This document discusses obstructive jaundice, providing definitions, pathophysiology, effects on various body systems, etiology, history and examination findings, laboratory investigations, imaging modalities, and causes of biliary obstruction. It defines obstructive jaundice as a failure of bile to reach the intestine due to mechanical obstruction. Pathophysiological changes include bile duct dilation, hepatic fibrosis, and portal hypertension. Causes include gallstones, strictures, tumors, and congenital anomalies. A thorough history, physical exam, and lab tests can localize the level and cause of obstruction, while imaging modalities like ultrasound and MRCP can identify and characterize obstructive lesions.
2. DEFINITION
Failure of normal amount of bile
to reach intestine
due to mechanical obstruction of the extra
hepatic biliary tree or within the porta hepatis
3. JAUNDICE
Jaundice (derived from French word ‘jaune’ for yellow) or icterus (Latin
word for Jaundice)
Yellowing of sclera at 3 mg%
Bilirubin has got high affinity for elastin and sclera has high elastin content
Yellowing of skin and mucous membrane at 6 mg%
D/D beta carotenemia,Quinacrine therapy malingering with picric acid
They doesn’t stain mucous membrane and sclera
Bilirubin level rise upto three weeks than stabilise
5. PHYSIOLOGICAL FACTS
Total bile flow-600ml/day(500-1000ml/day)
Hepatocyte component is -450ml/day
Can be bile salt dependent due to biliary glutathione and ductular bicarbonate
secretion
Cholangiocyte component-150ml/day
It depends on secretin stimulation
Total serum bilirubin is 0.3-1.2 mg/dl
With conjugated bilirubin<15 %
1mg/dl of bilirubin=17 mmol/l
6. PHYSIOLOGY OF OBSTRUCTION
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
7. PATHOPHYSIOLOGY
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. CHANGES IN LIVER BLOOD FLOW
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 EFFECTS
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
Decresed cardic function
Increased levels of ANP resulting in hypovolemia
Decreased effect of bile salts on kidney mediated by increased
prostaglandin E2
Endotoxemia
Resulting in
Renal vasoconstriction
Shunting of blood from cortex
Activation of complement system peritubular 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 ie Kupffer cells
13. WOUND HEALING
Delayed wound healing
High incidence of wound dehiscence
Decresed 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
Loss of calcium
Endotoxin induced damage to factor XI ,XII ,platelets
Low grade DIC with increased fibrin degradation
products
Thrombocytopenia from hyperspleenism
Decreased absroption of fat solube vitamins A,D,E,K
15. ITCHING
Retained bile salts
Levels does not correlete well
Itching disappears in terminal liver failure but bile salt
level still increased
Other theory
Due to endogenous opiate peptides
Inducing opiod receptor mediated scratching
activity of central origin
16. BIOCHEMICAL EFFECTS
Bilirubin
Rise by 25-43 micromol/litre/day
Mechanism of hyperbilirubinemia
Biliary venous & biliary regurgitation of conjugated bilirubin due to
disruption of tight intracellular junction
Trans hepatocytic regurgitation due to reversal of the secretory
polarity of hepatocytes
Rupture of dilated canaliculi in to sinusoids due to necrosis of
hepatocytes
18. Why Bilirubin levels plateau
Increased excretion of bile pigments by kidney by products other than bilirubin
not giving DIAZO reaction
With increasing levels of conjugated bilirubin
A portion get covalently bounded to serum albumin
This protein bound bilirubin-Delta bilirubin,is not measurable by routine
technique
21. The sensitivities of history, physical examination, and blood tests alone range
from 70% to 95%,whereas the specificities are approximately 75%.
The overall accuracy of clinical assessment of hepatic and posthepatic causes
of jaundice ranges from 87% to 97%.
6.Lindberg G, BjÃjrkman A, Helmers C: A description of diagnostic strategies in jaundice. Scand J
Gastroenterol 18:257, 1983
7. Lumeng L, Snodgrass PJ, Swonder JW: Final report of a blinded prospective study comparing current
non-invasive approaches in the differential diagnosis of medical and surgical jaundice. Gastroenterology
78:1312, 1980
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non-invasive approaches in the differential diagnosis of medical versus surgical jaundice.
Gastroenterology 84:1498, 1983
22. HISTORY
Previous dyspepsia, fat intolerance
Jaundice- onset, course, itching
Pain
Pyrexia
Weight loss
Dark urine and clay coloured stools
Travel to endemic area
Contact with jaundice patient
History of upper abdominal operation
Drug intake ie ATT
History of injection in preceding six months
23. CLINICAL EXAMINATION
Age
Anaemia - hemolysis, cancer , cirrhosis
Gross weight loss-malignancy
Hunched up position-chronic pancreatitis or ca pancreas
Fetor, flapping tremors,personality changes-impending hepatic coma
Skin changes-Bruising,purpuric spots,spider naevi,palmar erythema,white
nails,loss of secondary sexual characters
24. ABDOMINAL EXAMINATION
Dilated peri umbalical veins- cirrhosis & portal collateral
circulation
Ascitis-Cirrhosis or malignant disease
Nodular liver
Courvoisier’s Law-palpable non tender gall bladder in
jaundice patient-malignant biliary obstruction
Exceptions
Double impaction of stones
Impaction of pancreatic calculus at ampulla of vater
Mirizzi syndrome
26. ALKALINE PHOSPHATSE(ALP)
ALP levels are elevated in nearly 100 % of patients with extra hepatic
obstruction except in some cases of intermittent obstruction.
Values usually greater than 3 times the upper limit of reference range,
and in most typical cases, they exceed 5 times the upper limit.
An elevation less than 3 times the upper limit is evidence against
complete extra hepatic obstruction.
27. AST and ALT
Serum enzymes that provide evidence of hepato cellular damage.ALT found
primarily in the liver, where as AST also found in heart ,kidney, skeletal muscle
and brain
AST is less specific for liver function. The levels of AST and ALT should be
done simultaneously since ALT can confirm the hepatic origin of the less
specific but more sensitive AST.
In extra hepatic obstruction usually AST levels are not elevated(< 10 times the
upper reference limit)
28. GAMMA –GLUTAMYL TRANSPEPTIDASE(GGTP)
Correlates with ALP level
Most sensitive indicator of biliary tract disease
Better indicator of obstruction in children – levels are independent of age
Helpful in the diagnosis of acute biliary tract obstruction in contrast to ALP
because ALP requires synthesis of fresh ALP and hence lags behind the onset
of obstruction
29. 5- NUCLEOTIDASE
The principal value is to confirm the hepatic origin of an elevated
ALP
This is particularly helpful in children, pregnant women and patients
who may have bone disease resulting in rise of ALP
It is more useful than ALP/GGTP in detecting hepatic metastasis
30. OTHER LAB INVESTIGATIONS
Prothrobin time
Serum albumin
Stool for occult blood
Presence of occult blood in the stools of a patient with jaundice must raise the
suspicion of malignancy.
31. Obstructive jaundice Medical jaundice
Serum Bilirubun
conjugated
unconjugated
+++
+
+
+++
Urobilinogen ↓ ↑
Urinary Bilirubin + 0
Urinary Bile salts + 0
Serum ALP ↑ No change
Serum GGTP ↑ No change
Serum 5-
nucleotidase
↑ No change
Transaminases Mildly raised Markedly raised
34. INTERMITTENT OBSTRUCTION
Symptoms and typical biochemical changes
Clinically jaundice may or may not be present
Causes
CBD stones
Periampullary tumours
Duodenal diverticulum
Choledochal cyst
Biliary parasites
hemobilia
35. CHRONIC INCOMPLETE OBSTRUCTION
With or without classical symptoms or biochemical changes
Pathological changes in bile ducts or liver
Causes
Strictures of CBD
Stenosis of biliary-enteric anastamosis
Chronic pancreatitis
Cystic fibrosis
Sphincter of oddi stenosis
36. SEGMENTAL OBSTRUCTION
one or more segment of intrahepatic biliary tract obstructed
Causes
Traumatic
Intrahepatic stones
Sclerosing cholangitis
Cholangiocarcinoma
37. BILIARY OBSTRUCTION
INTRINSIC
Ductal calculi
Primary - Develop de novo in bile ducts
Secondary - Migrate from gall bladder
Acute Cholangitis
Biliary Strictures
Idiopathic
Iatrogenic
Sclerosing Cholangitis
Parasites
Haemobilia
Benign Biliary Tumours
Cholangiocarcinoma
Carcinoma of ampulla of vater and Periampullary tumours
Intraductal secondary tumour seeding
38. BILIARY OBSTRUCTION
EXTRINSIC
Mirizzi syndrome
Pancreatitis- acute and chronic
Pancreatic pseudocyst
Carcinoma of gall bladder
Carcinoma of pancreas
Cystic tumours of pancreas
Metastatic carcinoma
Hepatocellular carcinoma
39. BILIARY OBSTRUCTION
CONGENITAL AND GENETIC DISORDERS
Biliary atresia
Choledocal cyst
Caroli’s disease
Progressive familial intra hepatic cholestasis
Primary biliary cirrhosis
Alpha 1 antitrypsin defeciency
Tyrosinemia
Neonatal hepatitis
Wilson disease
Others - dyskinesia of sphincter of odi
40. IMAGING GOALS
To confirm the presence of an extrahepatic obstruction
To determine the level of the obstruction, to identify the specific cause of the
obstruction
To provide complementary information relating to the underlying diagnosis (eg.,
Staging information in cases of malignancy).
41. Ultrasonography
Ultrasound of the abdomen is an extremely useful and accurate method for
identifying gallstones and pathologic changes in the gallbladder consistent with
acute cholecystitis. Abdominal ultrasound, if performed by an experienced
operator, should be part of the routine evaluation of patients suspected of having
gallstone disease, given the high specificity (>98%) and sensitivity (>95%) of this
test for the diagnosis of cholelithiasis[1] ( Table 54-1 ). In addition to identifying
gallstones, ultrasound can also detail signs of cholecystitis such as thickening of
the gallbladder wall, pericholecystic fluid, and impacted stone in the neck of the
gallbladder. It is often the initial screening test for patients with suspected
extrahepatic biliary obstruction ( Fig. 54-7 ). Dilation of the extrahepatic (>10 mm)
or intrahepatic (>4 mm) bile ducts suggests biliary obstruction. Intraoperative
ultrasound is now used frequently to further evaluate intrahepatic lesions, assess
resectability, and determine involvement of vascular structures
42.
43.
44. .
MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP)
•Noninvasive test to visualize the hepato biliary tree
•No contrast
•Fluid found in the biliary tree is hyper intense on T2-weighted images. Surrounding
structures do not enhance and can be suppressed during image analysis.
•Sensitive in detecting biliary and pancreatic duct stones, strictures, or dilatations
within the biliary system.
•MRCP combined with conventional MR imaging of the abdomen can provide
information about surrounding structures (eg, pseudocysts, masses).
• ERCP and MRCP similarly effective in detecting malignant hilar and perihilar
obstruction
• MRCP is better able to determine the extent and type of tumor as compared to ERCP
45. Absolute contraindications
cardiac pacemaker
cerebral aneurysm clips
ocular or cochlear implants
Fluid stasis in the adjacent duodenum or ascitic fluid may produce image artifacts
on MRCP, making it difficult to clearly visualize the biliary tree.
46. ENDOSCOPIC ULTRASOUND (EUS)
Combines Endoscopy and US
Higher-frequency ultrasonic waves compared to traditional US (3.5 mhz vs 20
mhz) and allows diagnostic tissue sampling via EUS-guided fine-needle aspiration
(EUS-FNA).
EUS has been reported to have up to a 98% diagnostic accuracy in patients with
obstructive jaundice
The sensitivity of EUS for the identification of focal mass lesions in pancreas has
been reported to be superior to that of CT scanning, both traditional and spiral,
particularly for tumors smaller than 3 cm in diameter.
Compared to MRCP for the diagnosis of biliary stricture, EUS has been reported to
be more specific (100% vs 76%) and to have a much greater positive predictive
value (100% vs 25%), although the two have equal sensitivity (67%).
The positive yield of eus-fna for cytology in patients with malignant obstruction has
been reported to be as high as 96%.
50. WORKUP AND MANAGEMENT OF POSTHEPATIC JAUNDICE
three possible clinical scenarios:DUCTAL OBSTRUCTION
SUSPECTED CHOLANGITIS
SUSPECTED
CHOLEDOCHOLITHIASIS WITHOUT
CHOLANGITIS
SUSPECTED LESION OTHER THAN
CHOLEDOCHOLITHIASIS
51. SUSPECTED CHOLANGITIS
A clinical picture compatible with acute suppurative cholangitis (charcot's triad or
raynaud's pentad) the most likely diagnosis is choledocholithiasis.
Appropriate resuscitation, correction of any coagulopathies if present, and
administration of antibiotics
ERCP is indicated for diagnosis and treatment
If ERCP is unavailable or is not feasible (e.g., Because of previous roux-en-y
reconstruction), transhepatic drainage or surgery may be necessary
Mainstay of treatment of severe cholangitis is not just the administration of
appropriate antibiotics but rather the establishment of adequate biliary drainage.
52. SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS
Choledocholithiasis is the most common cause of biliary obstruction.
Strongly suspected if the jaundice is episodic or painful or if usg has shown
presence of gallstones or bile duct stones.
Patients with suspected cbd stones should be referred for lap cholecystectomy with
either preoperative ERCP, intra operative cholangiography
Preoperative ERCP in this setting of jaundice is prefered
Diagnostic yield is high
Therapeutic-clearing the CBD of stones in 95% of cases.
Many authors, however favor fully laparoscopic approach, in which CBD stone is
detected in the OR by means of intraoperative cholangiography and laparoscopic
biliary clearance is performed when choledocholithiasis is confirmed.
The optimal approach in a particular setting should be dictated by local expertise.
53. SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS
No gallstones are seen
Clinical presentation is less acute (e.g., constant abdominal or back pain)
Associated constitutional symptoms (e.g., weight loss, fatigue, and long-standing
anorexia)
Possible causes of may be classified into three categories depending on the location of
the obstructing lesion
the upper third of the biliary tree
the middle third
the lower (distal) third
54. Upper-third obstruction
Polycystic liver disease
Caroli diseas
HCC
Oriental cholangiohepatitis
Hemobilia(e.g.,afterbiliaryma
nipulation)
Iatrogenic bile duct injury
Cholangiocarcinoma
(Klatskin'stumor)
Sclerosing cholangitis
Papillomas of the bile duct
Mid-third obstruction
Cholangiocarcinoma
Sclerosing cholangitis
Papillomas of the bile duct
Gallbladder cancer
Choledochal cyst
Intrabiliary parasites
Mirizzi syndrome
Extrinsic nodal compression
(e.g., lymphoma)
Iatrogenic bile duct injury
Cystic fibrosis
Benign idiopathic bile duct
stricture
Lower-third obstruction
Cholangiocarcinoma
Sclerosing cholangitis
Papillomas of the bile duct
Pancreatic tumors
Ampullary tumors
Chronic pancreatitis
Sphincter of Oddi dysfunction
Papillary stenosis
Duodenal diverticula
Penetrating duodenal ulcer
Retroduodenal adenopathy
(e.g., lymphoma, carcinoid
ETIOLOGY
55. DIAGNOSIS AND ASSESSMENT OF RESECTABILITY
Involvement of the SUPERIOR MESENTERIC VEIN, THE PORTAL VEIN, THE
SUPERIOR MESENTERIC ARTERY, and the PORTA HEPATIS and on whether
there is evidence of significant LOCAL ADENOPATHY or EXTRAPANCREATIC
EXTENSION OF TUMOR indicates UNRESECTABILITY
The majority of lesions will be clearly unresectable, either because of tumor
extension or because of the presence of hepatic or peritoneal metastases
57. In the majority of patients with malignant obstructions, treatment is palliative rather
than curative.
Cholangiography and decompression of obstructed biliary system
In the absence of preexisting or concomitant hepatocellular dysfunction, drainage of
one half of the liver is generally sufficient for resolution of jaundice
58. Routine preoperative drainage of an obstructed biliary system does not benefit
patients who will soon undergo resection.90,91
There is evidence suggesting that in patients with either pancreatic 92,93 or hepatic
malignancies, routine preoperative direct cholangiography with decompression is
associated with a higher incidence of postoperative complications when tumor resection
is ultimately carried out.
90. Pitt HA, Gomes AS, Lois JF: Does preoperative percutaneous biliary drainage reduce operative
risk or increase hospital cost? Ann Surg 201:545, 1985
91. McPherson GA, Benjamin IS, Hodgson HJ, et al: Preoperative percutaneous transhepatic biliary
drainage: results of a controlled trial. Br J Surg 71:371, 1984
92. Povoski SP, Karpeh MS Jr, Conlon KC, et al: Preoperative biliary drainage: impact on
intraoperative bile cultures and infectious morbidity and mortality after pancreaticoduodenectomy. J
Gastrointest Surg 3:496, 1999
93. Sohn TA, Yeo CJ, Cameron JL, et al: Do preoperative biliary stents increase
postpancreaticoduodenectomy complications? J Gastrointest Surg 4:258, 2000
60. UPPER-THIRD OBSTRUCTION
PALLIATION.
Because the left hepatic duct has a long extrahepatic segment and is more
accessible, the preferred bypass -is a left hepaticojejunostomy
Laparoscopic bypass techniques that make use of segment 3 have been
developed, but their performance has yet to be formally assessed
61. RESECTION FOR CURE
The hilar plate is taken down to lengthen the hepatic duct segment available for
subsequent anastomosis.
A formal hepatectomy or segmentectomy is required to ensure an adequate proximal
margin of resection
If the resection is carried out proximal to the hepatic duct bifurcation, several
cholangiojejunostomies have to be done to anastomose individual hepatic biliary
branches.
The results of aggressive hilar tumor resections that included as much liver tissue as
was necessary to obtain a negative margin appear to justify this approach.
In cases of left hepatic involvement, resection of the caudate lobe is indicated as well.
62. MIDDLE-THIRD OBSTRUCTION
Palliation.
Surgical bypass of middle-third lesions is technically simpler
Hepaticojejunostomy is done distal to the hepatic duct bifurcation,
Exposure of the hilar plate or the intrahepatic ducts is unnecessary.
Resection for cure.
Tumors in this part usually quite amenable to resection along with the lymphatic chains
in the porta hepatis.
Mirizzi syndrome -extrinsic obstruction of the CBD, either by causing inflammation of
the gallbladder wall or via direct impingement.
Treatment of this syndrome - Hepaticojejunostomy
63. Lower-third obstruction
Palliation
The preferred bypass technique for lower-third lesions is a Roux-en-Y
choledochojejunostomy.
Cholecystojejunostomy carries a higher risk of complications and subsequent
development of jaundice
Resection for cure.
Resection of a lower-third lesion usually involves a pancreaticoduodenectomy though
transduodenal ampullary resection may be an acceptable alternative for a small
adenoma of the ampulla
For optimal results, pancreaticoduodenectomy is best performed in specialized centers.
postoperative adjuvant therapy may improve the prognosis after resection of a
pancreatic adenocarcinoma
64. PALLIATION IN PATIENTS WITH ADVANCED MALIGNANT DISEASE
When a patient has advanced malignant disease, drainage of the biliary system for
palliation is not routinely indicated, because the risk of complications related to the
procedure may outweigh the potential benefit
The best treatment for a patient with asymptomatic obstructive jaundice and liver
metastases may be supportive care alone.
Biliary decompression is indicated if cholangitis or severe pruritus interferes with quality
of life.
Stent placed with ercp to be the palliative modality of choice for advanced disease,
Upper-third lesions may be managed most easily through the initial placement of an
internal/external catheter at the time of ptc.
65. Metal expandable stents remain patent longer than large conventional plastic stents
RCTs suggest that surgical biliary bypass should be reserved for patients who are
expected to survive for 6 months or longer because bypass is associated with more
prolonged palliation at the cost of greater initial morbidity.
The role of prophylactic gastric drainage at the time of operative biliary drainage
remains controversial,101,102
RCTs demonstrated a reduced incidence of subsequent clinical gastric outlet
obstruction when this measure was employed.
When a pancreatic malignancy is present, intraoperative celiac ganglion injection
should be performed for either prophylactic or therapeutic pain
66. POSTOPERATIVE JAUNDICE
The development of jaundice in the postoperative setting is approximately 1% of all
surgical patients after operation.120
When jaundice occurs after a hepatobiliary procedure,
Attributable to specific biliary causes,
Retained cbd stones,
Postoperative biliary leakage (through reabsorption of bile leaking into the peritoneum)
injury to the cbd
Development of biliary strictures
67. JAUNDICE WITHIN 48 HOURS OF THE OPERATION
Breakdown of rbc –due to multiple blood transfusions ,
The resorption of a large hematoma,
Transfusion reaction.
Known underlying hemolytic anemia and may be precipitated specific drugs (e.G.,
Sulfa drugs in a patient who has G6PD deficiency).
Gilbert syndrome may first manifest itself early in the postoperative period.
Intraoperative hypotension or hypoxemia or the early development of heart failure
can lead to hyperbilirubinemia within 5 to 10 days after operation.
The hyperbilirubinemia may be associated with other end-organ damage (e.G.,
Acute tubular necrosis).
Impairment of renal function causes a decrease in bilirubin excretion and can be
responsible for a mild hyperbilirubinemia.
68. Jaundice developing 7 to 10 days after operation
In association with a medication-induced hepatitis attributable to an anesthetic agent.
Incidence of 1/10,000 after an initial exposure.
Administration of antibiotics or other medications used in the perioperative setting
Jaundice associated with intrahepatic cholestasis is often a manifestation of a sepsis,
particularly in patients with mods
Jaundice may occur in as many as 30% of patients receiving total parenteral nutrition
(tpn).
It may be due to steatosis, particularly with formulas containing large amounts of
carbohydrates.
Decreased export of bilirubin from the hepatocytes may lead to cholestasis
Acalculous cholecystitis or even ductal obstruction may develop as a result of sludge in
the gallbladder and the cbd.
69. Unsuspected hepatic or post-hepatic causes (e.G., Occult cirrhosis,
choledocholithiasis, or cholecystitis)
A rare cause of postoperative jaundice is the development of thyrotoxicosis.
A diagnosis of exclusion- is so-called benign postoperative cholestasis, a
primarily cholestatic, self-limited process with no clearly demonstrable cause that
typically arises within 2 to 10 days after operation.
Mechanism-combination of an increased pigment load, impaired liver function,
and decreased renal bilirubin excretion caused by varying degrees of tubular
necrosis.
The predominantly conjugated hyperbilirubinemia may reach 40 mg/dl and
remain elevated for as long as 3 weeks.