1. Obstructive Jaundice Dr. Mohammed H. Alarawi
Consultant General surgeon
Al- Iman General Hospital
FRCS, ED – ABCS

2. 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

3. Case Scenario
82 yr old male patient presents with progressive jaundice, itching, loss of weight .

4. 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

5. H/o past illness Personal History No h/o DM, HT, TB,
No past Surgical history
Personal History
Smoker – 25 yrs
Non-alcoholic

6. Physical Examination Abdomen Pulse 88/min, BP 110/70 –Afebrile
anemia +, Jaundice ++–
No Lymphadenopathy
Scratch marks
Abdomen
Soft non-tender– palpable gall bladder– No free fluid

7. 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 mg/dl
Direct Bilirubin < 0.4 mg/dl
The cause of the yellowish discoloration is the accumulation of the bile pigments (bilirubin) in the skin.
Most of the bilirubin in the blood is in the unconjugated form.

8. 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

9. 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

10. 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

11. Con’t
When the conjugated bilirubin reaches the terminal ileum and colon it will de-conjugated into urobilinogen and stercobillinogen. Urobilinogen controbutes for the enterohepatic circulation, and some will be filtered in the urine because it is slightly water soluble. Stercobillinogen will give the dark brown color of the stool.

12. Anatomy of the Hepatobiliary Tree
The gallbladder has 3 main parts the neck, Body and the fundus. The gallbladder has the function of concentrating the bile and has no role in the production process the bile. Cystic duct joins the common hepatic duct to form the common bile duct. And then the common bile duct will join the pancreatic duct and it will enter the second part of the duodenoum. The area of the insertion is called Ampulla of Vater.

13. Types of Jaundice Pre-hepatic Hepatic
Post-hepatic (Obstructive)(cholestatic)
Intrahepatic
Extrahepatic
Physiologic jaundice, affect the newborn because of the down regulation of the glucoronyltransferase enzyme. The reason for the down regulation is during fetal life the bilirubin must be in the unconjugated form so it can pass placenta and cleared by the mother liver. So the fetus doesn’t need to conjugate the bilirubin so it will loss its function for a while. But it will gain its function later.
Physiologic Jaundice???

14. Pre-hepatic
Excess extra-hepatic production of bilirubin raising unconjagated form.
Haemolytic anemias
- Malariae

15. Hepatic jaundice
liver disability to uptake, conjugate or excecrete bilirubin, raising unconjugated bilirubin
Acute :
Chronic :
Viral hepatitis A, B, C..
Other viruses: EBV, CMV
Drugs
Dose-dependant e.g. paracetamol
Idiosyncratic
Toxins
Autoimmune hepatitis
Alcoholic hepatitis
Tumours
Viral hepatitis B, C
Chronic AI hepatitis
Genetic (Crigler–Najjar, Gilbert syndroms)
End-stage liver disease (of any cause)
Alcoholic
Hepatitis B, C
Autoimmune
Haemochromatosis
Wilson’s disease
Hemochromatosis : it could be primary (HEF gene mutation) or secondary (multiple blood transfusions).

16. Post hepatic (Obstructive Jaundice)

17. Benign causes Choledocholithiasis Primary sclerosing cholangitis
Post-surgical stricture
Pancreatitis
Parasitic infections

18. Malignant Causes Carcinoma gall bladder Periampullary Carcinoma
Cholangiocarcinoma
Carcinoma of head of pancreas
Obstruction due to metastatic LN

19. 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
intrahepatic cholestasis (Intrahepatic biliary tree diseases or hepatocellular secretory failure cannot be treated surgically, and the patient’s condition may be worsened by an operative procedure. Thus, there is some urgency in identifying the cause of jaundice and cholestasis

20. What are the Causes of Cholestasis: Intrahepatic & Extrahepatic

21. Intrahepatic cholestasis
Cholestatic phase of AVH
Alcoholic H
Drug induced liver D
Primary biliary cirrhosis
Primary sclerosing cholangitis
TPN

22. Intrahepatic cholestasis
Cholestasis of pregnancy
Sepsis
Benign postoperative Cholestasis

23. Drugs that lead to Cholestasis Jaundice
Estrogen
Tamoxifen
Anabolic steroid
Azathioprine
Chlorpromazine
Carbamazepine
Antibiotics- Erythromycin, Rifampicin

24. 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

25. 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

26. Clinical presentation of obstructive jaundice
Jaundice, dark urine,pale stool, pruritus
RUQ pain, Nausea and vomiting
Fever
Charcot Triad???
Skin xanthomas
Symptoms related to intestinal mal-absorption and nutritional deficiency of fat soluble vitamins

27. History - sex - onset , duration - alcohol consumption
- 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

28. 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.
In presence of enlarged g b associated with jaundice ,the cause is unlikely to be gall stone

29. Laboratory Investigations
Blood test (Hemoglobin, WBC, Platelets)?
Coagulation Profile (PTT, INR,..)?
Hepatic profile
Hepatitis profile
Blood test (Hemoglobin, WBC, Platelets)? infections. Hemolysis
Coagulation Profile (PTT, INR,..)? in liver failure patients the tendency of bleeding is high, ( vit. K deficiency because this is lipid soluble vitamin so it will not be absorbed because of the live unable to produce bile which is responsible for lipid absorption. and unable to produce clotting factors)
Antibody assay? rule out infectious and autoimmune diseases
Surface antigen? look for hepatitis virus
Total and fractional Bilirubin see the summery slide

30. Laboratory Investigations
Hepatic Profile:
AST
(10-40)
ALT
Alkaline phosphatase
( U/L)
Albumin
(35-50 g/L)
Total bilirubin
(5-20 umol/L)
Direct bilirubin
(<5 umol/L)
Indirect bilirubin
(<12 umol/L)

31. 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

32. 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

33. 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

34. ALP  cholesterol  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.

35. 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

36. Radiology Determine: Extrahepatic obstruction level of obstruction
Cause of obstruction
Staging
Best therapeutic approach

37. 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
At PTC or ERCP, stents can be introduced (treatment during diagnosis)

38. 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
At PTC or ERCP, stents can be introduced (treatment during diagnosis)

39. 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.

40. 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

41. Oral Cholecystography (OCG):
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

42. ERCP
MRCP

43. 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

45. Treatment options for obstructive jaundice
Depends on the cause and severity .
Antibiotic therapy (if indicated for infection)
. ERCP, allows treatment of some bile duct problems including removal of gallstones causing obstruction
Intravenous fluids , pain medications and Nutritional support .
Surgery to repair anatomical defects or create alternative pathways for the flow of bile
Treatment for cancer, which may include surgery, chemotherapy, or radiation therapy

46. What are the Surgical Procedures done for Obstructive Jaundice?

47. 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: Hepatico-jejenostomy/

48. Periampullary Ca:
Whipple’s Procedure
Chronic Pancreatits with head Mass: Whipple/ bilio-enteric anastmosis

49. Whipple’s Procedure Pancreaticojejunostomy- end to end
Hepatico-jejunostomy – end to side
Gastrojejunostomy – end to side
Feeding Jejunostomy

50. Preoperative preparation
Oral H2 antagonist
Vit. K or FFP
Perioperative broad spectrum antibiotics
Rehydration and adequate diuresis
Furosemide/ Mannitol
Catheterization & CVP monitoring

51. Postoperative management
- 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