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Acute cholangitis- An overview of diagnosis and medical management

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Review Article
Acute cholangitis- An overview of diagnosis and medical management
1 2
Monica Gupta , Atul Sachdev
Professor
Department of Medicine1, Gastroenterology2
Government Medical College and Hospital, Chandigarh
INTRODUCTION
Acute cholangitis is a systemic disease resulting from
bacterial infection superimposed on partially or
completely obstructed biliary system. Acute cholangitis
is defined as a morbid condition with acute inflammation
and infection in the bile duct.1 Infectious cholangitis
encompass a wide spectrum of infectious processes
affecting biliary tree. It may present as a local biliary
infection or progressive systemic inflammatory
response syndrome (SIRS), or more rapidly advancing
sepsis with or without multi-organ dysfunction. Others
are indolent infections that may predispose a patient to
liver failure or cholangiocarcinoma. Viral cholangitides
primarily affect immune-compromised patients.
Parasitic cholangitis is generally seen in tropical
countries. Rapid diagnosis and severity estimation are
essential for proper management, including intensive
medical support and urgent biliary drainage.
Pathophysiology
Although bile is normally sterile, microorganisms gain
access to biliary tree by retrograde ascent from
duodenum or from portal venous system. Progressive
biliary obstruction causes an elevated intraluminal
pressure, that spreads the infection into the biliary
canaliculi, hepatic veins, and perihepatic lymphatics.2 In
absence of obstruction and raised intra-ductal pressures,
bile is unlikely to get infected and cause clinical
cholangitis. Increased bacterial colonization of small
bowel and diminished host immune defenses set the
stage for translocation of local bacteria into the systemic
circulation, resulting in potentially life-threatening
septicemia. The lack of endothelial lining between bile
Corresponding Author :
Dr. Monica Gupta
M. D., D.N.B. Medicine, Professor
Level 4, D Block, Department of General Medicine,
GMCH, Chandigarh
Email: drmg1156@gmail.com
1 Journal of Medical College Chandigarh, 2016, Vol. 6, No.2
canaliculi and liver capillaries also predisposes to early
septicemia.
HISTORY
Acute cholangitis was initially described in literature by
Dr. Jean-Martin Charcot as “hepatic fever” in 1877.
Charcot's triad is characterized by classical features of
acute cholangitis; intermittent fever with chills, right
upper quadrant pain, and jaundice.3 The Reynold's
pentad was coined in 1959 by Reynolds and Dragan,
who described a severe form of cholangitis with septic
shock and mental confusion, in addition to triad of
Charcot.4 However, the actual occurrence of Charcot's
triad is observed in 15.4% to 72% of patients with acute
cholangitis, and Reynolds' pentad is exceedingly
5,6
uncommon, reported in only 3.5%–7.7% of patients.
Epidemiology
Etiology
The circumstances leading to biliary stasis or obstruction
result in bacterial infection and cholangitis. Partial
blockage has a higher incidence of infection than
complete obstruction. Choledocholithiasis is the
commonest reason of acute cholangitis. The propensity
of bactibilia increases with presence of gallbladder or
common bile duct (CBD) stones. Bile cultures are
7
affirmative in 50% of patients with choledocholithiasis.
Earlier choledocholithiasis accounted for about 80%
cases of acute cholangitis. However, recently health care
associated acute cholangitis related to growing
endoscopic and radiological interventions and bilio-
pancreatic malignancy is becoming more frequent. The
incidence of acute cholangitis after endoscopic
retrograde cholangiopancreatography (ERCP) is
0.5–1.7%.8,9 Malignancies currently account for 10–30%
of all cases. South-east Asians are more prone to have
primary stones attributable to chronic biliary infections,
parasites, bile stasis, and biliary strictures.
In tropical countries like India or Latin America,
parasitic infestations of biliary tract are responsible for
Gupta and Sachdev
substantial cases of biliary obstruction and cholangitis.
This condition is known as recurrent pyogenic
cholangitis or Oriental cholangiohepatitis and is a
progressive disease characterized by recurrent episodes
of bacterial cholangitis. It is related to biliary ductal
ectasia, focal strictures, and development of intrahepatic
pigment stones.10 The causal parasites are Ascaris
lumbricoides, Clonorchis sinensis, Opisthorchis
viverrini, Opisthorchis felineus, and Dicrocoelium
11
dendriticum. Occasionally, Echinococcus granulosus
and Echinococcus multilocularis cysts may rupture or
fistulize into biliary system with resultant cholangitis.
Other uncommon etiologies are AIDS cholangiopathy
characterized by sclerosing chongitis like picture,
Mirizzi syndrome characterized by CBD stenosis caused
by stone impacted at the gall bladder neck or in the cystic
duct and Lemmel syndrome distinguished by presence of
cholestatic jaundice, cholangitis and pancreatitis
secondary to duodenal pancreatic diverticulum
compressing or displacing distal biliary opening. Table I
shows the common etiologies of acute cholangitis.
Causative agents
The infecting organisms are usually those of gut flora.
Bile cultures are often polymicrobial in 30-80% of
patients and gram-negative bacilli are seen in 88% of
these cases.12 The common gram-negative bacilli
cultured from the bile in acute suppurative cholagitis are
Escherichia coli, Klebsiella species, Enterococcus
species, Streptococcus species, Enterobacter species,
and Pseudomonas aeruginosa.13 Anaerobes consisting of
Bacteroides and Clostridium species are detected in
roughly 25% of patients. Hospital acquired cholangitis is
frequently caused by multiple resistant organisms, such
as Pseudomonas, methicillin resistant Staphylococcus
aureus, and vancomycin-resistant enterococci, whereas
infection in community-acquired cases are typically
associated with intestinal microorganism, such as
Escherichia coli, Klebsiella, or Enterococcus. Many
cases with culture positive cholangitis have the same
species of bacteria in blood as isolated from bile
14
cultures. The rates of blood culture-positivity in acute
cholangitis are reported to fluctuate between 21-71%.15
In AIDS -related cholangitis the causative agents may be
Cytomegalovirus or Cryptosporidium and is
characterized by extrahepatic biliary edema, ulceration,
and obstruction.
Journal of Medical College Chandigarh, 2016, Vol. 6, No.2
Clinical features
To suspect cholangitis, it is important to elicit the history
of gallstones or CBD stones, recent cholecystectomy or
biliary surgery, recent endoscopic procedures or invasive
radiological interventions. The presenting features may
be classical as Charcot's triad consisting of fever, right
upper quadrant (RUQ) pain, and jaundice. But a classical
presentation is usually not the case; although if present it
is very specific to the diagnosis of acute cholangitis.
Similarly the Reynold's pentad is much rarer. Fever and
abdominal pain are the core symptoms, with similar
incidence of 80% or more, whereas jaundice is observed
in 60–70% of cases.16,17 Other patients may present with
altered mental status (10-20%), hypotension (30%),
acute renal failure or cholestasis. Physical examination
may reveal fever, RUQ tenderness, mild hepatomegaly,
jaundice, disturbed consciousness, septic shock,
tachycardia and rarely peritonitis. The classic clinical
symptoms of fever and abdominal pain are often absent
or more difficult to recognize in elderly patients.18
Symptoms in elderly may not correlate with disease
severity therefore many with severe cholangitis present
with deceptively mild symptoms leading to delayed or
misdiagnosis.19 Moreover, elderly have relatively higher
prevalence of severe cholangitis, hypotension, altered
sensorium, peritonism and renal failure.
Laboratory studies
Laboratory data may indicate evidence of inflammation
in the form of abnormal WBC count (leucocytosis or
leucopenia), increase of serum C-reactive protein, and
erythrocyte sedimentation rate. There may be also
indication of biliary stasis (hyperbilirubinemia) and
raised liver enzymes (Increased alkaline phosphatase,
gamma-glutamyltranspeptidase, aspartate amino-
transferase and alanine aminotransferase). Electrolyte
panel with renal function should be performed. A
prolonged prothrombin time helps to assess severity of
disease. Both aerobic and anerobic blood cultures should
be done to detect bacteremia and antibiotic
susceptibility. Biliary cultures must be sent if a biliary
drainage procedure is considered. Hyperamylasemia is a
helpful parameter to identify complications such as
20
choledocholithiasis resulting in biliary pancreatitis.
Imaging findings
Imaging plays a pivotal role in diagnosis of cholangitis,
2

Table I
1
Etiology of acute cholangitis
sCholelithiasis
sBenign biliary stricture
sCongenital factors
sPostoperative factors (damaged bile duct, strictured
choledojejunostomy, etc.)
sInflammatory factors (oriental cholangitis, etc.)
sMalignant occlusion
w Bile duct tumor
w Gallbladder tumor
w Ampullary tumor
w Pancreatic tumor
w Duodenal tumor
sPancreatitis
sEntry of parasites into the bile ducts
sExternal pressure
sFibrosis of the papilla
sDuodenal diverticulum
sBlood clot
sSump syndrome after biliary enteric anastomosis
sIatrogenic factors
identifying predisposing factors, and revealing
complications. Ultrasonography (USG) is the most
frequently used first-line imaging modality. USG is
highly sensitive and specific for imaging gallbladder
and assessing bile duct dilatation. As compared to with
USG, computed tomography (CT) is more effective in
demonstrating the cause and site of biliary obstruction
(in particular distal common bile duct) and biliary
21
morphology. CT cholangiography is a novel modality
that utilizes contrast which is taken up by hepatocytes
and secreted into biliary system and its accuracy is
e q u i v a l e n t t o E R C P. M a g n e t i c r e s o n a n c e
cholangiopancreatography (MRCP) is a noninvasive
technique that detects dilatation and enhancement of
intrahepatic biliary ducts in majority (92%) of
cholangitis cases. The distribution can be segmental
(46%), central (38%) or diffuse (16%). In 85%, there is
associated smooth and symmetric wall thickening.
Pneumobilia can also be present in cases of acute
bacterial cholangitis, similarly complications include
liver abscesses and portal vein thrombosis which can
22
also be detected. Oriental cholangiohepatitis is
distinguished by stenosis or strictures of peripheral
ducts, with decreased branching and abrupt tapering
(“arrowhead appearance”) and disproportionate
dilatation of extrahepatic bile ducts.23 Diagnostic direct
cholangiography methods like percutaneous
transhepatic cholangiography (PTC) or ERCP can
3 Journal of Medical College Chandigarh, 2016, Vol. 6, No.2
Acute Cholangitis
demonstrate detailed biliary anatomy. Since they can
exacerbate cholangitis, whenever contemplated, these
procedures should always be accompanied by
therapeutic biliary drainage.
Diagnosis
In Tokyo April 2006, Evidence-Based Practice
Guidelines for Management of Acute Cholangitis and
Cholecystitis were developed and published by the
International Consensus Meeting for Management of
24
Acute Cholecystitis and Cholangitis. Based on
extensive review of large studies and consensus of World
experts, these guidelines have been established as
benchmark for the diagnosis, severity assessment and
management of acute cholangitis. Before these
guidelines were available, there were no standard
diagnostic criteria for acute cholangitis. Acute
cholangitis was defined by some authors based on
clinical signs such as Charcot's triad (fever and/or chills,
abdominal pain, and jaundice) while others emphasized
the properties of bile or presence of biliary obstruction
(acute suppurative cholangitis, acute obstructive
suppurative cholangitis.16,25 In 2013, these guidelines
were further updated to improve the diagnostic accuracy
and reliability in the assessment of severity of disease.26
Table II shows the diagnostic criteria for acute
27
cholangitis that were adopted in 2013. Diseases which
need to be differentiated from acute cholangitis are acute
cholecystitis, peptic ulcer, acute pancreatitis, acute
hepatitis, diverticulitis, mesenteric ischemia and
septicemia from other sources.
Table II
Diagnostic criteria for acute cholangitis27
A. Systemic inflammation
A-1. Fever and/or shaking chills
A-2. Laboratory data: evidence of inflammatory response
B. Cholestasis
B-1. Jaundice
B-2. Laboratory data: abnormal liver function tests
C. Imaging
C-1. Biliary dilatation
C-2. Evidence of the etiology on imaging (stricture, stone,
stent etc.)
Suspected diagnosis: One item in A plus one item in either
B or C
Definite diagnosis: One item in A, one item in B and one
item in C
Gupta and Sachdev

High risk patients cholangitis may prove fatal unless appropriately

Certain subgroups of patients are at high risk to succumb
to acute cholangitis. These include patients with higher
disease severity in the form of organ dysfunction, shock,
mental confusion, elevated serum creatinine, prolonged
prothrombin time, hyperbilirubinemia, cirrhosis and
reduced platelet count.7,15,28,29 Other risk factors include
high fever, leukocytosis, bacteremia, endotoxemia,
hypoalbuminemia, liver abscess, medical comorbidity,
female gender, elderly and patients with malignancies.
Based on new evidence, five predictive factors for poor
prognosis have been identified; these include
hyperbilirubinemia, high fever, leucocytosis, elderly
patient and hypoalbuminemia.27
Complications
Acute cholangitis may get complicated with
development of septicemia, liver abscesses, portal vein
thrombosis, and biliary peritonitis or may become
indolent and lead to biliary stricture, sclerosing
cholangitis, and cholangiocarcinoma. The mortality in
28,30
acute cholangitis varies from 2.5-65%. The mortality
rate has declined dramatically from over 60% in 1970's
to less than 7% by 1980s with newer antibiotics and
prompt biliary drainage.29,31,32 However, mortality may
escalate to 11- 27% in high risk group. Even today severe
managed.
Severity of cholangitis
Assessment of disease severity at presentation is an
essential component of management of acute
cholangitis. As already emphasized, acute cholangitis
may manifest itself from a localized self -limited disease
to overwhelming sepsis. Although most cases respond to
initial medical management, it is important to recognize
those which may prove hazardous. Two factors that are
important in grading severity are the 'onset of organ
33
dysfunction'and 'response to initial medical treatment'.
Even after initial medical treatment, frequent re-
evaluations are necessary, so as to re-stratify patients as
per their parameters.
Definitions of severity assessment criteria for acute
27
cholangitis
Grade III (Severe) acute cholangitis
''Grade III'' acute cholangitis is defined as acute
cholangitis that is associated with the onset of
dysfunction in at least one of any of the following
organs/systems:
1. Cardiovascular dysfunction: Hypotension requiring
dopamine ≥ 5 ug/kg per min, or any dose of

Table III
Comparison of various biliary drainage techniques in acute cholangitis

Authors Type of technique No. of Success rate Incidence of Mortality Conclusion

patients of drainage complications
Chen et al 41 PTBD 56 82.1%
Pessa et al 42 PTBD 42 100% 7% 5%
Lai et al 43 Endoscopic drainage 41 100% 34% 10% Endoscopy much more
Open (laparotomy with 41 100% 66% 32% safe
T-tube drainage)
Sugiyama and ENBD without EST 93 96% 2%
Atomi39 ENBD without EST 73 95% 11%
40
Hui et al Stent without EST 37 86% 3%
Stent with EST 37 89% 11%
44
Sharma et al ENBD 75 97.3% 2.7% Equally safe and
Stent 75 97.3% 2.7% effective
Goenka et al 45 ENBD 143 90.2% 3.5% ENBD is safe and
effective
Agarwal et al 19 ENBD 80 100 3% Both equally effective
Stent 92 100

Journal of Medical College Chandigarh, 2016, Vol. 6, No.2 4


norepinephrine
2. Neurological dysfunction: Disturbance of
consciousness
3. Respiratory dysfunction: PaO2/FiO2 ratio < 300
4. Renal dysfunction: Oliguria, serum creatinine > 2.0
mg/dl
5. Hepatic dysfunction: PT-INR > 1.5
6. Hematological dysfunction Platelet count <
100,000/mm
3 clavulanante; ceftriaxine plus tazobactam) is the
Grade II (moderate) acute cholangitis
''Grade II'' acute cholangitis is associated with any two of
the following conditions:
3 3
1. Abnormal WBC count (>12,000/mm , < 4,000/mm )
2. High fever (≥39°C)
3. Age (≥75 years old)
4. Hyperbilirubinemia (total bilirubin ≥5 mg/dL)
5. Hypoalbuminemia
Grade I (mild) acute cholangitis
''Grade I'' acute cholangitis does not meet the criteria of
''Grade III (severe)'' or ''Grade II (moderate)'' acute
cholangitis at initial diagnosis.
Goals of management
The International Guidelines developed based on best
clinical evidence and discussions at the International
Consensus Meeting (Tokyo 2006) have provided the
management approach for acute cholangitis. 3 4
Management is focused towards correction of the most
important components of disease: biliary infection and
obstruction and approach should be directed by grade of
severity of disease. However, early empirical broad-
spectrum antibiotics, parenteral fluids and appropriate
supportive and resuscitative procedures are mandatory
for all these patients.
Antibiotic regimen: The antimicrobial therapy should
be administered as soon as diagnosis of acute cholangitis
35
is suspected or established. Various comparative trials
have not shown the superiority of any one antimicrobial
agent. The choice of parenteral antibiotics is based on the
pathogenic bacteria, severity of cholangitis, and
5 Journal of Medical College Chandigarh, 2016, Vol. 6, No.2
Acute Cholangitis
presence of hepatic or renal disease, setting of infection,
patient allergies and local sensitivity patterns and biliary
36
penetration of antimicrobial. In the past, ampicillin and
gentamicin were commonly used as first-line drugs, but
with widespread resistance, they have limited role now.
Currently, a combination of ureidopenicillin with
metronidazole and an aminoglycoside or a combination
of penicillin/ß-lactamase inhibitor or third or fourth-
generation cephalosporins/ß-lactamase inhibitor
(piperacillin plus tazobactam or ticarcillin plus
34,35
preferred treatment. If these drugs are not useful,
fluorquinolones and carbapenems (imipenem,
meropenem) can be substituted. In severe cholangitis or
hospital acquired infections, antimicrobials efficacious
against methicillin resistant Staphylococcus aureus
(MRSA), vancomycin resistant enterococcus (VRE) and
pseudomonas are recommended. The presumptive
antibiotic regimen should be modified based on culture
and sensitivity reports.
About 90% of patients respond to antibiotics and
37
supportive measures within 24-48 hours. Response is in
the form of improvement of clinical signs and resolution
of fever, normalization of white blood cell count, C-
reactive protein and liver function tests, and subjective
well being. In moderate (grade II) or severe (grade III)
acute cholangitis, antimicrobials should be administered
for a minimum of 5–7 days. Prolonged therapy may be
planned, depending on patient's clinical response and
presence of bacteremia. In mild (grade I) acute
cholangitis, duration of antimicrobial therapy could be
shorter (2 or 3 days).35
Mild cases are often caused by a single pathogen, such as
E. coli, and single antibiotic, for instance, first or second
generation cephalosporin, penicillin/beta-lactamase
inhibitor is usually adequate. The disease is usually
managed by conservative medical management and a
good response is expected in more than 70%–80%
patients, permitting biliary decompression procedure to
be carried out electively.
Moderate cases are often infected with multiple and/or
resistant organisms. They should be treated with broad
spectrum third- and fourth generation cephalosporins or
penicillins with beta-lactamase inhibitors or
fluoroquinolones / carbapenems with metronidazole.
Once stable, patient should undergo appropriate
endoscopic or percutaneous drainage or even definite
Gupta and Sachdev
operative drainage.
Severe cases usually require resuscitation, such as
ventilatory or circulatory support in addition to empirical
medical management. The antibiotic therapy is
analogous to that used for moderate cholangitis, however
piperacillin/tazobactam is strongly suggested when
Pseudomonas is expected. Since relief of biliary
obstruction can significantly improve antimicrobial
penetration and survival, such patients should have
immediate endoscopic or percutaneous transhepatic
biliary decompression or an emergent operation with
decompression of bile duct with a T-tube as soon as they
35
are stabilized.
Biliary drainage
Biliary drainage is central to the management of acute
cholangitis. Biliary drainage can be achieved by three
different mechanisms: open surgical drainage, ERCP or
endoscopic ultrasound (EUS)-guided drainage or,
percutaneous transhepatic biliary drainage (PTBD).
Open drainage is more invasive and has obvious
drawbacks compared to endoscopic and percutaneous
routes; thus the latter have become the preferred methods
for urgent biliary drainage. Further, endoscopic drainage
is advocated as it is associated with a lesser discomfort,
lower morbidity rate, and shorter duration of
hospitalization.38 Choices for endoscopic drainage
during ERCP consists of biliary stent placement and
nasobiliary drain placement (ENBD), with or without
endoscopic sphincterotomy (EST). Studies have
scrutinized whether or not EST should be added to
ENBD or biliary tube stenting.39,40 However, no
significant difference was observed in the success rate or
effectiveness of drainage between the two techniques.
Complications in particular hemorrhage were higher in
39,40
patients who underwent EST. Table III shows the data
from various studies utilizing endoscopic techniques for
biliary drainage in acute cholangitis.
Surgical treatment
Open surgical drainage of biliary tree was the last resort
for patients with severe cholangitis before the advent of
interventional radiology and therapeutic endoscopy.
Surgical interventions consist primarily of stone
extraction, T-tube insertion, trans-hepatic intubation of
bile duct or bilio-enteric bypass. Open surgery for acute
cholangitis has traditionally been associated with high
morbidity and mortality. Emergency surgery mortality
Journal of Medical College Chandigarh, 2016, Vol. 6, No.2
46
varied from 20-60%. Age, medical co morbidities,
organ dysfunction, and malignant diseases are known
risk factors linked with higher peri-operative mortality.
Open drainage is thus reserved for patients who have
contraindications for endoscopic or percutaneous
transhepatic drainage or those in whom it has been
38
unsuccessful.
Percutaneous transhepatic biliary drainage (PTBD)
PTBD is the favored approach in cases of high biliary
obstruction, intrahepatic stones, previous biliary-enteric
47
surgery, or failed endoscopic decompression. PTBD
aims at establishing drainage in the acute emergency
phase of cholangitis, and in a recently reported series, it
could achieve successful biliary drainage close to 100%,
complications in less than 10% and mortality around
41,42
5%. However, puncturing the liver in severe sepsis is
unsafe considering clotting derangement and
thrombocytopenia with resulting bleeding,
hemoperitoneum and hemobilia. Biliary peritonitis and
external catheter related issues add to the morbidity. If
skilled interventionalist's expertise is available, this
procedure's success may be comparable to endoscopic
38,48
drainage, although no head to head trials are existing.
Endoscopic drainage
Endoscopic management has grown to be the best
possible mode of treatment for patients with acute
cholangitis. Numerous studies have documented and
established that endoscopy is far superior to surgery in
management of acute cholangitis. Lai et al in a
retrospective study, found that endoscopic drainage
using nasobiliary catheter resulted in lower morbidity
(40% vs 65%) and mortality (6.7% vs 20%) compared to
49
surgery. In another prospective randomized trial, the
same author observed that patients who were treated
surgically had notably higher complications (64% vs
34%) and hospital deaths (32% vs 10%) compared to
endoscopic treatment.43
Options for endoscopic drainage during ERCP consist of
biliary stent placement and nasobiliary drain placement,
with or without sphincterotomy. Three prospective
studies comparing ENBD and biliary tube stent
placement showed no significant difference in success
rate, effectiveness or morbidity.
19,44,50
However, there tube
related problems such as inadvertent removal of
nasobiliary tube by patients and appreciably higher
patient discomfort in ENBD group.50 Thus, in patients
6

who are likely to remove ENBD tube by themselves,
biliary stent placement is preferable. Table III shows the
comparison of various biliary drainage techniques used
by various research groups. Another area of debate is
whether or not EST should be added to ENBD or biliary
tube stent placement. Two case-series have indicated and
concluded that it does not increase the effectiveness of
drainage in any of the techniques, rather it increases
complications like hemorrhage.39,40 Pancreatitis, bowel
perforation, and bleeding are the main complications of
ERCP.
CONCLUSIONS
Acute cholangitis is a bacterial infection superimposed
on an obstructed biliary tree and is a potentially life
threatening condition. Prompt clinical recognition of this
entity and accurate diagnostic imaging are critical steps
in the optimal management of cholangitis. Treatment
needs to focus simultaneously on managing sepsis with
immediate and appropriate antimicrobial therapy and
emergent biliary drainage. Endoscopic biliary drainage
with stent placement and nasobiliary drainage are
established modes of biliary decompression that are
equally superior and efficacious.
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