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Obstructive Jaundice: Understanding the pathophysiology

Article  in  International Journal of Surgery and Medicine · August 2020

DOI: 10.5455/ijsm.2020-07-061-jaundice

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 SURGERY | REVIEW ARTICLE

OBSTRUCTIVE JAUNDICE: UNDERSTANDING THE

PATHOPHYSIOLOGY
Ketan Vagholkar∗,1
∗ Department of Surgery, D.Y.Patil University school of Medicine, Navi Mumbai-400706. MS. India.

ABSTRACT Jaundice is one of the most prevalent symptom in hepatobiliary disorders. The nature of jaundice may vary
from hepatocellular to obstructive pattern. In a few cases, it may be haemolytic in nature. Identifying and ascertaining
the type is pivotal for further investigation. A combination of haematological and radiological investigations will not
only provide information on the severity and the impact of obstructive jaundice on various organ systems of the body
but also help in determining the prognosis. Endoscopy can also provide diagnostic as well as a therapeutic benefit in
obstructive jaundice. The pathophysiology, clinical evaluation and investigations in a case of obstructive jaundice is
discussed in this paper.
KEYWORDS Jaundice, obstructive, causes, complications, investigations

Introduction
Obstructive jaundice is one of the most challenging types of jaun-
dice. It can be treated successfully once the cause is ascertained.
Understanding the basic physiology of bilirubin metabolism and
the structure of the extrahepatic biliary passages is essential for
the adequate diagnostic evaluation of a patient presenting with
obstructive jaundice. [1]
Surgical anatomy of the extrahepatic biliary passages
The intrahepatic ducts converge to form the right and left hepatic
ducts which exit from the liver and join to form the common hep-
atic duct. The cystic duct emerges from the gall bladder and joins
the common hepatic duct which then descends as the common
bile duct. The common bile duct has four parts, supraduodenal,
retroduodenal, intrapancreatic and intraduodenal. The common
bile duct is joined by the main pancreatic duct to open into the
ampulla of Vater situated in the second part of the duodenum.
The diameter of the normal CBD is less than 8mm, and the di-
ameter of the main pancreatic duct is less than 4 mm. The ducts
Copyright © 2020 by the Bulgarian Association of Young Surgeons
DOI:10.5455/ijsm.2020-07-061-jaundice
First Received: July 11, 2020
Accepted: July 23, 2020
Associate Editor: Ivan Inkov (BG);
1
Annapurna Niwas, 229 Ghantali Road. Thane 400602. MS. India; E mail:
kvagholkar@yahoo.com; Mobile: 9821341290
of Luschka are small biliary ducts that lie in the gall bladder
fossa and connect the liver and gall bladder directly. The normal
thickness of the gall bladder wall is less than 4 mm. Therefore
obstruction can occur at any level. It may be intraluminal or
due to extrinsic compression. Backpressure leads to dilatation
of the passages. Identifying the level and cause for obstruction
is, therefore, the main aim of clinical evaluation and imaging.
Physiology of bilirubin metabolism
Bilirubin is of two types, direct which is water soluble and indi-
rect, which is water insoluble. Identifying the rise of each type
is essential in the evaluation of the type of jaundice. Hence it is
essential to review the normal process of bilirubin formation and
clearance from the gastrointestinal tract. Fragile and senescent
RBC’s are broken down in the spleen. When the RBC membrane
ruptures, haemoglobin is released. The macrophages of the retic-
uloendothelial system phagocytose this. Haemoglobin is further
broken down into heme and globin. The heme component is
then further broken into free iron which combines with ferritin
and the straight remnant chain of four pyrrole nuclei that serves
as a substrate for the formation of bile pigments.
Biliverdin is formed which then gets converted into bilirubin.
Bilirubin is released into the plasma. In the plasma, it is bound
to albumin and transported to the liver. There it gets absorbed
across the hepatic cell membrane. During this process, it is
released from the albumin but remains attached to two proteins
Y and Z proteins inside the hepatocytes. Soon the bilirubin
is detached from these proteins and is conjugated. The end

Ketan Vagholkar / International Journal of Surgery and Medicine (2020) 6(4):26-31

products are bilirubin glucuronide (80%), bilirubin sulphate
(10%), and other substances (10%). An active transport process
then excretes bilirubin glucuronide into the bile canaliculi.
A small quantity of conjugated bilirubin enters the plasma.
Through the extrahepatic biliary passages, it inters into the in-
testine. Conjugated bilirubin is acted upon by the bacteria con-
verting it into urobilinogen. Urobilinogen undergoes oxidation
to stercobilinogen which is excreted into the stools as stercobilin.
Stercobilin imparts the yellowish colour to normal stools. A
part of urobilinogen is absorbed and passes to the kidneys from
where it is excreted into the urine as urobilin which imparts a
yellowish colour to normal urine.
Pathophysiology of Jaundice
Jaundice is best described as yellowish discolouration of the
sclera. Obstructive jaundice results from obstruction to the
free flow of bile from the liver to the gall bladder and then
to the small intestine. Jaundice or raised total bilirubin may be
due to an increase in either conjugated or unconjugated compo-
nent. This depends upon the level at which the normal bilirubin
metabolism is altered. This can happen at three levels Pre hep-
atic wherein there is increased production of bilirubin which
exceeds the capability of the liver to conjugate the bilirubin and
excrete it into the gut. There is a predominant increase in the
unconjugated bilirubin. The most frequent prehepatic cause is
haemolytic anaemia, where there is an excessive breakdown of
heme. [2]
Intrahepatic cause for hyperbilirubinaemia is usually due
to parenchymal liver disease, thereby causing an inability to
either conjugate or excrete bilirubin. This may initially cause a
transient increase in the conjugated component, followed by the
indirect component. This is seen in viral hepatitis, drug-induced
and primary biliary cirrhosis. [3]
Post hepatic causes lead to an impediment to the flow of bile,
which may be either due to partial or complete obstruction of the
extrahepatic biliary passages between the liver and duodenum.
There is predominantly conjugated hyperbilirubinaemia. This is
a characteristic feature of obstructive jaundice. [3]
Aetiology of biliary obstruction
Biliary obstruction may either be intrahepatic or extrahepatic in
origin. [4] Intrahepatic cholestasis could be at the level of the
hepatocyte or the canalicular bile membrane. The causes include
hepatitis (hepatitis A, B & C) leading to inflammation of the
liver with necrosis, cirrhosis (primary biliary cirrhosis) leading
to nodular regeneration and scarring, drug-induced (anabolic
steroids, chlorpromazine) and space-occupying lesions of the
liver such as cysts, abscesses and tumours. [5]
Extrahepatic causes can further be classified as intraductal,
which include choledocholithiasis, neoplasms (cholangiocarci-
nomas), biliary strictures and parasitic infestations (ascariasis,
liver flukes). [6] For better understanding extrahepatic causes of
obstructive jaundice can be classified into four types (Table 1)
Extra ductal causes include neoplasms, pancreatitis, pseu-
docysts of pancreas and portal hilar lymphadenopathy. Tu-
mours causing extra ductal compression deserve special men-
tion. These include pancreatic head tumours, cholangiocarci-
noma, ampullary carcinomas, gall bladder carcinomas extending
up to the CBD and metastatic lymphadenopathy. [7] Choledo-
cholithiasis, biliary strictures and malignant tumours are the
most important and common causes of obstructive jaundice. Un-
common postoperative causes need to be considered as well.
Ketan Vagholkar / International Journal of Surgery and Medicine (2020) 6(4):26-31
This includes sump syndrome seen in a side to side choledo-
choduodenostomy in which food, stones or debris accumulate
in the CBD and obstruct the normal biliary outflow. The other
such cause is seen in Roux-en Y limb wherein stasis may cause
biliary obstruction after biliary enteric anastomosis. [8]
Effects of biliary obstruction:
Complications of cholestasis are proportional to the duration
and intensity of jaundice. Jaundice has a negative impact on
various organ systems of the body.
Intestines:
Bile and bile acids have essential functions in maintaining the
normal integrity and function of the intestines. Bile and bile
acids contribute significantly to the normal gut barrier function.
It has positive effects on the intestinal immune function. In
experimental studies, it affects homing and distribution of T
lymphocytes in the gut-associated lymphatic tissue. Absence
of bile acids in the gut causes a fall in the CD4+ and CD8+
lymphocytes. It exerts a trophic effect on the intestinal mucosa
by increasing the villous density and inducing hypertrophy of
various components of the intestinal wall. Bile acids inhibit
the growth of certain bacteria such as Bacteroides, clostridia,
lactobacillus and streptococci. [9]
Absence of bile in the intestine has a series of deleterious
effects leading to septicaemia. Absence of bile salts leads to
disturbance of intestinal bacterial balance with overgrowth of
gram-negative bacteria. There is an alteration of intestinal tight
junction expression and increased intestinal apoptosis, causing
significant alterations in the intestinal oxidative state, thereby
exacerbating the gut injury. There is increased intestinal perme-
ability causing bacterial and endotoxin translocation leading to
septic and renal complications. Absence of bile causes suppres-
sion of clearing capacity of Kupffer cells, the main hepatocyte
macrophage population due to accumulation of bile acids in
the liver thereby permitting spillover of endotoxins from the
portal circulation into the systemic circulation with the release
of pro-inflammatory cytokines. These lead to the development
of “gut-derived sepsis”. [10, 11, 12]
Coagulation system:
The liver has a significant synthetic role to play in the coagu-
lation system. It synthesizes fibrinogen, prothrombin, factors
II, VII, IX and X. The production of these factors is dependent
on vitamin K, which is a fat-soluble vitamin requiring bile in
the intestine for absorption. Due to the absence of bile in the
intestine, this vitamin cannot be absorbed, leading to deficiency.
Hence glycosylation of lysyl residues cannot take place in the
liver, thereby leading to deficiency of factors II, VII, IX and X.
This causes disturbances in the extrinsic pathway of coagulation.
The liver also manufactures natural anticoagulants such as an-
tithrombin III, protein C, protein S and heparin cofactor II. With
respect to the fibrinolytic system, it produces plasminogen and
alpha two anti-plasmin. Therefore alteration in liver function
can lead to serious coagulation defects. If septic and pancreatic
complications develop then a prothrombotic state may develop
initially. Mucinous adenocarcinomas of the pancreas and hepa-
tocellular carcinomas can induce activation of the haemostatic
system. Thromboembolic events usually follow. Unresolved
cholestasis leads to a generalized alteration in the haemostatic
system. The effects are thrombocytopenia, decreased synthesis
Table 1 Classification of obstructive jaundice (Benjamin).
Type I : Complete obstruction
Tumours of the head of pancreas
Ligation of the CBD
Cholangiocarcinoma
Parenchymal liver disease
Type II: Intermittent obstruction
Choledocholithiasis
Cholodochal cyst
Duodenal diverticulum
Intrabiliary parasites
Haemobilia
Type III : Chronic incomplete obstruction
Strictures of the CBD
Stenosed biliary enteric anastomosis
Chronic pancreatitis
Stenosis of the sphincter of Oddi
Type IV: Segmental obstruction
Traumatic
Sclerosing cholangitis
Intrahepatic stones
Cholangiocarcinoma

Table 2 Types of jaundice.

Hepatocellular
Parameter Pre-hepatic Obstructive
(hepatic)
Haemolysis leading to excess Deficient uptake, conjugation or Deficient excretion due to
Mechanism of raised bilirubin
production excretion by hepatocytes obstruction in the biliary tract
Unconjugated+ Predominantly conjugated
Type of serum bilirubin affected Mainly unconjugated
conjugated (>50%)
Urine bilirubin absent present present

Urine urobilinogen increased variable absent

Abnormal that is not correctable Abnormal that is corrected with
Prothrombin time normal
by vitamin k vitamin k
Features of haemolysis on blood
smear Marked increase in ALT Marked increase in ALP > 3
Additional features
(reticulocytosis, low and AST times the normal upper limit
haptoglobin, low Hb)
Prototypes Haemolytic anaemia Viral hepatitis Common bile duct stones

Table 3 Prognostic factors (Pitt’s score)

Parameters (one point per factor)

Type of obstruction (benign or malignant)

Age >60 years
Serum albumin < 3gm/dl
Serum bilirubin > 10 mg%
Serum Alkaline phosphatase > 100 IU
Serum creatinine > 1.3 mg%

TLC > 10000/mm3

Haematocrit < 30%

Ketan Vagholkar / International Journal of Surgery and Medicine (2020) 6(4):26-31

Interpretation of scores
Factors
Up to 2
3 4%
4 7%
5 44%
6 67%
8 100%
and clearance of coagulation factors and inhibitors, dysfibrino-
genemia, hyperfibrinolysis, over DIC, portal vein stasis and
thrombosis. [13, 14]
Renal system
Jaundice alone independent of the parenchymal liver disease
affects the integrity of the cardiovascular system. [15] The effects
are
1. Reduction in peripheral vascular resistance resulting in
systemic hypotension.
2. Depression of myocardial function.
3. Profound natriuresis and diuresis, leading to volume deple-
tion.
In experimental models, renal complications are attributed to
pre-renal factors. Various factors related to liver parenchymal
damage associated with obstructive jaundice may have an inde-
pendent contribution to the pathogenesis of arterial underfilling,
which predisposes to pre-renal failure and acute tubular necro-
sis. Peripheral and renal haemodynamic effects of obstructive
jaundice are more marked than medical jaundice. High level of
bile acids in the circulation seen in obstructive jaundice has a
direct cardio depressant and hypovolemic effect. In addition to
the direct effects of bile acids on circulation, a higher concentra-
tion of circulating endotoxins has deleterious effects on both the
peripheral and renal microcirculation.
Liver:
High-grade biliary obstruction leads to increased intraductal
pressure. There is bacterial overgrowth leading to cholangitis
which eventually culminates to septic shock. Severe functional
derangements of the hepatic function lead to alteration of liver
regeneration. High-grade obstructive jaundice causes cell dam-
age. Bile acids cause liver cell apoptosis by directly activating
death receptors inducing oxidative damage and mitochondrial
dysfunction, which as a combination strongly sensitizes to apop-
tosis. The net result of gross hepatic dysfunction is endotox-
aemia. Long-standing biliary obstruction leads to secondary
biliary cirrhosis. [16]
CNS:
Long-standing jaundice leads to the formation of pseudo trans-
mitters which predispose to precoma and finally into a hepatic
coma.
Ketan Vagholkar / International Journal of Surgery and Medicine (2020) 6(4):26-31
Mortality
0%
Clinical evaluation:
Jaundice is the main presenting symptom. The main aims of
clinical evaluation are:
1. Determining the obstructive nature of jaundice.
2. Identifying the cause for obstructive jaundice.
3. Whether the aetiology is benign or malignant in nature.
4. If malignant then whether the disease is metastatic in na-
ture.
5. Impact of jaundice on other organ systems.
6. The need for multiorgan system support.
7. Postulate an investigation algorithm based on the clinical
findings.
Jaundice can be haemolytic, hepatocellular or obstructive in
nature. (Table 2) The onset duration and progress of the jaun-
dice is important. Rapidly developing jaundice associated with
symptoms of pruritus, the passage of clay coloured stools and
high coloured urine is seen in the obstructive pattern of jaundice.
Significant nausea, vomiting and loose motions are suggestive
of medical aetiology. History of alcoholism, intravenous drug
abuse and multiple tattoos over the body go in favour of medi-
cal causes of jaundice. Persistent anaemia with mild abdominal
symptoms is suggestive of the haemolytic pattern. History of
drug ingestion followed by jaundice is seen in the hepatocel-
lular type of jaundice. Multiple blood transfusions predispose
hepatitis B and cirrhosis. [17]
Pain as an associated symptom is important in identifying
the cause of obstructive jaundice. Jaundice associated with pain
and fever suggestive of cholangitis is seen in bile duct stones.
Jaundice typically shows waxing and waning. Intermittent at-
tacks of right upper abdominal pain accompanied by vomiting
is seen in cholecystitis. Severe pain and associated symptoms
suggestive of pancreatitis can also cause transient obstructive
jaundice. Painless progressive jaundice related to weight loss is
highly suspicious of malignant aetiology. The previous history
of biliary surgery presenting as jaundice is suggestive of a biliary
stricture. History of inflammatory bowel disease presenting as
jaundice is suggestive of primary sclerosing cholangitis. [18]
Weight loss, bone pains, and abdominal distension due to
ascites are suggestive of malignant aetiology. History of abdom-
inal masses is highly suggestive of malignancy.
Long-standing jaundice can affect other organ systems. Neu-
rological symptoms are suggestive of impending coma. Renal
dysfunction is a common accompaniment in severe jaundice. Co-
agulopathies are seen in advanced stages. Generalized oedema
due to hypoproteinaemia is a bad prognostic sign.
Physical examination reveals deepening of scleral icterus. Vi-
tal parameters may be altered if the patient presents late. Fever
is an important feature. Pain, fever and jaundice is Charcot’s
triad seen in cholangitis. In addition to these, if there is hypoten-
sion and mental obtundation, then that constitutes Reynold’s
pentad. Reynold’s pentad is seen in suppurative cholangitis.
Scratch marks of pruritus are commonly visible in obstructive
jaundice. Signs of hepatocellular failure are seen in advanced
cases. Flapping tremors and mental obtundation are red flags of
poor prognosis. Fullness due to a mass in the left supraclavicular
region is suggestive of an inoperable malignancy.
The abdominal examination needs to be done meticulously.
Tenderness in the right hypochondrium suggests cholecystitis. A
palpable gall bladder in a jaundiced patient is highly suggestive
of malignant obstruction. (Courvoisier law) Hepatomegaly may
be due to hepatitis or due to chronic cholestasis. Metastases
in the liver can also cause hepatomegaly. A mass in continuity
with the liver can be due to an advanced gall bladder tumour.
Free fluid in the abdomen due to ascites is a sign of advanced
malignant disease.
Investigations:
Investigations are aimed at
2. Level of obstruction and degree of back pressure changes.
3. Status of the liver and abdominal metastases in suspected
malignant obstruction.
4. Splenic enlargement.
5. Ascites.
Endoscopic ultrasound further helps in the assessment of
malignant obstruction. [20] Advantages are:
1. Helps in evaluating the distal CBD.
2. It is accurately diagnosing CBD calculi including small cal-
culi in a nondilated system which are missed on routine
ultrasonography.
3. Small resectable pancreatic masses can also be identified.
Magnetic resonance cholangiopancreatography (MRCP) is a
non-invasive investigation for evaluation of the biliary tract. It
has a sensitivity of 95% and a specificity of 95% as well. It helps
in diagnosing the cause and level of biliary obstruction.
Contrast-enhanced computed tomography (CECT) is the in-
vestigation of choice for staging the disease in cases of malignant
obstruction. [21] CECT reveals the following:

1. Determining the severity of illness 1. Site of obstruction

2. Urgency of intervention 2. Nature of obstruction, whether benign or malignant.

3. Level of care required 3. Extent or severity of backpressure changes

4. Echotexture of the liver.

Haematological investigations are very critical in the evalua-
tion of obstructive jaundice. A complete blood count will reveal
5. Presence of metastases
anaemia in malignant cases. Leucocytosis is seen in cholangitis.
Total bilirubin will be raised. There will be a predominant
increase in the direct reading component. Alkaline phosphatase 6. Ascites.
is a membrane-bound enzyme located in the bile canalicular
pole of the hepatocyte. A value of three times the upper limit 7. Vascular encasement in cases of pancreatic head cancers.
of normal value is seen in the obstructive pattern of jaundice.
It is elevated in almost all patients of biliary obstruction except
Endoscopic retrograde cholangiopancreatography (ERCP) is
for incomplete or intermittent obstruction. Gamma-glutamyl
the investigation of choice once a preliminary imaging assess-
transpeptidase is raised in bile duct obstruction. Its level paral-
ment has been done. ERCP can be both diagnostic and ther-
lels the level of alkaline phosphatase in patients with cholesta-
apeutic. The diagnostic role is to collect tissue for biopsy in
sis.
periampullary growths or brush cytology samples. The exact
Serum transaminases (ALT, AST) are mildly elevated in
level of the block and the severity of backpressure changes can
cholestasis while markedly elevated in cholangitis. PT/INR
also be ascertained. Therapeutic intervention is ideal for stones
is prolonged due to malabsorption of vitamin K. It is corrected
in the CBD, which saves unnecessary surgical exploration of the
by parenteral administration of vitamin K. If PT/INR improves
CBD. Preoperative stenting to relieve jaundice is of great help
with vitamin K injections, then it is more in favour of obstructive
in preparing the patient for surgery. In inoperable cases, pallia-
pattern while no improvement is seen in the liver parenchymal
tive stenting is useful to reduce the complications of jaundice.
disease.
However, one needs to be careful of the complications of the
Renal function is best assessed and monitored by evaluation
procedure, which include pancreatitis, perforation, haemorrhage
of serum creatinine, blood urea nitrogen and electrolytes.
and sepsis by causing cholangitis. [22]
Viral markers for hepatitis B and C should be done in all cases
Percutaneous transhepatic cholangiography (PTC) is an alter-
of obstructive jaundice.
native if ERCP fails as in hilar obstructions. It enables drainage
Ultrasound is a preliminary investigation. It enables docu-
of accumulated bile proximal to the obstruction. [23]
mentation of the presence, extent and level of obstruction. [19]
It helps in Prognosis in obstructive jaundice can be evaluated based on
haematological and radiological findings. [24] Pitt’s score can be
1. It is identifying the cause of obstruction. evaluated. Higher the score worst in the prognosis. (Table 3)

Ketan Vagholkar / International Journal of Surgery and Medicine (2020) 6(4):26-31

Conclusion
Understanding the pathophysiology of obstructive jaundice is
essential for proper evaluation in order to prevent a delay in
the diagnosis: a careful history and physical examination help
in ascertaining the obstructive aetiology of jaundice. Various
imaging modalities help in confirming the benign or malignant
nature of the obstruction. ERCP has an added advantage of
therapeutic intervention especially in choledocholithiasis. Once
this road map is available the surgeon can formulate a surgical
plan for the patient.
Acknowledgements
I would like to thank Parth Vagholkar for his help in typesetting
the manuscript.
Conflict of interest
None.
Funding
Nil
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