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Slide 1
Dr. Firas Obeidat, MD
Slide 2
Bilirubin metabolism
Slide 3
What causes bilirubin? overproduction by reticuloendothelial
system. failure of hepatocyte uptake. failure to conjugate or
excrete. obstruction of biliary excretion into intestine.
Slide 4
Prehepatic (hemolytic) jaundice Excessive production of
bilirubin. Ability of the liver to conjugate is overcame. Increase
plasma unconjugated bilirubin.
Slide 5
Slide 6
Intrahepatic jaundice Defect may be in: uptake. conjugation.
secretion. Reflects liver dysfunction. In addition to high bili,
biochemical liver markers are high.
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Slide 8
Posthepatic jaundice Secondary to biliary obstruction. Increase
of conjugated bilirubin. GGT, ALP Clinical: pale colored stool
(absence of fecal bilirubin ) dark urine ( increased conjugated
bilirubin ) itching
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Slide 10
Diagnosis of jaundice
Slide 11
Approach to the Jaundiced Patient Definition. Imbalance between
bili production and excretion appears as jaundice. The appearance
of jaundice also depends on: which type of bilirubin is elevated.
duration.
Slide 12
Clinical Evaluation and Investigative Studies History and
physical examination: examine the mucous membranes of the mouth,
the palms, the soles, and the sclerae in natural light. Why?
protected areas from photodegradation skin will be the only site of
coloration due to consumption of large quantities of food
containing lycopene or carotene or drugs such as rifampin. careful
inspection of elastic tissues reveal no jaundice.
Slide 13
Clinical Evaluation and Investigative Studies Direct versus
indirect hyperbilirubinemia: ask about urine and stool color.
pruritus. look for scratch marks. rarely, the clinical picture may
be secondary to a massive increase in both direct and indirect
bilirubin production.
Unconjugated (Indirect) Bilirubin In case of hemolysis:
excissive production of unconjugated bilirubin. normal liver will
handle extrabilirubin. slight rise in serum levels is observed.
Blood tests reveal that 60% to 85% of bilirubin is indirect.
Slide 16
Unconjugated (Indirect) Bilirubin The diagnosis of indirect
hyperbilirubinemia attributable to hemolysis is confirmed by:
elevated serum (LDH) level (abundant in RBCs). decreased serum
haptoglobin level. evidence of hemolysis on microscopic examination
of the blood smear.
Slide 17
Unconjugated (Indirect) Bilirubin In case of decreased hepatic
bilirubin conjugation: Gilbert syndrome, is the most common: benign
condition affecting up to 7% of the population. characterized by a
defect in glucuronyl transferase I gene. impairment of bilirubin
glucuronidation affected patients may have jaundice after stress or
infection.
Slide 18
Cholestatic Syndrome conjugated hyperbilirubinemia: hepatic
jaundice (nonobstructive or medical jaundice) due to defect in
hepatocellular function. posthepatic jaundice (obstructive or
surgical jaundice ) as a result of blockage somewhere in the
biliary tree.
Slide 19
Cholestatic Syndrome characteristics: conjugated hyperbili.
(dark urine, pale stools, pruritus ). chronic malabsorption of
fat-soluble vitamins.
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HEPATIC VERSUS POSTHEPATIC JAUNDICE After confirmation of the
presence of direct hyperbilirubinemia, the next step is to
determine whether the jaundice is hepatic or posthepatic. The
sensitivities of history, physical examination, and blood tests
alone range from 70% to 95. The overall accuracy : 87% to 97%.
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HEPATIC VERSUS POSTHEPATIC JAUNDICE Clinical manifestations:
hepatic jaundice: acute hepatitis. a history of alcohol abuse.
physical findings reflecting cirrhosis or portal hypertension.
posthepatic jaundice: abdominal pain. rigors, itching.
hepatomegaly. patients are usually younger.
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HEPATIC VERSUS POSTHEPATIC JAUNDICE Summary: clinical approach
supported by simple biochemical evaluation displays good predictive
ability to distinguish hepatic from posthepatic jaundice. clinical
approach alone does not accurately identify the level of biliary
obstruction in a patient with posthepatic jaundice.
Slide 23
Causes of Hepatic Jaundice Hepatitis (viral, autoimmune or
alcoholic). Drugs and hormones. Diseases of intrahepatic bile
ducts. Liver infiltration and storage disorders. Systemic
infections. Total parenteral nutrition. Postoperative intrahepatic
cholestasis. Cholestasis of pregnancy. Benign recurrent
intrahepatic cholestasis. Infantile cholestatic syndromes.
Inherited metabolic defects. No identifiable cause (idiopathic
hepatic jaundice).
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Hepatic Jaundice Hepatic jaundice may be either acute or
chronic. Acute hepatic jaundice: de novo or in the setting of
ongoing liver disease. Causes: medications or viral hepatitis.
Physical examination usually reveals little. treatment in most
cases remains supportive.
Slide 25
Hepatic Jaundice Chronic hepatic jaundice: patient may have
chronic hepatitis, with or without cirrhosis. causes : viral
infection, drug, autoimmune liver disease. Physical examination:
stigmata of chronic liver disease. Treatment: supportive. to
quantify hepatic reserve: Child-Pugh classification. end-stage
liver disease: liver transplantation.
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Child-Pugh Classification Variable123 EncephalopathyNil
(0)Slight to moderate (1, 2) Moderate to severe (3-5)
AscitesNilSlightModerate to severe Bilirubin, mg/dl (mol/L*) < 2
(< 34)2-3 (34-51)>3 (> 51) Albumin, g/dl (g/L*)> 3.5
(> 35)2.8-3.5 (28-35)< 2.8 (< 28) Prothrombin index>
70%40%-70%< 40% ** grade A, 5-6 points ** grade B, 7-9 points **
grade C, 10-15 points
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(MELD) score The Model for End-Stage Liver Disease. the most
accepted score for allocation of organs for liver transplantation.
This score is based on: serum bilirubin. creatinine concentrations.
international normalized ratio (INR). No subjective components of
the Child-Pugh score (e.g., ascites and encephalopathy).
Slide 28
IMAGING It is the next step after Hx, physical examination and
laboratory assessment. Goals: to confirm the presence of an
extrahepatic obstruction. to determine the level of the
obstruction. to identify the specific cause of the obstruction.
staging information in cases of malignancy).
Slide 29
IMAGING Direct cholangiography (ERCP, PTC): gold standard for
defining the level of a biliary obstruction. Ultrasonography:
ductal dilatation with or w/o GB distension, presence of liver
causes. MRCP, CT scan and EUS: location and nature of biliary
obstruction. Diagnosis and staging biliopancreatic tumors.
Slide 30
Workup and Management of Posthepatic Jaundice Once
ultrasonography has confirmed that ductal obstruction is present,
there are three possible clinical scenarios: suspected cholangitis.
suspected choledocholithiasis without cholangitis. suspected lesion
other than choledocholithiasis.
Slide 31
Workup and Management of Posthepatic Jaundice suspected
cholangitis: presence of (Charcot's triad or Raynaud's pentad), the
most likely diagnosis is choledocholithiasis. ERCP is indicated for
diagnosis and treatment. Antibiotics with adequate biliary drainage
is the mainstay of treatment.
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Workup and Management of Posthepatic Jaundice SUSPECTED
CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS: Choledocholithiasis is the
most common cause of biliary obstruction. It should be strongly
suspected if the jaundice is: episodic painful if ultrasonography
has demonstrated the presence of gallstones or bile duct
stones.
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Workup and Management of Posthepatic Jaundice SUSPECTED LESION
OTHER THAN CHOLEDOCHOLITHIASIS: clinical presentation is less acute
(back pain) associated constitutional symptoms (e.g., weight loss,
fatigue, and long-standing anorexia) Categories depending on the
level of obstruction: Upper-third obstruction Middle-third
obstruction Lower-third obstruction
Slide 34
Causes of Posthepatic Jaundice Upper-third obstruction:
Polycystic liver disease Caroli disease Hepatocellular carcinoma
Oriental cholangiohepatitis Hepatic arterial thrombosis ( after
liver transplantation or chemotherapy) Hemobilia (e.g., after
biliary manipulation) Iatrogenic bile duct injury (e.g., after
laparoscopic cholecystectomy) Cholangiocarcinoma (Klatskin's tumor)
Sclerosing cholangitis Papillomas of the bile duct
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Causes of Posthepatic Jaundice Middle-third obstruction:
Cholangiocarcinoma Sclerosing cholangitis Papillomas of the bile
duct Gallbladder cancer Choledochal cyst Intrabiliary parasites
Mirizzi syndrome Extrinsic nodal compression (e.g., from breast
cancer or lymphoma) Iatrogenic bile duct injury (e.g., after open
cholecystectomy) Cystic fibrosis Benign idiopathic bile duct
stricture
Slide 36
Causes of Posthepatic Jaundice Lower-third obstruction
Cholangiocarcinoma Sclerosing cholangitis Papillomas of the bile
duct Pancreatic tumors Ampullary tumors Chronic pancreatitis
Sphincter of Oddi dysfunction Papillary stenosis Duodenal
diverticula Penetrating duodenal ulcer Retroduodenal adenopathy
(e.g., lymphoma, carcinoid)
Slide 37
Diagnosis and Assessment of Resectability The following
structures should be carefully evaluated for assessment of the
resectability: superior mesenteric vein the portal vein superior
mesenteric artery porta hepatis local adenopathy extrapancreatic
extension metastasis
Slide 38
Nonoperative Management: Drainage and Cholangiography Most
malignant obstruction present in advance stage and the treatment is
usually palliative rather than curative. Decompression is by ERCP
or PTC though the PTC is preferable in obstruction near the
bifurcation.
Slide 39
Palliation in patients with advanced malignant disease
supportive care is the only method for treatment of asymptomatic
(cholangitis, pruritus ) malignant obstruction. metalic stent via
PTC or ERCP is the option for palliation. patients who expected to
live more than 6 months surgical bypass is preferable. prophylactic
gastric drainage is controversial. in patients with periampullary
tumor, celiac block.
Slide 40
Postoperative Jaundice Jaundice develops in approximately 1% of
all surgical patients after operation. Common causes of jaundice
within 24h after opertation: Hemolysis as a result of massive blood
transfusion, hematoma resorption, or transfusion reaction.
Inhereted disorders of bilirubin metabolism ( Gilberts syndrome and
others). Presence of underlying hemolytic anemia which may
exacerbate by administration of drugs.
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Summary Types of jaundice. Approach to the patient and
importance of history and physical examination. Role of imaging
modalities. Differentiation between surgical and medical jaundice.
Treatment options in surgical jaundice.