Download Jaundice and Posthepatic Jaundice

Obstructive Jaundice
Dr. Mohammed H. Alarawi
Consultant General surgeon
Al- Iman General Hospital
FRCS, ED – ABCS
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Objectives
• Case scenario
• Definition of Jaundice
• Bilirubin Biochemistry
• Anatomy of the Hepatobiliary Tree
• Types of Jaundice
• OBSTRUCTIV Jaundice.
• Clinical presentation
• Laboratory investigations
• Radiological investigations
• Treatment options
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Case Scenario
82 yr old male patient presents with
progressive jaundice, itching, loss of
weight .
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History of presenting illness
Gradually progressive jaundice
Recurrent episodes of itching
White stools for last 2 months
Dark yellow urine
Generalized weakness & fatigability- 6
months
• Weight loss in last 1 year
• Reduced appetite
• No fever
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H/o past illness
– No h/o DM, HT, TB,
– No past Surgical history
• Personal History
– Smoker – 25 yrs
– Non-alcoholic
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Physical Examination
– Pulse 88/min, BP 110/70 –Afebrile
– anemia +, Jaundice ++–
– No Lymphadenopathy
– Scratch marks
• Abdomen
– Soft non-tender– palpable gall bladder– No
free fluid
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Definition of Jaundice
• = icterus
• Yellowish pigmentation of the skin and
other Tissues (Sclera, mucous membrane,
deep tissue…)due to deposition of bile
pigment(bilirubin) when serum level
exceed 3mg/dl
• Normal Total serum bilirubin is 0.3-1.9 mg/dl
– Direct Bilirubin < 0.4 mg/dl
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Bilirubin Biochemistry
• 80% of Bilirubin is formed by the
degradation of Heme from Red blood cell.
• The reminder from Heme containing
enzymes (cytochromes, catalase,
peroxidase..)
• Is potentially Toxic
• Remains harmless by binding to albumin
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Unconjugated Bilirubin
(indirect bilirubin)
• Insoluble in water
• Tightly complex to albumin
• Not filtered through renal glomeruli, is
not excreted in urine
• Toxic substance
• The main form of bilirubin in the blood
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Conjugated Bilirubin
(Direct bilirubin)
• Bilirubin must be conjugated before its
excretion into bile
• Bilirubin is conjugated with glucuronic acid
by the enzyme glucuronyltransferase
• This changes the bilirubin into a water
soluble and thus facilitates rapid excretion
• Can be filtered through renal glomeruli
• Present in low concentration in the blood
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Con’t
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Anatomy of the Hepatobiliary Tree
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Types of Jaundice
A. Pre-hepatic
B. Hepatic
C. Post-hepatic (Obstructive)(cholestatic)
I. Intrahepatic
II. Extrahepatic
Physiologic Jaundice???
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Pre-hepatic
• Excess extra-hepatic production of
bilirubin raising unconjagated form.
– Haemolytic anemias
– - Malariae
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Hepatic jaundice
liver disability to uptake, conjugate or excecrete
bilirubin, raising unconjugated bilirubin
Acute :
• Viral hepatitis A, B, C..
• Other viruses: EBV,
CMV
• Drugs
– Dose-dependant e.g.
paracetamol
– Idiosyncratic
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Toxins
Autoimmune hepatitis
Alcoholic hepatitis
Tumours
Chronic :
• Viral hepatitis B, C
• Chronic AI hepatitis
• Genetic (Crigler–Najjar,
Gilbert syndroms)
• End-stage liver disease (of
any cause)
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Alcoholic
Hepatitis B, C
Autoimmune
Haemochromatosis
Wilson’s disease
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Post hepatic
(Obstructive Jaundice)
Benign causes
• Choledocholithiasis
• Primary sclerosing cholangitis
• Post-surgical stricture
• Pancreatitis
• Parasitic infections
Malignant Causes
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Carcinoma gall bladder
Periampullary Carcinoma
Cholangiocarcinoma
Carcinoma of head of pancreas
Obstruction due to metastatic LN
Cholestatic jaundice
• Cholestasis denotes a pathologic condition of
impaired bile formation and or bile flow.
– Extrahepatic cholestasis (biliary obstruction)
frequently is amenable to surgical correction.
– Intrahepatic cholestasis (Intrahepatic biliary tree
diseases or hepatocellular secretory failure
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What are the Causes of
Cholestasis:
Intrahepatic & Extrahepatic
Intrahepatic cholestasis
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Cholestatic phase of AVH
Alcoholic H
Drug induced liver D
Primary biliary cirrhosis
Primary sclerosing cholangitis
TPN
Intrahepatic cholestasis
• Cholestasis of pregnancy
• Sepsis
• Benign postoperative Cholestasis
Drugs that lead to Cholestasis
Jaundice
• Estrogen
• Tamoxifen
• Anabolic steroid
• Azathioprine
• Chlorpromazine
• Carbamazepine
• Antibiotics- Erythromycin, Rifampicin
Consequences of Cholestasis
Retention of bile salt in liver
• Decreased hepatocyte function
• Decreased Kuffer cell activity
• Decreased albumin & clotting factors synthesis
• Decreased collagen synthesis, impaired wound healing
Retention of bile constituents in serum
• Jaundice, dark urine and Pruritis
• CVS depression
• Nephrotoxicity
• Hypercholesterolemia, atheroma, Xanthoma
Consequences of Cholestasis
Absence of bile in Intestine
• Escape of endotoxins into portal blood
• Mal-absorption of fats and Vitamin A, D, E & K
• Clay colored stools
Clinical presentation of
obstructive jaundice
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Jaundice, dark urine,pale stool, pruritus
RUQ pain, Nausea and vomiting
Fever
Charcot Triad???
Skin xanthomas
Symptoms related to intestinal malabsorption and nutritional deficiency of fat
soluble vitamins
History
- age
- sex
- onset , duration
- alcohol consumption
- blood transfusion
- drug abuse
- medication
- recent surgery(post op complication)
- history of hemolytic disorders
- weight loss, loss of appetite
- pain ,fever ,fatty dyspepsia
- dark urine, pale stool.
- yellow discoloration(skin , sclera)
- symptoms & signs of chronic liver disease
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Courvoisier’s law
If the CBD is obst. due to
calculus , the GB is
usually not distended
owing to previous
inflammatory fibrosis.
If CBD is obstr. due to
malignant growth, the GB
becomes distended in
order to reduce the press.
in the biliary system.
Laboratory Investigations
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Blood test (Hemoglobin, WBC, Platelets)?
Coagulation Profile (PTT, INR,..)?
Hepatic profile
Hepatitis profile
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Laboratory Investigations
Hepatic Profile:
AST
(10-40)
ALT
(10-40)
Alkaline phosphatase
(40-100 U/L)
Albumin
(35-50 g/L)
Total bilirubin
(5-20 umol/L)
Direct bilirubin
(<5 umol/L)
Indirect bilirubin
(<12 umol/L)
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AST & ALT
• AST found in liver, cardiac muscle,
skeletal muscles, kidneys, brain, pancreas
• ALT found in liver, skeletal muscle
• Used as indicator of liver cell injury
• ALT is more specific
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Alkaline Phos.
• Can come from liver, bone, placenta and intestine
Used mainly as indicator of ductal causes: partial
obstruction of bile ducts, primary biliary cirrhosis,
sclerosing cholangitis
• Elevated in all patients with extra hepatic obstruction
with values greater 3-5 times the normal
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GGT
• Very sensitive for hepatobiliary disease.
• Mainly it increases in ductal injury
• In case of increase in Alkaline Phosp .
GGT is a good test to exclude the Bone
source of ALP
High Alkaline Phosph. Normal GGT  Bone is
more likely
High Alkaline Phosph . High GGT  Hepatic
source is more likely
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• Serum conjugated bilirubin
– > 50% of total: more suggestive of post
hepatic than hepatic jaundice
• ALP 
• cholesterol 
• Fecal urobilinogen (incomplete obstruction)
and absent (complete obstruction)
• Urobilinogenuria is absent in complete
obstructive jaundice with  bilirubinuria.
Case scenario Con’t
• Hb: 11.7• Hct: 35• WBC: 6000; Plt: 350,000
• Serum Creat: 1.2 mg• Total bil: 20
mg;B1(unconj): 2 mgB2 (conj): 18 mg•
Alkaline phosphatase: 990 U/L• Total
protein: 6.5 grams;
• CA 19-9: 350 units/ml
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Radiology
– Determine:
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Extrahepatic obstruction
level of obstruction
Cause of obstruction
Staging
Best therapeutic approach
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Radiology
• Ultrasound
– Best imaging for biliary tree –
non-invasive, cheap, high
accuracy esp in gallstones and
biliary dilatation.
– Disadvantege: distal bile duct
may be obscured by bowel gas
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Radiology
• Ultrasound
– Best imaging for biliary tree –
non-invasive, cheap, high
accuracy esp in gallstones and
biliary dilatation.
– Disadvantege: distal bile duct
may be obscured by bowel gas
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ENDOSCOPIC ULTRASOUND
(EUS)
• 98%diagnostic accuracy in obstructive jaundice
• It allows diagnostic tissue sampling (EUS-FNA)
• High sensitivity for identification of focal
pancreatic mass, SUPERIOR to CT.
• More specific to biliary stricture compared to
MRCP.
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• CT :
– Main role in malignancies for primary and
metastatic tumors
• MRCP:
– Non invasive to visualize the hepato biliary tree.
• ERCP:
– invasive, therapeutic (biopsy, brush cytology, Stone
extraction or stenting)
– Complications: Pancreatitis, Cholangitis, Hge, Sepsis
– limitations: Unfaverable anatomy
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• PTC indications:
– when ERCP either is inappropriate or has failed.
– Drainage of biliary obstructions.
• Oral Cholecystography (OCG):
• useful with symptomatic patients with negative US
• HIDA Scan: useful in acute cholecystitis
• Diagnostic Laparoscopy
• Angiography: Rule out abnormal vascular anatomy
• Tumor markers- CA19-9 , CEA
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ERCP
MRCP
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Scenario case con’t
• USG-Abd: solid mass in distal CBD,
dilated CBD, Intrahepatic Biliary
distension and distended GB
• CT abdomen show grossly dilated intra
and extra hepatic biliary channels With
distended gall bladder And possibility of
periampullary mass ADVISE ERCP
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Treatment options for obstructive
jaundice
Depends on the cause and severity .
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Antibiotic therapy (if indicated for infection)
. ERCP, allows treatment of some bile duct problems including removal of
gallstones causing obstruction
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Intravenous fluids , pain medications and Nutritional support .
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Surgery to repair anatomical defects or create alternative pathways for the
flow of bile
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Treatment for cancer, which may include surgery, chemotherapy, or
radiation therapy
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What are the Surgical Procedures
done for Obstructive Jaundice?
Ca GB: Radical
Cholecystectomy with
wedge resection and
CBD excision
Cholediocholithiasis:
ERCP removal,
mechanical lithotripsy ,
shock wave laser or
CBD exploration
Cholangio Ca: Liver
resection and or local
excision of the lesion or
Whipple or stenting by
ERCP or PTC
Biliary Stricture: Hepaticojejenostomy/
Periampullary Ca:
Whipple’s Procedure
Chronic Pancreatits
with head Mass:
Whipple/ bilio-enteric
anastmosis
Whipple’s Procedure
Pancreaticojejunostomy- end to end
Hepatico-jejunostomy – end to side
Gastrojejunostomy – end to side
Feeding Jejunostomy
Preoperative preparation
• Oral H2 antagonist
• Vit. K or FFP
• Perioperative broad spectrum antibiotics
• Rehydration and adequate diuresis
• Furosemide/ Mannitol
• Catheterization & CVP monitoring
Postoperative management
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Correct Fluid & Electrolyte imbalance
Correct hypothermia
Achieve CVS stability
Adequate analgesia & chest physiotherapy
Antibiotics + H2 receptor antagonist
Maintain urine output
Replace blood and blood products