The document provides an extensive overview of obstructive jaundice, including its causes, clinical features, and management options. Key points include intraluminal, mural, and extrinsic causes of obstructive jaundice, with diagnostic approaches such as ERCP and imaging studies emphasized for effective treatment. It details the clinical presentations, investigations, and algorithms for managing conditions like choledocholithiasis and pancreatic carcinoma, as well as understanding biliary atresia in infants.

1. OBSTRUCTIVE JAUNDICE
INTRODUCTION
Dr.B.Selvaraj MS;Mch;FICS;
Professor Of Surgery
Melaka Manipal Medical college
Melaka 75150 Malaysia

2. Must to know core clinical
problems
1.Acute RLQ pain
2.Acute RUQ pain
3.Acute epigastric pain
4.Acute LLQ pain
5.Dysphagia
6.Abdominal lumps
7.Upper GI haemorrhage
8.Lower GI haemorrhage
9.Obstructive Jaundice
10.Breast lumps, mastalgia & nipple discharge
11.Neck swellings- Thyroid & non thyroidal
12.Groin swellings
13.Scrotal swellings
14.Limb ischemia- Acute & Chronic
15.Varicose veins
16.Renal & ureteric colic
17.Hematuria
18.Acute retention of urine

3. Obstructive Jaundice- Introduction
Causes of obstructive jaundice
Anatomy of biliary tract
Physiology of jaundice
Labs in obstructive jaundice
Algorithm in obstructive jaundice

4. Obstructive Jaundice- Causes
• 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

5. Anatomy of Biliary Tract

6. Physiology of Jaundice

7. Labs in all types of Jaundice

8. Labs in Obstructive Jaundice
Bilirubin in the urine (characteristic
dark colouration) this occurs as the
bilirubin is conjugated and thus
water-soluble
No urobilinogen in the urine; due to
the obstruction, no bilirubin enters
the bowel to be converted to
urobilinogen.
Increased total bilirubin and direct
bilirubin(conjugated bilirubin)
 Increased canalicular enzymes: alkaline
phosphatase and GGT
Increased liver enzymes ALT and AST;
not as significant as seen in
hepatocellular causes, but biliary
backpressure inevitably leads to mild
hepatocyte damage.

9. Obstructive Jaundice-
Diagnostic Algorithm

10. THANK YOU
To watch the video version go
to:
youtube.com/c/surgicaleducator

11. OBSTRUCTIVE JAUNDICE
Dr.B.Selvaraj MS;Mch;FICS;
Professor Of Surgery
Melaka Manipal Medical college
Melaka 75150 Malaysia
CHOLEDOCHOLITHIASIS

12. Choledocholithiasis- Overview
Causes of obstructive jaundice
Classical clinical vignette
Etiopathogenesis
Clinical features & complications
Investigations
Treatment
Mindmap of Choledocholithiasis
Diagnostic Algorithm in obstructive jaundice
Management algorithm in choledocholithiasis

13. Obstructive Jaundice- Causes
• 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

14. Classical Clinical
Vignette
A 40-year-old female presents with a 24 hour history of right upper
quadrant (RUQ) and epigastric pain, associated with nausea and
vomiting. She has had similar pain in the past, particularly after
eating fatty foods. According to her family, over the last few hours,
the patient has become slightly confused. Past medical history is
negative.
O/E: She is moderately tender in the RUQ to deep palpation. She has
slight scleral icterus. She has noted dark- coloured urine. The
remainder of her abdominal exam is negative.
 Vitals: BP-90/60 mms of Hg; PR-110/mt; RR-16/mt;T:102*F

15. Classical ClinicalVignette
Laboratory examination:
 TWBC- 15,000/µL(4 to 11,000/µL),
 Total bilirubin-4mgm/dl(0.1 to 1.2mgm/dl) Direct bili- 3mgm/dl
 ALP- 350µ/L (33-131µ/L); GGT- 330µ/L (8-88µ/L)
 AST- 300µ/L(5-35µ/L); ALT- 280µ/L(7-56µ/L)
 Sr Amylase- 100µ/L( 30-110µ/L)
Urine is positive for bilirubin
CHOLEDOCHOLITHIASIS WITH
CHOLANGITIS

16. Choledocholithiasis-Etiology
It is stones in the CBD and biliary tree.
Primary—Rare 5%—brown pigment stones. They are formed in
CBD and biliary tree itself, and are multiple, often sludge like,
commonly pigment or mixed type, extends into hepatic ducts.
Causes: Biliary stasis, biliary dyskinesia, caroli’s disease,
choledochal cyst, clonorchiasis, ascariasis Etc
Secondary—Common 95%—black pigment stones/cholesterol
stones. It is seen in 15% of gallstone disease; 75% are cholesterol
stones, 25% are pigment stones.

17. Choledocholithiasis-Etiology

18. Clinical Features
50% asymptomatic
Biliary colic because of CBD obstruction by stone-
pain in RHC & epigastrium
 Intermittent chills, fever, or jaundice
accompanies biliary colic Charcot’s triad
Ascending cholangitis
 Suppurative cholangitis Reynold’s pentad
Persistent pain, fever, jaundice, shock & AMS
 Painful jaundice with dark color urine, clay
colored stool and pururitus.
Features of Ac Pancreatitis in distal CBD stone
impaction

19. Clinical Features
 Patient may be icteric and toxic, with high fever and chills, or may
appear to be perfectly healthy.
A palpable gallbladder is unusual in patients with obstructive
jaundice from common duct stone because the obstruction is
transient and partial, and scarring of the gallbladder renders it
inelastic and non distensible.
Courvoisier’s Law: “ In a jaundiced patient if GB is palpably
enlarged it is not due to Gall stone”
Tenderness in the right upper quadrant is not often as marked as in
acute cholecystitis, DU perforation or Ac Pancreatitis
 Tender enlarged liver +

20. Differential diagnosis
Obstructive jaundice due to other causes:
Carcinoma of head of pancreas
 Periampullary carcinoma
Carcinoma of biliary tree- cholangiocarcinoma
Biliary stricture- Scelerosing cholangitis
Intrahepatic cholestasis from drugs, pregnancy, chronic active
hepatitis, or primary biliary cirrhosis may be difficult to distinguish
from extrahepatic obstruction. ERCP would be appropriate to make
the distinction.

21. COMPLICATIONS
 Liver dysfunction and biliary
cirrhosis.
 White bile formation and liver
failure.
 Suppurative cholangitis.
Liver abscess.
 Septicaemia.
 Pancreatitis if CBD stone is near
sphincter of Oddi blocking drainage of
bile and pancreatic duct.

22. Investigations- Labs
 In cholangitis, leukocytosis of 15,000/mL is usual, and values above
20,000/mL are common.
T bilirubin level usually remains under 10 mg/dL, and most are in
the range of 2-4 mg/dL. The direct fraction exceeds the indirect, but
the latter becomes elevated in most cases.
Bilirubin levels do not ordinarily reach the high values seen in
malignant tumors because the obstruction is usually incomplete and
transient. In fact, fluctuating jaundice is so characteristic of
choledocholithiasis.
Serum alkaline phosphatase & GGT levels usually rises
Mild increases in AST and ALT are often seen

23. Investigations-Imaging
 AXR & USG abdomen- ineffective to pick up CBD stones
 USG abdomen may indicate dilated CBD >1cm
 CECT- can pick up CBD stone
 MRCP- best non-invasive diagnostic investigation
 ERCP- Gold standard- diagnostic & therapeutic
 EUS- can pick up CBD stone and can take biopsy if there is a mass

24. Investigations-Imaging
ERCP MRCP

25. TREATMENT
 In absence of cholangitis:
ERCP, Sphincterotomy, CBD stone removal by dormia basket or
balloon followed by Lap cholecystectomy.
Lap cholecystectomy with Lap CBD exploration
 In presence of cholangitis:
ERCP with sphincterotomy and stone extraction or stent placement-
decompression
 PTBD- Percutaneous transhepatic biliary drainage in ERCP failed
cases
Surgical treatment: Only when above two procedures not possible.
Decompression of CBD with T tube.

26. TREATMENT

27. TREATMENT
 Open cholecystectomy, intra op cholangiogram, choledocholithotomy
with T tube placement.
 Remove T tube—10 to 14 days after T tube cholangiogram
Missed/retained/residual stones (< 2 years):
If T tube present Percutaneous stone extraction via T tube tract
after 4-6 weeks (Burhenne technique) using choledochoscope
If T tube absent ERCP stone removal
Recurrent stones (> 2 years):
ERCP—first approach
If duct dilated > 2 cm—choledochoduodenostomy or transduodenal
sphincteroplasty

28. TREATMENT
Burhenne Technique

29. Cholelithiasis Vs Choledocholithiasis

30. Choledocholithiasis - Mindmap

31. Obstructive Jaundice- Diagnostic Algorithm

32. Choledocholithiasis Treatement Algorithm

33. THANK YOU
Subscribe to get notified
regarding my latest
uploads

34. PANCREATIC CARCINOMAPANCREATIC CARCINOMA
Dr.B.Selvaraj MS;Mch;FICS
Professor of surgery
Melaka Manipal Medical College
Melaka 75150 Malaysia
OBSTRUCTIVE JAUNDICE

35. Pancreas- Anatomy

36. Pancreas- Blood supply

37. Classical Clinical
Vignette
• 72 yrs old man presents with jaundice for 7days
with dull abdominal discomfort for 2 months. He
gives H/O loss of appetite and loss of weight.
• His stools have become lighter in color and his
urine is much darker than before
• He has a 50+ pack-year smoking history before
quitting last year
• He was recently diagnosed with type 2 diabetes,
but has no other medical problems

38. Classical Clinical
Vignette
• O/E: he has a yellow hue to his eyes and tongue,
along with scratch marks on his skin.
• A non-tender globular mass is palpated in the
right upper quadrant (RUQ) of the abdomen
• Labs: Laboratory testing reveals total and direct
bilirubin of 18 mg/dL (normal 0.2–1.3 mg/dL) and
17.2 mg/dL (<0.3 mg/dL), respectively.
• Alkaline phosphatase (ALP) elevated at 215 µ/L
(33–131 µ/L). AST & ALT mildly elevated

39. • 3rd most common GIT cancer.
• 4th most common cause of cancer death
• Death to incidence ratio is one.
( lowest among all types of cancer). why???
• Male:Female ratio 2:1
• Peak age 65 to 75 yrs
• Common in black americans
Introduction

40. Risk factors
• Cigarette smoking.
• Increased age.
• Chronic pancreatitis.
• Family H/O Pancreatic Cancer in more
than 2 first degree relatives
• Increased saturated fat intake.
• Exposure to non chlorinated solvents

41. Genetic Risk factors
• Chronic familial relapsing pancreatitis.
• Familial breast cancer ( BRCA2).
• Peutz –Jeghers syndrome.
• HNPCC (Hereditary non polyposis colorectal
cancer)
• Gardener syndrome.
• Familial atypical mole and melanoma
syndrome.

42. Genetic progression

43. Pathology
• Site :55% head of pancreas;25% body
15% tail; 5% periampulary
• Macroscopic : growth is hard & infiltrating
• Histology :90% ductal adeno ca;
9% cystic neoplasms
1% endocrine neoplasms
• Spread :Lymphatics to peritoneum & regional
nodes
Blood to liver & lung
Perineural spread Back pain

44. Clinical features
• Head&Periampulary : Painless progressive
jaundice with palpable GB- “Courvoisier’s Law”;
Vomiting due to duodenal block
Tea color urine, clay color stool & pruritus
• Body : back pain,anorexia,weight loss &
steatorrhea
• Tail : often presents with metastases,malignant
ascites or unexplained anemia

45. Investigations
• Lab : Elevated total & direct bilirubin
High Alk Phosphatase& GGT
Tumor marker CA19-9 >200U/ml
• USG Abd : can detect huge tumors
can’t pickup small mass
• MDCT : Triple phase CT abdomen: with arterial &
portal venous phase is sensitive to pickup
even small hypodense lesions

46. Investigations
• ERCP & MRCP : “Dual duct sign”
Therapeutic ERCP for palliative stent in CBD
& Duodenum
• Endoscopic Ultrasound:(EUS)
Excellent for staging the tumor
EUS guided pancreatic biopsy

47. CT Abdomen

48. ERCP “Dual Duct Sign”

49. Periampulary Mass
&EUS

50. Staging
Stage1 :Tumor is limited to pancreas with no
nodes or metastases
Stage2 :Tumor extends into bile duct,
peripancreatic tissues or duodenum. No nodes or
metastases
Stage3 :as stage 2 + positive nodes or celiac or
SMA involvement

51. Staging
Stage4a : Tumor extends to stomach,colon,spleen
or major vessels with any nodal status and
no distant metastases
Stage4b : Distant metastases with any nodal
status or tumor size

52. Staging & Prognosis

53. Treatment
• Rescectable tumors
• Borderline resectability
• Unresectable tumors

54. Resectable tumors
• Normal fat planes between tumor and
SMA, SMV
• Absence of extrapancreatic disease
• Patent SMPV confluence
• No direct extension to celiac axis or SMA

55. Borderline tumors
• Short segment occlusion of SMPV
confluence with an adequate vessel for
grafting
• Short segment (< 1 cm ) abutment of the
common or proper hepatic artery or SMA on
high quality CT

56. Unresectable tumors
• Extrapancreatic disease- distant metastases
• Encasement of coelic axis or SMA
( anything more than short
abutment)

57. Treatment Algorithm

58. Whipple’s Operation

59. Complications
• Delayed gastric emptying
• Pancreatic fistula
• Intra-abdominal abscess
• Operative site hge
• GI Hemorrhage

60. Palliative Surgery
• Biliary obstruction:
 Biliary enteric bypass
 Endoscopic biliary stent
placement
 Radiographic transhepatic
stent placement

61. Palliative Surgery
• Gastric outlet obstruction:
 Gastroenteric bypass
 Endoscopically placed
duodenal stent

62. Palliative Bypass

63. Adjuvant therapy
• 85% local recurrence .→ RT
• 70% liver metastasis.→CT
• 5 FU is the only active agent.
• Gemcitabine.
• 5 FU + Gemcitabine

65. Mindmap

66. Treatment Algorithm

68. OBSTRUCTIVE JAUNDICE
Dr.B.Selvaraj MS;Mch;FICS;
Professor Of Surgery
Melaka Manipal Medical college
Melaka 75150 Malaysia
BILIARY ATRESIA

69. BILIARY ATRESIA- Objectives
To be aware of possible causes of surgical jaundice in infancy
To be aware of clinical features of biliary atresia
To be familiar with the methods of investigation
To understand the management options
To be aware of the surgical outcome and results

70. BILIARY ATRESIA
Biliary atresia is also known as progressive obliterative
cholangiopathy
Biliary atresia causes a progressive damage of the extrahepatic and
intrahepatic bile ducts with cholestasis because of obstructive
cholangiopathy secondary to inflammation, leading to fibrosis, and if
not recognized and treated, it leads to biliary cirrhosis and liver
failure.
The incidence of biliary atresia is 1:10,000 to 1:15,000 live births
Biliary atresia affects girls more often than boys.

71. BILIARY ATRESIA
Asians and African-Americans are affected more frequently than
Caucasians - more common in Chinese and Japanese.
Biliary atresia should be recognized and distinguished from neonatal
jaundice. Infants with prolonged jaundice should be thoroughly
investigated for biliary atresia.
Biliary atresia should be considered in all neonates with direct
hyperbilirubinemia
A high index of suspicion is important to make the diagnosis of
biliary atresia because surgical treatment by age 2 months has
clearly been shown to improve the outcome and establishment of bile
flow and to prevent the development of biliary cirrhosis.

72. BILIARY ATRESIA-Etiology
The exact cause of biliary atresia is not known and many factors
have been incriminated
1. Reovirus 3 infection.
2. Congenital malformation. Early studies postulated a congenital
malformation of the biliary ducts leading to their obstruction.
3. Congenital cytomegalovirus (CMV) infection.
4. Autoimmunity
5. A possible association with the gene GPC1, which is located on the
longarm of chromosome 2 (2q37).
6. Identification of active and progressive inflammation and
destruction of the biliary system

73. BILIARY ATRESIA-Types
Clinically, biliary atresia occurs in two distinct forms:
 The fetal-embryonic form:
− Appears in the first 2 weeks of life.
− About 10–20 % of affected neonates have associated congenital
defects.
 The postnatal form:
− Appears in neonates and infants aged 2–8 weeks.
− Progressive inflammation and obliteration of the extrahepatic bile
ducts occur after birth.
− Not associated with congenital anomalies.
− Infants may have a short jaundice-free interval.

74. BILIARY ATRESIA-Types
Type I: atresia of the common bile duct
Type IIa: atresia of the common hepatic
duct
Type IIb: atresia of common bile duct,
cystic duct, and common hepatic duct
Type III: atresia of the common bile duct,
cystic duct, and hepatic ducts up to the
porta hepatis. This is the subtype present
in over 90% of patients with biliary
atresia

75. ASSOCIATED ANOMALIES
Associated anomalies are seen in 10 to 20 % of biliary atresia cases.
 Polysplenia syndrome:
 These include:
− Cardiac malformations
− Polysplenia
− Situs inversus
− Absent vena cava
− A preduodenal portal vein
-- Bilobed symmetric liver
-- Bilobed lungs
BASM
Syndrome

76. Clinical Features
Infants with biliary atresia are typically full term
The symptoms are seen usually between 1 and 6 weeks of life
 Conjugated Jaundice which is prolonged
Dark urine because of bilirubin in urine
Clay-colored stools because of absence of stercobilin.- acholic stools
Vitamin K deficiency and coagulopathy
Antenatally detected subhepatic cyst
Cirrhosis (ascites and hepatosplenomegaly), rarely younger than 3
months

77. Biliary Atresia- Investigations
 LFT: Total bilirubin and direct bilirubin are elevated
ALP & GGT are elevated; AST & ALT mildly elevated
Medical causes, such as a1-antitrypsin deficiency, Alagille’s
syndrome, cystic fibrosis and neonatal hepatitis, should be
excluded.
 Biliary USG: whether the gallbladder is atrophic, dilated or
abnormal.
 to exclude other etiologies like choledochal cyst
 Triangular cord sign: Presence of fibrous cone of bile duct
remnant at porta hepatis

78. Triangular Cord Sign
Triangular Cord Sign Micky Mouse Sign

79. Biliary Atresia- Investigations
 Hepatobiliary isotope scan- HIDA scan: In biliary atresia,
there is normal uptake by the liver and failure of secretion of the
isotope, while in neonatal hepatitis there is poor liver uptake of
isotope. Intestinal excretion of the isotope confirms patency of the
extrahepatic bile ducts
Percutaneous liver biopsy: bile ductular proliferation; bile duct
plugs; inflammatory cell infiltrate, hepatocyte giant cell
transformation
Intraoperative cholangiography: this procedure definitively
demonstrates anatomy and patency of the extrahepatic bile ducts

80. Investigations- HIDA Scan

81. Investigations- IOC
Intra Operative Cholangiogram

82. Biliary Atresia- Treatment
 Kasai’s portoenterostomy: Once biliary atresia is suspected,
surgical intervention in the form of intraoperative cholangiogram and
Kasai portoenterostomy is indicated.
This procedure is not usually curative, but ideally does buy time until
the child can achieve growth and undergo liver transplantation
A considerable number of these patients, even if Kasai
portoenterostomy has been successful, eventually undergo liver
transplantation

83. Kasai’s Portoenterostomy

84. Kasai’s Portoenterostomy

85. Biliary Atresia- Postop care
 In the immediate postoperative period, Methylprednisolone should
be given for it’s anti-inflammatory and choleretic effects
Ursodeoxycholic acid has also been shown to enhance bile flow.
In order to prevent cholangitis postoperatively, immediate postop
give IV antibiotics, then prophylaxis with trimethoprim–
sulfamethoxazole has been used on a long-term basis.

86. Biliary Atresia- Outcome
 Prognosis is good if operated before 2 months of age
 Risk factors for failure liver fibrosis &Post op cholangitis episodes
1/3rd of pts remain asymptomatic No transplant
1/3 never have bile flow and require early transplant
1/3 initially have good bile flow but subsequently develop cirrhosis
Without surgery or liver transplant life span – 19 months
Death is due to liver failure, bleeding esophageal varices and sepsis

87. Biliary Atresia - Mindmap

88. Differential Diagnosis

89. Infantile Surgical Jaundice- Algorithm

90. THANK YOU
Subscribe to get notified
regarding my latest
uploads