Every year, approximately 50,000 infants are born who are under 32 weeks in gestational age and who weigh less than 1,500 g

The Pediatric Patient with Jaundice
Henrietta Kotlus Rosenberg, MD, FACR, FAAP
Englewood, New Jersey, USA
High-resolution real-time ultrasonography (US) serves as an important tool for differentiation of obstructive and nonobstructive causes of jaundice in infants and children, independent of liver function. Unconjugated hyperbilirubinemia occurs in approximately 60% of normal term infants and in 80% of preterm infants. Persistence of neonatal jaundice beyond 2 weeks of age demands US evaluation to differentiate between the three most common causes: hepatitis, biliary atresia, and choledochal cyst. In all three conditions, the hepatic echotexture is diffusely coarse and hyperechoic, but this appearance may be seen in a variety of hepatic inflammatory, obstructive, and metabolic processes. Thus, scintigraphy and at times percutaneous liver biopsy are necessary to narrow the differential diagnosis and to identify patients who require more invasive techniques (e.g. intraoperative cholangiography). US is useful for demonstrating inspissated bile and biliary duct stones. In infants, stones are usually secondary to obstructive congenital anomalies of the biliary tract, total parenteral nutrition, furosemide treatment, phototherapy, dehydration, infection, hemolytic anemia, and short-gut syndrome, whereas in older children, stones are usually associated with sickle cell disease, bowel resection, hemolytic anemia, and choledochal cyst. Jaundice in infants and children may also be due to cirrhosis, benign strictures, and neoplastic processes. Introduction

Unconjugated hyperbilirubinemia is a normal physiologic event that occurs in approximately 60% of normal full-term infants and in 80% of preterm infants. The bilirubin level normally increases by day 2-3 and peaks by day 5-7, reaching as high as 12 mg/dL in normal premature infants by the end of the first week of life. Breast-fed babies may normally have an elevated bilirubin level until the end of the second week of life. However, the onset of jaundice within the first 24 hours of life, rate of rise of serum bilirubin levels greater than 5 mg/dL in 24 hours, direct bilirubin level greater than 1 mg/dL at any time, or the persistence or new onset of jaundice in infants 2 weeks of age or older may no longer be physiologic. In these cases, clinical and laboratory work-up is needed to identify the underlying infectious, metabolic, or structural causes of jaundice for which early therapy might improve outcome. Laboratory work-up may include liver function tests, testing for hepatitis B antigen, TORCH (toxoplasmosis, other [syphilis, hepatitis, zoster], rubella, cytomegalovirus, and herpes simplex [maternal infections]), titers, work-up for sepsis (blood, urine, cerebrospinal fluid), metabolic screening (α-1-antitrypsin phenotype testing, and sweat test. The advent of high-resolution real-time sonography has revolutionized the work-up of jaundice in infants and children. This noninvasive, nonionizing imaging modality is independent of liver function and serves as an important tool for differentiating between obstructive and nonobstructive causes of jaundice and is the imaging modality of choice for screening this patient population. This lecture will present a broad overview of causes of jaundice (congenital, heritable, and acquired) in the pediatric patient and descriptions of the ultrasonographic (US) findings and those of correlative imaging studies when needed. A systematic approach for the US examination of these patients will be discusses. By combining meticulous scanning with a thorough knowledge of the myriad of causes of jaundice in the pediatric patient, the radiologist can help provide an organized approach to the work-up of jaundice and thereby prevent unnecessary tests and facilitate prompt treatment. US Examination
The US evaluation of infants and children with jaundice should consist of a systematic, thorough examination of the right upper quadrant, including the live, bile ducts, gallbladder, pancreas, spleen, and portal vein. The US examination should also cover the entire abdomen and pelvis. Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
The size and texture of the liver should be thoroughly evaluated. The right hepatic lobe should not extend more than 1 cm below the costal margin in a young infant without pulmonary hyperaeration and should not extend below the right costal margin in older infants and children. The normal echotexture of the hepatic parenchyma in the pediatric liver does not differ from that seen in normal adult livers. The echogenicity is normally low to medium and homogeneous, and the peripheral portal venous vasculature is clearly seen. Intra- and extrahepatic biliary ducts should be carefully measured to exclude ductal dilatation. The common bile duct should measure less than 1 mm in neonates, less than 2 mm in infants up to 1 year old, less than 4 mm in older children, and less than 7 mm in adolescents and adults. The gallbladder size and wall thickness should be measured and should not exceed 2-3 mm. A normal gallbladder length is 1.5-3 cm in infants (<1 year old) and 3-7 cm in older children. The length of the gallbladder should not exceed that of the adjacent kidney, assuming the renal length is normal. The gallbladder should also be evaluated for stones, sludge, sludge balls, pericholecystic fluid, and a sonographic Murphy’s sign. The pancreas should be examined for size, echotexture, and evidence of dilatation of the pancreatic duct. The pancreatic head should measure 1.0-2.2 cm; the body 0.4-1.0 cm; and the tail, 0.8-1.8 cm. The size of the pancreas should increase with the child’s age. The normal pediatric pancreas is isoechoic or minimally hyperechoic compared with the liver. The cross-sectional diameter of the pancreatic duct should not exceed 1-2 mm. The spleen size and texture must also be evaluated. The upper limits of normal splenic length ranges from 6.0 cm in infants 0-3 months old to 12.0 cm in females and 13.0 cm in males 12-15 years old. The cross-sectional diameter of the portal vein is a helpful measurement in the diagnosis of portal hypertension. The mean portal vein measurement is 8.5 mm in children less than 10 years of age and 10 mm in patients 10-12 year old. Duplex and color Doppler sonography should be used to determine the presence and direction of flow. A complete duplex and color Doppler examination of the biliary ducts and vessels is essential. A search for collateral channels (varices) and ascites should also be performed. The remainder of the abdomen and pelvis should be thoroughly examined to exclude any evidence of neoplasia or lymphadenopathy. Causes and Diagnosis of Neonatal Jaundice
The three most common causes of jaundice in neonates are hepatitis, biliary atresia, and choledochal cyst. US is the imaging modality of choice for differentiating amongst these conditions. Because some of the US findings of hepatitis and biliary atresia overlap, the differential diagnosis of these entities is discussed in detail. Neonatal Hepatitis
Neonatal hepatitis manifests at 1-4 weeks of age and is seen more commonly in male infants. There are multiple causes of neonatal hepatitis including infections (virus, protozoa, spirochete, toxoplasmosis, rubella, cytomegalovirus, herpes, syphilis), metabolic disorders (α1-antiprypsin deficiency), familial recurrent cholestasis, errors of metabolism such as nesidioblastosis (idiopathic hyperinsulin hypoglycemia of infancy), or idiopathic causes. On sonography, the liver may be normal size or enlarged. The parenchymal echogenicity is increased, with decreased visualization of the peripheral portal venous vasculature. The biliary ductal system is unremarkable with a normal size gallbladder. In cases of severe hepatocellular dysfunction, the gallbladder may be reduced in size because of the decreased volume of bile. In infants with poor biliary excretion and resultant underfilling of the gallbladder, sonographic differentiation between neonatal hepatitis and biliary atresia may be difficult, unless the common bile duct is clearly seen and amenable to accurate measurement. Thus, in unclear cases, Hepatobiliary scintigraphy should be performed to assess whether there is normal bile excretion into the small intestines. Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
Biliary Atresia
Biliary atresia is seen twice as often in male infants as in female infants and is thought to result from inflammation of the Hepatobiliary system. The three types of biliary atresia include: Type I which is a focal extremely rare focal type that is thought to result from an intrauterine vascular insult. Type II is intrahepatic biliary atresia which is uncommon and consists of a paucity of intrahepatic bile ducts. Type III is the extrahepatic type of biliary atresia affecting the common bile duct with the intrahepatic biliary system remaining patent. There are 2 subtypes of Type III. Subtype 1 (perinatal type) which occurs in 66% of cases late in fetal life or postnatally with jaundice developing after regression of the expected physiologic jaundice, a bile duct remnant is seen in the porta hepatis. Subtype 2 (embryonic or fetal type) occurs in 34% of cases, and is suspected when the normal decline in bilirubin levels in the perinatal period does not occur. There is no bile duct remnant in the porta hepatis. Subtype 2 os associated with multiple congenital abnormalities including polysplenia, intestinal malrotation, azygous continuation of the inferior vena cava, symmetric bilobed liver, situs inversus, preduodenal portal vein, anomalous hepatic artery supply, bilobed right lung, and complex heart disease. A spectrum of changes may be seen sonographically in cases of biliary atresia, depending on the type and severity. The liver size may be either normal or increased. As with hepatitis, the echogenicity of the liver parenchyma may be either normal or increased, with decreased visualization of the peripheral portal venous vasculature (a finding suggesting fibrosis). The intrahepatic bile ducts are typically not dilated. A bile duct remnant may be identified in the porta hepatis depending on the type of biliary atresia. A triangular or tubular, echogenic structure may be visualized in the porta hepatis. This finding has been called the ultrasonic “triangular cord” and correlates with fibrous tissue found in the porta hepatis at surgery. This sign is relatively specific for extrahepatic biliary atresia. Although the findings of a normal size gallbladder usually implies neonatal hepatitis, it may also be seen when the atretic common bile duct is distal to the insertion of the cystic duct. The finding of a small (<1.5 cm) gallbladder is non-specific and may be seen with either hepatitis or biliary atresia. Change in gallbladder size after a milk feeding suggests patency of the common hepatic and common bile ducts and is seen only with neonatal hepatitis. A careful search for polysplenia should be made because of its association with biliary atresia in 10-12% of cases. The abdomen should be examined for signs of end-stage liver disease, including ascites, hepatofugal flow in the portal and splenic veins, and collateral venous channels. Hepatobiliary scintigraphy is often indicated to distinguish between neonatal hepatitis and biliary atresia. Patient with Alagille syndrome (arteriohepatic dysplasia) may also present with jaundice in the newborn period and with US findings similar to those of biliary atresia. In these patients, the
histologic analysis reveals paucity and hypoplasia of the interlobar ducts. The presence of associated
congenital anomalies (abnormal facies, butterfly vertebrae, pulmonic stenosis, and complex congenital
heart disease) should help distinguish this entity from biliary atresia.

Differential diagnosis between Hepatitis and Biliary Atresia
Infants with biliary atresia less than 3 months of age typically have a normal hepatic extraction fraction; however, there is no excretion of the radionuclide into the small intestine. In affected infants older than 3 months, hepatic extraction of the radionuclide is decreased and there is no passage of radiopharmaceutical into the small intestine. The presence of small bowel activity excludes biliary atresia as the diagnosis; however, differentiation between biliary atresia and neonatal hepatis is nearly impossible in the absence of small bowel activity when there is poor hepatocellular function. Administration of Phenobarbital before the procedure may be useful in enhancing hepatocellular function in patients with hepatitis, thus allowing small bowel activity to be seen. MR Imaging
MR cholangiopancreatography may also provide useful information for evaluating the patency of intra- and extrahepatic biliary ducts. MR cholangiography uses signal from the bile within the ducts to allow visualization of the biliary system. Therefore, MR imaging is best used to evaluate Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
the extrahepatic biliary system. Complete visualization of the extrahepatic biliary system excludes biliary atresia as a diagnosis. Liver Biopsy
When neonatal hepatitis and biliary atresia cannot be differentiated with imaging studies, percutaneous liver biopsy may be necessary, especially when small bowel activity cannot be demonstrated at Hepatobiliary scintigraphy. In neonatal hepatitis, there are multinucleated giant cells with hepatic parenchymal disruption and relatively little bile within the bile duct canaliculi. In biliary atresia, proliferation of the small intrahepatic bile ducts, periportal fibrosis, and occasionally multinucleated giant cells may be seen. There may be acute or chronic inflammation, degeneration of the duct epithelium, or frank scarring in the extrahepatic biliary remnant. Cholangiography
Cholangiography is indicated when the imaging and pathologic findings suggest the diagnosis of biliary atresia. Cholangiography may be performed percutaneously, endoscopically, or intraoperatively via the gallbladder. When extrahepatic biliary atresia is confirmed intraoperatively, a Kasai portoenterostomy is performed. The best results are achieved in infants who are operated on before 60 days of age, with a success rate of 91%. Dramatically poor results (17% success rate) are seen when surgery is performed beyond 90 days of age because of the presence of cirrhosis. Liver transplantation becomes the only option in these older infants and in babies with intrahepatic biliary atresia. Choledochal Cyst
Choledochal cyst is an uncommon cause of obstructive jaundice. It is more frequently seen in female and Asian infants. Patients may be asymptomatic or may present with any or all of the classic triad of pain, jaundice, and a right upper quadrant mass. There are 3 main types of choledochal cysts. Type I (80-90% of cases) has 3 subtypes: IA, cystic dilatation of CBD, 1B, focal segmental CBD dilatation, and 1C which is fusiform dilatation of the CBD. Type II (2% of cases) is a true choledochal diverticulum. This condition is thought to be related to an abnormal insertion of the common bile duct into the pancreatic duct, which causes reflux of pancreatic enzymes into the pancreatic duct, which causes reflux of pancreatic enzymes into the pancreatic duct. This reflux causes a chemical cholangitis and eventually leads to dilatation of the common bile duct as well as the entire biliary tree. The remaining 2 subtypes of choledochal cysts include Type IV which includes 2 subtypes, IVA, multiple intra-and extrahepatic biliary cysts and IVB, normal intrahepatic bile ducts, multiple extrahepatic biliary cysts; and Type V which consists of Caroli disease. In Caroli disease, there are single or multiple intrahepatic cysts that converge toward the porta hepatis and represent saccular dilatation of the bile ducts. The portal radical may be either partially or completely surrounded by dilated ducts (“central dot sign”), and there may be dilatation of the common bile duct. Hepatic fibrosis, portal hypertension, and polycystic kidney disease are associated. Most patients present as young adults with fever, pain, and transient jaundice. Rarely, patients may present in the neonatal period. Complications of choledochal cysts include cholelithiasis, choledocholithiasis, pancreatitis, At US, choledochal cysts of types I, II, and III appear as a simple cyst in the region of the common bile duct, which can be separated from the gallbladder. The communication with the biliary ductal system must be demonstrated in order to make the diagnosis of choledochal cyst. The intrahepatic ducts may or may not be dilated. Depending on the type of choloedochal cyst, other intrahepatic cysts may or may not be demonstrated. The pancreas and pancreatic duct should be examined for evidence of Pancreatitis or ductal dilatation. Although Hepatobiliary scintigraphy may demonstrate accumulation of radiopharmaceutical within a cyst and lack of passage in the small intestine, at times the choledochal cyst does not fill with the radionuclide and the diagnosis can be missed. Therefore, when a choledochal cyst is demonstrated sonographically, cholangiography should be the next step. MR cholangiography may also be useful in preoperative assessment of these lesions. Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
A choledochal cyst may be confused with several other cystic lesions, including hepatic cyst, enteric duplication cyst, pancreatic pseudocyst, hepatic artery aneurysm, and spontaneous perforation of the common bile3 duct. These entities can all be differentiated with a careful scanning approach and the use of duplex and color Doppler imaging. An enteric duplication cyst most often has the characteristic intestinal signature, the “muscular rim sign”, which consists of a brightly echoic inner rim (mucosa) and a hypoechoic outer rim (muscular layer). Hepatic artery aneurysm may be differentiated with Doppler. Inspissated Bile Syndrome
Inspissated bile syndrome is an uncommon cause of jaundice in neonates. Sludge may be seen within the gallbladder as low-level echoes within the lumen, at times dependent. Inspissated bile is slightly more echogenic but does not cause shadowing. It may also be seen within the biliary ducts associated with partial or complete biliary ductal obstruction. The affected ducts may blend with the surrounding hepatic parenchyma, causing silhouetting of the bile ducts and thus difficulty in determining that the ducts are dilated. Inspissated bile syndrome may be associated with massive hemolysis (Rh incompatibility), hemorrhage (intraabdominal, intracranial, or retroperitoneal), and increased enterohepatic circulation
in various intestinal diseases (Hirschsprung disease, intestinal atresia, and stenoses).

Causes and Diagnosis of Jaundice in Older Children
The multiple causes of jaundice in older children can be divided into primary diseases of the Hepatocellular disease can be subdivided into hepatitis (both acute and chronic) and metabolic. Acute hepatitis may be causes by infection, toxic agents, or drugs. Its US appearance depends more on the severity and stage of disease than on the causative agent. The liver size may be normal or enlarged, with diffuse decrease in the parenchymal echogenicity and brightly echogenic portal venous walls due to edema in the hepatocytes. The gallbladder wall may be diffusely thickened. In patients with chronic active hepatitis, sonograms generally show increased echogenicity of the hepatic parenchyma, with a coarsened echotexture and decreased visualization of the peripheral portal venous vasculature. Metabolic causes of jaundice include Wilson disease, cystic fibrosis, glycogen storage disease, tyrosinemia, and α1-antiprypsin deficiency. The US appearances of all of these disorders are non-specific, with the liver often appearing hyperechoic with decreased visualization of the peripheral portal venous vasculature. The sonographic findings should be correlated with clinical information and laboratory results. At times, liver biopsy may be necessary to confirm the diagnosis. Biliary obstruction resulting in jaundice may be related to neoplasms, benign strictures (rare in children), or stone disease. Hepatic masses are relatively rare in children and account for approximately 5%-6% of all pediatric intraabdominal masses. Although hepatic malignancies are the most common gastrointestinal malignancy in children, they account for less than 2% of all pediatric malignancies. US is the modality of choice for the examination of children suspected of having an abdominal mass. Neoplasms
Hepatoblastoma is the most common primary liver tumor in children and is usually seen in infants and children less than 3 years old. Typically, patients present with a palpable mass, but jaundice, pain, anorexia, or weight loss may be present as well. The mass is typically large, solid, and well defined, with variable echogenicity and often including calcifications. Hepatocellular carcinoma is seen in older children, with a peak prevalence at 12-14 years of age, and less commonly in children less than 4-5 years old. Approximately 50% of children who develop hepatocellular carcinoma have a preexisting liver condition such as hepatitis, glycogen storage disease, tyrosinemia, cirrhosis, hemochromatosis, or α1-antiprypsin deficiency. Hepatocellular carcinoma has variable echogenicity, either hypo-, iso-, or hyperechoic relative to the surrounding liver Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
parenchyma. Calcifications are rare. In the presence of underlying liver disease, the surrounding liver parenchyma may be abnormal. Other hepatic malignancies in children are even more rare and include angiosarcoma, fibrolamellar hepatocellular carcinoma, rhabdomyosarcoma of the biliary tree, undifferentiated embryonal sarcoma, angiosarcoma, rhabdoid tumor, lymphosarcoma, and endodermal sinus tumor. The sonographic appearances of these lesions are nonspecific, and definitive diagnosis is made with biopsy. Infantile hemangioendothelioma is a benign liver lesion seen in young infants. These infants usually present with high output congestive heart failure and may also have thrombocytopenia. These lesions are typically heterogeneous and may be either hypo- or hyperechoic, with calcifications noted in up to 50% of cases. Duplex and color Doppler US evaluation is extremely helpful in demonstrating the vascular components of the mass. Sonography is the ideal imaging modality for serial imaging of these often large masses because they spontaneously involute. Multiple smaller hemangiomas with variable echogenicity (usually hypo- or hyperechoic) may also be demonstrated throughout the liver. These lesions may also resolve spontaneously. Mesenchymal hamartoma most often occurs in children less than 2 years of age and is most often a complex mass with cystic elements and possible calcifications. Hepatocellular adenomas are rare in children but may be seen in patients with glycogen storage disease and Fanconi anemia. These lesions may have variable echogenicity, with the hyperechoic lesions having a well-defined rim of decreased echogenicity. Metastatic disease to the liver may rarely manifest with jaundice. In children, secondary tumors are most often due to neuroblastoma or Wilms tumor, but they may also be seen with leukemia
and lymphoma. Stage IV-S neuroblastoma may manifest with diffuse heterogeneous involvement of
the entire liver, along with a primary adrenal mass, Lymphadenopathy, and bone marrow involvement
but no skeletal metastases.

Cholelithiasis and Choledocholithiasis
Cholelithiasis and choledocholithiasis are uncommon causes of jaundice in children and are even more rare in neonates. Stones are typically brightly echoic shadowing foci, which are freely mobile when located within the gallbladder lumen. Tumefactive sludge is an echogenic, nonshadowing, mobile structure within the gallbladder lumen. Associated intra- and extrahepatic biliary ductal ectasia including the “parallel channel sign” should be looked for. Cholelithiasis in neonates and young infants is usually secondary to predisposing conditions such as obstructive congenital anomalies of the biliary tract; a history of total parenteral nutrition, furosemide treatment, or phototherapy; dehydration; infection; hemolytic anemias; and short-gut syndrome. In older children, causes of biliary stones include sickle cell disease, cystic fibrosis, malabsorption, total parenteral nutrition, Crohn’s disease, intestinal resection, hemolytic anemia, and choledochal cyst. Choledocholithiasis manifests as brightly echogenic shadowing structures within the biliary ducts and is usually associated with ductal dilatation. Hydrops of the gallbladder may manifest as either a mass or pain in the right upper quadrant. The gallbladder is massively distended but has a normal wall thickness. The gallbladder measures more than 3 cm in infants less than 1 year old and more than 7 cm in length in older children and changes from an ovoid shape to a biconvex configuration. Typically, there is no evidence of either intra- or extrahepatic biliary ductal dilatation. The gallbladder distention may be due to thickened bile, which causes transient obstruction, but most commonly results from biliary stasis secondary to dehydration or prolonged fasting. Other conditions associated with gallbladder hydrops include Kawasaki syndrome (mucocutaneous lymph node syndrome), a history of total parenteral nutrition, scarlet fever, sepsis, leptospirosis, ascariasis, typhoid fever, and familial Mediterranean fever. Once the underlying condition is corrected, the hydropic gallbladder may resume its normal configuration. Acute cholecystitis is uncommon in infants and children. As in adults, it may be either calculous or acalculous. Fifty percent of pediatric cases are caused by stones obstructing the cystic duct. Acalculous cholecystitis is often associated with recent surgery, burns, sepsis, debilitation, and prolonged bile stasis with cystic duct obstruction. Cholecystitis is causes by organisms that invade the mucosa of the gallbladder wall and cause inflammation. Complications of acute cholecystitis include gangrene, emphysema, and perforation. Henrietta Kotlus Rosenberg, MD, FACR, FAAP
The Pediatric Patient with Jaundice
In cholecystitis, the gallbladder wall may or may not be thickened (>3 mm); thus, the finding of a positive sonographic Murphy sign is an important observation. It is also important to examine the wall for irregularities that might suggest gangrenous changes, for brighter areas with “dirty” shadowing indicative of emphysema, and for pericholecystic fluid suggestive of perforation. Hepatobiliary scintigraphy may be useful in suspected cases of acute cholecystitis in which the US findings are equivocal. Cirrhosis
Cirrhosis is rare in neonates but may occur in older children and cause jaundice. This chronic destruction of hepatic parenchyma with replacement by fibrosis and nodular regeneration may be caused by chronic hepatitis, congenital hepatic fibrosis, biliary atresia, cystic fibrosis, metabolic disease (Wilson disease, glycogen storage disease, tyrosinemia, galactosemia, α1-antiprypsin deficiency), Budd-Chiari syndrome, and total parenteral nutrition. At US, the right hepatic lobe and medial segment of the left lobe are often small, with compensatory hypertrophy of the lateral segment of the left and caudate lobes. The hepatic echotexture is coarsened and often heterogenous with a nodular parenchymal pattern. There is decreased penetration of the sound beam through the hepatic parenchyma, which contains fibrous tissue and at times multiple regenerating nodules. Secondary signs of cirrhosis, including ascites and portal hypertension, are often seen. Duplex and color Doppler evaluation of biliary vessels is important in pediatric patients with chronic liver disease to establish whether the flow is hepatopedal or hepatofugal in the portal vein and its tributaries, if there are varices and collateral venous channels, if spontaneous portosystemic shunts have formed, if “portalization” of the hepatic veins is evident, and if satisfactory flow is seen in the hepatic artery and inferior vena cava. US plays an indispensable role in the evaluation and follow-up of infants and children with jaundice and in the differentiation of obstructive and nonobstructive jaundice. Without being dependent on ionizing radiation or liver function, US provides important information about liver size and texture, the size and clarity of the biliary ducts, the presence and direction of blood flow in the biliary vessels and collateral channels, and pertinent abnormalities in related organs and other abdominal and pelvic soft tissues. Reference
1. Gubernick JA, Rosenberg HK, Ilaslan H, Kessler A. US Approach to Jaundice in Infants and
Children. RadioGraphics 2000;20:173-195. 2. Teele RL, Share JC. The liver. In: Teele RL, Share, JC, eds. Ultrasonography of infants and children. Philadelphia, Pa: Saunders, 1991;416-451. 3. Bezerra JA, Balstreri WF. Cholestatic syndromes of infancy and childhood. Semin Gastrointest 4. Subramanyam BR, Balthzar EY, Madamba MA, Raghavendra BN, Horii SC, Lefleur RS. Sonography of portosystemic venous collaterals in portal hypertension. Radiology 1982;146:161-166.

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