):11-15. doi:10.1016/j.diii.2013.08.009.

Figure 7: Successfully placed 10 X 68 mm Wallstent dilated with 10 mm X 4 cm balloon. From


Novelli PM. Transjugular Intrahepatic Portosystemic Shunt in Radiology. Medscape 2017.
Available at: http://emedicine.medscape.com/article/420343-overview#a5. Accessed April 9,
2017.

23
Quiz
1. Which liver ligament is a remnant of the umbilical vein?
a. Falciform Ligament
b. Round Ligament
c. Coronary Ligament
d. Right Triangular Ligament
2. Which vessel is NOT in the portal triad?
a. Proper Hepatic Artery
b. Portal Vein
c. Common Bile Duct
d. Common Hepatic Artery
3. Which cells in the liver are responsible for removing bacteria from the blood?
a. Kuppfer Cells
b. Hepatocytes
c. Islets of Langerhans
d. Sinusoids
4. Which structure helps prevent the backflow of chyme into the bile duct?
a. Ampulla of Vater
b. Major Duodenal Papilla
c. Sphincter of Oddi
d. Minor Duodenal Papilla
5. What is the ideal measured pressure gradient when performing a Transjugular Liver
Biopsy (TJLB)?
a. 3 mmHg
b. 10 mmHg
c. 12 mmHg
d. 5 mmHg
6. Which of the following is NOT a contraindication for a Transjugular Intrahepatic
Portosystemic Shunt (TIPS) procedure?
a. Portal Hypertension
b. Sepsis
c. Liver Failure
d. Biliary Obstruction
7. Hepatomas are the _____ most common cause of cancer death in the US?
a. 4th
b. 6th
c. 8th
d. 9th
8. This substance makes Transarterial Chemoembolization (TACE) visible under
fluoroscopy?
a. Yttrium-90
b. Lipiodol
c. CO2
d. Theraspheres

24
9. This procedure has replaced Percutaneous Transhepatic Cholangiography (PTC) and
Percutaneous Biliary Drainage (PBD) as the preferred diagnostic and therapeutic methods
for biliary obstruction?
a. TIPS
b. TJLB
c. ERCP
d. Stent Placement
10. The following are causes of biliary obstruction EXCEPT:
a. Jaundice
b. Cholelithiasis
c. Gallbladder Carcinomas
d. Cirrhosis

25
Quiz Answers
1. B
2. D
3. A
4. C
5. D
6. A
7. D
8. B
9. C
10. A

26

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