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Surgical JAUNDICE
Presented by: Hassan fares , Jamal aljamal, hamam
alazzam , mothana alrfo’u, morad kawaldah
Supervised by: Dr Mohammad nofel
 Definition
 Bilirubin metabolism
 Classification
 Diagnosis
 Special investigations
 Management.
 Jaundice is not a disease
but rather a sign that can
occur in many different
diseases.
 Jaundice is the yellowish
staining of the skin ,
sclerae (the whites of the
eyes) and other mucous
membranes that is caused
by high levels in blood of
the chemical bilirubin.
 The color of the skin and
sclerae vary depending on
the level of bilirubin. When
the bilirubin level is mildly
elevated, they are
yellowish. When the
bilirubin level is high, they
tend to be brown.
What is jaundice?
 Normal serum total bilirubin is >>5-17 μmol/L (< 1 mg/dL)
 Jaundice is clinically evident when serum total bilirubin > 2-3x normal
(2.5 mg/dL)
Heme
Heme oxygenase
Biliverdin reductase
Hemoglobin
(70 to 80%)
Heme proteins
myoglobin, cytochromes
(20 to 25%)
Biliverdin
Bilirubin
indirect
unconjugated
pre-hepatic
albumin
Bilirubin Excretion
Bilirubin diglucuronide
80%
Stercobilinogen
Bacterial enzymes
Bilirubin
Bacterial enzyme
2 glucuronate
Bacterial enzyme
Urobilinogen
90% liver
Urobilin
10% kidneys
urine
Stercobilin feces
intestines
-------->
20%
 Disruption of bilirubin metabolism and excretion can cause
hyperbilirubinaemia and subsequent jaundice
 Hyperbilirubinaemia maybe unconjugated (indirect) or conjugated
(direct) depending on the cause
 Some inherited syndromes of bilirubin handling can result in
hyperbilirubinaemia
 Gilbert’s syndrome – reduced activity of glucuronyl transferase
therefore reduced conjugated bilirubin therefore elevated
unconjugated bilirubin
 Criggler-Najjar – reduction in amount of glucoronyl transferase
therefore elevated unconjugated bilirubin
 Rotor’s/Dubin-Johnson syndrome – defective excretion of conjugated
bilirubin into the biliary cannaliculi therefore elevated conjugated
bilirubin
PREHEPATIC JAUNDICE
Hemolytic disorders
 Thalassemias
 G6PD deficiency
 Hereditary spherocytosis
 Autoimmune hemolytic anemias
 Incompatible blood transfusion
“A healthy liver can excrete 6x the normal load of bilirubin before
unconjugated bilirubin starts to accumulate”
 Gilbert syndrome, Criggler-Najjar syndrome
HEPATOCELLULAR JAUNDICE
INTRA-HEPATIC
 Basically any acute or chronic liver disease!
 Viral hepatitis Drug-induced hepatotoxicity Alcoholic and non-
alcoholic liver disease (NASH) PBC PSC Autoimmune hepatitis
Hemochromatosis Wilson’s disease Cirrhosis Liver tumors
 All the causes of hepatitis/cirrhosis (e.g. Alcohol, viral, auto-immune,
primray biliary cirrhosis , Primary sclerosing cholangiti
haemochromatosis, wilsons, alpha-1 antitrypsin deficiency , Drug-
induced, )
 Rotor’s syndrome, Dubin-Johnson syndrome
Can result in hepatocyte destruction and therefore unconjugated
hyperbilirubinaemia or in bile cannaliculi destruction and therefore
conjugated hyperbilirubinaemia or both
 Is caused by an interruption to the drainage of bile containing conjugated bilirubin
in the biliary system.
 The most common causes are gallstones in the CBD, and cancer head of the
pancreas.
 Also, a group of parasites known as "liver flukes" can live in the CBD, causing
obstructive jaundice. Other causes include strictures of the CBD, biliary atresia,
cholangiocarcinoma, pancreatitis, cholestasis of pregnancy, and pancreatic
pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.
 The presence of pale stools and dark urine suggests an obstructive or post-
hepatic/liver cause as normal feces get their color from bile pigments. They can,
however, occur in many liver conditions and are therefore not a reliable clinical
feature to distinguish obstruction from liver causes of jaundice.
 People also can present with elevated serum cholesterol, and often complain of
severe itching or "pruritus" because of the direct and indirect effects of pruritogens
in bile such as bile salts.
 A combination of liver function tests is essential to arrive at a diagnosis.
PAINFUL VS. PAINLESS
 One of the main distinguishing symptoms between
benign and malignant causes is pain.
 Painful obstructive jaundice is usually related to
gallstones, while painless obstructive jaundice tends
to be related to tumors (red flag).
 The reason for this difference is that stones tend to
harbour bacteria and cause bile duct infection,
resulting in pain and fever.
 Interestingly, as pain is not a key feature for
malignant causes, patients with tumors tend to seek
expert help later. These patients may also have
worrisome symptoms of weight loss and loss of
appetite.
Intraluminal obstruction: stones, hydatid cysts worms
Wall pathologies “Intra-mural”
 Benign stricture
1. Congenital BILIARY ATRESIA
2. IATROGENIC: BILIARY SURGERY , GASTRECTOMY, HEPATIC RESECTION
,LIVER TRANSPLANT
3. INFLAMMATORY; CHOLANGITIS, PANCREATITIS, SCLEROSING CHOLANANGITIS.
4. TRAUMA
5. IDIOPATHIC
6. RADIOTHERAPY
 Malignant stricture: cholangiocarcinoma
External compression: pancreatitis, tumor of the head of the pancreas, pancreatic pseudocyst, tumor of the
ampulla of Vater, Mirizzi syndrome.
STONE VS. MALIGNANCY
It is important to distinguish between the possible
causes of obstructive jaundice.
While the common causes are related to gallstone
disease, the more frightening causes are related to
cancer (pancreatic cancer, bile duct cancer,… ).
Benign causes: Gallstones, choledochal cyst,
benign bile duct strictures
Malignant causes: malignant tumors in the
pancreas, bile duct, gallbladder
 STONE SLIPPING INTO THE BILIARY TREE “Choledocholithiasis”
 Common bile duct stone, may be small or large and single or
multiple, and are found in 6% to 12% of patients with stones in
the gallbladder.
 There are two possible origins for common duct stones;
 secondary stones (cholesterol stones) : most cholesterol stones
develop within the gallbladder and reach the duct after traversing
the cystic duct.
primary common duct stone (Brown pigment stones)
 Elevation of serum bilirubin, alkaline phosphatase, and transaminases are
commonly seen in patients with bile duct stones (almost 2/3).
 US, MRC, PTC, Endoscopic cholangiography is the gold standard for diagnosing
common bile duct stones.
 TT:sphincterotomy and ductal clearance of the
stones, followed by a laparoscopic cholecystectomy
MALIGNANCY CAUSES OF
JAUNDICE
in malignant causes of jaundice, the jaundice is
painless and progressive.
Malignancy causing complete blockage of bile can
result in significant itching due to accumulation of
bile pigments within the skin, and malnutrition as
bile is part of the digestive system.
 About two-thirds of pancreatic adenocarcinomas arise within the
head or uncinate process of the pancreas; 15% are in the body,
and 10% in the tail
 For potentially resectable pancreatic head cancer, the standard operation is
pancreaticoduodenectomy (the Whipple procedure)
 is an adenocarcinoma of the bile ducts; it forms in the biliary
epithelial cells
 About two thirds are located at the hepatic duct bifurcation.
 Painless jaundice is the most common presentation.
 Pruritus, mild right upper quadrant abdominal pain,
anorexia, fatigue, and weight loss also may be present.
 Diagnosis : CT and MRI
 Risk factors
 primary sclerosing cholangitis, choledochal cysts, ulcerative colitis,
hepatolithiasis, biliary-enteric anastomosis, and biliary tract
infections.
 Other risk factors: dietary nitrosamines, thorotrast, and exposure to
dioxin.
 Surgical resection offers the only chance for cure; however, many
patients have advanced disease at the time of diagnosis.
 Most patients with unresectable disease die within 1 year of
diagnosis.
 is a cancer that forms in The ampulla of Vater ( a small opening
that enters into the duodenum)
 the most common presenting symptom is obstructive jaundice
(80%), caused by compression of the distal bile duct by the tumor.
 Additional symptoms may include diarrhea due to fat malabsorption
(steatorrhea), mild weight loss, and fatigue
 ERCP is the single most useful endoscopic study for diagnosing
ampullary carcinoma because it permits identification of the
tumor, biopsy, and decompression, if needed.
 Whipple procedure (pancreaticoduodenectomy)
BILE DUCT STRICTURES
Benign causes :
operative injury, most commonly by laparoscopic cholecystectomy
fibrosis due to chronic pancreatitis, common bile duct stones, acute
cholangitis, biliary obstruction due to cholecystolithiasis (Mirizzi’s
syndrome), sclerosing cholangitis
Malignant causes :
cholangiocarcinoma, adenocarcinoma of the pancreas and ampullary
tumors
 most commonly present with episodes of cholangitis
 An ultrasound or a CT scan will show dilated bile ducts
proximal to the stricture, as well as provide some information
about the level of the stenosis.
 Treatment depends on the location and the cause of the
stricture.
 Roux-en-Y choledochojejunostomy or hepaticojejunostomy is the
standard of care with good or excellent results in 80% to 90% of
patients
 Percutaneous or endoscopic dilatation and/or stent placement
• the cystic duct is densely adherent to the
common bile duct
• (a stone ulcerating through the neck of the
gallbladder into the common hepatic duct)
• the infundibulum of the gallbladder should be
opened, the stone removed and the
infundibulum over sewn.
• Attempts to dissect out the cystic duct
completely will only lead to injury to the
common hepatic or common bile duct.
History
Physical examination
Investigations
Labs
Imaging
Pathology (biopsy)
Personal profile
Name , Age (and date of birth) , Sex ,
Marital status , Occupation , Address ,
Admission (Date , time and route) ,
referral (if apply)
Chief complaint
Complaint + duration
Analyze the jaundice
Distribution: skin , eyes or both
 Carotenemia spares the eyes
Onset: sudden vs gradual
 Sudden in Hepatitis A , Hepatitis secondary to alcohol use
, Autoimmune hepatitis , Gallstone diseases ,
 Gradual in Carcinoma (pancreatic or biliary)
Duration
Course: intermittent vs continuous (progressive vs
constant)
 Intermittent in Gallstone diseases ,
 Continuous in Carcinoma ,
Accompanying symptoms:
fever, chills, rigors and RUQ pain  acute
cholangitis
anorexia, malaise, and myalgias  viral hepatitis
Acholic stool (clay colored) & Dark urine (tea or
cola colored)  cholestasis (gallstones , cancer ,
viral hepatitis)
Skin itching
Weight loss  cancer
Start with the involved system (in case of
jaundice it is the alimentary system and
abdomen):
Appetite. Diet. Weight. Nausea. Dysphagia.
Regurgitation. Flatulence. Heartburn. Vomiting.
Hematemesis. Indigestion pain. Abdominal pain.
Abdominal distension. Bowel habit. Nature of stool.
Rectal bleeding. Mucus. Slime. Prolapse.
Incontinence. Tenesmus
Then review the RS , CVS , GUS , NS , MSS
for a full history
History of inherited disorders, including liver
diseases and hemolytic disorders
A past history of hepatitis  chronic active
hepatitis
History of abdominal operations, including
gallbladder surgery  acute cholangitis
Drug Hx:
Drugs associated with jaundice and contraindicated in
jaundice include: amitriptyline, chlorpromazine,
erythromycin, halothane, imipramine, indomethacin,
isoniazid, methyldopa, monoamine oxidase inhibitors
(MAOIs), oral contraceptive pill, rifampicin, salicylates,
sulfonamides, thiouracil.
Recent blood transfusions  viral hepatitis ,
incompatibility reaction , hemolytic disease
Use of alcohol
Recent contact with jaundiced person 
hepatitis
Recent travel  hepatitis
Immunization history  hepatitis
Family history of jaundice
Occupational history as sewerage
workers or people exposed to hepatotoxic
chemicals.
 Jaundice
 Abdominal examination
 Examine the jaundice (on the sclera , skin , under the tongue)
 Check for signs of liver disease:
spider nevi,
clubbing,
palmar erythema,
gynecomastia ,
testicular atrophy ,
flapping tremor ,
splenomegaly ,
ascites ,
peripheral edema ... etc.
Jaundice
1- Sclera 2- Skin 3- Mucous membranes
Early signs :
 Finger clubbing
 Leukonychia
 Spider naevi
 Body hair loss
 Palmer erythema
 Duputyrens contracture
Late signs :
 Jaundice
 Ill looking
 Teticular atrophy
gynaecomastia
 Ascites
 Flapping tremor ( asterixis )
 caput medusa
 Encephalopathy
 Intellectual change
 Convulsions
 Coma
Early signs :
Leukonychia Finger clubbing
Palmer erythema
Duputyrens contracture Spider naevi
EXAMINATION
 Abdominal examination ::
 Palpation: liver edge:
 The liver edge in cirrhosis >> is firm
 An irregular liver edge  malignant disease
 Gallbladder
 If the gallbladder is palpable, it is probable that the cause of jaundice is not
a stone (Courvoisier's law)
 spleen
 Splenomegaly is suggestive of cirrhosis, hematological disorders or
reticulosis.
Percussion: liver span ,, ascites ..
 Auscultation.
Late signs :
caput medusa
Ascites
Labs:
 LFT(Bilirubin ,ALT ,AST ALP,GGT,INR/PT)
 Urine analysis (color, bilirubin ,urobilinogen)
 Stool analysis(color)
Imaging:U/S , CT, MRCP, ERCP, PTC.
Test with normal
range
Pre-hepatic Hepatic Post-hepatic
Total bilirubin
0.1to 1.2 mg/dl
+ ++ +++
Conjugated
bilirubin less than
0.3 mg/dl
Normal Increased Increased
Unconjugated
bilirubin 0.2 to 0.8
mg/dl
Increased Increased Normal
 Total bilirubin and its conjugated and
unconjugated levels help to determine nature of
jaundice
 Liver Enzymes
 ALT/AST mainly present in hepatocytes
 ALP/GGT mainly present in bile cannaliculi biliary tree
Test Pre-hepatic Hepatic Post-hepatic
ALT 7to 55 u/l
AST 8 to 48 u/l
Normal +++ raised +
ALP 40 to 129 u/l
GGT 8to 61 u/l
Normal + +++ raised
Test Pre-hepatic Hepatic Post-hepatic
Urine colour Normal Normal
If Dark (urobilinogen +
conjugated bilirubin )
Dark
(conjugated bilirubin )
Urine Bilirubin negative Negative Increased
Urine urobilinogen
0.2to 1 mg/dl
Increased Normal present Decreased/negative
Stool colour Normal Normal Pale
Test Prehepatic Hepatocellular Obstructive
Urine Urobilinogen Urobilinogen Bilirubin
Serum bilirubin Unconjugated Mixed Conjugated
AST and ALT Normal Raised Normal – raised
ALP Normal Normal – raised Raised
Blood glucose Normal Low if liver failure May be raised in
pancreatic CA
Reticulocyte count Raised in
hemolysis
Normal Normal
Haptoglobin Low Normal or low if
liver failure
Normal
PT/INR Normal Prolonged Prolonged
U/S Normal May show
abnormal liver
texture
Dilated bile ducts
 Initial: U/S
 Secondary line imaging(incoclusive U/S): CT , MRCP , EUS
 Theraputic:ERCP(low obstruction)+PTC(high obstruction,intrahepatic biliary
dilatatin)
 Commonly obtained for initial evaluation of all patients with jaundice
 Preferred initial image for suspected cholestasis
 Cheap, noninvasive, good sensitivity , readily available, inexpensive and quick to perform
 Best initial test for gallstones. Also useful for biliary dilation due to any cause, and screen for liver
tumors
 Operator dependent. Limited visualization of stones in CBD, limited in obese patients & in
intraluminal bowel gases.
 Endoscopic U/S provides accurate imaging of stones in CBD, diagnosing and staging pancreatic and
periampullary cancers. FNA can be used with the advantage of avoiding spillage of tumor cells into
the peritoneal cavity
 Ct Is indicated if we suspect malignancy ( painless jaundice)
 Very useful for hepatic and pancreatic masses, may be used with guided biopsy
 MRI may be a good alternative (e.g. patients who can’t take contrast)
 Noninvasive visualization of biliary tree
 It avoid the complications of diagnostic ERCP & PTC ( but these methods should
be done if there is therapeutic need )
 Not theraputic
 Diagnostic and therapeutic
 Used for biliary obstruction distal to the bifurcation of hepatic ducts, when
intervention is anticipated.
 Theraputic: -sphincterotomy(stone in lower CBD) -stent(exernal
compression/stricture) – drainage(pancreatitis and cholangitis)
 Check coagulation profile and give prophylactic antibiotics
 Complications: Pancreatitis, cholangitis, bleeding, duodenal perforation.
 May be used when ERCP is not possible (e.g. patient had done a gastrectomy/
pancreatoduodencectomy)
 “In general, in the jaundiced patient, if a malignant stricture at the level of the
confluence of the right and left hepatic ducts or higher is suspected, a PTC is
preferred to ERCP as successful drainage is more likely”
 Complications: intraperitoneal hemorrhage, subphrenic abscess, sepsis
 I.V.F
 Prophylactic broad spectrum antibiotic????
 Parenteral vitamin K +/- fresh frozen plasma.
 Cholestyramine and antihistamine for symptomatic relief of pruritis
12. Obstructive Jaundice copy (1).pptx

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12. Obstructive Jaundice copy (1).pptx

  • 1. Surgical JAUNDICE Presented by: Hassan fares , Jamal aljamal, hamam alazzam , mothana alrfo’u, morad kawaldah Supervised by: Dr Mohammad nofel
  • 2.  Definition  Bilirubin metabolism  Classification  Diagnosis  Special investigations  Management.
  • 3.  Jaundice is not a disease but rather a sign that can occur in many different diseases.  Jaundice is the yellowish staining of the skin , sclerae (the whites of the eyes) and other mucous membranes that is caused by high levels in blood of the chemical bilirubin.  The color of the skin and sclerae vary depending on the level of bilirubin. When the bilirubin level is mildly elevated, they are yellowish. When the bilirubin level is high, they tend to be brown. What is jaundice?
  • 4.  Normal serum total bilirubin is >>5-17 μmol/L (< 1 mg/dL)  Jaundice is clinically evident when serum total bilirubin > 2-3x normal (2.5 mg/dL)
  • 5.
  • 6.
  • 7.
  • 8. Heme Heme oxygenase Biliverdin reductase Hemoglobin (70 to 80%) Heme proteins myoglobin, cytochromes (20 to 25%) Biliverdin Bilirubin indirect unconjugated pre-hepatic albumin
  • 9.
  • 10. Bilirubin Excretion Bilirubin diglucuronide 80% Stercobilinogen Bacterial enzymes Bilirubin Bacterial enzyme 2 glucuronate Bacterial enzyme Urobilinogen 90% liver Urobilin 10% kidneys urine Stercobilin feces intestines --------> 20%
  • 11.  Disruption of bilirubin metabolism and excretion can cause hyperbilirubinaemia and subsequent jaundice  Hyperbilirubinaemia maybe unconjugated (indirect) or conjugated (direct) depending on the cause  Some inherited syndromes of bilirubin handling can result in hyperbilirubinaemia  Gilbert’s syndrome – reduced activity of glucuronyl transferase therefore reduced conjugated bilirubin therefore elevated unconjugated bilirubin  Criggler-Najjar – reduction in amount of glucoronyl transferase therefore elevated unconjugated bilirubin  Rotor’s/Dubin-Johnson syndrome – defective excretion of conjugated bilirubin into the biliary cannaliculi therefore elevated conjugated bilirubin
  • 12. PREHEPATIC JAUNDICE Hemolytic disorders  Thalassemias  G6PD deficiency  Hereditary spherocytosis  Autoimmune hemolytic anemias  Incompatible blood transfusion “A healthy liver can excrete 6x the normal load of bilirubin before unconjugated bilirubin starts to accumulate”  Gilbert syndrome, Criggler-Najjar syndrome
  • 13. HEPATOCELLULAR JAUNDICE INTRA-HEPATIC  Basically any acute or chronic liver disease!  Viral hepatitis Drug-induced hepatotoxicity Alcoholic and non- alcoholic liver disease (NASH) PBC PSC Autoimmune hepatitis Hemochromatosis Wilson’s disease Cirrhosis Liver tumors  All the causes of hepatitis/cirrhosis (e.g. Alcohol, viral, auto-immune, primray biliary cirrhosis , Primary sclerosing cholangiti haemochromatosis, wilsons, alpha-1 antitrypsin deficiency , Drug- induced, )  Rotor’s syndrome, Dubin-Johnson syndrome Can result in hepatocyte destruction and therefore unconjugated hyperbilirubinaemia or in bile cannaliculi destruction and therefore conjugated hyperbilirubinaemia or both
  • 14.  Is caused by an interruption to the drainage of bile containing conjugated bilirubin in the biliary system.  The most common causes are gallstones in the CBD, and cancer head of the pancreas.  Also, a group of parasites known as "liver flukes" can live in the CBD, causing obstructive jaundice. Other causes include strictures of the CBD, biliary atresia, cholangiocarcinoma, pancreatitis, cholestasis of pregnancy, and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.  The presence of pale stools and dark urine suggests an obstructive or post- hepatic/liver cause as normal feces get their color from bile pigments. They can, however, occur in many liver conditions and are therefore not a reliable clinical feature to distinguish obstruction from liver causes of jaundice.  People also can present with elevated serum cholesterol, and often complain of severe itching or "pruritus" because of the direct and indirect effects of pruritogens in bile such as bile salts.  A combination of liver function tests is essential to arrive at a diagnosis.
  • 15. PAINFUL VS. PAINLESS  One of the main distinguishing symptoms between benign and malignant causes is pain.  Painful obstructive jaundice is usually related to gallstones, while painless obstructive jaundice tends to be related to tumors (red flag).  The reason for this difference is that stones tend to harbour bacteria and cause bile duct infection, resulting in pain and fever.  Interestingly, as pain is not a key feature for malignant causes, patients with tumors tend to seek expert help later. These patients may also have worrisome symptoms of weight loss and loss of appetite.
  • 16. Intraluminal obstruction: stones, hydatid cysts worms Wall pathologies “Intra-mural”  Benign stricture 1. Congenital BILIARY ATRESIA 2. IATROGENIC: BILIARY SURGERY , GASTRECTOMY, HEPATIC RESECTION ,LIVER TRANSPLANT 3. INFLAMMATORY; CHOLANGITIS, PANCREATITIS, SCLEROSING CHOLANANGITIS. 4. TRAUMA 5. IDIOPATHIC 6. RADIOTHERAPY  Malignant stricture: cholangiocarcinoma External compression: pancreatitis, tumor of the head of the pancreas, pancreatic pseudocyst, tumor of the ampulla of Vater, Mirizzi syndrome.
  • 17.
  • 18. STONE VS. MALIGNANCY It is important to distinguish between the possible causes of obstructive jaundice. While the common causes are related to gallstone disease, the more frightening causes are related to cancer (pancreatic cancer, bile duct cancer,… ). Benign causes: Gallstones, choledochal cyst, benign bile duct strictures Malignant causes: malignant tumors in the pancreas, bile duct, gallbladder
  • 19.  STONE SLIPPING INTO THE BILIARY TREE “Choledocholithiasis”  Common bile duct stone, may be small or large and single or multiple, and are found in 6% to 12% of patients with stones in the gallbladder.  There are two possible origins for common duct stones;  secondary stones (cholesterol stones) : most cholesterol stones develop within the gallbladder and reach the duct after traversing the cystic duct. primary common duct stone (Brown pigment stones)
  • 20.  Elevation of serum bilirubin, alkaline phosphatase, and transaminases are commonly seen in patients with bile duct stones (almost 2/3).  US, MRC, PTC, Endoscopic cholangiography is the gold standard for diagnosing common bile duct stones.  TT:sphincterotomy and ductal clearance of the stones, followed by a laparoscopic cholecystectomy
  • 21. MALIGNANCY CAUSES OF JAUNDICE in malignant causes of jaundice, the jaundice is painless and progressive. Malignancy causing complete blockage of bile can result in significant itching due to accumulation of bile pigments within the skin, and malnutrition as bile is part of the digestive system.
  • 22.  About two-thirds of pancreatic adenocarcinomas arise within the head or uncinate process of the pancreas; 15% are in the body, and 10% in the tail
  • 23.  For potentially resectable pancreatic head cancer, the standard operation is pancreaticoduodenectomy (the Whipple procedure)
  • 24.  is an adenocarcinoma of the bile ducts; it forms in the biliary epithelial cells  About two thirds are located at the hepatic duct bifurcation.  Painless jaundice is the most common presentation.  Pruritus, mild right upper quadrant abdominal pain, anorexia, fatigue, and weight loss also may be present.  Diagnosis : CT and MRI
  • 25.
  • 26.  Risk factors  primary sclerosing cholangitis, choledochal cysts, ulcerative colitis, hepatolithiasis, biliary-enteric anastomosis, and biliary tract infections.  Other risk factors: dietary nitrosamines, thorotrast, and exposure to dioxin.  Surgical resection offers the only chance for cure; however, many patients have advanced disease at the time of diagnosis.  Most patients with unresectable disease die within 1 year of diagnosis.
  • 27.  is a cancer that forms in The ampulla of Vater ( a small opening that enters into the duodenum)  the most common presenting symptom is obstructive jaundice (80%), caused by compression of the distal bile duct by the tumor.  Additional symptoms may include diarrhea due to fat malabsorption (steatorrhea), mild weight loss, and fatigue  ERCP is the single most useful endoscopic study for diagnosing ampullary carcinoma because it permits identification of the tumor, biopsy, and decompression, if needed.  Whipple procedure (pancreaticoduodenectomy)
  • 28. BILE DUCT STRICTURES Benign causes : operative injury, most commonly by laparoscopic cholecystectomy fibrosis due to chronic pancreatitis, common bile duct stones, acute cholangitis, biliary obstruction due to cholecystolithiasis (Mirizzi’s syndrome), sclerosing cholangitis Malignant causes : cholangiocarcinoma, adenocarcinoma of the pancreas and ampullary tumors
  • 29.  most commonly present with episodes of cholangitis  An ultrasound or a CT scan will show dilated bile ducts proximal to the stricture, as well as provide some information about the level of the stenosis.  Treatment depends on the location and the cause of the stricture.  Roux-en-Y choledochojejunostomy or hepaticojejunostomy is the standard of care with good or excellent results in 80% to 90% of patients  Percutaneous or endoscopic dilatation and/or stent placement
  • 30. • the cystic duct is densely adherent to the common bile duct • (a stone ulcerating through the neck of the gallbladder into the common hepatic duct) • the infundibulum of the gallbladder should be opened, the stone removed and the infundibulum over sewn. • Attempts to dissect out the cystic duct completely will only lead to injury to the common hepatic or common bile duct.
  • 32. Personal profile Name , Age (and date of birth) , Sex , Marital status , Occupation , Address , Admission (Date , time and route) , referral (if apply) Chief complaint Complaint + duration
  • 33. Analyze the jaundice Distribution: skin , eyes or both  Carotenemia spares the eyes Onset: sudden vs gradual  Sudden in Hepatitis A , Hepatitis secondary to alcohol use , Autoimmune hepatitis , Gallstone diseases ,  Gradual in Carcinoma (pancreatic or biliary) Duration Course: intermittent vs continuous (progressive vs constant)  Intermittent in Gallstone diseases ,  Continuous in Carcinoma ,
  • 34. Accompanying symptoms: fever, chills, rigors and RUQ pain  acute cholangitis anorexia, malaise, and myalgias  viral hepatitis Acholic stool (clay colored) & Dark urine (tea or cola colored)  cholestasis (gallstones , cancer , viral hepatitis) Skin itching Weight loss  cancer
  • 35. Start with the involved system (in case of jaundice it is the alimentary system and abdomen): Appetite. Diet. Weight. Nausea. Dysphagia. Regurgitation. Flatulence. Heartburn. Vomiting. Hematemesis. Indigestion pain. Abdominal pain. Abdominal distension. Bowel habit. Nature of stool. Rectal bleeding. Mucus. Slime. Prolapse. Incontinence. Tenesmus Then review the RS , CVS , GUS , NS , MSS for a full history
  • 36. History of inherited disorders, including liver diseases and hemolytic disorders A past history of hepatitis  chronic active hepatitis History of abdominal operations, including gallbladder surgery  acute cholangitis
  • 37. Drug Hx: Drugs associated with jaundice and contraindicated in jaundice include: amitriptyline, chlorpromazine, erythromycin, halothane, imipramine, indomethacin, isoniazid, methyldopa, monoamine oxidase inhibitors (MAOIs), oral contraceptive pill, rifampicin, salicylates, sulfonamides, thiouracil. Recent blood transfusions  viral hepatitis , incompatibility reaction , hemolytic disease Use of alcohol
  • 38. Recent contact with jaundiced person  hepatitis Recent travel  hepatitis Immunization history  hepatitis Family history of jaundice Occupational history as sewerage workers or people exposed to hepatotoxic chemicals.
  • 40.  Examine the jaundice (on the sclera , skin , under the tongue)  Check for signs of liver disease: spider nevi, clubbing, palmar erythema, gynecomastia , testicular atrophy , flapping tremor , splenomegaly , ascites , peripheral edema ... etc.
  • 41. Jaundice 1- Sclera 2- Skin 3- Mucous membranes
  • 42. Early signs :  Finger clubbing  Leukonychia  Spider naevi  Body hair loss  Palmer erythema  Duputyrens contracture Late signs :  Jaundice  Ill looking  Teticular atrophy gynaecomastia  Ascites  Flapping tremor ( asterixis )  caput medusa  Encephalopathy  Intellectual change  Convulsions  Coma
  • 43. Early signs : Leukonychia Finger clubbing Palmer erythema
  • 44.
  • 46. EXAMINATION  Abdominal examination ::  Palpation: liver edge:  The liver edge in cirrhosis >> is firm  An irregular liver edge  malignant disease  Gallbladder  If the gallbladder is palpable, it is probable that the cause of jaundice is not a stone (Courvoisier's law)  spleen  Splenomegaly is suggestive of cirrhosis, hematological disorders or reticulosis. Percussion: liver span ,, ascites ..  Auscultation.
  • 47. Late signs : caput medusa Ascites
  • 48.
  • 49. Labs:  LFT(Bilirubin ,ALT ,AST ALP,GGT,INR/PT)  Urine analysis (color, bilirubin ,urobilinogen)  Stool analysis(color) Imaging:U/S , CT, MRCP, ERCP, PTC.
  • 50.
  • 51. Test with normal range Pre-hepatic Hepatic Post-hepatic Total bilirubin 0.1to 1.2 mg/dl + ++ +++ Conjugated bilirubin less than 0.3 mg/dl Normal Increased Increased Unconjugated bilirubin 0.2 to 0.8 mg/dl Increased Increased Normal  Total bilirubin and its conjugated and unconjugated levels help to determine nature of jaundice
  • 52.  Liver Enzymes  ALT/AST mainly present in hepatocytes  ALP/GGT mainly present in bile cannaliculi biliary tree Test Pre-hepatic Hepatic Post-hepatic ALT 7to 55 u/l AST 8 to 48 u/l Normal +++ raised + ALP 40 to 129 u/l GGT 8to 61 u/l Normal + +++ raised
  • 53. Test Pre-hepatic Hepatic Post-hepatic Urine colour Normal Normal If Dark (urobilinogen + conjugated bilirubin ) Dark (conjugated bilirubin ) Urine Bilirubin negative Negative Increased Urine urobilinogen 0.2to 1 mg/dl Increased Normal present Decreased/negative Stool colour Normal Normal Pale
  • 54. Test Prehepatic Hepatocellular Obstructive Urine Urobilinogen Urobilinogen Bilirubin Serum bilirubin Unconjugated Mixed Conjugated AST and ALT Normal Raised Normal – raised ALP Normal Normal – raised Raised Blood glucose Normal Low if liver failure May be raised in pancreatic CA Reticulocyte count Raised in hemolysis Normal Normal Haptoglobin Low Normal or low if liver failure Normal PT/INR Normal Prolonged Prolonged U/S Normal May show abnormal liver texture Dilated bile ducts
  • 55.  Initial: U/S  Secondary line imaging(incoclusive U/S): CT , MRCP , EUS  Theraputic:ERCP(low obstruction)+PTC(high obstruction,intrahepatic biliary dilatatin)
  • 56.  Commonly obtained for initial evaluation of all patients with jaundice  Preferred initial image for suspected cholestasis  Cheap, noninvasive, good sensitivity , readily available, inexpensive and quick to perform  Best initial test for gallstones. Also useful for biliary dilation due to any cause, and screen for liver tumors  Operator dependent. Limited visualization of stones in CBD, limited in obese patients & in intraluminal bowel gases.  Endoscopic U/S provides accurate imaging of stones in CBD, diagnosing and staging pancreatic and periampullary cancers. FNA can be used with the advantage of avoiding spillage of tumor cells into the peritoneal cavity
  • 57.
  • 58.  Ct Is indicated if we suspect malignancy ( painless jaundice)  Very useful for hepatic and pancreatic masses, may be used with guided biopsy  MRI may be a good alternative (e.g. patients who can’t take contrast)
  • 59.  Noninvasive visualization of biliary tree  It avoid the complications of diagnostic ERCP & PTC ( but these methods should be done if there is therapeutic need )  Not theraputic
  • 60.
  • 61.  Diagnostic and therapeutic  Used for biliary obstruction distal to the bifurcation of hepatic ducts, when intervention is anticipated.  Theraputic: -sphincterotomy(stone in lower CBD) -stent(exernal compression/stricture) – drainage(pancreatitis and cholangitis)  Check coagulation profile and give prophylactic antibiotics  Complications: Pancreatitis, cholangitis, bleeding, duodenal perforation.
  • 62.
  • 63.  May be used when ERCP is not possible (e.g. patient had done a gastrectomy/ pancreatoduodencectomy)  “In general, in the jaundiced patient, if a malignant stricture at the level of the confluence of the right and left hepatic ducts or higher is suspected, a PTC is preferred to ERCP as successful drainage is more likely”  Complications: intraperitoneal hemorrhage, subphrenic abscess, sepsis
  • 64.
  • 65.  I.V.F  Prophylactic broad spectrum antibiotic????  Parenteral vitamin K +/- fresh frozen plasma.  Cholestyramine and antihistamine for symptomatic relief of pruritis

Editor's Notes

  1. Gilbert syndrome: Mildly low UGT activity; autosomal recessive. >> Jaundice during stress (e.g., severe infection); otherwise, not clinically significant. Criggler-Najjar syndrome: Absence of UGT>> usually seen in the fetus>> Kernicterus; usually fatal
  2. PBC: Primary biliary cirrhosis. PSC: Primary sclerosing cholangitis. Dubin-Johnson syndrome: Deficiency of bilirubin canalicular transport protein; autosomal recessive, the liver is dark. Rotor’s is the same but the liver is not dark.
  3. Urine bilirubin Normally, tiny amount bilirubin (conjugated) excreted in urine * Pre-hepatic jaundice: Haemolysis causes rise in unconjugated bilirubin (water insoluble) and this is not excreted by the kidney therefore there is no rise in urine bilirubin * Some causes of Hepatic jaundice: result in damage to biliary cannaliculi and therefore result in poor biliary drainage and therefore elevated conjugated bilirubin levels in blood, excreted into urine (giving dark urine) * Post-Hepatic juandice: Obstruction to biliary drainage and so conjugated bilirubin (water soluble) levels in the blood increase and appear in the urine (giving dark urine) Urine urobilinogen Pre-hepatic jaundice: Haemolysis results in increased bilirubin production and subsequent increase bilirubin metabolism and urobilinogen in stool and therefore in the urine. Some causes of Hepatic jaundice : result in hepatocellular destruction and therefore reduced re-excretion of re-absorbed urobilinogen (i.e. Reduction in entero-hepatic circulation of urobilinogen) resulting in elevated levels in urine Post-Hepatic jaundice: Less bilirubin reaching intestine therefore reduction in urobilinogen therefore reduction in urine urobilinogen
  4. Four Fs”: Female Fat Forty Fertile (multiparity) What are the types o stones? Cholesterol stones (75%) / Pigment stones (25%) What are the types of pigmented stones? Black stones (contain calcium bilirubinate) Brown stones (associated with biliary tract infection) What are the causes o black pigmented stones? Cirrhosis, hemolysis What is the pathogenesis of cholesterol stones? Secretion of bile supersaturated with cholesterol (relatively decreased amounts of lecithin and bile salts); then, cholesterol precipitates out and forms solid crystals, then gallstones
  5. is a cancer of the cells that make up the ducts in the pancreas
  6. Cholangicarcinoma is a rare malignancy. The overall annual incidence is 1–1.5 per 100 000 Male : female ratio is approximately 1.5:1. Risk factors for cholangiocarcinoma Chronic inflammatory conditions ●● Primary sclerosing cholangitis (PSC) 20 fold ●● Hepatitis C infection Congenital ●● Choledochal cysts ●● Caroli’s disease Chemical agents ●● Thorium dioxide (Thorotrast) ●● Vinyl chloride ●● Dioxin ●● Asbestos Post surgical ●● Biliary–enteric anastomosis Most patients present with abnormal liver function tests or puritus + jaundice, wt loss, anorexia , abd. pain ●Diagnosis by ultrasound, CT or MRCP scanning ●The majority of patients receive palliative care only ●Complete surgical excision possible in <10% ●Prognosis poor: 90% die within 1 year, from hepatic failure or biliary sepsis ●Adjuvant chemoradiation therapy has a limited role
  7. Surgery involves excision of the extrahepatic biliary tree with or without a liver resection and a Roux loop reconstruction
  8. Complication if left untreated : recurrent cholangitis, secondary biliary cirrhosis, and portal hypertension
  9. Less commonly, they may present with jaundice without evidence of infection Surgery with
  10. Haptoglobin binds free Hb
  11. Ultrasound examination. Gallstones noted at the neck of the gallbladder with associated acoustic shadowing. Ultrasound examination. Multiple gallstones noted within the gallbladder. Endoscopic ultrasonography. CBD, common bile duct; PD, pancreatic duct.
  12. Magnetic resonance cholangiopancreatography
  13. Magnetic resonance cholangiopancreatography: projectional images demonstrating stones and hilar obstruction (arrow). Magnetic resonance cholangiopancreatography: cross-sectional image demonstrating a hilar mass (thick arrow) and gallstones (thin arrow).
  14. Endoscopic retrograde cholangiopancreatography (ERCP)
  15. Endoscopic retrograde cholangiopancreatography: normal cholangiogram. Endoscopic retrograde cholangiopancreatography: common duct obstruction (arrow). Endoscopic retrograde cholangiopancreatography: partial occlusion of the bile duct by a malignant stricture (arrow).
  16. Percutaneous transhepatic cholangiography