SURGICAL OBSTRUCTIVE JAUNDICE1

INTRODUCTION
Jaundice (French: yellow) is a generic term for the yellow pigmentation of the skin,
mucous membranes or sclera that is caused by a heterogeneous group of disorders.
The importance of jaundice for a surgeon is to decide weather the jaundice is ‘medical
‘or ‘surgical’, with surgical jaundice being the type caused by obstruction that must be
relieved by a surgical procedure.
A rational approach to management of jaundice requires a thorough understanding of
billirubin metabolism.
Surgical jaundice can be distinguished from medial jaundice by a thorough history,
complete physical examination and simple lab tests.
Surgery in presence of jaundice results in a higher mortality and morbidity

BILIRUBIN METABOLISM

Billirubin is a product of breakdown of iron containing pigments

Total daily production is 300 mg under normal circumstances
15-20% of bilirubin comes from the destruction of RBC’s maturing in the liver and
breakdown of non-heme pigments the so-called early labelled fraction after
radiolabeled glycine administration, the rest coming from the destruction of senescent
RBC in the RE system.

Haemoglobin

Goblin haeme

Haem oxygenase
Biliverdin

Biliverdin reductase

Bilirubin

Bilirubin albumin complex transported to the liver

Liver takes up bilirubin

Conjugation with glucuronic acid

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Gaurav Kumar, Rohit Sharma & Ajay Bisht. Oct 1999

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 Urobilinogen

Stercobilinogen

Billirubin is produced from the destruction of senescent RBC’s by the removal of the
of iron by the action of the enzyme haem oxygenase; the reaction liberates carbon
monoxide, the only reaction in the body releasing carbon monoxide. The intermediate
product being Biliverdin
Bilirubin a water insoluble compound is transported to the liver bound to albumin
In the liver the bilirubin is taken up actively by two mechanisms. The first being a
membrane bound carrier protein and the second being by two cytoplasmic proteins
namely protein Y and Z. These proteins pick up the bilirubin diffusing into the
cytoplasm.
Once in the hepatocyte the bilirubin is bound to glucuronic acid thus forming bilirubin
mono and di glucuronide by the enzyme UDP glucuronyl transferase. The enzyme is
located on the endoplasmic reticulum, both smooth and rough.
The conjugated bilirubin is excreted into the biliary canaliculus by an enzyme located
on the canalicular membrane. The excretion is the rate-limiting step of billirubin
disposal.
The conjugate bilirubin passes unchanged through the ileum till it reaches the
ileocaecal region and the colon where the glucuronic acid moiety is split from it.
The free billirubin so formed undergoes a series of reduction reactions. 80% of these
reduced products get excreted as stercobilinogen. The kidneys excrete a part of the
absorbed billirubin as urobilinogen and the rest enters the enterohepatic circulation.

CLASSIFICATION

There are a number of classification systems available for the classification of

obstructive jaundice. The commonest one in use is the Benjamin classification.

Benjamin classification

Type I: Tumors specially pancreatic head

complete obstruction (produce Ligation of CBD
jaundice) Cholangiocarcinoma
Parrenchymal liver tumors primary, secondary

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Type II: Choledocholithiasis
intermittent obstruction Periampullary carcinoma
(produces symptoms and Duodenal diverticula
biochemical changes of Papillomas of bile duct
obstruction but may or may not Choledochal cyst
produce jaundice) Polycystic liver disease
Intrabilliary parasites
Haemobilia
Type III: Strictures of CBD
chronic incomplete obstruction Stenosed biliary enteric anastomosis
(with or w/o symptoms or Chronic pancreatitis
biochemical changes but will Cystic fibrosis
eventually produce pathological Stenosis of sphincter of Oddi
changes in the liver, ducts) ? Dyskinesis (sphincter of Oddi dysfunction)
Type IV: Traumatic
segmental obstruction Hepatodocholithiasis
(one or more anatomical segments Sclerosing cholangitis
are involved with either of the Cholangiocarcinoma
above types)

AETIOLOGY (PGI) INDIAN DATA

Benign 38%
CBD stone 30%
Intrabiliary rupture of hydatid cyst 3%
Stricture CBD 2%
Misc 2.7%
Malignant 62%t
Ca pancreas 28.6%
Periampullary 6.8%
Extrahepatic ductal carcinoma 9.5%
Ca gall bladder 11.3%
Secondaries in porta 4.5%

CONSEQUENCES OF BILIARY OBSTRUCTION

Proximal dilatation of the biliary tree. It is more marked in acute complete obstruction
and may be completely reversible.
Increased secretory pressure of bile. N=5-10 cm mm water. Stabilizes at around 30 cm
in biliary obstruction. High pressure opens tight junctions between hepatocytes and
bile canaliculi. This can cause reflux, inflammation and fibrosis.
In prolonged obstruction leads to fibrosis of the biliary tract and the dilatation may not
be evident. This is a grave sign and fibrosis makes anastomosis difficult

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In obstruction, cholesterol and PL secretions are reduced more than bile acids thus
bile becomes less lithogenic bile. When obstruction is relieved, cholesterol and
phospholipids are rapidly secreted leading to lithogenic bile, which can not block
stents.
Increased pressure alters liver perfusion which can lead to hepatocyte dysfunction.
At pressures above 20 cm H2O, excretory biliary components can reflux into
circulation leading to systemic toxicity.
Bile acids inhibit cyto P450, convert it to inactive cyto P 420. This slows down
degradation of drugs and toxins.
A serum bilirubin higher that 12 mg% significantly increases risk of surgical
complications

PATHOLOGICAL EFFECTS OF BILIARY OBSTRUCTION

Liver:
 Dilated biliary canaliculi (centrilobular) with swollen, tortuous villi
 Bile thrombi
 Inflammatory reaction around the canaliculi due to recurrent cholangitis
which may further aggravate the obstruction
 Canalicular proliferation; later there may be changes of secondary biliary
cirrhosis
 Dilatation of microvilli of the bile canaliculi
 Destruction of layers of hepatocytes around the portal tract
 Periportal inflammatory exudate which connects the portal tracts
 Kuppfer cells (tissue macrophages) remove micro-organisms, damaged blood
cells, cellular debris, FDP and endotoxin. They also modulate synthesis of
proteins, expression of MHC-II antigens and phagocytosis. SOJ depresses
these function of Kupffer cells.
Kidney
 Causes renal failure the reasons for which are-
1. Direct toxic effect of elevated bilirubin
2. Endotoxemia
3. Absence of bile acids from the small intestine
4. Alteration in mitochondrial oxidative phosphorylation
5. Renal vascular fibrin deposition
6. Increased sensitivity of -adrenergic effects of nor adrenaline

 Incidence: ~ 10%
 Mortality: 70%

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  Endotoxin causes renal vasoconstriction and redistribution of internal blood
flow away from the cortex
 Hence aim for a urine output > 1.5-2 L/day for a few days prior to surgery
 External biliary drainage does not reduce mortality from ARF following
surgery for obstructive jaundice

Wound healing
 Wound dehiscence in 2-4%
 Incisional hernia in 10-12.5% skin prolyl hydroxylase activity is low
 Not known if this is due to malnutrition or hyperbilirubinemia.

Endotoxemia
 Absence of bile salts encourages the endotoxin production by loss of specific
binding function of bile salts and alteration of small bowel microflora
 Depressed hepatic RE cell function and thus decreased clearance of
endotoxins
 Cimetidine prevents endotoxin absorption
 A direct anti-endotoxic effect of lactulose has been proposed (indirect effect
by altering the gut flora)
 Kaolin ,pectin and cholestyramine have been shown to bind endotoxins in
animal models
 There is an increase in the incidence of infection of bile. It ranges from 36% in
the case of malignant obstruction to 80% in benign biliary strictures

Coagulation defects
 There is a decrease in the levels of vit K dependent coagulation factor
synthesis (II, VII, IX, X). Impairment of hepatic function, especially in
prolonged jaunice reduces secretory function, leading to reduction in
fibrinogen, prothrombin, prekallekrien, HMWK and factor XI
 Similarly there is reduced synthesis of natural coagulation inhibitors like
Protein C, S and antithrombin C
 There is failure to clear activated coagulation factors from circulation. This
along with endotoxaemia probably predisposes to a higher incidence of DIC.

Hemodynamic changes
 Decreased systemic arterial pressure
 Decreased peripheral vascular resistance
 Decreased responsiveness to norepinephrine
 Increased atrial natriuretic peptide

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  These patients have a reduced interstitial volume and marginally reduced
plasma volume

CLINICAL MANIFESTATIONS
 Ductal stones are more common in females and cancers in males
 Pain, a continuous dull boring pain in the upper abdomen. Usually precedes
the onset of jaundice. Pain before jaundice is more common in benign
obstruction than in malignancies. Pain radiating to back is seen in chronic
pancreatitis and pancreatic cancers
 Icterus (may or may not be present- see classification). The level may
fluctuate as seen in CBD stones, periampullary tumours where it is due to
sloughing of a part of the tumour. This may be accompanied by an
intermittently palpable gall bladder. Scleral icterus begins to appear with a
serum bilirubin of 2.5 and yellowing of skin and mucosa does not appear until
the serum bilirubin is around
 Pruritus (irritation of cutaneous nerve endings by bile salts). ? Centrally
mediated
 Weight loss is frequent and results from sitophobia, malabsorption and effects
of cancer
 Clay coloured stools due to absence of bile from intestine
 Cholangitis i.e. fever with chills and rigor. Usually occurs in benign
conditions and is rare in malignant obstruction. (As the malignant obstruction
is usually a complete block) The chills and rigors are due to a
cholangiovenous and cholangiolymphatic reflux of bacteria from the
obstructed & infected ducts
 Courvoisier’s law in the cases of malignancy causing obstructive jaundice the
gall bladder is usually palpable (as the GB is usually thickened and non
distensible due to recurrent attacks of cholangitis)
 Chung- the palpable GB simply represents a chronically elevated ductal
pressure which is more likely to result from a high grade malignant
obstruction
 Steatorrhoea: Maldigestion of fatty foods due to

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  absence of bile
 Due to alteration of the gut flora
 Also causes a deficiency of fat soluble vitamins

History and examination

LFT
Unconjugated hyperbilirubinemia Conjugated hyperbilirubinemia

Normal Hepatic enzymes Cholestasis Hepatocellular disease

USG Viral/drugs etc

Duct dilatation no duct dilatation

CT ? Viral

Proximal duct dilatation distal duct dilatation

PTC ERCP

INVESTIGATION PROTOCOL FOR A JAUNDICED PATIENT

Biochemical parameters

Serum bilirubin (0.6-1 mg/dL)

There is an increase in the conjugated bilirubin. The increase may be marginal
especially in incomplete or intermittent obstruction. It can be very difficult to
differentiate between obstructive and hepatocellular jaundice solely on the basis of
serum bilirubin

Alkaline phosphatase (60-170 IU/L; 3-13 KAU/mL)

This enzyme is elevated in SOJ. The enzyme is actively secreted into the biliary
canaliculi. Increased levels in obstruction are due to back diffusion or leak from the
ducts. The level of rise is not proportional to the degree of obstruction. The levels of
the enzyme start to reduce after the relief of obstruction but it may take time. The
measurement of the biliary isozyme (the other being the hepatic) may allow for a
better differentiation between complete or minimal biliary obstruction.

Transaminases (0-49 IU/L)

These are elevated initially even before the rise of serum bilirubin and ALP but return
to normal later. In prolonged obstruction they may get elevated again and this is a
poor prognostic factor.

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Serum albumin (TP: 6-8 g/dL; Alb: 3.8-5 g/dL; Glb: 1.8-3.5 g/dL)
Used as an indicator of hepatic synthesis. But due to its long half life it is not a very
useful measure of acute hepatic dysfunction. Decreased levels are commonly seen in
malignant obstruction. Half life of albumin is 10-14 days

Lipoprotein X
This is an abnormal lipoprotein. Elevated levels may be seen in biliary obstruction.

Coagulation profile
There is deranged prothrombin time, which promptly returns to normal after
administration of vitamin K (as opposed to hepatocellular jaundice when the PT
shows poor response to vit K).

Urinary bilirubin and urobilinogen

There is absence of urinary urobilinogen and there may be bilirubnuria
Gamma glutamyl transpeptidase
Alternative to ALP estimation
Antipyrine clearance test
This is an analgesic oxidised by the liver.

Radiological investigations

Plain X ray abdomen

has limited if any value. Calcified stones may be seen in 20-30% of
Choledocholithiasis. Speckled calcification in the region of the head of pancreas
may be seen in chronic pancreatitis.

Hypotonic duodenography
Done using a double lumen Derringer tube. Rarely used now. Gives a mucosal relief
and can be used to pick up periampullary tumors

Abdominal USG:
Non invasive and free of risk
Defines the presence of a dilated biliary tree, calculi, abnormal hepatic anatomy and
pancreatic abnormality
Can determine the site of obstruction in 60-80% and the cause of obstruction in 50%
Can not reliably exclude extra hepatic obstruction
More sensitive than CT for detecting Cholelithiasis

Endoscopic USG:
May be more accurate than combined ERCP and CT scan in defining the nature and
extent of biliary obstruction

CT :
Can establish the level in 90% and the cause in 75-94%
The dilated biliary system is divided into 4 parts
 Hepatic
 Supra pancreatic
 Pancreatic
 Ampullary

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An abrupt change in calibre of a grossly dilated CBD is indicative of malignancy. The
terminal end of the CBD may be irregular, rounded or nipple shaped but the end is
always abrupt
Calculi are visible in 80-90%
More sensitive than USG in detecting Choledocholithiasis
Can visualise small (1-2 cm) hepatic parenchymal lesions
Assesses the distal CBD which can not be done by USG
Can evaluate inflammatory process

Cholecyntigraphy:
Uses Tc 99m labelled iminodiacetic acid derivatives
Images are influenced by hepatic blood flow, RE function, and biliary excretion
Focal hepatic abnormalities appear as photopenic areas
Poor recognition of morphologic detail
Constantly increasing visualization intensity of the biliary tract accompanied by
decreasing liver parenchyma activity is very sensitive for partial obstruction
Time and extent of entry of activity into the duodenum is of importance in
differentiating incomplete and complete obstruction

PTC:

Technique
Now done with a thin flexible CHIBA needle 22 gauge
A brisk puncture is more likely to be successful than intermittent advance
When the needle enters the duct the contrast moves slowly away from the needle tip
unlike the washout seen in the puncture of the vessels
If the contrast is outside the duct and tracks along the duct then the margins are not
sharp and well defined
Lymphatics appear as irregular linear structures which do not wash out and form a
organised branching pattern
Results
In dilated systems upto 99% success
In non dilated system upto 80% success
Complications – 5% serious complications overall
Precautions
Antibiotic cover especially in the presence of cholangitis
In the presence of cholangitis aspirate some bile before injecting and inject a
small amount
Advantages
Accurate pre op delineation of stricture
Can plan surgery
Percutaneous needle biopsy under fluoroscopic guidance
Therapeutic placement of stent, drainage catheters

PTC pictures in various diseases

Sclerosing cholangitis: alternative dilatations and strictures throughout the biliary tree
Intra luminal filling defects
Ascaris: long linear filling defects

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Echinococcus: large grape like filling defects
Haemobilia : large irregular filling defects
Caroli’s disease: multiple contrast filled spaces in line with the intrahepatic ducts
Fluffy contrast collections in the ends of the ducts is seen in abscesses complicating
cholangitis
Calculus: a steeply curved margin or claw shaped end
Malignant obstruction: a shapr cut off below a grossly dilated duct
Benign stricture: incomplete obstruction. Long narrowing with smooth margins
Extrinsic compression: extrinsic scalloped margin with forward displacement

ERCP: endoscopic retrograde cholangio pancreatography

Complimentary to PTC
Shows the distal part of an obstructive lesion
Success ranges from 60-92%
Should be carried out with preparedness to do a laparotomy if required
Advantages
Frequent opacification of the pancreatic duct
Direct visualization of stomach and duodenum
Can biopsy Ampullary lesion and obtain fluid for cytology
Therapeutic applications
Endoscopic sphincterotomy
External drainage of obstructed bile ducts NBD
Internal biliary stents

MRI:
Role is controversial
MRCP is being used increasingly in the management of obstructive jaundice
It is a non-invasive test
Gadolinium enhanced images are used

Interventional biopsy procedures:

There various procedures that can be used are

Percutaneous fine needle aspiration biopsy
Either blind or guided by USG or CT can be used to obtain a tissue diagnosis. This
can obviate the need for surgery in patients who have unresectable tumours. It can
also allow proper radical surgery in resectable malignant tumours.

Percutaneous brush or forceps biopsy

Done through a percutaneous catheter. Upto 47% of times a positive diagnosis can be
obtained from the bile so aspirated.

Transpapillary brush or forceps biopsy

The results of endoscopic bile duct brush cytology are similar to that obtained
percutaneously.

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Transgastric or transduodenal aspiration biopsy
Done during endoscopy and helps in the diagnosis of pancreatic or periampullary
carcinoma.

Angiography
Now is rarely required with the advent of CECT and USG, which can give an accurate
diagnosis.

Barium meal and follow through

Was used earlier in the diagnosis of lesions in the region of the head of pancreas .The
findings are
Widening of the duodenal C loop The pad sign
If there is a pseudocyst in the head of the pancreas there will be widening of the
duodenal C.

TREATMENT
The treatment of obstructive jaundice depends on the specific condition causing it
The perioperative morbidity and mortality for surgery in patients with obstructive
jaundice approaches 50% and 25% respectively.
The basic considerations in the management of obstructive jaundice are
Establishing a diagnosis
Amelioration of symptoms
Relief of the obstruction

Amelioration of symptoms
Pruritis:
This is a distressing symptom mediated centrally through opoid receptors agonism. It
is not due to deposition of bile pigments in the skin. Establishment of a biliary
drainage best relieves pruritus.
Cholestyramine may be effective in reducing pruritis due to partial biliary obstruction.
It has no effect in complete biliary obstruction
Drugs used include the anion exchange resins, cholestyramine and colestipol, and
hepatic enzyme inducing drugs, such as rifampin, phenobarbital, and flumecinol.
More invasive examples include plasmapheresis, charcoal hemoperfusion, and partial
external diversion of bile.
Antihistamines are often administered. However no skin changes consistent with
histamine-mediated effects are found and antihistamines do not appear to be
efficacious.
Sedatives, such as phenobarbital, benzodiazepines, and antihistamines may have a
nonspecific beneficial effect by facilitating sleep, but may impair activities that
require mental concentration.
Miscellaneous therapies that have been tried include ultraviolet light, lignocaine,
androgens, and hydroxyethylrutosides. None of these therapies have a clear rationale
and none have been shown convincingly to be efficacious.
Other drugs used include naloxone and glucagon on experimental basis

Relief of obstruction
The ideal situation is to provide internal drainage
The factors to be considered are

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  Nature of the underlying problem / lesion
 Biliary and GI anatomy
 Desired goal
 Local expertise

It can be done by the following methods

 Radiological and percutaneous drainage techniques
 Endoscopic techniques
 Surgery

All these techniques are complementary

Patients are best managed by a multidisciplinary approach.
When a procedure is being done as a palliative measure then the non surgical methods
are preferred

Factors associated with poor risk are

Clinical
Depth of jaundice
Cholangitis
Malignancy
Malnutrition
Lab
Hyperbillirubinemia
Immune suppression
Prothrombin time
Delayed antipyrine clearance
GTT (linear GTT curves have a poorer prognosis as compared to parabolic
curves)

Radiological and percutaneous drainage technique

PTC:
 It is imperative to drain the system completely else acute suppurative cholangitis
 Technique as described earlier
 Antibiotics for 24-48 hours
 After the cholangiogram a guide-wire can usually be passed through the
obstruction and in most cases a Cope loop type self retaining catheter can be
passed to provide internal drainage
 Balloon dilatation can be done and an endoprosthesis can then be passed (the
common self expanding ones being Gianturco Z or Wallstent stents) . these stents
have a maximum life of upto 15 months

Indications of PTBD
 Decompression of biliary tract in cases of tumor obstruction
 Drainage in cases of biliary lithiasis and septic cholangitis
 Transtumoral biliary drainage with positioning of iridium particles for internal
radiotherapy
 Permits biopsy and scraping for cytological study

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  procedure of choice in patients with proximal tumors who are poor candidates for
surgery due to high operative risk or unresectibility

ROLE OF PREOPERATIVE PERCUTANEOUS BILIARY DRAINAGE

Controversial three studies have shown that it has no effect and only one study
has shown that though as a procedure it is useful but the effect is offset by the
drainage related complications

Complications of transhepatic intubation

1. Sliding of tube ( less common if secured below the obstruction)
2. Haemorrhage
3. Sepsis
4. Irritative skin lesion
5. External leak of ascitic fluid
6. Tumoral invasion

Endoscopic technique

Endoscopic sphincterotomy with or without placement of stents

 Use a 10F ( ext dia 3.4 mm) tube as the smaller 1.7 mm tube gets blocked early
 Papilotomy prior to insertion
 If the tube gets blocked then it can be easily changed

Naso biliary drainage: useful for short term drainage

 Done using a 250 cm long WURB’S tube external dia1.7 or 2.2 mm. It has a
preformed tip which prevents slipping
 Tube is passed through the instrumentation channel of a side viewing
endoscope after carrying out a papilotomy and advanced proximal to the
obstruction and the scope is then removed. The tube is then taken out through
the nose and fixed to the cheek.

SURGERY

Decide on the most appropriate procedure

The mainstay of therapy for biliary tract malignancies
In case of hilar obstruction drainage of one side achieves the same effect as
that of bilateral
Drainage
The specific surgical procedure performed will vary with the pathology causing the
obstruction

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 The specific procedures are: -

1. Sphincterotomy/ sphincteroplasty
2. Choledochoduodenostomy / choledochojejunostomy
3. Pancreaticoduodenectomy
a. Whipple’s procedure
b. Pylorus preserving Whipple’s
4. Hepaticojejunostomy
5. Pancreaticojejunostomy (Puestow’s procedure)
6. Coring of the head of pancreas
7. Hepatolithotomy
8. Cystoentrostomy

The indications of these procedures are as follows

(provided the growth is resectable in the malignant group)

Benign
1. Choledocholithiasis choledocholithotomy /
Choledochoduodenostomy
2. Hepatotithiasis hepaticolithotomy
3. Chronic calculus pancreatitis Pancreaticojejunostomy
4. Biliary strictures Choledochoduodenostomy /
Hepaticojejunostomy
5. Pancreatic pseudocyst cystogastrostomy / cystojejunostomy
6. Intrabilliary rupture of hydatid cyst drainage of liver cyst

Malignant

1. Whipple’s / pylorus preserving Whipple’s / total pancreatectomy

2. Periampullary carcinoma Whipple’s / pylorus preserving Whipple’s
3. Cholangiocarcinoma Hepaticojejunostomy
4. Ca gall bladder extended/ radical cholecystectomy

Perioperative Problems

a. Endotoxemia
b. Renal failure
c. Wound healing
d. Gastrointestinal haemorrhage
e. Coagulation disorders
Gastrointestinal haemorrhage

Seen post op in 6-24%

Accounts for 20% of post op deaths
The commonest cause is gastric erosions probably caused by
Endotoxemia

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 Increase gastric secretion
Intragastric bile reflux
Ischemia
Reduced intestinal blood flow

Factors as postulated by Dixon for poor prognosis

1. Initial Haematocrit < 30
2. Initial leucocyte count > 10* 10*9/L
3. Malignant obstructing lesion

Surgical obstructive jaundice in newborn and infancy

1. Biliary atresia
2. Choledochal cyst
3. Inspissated bile plug syndrome
4. Spontaneous perforation of CBD
5. Biliary hypoplasia
BILIARY ATRESIA:
 Highest incidence is in Japan
 1:12000 live births
 Histologically there is bile duct proliferation, bile stasis, portal fibrosis
with preserved hepatic architecture
 It is of two types
1. Correctable (ducts are formed till the porta)
2. Non correctable
 Has been divided into 3 types by KIMURA et al
 Type I atresia of CBD only
 Type II atresia of both hepatic ducts but patent GB
 Type III complete obliteration

 Treatment in the correctable types is by the KASAI procedure (Porto

enterotomy)

CHOLEDOCHAL CYST

Presents with jaundice, fever and mass

Divided into 5 types
I. saccular cysts of the CBD
II. fusiform dilatation of CBD
III. dilatation of lower end of CBD
IV. dilatation of IHBR and EHBR
V. CAROLI’S disease

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