The document discusses obstructive jaundice, including its causes, pathophysiology, clinical presentation, investigations, and treatment. The most common causes are gallstones and cancer of the head of the pancreas. Obstructive jaundice results from the blockage of bile flow from the liver to the small intestine, leading to increased bilirubin levels and yellowing of the skin and eyes. Investigations include blood tests, imaging like ultrasound and CT/MRCP, and invasive procedures such as ERCP. Surgical treatment aims to relieve the obstruction by removing gallstones or tumors.

1. OBSTRUCTIVE JAUNDICE
By De Pope
9/1/2023 De Pope 1

2. OUTLINE
• INTRODUCTION
• AETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• INVESTIGATIONS
• PRE-OPERATIVE TREATMENT
• TREATMENTS
• PROGNOSIS
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3. INTRODUCTION
• Is the yellowish discoloration of the skin, mucus membranes and
sclera due to hyperbilirubinea.
• Obstructive jaundice is caused by conditions that block the normal
flow of bile from the liver into the intestines
• Gallstones are the most common cause of biliary obstruction followed
by cancer of the head of the pancreas
• Normal serum bilirubin level is 0.2 - 1 mg/dl of which no more than
0.2 mg/dl are directly reacting.
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4. Continua…………
• Surgical jaundice is any jaundice amenable to surgical treatment.
Majority are due to extra-hepatic biliary obstruction.
• Not all surgical jaundice is due to obstruction e.g. congenital
spherocytosis, here surgical treatment can be offered as splenectomy.
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5. AETIOLOGY
• Intraluminal causes:
- Choledocholithiasis
- Clonorchis sinensis
- Ascariasis & Schitosomiasis
• Mural causes:
- Malignant stricture
- cholangiocarcinoma
- Benign stricture
- Scelerosing cholangitis
• Extrinsic Causes:
- Ca Head of Pancreas
- Periampullary Carcinoma, Portal LN
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6. BENJAMIN’S CLASSIFICATION
Type 1 ( complete obstruction)
• Primary or secondary liver tumors
• Iatrogenic ligation of CBD
• Pancreatic tumors,
cholangiocarcinoma
Type 2 ( intermittent obstruction)
• Choledocholithiasis
• Periampullary tumor
• Choledochal cyst
• Bile duct papilloma
• Hemobilia, Duodenal diverticula
Type 3 ( chronic complete
obstruction)
• Bile duct stricture
• Biliary atresia
• Post radiotherapy
• Chronic pancreatitis
• Cystic fibrosis
Type 4 ( segmental obstruction)
• Sclerosing cholangitis
• Traumatic
• Hepatolithisis
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7. DIFFERENT CAUSES
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8. PATHOPHYSIOLOGY
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9. Continua……....
• Bile is produced continuously by hepatocytes. It contains cholesterol
and waste products, such as bilirubin and bile salts, which aid in the
digestion of fats.
• Half the bile produced runs directly from the liver into the duodenum
via a system of ducts, ultimately draining into the common bile duct
(CBD). The remaining 50% is stored in the gallbladder. 12Hrs
• Biliary obstruction prevents carriage of bile to the small intestine
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10. Continua………
• Normal secretory pressure of bile is 15-25 cm of water
• At 35 cm of water there is suppression of bile flow
• High pressure leads to cholangiovenous and cholangiolymphatic
reflux of bile
• Dilatation of bile duct and intra hepatic biliary radicals(IHBR)
• IHBR dilatation may be absent if there is secondary hepatic fibrosis or
cirrhosis
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11. Continua………….
• Increase in biliary pressure leads to disruption of tight junctions
between hepatocytes and bile duct cells with increased permeability
• Reflux of bile contents in liver sinusoids
• Neutrophil infiltration,increased fibrinogenesis and deposition of
reticulin fiberes in portal triad
• Reticulin fibers gets converted in to type 1 collagen
• Laying down of collagen fibers leads to hepatic fibrosis, obstruction
of sinusoids and secondary biliary cirrhosis and portal hypertension
• Fibrosis can also lead to atrophy of obstructed liver.
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12. SYSTEMIC EFFECTS
CHANGES IN LIVER BLOOD FLOW
In Acute obstruction
increase in hepatic arterial blood flow
No change in portal venous blood flow
Chronic obstruction
Decrease in total liver blood flow , dilatation of sinusoids and
elevation of portal pressure
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13. Continua………
CARDIOVASCULAR SYSTEM
Decreased cardiac contractability
Reduced left ventricular pressure
 Impaired response to beta agonist drugs
 Decreased peripheral vascular resistance
 Bradycardia due to direct effect of bile salts on SA node.
Net result: Hypotensive patient, Exaggerated hypotensive response to
bleeding, More prone to postoperative shock.
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14. Continua……….
RENAL FAILURE
10 % incidence with 70 % mortality, Factors responsible are:
 Decreased cardiac function
 Increased levels of ANP resulting in hypovolemia
Decreased effect of bile salts on kidney mediated by increased
prostaglandin E2
 Endotoxemia
Bile salt deposition
Result: in renal vasoconstriction, shunting of blood from cortex, Activation of
complement system, peri-tubular and glomerular fibrin deposition leading to
tubular and cortical necrosis
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15. Continua………
IMMUNE SYSTEM
Defects in cellular immunity
 Impaired T cell proliferation
Decreased neutophil chemotaxis
Defective bacterial phagocytosis
Depressed function of RE system i.e Kupffer cells
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16. Continua………..
WOUND HEALING
Delayed wound healing
High incidence of wound dehiscence
Decreased activity of enzyme Propyl hydroxylase in the skin -This
helps in incorporation of proline in collagen
 Defective synthesis of collagen
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17. Continua……….
COAGULATION FACTOR DEFECTS
Prolongation of Prothrombin time
Decreased absorption of fat soluble vitamins A,D,E,K (vitamin K dependent
clotting factors not formed- II, VII, IX and X)
 Endotoxin induced damage to factor XI ,XII ,platelets
Low grade DIC with increased fibrin degradation products
ITCHING
Retained bile salts stimulate nerve endings.
Other theory: Due to endogenous opiate peptides
Inducing opiod receptor mediated scratching activity of central origin
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18. CLINICAL PRESENTATION
The features that suggest obstructive jaundice are as follows:
• Jaundice
• Generalized pruritus
• Pale, bulky and oily stool
• Dark urine
However their mode presentation depends on the aetiology of the
jaundice.
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19. SUGGESTING CA HEAD OF PANCREAS
OBSTRUCTING CBD
• An older patient
• Vague Epigastric pain
• Usually painless obstructive jaundice. (presents with jaundice then later
pain. Pain is due to; involvement of the retropancreatic nerve, obstruction
of pancreatic duct, or disruption of the nerve sheeth by tumour )
• Weight loss, New onset type2 DM
• Progressive deepening jaundice associated with ca pancreas.
• Gall-bladder is palpably enlarged, Courvoisier’s Sign strongly suggests a
malignant obstruction at the lower end of the common bile-duct, but its
absence does not exclude this.
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20. SUGGESTING AMPULLARY CA
• Fluctuating obstructive jaundice (necrosis of the tumour with
sloughing with temporary relief of jaundice).
• Silver coloured stools
• Weight loss and pain is a late feature
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21. SUGGESTING GALLSTONES
• Severe intermittent colicky pain (painful jaundice- develop pain
before jaundice).
• A long history of intermittent varying jaundice (fluctuating jaundice)
• Fever, chills, and rigors (suggesting cholangitis, often complicate the
jaundice of gallstones)
• Little or no weight loss
• Flatulent dyspepsia
• A non-palpable gall-bladder.
• A raised white count suggests cholecystitis
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22. SUGGESTING A CARCINOMA OF STOMACH
WITH SECONDARIES TO PORTA HEPATIS
• Pain
• Anorexia
• Vomiting
• An upper abdominal mass, and Visible peristalsis of pyloric stenosis.
• Anaemia is common
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23. SUGGESTING HEPATOMA
• A large, hard, irregular liver
• A bruit is often present
• Ascites is common, and is often bloodstained.
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24. SUGGESTING CARCINOMA OF THE GALL-
BLADDER
• The patient is a woman with an enlarged liver and a hard, irregular
mass in her right hypochondrium.
• Cirrhosis – Alcohol intake
• Hepatitis – injections and transfusions
• Hereditary spherocytosis – Family Hx of anaemia, splenectomy and
gallstones
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25. COMPLICATIONS
• ASCENDING CHOLANGITIS
• HEPATORENAL SYNDROME
• HYPOGYCEMIA
• ANAEMIA
• MALNUTRITION
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26. ASCENDING CHOLANGITIS
• Acute cholangitis results from bacterial superimposed infection on
biliary obstruction. The infection ascends into the hepatic duct
causing serious infection.
• The classical triad – Charcot triad- RUQ pain, fever, and jaundice. A
pentad – Raynold’s pentad- in which alter sensorium and hypotension
is added to the triad.
• Most common organisms; E coli, Klebsiella, Enterococcus,
Streptococcus, Enterobacter, Pseudomonas aeruginosa.
• Treatment involve iv fluids, antibiotics, analgesics then non-surgical
decompression (ERCP or PTC).
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27. HEPATORENAL SYNDROME
• Renal failure occurring in the setting of a Hepatic disease. It is an
acute, progressive, oliguric renal failure occurring in the absence of
any other apparent clinical cause.
Cause of Hepatorenal Syndrome in Obstructive Jaundice:
• Extracellular water depletion
• Gram negative endotoxaemia
• Myocardial dysfunction
• Increased plasma level of atrial natriuretic peptide (ANP)
• Bile deposit in the renal tubules
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28. Sclera of the patient with obstructive jaundice
is greenish yellow in colour.
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VIRCHOW`S NODE
Or troisier’s sign
BRUISING
VIT.K DEF.
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29. Urine in obstructive jaundice
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30. INVESTIGATIONS
• LABORATORY
• IMAGING
• INVASIVE PROCEDURES
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31. LABOROTORY
URINALYSIS
• Presence of bilirubin in the urine
• Absent urobilinogen
LIVER FUNCTION TEST
• Hepatic causes of jaundice (such as hepatocellular injury from hepatitis)
are usually nonsurgical problems, whereas posthepatic causes (such as
biliary obstruction from acute cholangitis) are typically surgical.
Distinguishing between the two is not always straightforward.
• Both will have some degree of elevation in total bilirubin, AST, ALT,
gammaglutamyl transpeptidase (GGT), and AP.
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32. Continua………
• AST and ALT are enzymes within the liver cells (though AST is also
found in muscle and other cells). With hepatocellular injury, these
enzymes are released.
• AP is present in the cells that line the bile ducts. A marked rise in ALP,
out of proportion to the AST and ALT, is therefore indicative of
posthepatic (biliary obstruction) pathology such as tumors or
choledocholithiasis.
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33. Continua……….
CLOTTING PROFILE:
• PT is prolonged
NB; parenteral administration of Vitamin K improves PT, unlike in
hepatocellular failure.
Other laboratory tests:
• Hepatitis serology
• Antimicrobial antibody level
• FBC
• U/ECR
• FBS, GXM
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34. IMAGING STUDIES
ULTRASONOGRAPHY:
• Accuracy is close to 95%
• Dilated CBD > 10mm
• Dilated intrahepatic duct > 4mm
• Distended gall bladder.
• Pancreatic mass.
• Has limited ability in detecting specific causes
• Poorly visualize the CBD and cystic duct due to intervening bowel.
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35. Continua………
ABDOMINAL CTSCAN:
• More accurate in determining the cause
• Visualizes structures more consistently than the USS
• Determine the involvement of the SMV, portal vein
MRCP:
• Non invasive and sensitive method of visualizing pathologies of the
hepatobiliary system.
• Better able to determine the type and extent of tumour than ERCP, Does
not require contrast.
• Unlike ERCP has only diagnostic potential rather than therapeutic
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37. INVASIVE PROCEDUES
ERCP (Endoscopic retrograde cholangiopancreatography):
• It is especially useful in lesions distal to bifurcation of the hepatic duct
• Has diagnostic and therapeutic application
• Obstruction can be relieved by removal of stones, sphincterotomy,
placement of stent and drains.
• Allows for brush cytology.
• Has limited capacity to image site proximal to the site of obstruction
• Cannot be performed in altered anatomy that prevent access to the
ampulla e.g Roux loop Complications; pancreatitis, perforation, biliary
peritonitis, sepsis, hemorrhage, stricture.
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39. Continua…………..
PTC (Percutaneous transhepatic cholangiogram):
• Especially useful in lesions proximal to the common hepatic duct
• Has both diagnostic and therapeutic application
• Can be used to decompress the biliary system
• The liver is punctured to enter the peripheral intrahepatic bile system.
• Iodine based contrast medium is injected into the biliary system.
• Performed under fluoroscopic guidance
• ERCP still preferred, it is reserved for failed ERCP or altered anatomy
preclude assess to the ampulla.
Complications; reaction to contrast, peritonitis, hemorrhage, sepsis,
cholangitis, subphrenic abscess, lung collapse.
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41. PREOPERATIVE CARE
1. Coagulation: Vitamin K iv
10mg 0.d 5/7 until INR = 1.3, If
> 1.3 give FFP 4units pre – op.
2. Reduced glycogen stores: iv
dextrose 10% IL 0.d
3. Infection; Prophylactic
antibiotics-Quinolones.
4. Endotoxemia: Lactulose, Oral
Bile acid. Metronidazole
5. Hepatorenal syndrome: Iv
fluids Mannitol, Achieve a urine
output > 60ml/hour.
6. Nutritional problems:
Avitaminosis – give pabrinex 1 and
2 , Calories – give Iv dextrose 10%
Serum protein – High pro diet Iv
nutrition.
7. Pruritus –
cholestyramine/Antihistamine
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42. TREATMENT
Treatment depends on the cause;
Stone in the biliary tract:
• Cholecytectomy + common bile duct exploration
• ERCP
Biliary stricture:
• Roux-en Y hepatico-jejunostomy
• Stenting for short stricture
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43. Periampullary and pancreatic head tumours
Early – whipple procedure
Late:
• Endoscopic biliary stenting
• Percutaneous transhepatic endobiliary radiofrequency ablation + stent
• Photodynamic therapy (PDT) + stent
Bypass procedure;
• triple bypass, double bypass.
• Cholecysto-jejunostomy/choledoco-jejunostomy
• Gastro-jejunostomy
• Jejuno-jejunostomy
• Liver transplant; ESLD, PSC, HCC, Secondary biliary cirrhosis and portal
hypertension, congenital biliary atresia
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44. PROGNOSIS
• Better with benign causes of obstruction
• Poor prognosis for malignant causes
• Upto 90% die within the first year of diagnosis (especially proximal tumours)
• Prognosis is better with distal tumours
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45. Whipple’s operation in early ca head of the
pancreas
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46. STENT for ca head of the pancreas
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47. Post op mgt
• Monitoring with prothrombin time, bilirubin, albumin, creatinine,
electrolyte estimation.
• FFP or blood transfusion.
• Antibiotics.
• Observation for septicaemia, haemorrhage, pneumonia, pleural
effusion, bile leak.
• Care of T-tube and drains.
• T-tube cholangiogram in 10-14 days.
• TPN, CVP line, nasogastric tube, urinary catheter.
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48. Complications (secondary to causes above)
• Steatorrhea
• Bleeding tendencies
• Malabsorption
• Pancreatis due to the stone
• Cholangitis
etc
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