Obstructive jaundice

Katatwire Jr.
MD
2
 Introduction
• Biliary obstruction refers to the blockage of any duct that carries
bile from the liver to the gallbladder or from the gallbladder to the
small intestine. This can occur at various levels within the biliary
system.
• The major signs and symptoms of biliary obstruction result directly
from the failure of bile to reach its proper destination.
• Jaundice (derived from French word ‘jaune’ for yellow) or icterus
(Latin word for jaundice) is a yellowish staining of the skin, sclera
and mucous membranes by deposition of bilirubin (a yellow orange
bile pigment) in these tissues.
 Cont……….
• Clinically apparent when the bilirubin level exceeds 2mg/dl(34.2
μmol/L).
• Fair skin patients; most noticeable on the face, trunk, and sclerae;
• Dark-skinned patients; noticeable on the hard palate, sclerae, and
conjunctivae.
• Pseudo - jaundice may be found in black patients with pigmented
sclera, from carotinemia, uraemia (a sallow yellowish pallor), and
quinacrine (a yellow-green colour).
• The first sign of jaundice is scleral icterus (appears when the
serum concentration of bilirubin exceeds 25mg/L= 42.75umol/L).
 Cont…….
• If serum bilirubin level continues to increase jaundice
represents at skin (more than 50 mg/L).
• Jaundice is not a disease but it is a sign of other diseases.
• The urine becomes dark for the presence of conjugated bilirubin.
• The stool becomes white (aholic), because bile is absence in
intestine.
• The skin itching usually follows after jaundice.
 Definition;
• The term “obstructive jaundice” implies the partial or complete
obstruction of the flow of bile and its components into the
intestinal tract resulting in yellowish staining of the skin, sclera and
mucous membranes by deposition of bilirubin.
• The normal bilirubin levels in serum is 0.2-1.2mg/dl
• Jaundice is clinically recognizable when the serum levels rise to at
least 3mg/dl
 Surgical Anatomy of the Hepatobiliary
system
• An accurate knowledge of the anatomy of the liver and biliary tract,
and their relationship to associated blood vessels is essential for the
performance of hepatobiliary surgery because wide anatomic
variations are common.
• The classic anatomic description of the biliary tract is only present
in 58% of the population.
• The liver, gallbladder, and biliary tree arise as a ventral bud (hepatic
diverticulum) from the most caudal part of the foregut early in the
fourth week.
 Cont…..
• This divides into two parts as it grows between the layers of the
ventral mesentery: the larger cranial part (pars hepatica) is the
primordium of the liver, and the smaller caudal part (pars cystica)
expands to form the gallbladder, its stalk becoming the cystic duct.
• The initial connection between the hepatic diverticulum and the
foregut narrows, thus forming the bile duct.
• As a result of the positional changes of the duodenum, the entrance
of the bile duct is carried around to the dorsal aspect of the
duodenum.
• The biliary system can be broadly divided into two components, the
intra-hepatic and the extra-hepatic tracts.
 Cont……
• The secretory units of the liver (hepatocytes and biliary epithelial
cells, including the peribiliary glands), the bile canaliculi, bile
ductules (canals of Hering), and the intrahepatic bile ducts make up
the intra-hepatic tract while the extrahepatic bile ducts (right and
left), the common hepatic duct, the cystic duct, the gallbladder, and
the common bile duct constitute the extra-hepatic component of
the biliary tree.
 Cont…..
• The cystic and common hepatic ducts join to form the common bile
duct. The common bile duct is approximately 8 - 10 cm in length
and 0.4 - 0.8 cm in diameter.
• The common bile duct can be divided into three anatomic
segments: supraduodenal retroduodenal, and intrapancreatic.
• The common bile duct then enters the medial wall of the
duodenum, courses tangentially through the submucosal layer for 1
to 2 cm, and terminates in the major papilla in the second portion
of the duodenum.
 Cont…..
• The distal portion of the duct is encircled by smooth muscle that
forms the sphincter of Oddi. The common bile duct may enter the
duodenum directly (25%) or join the pancreatic duct (75%) to form
a common channel, termed the ampulla of Vater.
• The biliary tract is supplied by a complex vasculature called the
peribiliary vascular plexus. Afferent vessels of this plexus derive
from hepatic arterial branches, and this plexus drains into the portal
venous system or directly into hepatic sinusoids
 Bilirubin Metabolism
• Bile is a substance produced in the liver and contains bile salts,
water, cholesterol, electrolytes, and bilirubin, which is a
breakdown product of hemoglobin.
• The formation of bilirubin from heme is essential for mammalian
life, because it provides the body with the main means of
elimination of heme.
• 80% of the circulating bilirubin is derived from heme of hemoglobin
from senescent red blood cells destroyed in the
reticuloendothelium of the bone marrow, spleen, and liver.
 Cont…….
• 10-20% of the bilirubin comes from other sources such as
myoglobin, cytochromes, and other heme containing proteins
processed in the liver.
• Bilirubin is the result of haem breakdown.
• Initially, heme(red compound) is oxidized at the alpha position to
the green pigment biliverdin by the enzymes heme oxygenase
and heme reductase, which is then reduced at the gamma position
to orange bilirubin by biliverdin reductase.
 Cont…….
• Circulating bilirubin is bound to albumin, since it is insoluble in
aqueous solutions.
• The bilirubin-albumin complex enters hepatic sinusoidal blood,
where it enters the space of Disse through the large sinusoidal
fenestrations.
• The bilirubin-albumin complex is disassociated in this space.
• Free bilirubin is then internalized into the hepatocyte, where
it is conjugated to glucuronic acid. ……. The concept and role of
glucuronosyltransferase.
 Bilirubin formation
120ds Iron
RBCs Senecent RBCs
hemoglobin
Globin
Chiefly
70+% R
Bilirubin Biliverdin C heme
CBR MHO

Bilirubin 20%
nonhemoglobin heme
Hepatic Hemoproteins
nonhemoglobin hemoprotein

1-5%

Premature destruction of newly formed RBCs

 Transport of Bilirubin in Plasma
Albumin + UB UB ~ Albumin Complex

H affinity binding sites

2:1 Bilirubin
Molar Plasma protein
Ratio Albumin
L affinity binding sites
>2:1 Bilirubin

Other organic anions

can be replaced by
PH UB
 Hepatic Bilirubin Transport
1. Hepatic uptake of Bilirubin
UCB~Albumin Complex Separated

Bilirubin(be) taken up
Plasma membrane of the liver
MTA (receptor ?)
2.Conjugation of Bilirubin

ligation (Y protein)
(be) bound to carrier transfer
UCB ER
protein
(lipid soluble) Conjugation
Z protein (catalized by
UDPGT)
CB CBGA
3.Biliary Excretion of Bilirubin
(water soluble)

Transfer across
CB Bile canaliculus
Microvillar membrane
• UDPGT: Uridine Diphosphate Glucuronyl Transferase
• UCB: because of its tight albumin binding and lipid solubility, it
is not excreted in urine.
• CB: is less tightly bound to albumin and is water soluble, so it is
filtered at the glomerulus and appears in the urine.
 Entero-hepatic circulation
T be degraded
CB B and I Urobilinogens (coloress)
Bacterial Enzymes

feces (fecal urobilinogens) 50-200 mg/d

mostly
re-excreted excreted
90% liver Bile feces
20% Reabsorbed plasma
trace
circulation kidneys

4 mg/d urine urobilinogen

•The serum of normal adults contains 1 mg of bilirubin per 100 ml.

•In healthy adults The direct fraction is usually <0.2 mg/100 ml
The indirect fraction is usually <0.8 mg/100 ml
 Cont…..
• The processing of the serum bilirubin load by the hepatocytes occurs in
four steps. These are: uptake, cytosolic binding, conjugation, and
secretion.
• Hepatic uptake of bilirubin occurs with the dissociation of the albumin-
bilirubin complex facilitated by plasma membrane proteins with
subsequent translocation of bilirubin into the hepatocyte through a
saturable protein carrier, which also binds other organic anions, but
not bile salts.
• In the hepatocytes, bilirubin binds to two cytosolic proteins: ligandin
and Z protein. The binding limits the reflux of bilirubin back to the
plasma and delivers it to the endoplasmic reticulum for conjugation.
• Conjugation of bilirubin involves its esterification with glucuronic acid
to form, first, a monoglucuronide, then a diglucuronide.
 Cont…..
• The principal enzyme involved is uridine diphosphate (UDP)-
glucuronyl transferase.
• Conjugation renders bilirubin water-soluble and is essential for its
elimination from the body in bile and urine.
• Most of the conjugated bilirubin excreted into bile in humans is
diglucuronide with a lesser amount of monoglucuronide.
• Secretion of conjugated bilirubin from the hepatocyte to the bile
canaliculi involves a specific carrier and occurs against a
concentration gradient.
 Cont……..
• Conjugated bilirubin is then secreted in an energy-dependent
fashion into canalicular bile against a large concentration gradient.
• Bilirubin is then secreted with bile micellar complex with
cholesterol, phospholipids, and bile salts, through the biliary and
cystic ducts to enter the gallbladder, where it is stored or it passes
through Vater’s ampulla to enter the duodenum.
• Inside the intestines, some bilirubin is excreted in the stool, while
the rest is metabolized by the gut into the gastrointestinal tract.
 Cont…….
• Within the gastrointestinal tract, bilirubin is deconjugated by
intestinal bacteria to a group of compounds known as
urobilinogens……. there, colonic bacteria deconjugate and
metabolize the bilirubin into colourless urobilinogens, which can be
oxidized to form urobilin and stercobilin……. these give stool its
characteristic brown color.
 Cont……..
• These urobilinogens are further oxidized and reabsorbed into
the enterohepatic circulation and secreted into bile.
• A trace (~1%) of the urobilinogen is reabsorbed into the
enterohepatic circulation to be re-excreted in the bile: some of this
is instead processed by the kidneys, coloring the urine yellow.
• It is these oxidized urobilinogens that account for the coloured
compounds that contribute to the yellow color of urine and the
brown color of stool.
 Cont……
• A number of disorders can result in a serum unconjugated
hyperbilirubinemia, such as the aforementioned neonatal
hyperbilirubinemia, increased bilirubin load (haemolytic
syndromes), and inherited enzymatic deficiencies such as
Crigler-Najjar syndrome(deficiency of the enzyme) and Gilbert
syndrome(Deficiency of the enzyme +/- defective excretion of
bilirubin by liver).
• Disorders presenting with serum conjugated hyperbilirubinemia
include cholestasis syndromes, Dubin-Johnson syndrome(defective
canalicular bile transport), and Rotor's syndrome
Heme metabolism
 Pathophysiology of obstructive jaundice;
• Bile is a multipurpose secretion with an array of functions,
1. Intestinal digestion
2. Intestinal absorption of lipids
3. Elimination of environmental toxins, carcinogens, drugs, and their
metabolites (xenobiotics)
4. Serving as the primary route of excretion for a variety of
endogenous compounds and metabolic products, such as
cholesterol, bilirubin, and many hormones.
 Cont…...
• In obstructive jaundice, the pathophysiologic effects reflect the
absence of bile constituents (most importantly, bilirubin, bile salts,
and lipids) in the intestines, and their backup, which causes spillage
into the systemic circulation.
• Stools are often pale because less bilirubin reaches the intestine.
Absence of bile salts can produce malabsorption, leading to
steatorrhea and deficiencies of fat-soluble vitamins (particularly A,
K, and D); vitamin K deficiency can reduce prothrombin levels. …….
It is corrected by injection vitamin K, 10 mg 1M 00 for 5 days or by
FFP 5 - 10 units
• In long-standing cholestasis, concomitant vitamin D and Ca
malabsorption can cause osteoporosis or osteomalacia.
 Cont……
• Bilirubin retention produces mixed hyperbilirubinemia.
• Some conjugated bilirubin reaches and darkens the urine.
• High levels of circulating bile salts are associated with, but may not
cause, pruritus.
• Cholesterol and phospholipid retention produces hyperlipidemia
despite fat malabsorption (although increased liver synthesis and
decreased plasma esterification of cholesterol also contribute);
triglyceride levels are largely unaffected.
 Cont…….
• The lipids circulate as a unique, abnormal, low-density
lipoprotein(LDL) called lipoprotein X .
• Cholestatic liver diseases are characterized by accumulation of
hepatotoxic substances, mitochondrial dysfunction and impairment
of liver antioxidant defense.
• The storage of hydrophobic bile acids has been indicated as the
main cause of hepatotoxicity with alteration of some important cell
functions, such as the mitochondrial energy production.
• Both mitochondrial metabolism impairment and hydrophobic bile
acids accumulation are associated with increased production of
oxygen free radical species(ROS) and development of oxidative
damage.
 Cont………
• Accumulation of bilirubin in the bloodstream and subsequent
deposition in the skin causes jaundice (icterus). Conjunctival icterus
is generally a more sensitive sign of hyperbilirubinemia than
generalized jaundice.
• Urine bilirubin is normally absent. When it is present, only
conjugated bilirubin is passed into the urine.
• This may be evidenced by dark - coloured urine seen in patients
with obstructive jaundice or jaundice due to hepatocellular injury.
However, reagent strips are very sensitive to bilirubin, detecting as
little as 0.05 mg/dL.
 Cont……
• Thus, urine bilirubin may be found before serum bilirubin reaches
levels high enough to cause clinical jaundice.
• The lack of bilirubin in the intestinal tract is responsible for the pale
stools typically associated with biliary obstruction.
• The cause of itching (pruritus) associated with biliary obstruction is
not clear. Some believe it may be related to the accumulation of
bile acids in the skin.
• Others suggest it may be related to the release of endogenous
opioids.
 Aetiology;
• Intrahepatic cholestasis generally occurs at the level of the
hepatocyte or biliary canalicular membrane.
• Causes include;
1. Hepatocellular disease (eg, viral hepatitis, drug-induced hepatitis)
2. Drug-induced cholestasis
3. Biliary cirrhosis
4. Alcoholic liver disease.
• In hepatocellular disease, interference in the 4 major steps of
bilirubin metabolism, ie, uptake, cytosolic binding, conjugation, and
excretion, usually occurs.
• Excretion is the rate-limiting step and is usually impaired to the
greatest extent. As a result, conjugated bilirubin predominates in
the serum.
 Cont……
• Extrahepatic obstruction; may occur within the ducts or 2o to
external compression.
1. Gallstones (most common cause)
2. Malignancy
3. Infection; Ascending cholangitis, sclerosing cholangitis.
4. Biliary cirrhosis.
5. Cancer of the Pancreas(especially that of the head of the
pancrease)
6. Biliary strictures.
7. Biliary atresia.
8. Choledochal cyst
• External compression of the ducts may occur secondary to
inflammation (eg, pancreatitis) and malignancy. Regardless of the
cause, the physical obstruction causes predominantly conjugated
hyperbilirubinemia.
 Cont……
9. Carcinoma of head and periampullary region of the pancreas.
10. Cholangiocarcinoma.
11. Klatskin tumour (Carcinoma at the confluence of hepatic ducts above
the level of the cystic duct and so will cause hydro hepatosis without
GB enlargement ).
12. Extrinsic compression of CBD by lymph nodes or tumours.
13. Parasitic infestations.
 Cont……
CLASSIFICATION OF CAUSES OF OBSTRUCTIVE JAUNDICE :
1. Congenital: Biliary atresia, choledochal cyst.
2. Inflammatory: Ascending cholangitis, sclerosing cholangitis.
3. Obstructive: CBD stones, biliary stricture, parasitic infestation.
4. Neoplastic: Carcinoma of head or periampullary region of
pancreas, cholangiocarcinomas, Klatskin tumour.
5. Extrinsic compression of CBD by lymph nodes or tumours
 Clinical Features;

• Good history taking from the patient

• Physical examination
• Diagnostic tests are the requisites for the evaluation of the
jaundiced patient.
• Hallmark of obstructive jaundice are; i. Jaundice ii. Dark urine iii.
Pale stools iv. Generalized pruritus.
• +/- Fever(Role of ascending cholangitis).
• History of fever, biliary colic and intermittent jaundice may be
suggestive of cholangitis/ choledocholithiasis.
 Cont……
• Weight loss, abdominal mass, pain radiating to the back and
progressively deepening jaundice may be suggestive of pancreatic
cancer.
• pain, due to gallbladder disease, malignancy, or stretching of the
liver capsule
• Deep jaundice (with a greenish hue) that appears to fluctuate in
intensity may be due to a peri ampullary cancer. A palpably
enlarged gall bladder in a jaundiced patient is also suggestive of an
extrahepatic malignancy (Courvoisier’s statement)
 General signs of cholestasis
• xanthomas: palmar creases, below the breast, on the neck.
They indicate raised serum cholesterol of several months.
Xanthomas on the tendon sheaths are uncommonly associated
with cholestasis.
• xanthelasma on the eyelids
• scratch marks: excoriation
• finger clubbing
• loose, pale, bulky, offensive stools
• dark orange urine
 Courvoisisers sign/law
Courvoisier law;

painless enlargement of the gallbladder with jaundice is likely to

result from carcinoma of the head of the pancreas and not from a

stone in the common duct, because in the latter the gallbladder is

usually scarred from infection and does not distend.

 Investigations;
1. Biochemistry/ Haematology
• Elevated serum bilirubin level with a preponderance of the
conjugated fraction is the rule.
• The serum gamma glutamyl transpeptidase (GGT) level is also raised
in cholestasis.
• In general, patients with gallstone disease have less
hyperbilirubinemia than those with extra-hepatic malignant
obstruction.
• The serum bilirubin is usually less than 20 mg/dL.
• The alkaline phosphatase may be elevated up to ten times normal.
• The transaminases may abruptly rise about ten times normal and
decrease rapidly once the obstruction is relieved.
 Obstructive Jaundice
Lab Findings
• Serum Bilirubin
• Feceal urobilinogen (incomplete obstruction)
• Feceal urobilinogen absence (complete obstruction)
• urobilinogenuria is absent in complete obstructive jaundice
• bilirubinuria 
• ALP 
• cholesterol 
 Cont…….
• Elevated WBC may be present in cholangitis.
• In pancreatic cancer and other obstructive cancers, the serum
bilirubin may rise to 35 - 40 mg/dL, the alkaline phosphatase may
rise up to ten times normal, but the transaminases may remain
normal.
• Tumor markers like CA 19-9, CEA and CA-125 are usually elevated
in pancreatic cancers, cholangiocarcinoma and peri-ampullary
cancers, but they are non specific and may be elevated in other
benign diseases of the hepatobiliary tree.
2. Urine tests: Fouchet's test for bile pigments, Hay's test for bile salts
and test for urobilinogen in urine.
 Cont……
• FOUCHET'S TEST: 10 ml of urine + 5 ml of BaCb + pinch of MgS04
causes formation of BaS04 which is filtered over a filter paper and
few drops of Fouchet's reagent is added. Green or blue colour
signifies presence of bile pigments in the urine.
• HAY'S TEST FOR BILE SALT: Sprinkle sulphur to 2 ml of urine. In
presence of bile salts sulphur sinks to the bottom.
• EHRLICH'S TEST: 5 ml of freshly voided urine + 1 ml of Ehrlich
reagent (p‐dimethyl amino benzaldehyde) and wait for 5 minutes.
Formation of red colour signifies presence of urobilinogen in urine.
Normally it is present in traces, in obstructive jaundice it is absent
and in haemolytic jaundice it is in excess.
 Imaging;
• The goals of imaging are:
(1) to confirm the presence of an extrahepatic obstruction (i.e., to
verify that the jaundice is indeed post-hepatic rather than hepatic)
(2) to determine the level of the obstruction
(3) to identify the specific cause of the obstruction
(4) to provide complementary information relating to diagnosis (e.g.,
staging information in cases of malignancy)
 Cont……..
• Plain abdominal x ray; calcified gallstones, porcelain gallbladder, air
in the biliary tract or air in the gallbladder wall.
• USS; size of the bile ducts, may define the level of the obstruction,
may identify the cause and gives other information related to the
disease (e.g. hepatic metastases, gallstones, hepatic parenchymal
change)……. It identifies bile duct obstruction with 95% accuracy
though results are largely operator dependent…… It will also show
stones in the gallbladder and dilated bile duct, but it is unreliable
for small stones or strictures in the bile ducts…… It may also
demonstrate tumors, cysts, or abscesses in the pancreas, liver, and
surrounding structures. +
• Ultrasonography also assess the operability of the tumour.
 Cont…….
• CT scan of the abdomen provides excellent visualization of the liver,
gallbladder, pancreas, kidneys, and retroperitoneum…… It can
differentiate between intra- and extra-hepatic obstruction with 95%
accuracy. However, CT may not define incomplete obstruction
caused by small gallstones, tumors, or strictures.
• Contrast-enhanced multi-slice CT is very useful for assessment of
biliary malignancies. Contrast agents given orally or intravenously
are used and imaging done in unenhanced, arterial and venous
phases.
• ERCP and PTC (Percutaneous transhepatic cholangiography) provide
direct visualization of the level of obstruction. However they are
invasive and associated with complications like cholangitis, biliary
leakage, pancreatitis and bleeding.
 Cont…….
• Endoscopic ultrasound: Endoscopic ultrasonography has various
applications, such as staging of gastrointestinal malignancy,
evaluation of submucosal tumors, and has grown to be an
important modality in evaluating the pancreaticobiliary system.
With regard to the biliary system, EUS is useful for the detection
and staging of ampullary tumors, detection of microlithiasis,
choledocholithiasis and evaluation of benign and malignant bile-
duct strictures…… It can further evaluate relationships to vascular
structures. It may help define benign lesions mimicking cancer (e.g.
sclerosing pancreatitis) if there is diagnostic doubt.
• Endoscopic ultrasound enables the aspiration of cysts and biopsy of
solid lesions, but is operator-dependent.
 Cont……..
• Magnetic resonance cholangiopancreatography (MRCP) is a newer,
noninvasive technique for visualization of the biliary and pancreatic
ductal system. It is especially useful in patients who have
contraindications for endoscopic retrograde
cholangiopancreatography (ERCP). Excellent visualization of biliary
anatomy is possible without the invasiveness of ERCP…… Unlike
ERCP, it is purely diagnostic.
• Other imaging tests include Cholescintigraphy, radionuclide
scanning (Tc 99) angiography and staging laparoscopy.
 Preoperative preparation of patient with
obstructive jaundice:
• Proper diagnosis and assessment.
• Injection vitamin K 1M 10 mg for 5 days.
• Fresh Frozen plasma‐often requires 6 bottles or more.
• Blood transfusion in case of anaemia.
• Oral neomycin, lactulose.
• Mannitol 100‐200 ml BD IV to prevent hepato renal syndrome.
• Hydration
• Repeated monitoring by doing prothrombin time, electrolytes.
• Antibiotics like third generation cephalosporins.
• Calcium supplements as calcium chloride IV
 TREATMENT OF OBSTRUCTIVE JAUNDICE:
• CBD stones ‐ ERCP stone removal, choledocholitho‐tomy,
transduodenal sphincteroplasty, choledocho jejunostomy or
choledocho duodenostomy .
• Carcinoma periampullary or head of pancreas ‐ Whipple's operation
or triple bypass or ERCP stenting.
• Biliary stricture ‐ Stenting, choledochojejunostomy, Roux‐en‐ Y
hepatico jejunostomy.
• Klatskin tumour ‐ Radical resection or palliative stenting.
• Biliary atresia ‐ Kasai's operation or liver transplantation.
• Choledochal cyst ‐ Excision, hepaticojejunostomy, mucosal
resection.
 POSTOPERATIVE MANAGEMENT:
• Monitoring with prothrombin time, bilirubin, albumin, creatinine,
electrolyte estimation.
• FFP or blood transfusion.
• Antibiotics.
• Observation for septicaemia, haemorrhage, pneumonia, pleural
effusion, bile leak.
• Care of T ‐tube and drains.
• T‐tube cholangiogram in 10‐14 days..
• TPN, CVP line, nasogastric tube, urinary catheter.