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1.6 · Pancreatitis
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1
11. Pancreatic abscess is seen as a cavity fi lled with
air–fl uid level, while the pseudocyst is a
fl uid-fi lled cavity without air. Gas is the only
reliable sign for abscess diagnosis in CT (30–50 %)
(
. Fig. 1.6.5 ).
a
12. Juxtapapillary diverticulum is typically found within a
radius of 2–3 cm from papilla of Vater and is seen as a
thin-walled pouch of intestinal dilatation that is fi lled
with air or air–fl uid level (
diagnoses include pancreatic abscess.
b
. Fig. 1.6.8 ). Diff erential
. Fig. 1.6.8 Axial ( a ) and coronal ( b ) abdominal, postcontrast CT images that show duodenal diverticulum ( arrows )
Chronic Pancreatitis
condition and occurs in 4 % of chronic pancreatitis cases.
Focal pancreatitis is considered as carcinoma of the head
Chronic pancreatitis is de ned as prolonged in ammation
of the pancreas that is characterized by irreversible pancreatic damage with brosis, calci cation, and loss of exocrine
and/or endocrine functions. e most common cause is
alcoholism (70 % of cases). Complications of chronic pancreatitis include pancreatic pseudocyst formation, diabetes
mellitus, portal hypertension, and pleuropancreatic stula.
A pleuropancreatic stula is a very rare complication of
chronic pancreatitis characterized by pancreatic ductal disruption with leakage of pancreatic uid not contained by the
in ammatory response of the surrounding tissues in the retroperitoneum or the lesser sac. When the ductal disruption
occurs posteriorly, the pancreatic uid may track through the
retroperitoneum via the aortic hiatus into the mediastinum
and eventually into the pleural space, typically on the le side.
Patients typically present with le -sided isolated pleural e usion. Up to 50 % of these patients may give a previous history
of previous episodes of pancreatitis within the 12 months
preceding this admission. Rare forms of chronic pancreatitis
include:
(a) Focal pancreatitis is an acute pancreatitis that occurs on
top of a chronic pancreatitis causing pancreatic head
focal contour abnormality, common bile duct obstruction, and dilatation (biliary obstruction). It is a rare
of the pancreas when it is seen. It is diagnosed as focal
pancreatitis when the biopsy returns negative for tumor
cells and only in ammatory cells are found. Also, it can
be suspected when pancreatic calci cations are found,
which are not commonly seen in pancreatic tumors
(except in endocrinal pancreatic tumors).
(b) Hereditary pancreatitis is a rare autosomal dominant
cause of chronic pancreatitis characterized by recurrent
attacks of acute pancreatitis, usually since infancy.
Patients present with recurrent attacks of acute
pancreatitis that will progress with time into chronic
pancreatitis in 50 % of patients. Patients with hereditary
pancreatitis have high risk of developing pancreatic
carcinomas (50–60 times greater than normal
population).
(c) Autoimmune pancreatitis (AIP) is a special form of
chronic pancreatitis that can be primary or associated
with other autoimmune disorders (e.g., Sjögren’s
syndrome).
AIP is characterized by (1) elevated serum levels of
autoimmune antibodies (e.g., high ANA titers ); (2)
increased serum γ-globulin or IgG levels; (3) di use or
focal enlargement of the pancreas on US, CT, or MRI
that mimics carcinoma ( focal type ); (4) di use irregular
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Chapter 1 · Gastroenterology
narrowing of the main pancreatic duct; (5) brotic
1
changes of the pancreas with lymphatic in ltration on
histological examination; (6) obstructive jaundice due to
stenosis of the common bile duct; (7) mild symptoms
with the absence of acute attacks of pancreatitis; (8) association with other autoimmune disorders; and (9) good
response to steroid therapy.
Patients with AIP o en present with signs of obstructive jaundice, hypergammaglobulinemia, and type 2 diabetes mellitus (>50 % of patients). Diagnosis is established
by detecting di use or focal narrowing of the main pancreatic duct with focal or di use pancreatic enlargement
in radiological modalities, in association with other two
criteria from the past nine criteria.
(d) Groove pancreatitis , also known as paraduodenal
pancreatitis with duodenal cystic dystrophy , is a rare
form of pancreatitis that arises from ectopic pancreatic
tissues located in the groove between the pancreas and
the duodenum. Patients with groove pancreatitis
present with the same clinical history of the classical
chronic pancreatitis (e.g., alcoholism , recurrent
pancreatitis attacks ). Peptic ulcer is markedly associated
with groove pancreatitis.
Groove pancreatitis is commonly mistaken for pancreatic head carcinoma because of the radiological features and because it is usually associated with mild
elevation in CA19-9 levels ( a marker for pancreatic carci-
noma ). Diagnosis can be suggested radiologically; however, diagnosis has to be con rmed by biopsy, unless the
radiological features and clinical history are so typical.
Two types of groove pancreatitis are distinguished histologically, “pure” and “segmental.” Pure groove pancreatitis is characterized by scarring due to chronic
in ammation that is located exclusively in the space
between the pancreas and the duodenum. In contrast,
the segmental groove pancreatitis is characterized by
scarring of the pancreaticoduodenal groove with a ection of the dorsocranial parts of the pancreas.
(e) Idiopathic brosing pancreatitis ( IFP ) is a rare form of
chronic pancreatitis predominantly seen in childhood
and adolescence with a male predominance. Two major
forms of IFP have been described: the calcifying and the
noncalcifying. e calcifying form is associated with
hereditary or juvenile tropical pancreatitis. e
noncalcifying or obstructive form is less common and
causes pancreatic and biliary duct obstruction. IFP is a
diagnosis that can only be made once other causes of
chronic pancreatitis such as hereditary pancreatitis,
cystic brosis, hypercalcemia, hyperlipidemia,
sclerosing cholangitis, and congenital anomalies of the
pancreatic and biliary trees are excluded. Histologically,
IFP is characterized by di use brosis of the pancreatic
parenchyma, with relative sparing of the islets of
Langerhans and occasional sparing of pancreatic acini.
Diagnosis can be suggested clinically especially if IFP is
associated with other form of multicentric brosis
diseases (e.g., Riedel’s thyroiditis ). Patients with IFP are
typically children or adults presenting with abdominal
pain, obstructive jaundice, passing dark urine, and pale
stool, with normal amylase and lipase levels.
Signs on Plain Radiograph
The presence of calcifi cations within the mid-abdomen at
the region of the pancreas is highly specifi c for chronic
pancreatitis (
a
. Fig. 1.6.9 Plain abdominal radiograph ( a ) and plain axial CT image ( b ) of a patient with chronic pancreatitis showing dense
calcifi cation at the head of pancreas ( arrowheads )
. Fig. 1.6.9 ).
b
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Signs on US
1. There is irregular shape or contour of the pancreas
with atrophic changes of the pancreas (more
hyperechoic due to fat infi ltration).
2. Pancreatic calcifi cations ( seen as hyperechoic clumps
within the pancreas ).
3. Dilatation of the pancreatic duct is the most reliable
sign (>2 mm in width) of chronic pancreatitis.
4. In autoimmune pancreatitis, there is diff use or focal
pancreatic enlargement with hypoechoic texture
(sausage appearance), with complete compression of
the pancreatic duct (of Wirsung).
5. In groove pancreatitis, there is a hypoechoic,
band-like area typically seen between the pancreas
and the duodenum ( represents the infl ammation with
edema ) and duodenal wall thickening with or
without evidence of surrounding infl ammation. The
pancreatic head typically shows enlargement and
hypoechoic texture due to infl ammation and edema.
Signs on CT
1 . Chronic pancreatitis : stigmata in CT include the
presence of pancreatic calcifi cation (50 % of cases)
(
. Fig. 1.6.9 ), pancreatic atrophy due to chronic
infl ammation with fatty infi ltration and fi brosis, and
dilated pancreatic duct with multiple strictures
giving beaded shape appearance (
2 . Autoimmune pancreatitis : it is detected as focal or
diff use pancreatic enlargement with decreased
pancreatic enhancement mimicking pancreatic
adenocarcinoma. The lack of vascular invasion plus
the history of associated autoimmune disease helps
in establishing the diagnosis. However, defi nite
diagnosis requires biopsy.
3 . Groove pancreatitis : because of the chronic
infl ammation and the formation of scar tissue within
the pancreaticoduodenal groove (
groove pancreatitis is classically seen as a triad of a
mass of soft tissue located between the pancreas
head and duodenum with duodenal wall thickening,
cystic changes of the second part of the duodenum’s
wall with or without air–fl uid level, and dilatation of
the proximal part of the common bile duct with or
without intrahepatic biliary radical dilatation due to
distal obstruction by the fi brous mass (
The fi brous mass enhances after contrast injection.
The enhancing fi brous mass, duodenal infl ammation
and cystic changes, and vascular sparing are features
that may be useful in diff erentiating groove
pancreatitis from pancreatic carcinoma. Moreover,
groove pancreatitis shows patchy enhancement in
the portal venous phase, with displacement of the
. Fig. 1.6.10 ).
. Fig. 1.6.11 ),
. Fig. 1.6.12 ).
gastroduodenal artery leftward. In contrast
pancreatic groove carcinoma often shows rim
enhancement because the tumor cells are located
more in the peripheral and the center may show
necrosis, and the gastroduodenal artery is usually
infi ltrated by the mass or located within the mass
rather than displaced.
4 . Idiopathic fi brosing pancreatitis : there is typically
pancreatic mass that mimics carcinoma, with dilated
proximal common bile duct (CBD) due to distal CBD
stenosis or obstruction and dilated intrahepatic
biliary radicals ( mimicking pancreatic carcinoma ). The
pancreatic duct usually is not seen.
. Fig. 1.6.10 Axial abdominal, postcontrast CT image of a
patient with chronic pancreatitis showing massive dilatation of
the pancreatic duct ( arrowhead )
. Fig. 1.6.11 Axial abdominal, postcontrast CT image that
demonstrates the pancreaticoduodenal grove location ( arrow )
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Chapter 1 · Gastroenterology
Ishigami K, etal. Di erential diagnosis of groove pancreatic
1
5 . Pleuropancreatic fi stula : it is seen as a fl uid collection
between the diaphragmatic crus and the posterior
abdominal wall near the aorta, typically on the left
side.
carcinoma vs. groove pancreatitis: usefulness of the portal
venous phase. Eur J Radiol. 2010;47:e95–100.
Ju S, etal. Value of CT and clinical criteria in assessment of
patients with acute pancreatitis. Eur J Radiol. 2006;57:
102–7.
Ketikoglou I, etal. Autoimmune pancreatitis. Dig Liver Dis.
2005;37:211–5.
Khan AZ, et al. Pleuropancreatic stulae: specialist center
management. J Gastrointest Surg. 2009;13:354–8.
Kimot WA, et al. Cholesterolosis in patients with chronic
acalculous biliary pain. Br J Surg. 1994;81:112–5.
Macari M, etal. Duodenal diverticula mimicking cystic neo-
plasms of the pancreas: CT and MR imaging ndings in
seven patients. AJR Am J Roentgenol. 2003;180:195–9.
Schneider A, et al. Hereditary pancreatitis: a model for
in ammatory diseases of the pancreas. Best Pract Res
Clin Gastroenterol. 2002;16(3):347–63.
Sclabas G, etal. Juvenile idiopathic brosing pancreatitis. Dig
Dis Sci. 2002;47(6):1230–5.
Segal D, etal. Acute necrotizing pancreatitis: role of CT-
. Fig. 1.6.12 Axial abdominal, postcontrast CT illustration
that demonstrates the fi ndings of groove pancreatitis
guided percutaneous catheter drainage. Abdom Imaging.
2007;32:351–61.
Siddiqi AJ, etal. Chronic pancreatitis: ultrasound, computed
tomography, and magnetic resonance imaging features.
Semin Ultrasound CT MR. 2007;28:384–94.
Whitcomb DC, etal. Hereditary pancreatitis: new insights,
Signs on MRCP
1. In groove pancreatitis, there is tapering or
obstruction of the distal CBD with proximal CBD
dilatation, with cystic dilatation (>1 cm in diameter)
aff ecting the second part of the duodenum. If cystic
dilatation is <1 cm in diameter, the duodenum
appears thickened only.
2. A pleuropancreatic fi stula is seen as a fl uid signal
fi stula that arises from the pancreatic duct and
ascends superiorly to the mediastinum on coronal
MIP images.
new directions. Baillieres Clin Gastroenterol.
1999;13(2):253–63.
1.7 Jaundice
Jaundice is a clinical condition characterized by yellowish
discoloration of the skin and the conjunctival membrane
over the sclera due to high serum bilirubin level (hyperbilirubinemia). Jaundice comes from the French word jaune ,
meaning yellow.
Mature red blood cells (RBCs) are renewed every 3
months ( life span of RBCs is approximately 120 days ). When
RBCs die due to normal apoptosis or destructed due to
Selected References
Atkdnson GO, etal. Idiopathic brosing pancreatitis: a cause
of obstructive jaundice in childhood. Pediatr Radiol.
1988;18:28–31.
Balci NC, etal. Juxtapapillary diverticulum. Findings on CT
and MRI.J Clin Imaging. 2003;27:82–8.
Bollen TL, etal. Updates on acute pancreatitis: ultrasound,
computed tomography, and magnetic resonance imaging
features. Semin Ultrasound CT MR. 2007;28:371–83.
Delrue LJ, etal. Acute pancreatitis: radiologic scores in pre-
senting severity and outcome. Abdom Imaging.
2010;35:349–61.
Harb R, etal. Idiopathic brosing pancreatitis in a 3-year-old
girl: a case report and review of the literature. J Pediatr
Surg. 2005;40:1335–40.
hemolysis, the cellular content of the RBCs including hemoglobin is released into the bloodstream and engulfed by macrophages in the reticuloendothelial system ( liver, spleen, and
bone marrow ). Macrophages degrade the hemoglobin into
the globulin (protein) portion and the heme portion. e
globulin is further degraded into amino acids and plays no
portion in jaundice. e heme molecule is converted rst
into biliverdin, a green color pigment, by oxidation, and then
into bilirubin, which is a yellow color pigment, by reduction.
e newly formed bilirubin is insoluble in water (unconjugated/indirect) and requires a special transport mechanism
to reach the liver for further modi cation. Albumin molecules serve as a carrier for the unconjugated bilirubin to the
liver by binding to unconjugated bilirubin creating a bilirubin–albumin complex in the intravascular compartment.
is bilirubin–albumin complex retains the yellowish
1.7 · Jaundice
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bilirubin pigment within the plasma. e albumin-binding
capacity is reduced when the serum albumin is reduced (e.g.,
hypoalbuminemia ), when albumin capacity is diminished by
competition of other organic anion (e.g., sulfonamides ,
salicylate ), and when albumin a nity is diminished by acido-
sis.
When the unconjugated bilirubin reaches the liver, the
free bilirubin molecules are taken up by the hepatocytes and
bind to special proteins within the hepatocytes called Y
(ligandin) and Z proteins. ese proteins are responsible for
aggregating bilirubin molecules within the hepatocytes for
conjugation. Ligandin is the preferential bilirubin-binding
protein at low bilirubin concentration, whereas Z protein
becomes more important binding protein as bilirubin concentration increases. Conjugation of bilirubin takes place
within the endoplasmic reticulum, which is a process characterized by changing the chemical properties of bilirubin to be
water soluble (conjugated) instead of lipid soluble (unconjugated). e bilirubin is converted to bilirubin glucuronide by
the action of the enzyme uridine 5- diphosphateglucuronosyl
transferase (UDPG-T).
e conjugated bilirubin is actively excreted by the hepatocytes to the biliary sinusoids in the liver, which in turn
drain the bile into the biliary tree. A part of the conjugated
bilirubin is stored in the gallbladder and a part enters the
duodenum via ampulla of Vater. e conjugated bilirubin is
converted to urobilinogen by the intestinal bacterial ora. A
part of urobilinogen is reabsorbed by the intestine and enters
the portal system back to the liver to complete the bilirubin
intestinal–hepatic cycle, and the rest is excreted in the stool
giving the stool its brown pigment. When the urobilinogen
reaches the liver, it is further excreted from the body later via
the kidneys into the urine. ere is no intestinal absorption
of conjugated bilirubin.
A group of disorders and rare hereditary syndromes
results from disturbance of one or two steps in the bilirubin
metabolism mechanism described above. Some of these conditions are benign and some are fatal as the following:
1 . Neonatal jaundice is a term used to describe jaundice in
neonates a er birth that arises when the binding capacity
of the albumin is exceeded. Also, the amount of Z protein
in the liver a er birth is comparable to that in the adult,
but adult levels of ligandin are not attained until several
weeks a er birth. Both previous factors contribute to the
development of the physiological jaundice in neonates.
e condition is self-limited and lasts 8 days in normal
births and approximately 14 days in premature births.
2 . Gilbert syndrome is a rare disease characterized by
isolated serum unconjugated hyperbilirubinemia (usually
up to 6.0mg/dL). e other liver serum biochemical tests
are normal. e unconjugated hyperbilirubinemia can be
precipitated by fatigue, alcohol consumption, stress
situations, and diseases like in uenza. e disease a ects
1 % of the population. Gilbert syndrome is believed to be
caused at least by the de ciency of ligandin and Z
proteins in hepatocytes. e serum unconjugated
hyperbilirubinemia is reduced by phenobarbital therapy.
3 . Crigler–Najjar syndrome is a very rare disease
characterized by complete or partial absence of the
enzyme UDPG-T, which is responsible for bilirubin
conjugation within hepatocytes. Neonates with Crigler–
Najjar syndrome present with severe serum
unconjugated hyperbilirubinemia that o en leads to
kernicterus. e disease is classi ed into type I and type
II.Type I Crigler–Najjar syndrome is the most severe
type and it is due to the complete absence of the enzyme
UDPG-T action, and serum unconjugated
hyperbilirubinemia is not responsive to phenobarbital
therapy. In contrast, type II Crigler–Najjar syndrome
arises due to partial absence of the enzyme UDPG-T
action, and serum unconjugated hyperbilirubinemia is
reduced by phenobarbital therapy. Type I Crigler–Najjar
syndrome is inherited as autosomal recessive, whereas
type II Crigler–Najjar syndrome is inherited as
autosomal dominant.
4 . Lucey–Driscoll syndrome is a rare disease characterized
by serum unconjugated hyperbilirubinemia due to
inhibition of the enzyme UDPG-T action in neonates
due to serum factor coming from mother’s breast milk.
Infants become jaundiced when breastfed with their
mother’s milk but recover on withdrawal from
breastfeeding.
5 . Dubin–Johnson syndrome is a rare, autosomal recessive
disease characterized by serum conjugated
hyperbilirubinemia due to congenital abnormality in the
active conjugated bilirubin excretion from the
hepatocytes to the biliary canaliculi. e disease also is
characterized by deposition of a melaninlike pigment
within the liver causing the liver to be dark in gross
examination. Patients’ laboratory tests show conjugated
hyperbilirubinemia plus mild elevation in liver enzymes.
ere are no purities or steatorrhea.
6 . Rotor syndrome is a rare variant of Dubin–Johnson
syndrome characterized by serum conjugated
hyperbilirubinemia with the absence of purities or
steatorrhea. Unlike Dubin–Johnson syndrome, there is
no melaninlike pigment deposition within the liver.
Approximately 4mg/kg of bilirubin is produced every
day. e normal serum level of bilirubin is 0.5mg/dL.Serum
bilirubin level must exceed 1.5mg/dL for the yellowish coloration to start visible on the patient. Jaundice itself is not a
disease but rather a sign of an underlying condition.
Conditions that predispose to jaundice can be categorized
into three main categories:
1 . Prehepatic jaundice : this type of jaundice arises due to
increase rate of hemolysis with increased production of
unconjugated bilirubin. Prehepatic jaundice is typically
seen in hemolytic anemia, malaria, glucose-6-phosphate
dehydrogenase de ciency, rat fever (leptospirosis), and
hemolytic uremic syndrome. ere is increased serum
unconjugated bilirubin level with normal urinary color
and bilirubin concentration, stool color, and serum liver
enzymes.
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Chapter 1 · Gastroenterology
2 . Hepatic jaundice : this type of jaundice arises due to
1
hepatocyte disease or liver enzyme failure. Hepatic
jaundice is typically seen in hepatitis, hepatic failure, liver
cirrhosis, Gilbert’s syndrome, Crigler–Najjar syndrome,
and Niemann–Pick disease type C.Laboratory
investigations show abnormal liver enzyme pro le and
increased urinary urobilinogen level.
3 . Posthepatic jaundice : this type of jaundice arises due to
interruption to the drainage of the bile within the biliary
tree. Posthepatic jaundice is typically seen in biliary
gallstones (choledolithiasis), carcinoma of the pancreatic
head, cholangiocarcinoma, biliary atresia, and Mirizzi
syndrome. Laboratory investigations show
hypercholesterolemia, abnormal liver enzyme pro le,
and increased urinary urobilinogen level. Patients may
present with purities due to the neuronal irritation of the
dermal nerve endings by the urobilinogen in the skin.
Radiological modalities can be used as tools to de ne the
cause or asses complications of jaundice. e following discussed diseases show well-documented radiological signs
that can be looked for in assessing a patient with jaundice.
Kernicterus
Kernicterus is a pathological condition characterized by choreoathetoid cerebral palsy, hearing loss, and mental retardation due to bilirubin accumulation in the subthalamic
nucleus, hippocampus, globus pallidus, putamen, cranial
nerves ( especially III, IV, and VI ), and thalami.
Up to 50 % of patients with kernicterus die, while survivors develop bilirubin encephalopathy with the previous
described manifestations. In the early form of the disease,
symptoms may mimic sepsis, asphyxia, or hypoglycemia.
Signs on MRI
On T2W and FLAIR images, there is typically high signal
intensity observed in the globus pallidus bilaterally ( the
preferential site of bilirubin deposition in the brain )
(
. Fig. 1.7.1 ). Diff erential diagnosis of this MRI fi nding
includes carbon monoxide poisoning, hypoglycemia,
and hypoxia.
. Fig. 1.7.1 Axial, T2W MR illustration that demonstrates the
brain fi ndings in kernicterus. Diff erential diagnoses of such a
sign include carbon monoxide poisoning, hypoglycemia, and
hypoxia
Obstructive Jaundice
Obstructive jaundice is a clinical condition characterized by
systemic jaundice due to extrahepatic biliary duct drainage
obstruction, with subsequent dilatation of the intrahepatic
biliary tree radicals. e most common causes of obstructive
jaundice are choledocholithiasis (bile ducts stones), pancreatitis, carcinoma of the ampulla of Vater, and choledochal
cyst. Choledocholithiasis is found in approximately 15 % of
patients undergoing cholecystectomy and usually results
from migration of stones from the gallbladder to the
CBD. Predisposing factors for choledocholithiasis include
female sex, obesity, and older age.
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Signs on US
Cholestasis or intrahepatic biliary dilatation is diagnosed
when the intrahepatic biliary radicals show dilatation
(>2 mm in diameter) (
. Figs. 1.7.2 and 1.7.3 ).
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1
. Fig. 1.7.2 Ultrasound liver image that shows dilatation of
the main left hepatic duct ( LHD ) and right hepatic duct ( RHD )
( arrowheads ) in a patient with obstructive jaundice
a
b
. Fig. 1.7.3 B-Mode ( a ) and Doppler ( b ) ultrasound liver image of a patient with obstructive jaundice that
shows dilatation of the intrahepatic biliary radicals and main duct with a biliary stone detected inside the
intrahepatic bile duct ( arrow )
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Chapter 1 · Gastroenterology
BPS typically occurs in the absence of any anatomical
1
Signs on CT and MRI
1. The key radiological sign of obstructive jaundice is
intrahepatic biliary plus extrahepatic biliary
dilatation (
2. The presence of gallbladder mild of calcium or stones
further strengthens the diagnosis of obstructive
jaundice due to choledocholithiasis (
3. Signs of pancreatitis or carcinoma in the second part
of duodenum may be detected.
4. Choledochal cyst is diagnosed by the presence
of cystic lesion within the porta hepatis or within
the CBD.
. Fig. 1.7.4 ).
. Fig. 1.7.4 ).
abnormalities of the extrahepatic bile ducts. Newborns with
BPS present with hepatomegaly, jaundice, and conjugated
hyperbilirubinemia.
Signs on US
BPS is commonly associated with enlarged gallbladder
full of sludge observed in 20–30 % of ill newborns with
jaundice and history of maternal Rh and ABO blood
group incompatibility.
. Fig. 1.7.4 Axial liver CT postcontrast illustration that
demonstrates the fi ndings in pyogenic cholangitis; the image
illustrates dilatation of the internal biliary radicals with wall
contrast enhancement ( arrowhead ) and the presence of biliary
stones inside the dilated biliary ducts ( arrow )
Signs on MRCP
1. The CBD is dilated (>10 mm in diameter) with a
fi lling defect inside the CBD representing stone if
the cause of the obstructive jaundice is
choledocholithiasis.
2. Choledochal cyst is detected as cystic dilatation of
the CBD or the biliary radicals at the porta hepatis.
Bile Plug Syndrome
Infectious Ascending Cholangitis
Infectious ascending cholangitis (IAC) is a condition characterized by in ammation of the extra- and intrahepatic bile
duct dilatation due to infections, usually accompanied by the
formation of infected, brown bile duct stones (choledocholithiasis). e main pathology in IAC is related to bile stasis,
usually due to a stone, with superimposed infection
Patients with IAC typically present with right upper
quadrant pain, fever, and jaundice ( Charcot’s triad ), may be
in association with confusion and hypotension ( Reynold’s
pentad ). Other symptoms include abdominal pain and discomfort and chills. IAC commonly a ects male between 20
and 40 years of age. Suppurative cholangitis refers to the pres-
ence of pus within the biliary tree. Di erentiation between
suppurative and nonsuppurative cholangitis is crucial as the
former requires urgent medical or surgical decompression.
Discrimination can be established by CT.
Oriental cholangitis , also known as recurrent pyogenic
cholangitis , is a rare disease characterized by recurrent or
chronic infection of the bile ducts. e disease is usually
found in Asian countries and arises due to parasitic infection
with Clonorchis sinensis (Clonorchiasis).
Signs on US
1. There is dilatation of the intrahepatic biliary ducts
(>2 mm) (
2. Stones may be found within the intrahepatic ducts
(
. Fig. 1.7.3 ).
3 . Suppurative pyogenic cholangitis : the CBD is dilated
(>10 mm) and may show internal sludge, and the portal
vein may show internal echoes due to thrombosis.
. Fig. 1.7.2 ).
Bile plug syndrome (BPS) is a disease characterized by extrahepatic biliary obstruction by inspissated pigmented bile
sludge; BPS was rst described in infants with maternal Rh
and ABO blood group incompatibility, complicated by massive hemolysis. BPS can occur also in certain systemic conditions such as dehydration, hemolysis, and increased
enterohepatic circulation in various intestinal diseases like
Hirschsprung’s disease, intestinal atresias, and stenoses.
Signs on CT and MRI
1. Typical imaging features of infectious ascending
cholangitis include dilatation of the intra- and
extrahepatic biliary ducts, thickening of the
intrahepatic biliary radical walls with enhancement,
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and the presence of stones within the biliary radicals
(
. Fig. 1.7.4 ). In the arterial phase of the liver scan,
the liver may show heterogeneous parenchymal
enhancement that may disappear in the portal or
equilibrium phase; this heterogeneous enhancement
is seen as patchy, nodular, geographical, or
wedge-shaped parenchymal enhancement
(
. Fig. 1.7.5 ). This fi nding is often seen in
suppurative cholangitis. The mechanism of this
heterogeneous enhancement is related to the
presence of arterioportal shunt, which can be also
observed in other conditions like Budd–Chiari
syndrome, hepatic congestion, acute cholecystitis,
hepatic tumors, or hepatic abscesses.
2. In suppurative cholangitis, the duodenal papilla
shows bulging into the second part of the
duodenum and enhancement in a ringlike pattern
(papillitis) due to the presence of pus within the
CBD. This fi nding is characteristic to suppurative
cholangitis and helps diff erentiating suppurative
from nonsuppurative cholangitis.
. Fig. 1.7.5 Axial liver CT arterial-phase, postcontrast
illustration that demonstrates heterogeneous, patchy, nodular,
geographical, or wedge-shaped liver parenchymal
enhancement due to arterial shunting; this fi nding can be seen
in pyogenic cholangitis among other diff erentials ( see text )
Choledochal Web
Choledochal web is de ned as the presence of a mucosal
web within the CBD that results in intermittent obstructive jaundice in neonates and children. Choledochal web is
a rare cause of childhood intermittent jaundice. Obstructive
jaundice may develop due to biliary sludge formation, mucus
plugs, and choledocholithiasis.
Signs on MRCP
Choledochal webs are detected as thin horizontal
intraductal linear structures within the CBD with
dilatation of the extra- and intrahepatic biliary radicals.
Selected References
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mogenous enhancement of the liver. AJR Am J Roentgenol.
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Bader TR, etal. MR imaging ndings of infectious cholangi-
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Badley BWD. A physiological approach to jaundice. Clin
Biochem. 1976;9(3):144–8.
Brown DM, etal. Bile plug syndrome: successful manage-
ment with mucolytic agent. J Pediatr Surg. 1990;25:251–2.
Cebecauerova D, etal. Dual hereditary jaundice: simultane-
ous occurrence of mutations causing Gilbert’s and DubinJohnson syndrome. Gastroenterology. 2005;129:315–20.
Germiller JA, et al. Early presentation of choledocal cyst
transiently obstructed by an impissated bile plug. J Pediatr
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Hawes DA, etal. Imaging of the biliary sump syndrome. AJR
Am J Roentgenol. 1992;158:315–9.
Kirks DR, etal. An imaging approach to persistent neonatal
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Lee NK, etal. Discriminating of suppurative cholangitis from
nonsuppurative cholangitis with computed tomography
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Mavrogiannis C, etal. Sump syndrome: endoscopic treat-
ment and late recurrence. Am J Gastroenterol.
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cholestasis: assessment with magnetic resonance cholangiography and fast MRI. Abdom Imaging. 2004;29:
87–99.
Muhletaler CA, etal. Diagnosis of obstructive jaundice with
nondilated bile duct. AJR Am J Roentgenol.
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Nazer H, etal. Crigler-Najjar syndrome in Saudi Arabia. Am
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Parekh HP, etal. Recurrent pyogenic cholangitis. Eur J Radiol
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Shah Z, etal. MRI in kernicterus. Aust Radiol. 2003;47:55–7.
Shanser JD, et al. Computed tomographic diagnosis of
obstructive jaundice in the absence of intrahepatic ductal
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54
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Chapter 1 · Gastroenterology
1
1.8 Diarrhea and Malabsorption
Diarrhea is de ned as passing loose stool >200g/day. Chronic
diarrhea is de ned as diarrhea that persists >4 weeks, while
severe diarrhea is de ned as passing loose stool more than 6
times/day. Pathological diarrhea with serious cause is usually
nocturnal, is associated with weight loss, contains bloody
content, and is accompanied by fever. Lesions to the small
intestine cause large volume watery diarrhea, whereas large
intestine lesions cause small volume diarrhea with bloody or
mucus contents.
Malabsorption syndrome is a term used to describe a
group of disorders characterized by defective absorption of
the main food elements ( carbohydrates, fat, and proteins )
from the small intestine, resulting in the passage of bulky,
fatty, and foul-smell stool. Malabsorption syndrome can be
due to:
1 . Sprue group : including celiac disease and tropical sprue
2 . Constitutional diseases : like Whipple’s disease,
scleroderma, and diabetes mellitus
3 . Small bowel diseases : like intestinal lymphangiectasia
4 . Surgical operations : like subtotal gastrectomy and small
bowel resection
Normal Anatomy
e cells of the small and the large intestine can be divided
into three main functional cells:
1 . Absorptive epithelial cells are composed of columnar epi-
thelium that is found in the intestinal villi and absorb
sodium, chloride, and nutrients. Generally, water absorption follows sodium absorption (up to 95 %).
2 . Secretory cells are composed of goblet cells that are found
in the intestinal crypts of Liberkühn and secrete chloride
and bicarbonate in the intestine and chloride,
bicarbonate, and potassium in the colon. Mucus is the
largest component of colonic secretion by goblet cells,
which protects the colonic epithelium from the fecal
material.
3 . Enterochroma n cells are endocrine cells that secrete
multiple neurotransmitters and endocrine peptides; they
are found in the crypts of Liberkühn in the small
intestine and colon. ese cells are found in the small
intestine only, not in the colon.
Pathophysiology
Diarrhea is divided generally into two main types, watery and
osmotic. Watery diarrhea arises due to increased chloride
secretion, low sodium absorption, and increased intestinal
motility. In contrast, osmotic diarrhea arises due to ingestion
of osmotic, nonabsorbable material (e.g., excess vitamin C
intake diarrhea ) or the absence of brush-border enzyme
required for digestion of food (e.g., lactose intolerance ).
ree mechanisms of diarrhea have been described:
1 . Abnormal intestinal motility : the enteric nervous system
supplies the nervous supply to the smooth muscles in the
intestinal and colonic walls. In ammation of the neurons
of the enteric system causes dysfunction of the intestinal
wall’s muscle movement, causing diarrhea or constipation. In intestinal in ammation, many in ammatory
mediators such as serotonin , acetylcholine , histamine , sub-
stance P , opioids , and dopamine act like neurotransmitters
for the enteric nervous system, augmenting the diarrhea
e ect by increasing intestinal motility.
2 . Decreased absorption : any pathological condition that
impedes the function of the absorptive cells in the small
intestine will cause elevated water ux into the colon.
When this water ux exceeds 4.5l/day, diarrhea arises.
Decreased absorption of sodium or other osmolar
metabolites (e.g., lactose ) can induce diarrhea by drawing
the water from the blood in the intestinal walls into the
lumen, increasing the water ux into the colon. Common
osmolar agents that cause diarrhea include bile acids and
their bacterial metabolites, gluten from wheat (celiac
disease), and ascorbic acid (vitamin C).
3 . Increased secretion : this mechanism involves increased
secretion of chloride into the colonic lumen, which will
cause drawing of water from the blood in the colonic
wall into the colonic lumen, causing diarrhea. Any
pathological condition that increases chloride secretion
in the colon will cause “secretory diarrhea.” Chloride
secretion is increased by any pathological process that
increases “cyclic nucleotides” (cAMP and cGMP) and/or
“intracellular calcium” levels in the colonic cells, which
will open the “cystic brosis transmembrane
conductance regulator” (CFTR). Vasoactive intestinal
peptide (VIP) is a molecule that works as a
neurotransmitter causing increased chloride channel
opening by raising cyclic AMP within the colonic and
intestinal secretory cells; this form of diarrhea can be
seen due to pancreatic neuroendocrine tumor (VIPoma).
Common Causes of Diarrhea and Their
Mechanism of Action
1 . Cholera : cholera toxin also causes secretory diarrhea via
raising cAMP in the secretory cells, like VIPoma.
2 . Celiac disease : the gluten from the wheat is converted by
the intestinal bacteria into a toxic metabolite called
“gliadin.” Gliadin causes in ammatory destruction of the
intestinal villi, reducing absorption and causing osmotic
diarrhea.
3 . Food allergy : food allergy causes the release of histamine,
which raises cAMP in secretory cells causing secretory
diarrhea.
4 . Short bowel syndrome : bile salts are absorbed in the
terminal ileum and the ileocecal valve. Any disease that
a ects the terminal ileum (e.g., Crohn’s disease ,
tuberculosis , ileocecal valve syndrome ) will cause
reduction of bile salt absorbance, causing bile salts to
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