obstructive jaundice, cholestasis, cholangitis, pancreatic head tumour, periampullary tumour, cholangiocarcinoma,

1. AN OVERVIEW ON
OBSTRUCTIVE JAUNDICE
DR BASHIR BN YUNUS
General surgery

2. OUTLINE
• INTRODUCTION
• AETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL FEATURES
• INVESTIGATIONS
• PRE-OPERATIVE TREATMENT
• TREATMENTS
• PROGNOSIS

3. INTRODUCTION
• In obstructive jaundice, there is the failure of normal amount of bile
to reach the intestine due to the impediment of bile flow along the
hepato-biliary tree.
• 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.

4. AETIOLOGY
INTRAHEPATIC: Cirrhosis, Hepatitis
EXTRAHEPATIC
a. Intraductal causes
• stone disease (Choledocholithiasis- CBD stones ),
• Neoplasms (cholangiocarcinoma-CBD Ca),
• Traumatic bile duct stricture,
• parasites (Ascaris),
• primary sclerosing cholangitis (PSC),
• AIDS-related cholangiopathy and biliary tuberculosis.
b. Extraductal obstruction
• Neoplasms
Primary; ca head of pancreas, Carcinoma ampulla of Vater, Primary duodenal cancer
Secondary; Tumour in the porta hepatis, usually from a primary in the stomach
• Chronic pancreatitis,
• Cystic duct stones with subsequent gallbladder distension (Mirizzi syndrome)

5. PATHOPHYSIOLOGY

6. • 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.
• Biliary obstruction prevents carriage of bile to the small intestine

7. • 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

8. • 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.

9. 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

10. 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.

11. 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

12. 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

13. 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

14. COAGULATION FACTOR DEFECTS
Prolongation of Prothrombin time;
• Decreased absorption of fat soluble vitamins A,D,E,K (vitamin K
dependent clotting factors nor formed- II, VII, IX and X)
• Endotoxin induced damage to factor XI ,XII ,platelets
• Low grade DIC with increased fibrin degradation products

15. ITCHING
• Retained bile salts stimulate nerve endings.
• Other theory
• Due to endogenous opiate peptides
• Inducing opiod receptor mediated scratching activity of central origin

16. CLINICAL FEATURES
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.

17. 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
• Progressive deepening jaundice associated with ca pancreas.
• Gall-bladder is palpably enlarged, strongly suggests a malignant obstruction at
the lower end of the common bile-duct, but its absence does not exclude this.

18. 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

19. 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

20. 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

21. SUGGESTING HEPATOMA
• A large, hard, irregular liver
• A bruit is often present,
• Ascites is common, and is often bloodstained.

22. 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

23. • PANCREATIC CANCER RELATED DIABETES MELITUS
• Longstanding diabetes is an aetiologic factor for pancreatic cancer
• New-onset diabetes (<24months) is also a manifestation pancreatic cancer
• The pancreatic cancer cells produce soluble factors that can impair glucose
metabolism and causes hyperglycemia.
• Resent onset diabetes tends to improve following resection.
• It is unlikely due to destruction of the gland by tumour; high prevalence in
tumours < 2cm and early stage tumour or radiological undetectable

24. COMPLICATIONS
• ASCENDING CHOLANGITIS
• HEPATORENAL SYNDROME
• HYPOGYCEMIA
• ANAEMIA
• MALNUTRITION

25. 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).

26. 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

27. INVESTIGATIONS
• LABORATORY
• IMAGING
• INVASIVE PROCEDURES

28. LABORATORY
• URINALYSIS
• Presence of bilirubin in the urine
• Absent urobilinogen

29. • LIVER FUNCTION TEST
• Alkaline phosphatase(ALP); markedly elevated (heat stable type) The value is
not specific to cholestasis, however, to determine if the value is hepatic in
origin, measure GGT or 5’ nucleotedase. These values parallel that of ALP in
liver disease.
• The values are usually morethan 3X the upper limit of the reference range,
and most typically > 5X the upper limits.
• Values < 3X the upper limits indicate partial obstruction or intrahepatic
obstruction

30. • AST and ALT
• Are not elevated unless secondary parenchymal damage
• Mild to moderate elevation (<10X the upper limit of the reference range)
• Occassionally markedly elevated in cholangitis
• A ≥ 3X increase in ALT strongly suggest pancreatitis
• ALT predominates in the liver and more specific than AST
• GGT
• Levels parallel the level of ALP and 5’-nucleotidase
• More sensitive
• The levels would distinguish hepatobiliary disease as a cause of isolated ALP
elevation.

31. • 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

32. 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.

33. • ABDOMINAL CTSCAN
• More accurate in determining the cause
• Visualizes structures more consistently than the USS
• Determine the involvement of the SMV, portal vein

34. ABD CTSCAN
Demonstrate a resectable
pancreatic adenocarcinoma of the
head of pancreas with SMV
abutment of less than 180⁰ and a
clear fat plane between the tumour
and the SMA
NCCC definition of a resectable
tumour; any tumour with ≤ 180⁰
contact of the superior mesenteric
–portal vein but without any vein
contour irregularity

35. Outline of the pancreas with a tumour of the
head

36. Locally advanced disease with obliteration of
the SMV
Locally advance is defined as tumour > 180⁰
contact with the SMA, CA or 1st jejunal
branch of the SMA
No technical option for reconstruction

37. A borderline resectable pancreatic
adenocarcinoma with SMV abutment of
approximately 180⁰ and subtle haziness
posterior to the SMA.
Borderline are group of patient at high risk
for margin positive and for whom
neoadjuvant therapy should be considered
Definitions;
• ≤ 180⁰ contact with the SMA
• >180⁰ contact with the SMV-PV
• ≤180⁰ contact with the SMV-PV with
irregularity or thrombus amenable to
resection and reconstruction

38. • 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

39. MRCP

40. MRCP

41. 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

42. ERCP

43. • 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.

44. PTC

45. 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

46. 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

47. • 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

48. 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

49. REFERENCES
• 1. Long W, Wei-Feng Y. Obstructive and perioperative management.
Acta Anaesthesiology Taiwanica 2014;52: 22-29.
• 2. Jennifer LB. (2019, October 16). Biliary obstruction. Retrieve from
https://www.emedicine.Medscape.com
• 3. NCCN Guidelines. Pancreatic cancer, 2019.
• 4. Rahul P et al. New-onset diabetes: A potential clue to the early
diagnosis of pancreatic cancer. Lancet Oncol. 2009; 10(1);88-95