1. Obstructive Jaundice
M K Alam MS; FRCS Ed

2. Objectives Definition Anatomy of the hepatobiliary tree
Biochemistry of bilirubin
Types of Jaundice
Causes of OBSTRUCTIVE Jaundice.
Clinical presentation
Laboratory investigations
Radiological investigations
Treatment options

3. Definition of Jaundice
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 (50 µmol/L)
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.

4. 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.

5. Bilirubin Biochemistry
80% of bilirubin is formed by the degradation of Heme from RBC.
The reminder Heme containing enzymes (cytochromes, catalase, peroxidase..)
Potentially toxic
Remains harmless by binding to albumin

6. Unconjugated Bilirubin (indirect bilirubin)
Insoluble in water
Tightly complex to albumin
Not filtered through renal glomeruli
Not excreted in urine
Toxic substance
The main form of bilirubin in the blood

7. Conjugated Bilirubin (Direct bilirubin)
Bilirubin conjugated in the liver before its excretion into bile
Conjugated with glucuronic acid
Changes bilirubin into water soluble
Can be filtered through renal glomeruli
Present in low concentration in the blood

8. 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.

9. Types of Jaundice Pre-hepatic Hepatic Post-hepatic (Obstructive)
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.

10. Pre-hepatic
Excess extra-hepatic production of bilirubin raising unconjugated form.
Haemolytic anemias: congenital spherocytosis, sickle cell disease

11. Hepatic jaundice
Disability of liver to uptake/ conjugate bilirubin (hepatocellular), or excrete bile from the liver (cholestatic)
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).

12. Cholestatic jaundice
Cholestasis denotes a pathologic condition of impaired bile formation and or bile flow.
Intrahepatic cholestasis (Intrahepatic biliary tree diseases or hepatocellular secretory failure
Extrahepatic cholestasis (biliary obstruction) frequently is amenable to surgical correction.
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

13. Consequences of Cholestasis
Retention of bile salt in liver
Decreased hepatocyte function
Decreased Kupffer 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

14. 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

15. Intrahepatic cholestasis
Cholestatic phase of AVH
Alcoholic Hepatitis
Drug induced liver disease
Primary biliary cirrhosis
Primary sclerosing cholangitis
TPN
Cholestasis of pregnancy
Sepsis
Benign postoperative Cholestasis

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

17. Post hepatic (Obstructive Jaundice)

19. Benign Choledocholithiasis* Primary sclerosing cholangitis
Post-surgical stricture
Pancreatitis
Parasitic infections

20. Malignant Carcinoma gall bladder Periampullary carcinoma
Cholangiocarcinoma
Carcinoma of the head of pancreas
Obstruction due to metastatic LN

21. History - Age, gender - Pain / painless ,onset , duration
- Fever ,fatty dyspepsia
- Jaundice, dark urine, pale stool
- Alcohol, blood transfusion
- Medication , drug abuse
- Surgery(post op complication)
- Hemolytic disorders
- Weight loss, loss of appetite

22. Clinical presentation
RUQ pain/painless, nausea, vomiting, fever, jaundice, dark urine , pale stool, pruritus
Charcot triad: pain, jaundice, fever
Reynold’s pentad: triad+ confusion, shock
Skin xanthomas
Symptoms of intestinal mal-absorption
Deficiency of fat soluble vitamins

23. Calculous obstruction: Younger patient, intermittent abdominal pain, fatty dyspepsia, fluctuant jaundice, dark urine, pale stool, pruritus (bile salt deposits)
Neoplasia: Older age, painless/ mild discomfort, weight loss, progressive jaundice, dark urine, pale stool, pruritus, Courvoisier sign, hepatomegaly
Hepatocellular: Stigmata of CLD- liver palm, spider naevi, gynecomastia, signs of PH (splenomegaly, ascitis, caput medusae), hepatomegaly

24. Courvoisier’s law/sign
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

25. Laboratory Investigations
Blood test (Hemoglobin, WBC, Platelets)?
Coagulation Profile
Hepatic profile
Hepatitis profile
Tumour marker
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

26. 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)

27. Alkaline Phosphatase 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 extra hepatic obstruction with values greater 3-5 times the normal

28. GGT Very sensitive for hepatobiliary diseases.
Mainly it increases in ductal injury
In case of increase in alkaline phosphatase GGT is a good test to exclude the bone source of ALP
High Alkaline Phosph. Normal GGT  Bone source likely
High Alkaline Phosph . High GGT  Hepatic source likely

29. AST & ALT
AST (aspartate aminotransferase) : liver, cardiac muscle, skeletal muscles, kidneys, brain, pancreas
ALT (alanine aminotransferase) liver, skeletal muscle
Used as indicator of liver cell injury
ALT is more specific

30. Haemolytic jaundice High unconjugated (indirect) serum bilirubin
No bilirubin in urine
Normal liver enzymes

31. Obstructive jaundice ALP  Transaminases: normal/ moderately elevated
Serum conjugated bilirubin
> 50% of total: more suggestive of post hepatic than hepatic jaundice
ALP 
Transaminases: normal/ moderately elevated
Fecal urobilinogen:  -incomplete obstruction , absent - complete obstruction
Urobilinogen in urine: absent in complete obstructive jaundice with  bilirubinuria.

32. Case Scenario
82-yr old, male Presents with: Progressive jaundice Itching Loss of weight .

33. History of presenting illness
Gradually progressive jaundice
Recurrent episodes of itching
White stools for 2 months
Dark yellow urine
Generalized weakness & fatigability- 6 months
Weight loss - 1 year
Reduced appetite
No fever

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

35. Physical Examination Abdomen Pulse 88/min, BP 110/70 mmHg, afebrile
Anemia +, Jaundice ++
No lymphadenopathy
Scratch marks
Abdomen
Soft non-tender–
Palpable gall bladder
No free fluid

36. Investigations Hb. 11.7, Hct. 35 WBC: 6000, Platelet: 350,000
Serum creatinine: 1.2 mg
Total bilirubin: 20 mg; (unconj. 2 mg, conj. 18 mg)
Alkaline phosphatase: 990 U/L
Total protein: 6.5 grams;
CA 19-9: 350 units/ml

37. Imaging studies To determine: Extrahepatic obstruction
Level of obstruction
Cause of obstruction
Staging
Best therapeutic approach

38. ULTRASOUND
Best imaging for biliary tree, non-invasive, cheap, high accuracy esp. in gallstones and biliary dilatation.
Disadvantage: 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. Imaging/ ERCP CT : MRCP: ERCP:
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: Unfavorable anatomy

42. ERCP
MRCP

43. 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

45. Scenario case (cont.)
USG- 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. Possibility of periampullary mass.
Advised ERCP.

47. Treatment options for obstructive jaundice
Antibiotic therapy (if indicated for infection)
Intravenous fluids
Pain medications, nutritional support
ERCP: biopsy, stone removal ,dilatation, stent placement
Surgery: Curative resection, palliative by-pass
Adjuvant therapy for cancer: chemotherapy, or radiotherapy

48. ERCP (Stone CBD, Periampullary carcinoma)

49. CBD stone extraction

50. Surgical Procedures for
Obstructive Jaundice

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

52. Carcinoma gallbladder: Radical Cholecystectomy with wedge resection & CBD excision
Cholediocholithiasis: ERCP removal, CBD exploration
Cholangio Ca: Liver resection, Whipple operation,
Stenting by ERCP or PTC- palliative
Biliary Stricture: Hepatico-jejenostomy/

53. Periampullary Ca: Whipple’s operation
Carcinoma head pancreas: Whipple op.
Bilio-enteric bypass (palliative)

54. Whipple’s Procedure

55. 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

56. Thank you!