Radiography of the Biliary System


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Radiographic imaging of the biliary system is commonly performed in radiology departments. This article explores how different radiology modalities image the biliary system. It includes discussions on the nuclear medicine IDA scan, ultrasound imaging, ERCP, and operative and T-tube cholangiography, CT imaging, and magnetic resonance cholangiography (MRCP).


Author: Nicholas Joseph, Jr. R.T (R)(CT)
Credits: 3

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Instructions:

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Objectives

Introduction

Anatomy and Physiology of the Liver, Pancreas, and Biliary Tract

The Gallbladder

The Pancreas

Anatomy and Function of the Biliary Tree

Gallstones and Biliary Tree Stones

Radiographic Imaging of the Biliary System

Computed Tomography

Oral Cholecystography

Percutaneous Transhepatic Cholangiography (PTC)

Operative and T-tube cholangiogram

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Magnetic Resonance Cholangiopancreatography (MRCP)

Ultrasound of the Gallbladder and Biliary Ducts

Nuclear IDA scan

Pathology of the Biliary System

Conclusions

Summary Points

References

Bottom


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Objectives:

  • Identify the right, left, caudate, and quadrate lobes of the liver and describe Riedel lobe.
  • Label the three parts of the gallbladder and describe the function of the spiral valve of Heister within the cystic duct.
  • Describe the location of Hartmann pouch and its significance to gallstone formation.
  • Draw and label the biliary ducts from the liver, pancreas, and gallbladder to the duodenum.
  • List at least 4 functions of the liver; name and discuss four liver function test the technologist routinely records on study sheets.
  • State which fat-soluble vitamins are stored in the liver, and which one affects blood coagulation factors.
  • Discuss the location of the porta hepatic and list the structures found in this region of the liver.
  • Name the vessels that form the portal vein and discuss the duel blood supply to the liver.
  • Discuss the counter-current system for bile formation within the liver sinusoids.
  • Discuss the function of the structure and function of the cystic duct in regulating bile flow.
  • Define enterohepatic circulation and give the correct order of absorption/secretion bile cycle.
  • State the two main functions (endocrine and exocrine) of the pancreas.
  • Discuss the role of the duct of Wirsung in the exocrine function of the pancreas.
  • Label a diagram of the biliary tree and discuss the flow of bile in the biliary tree.
  • Define the term cholesecretagogue and discuss the role of CCK in bile flow.
  • Define the terms cholangitis, cholecystitis, cholelith, cholelithiasis, choledocholithiasis, and jaundice.
  • Discuss the use of the operative and T-tube cholangiogram in detecting biliary stones.
  • Discuss the role of ERCP in diagnosing and treating biliary and pancreatic duct disorders.
  • State why ultrasound imaging is used to diagnose liver and pancreas disorders.
  • Discuss the normal values for gallbladder wall thickness, and common bile duct diameter measured during ultrasound imaging following cholecysectomy.
  • State why CT us useful in diagnosing liver and pancreas disorders.
  • Name two nuclear medicine studies of the gallbladder and tell the difference between them.
  • Define the following: cirrhosis, ascites, jaundice, gallstones, cholecystitis, cholelithiasis, acute pancreatitis, hepatitis, hepatoma, and cholangitis
  • Define the term cholecystagogue and tell why these are used in diagnostic imaging.
  • Discuss the role of MR imaging of the biliary tract.e.g. MRCP.
  • State why MRCP is used to determine if an ERCP is needed.
  • List the structures demonstrated by the MRCP study.
  • Discuss why MRCP is used as a pre-screening for ERCP
  • Discuss why ultrasound imaging of the gallbladder is used and what can be visualized on the scan.



Introduction

There are many disorders of the biliary system that include gallstones, cholangitis, cholecystitis, and bile duct cancer. Gallstones can reside in the gallbladder, a condition called cholelithiasis, or is present in the bile ducts-choledocholithiasis. Obstruction by gallstones can lead to life-threatening infection of the pancreas, liver, or the bile ducts. The clinician must also make sure a bile tract obstruction is not caused by cancer. Women between 20 and 60 are twice as likely to develop gallstones as men in the same age group. Gallstones are more common in persons over the age of 60 and in Native Americans of all ages. Obesity is another factor that along with increased estrogen affects women primarily. Other factors in the genesis of gallstones include long periods of fasting, rapid weight loss, cholesterol lowering drugs, diabetes, and sickle cell disease.

Gallstones may affect as many as 1 in 12 Americans and is perhaps the most common reason for radiographic imaging of the gallbladder and biliary system. Biliary stones can be treated; however, left untreated can be serious and in rare cases fatal. About 10,000 persons die each year from gallstones and complication of gallstones. When gallstones block the biliary tract, or worse the pancreas, the condition is more serious. Blockage of the pancreas can cause pancreatitis that can be life-threatening Today there are many treatments that make recovery from gallstones relatively quick in most cases. Radiographers and sonographers play an important role in imaging the gallbladder and biliary tract. Some imaging procedures used to diagnosis gallstones and biliary tract disorders are the operative cholangiogram, computed tomography (CT), ultrasound (US), nuclear imino diacetic acid (IDA) scan, and retrograde cholangiopancreatography (ERCP). There are advantages to each of these imaging methods and some disadvantages that we will discuss. Often the patient undergoes several imaging procedures that complement each other and augment diagnostic confidence. This module will discuss the role of each of the mentioned imaging modalities and how these procedures aid the physician in diagnosing and treating diseases of the gallbladder and biliary system. This module focuses on the liver, pancreas, gallbladder, and biliary ducts and their relationship to biliary disease.




Anatomy and Physiology of the Liver, Pancreas, and Biliary Tract

Before we begin our discussion on biliary disorders let’s review the basic anatomy and physiology of the gallbladder and biliary system. The liver, gallbladder, and pancreas share intimate anatomical and physiological codependence and therefore, will be discussed together in this section. The liver lies just below the diaphragm occupying the entire right hypochondrium, epigastrium, and a portion of the left side of the abdomen. Although it lies below the diaphragm it is attached to it moving up and down with ventilations. Under the cover of the 5th to 10th ribs it is easily injured by rib fractures resulting from high impact trauma. The liver is the largest organ and gland in the body weighing approximately 1500-1700 grams. Its surface anatomy consists of four lobes that can be plainly seen at dissection. Only two major lobes, the right and left lobes, which are separated by the falciform ligament, are seen on the anterior surface. The falciform ligament is a remnant of the umbilical vein; it attaches the liver to the anterior abdominal wall and diaphragm. Posteriorly the liver presents the left lobe and the right lobe that is divided into three lobes: the right lobe proper, and two minor lobes, the caudate and quadrate lobes. Frequently seen in women is a normal variation of the right lobe that gives the appearance of an additional lobe that has become known as the Riedel lobe. The liver’s diaphragmatic surface is dome shaped conforming to the shape of the inferior surface of the diaphragm. The gallbladder usually lies in a shallow surface on the posterior aspect of the right lobe.

Liver lobes are composed of cells called hepatocytes that are arranged into lobules. Liver cells perform over 100 known functions among which are forming blood cells, detoxifying poisons (alcohol and drugs), and metabolizes foodstuff (carbohydrates, fats, proteins). The liver also stores fat soluble vitamins A, D, E, K, and B12 but no water-soluble vitamins like vitamin C. Special cells called Kuppfler cells are found within the liver’s parenchyma. They engulf spent red blood cells (phagocytosis) and recycle hemoglobin in the form of bilirubin making it available for newly formed red blood cells. All hepatocytes make bile from substrates like bilirubin and cholesterol. The liver also makes many essential blood proteins products like albumin and fibrinogen for clotting blood. Urea excreted in urine comes from protein metabolism in the liver, and the liver can even make glucose when blood sugar becomes low. With so many functions it is easy to see why any process that diminishes the liver’s functions will be felt systemically. This remarkable organ can maintain the body’s physiological needs even when up to 70% of it is removed. It also has remarkable regenerative properties to replace hepatocytes lost due to liver resection, which is something other organs cannot do.

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This coronal CT image demonstrates the liver’s position in the right hypochondrium. Blood is supplied to the liver by the portal vein and hepatic artery (white arrow).
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This coronal reconstructed MR image demonstrates the anatomical position of the liver in the right hypochondrium. The portal vein (white arrow) distributes deoxygenated nutrient rich blood to the liver from the gut that mixes with oxygenated blood from the hepatic artery.
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This coronal CT image shows the surface beneath the liver. The gallbladder usually lies in the shallow fossa on the diaphragmatic surface of the liver. Gallstones are seen in the gallbladder (white arrow) on this post-processed coronal CT image with cephalic tilt.

Deep fissures on the posterior surface form an “H-shaped” groove further dividing the liver into four lobes. The crossbar of the H is called the porta hepatis; it separates the caudate and quadrate lobes. This area is important to radiologists, surgeons, and to imaging professions because it contains the portal vein, hepatic artery, and hepatic ducts. Though it is only about 5 cm in length it is very compact with anatomical structures that include nerves and lymphatics.

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This highly schematic drawing of the liver shows structures that are seen on the posterior surface. Most noticeable is the area called the porta hepatis. The portal vein and bile duct is demonstrated within the porta hepatis. Also shown are the caudate lobe, quadrate lobe, and inferior vena cava.

The liver performs several important roles in the digestive system. One is the removal of toxins and bacteria that enter the blood during absorption of raw foods (lipids, carbohydrates, and proteins) through the gut mucosa. Purification of nutrients occurs before they are released into the systemic circulation and made available to the body’s cells. The liver is therefore a defense organ of the body’s immune system protecting it against microorganism invasion. The importance here is in the absorption of nutrients to supply the energy needs of the body. This function is dependent on a good blood supply, which the liver has. Moreover, the liver is special in that it receives a double blood supply. The portal vein supplies most of the blood (70%) and the hepatic artery gives the remainder (30%); this duel supply is important to the unique metabolic needs of the liver. The portal vein is formed just posterior to the neck of the pancreas by the union of the superior mesenteric and splenic veins. The portal vein carries nutrients it receives from the gut (via the superior mesenteric vein) to the liver for detoxification.

Hepatocytes require lots of energy and oxygen when detoxifying nutrients received from the portal vein. The hepatic artery brings oxygenated blood that mixes with deoxygenated blood from the portal vein to supply the additional oxygen hepatocytes need for detoxification. This happens within the sinusoids of the liver parenchyma where the hepatocytes are bathed with unidirectional blood flow. The hepatic artery is a distal branch of the hepatic artery proper that branches from the celiac trunk on the anterior surface of the aorta. Hepatocytes are stacked hexagonally to form the architecture of the sinusoids. The apposing membranes of hepatocytes form channels for bile to flow called canaliculi. The functional unit is the lobule where detoxification and bile secretion occurs in a counter current type flow, an arrangement that maximizes cellular contact with blood. These rich vascular beds perfuse the liver allowing hepatocytes to perform metabolic functions like detoxification of nutrients. Once these foods are “cleaned” they leave the liver via hepatic veins. The hepatic veins join the inferior vena cava, which carries blood to the right atrium of the heart.

Blood in the sinusoids travel towards the hepatic veins, while bile moves in the opposite direction within the hepatic plates, so blood and bile never mix in the liver lobules. Bidirectional flow allows for what is called enterohepatic circulation. As blood moves along in the sinusoids hepatocytes absorb and secrete a variety of exogenous compounds. Many medications used to treat illnesses are removed from the liver by this mechanism too. The removal of drugs from the blood by the liver is called the first-pass effect, or first-pass metabolism. During first-pass metabolism an ingested drug is absorbed through the bowel mucosa into the blood. The superior mesenteric vein takes the drug to the liver via the portal vein where some, but not all of it is absorbed by hepatocytes and secreted into the bile. This accounts for the low bioavailability of many drugs. Drugs administered by intravenous, intramuscular, or sublinguinal routes can avoid the first-pass effect. What is interesting about the liver is that hepatocytes can recognize sugars, proteins, amino acids, and lipids and do not filter food vital to the body for energy production. Bile is released into the gut through the duodenum returning drugs to the gut to be reabsorbed and a portion released in stool.

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This highly schematic drawing demonstrated the microstructure of the hepatic lobule. Blood mixes as it enters the hepatic sinusoids from branches of the hepatic artery and portal vein. From the sinusoids mixed blood flows in the direction of the central vein. Each lobule has a central vein that flows into the hepatic veins. Products in the blood entering the central vein will be distributed to body cells via the systemic circulation. Hepatocytes secrete bile into the bile canaliculi between adjacent hepatocytes that ultimately empty into the hepatic ducts. Drugs entering the hepatic circulation are secreted in bile to be reabsorbed in the gut and returned to the liver in a process called enterohepatic circulation. This diminishes drug bioavailability and is called the first-pass effect.

All hepatocytes synthesize and secrete bile into small ducts called canaliculi, which lie between the hepatic plates. These canaliculi anastomose to form networks throughout the liver parenchyma. Bile canaliculi have no structure of their own; the membranes of adjacent hepatocytes form channels that are the bile canaliculi. These many small microscopic intrahepatic bile canaliculi form a network of ducts that become progressively larger becoming the hepatic ducts that drain the liver. A normal liver will secrete between 700 and 1200 ml of bile into these ducts daily. Bile is collected from both main lobes of the liver into the large right and left hepatic ducts that come together to form the extrahepatic common hepatic duct. The biliary tree is formed by the right and left hepatic ducts, common hepatic duct, cystic duct, common bile duct, the ampula of Vater. The biliary duct system shunts bile to the gallbladder to be concentrated and stored, and ultimately to the duodenum.





The Gallbladder

The gallbladder is a pear-shaped sac that lies in a shallow fossa on the posterior inferior surface of the gallbladder. Only a small portion (the fundus) can be seen from the anterior surface. The gallbladder’s surface anatomy is quite simple consisting of three parts: fundus, body, and neck. The neck of the gallbladder is continuous with the cystic duct that receives and empties bile from the common bile duct. The mucosa of the cystic duct is thrown into rugae that form spiral tracts called the spiral valve of Heister. The valve performs like a sphincter to regulate substances entering and leaving the gallbladder. Some individuals have a prominent pouch just posterior to the neck of the gallbladder called a Hartmann pouch. This is a prime site for gallstones to lodge possibly obstructing the gallbladder. A Hartmann pouch can best be seen with ultrasound when imaging the gallbladder.

The function of the gallbladder is to concentrate and store bile. The liver produces up to 20 times more bile than the capacity of the gallbladder. The cells of the gallbladder absorb water returning it to surrounding capillaries. Water, sodium, chloride and most electrolytes are absorbed from bile concentrating bile salts, cholesterol, lecithin, and bilirubin. Bile in the gallbladder is concentrated by a factor of 12 to 18 fold its liver secretion. The capacity of the gallbladder is between 30 and 60 ml. The mucosa of the gallbladder is formed into rugae that expand as it receives bile. Within its wall is a smooth muscle layer called the muscularis, which contracts when stimulated providing the force to eject bile. Contractions of the gallbladder eject concentrated bile into the biliary tree. This is coordinated with relaxation of the sphincter of Oddi to allow bile to pass into the duodenum without resistance.


COMPOSITION OF BILE (partial chart)
  Bile in the Liver Bile in the Gallbladder
Water 97.5 gm % 92 gm %
Bile Salts 1.1 gm % 6 gm %
Cholesterol 0.1 gm % 0.3 to 0.9 gm %
Bilirubin 0.04 gm % 0.3 gm %
Lecithin 0.04 gm % 0.3 gm %
Bicarbonate 28 mEq/l 10 mEq/l

It is important for radiographers to understand the role of bile salts. There are two main functions of bile salts (bile acids), emulsification of fats and facilitating absorption of lipids and fat-soluble vitamins. Bile is composed of bile salts, bile pigments, cholesterol, bilirubin, inorganic ions (sodium, potassium, chloride, and calcium), and substances that give alkalinity to bile. Bile salts are made from cholesterol that is either supplied in the diet or is synthesized in the liver. Cholesterol is converted in the liver to two bile salts: cholic acid and chenodeoxycholic acid. Bacteria in the gut convert a portion of these primary bile acids to secondary bile acid: deoxycolic and lithocholic acids. Bile salts cannot perform their function of emulsifying fat in the intestine until they are conjugated to either glycine or to taurine (amino acids) to form glycol-conjugated bile acids or taurine-conjugated bile acids. Conjugation of bile acids takes place in the liver. Calcium or potassium is added to conjugated bile acids to form a bile salt. Conjugated bile salts when secreted from the liver are able to emulsify lipids. The emulsification action of bile on lipids has been called the detergent function of bile. This is because bile breaks lipids apart causing them to foam when agitated by peristalsis. Emulsified lipids look a lot like soapy foam produced by dishwashing liquid. At the molecular level, we would see small structures called micelles formed in the emulsification process. Micelles are small “bubbles” of lipids that have cholesterol and fat inside and bile acids on the outside. This arrangement gives lipids solubility in water; otherwise lipids are insoluble and float on water. This arrangement also facilitates the transport of lipids to the gut mucosa and causes them to stick to it. This is an effective and efficient method of absorption of fats from the diet.

As you can see bile plays an important role in providing nutrients to the body. Here are a few other important reasons bile salts must be available in the gut to aid in digesting lipids. Without bile salts about 40% of lipids are lost in the stool creating a deficit of essential lipids. Essential lipids are those needed by the body for normal bodily functions, but cannot be endogenously synthesized by the body. Linoleate and linolenate are the two essential fatty acids that must be taken in through the diet. Fat-soluble vitamins A, D, E, and K are absorbed with lipids from the gut; excess fat-soluble vitamins are also stored in the liver. Of these, only vitamin K is not stored in sufficient quantity by the liver. In just a few days vitamin K deficiency will develop if insufficient amount is not absorbed from the diet. Vitamin K is a necessary nutrient for the liver to synthesize blood clotting agents. In just a few days without vitamin K, prothrombin, and coagulation factors VII, IX, and X become deficient. Therefore, bile formation and flow are very important for homeostasis of the blood coagulation system.

Bile salts are physiologically conserved; approximately 95% of bile salts are reabsorbed in the small intestine terminal ileum. Only a small amount of bile is newly synthesized daily, approximately about 0.2-0.5 grams per day. The circulating bile pool is roughly 2-3 grams, which recycles in enterohepatic circulation at a rate of twice per meal, or 6 times a day. In the liver bile is reabsorbed by hepatocytes almost 100% in the first pass and secreted into the bile canaliculi. It is estimated that bile salts circulate some 18 times in the enterohepatic cycle before being excreted in feces. The small quantity of bile salts (less than 5 %) that is lost in feces is replaced with newly synthesized bile salts by hepatocytes. Any impairment of enterohepatic bile circulation, such as obstruction of the biliary ducts by cholelith or chronic cirrhosis of the liver is a significant medical problem.

Enterohepatic circulation is defined as the recurrentcycle in which bile salts and other substances excreted by the liver pass through the intestinal mucosa and become reabsorbed by the hepatic cells and re-excreted. Any impairment of enterohepatic bile circulation, such as obstruction of the biliary ducts by cholelith or chronic cirrhosis of the liver is a significant medical problem.

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This fluorospot radiograph taken of the distal ileum using a compression paddle to spread apart the small intestine. This is the area were most of the bile is absorbed from the gut along with fatty acids and fat-soluble vitamins. This area is studied during the small bowel radiographic study when oral contrast reaches the terminal ileum. This is an important area for study when enterohepatic circulation is impaired for reasons other than bile duct obstruction.




The Pancreas

The pancreas is positioned horizontally along the posterior abdominal wall adjacent to lesser curvature of the stomach. It is a retroperitoneal organ located mainly in the epigastrium. It consists of a head, neck, body, and tail. The head is the expanded part found within the C-loop of the duodenum. Inferiorly the head constricts forming an uncinate process before tapering slightly forming the neck. The head and neck lie anterior to the inferior vena cava. The body is the longest part lying transversely across the posterior abdominal wall. The tail tapers along its course ending in or near the hilum of the spleen. It is a soft spongy organ about 12 cm long and 2.5 cm thick. The pancreas is both an endocrine and exocrine gland. Clusters of cells called the pancreatic islets (a.k.a. islets of Langerhans) carry out endocrine functions. The pancreatic islets produce insulin and glucagons. Both insulin and glucagon are secreted into the blood directly and are distributed systemically by the superior mesenteric vein to the portal vein. Because these hormones are secreted into the blood they are not affected by biliary duct obstruction. These hormones participate in carbohydrate metabolism and help regulate blood glucose level. Special exocrine cells called alpha 2 and beta cells comprise about 2% of the pancreas parenchyma. Alpha 2 cells secrete glucagons, and beta cells of the islets produce insulin. Endocrine cells comprise about 2% of the pancreas and exocrine cells make up about 98% of the pancreas. The biliary system consists of the liver, gallbladder and biliary ducts. The pancreas is not considered part of the biliary system based on its role of secreting inactive digestive juices into the duodenum. Inability to secrete digestive juices into the duodenum due to biliary obstruction can adversely affect the pancreas.

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This is a radiograph of the stomach and duodenum shows the C-loop of the duodenum where the head of the pancreas lies. Within the C-loop the head of the pancreas is attached to the duodenum by the ligament of Trietz holding it in place. The main pancreatic duct and common bile duct unite to form a short ampulla that empties bile and pancreatic juices into the duodenum.

What we are concerned with in this module is the exocrine functions of the pancreas, which produces digestive enzymes. Pancreatic juice contains enzymes to digest all three major foods: proteins, carbohydrates, and lipids. The pancreas also secretes sodium bicarbonate at a concentration of nearly 5 times that in serum. Strong digestive juices produced by the pancreas are capable of digesting it so these enzymes are secreted into ducts. Pancreatic enzymes are produced in an inactive form called a zymogen. Once they enter the protected mucosa of the duodenum they become activated and can digest proteins, lipids, and carbohydrates. Pancreatic enzymes are secreted into two main ducts of the pancreas. The main pancreatic duct called Wirsung’s duct runs transversely from the head to the tail of the pancreas. It joins the common duct that partially passes through the head of the pancreas as it transports bile to the duodenum. A minor accessory duct is seen in about 15% of the population; it drains the head of the pancreas into a minor duodenal papilla. Pancreatic enzymes are necessary to help digest food for absorption across the bowel mucosa. Pancreatic enzymes are alkaline so that when they are secreted into the duodenum acidic chyme is neutralized. Neutralization of acids from the stomach protects the rest of the gut from self-digestion. Enzymes from the pancreas include amylase to metabolize sugars, lipase to digests lipids, and trypsin, which digest proteins. These enzymes are inactive until they enter the duodenum where catalytic enterokinase activates them. This protects the pancreas and biliary ducts for self-digestion. Acute pancreatitis can be caused by reflux of active pancreatic enzymes from the duodenum back into the pancreatic duct. Enzymatic necrosis is a type of inflammation that is unique to the pancreas and is seen in acute pancreatitis. Active pancreatic digestive enzymes’ entering the main pancreatic duct digesting the pancreas causes this condition.

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These two axial CT images demonstrate the relative location of the pancreas. The pancreas lies transversely in the abdomen at the level of the first lumbar vertebrae. The arrow in the left CT image demonstrates the head of the pancreas. The body and tail are shown in the right image (arrows). Notice the inflammation and edema surrounding the pancreas caused by acute pancreatitis.
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These two axial CT images demonstrate the tail of the pancreas and its relative location to the spleen (white arrows). Again, edema around the pancreas is seen denoting acute pancreatitis. The spleen is labeled with a white arrowhead.




Anatomy and Function of the Biliary Tree

The biliary tree conducts bile and pancreatic digestive enzymes to the duodenum. The gross anatomy of the biliary tree begins with the right and left hepatic ducts that drain bile from the two halves of the liver. These become the common hepatic duct that is joined by the cystic duct from the gallbladder. The union of the common hepatic and cystic ducts form the common bile duct. The common bile duct is about 7.5 cm long. It passes posterior and often through the pancreas to join the main pancreatic duct (duct of Wirsung). The union of the main pancreatic duct and common bile duct form a short ampula called the hepatopancreatic ampula (a.k.a. ampula of Vater). The ampula inserts on the major duodenal papilla, which is guarded by the hepatopancreatic sphincter (a.k.a. sphincter of Oddi). A minor accessory duct called Santorini’s duct, when present may drain a portion of the pancreatic head into the minor duodenal papilla. The accessory duct is not present in most individuals.

The physiology of the biliary tract causes bile to be concentrated in the gallbladder in the absence of fat in the diet. Likewise, bile is released when fat and some proteins are present in the diet. The mechanism for bile concentration, storage and release is controlled primarily by the hormone cholecystokinin (CCK); other hormones gastrin and secretin along with vagal stimulation play minor roles. When the sphincter of Oddi is closed, hydrostatic pressure forces bile through the cystic duct into the gallbladder (retrograde filling). When chyme-containing fat reaches the duodenum, cells in the duodenum secrete CCK into the blood. Cholecystokinin is a hormone that when it reaches the gallbladder it causes it to contract. The action of CCK on the duodenal sphincter is to relax allowing muscular contractions of the gallbladder moves bile without resistance. The time from ingestion of lipids to stimulation of the gallbladder to contract is roughly 30 minutes. Complete emptying of the gallbladder takes about 1 hour. The hormones CCK, gastrin and secretin are cholesecretagogues. A secretagogue is a substance that stimulates secretion. Cholesecretagogues stimulate secretion of bile by the gallbladder.

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This highly schematic diagram of the liver, gallbladder, duodenum, pancreas and spleen demonstrates the relative positions of these organs. The relationship of the biliary tree to these organs is also demonstrated. The union of the main pancreatic duct and common bile duct is seen along with the opening of the sphincter of Oddi at the duodenum.
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This radiograph taken during an ERCP procedure demonstrates the hepatic ducts; common hepatic duct, cystic duct, and common bile duct are demonstrated. Note the spiral appearance of the cystic duct due which is the valve of Heister. The pancreatic ducts and ampulla of Vater are not demonstrated.



Gallstones and Biliary Tree Stones

Diseases of the pancreas and biliary system affect millions of Americans each year. According to the National Health and Nutrition Survey, gallbladder disease affects approximately 6.3 million men and 14.2 million women in the United States mainly between the ages of 24 and 74. Approximately one million new cases of cholelithiasis, the medical term for gallstones, are diagnosed each year. The incidence of gallstones is higher among women; adults over the age of 40; and people who are obese. Cholangitis, a term for inflammation of the bile ducts occurs at a rate of two to seven cases per 100,000 persons. The rate of gallbladder cancer is approximately 2.5 out of 100,000 persons. In addition, approximately 87,000 cases of pancreatitis and 30,000 cases of pancreatic cancer are diagnosed each year in the United States. Our focus will be on gallstones and biliary duct stones, but first we should review the dynamics of gallstone formation.

There are two main types of gallstones, cholesterol stones and pigment stones. About 85% of gallstones are cholesterol type stones. The composition of cholesterol stones is mostly cholesterol, and some minor amounts of bilirubin, bile salts, inorganic salts, proteins, and calcium that give radiographic density to stones. Pigmented stones are composed primarily of bilirubin and are generally radiolucent. There can be an array of stone compositions that fall into the category of mixed stones, but cholesterol stones are the most common. In terms of stone formation the amount of cholesterol that is soluble in bile is dependent primarily on the amount of bile salt present, and to a much lesser extent the amount of lecithin.

The formation of gallstones is a slow process that occurs in three recognizable stages. First bile becomes super saturated, 2) then there is nucleation or formation of a small crystal precursor to a stone, and 3) the small stone grows by a process called accretion. The critical stage in the formation bile stones, especially those formed by cholesterol is super saturation of bile with cholesterol. Normally cholesterol is formed into micelles. Bile salts orient to the outside of the micelle because they can interact with water. Cholesterol is packed inside the micelle protected from interacting with water making it soluble. Lecithin helps the micelle absorb cholesterol adding to the solubility of cholesterol. Lithogenesis can occur when any of these three conditions exists: 1) deficient secretion of bile salts and lecithin, 2) supersaturation of cholesterol in bile, or 3) inflammation of the epithelium of the gallbladder.

One of the functions of the gallbladder is to reabsorb water from bile. This does not normally cause supersaturation of bile; likewise, super saturation alone is not a mechanism that will produce gallstones. Gallbladder stasis and reabsorption of water may be a factor that can cause supersaturation of cholesterol. It appears that nucleation, or initiation of stone formation must also occur. The nucleation theory is supported by findings that an absence of a cheating agent or increase secretion of mucus type glycoproteins causes bile supersaturates to clump. Some studies have shown that when mucin combines with cholesterol a sludge-like material can be formed. Sludge is the seed for crystallization of cholesterol. Another theory that is gaining some popularity is the idea that prostaglandins may play a role in sludge formation. Some studies have shown that aspirin can reverse cholesterol lithogenesis of supersaturated bile. The driving forces in lithogenesis are cholesterol supersaturation and hemolysis. Both cholesterol and unconjugated bilirubin are insoluble in water, conditions that favor supersaturation.

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This sagittal ultrasound section of the gallbladder shows leveling of bile-sludge. Sludge is a collection of calcium carbonate granules and cholesterol crystals. Sludge often dissolves with normal diet and activity. Some speculate sludge is a precondition of stone formation. It is often seen in patients receiving parenteral nutrition and after gastrointestinal surgery and when the diet is altered to exclude fat.
image014a
This axial CT image demonstrates a large gallstone (arrow) in the gallbladder. The gallbladder is not enlarged, nor is there edema around the gallbladder. CT us useful for determining the type of stone, for example, this is a calcium dense cholesterol stone. Calcium makes it possible to see this stone on CT. Other radiographic studies will be needed to determine if the cystic duct is patent.
image014b image014c
Normally a balance of bile salts, lecithin and cholesterol keep gallstones from forming. If there are abnormally high levels of bile salts or, more commonly, cholesterol, stones can form. Symptoms usually occur when the stones block one of the biliary ducts, otherwise benign gallstones may be discovered on x-ray or abdominal CT.

In summary, the precursor molecule for gallstones is cholesterol. Bile salts are made from cholesterol; however, the role of pure cholesterol secreted in bile is unknown. It may be that secreted cholesterol is excess, or just a byproduct of bile salt formation. The problem with cholesterol being secreted in bile it that it is insoluble in water, but when combined with bile salts and lecithin it is soluble in the form of a micelle. Therefore, in addition to being an emulsification agent, bile salts and lecithin are responsible for the solubility of cholesterol in water (bile). Earlier we mentioned that the duodenum also secretes a hormone called secretin into the blood. Secretin causes bile ducts to secrete about 200 ml of highly concentrated alkaline (sodium bicarbonate) solution. This is important because micelles do not form in an acidic environment, a condition that releases cholesterol in the gut. With retrograde flow of bile concentrated sodium bicarbonate moves into the gallbladder to provide an environment for keeping cholesterol soluble. Fat in the diet is partially responsible for cholesterol secretion by the liver. Cholesterol is a product of lipid metabolism so that excessive dietary fat and cholesterol rich food ingestion for many years could precipitate gallstones.

Chronic low-grade inflammation of the epithelium of the gallbladder can also be a cause of gallstone formation. Mild chronic inflammation of the gallbladder can cause it to reabsorb bile salts, lecithin, and water. This too will cause supersaturation of cholesterol and sludge forms. Sludge begins to crystallize in a process called accretion and cholesterol bile lithogenesis begins. Pure cholesterol stones are generally yellow when viewed through an endoscope, and are radiolucent. Gallstones having calcium carbonate, phosphates, and billirubin are mixed stones and are variable in color from mildly yellow to gray-white, to black. Calcium gives gallstones the radiopaque appearance seen on x-rays. Black stones are pigmented stones composed of pure calcium bilirubinate. Gallstones are threatening because they can enter the common bile duct and can cause biliary colic. Calculous acute cholecystitis is a term referring to impaction of a gallstone within the neck of the gallbladder or cystic duct. It is often the result of cholelithiasis. Gram-negative aerobic bacteria like E.coli or Clostria can be found in the bile in about 80% of cases of cholecystitis. Whether or not these organisms play a role in causing gallstones is not clear. It is important to deduce the cause of gallstones and treat them since approximately15% of those with gallstones will develop choledocholiathiasis.

Gallstones, when they obstruct biliary flow can cause a type of jaundice called obstructive jaundice or surgical jaundice. Jaundice or icterus is the medical term for a yellowish tint to the skin and sclera of the eyes caused by excess bilirubin in the blood. Obstructive jaundice must be differentiated from medical jaundice. Medical jaundice is cause by liver disease not obstruction. For example, hemolytic jaundice is caused by excessive destruction of red blood cells causing more bilirubin to be formed than the liver can excrete. Another type of jaundice is hepatic jaundice that is caused by a diseased liver, which is incapable of excreting bilirubin at a rate to meet physiological demands.

Because the liver performs so many functions there is no single test that can differentiate liver disease. Certainly measuring serum bilirubin and bile pigment in urine can help. Also liver enzyme levels and test such as serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), and alkaline phosphatase can help the clinical physician differentiate cause of jaundice. When obstructive jaundice is suspected, radiological studies can pinpoint the location of biliary stones and can also provide diagnostic imaging during removal of them.




Radiographic Imaging of the Biliary System

Radiographic imaging of the biliary system and the biliary tree is commonly performed in most radiology departments. These studies include all radiology modalities especially computed tomography (CT), magnetic resonance imaging (MRI), ultrasound, nuclear medicine, interventional procedures, and fluoroscopy imaging. We will look at how all of these subspecialties image the gallbladder and biliary ducts and discuss their advantages and disadvantages.




Computed Tomography

Computed tomography is not performed specifically to evaluate the gallbladder except when it is known that the gallbladder wall is diseased. CT can demonstrate some gallstones, and pancreatic disease. The specificity for biliary duct stones is low with CT, but CT can demonstrate some of them and associated acute and chronic pancreatitis. One of the advantages of CT is that the scan can help determine the type of gallstones (e.g. cholesterol, pigmented, etc), identify pathological dilation of the extrahepatic bile ducts, and can detect pancreatic cancer with 100% accuracy. While CT is not the imaging modality of choice for visualizing the biliary tree directly it is useful in diagnosing liver, gallbladder, and pancreatic disease. The sensitivity for identifying bile duct stones is low; however, in a few cases a stone in the bile ducts can be identified.

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These two CT images demonstrate gallstones within the gallbladder. The CT on the left shows multiple distinct large stones. The axial CT image on the right shows layering of small stones and sludge within the gallbladder. While CT is not the primary imaging modality for evaluating gallstones because it does not answer the question of whether or not the stones are obstructing.
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These two thin slice axial CT images show a necrotic gallbladder. In this case thin slice CT imaging is extremely valuable in diagnosing the gallbladder. This condition is not thought to be caused by gallstones. The irregularity of the gallbladder wall indicates need for further evaluation with MRI and Ultrasound.
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CT is also valuable for diagnosing the common duct following cholecysectomy. The biliary tree dilates to hold bile and maintain enterohepatic circulation. The dilated bile duct can be seen within the parenchyma of the pancreas (yellow arrows). When the bile ducts are dilated in the absence of a cholecystectomy a bile duct stone may be identified in rare cases.



Oral Cholecystography

The oral cholecystogram (OCG) is a purely historical examination that studied the opacification of the gallbladder. This study was once the diagnostic standard for imaging the gallbladder before ultrasound and CT reached the current level of image quality. The basic process involved the patient not eating any fatty foods, or being N.P.O (nothing by mouth) about 6 hours before ingesting oral contrast media. This was in the form of tablets (brand name-Telopaque), that when dissolved the media is absorbed into the liver and secreted in bile. This study had a relatively good specificity for demonstrating a patent gallbladder and cystic duct. If the cystic duct was patent, cholelithiasis when present could be demonstrated. However, conditions like blockage of the cystic duct, hepatitis, or blockage of the hepatic ducts could cause nonvisualization of the gallbladder. The most common cause of nonvisualization of the gallbladder by OCG was poor patient preparation. Often the patient had to take a second dose of oral contrast agent to narrow the differential causes of non-visualization of the gallbladder. With newer imaging techniques patient preparation is almost always satisfactory. Another disadvantage of the OCG study is that the gallbladder will not visualize if the serum bilirubin is greater than 4 mg/100 mL. This is because high serum bilirubin indicates impaired enterhepatic circulation, thus poor absorption and secretion of telepaque.

Radiographs of the gallbladder are taken with the patient upright, as gallstones tend to layer in the most dependent portion of the gallbladder. Layering is also seen when the patient is positioned in the lateral decubitus position using a horizontal x-ray beam. The OCG could also be used to determine function of the gallbladder. A cholecystagogue preparation such as Bile-Evac, Neo-Cholex, or a fatty meal is administered to stimulate contraction of the gallbladder. Cholecystagogues like Neo-Cholex causes the duodenum to secrete cholecystokinin. When the gallbladder contracts contrast is forced out of the gallbladder documenting patency of the cystic duct.

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The four-fluorospot images seen on the left are taken from an oral cholecystogram. This study is purely historical and is not currently used to evaluate the gallbladder. The body of the gallbladder (arrowhead) and fundus (arrow) are clearly seen. One challenge while obtaining radiographs with the patient upright was to make sure an air bubble in the bowel is not mistaken for a radiolucent gallstone. Demonstrating the neck of the gallbladder was also an imaging challenge. This was a relatively safe study because it was not invasive. A non-visualizing gallbladder could indicate blockage of the cystic duct, or biliary tree. The oblique view seen on the right demonstrates bowel gas below the gallbladder.
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Occasionally opacification of the gallbladder is seen on routine x-rays. This is because up to 20% of intravenous iodinated radiocontrast is excreted through the gallbladder and intestine. This is seen 2 to 8 hours after intravenous injection like for angiography or a CT scan. This is not a reliable method for diagnosing the gallbladder; however it can indicate that enterohepatic circulation is working properly. Low renal output is thought to be the cause of iodinated excretion by alternate pathways such as through the bile or intestines in high enough concentration to be seen on a radiograph.




Percutaneous Transhepatic Cholangiography (PTC)

This is another radiographic study that is purely historical and is not done in modern radiographic imaging. It was both a diagnostic procedure in cases of suspected obstructive jaundice, and therapeutic in that dilated bile ducts could be drained during the procedure. Occasionally a stone could be removed by this procedure eliminating the risk of open surgical intervention. Today there are many other invasive procedures with lower risk than PTC. This study was a type of invasive cholangiography that involved direct puncture of the biliary ducts. A fine needle was passed from the skin surface through the liver into a biliary duct. Risk of the procedure included possible puncture of the lung, bleeding from the liver and vascular injury. This was not an easy procedure to perform so benefit of the procedure had to far outweigh its risk before it was performed.

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These two radiographs demonstrate the “skinny needle” used to puncture the bile duct during percutaneous transhepatic cholangiography. Using surgical asepsis a thin needle is passed into the bile duct and iodinated contrast media injected. The biliary tree is demonstrated as well as any obstruction. The radiograph on the left shows contrast in the bile duct as a positive image; the right is the same radiograph as a negative image. Note the thin needle on both radiographs (white arrows).



Operative and T-tube cholangiogram

The operative cholangiogram is also called the immediate cholangiogram because it is performed during cholecystectomy. When the surgeon suspects' residual cholelith may be in the biliary ducts the operative cholangiogram is performed. It can be performed either before or after removal of the gallbladder. The cystic duct is tied off just proximal to the neck of the gallbladder and a catheter is inserted into the cystic duct near its joining the common hepatic duct. Approximately 6 to 10 ml of water soluble iodinated radiocontrast is injected. The surgeon is careful not to inject air since even a small quantity of air can mimic a radiolucent biliary stone. The entire biliary tree should be demonstrated with contrast spilling into the duodenum.

The operative cholangiogram can also demonstrate patency of the biliary tract and hepatopancreatic ampulla. Strictures, mass lesions, and dilatations of the biliary ducts can also be assessed. Unlike the ERCP this is not a therapeutic study for removing stones from the biliary tree. Radiographs are taken using fluoroscopic C-arm so that they can be evaluated. Fluoroscopic C-arm imaging is preferred to plain films because the time to process images is long with plain films. Also images from the C-arm can be sent via Ethernet connection to PACS (picture archiving and communication system) so that consultation with a radiologist is available if needed. This saves valuable time when the patient is under anesthesia and the technologist is not required to make trips in and out of the surgical suite to currier films. An operative cholangiogram procedure can be performed with open surgery, or through a laparoscope.

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This image taken with a C-arm demonstrates the operative cholangiogram. The catheter is inserted into the cystic duct and iodinated contrast media injected as radiographs are taken. The entire distal biliary tree is demonstrated without stone or dilation of the ducts. This confirms that stones are limited to the gallbladder, which was removed following this operative cholangiogram.
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These two radiographs demonstrate the T-tube cholangiogram. The t-tube is named for the shape of the tube inserted into the common bile duct. As you can see the tube is long extending to the outside of the body. Notice the surgical clips in both radiographs indicating this is a post operative study.



Endoscopic Retrograde Cholangiopancreatography (ERCP)

The term endoscopy refers to the illumination of the lumen of an organ using an endoscope. The term cholangiopancreatography refers to imaging the biliary ducts and pancreatic duct. The term endoscopic retrograde cholangiopancreatography (ERCP) refers to imaging the biliary ducts and pancreatic duct using a retrograde approach through an endoscope. ERCP is both a diagnostic tool and a therapeutic procedure for certain conditions. It is usually performed following other radiologic studies that are inconclusive (i.e. ultrasound or MRCP). It is used as a preoperative study to plan a cholecystectomy or postoperative to remove stones that have become lodged in the biliary ducts. Examples of therapeutic treatments with ERCP include but are not limited to dilating stenosed biliary or pancreatic ducts, removal of biliary or pancreatic duct stones, opening the sphincter of Vater by cutting to increase narrowing (sphincterotomy), taking tissue sample by brushing or biopsy, or placement of a stent to facilitate bile flow.

As stated earlier a special type of endoscope called a duodenoscope is used to perform cholangiopancreatoscopy. It allows for detection of indeterminate ductal strictures, pancreatitis, treat large intraductal stones, and can identify and take tissue samples to diagnose ductal diseases like intraductal papillary mucinous tumors, and hemobilia. The patient is sedated and the back of the throat sprayed to numb the gag reflex, and the endoscope passed through the mouth down the esophagus into the stomach. The gastroenterologist is able to see the inside of the gastrointestinal tract through the endoscope allowing the advancement of the endoscope through the pyloric sphincter into the descending duodenum. A cannula is threaded through the duodenoscope into the papilla of Vater into the common bile or main pancreatic duct. Placement of the cannula is verified under fluoroscopy.

Nursing personnel assist the gastroenterologist in tending to the patient. This includes checking for allergies to medicines used during the procedure, getting the patient’s consent for the procedure, charting the procedure for the medical record, grounding the patient in case of a sphincterotomy, monitoring vital signs and blood oxygen saturation, administering medications, and monitoring the electrocardiogram. During the procedure the patient is given sedatives such as meperdine (Demerol), diazepam (Valium), and midazolam (Versed) and others until the desired amount of sedation is achieved. Antibiotics may also be given before the procedure to reduce the risk of pancreatitis. The patient is slightly sedated but able to cooperate during the procedure. An antispasmodic drug like glucagon is given to reduce spasms of the duodenum and relax the sphincter of Oddi for passage of the endoscope and cannula insertion. Air is introduced into the gut to expand the stomach and bowel for passage of the endoscope. The radiographer operates fluoroscopic equipment and exposes fluorospot images to document radiographs for interpretation. Nursing personnel tend to the patient and assist the gastroenterologist, as two persons are needed to change and flush catheters. After the procedure the patient is kept NPO (nothing by mouth) 4-10 hours since the throat is paralyzed. This will reduce the risk of liquid or food aspiration until general and local anesthetics wear off.

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The endoscope transmits dynamic images of the lumen of the gut allowing the physician to carefully examine the lining. During the procedure air is blown into the digestive tract to expand mucosal folds making examination thorough.
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The ERCP is usually performed in the radiology department under fluoroscopic guidance. The patient is sedated, the throat numbed, and the endoscope inserted through the mouth into the duodenum. The physician looks for the major duodenal papilla to insert the guide catheter into to perform the retrograde study of the biliary tree.

In order to examine the biliary tree the physician must thread a small catheter from the endoscope into the major duodenal papilla. The papilla is variable in its location and must be visualized in an orientation that allows it to be catherized. The ERCP procedure best visualizes the main pancreatic duct and ampula of Vater. This is because the ampula is directly catherized and radiopaque iodinated contrast media is injected into it. Usually a CT scan, ultrasound, and/or MRCP are performed prior to the ERCP exam. ERCP is contraindicated when the patient has a pseudocyst of the pancreas. This is because injection of contrast retrograde into a pseudocyst can cause infection. Acute pancreatitis is a potential adverse outcome of an ERCP, and ERCP is contraindicated when preexisting acute pancreatitis is known.

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This schematic drawing shows the endoscope as it is passed through the stomach into the duodenum. A guide catheter is placed into the major duodenal papilla. This allows the physician to perform a retrograde fluoroscopic cholangiogram of the biliary tree.
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These two pictures were taken with the camera on the endoscope. The picture on the left shows the major duodenal papilla before the endoscope is inserted. The picture on the right shows the catheter from the endoscope within the papilla. This allows the physician to perform a retrograde filling of the biliary tree.

During the retrograde cholangiopancreatogram the physician uses a catheter through the endoscope to administer iodinated contrast media such as ultravist or omnipaque into the biliary tree and pancreatic duct. Fluoroscopy is used to image the biliary tree during the procedure. During the procedure the physician looks for biliary stones, strictures, or a mass that causes obstruction of the biliary ducts.

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This picture demonstrates the importance of fluoroscopy and endoscope synchronization during the procedure. The endoscope image (white arrow) shows the catheter in the common bile duct. Using fluoroscopy (white arrowhead) the physician is able to image retrograde filling of the biliary tree and identify any pathology intrinsic or extrinsic to the duct system. Last-image-hold fluoroscopy allows the physician to study radiographic images on the monitor while practicing as low as reasonable achievable (ALARA) radiation dose to the patient.
image026a image026b
These two radiographs show a stricture of the common bile duct. This can be a cause of obstructive jaundice as the flow of bile is stagnated. ERCP can demonstrate stricture in almost all cases and can determine if the stricture is intrinsic or extrinsic to the affected duct. A brush is inserted into the duct to take a brush tissue scraping, or a biopsy of the duct is made. Histological slides are made of the tissue sample and reviewed by a pathologist to determine whether the duct is healthy or not.
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This fluorospot image demonstrates the use of the endoscope to collect a tissue sample for histological analysis. These two radiographs are the same; the one on the right is a magnified view to better show the claw used to take tissue samples. It can also be used to clasp a stone for removal from a biliary duct.
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This endoscope image revealed inflammation of the duodenum. Compare the picture on the left (duodenitis) to the healthy lining of the duodenum on the right. The point here is that endoscopy can demonstrate pathology of the lining of the gastrointestinal tract, in this case the duodenum and the ERCP can demonstrate pathology of the biliary tree. Together these imaging techniques make the ERCP the most reliable diagnostic procedure for imaging the biliary duct system.

There are several ways a stricture can be temporarily opened while doing an ERCP. Either a stent or a wire mesh stent can be placed in the duct to keep it opened. Depending on the result of the tissue biopsy other treatments or even surgical intervention may be necessary.

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These two fluorospot radiographs show a wire mesh type bridge within the common bile duct. This is one of the methods used in treating strictures of the biliary tree using ERCP. ERCP is a diagnostic and therapeutic procedure. Other imaging test will be needed to determine if the stricture is caused extrinsically by a mass.

The most likely reason for performing an ERCP is to diagnose and treat choledocolithasis (stone in the biliary ducts). ERCP not only demonstrates these stones, they can be removed using the duodenoscope. Biliary duct stones are relatively common, about 20 million Americans have gallstones and over 500,000 cholecestectomies are performed annually. These stones can form or be carried into the bile ducts obstructing them. ERCP can demonstrate biliary stones during the injection of iodinated contrast media. Cholesterol stones are black and are radiolucent within the boundary of the duct when surrounded with iodinated contrast media. It is important that air is not injected with the contrast media, which can mimic stones. Air will have a distinct layering effect whereas stones will be irregular.

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These two fluorospot images taken during an ERCP demonstrates stones in the common bile duct on the left radiograph, and cystic duct on the right radiograph (arrows). Cystic duct stones are difficult to remove during ERCP because the valve spirals. Stones in the common bile duct are quite removable by ERCP, but some can be too large to be pulled through the sphincter of Oddi. Sphincterectomy of the sphincter of Oddi may be needed to widen the opening into the duodenum to remove larger stones.

Some stones are large and cannot be adequately griped with a clasp through the endoscope. The physician may elect to pass a wire basket through the endoscope to capture these larger stones. Once the stone is in the basket it can be tightened to hold the stone effectively pulling it into the duodenum. Once in the gut these stones pass in the stool without incident. During ERCP stones and sludge are removed and the biliary tree checked for patency. A temporary stent may be needed to facilitate bile flow in cases where duct stasis has been prolonged.

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These two fluorospot images demonstrate the use of a wire basket to capture larger stones. The radiograph on the right is a magnified version of the picture on the left to better demonstrate the basket. Notice it contains a stone that will be drawn into the duodenum.
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These two pictures were taken with the endoscope. A large cholesterol stone (white arrow) is released from a wire basket into the duodenum (left picture). An sphincterectomy (blue arrow) was performed to allow a stone to be removed and release stagnated bile into the duodenum (right). In this case the bile duct was deeply cannulated with a short-nosed traction sphincterotome. A sphincterotome is an instrument used to lance a small sphincter to enlarge it. A sphincteroctomy is performed with the sphincterotome passed through the endoscope.

The physician may place a stent into the common bile duct after a stone is removed to keep it open and enhance bile flow into the duodenum. Stagnated supersaturated bile may have sludge or small crystals of stones so a preventive stent may be placed. The pancreatic duct may also be catherized to make sure it is patent. A pancreatic duct stent can also be placed if necessary.

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This fluorospot image demonstrates the completion of the ERCP. A stent has been placed in the common bile duct (white arrow). After a stone was removed and the stent placed, bile flowed freely into the duodenum as observed with the endoscope.
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These two pictures taken through the endoscope camera show the insertion of a stent (left) and bile draining from the stent (right) picture. Sometimes a stent can be placed to help drain the biliary ducts and gallbladder without performing a sphincteroctomy.
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At times the gastroenterologist may image the main pancreatic duct for stones or patency. These two fluorospot images demonstrate the main pancreatic duct (duct of Wirsung). During the ERCP procedure the physician usually catherizes and demonstrates the pancreatic duct to determine its patency. Both fluorospot images show the main pancreatic duct of two different patients (white arrows).
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Once gallstones are removed from the common duct the pancreatic duct is evaluated by injecting iodinated contrast into it. The study is complete when contrast media is injected into the biliary tree and unrestricted draining into the duodenum is demonstrated. Notice the filling of the intrahepatic ducts and biliary tree with iodinated contrast media. The ampulla of Vater and patency of the sphincter of Oddi are also seen as contrast media is seen entering the duodenum. ERCP is the best way to image, diagnose, and treat biliary tract stones in a single study; however, it is an invasive procedure.



Magnetic Resonance Cholangiopancreatography (MRCP)

In the past to demonstrate choledocholithiasis the only available techniques were cholecystectomy with operative cholangiography and percutaneous cholangiography, and ERCP. Today the MRCP is an available non-invasive magnetic resonance imaging exam that visualizes the entire gallbladder, biliary tree, and the pancreatic duct. It is often performed before an endoscopic retrograde cholangiopancreatogram (ERCP) to determine if therapeutic ERCP is needed. By contrast, ERCP is both a diagnostic and therapeutic imaging tool for identifying and removing biliary tract stones. MRCP is a good alternative for those patients who need biliary imaging, but have renal complications or allergy to iodinated contrast media.

The MRCP is a current topic in radiographic imaging practice and research. While image resolution of the MR cholangiogram is comparable to ERCP it is not as good. On the other hand, MRCP can demonstrate areas of the hepatic and biliary duct that may not be seen when there is obstruction. MRCP has risen to the level of clinical relevance as a preoperative and pre-ERCP diagnostic tool for evaluation of choledocholithiasis. The statistics on MRCP look good, for example, retrospective studies show a positive predictive value of 0.95 and a negative predictive value of 0.97 for bile duct stones. Research has shown that about 74% of clinically suspected bile duct stones are proven negative using MRCP, a finding that significantly reduces the risk of unnecessary ERCP. MRCP is also an excellent way to image the pancreatic duct to assess its size, detect normal or obstructed Wirsung duct, and determine etiology of ductal obstruction or disease. The specificity and sensitivity of MRCP in evaluating the normal pancreatic duct is 98% and 94%, respectively. The same correlation for ERCP is 100%; however, ERCP does not adequately demonstrate pancreatic neoplasms. Pancreatic neoplasm is not seen with ERCP; however, MRCP identifies pancreatic neoplasm nearly 100% of the time and correctly identifies chronic pancreatitis.

MRCP images are taken in axial, coronal, and 3-D formats providing imaging referencing in multiple planes. It is important that the entire gallbladder, biliary ducts, and pancreas are included in the axial, coronal, and 3-D images. Two techniques are combined for imaging the biliary tract: multisection thin-slice and single-slice thick-slab MRCP. Studies show that these techniques should be combined in the imaging protocol to get the most out of the unenhanced and enhanced MR scan. Intravenously administered fentanyl before MRCP has been shown to improve the qualitative and quantitative visualization of the biliary tree. The reason for both techniques is that single-shot thin-slice imaging is superior to multisection thin slice for bile duct imaging.

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These two axial MR images are taken from a series of images in the MRCP exam. They demonstrate a portion of the liver and gallbladder. The gallbladder is opacified due to the uptake of gadolinium. The MR image on the left is a slice taken through the gallbladder demonstrating the neck and beginning of the cystic duct. The gallbladder is round and pear-shaped, which is the normal shape of the gallbladder.
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These two MR images are taken from a series of coronal slices. Demonstrated are the entire gallbladder (left) and the cystic duct (right). The cystic duct (white arrow) is seen joining the common bile duct on the right MR image as well as numerous intrahepatic bile ducts.
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This coronal image demonstrates the common bile duct filled with contrast media (left). On the right is a 3-D image of the right and left hepatic ducts, cystic duct and common bile duct. 3-D imaging of the biliary tree is another very useful tool that is unique to MR biliary imaging.
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This 3-D image of the gallbladder and biliary tree shows good contrast enhancement and flow of bile into the duodenum. Notice the visualization of the extensive hepatic bile ducts within the liver; these are not comprehensively seen with ultrasound or with CT.
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This single-shot thick-slice MR image demonstrates patent hepatic, cystic, and common bile ducts. The single-shot thick-slab technique shows better detail than multisection imaging only. MR imaging is emerging as a strong tool for biliary duct imaging and prescreening for ERCP.



Ultrasound of the Gallbladder and Biliary Ducts

Ultrasound is used to evaluate patients for biliary stones and cholecystitis. It can detect cystic duct and neck of the gallbladder obstruction as well as distension and inflammation of the gallbladder. It can identify carcinoma of the gallbladder, which is highly malignant and metastasizes quickly. Ultrasound is important because gallbladder cancer has a very low prognosis; therefore, any early diagnosis of this condition is potentially lifesaving. The gallbladder on ultrasound can usually be found between the quadrate and right lobe of the liver on the underside. The fundus may be folded giving a Phrygian cap appearance, which makes the gallbladder look septated on ultrasound. When seen, this should be differentiated from a septate or double gallbladder that it could mimic. The cystic duct that joins the neck of the gallbladder to the common bile duct is only about 2-4 cm. The common hepatic duct (CHD) is only about 2.5 cm in length and runs to the right of the portal vein and hepatic artery. The common bile duct (CBD) is generally long, 7.5 to 10 cm. It runs posterior to the head of the pancreas and can be enclosed in the pancreas distally. Conventionally the union of the CHD and CBD is called the common duct (CD).

The patient should be NPO (nothing-by-mouth) for imaging the biliary tract with ultrasound. Fasting distends the gallbladder and bile ducts and reduces bowel gas that may obscure visualization of portions of the gallbladder. Food may increase the thickness of the gallbladder wall imitating pathological wall thickening. Four hours is sufficient fasting for small children, and 6-8 hours for age 12 to adult. They should be told not to smoke during the fasting period since smoking causes the bile ducts to contract. Ultrasound should be performed before any barium is administered for gastrointestinal (G.I.) imaging, or when the stomach and hepatic flexure is clear of barium is order after G.I. imaging procedure.

The scan protocol may vary based on the patient’s condition and pathological indications for the scan. Real time imaging in the sagittal, coronal, transverse, and appropriate oblique planes are made. The sonographer takes a patient history to include prior abdominal surgery, especially cholecystectomy or cholecystostomy for removal of stones. The sonographer also makes a physical assessment of the patient looking for surgical scars not accounted for in the patient history, jaundice, and may palpate the abdomen when a mass is felt for solidness or pulsatility, or tenderness. During the scan the patient may be positioned in the supine, left posterior oblique, left lateral decubitus, or upright positions as needed.

Longitudinally, the gallbladder appears as a pear-shaped structure with thin white walls surrounding a black fluid. The normal gallbladder wall is thin, echogenic and an anechoic lumen, and mild posterior enhancement. Bile is near the consistency of water so its acoustic impedance is low, as bile does not attenuate the sound waves. Generally there is no acoustic shadowing posterior to the gallbladder so when imaging near the neck an acoustic shadow may represent a stone in the cystic duct. The gallbladder and bile ducts are evaluated for size and shape, wall thickness, contents, course, and caliper. During the procedure the sonographer checks for a positive Murphy’s sign. The thumb or transducer is placed over the costal margin of the gallbladder. When the patient takes a deep inspiration they may pause abruptly due to a sharp pain before “catching” their breath, which is a positive Murphy’s sign. The sonographer may image the gallbladder during the elicited response to document a positive finding.

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These two ultrasound images demonstrate the normal gallbladder in the supine position (left) and decubitus (right). The thin wall of the gallbladder is seen as a white ring surrounding bile, which appears as a black low attenuated fluid. The wall thickness should be less than 3 mm in adults. There is no acoustic shadowing posterior to the gallbladder, or near the neck.

Dimensions of the Normal Adult Gallbladder on Ultrasound
   
Length
Diameter
Wall thickness
 
7-10 cm
3-4 cm
< 3 mm

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These two ultrasound images demonstrate normal gallbladder wall thicknesses. These are different patients’ notice the gallbladder on the left is imaged in the decubitus position. The gallbladder wall of this full gallbladder measures 2.2 mm on transverse section (left). Normal wall thickness should be less than 3 mm, but may increase in thickness in disease states such as cholecystitis, or biliary tract stone. The wall thickness can increase temporarily following a meal. Wall thickness is usually measured on both the transverse and longitudinal sections. The ultrasound image on the right is taken with the patient in the left posterior oblique position following a fatty meal. The wall thickness is 2.9 mm, just within normal limits.

The shape of the gallbladder is equally important when diagnosing gallbladder disease. It should be pear-shaped not round and tense, which indicates a pathological condition. What is interesting is that the size of the gallbladder increases with age, but the wall thickness is rather constant. The common bile duct does change with age, pregnancy, and following cholecysectomy. When choledocholithiasis is present the common duct may measure 7 mm or more in diameter. The common bile duct is imaged and measured as part of the ultrasound scan.


Some conditions where diffuse gallbladder wall thickening >3 mm is seen
  • AIDS
  • Ascites
  • Cholecystitis
  • Congestive heart failure
  • Hepatitis

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This ultrasound image of the gallbladder shows a normal shaped gallbladder. Even though it is not pear-shaped it is not rounded and tense. The shape of the gallbladder is an important diagnostic criterion since a rounded tense shape can indicate pathology. A large gallbladder (called hydrops) is large, rounded, and tense having a transverse diameter of greater than 5 cm and a length greater than 20 cm on ultrasound.
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This gallbladder is normal in size. No gallstones, gallbladder wall thickening, or pericholecystic fluid are identified. The patient did not demonstrate tenderness over the gallbladder during the exam (negative Murphy’s sign).
image045
These two ultrasound images demonstrate the common bile duct (CBD) in a normal patient (white arrow). The entire common bile duct is not usually visible with ultrasound; however, portions of it should be imaged and measured. The CBD measures 2.22 mm in this patient. Color Doppler image on the left proves this is not a vessel containing blood and is in fact the common bile duct. The CBD of this patient is measured on the supine longitudinal view (right ultrasound image); it may also be measured in the posterior oblique or decubitus positions.

Most pathology of the gallbladder and bile ducts can be seen on ultrasound. The two charts below lists pathology the sonographer looks for during the scan. While there are many pathologies of the gallbladder we will limit this discussion to gallstones and bile duct stones. This is because the imaging is the same for these pathologies as for most pathology of the gallbladder.


Gallbladder Pathology Demonstrated on Ultrasound
  • Acute and chronic Cholecystitis
  • Adenomyomatosis
  • Biliary ascaris
  • Carcinoma
  • Diffuse wall thickening
  • Empyema
  • Gallstones
  • Gangrenous and emphysematous cholecystitis
  • Non-visualized & micro gallbladder
  • Sludge (viscid bile)
  • Polyps
  • Porcelain gallbladder


Some conditions where diffuse gallbladder wall thickening >3 mm is seen
  • Air in bile ducts
  • Biliary
  • Choledochal cyst
  • Caroli’s disease
  • Choledocholithiasis
  • Klatskin tumor
  • Obstruction of ducts
    • Papilloma
    • Cystadenoma
  • Sclerosing cholangitis

image046
These two ultrasound images show gallstones in the gallbladder. The ultrasound image on the left demonstrates multiple stones imaged with the patient in the left lateral decubitus position. The right ultrasound image demonstrates these stones in the transverse section. Note the acoustic shadowing posterior to the stones in both images.
image047
This ultrasound image is taken with the patient in the left lateral decubitus position (LLD). The common bile duct is dilated; however, it can be up to 10 mm in patients who have undergone a cholecystectomy, are elderly, or during pregnancy. A good clinical history should be included in all cases and especially if the CBD is larger than 7 mm.
image048
This ultrasound image demonstrates a normal dilated CBD. Color Doppler indicates it is the duct not a vascular structure. Again, this is within the upper limits of normal but may be a pathological finding if the patient is not elderly or had a previous cholecystctomy. While a cholelith is not identified if the patient has other clinical signs of bile duct obstruction a MRCP or ERCP may be needed to differentiate cause of dilation.



Nuclear IDA scan (Cholescintigraphy)

The nuclear hepatobiliary (IDA) scan, which is also known as cholescintigraphy uses the radioisotope imino diacetic acid (IDA) to image part of the biliary system. In the past the IDA scan has been called the HIDA scan. The most common reason for physicians requesting this scan is to evaluate the functioning of the cystic duct in case of suspected cholecystitis. The IDA scan can also detect biliary obstruction, bile leak, and atresia. The IDA scan is a dynamic scan that assesses function of the gallbladder and cystic duct patency. Technetium-99m-IDA agents such as Choletec or Hepatolite are administered intravenously. These agents are bilirubin analogues having the same biliary uptake as bilirubin used to make bile, but are not conjugated to bilirubin. Then they are secreted into the biliary tract allowing them to be taken up by the liver and secreted into the biliary tract and concentrated in the normal functioning gallbladder. When the biliary tract is functioning properly the entire bilirubin pathway from filling of the gallbladder to passage into the common bile duct and duodenum should be visualized.

Patient preparation for the exam includes a good clinical history for compatibility for the study and mild fasting. The patient is required to fast 4-6 hours before the exam. Small amounts of water may be taken, but no narcotic medications are permitted 4 to 12 hours before the exam because they cause constriction of the sphincter of Oddi. Prolonged fasting is not recommended because it can cause false positive scan results, especially if the patient has been NPO more than 24 hours. The patient history should include prior cholecysectomy, morphine tolerance, and whether or not the patient currently has pancreatitis. Morphine is sometimes given during the test and morphine allergy or morphine with pancreatitis is contraindicated.

The adult study is initiated with 1.5 to 5 mCi IDA administered intravenously. The scintillation camera collects serial images over the liver and gallbladder acquired at 5 min intervals for one hour. If the gallbladder and duodenum are visualized on the one-hour scan the study is complete. When the gallbladder is not visualized after one hour the cause can include acute or chronic cholecystitis and the study is continued. After 2-4 hours of failed visualization of the gallbladder the specificity for acute cholecystitis is greater than before. Delay imaging may continue to 24 hours in cases of severe liver impairment to get a better diagnostic study.

There are several alternative methods of performing the IDA scan, for examples, Cholecystokin can be administered to contract the gallbladder, or morphine sulfate given to constrict the sphincter of Oddi. The ejection fraction of bile from the gallbladder as it contracts can also be assessed. The diagnostic specificity for acute cholecystis with partial or complete obstruction of the cystic duct can be improved by using CCK. When appropriate, 0.01-0.02 microgram per kilogram body weight is given intravenously over 3-5 minutes. The scan parameter can include the percentage of bile released with gallbladder contraction, called the ejection fraction. Morphine sulfate (0.04-0.01 mg/kg) intravenously causes constriction of the duodenal papilla. This enhances retrograde flow of bile laden with radiopharmaceutical into the gallbladder when the cystic duct is patent. This lowers the exam time for gallbladder filling; however, the patient must not have pancreatitis, or morphine allergy.

image049
These two images from the IDA scan demonstrate hepatic uptake of the radiopharmaceutical agent. The image is shown as a negative (left) and as a positive (right) just for comparative viewing. Hepatic extraction of IDA radiopharmaceutical from the blood is demonstrated. In order to evaluate the gallbladder and biliary bile flow there must be uptake of the radiopharmaceutical by the liver and excretion of it into the biliary ducts.
image050
These two IDA nuclear scan images (left) negative, (right) positive show a filled gallbladder following uptake of radioisotope IDA. Filling of the gallbladder indicates a patent cystic duct and normal hepatic billirubin uptake. Most of the radiocontrast is concentrated in the gallbladder since the patient is fasting and hepatic uptake and secretion is nearly completed.
image051
This patient presented to be evaluated for acalculous cholecystitis or gallbladder dysfunction. The study was performed with 8.5 mCi of Tc99m Choletec followed with 1.3 mcg CCK given two hours post injection. Initial images demonstrate normal extraction of the radiopharmaceutical. The gallbladder is seen at 20 minutes with the common duct visualized at 15 minutes. After injection of CCK the ejection fraction is 13%. These findings are consistent with gallbladder dysfunction and possibility of narrowing at the ampula. A MRCP or ERCP will be necessary to further differentiate the cause of the delayed filling of the biliary ducts.
image052
This scan taken at 55 and 60 min post injection of IDA shows good hepatic uptake and secretion into the bile to demonstrate the gallbladder. The cystic duct and common duct are partially demonstrated; however the entire course of the common bile duct is not seen. Delay images were needed to complete the study and point to the correct diagnosis.
image053
These images are taken from a series of images at 70 and 95 minutes. They show adequate contraction of the gallbladder, but the ejection fraction is only approximately 13%. These images do not show the distal biliary tract as these were not demonstrated on the 60 min IDA scans. This study concluded a possible obstruction due to stricture of the common duct near the ampula of Vater.
image054
This IDA scan to evaluate for acalculus cholecystitis was obtained following administration of 8.2 mCi Tc-99m Choletec. These images of the right upper quadrant were obtained at 5-minute intervals. The patient then received 1.4 micrograms of CCK and additional images were obtained. The gallbladder ejection fraction was then calculated.
image055
This scan was made following the intravenous injection of 8.7 mCi of Tc99m Choletec. The abdomen was imaged for one hour. There is a normal appearance to the liver. The intrahepatic ducts are visualized between 5-10 minutes with excretion into the bowel occurring in this same time period.
image056
The gallbladder is visualized in the 20-25 minute time range with continued excretion of activity into the bowel. After 60 minutes, most of the activity is cleared from the liver and contained primarily within the gallbladder and intestinal tract.
image057
These IDA uptake images show radiocontrast in the gallbladder at 40 min. The liver is nearly completely cleared of radiopharmaceutical and concentrated in the gallbladder. This confirms the cystic duct is patent and the next phase of the study to determine ejection fraction is performed.
image058
To determine the ejection fraction of the gallbladder the patient was then administered 1.8 mcg of cholecystokinin. Imaging was continued for an additional 30 minutes shown in the six images above. A time activity curve of gallbladder activity was created and is shown below. A time activity curve is generated from these images and the ejection fraction calculated.
image059
CCK was given to contract the gallbladder and generate this time activity curve. This is a normal time activity curve showing an ejection fraction of 80-82% during the twenty-eight minute time period. An ejection fraction greater than 35% is considered a normal gallbladder contraction and ejection fraction. Keep in mind that if CCK is administered too rapidly the gallbladder may spasm causing a false low ejection fraction. The proper rate of CCK infusion is to dispense it over a 30-45 minutes, which is closer to physiological secretion.
image060
The scintillation computer software can calculate the ejection fraction and plot the time activity curve. This is a summary of the scan data provided the radiologist who reads the scan and dictates the final report.

The IDA scan can be quite informative. How the liver extracts radiopharmaceutical from the blood can be assessed. The timing of intrahepatic biliary secretion into the gallbladder can also be rapidly assessed with the IDA scan since the radiopharmaceutical should be seen in the gallbladder and duodenum within an hour. The pattern of the scan indicates pathological versus normal processes. For example, a non-visualizing gallbladder especially after 4 hours indicates blockage of the cystic duct. Obstruction of the cystic duct can be quickly assessed by administering morphine. When the radiopharmaceutical is seen in the duodenum but not in the gallbladder 3 minutes after administering morphine a diagnosis of cystic duct stone is certain. A diagnosis of chronic cholecystitis can be made when the gallbladder does not fill within 1 hour, but fills after 4 hours. Chronic cholecystitis is also suggested when the morphine augmented study demonstrates the radiopharmaceutical entering the duodenum before the gallbladder of sequence images. A “rim” sign may be noted when radiotracer forms a rim around a non-visualized gallbladder. This indicates a possible perforation of the gallbladder, which is a complication of cholecystitis.

An obstruction of the distal biliary tree produces a high-grade obstructive pattern in which there is good hepatic extraction of the radiopharmaceutical, but the intrahepatic bile ducts, gallbladder, common bile duct, and duodenum is not visualized. An intrahepatic cholestasis pattern must be proven to be due to retrograde pressure obstruction rather than from drug effects. Certain drugs like Dilantin, oral contraceptives, or phenothiazines can be a cause of a false-positive study for high-grade obstruction. So each patient should be screened before the test is performed for compatibility to get a differential diagnosis from the IDA scan. It the biliary system is not visualized it is not possible to determine if the patient has cholecystitis or cystic duct obstruction. When there is partial hepatobiliary obstruction, radiopharmaceutical secretion may end bluntly just proximal to the obstruction. Keep in mind the IDA scan is a functional scan that can also indicate the anatomical location of a functional impairment.

image061
This is an older version of the IDA scan called the HIDA scan. These images are from our archive films of the year 1982. This is a very diagnostic study for its day with good resolution of the images. Notice the liver, bile ducts and radioisotope in the small intestine. This scan indicates normal extraction of bile from the enterohepatic circulation and emptying into the duodenum.


Pathology of the Biliary System

Certain conditions of the biliary system can be seen during radiographic imaging such as with ultrasound, CT, MRI, or nuclear radioisotope imaging. These include biliary atresia, choledochal cysts, biliary sludge, cholelithiasis, acute cholecystitis, chronic cholecystitis, and gallbladder neoplasm. Biliary atresia is the most common obstruction seen in infants and young children. It has two main causes, either congenital or as a result of viral infection shortly after birth. This disorder is caused by progressive obliliteration of the extrahepatic ducts and progresses to the intrahepatic ducts. The course of the disease is from distal to proximal parts of the biliary tree. This disorder is quite serious and needs to be diagnosed and treated as soon as possible. It causes scarring and fibrosis of the intrahepatic ducts if the disease progresses. About 50% of neonates present with mild jaundice that clears up in a few days, biliary atresia is a condition that most often begins a week or two after birth. It is marked by a sudden onset of jaundice and high serum bilirubin level. The two most serious conditions that are seen with sudden onset jaundice in neonates are biliary atresia and neonatal hepatitis. Other less serious causes are inspissated bile syndrome, enzyme deficiencies or metabolic disorders, and choledochal cysts. Biliary atresia is twice as common in males as females; however, neonatal hepatitis is four times more common in females than males. Although there is surgical options for biliary atresia the victim usually dies within a few years as there is no cure. Liver transplant has shown some promise towards a longer live expectancy.

Biliary atresia is generally diagnosed with ultrasound. An important indicator in the neonatal is the diameter of the common bile duct, which is less than 1 mm diameter. Inability to demonstrate the common bile duct combined with a finding of intrahepatic duct dilatation is highly suggestive of the diagnosis. Demonstration of dilatation of both the intrahepatic and extrahepatic ducts excludes a diagnosis of biliary atresia and favors a diagnosis of biliary obstruction.

Neoplasms of the gallbladder can be benign or malignant. Benign neoplasms are usually pedunculated and are non-gravity-dependent homogenous mass. Polyps for example, protrude into the lumen on a stalk that can be seen with ultrasound. Adenomas and polyps are benigned neoplasms that do not shadow on ultrasound, a feature that distinguishes them from stones. Other characteristics of adenomas and polyps are their attachment to the gallbladder wall, and they may sway with change in body position. Malignant neoplasm of the gallbladder accounts for 4% of all cancers. It mainly affects women over the age of 60 years. It is highly associated with gallstones as they are seen in 70-98% of cases. A porcelain gallbladder is seen in 25% of cases. Primary gallbladder cancer is strongly associated with gallstones and inflammation of the gallbladder. Eighty percent of primary carcinomas of the gallbladder are adenocarcinomas; 20% are differentiated or squamous cell cancers. Primary seeding from the gallbladder is to the liver and secondarily to the lungs, and intraductally to the pancreas. The gallbladder is affected by metastases mainly by embolic hematogenous spread from malignant melanomas. Other bloodborne metastasis from the kidneys, esophagus and lung do occur.

When a portion or the entire gallbladder wall is calcified it is called a porcelain gallbladder. This condition is highly associated with gallbladder cancer. An enlarged, highly distended, nontender gallbladder in a jaundiced patient is called a Courvoisier gallbladder. The cause of this condition is usually obstruction of the common bile duct due to pancreatic cancer. The gallbladder enlarges first, and then the CBD follows with progression of the disease. Hydrops is an abnormal distension of the gallbladder due to thickened bile, pus, or mucus. Hydrops is most commonly caused by obstruction of the cystic or CBD.



Conclusions

Radiographic imaging of the biliary system offers the clinical physician many diagnostic tools in the diagnosis of biliary tract disease. All imaging modalities: nuclear medicine, ultrasound, computed tomography, magnetic resonance imaging, interventional radiology, and general diagnostic imaging offer specific specialized test that individually and together has advanced the diagnosis of biliary disorders. Radiographers play an important role in imaging the biliary system. Therefore, it is important that we understand what patient’s go through when they have biliary system disorders. Hopefully this article will increase our apathy towards our patients. It is hoped that this article gives x-ray technologists, nuclear medicine technologist, ultrasonographers, nurses, healthcare workers, and lay persons a better understanding biliary system radiography.




Summary Points

  • There are many disorders of the biliary system that include gallstones, cholangitis, cholecystitis, and bile duct cancer. Gallstones can reside in the gallbladder, a condition called cholelithiasis, or present in the bile ducts-choledocholithiasis. Obstruction by gallstones can lead to life-threatening infection of the pancreas, liver, or the bile ducts.
  • Lobes are composed of liver cells called hepatocytes that are arranged into lobules. The liver performs over 100 known functions. Among them are forming blood cells, detoxifying poisons (alcohol and drugs), and metabolizes foodstuff (carbohydrates, fats, proteins). It stores several vitamins (A, D, E, K, and B12). Special cells within the liver parenchyma called Kuppfler cells are phagocytes that engulf spent red blood cells and recycle the hemoglobin in the form of bilirubin.
  • All hepatocytes have the function of converting the substrate bilirubin to bile. The liver also makes many protein products among which is albumin and blood clotting factors like fibrinogen. It produces urea from protein metabolism, which is a major component of urine. The liver can even make glucose when blood sugar becomes too low.
  • The liver has a double blood supply. The portal vein supplies most of the blood (70%) and the hepatic artery gives the remainder (30%); this duel supply is important to the unique metabolic needs of the liver. The portal vein is formed just posterior to the neck of the pancreas by the union of the superior mesenteric and splenic veins. The portal vein carries nutrients it receives from the gut (via the superior mesenteric vein) to the liver for detoxification.
  • The hepatic artery is a distal branch of the hepatic artery proper that branches from the celiac trunk on the anterior surface of the aorta. Hepatocytes are stacked hexagonally to form the architecture of the sinusoids. The apposing membranes of hepatocytes form channels for bile to flow called canaliculi. The functional unit is the lobule where detoxification and bile secretion occurs in a counter current type flow, an arrangement that maximizes cellular contact with blood. Drug bioavailability is reduced by this processing too is called the first-pass effect, or first-pass metabolism.
  • The mucosa of the cystic duct is thrown into rugae that form spiral tracts called the spiral valve of Heister. The valve performs like a sphincter to regulate substances entering and leaving the gallbladder. Some individuals have a prominent pouch just posterior to the neck of the gallbladder called a Hartmann pouch. This is a prime site for gallstones to lodge possibly obstructing the gallbladder. Ultrasound imaging of the neck of the gallbladder can document a Hartmann pouch.
  • The liver produces up to 20 times more bile than the capacity of the gallbladder. The cells of the gallbladder absorb water returning it to surrounding capillaries. Water, sodium, chloride and most electrolytes are absorbed from bile concentrating bile salts, cholesterol, lecithin, and bilirubin. Bile in the gallbladder is concentrated by a factor of 12 to 18 fold its liver secretion.
  • Bile is composed of bile salts, bile pigments, cholesterol, bilirubin, inorganic ions (sodium, potassium, chloride, and calcium), and substances that give alkalinity to bile.
  • Cholesterol is converted in the liver to two bile salts: cholic acid and chenodeoxycholic acid. Bacteria in the gut convert a portion of these primary bile acids to secondary bile acid: deoxycolic and lithocholic acids. Bile salts cannot perform their function of emulsification of fat in the intestine until they are conjugated to either glycine or to taurine (amino acids) to form glycol-conjugated bile acids or taurine-conjugated bile acids. Conjugation of bile acids takes place in the liver.
  • Without bile salts about 40% of lipids are lost in the stool creating a physiological deficit of essential lipids. Fat soluble vitamins A, D, E, and K are absorbed with lipids from the gut. Of these, only vitamin K is not stored in sufficient quantity by the liver. In just a few days vitamin K deficiency will develop if insufficient amount is not absorbed from the diet. Vitamin K is a necessary nutrient for the liver to synthesize blood clotting agents. In just a few days without vitamin K, prothrombin, and coagulation factors VII, IX, and X become deficient.
  • Bile salts are physiologically conserved; approximately 95% of bile salts are reabsorbed in the small intestine terminal ileum. Only a small amount of bile is newly synthesized daily, approximately about 0.2-0.5 grams per day. The circulating bile pool is roughly 2-3 grams, which recycles in enterohepatic circulation at a rate of twice per meal, or 6 times a day.
  • Bile salts are physiologically conserved; approximately 95% of bile salts are reabsorbed in the small intestine terminal ileum. Enterohepatic circulation is defined as the recurrent cycle in which bile salts and other substances excreted by the liver pass through the intestinal mucosa and become reabsorbed by the hepatic cells and re-excreted.
  • The biliary system consists of the liver, gallbladder and biliary ducts. The pancreas is not considered part of the biliary system, it merely secretes inactive digestive juice into the duodenum through a shared duct the ampula of Vater. Inability to secrete digestive juices into the duodenum can adversely affect the pancreas.
  • The main pancreatic duct called Wirsung’s duct runs transversely from the head to the tail of the pancreas. It joins the common duct that partially passes through the head of the pancreas as it transports bile to the duodenum.
  • The gross anatomy of the biliary tree begins with the right and left hepatic ducts that drain bile from the two halves of the liver. These become the common hepatic duct that is joined by the cystic duct from the gallbladder. The union of the common hepatic and cystic ducts form the common bile duct. The common bile duct is about 7.5 cm long. It passes posterior and often through the pancreas to join the main pancreatic duct (duct of Wirsung). The union of the main pancreatic duct and common bile duct form a short ampula called the hepatopancreatic ampula (a.k.a. ampula of Vater). The ampula inserts on the major duodenal papilla, which is guarded by the hepatopancreatic sphincter (a.k.a. sphincter of Oddi).
  • The hormones CCK, gastrin and secretin are cholesecretagogues. A secretagogue is a substance that stimulates secretion. Cholesecretagogues stimulate secretion of bile by the gallbladder.
  • About 85% of gallstones are cholesterol type stones. The composition of cholesterol stones is mostly cholesterol, and some minor amounts of bilirubin, bile salts, inorganic salts, proteins, and calcium that give radiographic density to stones. Pigmented stones are composed primarily of bilirubin and are generally radiolucent. There can be an array of stone compositions that fall into the category of mixed stones, but cholesterol stones are the most common. Calcium gives gallstones the radiopaque appearance seen on x-rays. Black stones are pigmented stones composed of pure calcium bilirubinate.
  • One of the advantages of CT is that the scan can help determine the type of gallstones (e.g. cholesterol, pigmented, etc), identify pathological dilation of the extrahepatic bile ducts, and can detect pancreatic cancer with 100% accuracy.
  • Occasionally opacification of the gallbladder is seen on routine x-rays. This is because up to 20% of intravenous iodinated radiocontrast is excreted through the gallbladder and intestine. This is seen 2 to 8 hours after intravenous injection like for angiography or a CT scan.
  • The oral cholecystogram (OCG) opacificies the gallbladder when ingested tablets (brand name-Telopaque) are dissolved and absorbed into the liver and secreted in bile. A fine needle was passed from the skin surface through the liver into a biliary duct allowing iodinated contrast media to be injected into the bile ducts is called a percutaneous transhepatic cholangiogram.
  • The operative cholangiogram is also called the immediate cholangiogram because it is performed during cholecystectomy. The T-tube cholangiogram is performed in the interventional radiology suite. This procedure is also known as a delayed cholangiogram. When the surgeon is suspicious of stones in the biliary tree and there is an uncertain radiology confirmation a T-tube may be inserted in the common duct. The tube extends to the outside of the body and is covered in a surgical dressing. The purpose of this is to perform the study 1 or 2 days after the cholecysectomy to see if there are biliary stones.
  • Cholangiopancreatography refers to imaging the biliary ducts and pancreatic duct. The term endoscopic retrograde cholangiopancreatography refers to imaging the biliary ducts and pancreatic duct using a retrograde approach through an endoscope.
  • Examples of therapeutic treatments with ERCP include but are not limited to dilating stenosed biliary or pancreatic ducts, removal of biliary or pancreatic duct stones, opening the sphincter of Vater by cutting to increase narrowing (sphincterotomy), taking tissue sample by brushing or biopsy, or placement of a stent to facilitate bile flow.
  • Nursing personnel assist the gastroenterologist in tending to the patient. This includes checking for allergies to medicines used during the procedure, getting the patient’s consent for the procedure, charting the procedure for the medical record, grounding the patient in case of a sphincterotomy, monitoring vital signs and blood oxygen saturation, administering medications, and monitoring the electrocardiogram.
  • During the procedure the patient is given sedatives such as meperdine (Demerol), diazepam (Valium), and midazolam (Versed). Antibiotics may also be given before the procedure to reduce the risk of pancreatitis. An antispasmodic drug like glucagon is given to reduce spasms of the duodenum and relax the sphincter of Oddi for passage of the endoscope and cannula insertion.
  • Without bile salts about 40% of lipids are lost in the stool creating a deficit of essential lipids. Essential lipids are those needed by the body for normal bodily functions, but cannot be endogenously synthesized by the body. Linoleate and linolenate are the two essential fatty acids that must be taken in through the diet
  • The formation of gallstones is a slow process that occurs in three recognizable stages. First bile becomes super saturated, 2) then there is nucleation or formation of a small crystal precursor to a stone, and 3) the small stone grows by a process called accretion. The critical stage in the formation bile stones, especially those formed by cholesterol is super saturation of bile with cholesterol.
  • Lithogenesis can occur when any of these three conditions exists: 1) deficient secretion of bile salts and lecithin, 2) supersaturation of cholesterol in bile, or 3) inflammation of the epithelium of the gallbladder.
  • Gallstones, when they obstruct biliary flow can cause a type of jaundice called obstructive jaundice or surgical jaundice. Jaundice or icterus is the medical term for a yellowish tint to the skin and sclera of the eyes caused by excess bilirubin in the blood.
  • Obstructive jaundice must be differentiated from medical jaundice. Medical jaundice is cause by liver disease not obstruction. Two examples of medical jaundice are hemolytic and hepatic jaundice caused by a diseased liver.
  • Up to 20% of intravenous iodinated radiocontrast is excreted through the gallbladder and intestine. This is seen 2 to 8 hours after intravenous injection like for angiography or a CT scan.
  • The percutaneous transhepatic cholangiogram (PTC) is a historical radiographic exam. This study was a type of invasive cholangiography that involved direct puncture of the biliary ducts. A fine needle was passed from the skin surface through the liver into a biliary duct and intravenous contrast media injected to opacify the biliary tree.
  • The operative cholangiogram is performed during cholecystectomy when the surgeon suspects residual cholelith in the biliary tree. The cystic duct is tied off just proximal to the neck of the gallbladder and a catheter is inserted into the cystic duct. Approximately 6 to 10 ml of water soluble iodinated radiocontrast is injected to opacify the biliary tree.
  • The ERCP is both diagnostic and therapeutic. Some therapeutic uses of ERCP are to dilating stenosed biliary or pancreatic ducts, removal of biliary or pancreatic duct stones, opening the sphincter of Vater by cutting to increase narrowing (sphincterotomy), taking tissue sample by brushing or biopsy, or placement of a stent to facilitate bile flow.
  • The MRCP is a non-invasive magnetic resonance imaging exam that visualizes the entire gallbladder, biliary tree, and the pancreatic duct. MRCP is a good alternative for those patients who need biliary imaging, but have renal complications or allergy to iodinated radiocontrast.
  • MRCP has a positive predictive value of 0.95 and a negative predictive value of 0.97 for bile duct stones. Research has shown that about 74% of clinically suspected bile duct stones are proven negative using MRCP, a finding that significantly reduces the risk of unnecessary ERCP. The specificity and sensitivity of MRCP in evaluating the normal pancreatic duct is 98% and 94%, respectively.
  • Pancreatic neoplasm is not seen with ERCP; however, MRCP identifies pancreatic neoplasm nearly 100% of the time and correctly differentiates acute and chronic pancreatitis.
  • The patient should be NPO (nothing-by-mouth) for imaging the biliary tract. Fasting distends the gallbladder and bile ducts and reduces bowel gas that may obscure visualization of portions of the gallbladder. Food may increase the thickness of the gallbladder wall imitating pathological wall thickening. Four hours is sufficient fasting for small children, and 6-8 hours for age 12 to adult. They should be told not to smoke during the fasting period since smoking causes the bile ducts to contract.
  • Ultrasound should be performed before any barium is administered for gastrointestinal (G.I.) imaging, or when the stomach and hepatic flexure is clear of barium is order after G.I. imaging procedure.
  • The gallbladder appears as a pear-shaped structure with thin white walls surrounding a black fluid. The normal gallbladder wall is thin, echogenic and an anechoic lumen, and mild to no posterior enhancement. Bile is near the consistency of water so its acoustic impedance is low, as bile does not attenuate the sound waves. Generally there is no acoustic shadowing posterior to the gallbladder.
  • The nuclear hepatobiliary (IDA) scan, which is also known as cholescintigraphy uses the radioisotope imino diacetic acid (IDA) to image part of the biliary system. In the past the IDA scan has been called the HIDA scan. The scan parameter can include the percentage of bile released with gallbladder contraction, called the ejection fraction.
  • Morphine sulfate (0.04-0.01 mg/kg) intravenously causes constriction of the duodenal papilla. This enhances retrograde flow of bile laden with radiocontrast into the gallbladder when the cystic duct is patent. This shortens the exam time for gallbladder filling. Contraindications to morphine include pancreatitis and morphine allergy.
  • Biliary atresia is the most common obstruction seen in infants and young children. It has two main causes, either congenital or as a result of viral infection shortly after birth. This disorder is caused by progressive distal to proximal obliliteration of the extrahepatic and intrahepatic ducts.



References

  1. James Askew. (2005) A survey of the current surgical treatment of gallstones in Queensland. ANZ Journal of Surgery 75:12, 1086–1089.
  2. Lilian Kow , FRACS. (2004) Magnetic resonance imaging in the diagnosis of choledocholithiasis. ANZ Journal of Surgery 74:8, 618–618
  3. Kejriwal RBBH, Liang JBHB, Anderson GF, Hill A . Magnetic resonance imaging of the common bile duct to exclude Choledocholithiasis. ANZ J. Surg. 2004; 74: 619- 21.
  4. Fuller A . Magnetic Resonance Cholangiopancreatography: is it becoming the study of choice for evaluating obstructive jaundice? J. Clin. Gastroenterol. 2004; 38: 839- 40.
  5. Kawamura, D.A., Diagnostic Medical Sopnography-Abdomen and Superficial Structures Liver, Gallbladder, and Biliary System, 2ND Ed., Lippencott (1997) (PP. 537-572.
  6. Ganong, W.F., Review of Medical Physiology 13th ed., Chapter 26-Regulation of Gastrointestional Function (pp. 441-422), Appleton & Lange, 1987.
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Copyright image Copyright 2007 Nicholas Joseph Jr.






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