Presentation is loading. Please wait.

Presentation is loading. Please wait.

Obstructive Jaundice M K Alam MS; FRCS Ed.

Similar presentations

Presentation on theme: "Obstructive Jaundice M K Alam MS; FRCS Ed."— Presentation transcript:

1 Obstructive Jaundice M K Alam MS; FRCS Ed

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

3 Definition of Jaundice
Yellowish discoloration of the skin and other tissues (sclera, mucous membrane, deep tissues…) due to deposition of bile pigment(bilirubin) when serum level exceed 3mg/dl (50 µmol/L) Normal : Total serum bilirubin 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 remainder ‘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 The main form of bilirubin in the blood

7 Conjugated Bilirubin- (Direct 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: Acute : Chronic :
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 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 pruritus 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 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

22 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

23 Courvoisier’s law/sign
If the CBD is obstructed due to calculus , the GB is usually not distended owing to previous inflammatory fibrosis. If CBD is obstructed 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

24 Laboratory Investigations
Blood test (Hemoglobin, WBC, Platelets) Coagulation Profile – PT, aPTT, INR Hepatic profile (Bilirubin, transaminase, ALP, GGT, albumin) Hepatitis profile (HAV, HBV, HCV) Tumour markers (AFP, CEA, CA 19-9) 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

25 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)

26 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

27 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 Phosphatase, Normal GGT  Bone source likely High Alkaline Phosphatase, High GGT  Hepatic source likely

28 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

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

30 Transaminases: normal / moderately elevated
Obstructive jaundice Serum conjugated bilirubin >50% : 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.

31 Investigation results of the patient
Hemoglobin , WBC: 6000, Platelet: 350,000 Serum creatinine: 1.2 mg Total bilirubin: 20 mg; (unconjugated- 2 mg, conjugated- 18 mg) Alkaline phosphatase: 990 U/L Total protein: 6.5 grams CA 19-9: 350 units/ml (Normal U/mL)

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

33 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)

98%diagnostic accuracy. Diagnostic tissue sampling (EUS-FNA) High sensitivity for- focal pancreatic mass (superior to CT). More specific to biliary stricture compared to MRCP.

35 Other Investigations CT : MRCP: ERCP:
Detects primary and metastatic tumors MRCP: Non invasive visualization of hepato biliary tree. ERCP: invasive therapeutic (biopsy, brush cytology, Stone extraction or stenting) Complications: Pancreatitis, Cholangitis, Hge, Sepsis limitations: Unfavorable anatomy

36 HIDA Scan: useful in acute cholecystitis Diagnostic Laparoscopy
PTC indications: when ERCP either is inappropriate or has failed. Drainage of biliary obstructions. HIDA Scan: useful in acute cholecystitis Diagnostic Laparoscopy Angiography: Rule out abnormal vascular anatomy Tumor markers- CA19-9 , CEA

37 CT- Tumour pancreas


39 PTC

40 ERCP Periampullary carcinoma CBD stone

41 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

42 CBD stone extraction

43 Surgical Procedures for
Obstructive Jaundice

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

45 Carcinoma gallbladder:
Radical Cholecystectomy with wedge resection & CBD excision Choledocholithiasis: ERCP removal, CBD exploration Cholangio carcinoma: Liver resection and or local excision of the lesion or Whipple operation or stenting by ERCP or PTC Biliary Stricture: Hepatico-jejenostomy

46 Whipple’s operation Periampullary Ca: Carcinoma head of pancreas:
Bilio-enteric bypass for unresectable tumour

47 Whipple’s Operation

48 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

49 Thank you!

Download ppt "Obstructive Jaundice M K Alam MS; FRCS Ed."

Similar presentations

Ads by Google