The Journal of Emergency Medicine, Vol. 54, No. 1, pp.

64–72, 2018
Published by Elsevier Inc.
0736-4679/$ - see front matter

http://dx.doi.org/10.1016/j.jemermed.2017.06.039

Clinical
Review

THE EMERGENCY MEDICINE FOCUSED REVIEW OF CHOLANGITIS

Rachel Ely, DO, MHA, NRP,* Brit Long, MD,* and Alex Koyfman, MD†
*Department of Emergency Medicine, San Antonio Military Medical Center, Fort Sam Houston, Texas and †Department of Emergency
Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas
Reprint Address: Brit Long, MD, Department of Emergency Medicine, San Antonio Military Medical Center, 3841 Roger Brooke Drive,
Fort Sam Houston, TX 78234

, Abstract—Background: Cholangitis is a life-threatening recognition, early broad-spectrum antibiotics, and fluid

infection of the biliary tract. Historically, the mortality sec-
ondary to cholangitis approached 100%. However, with
early recognition, antibiotics, resuscitation, and surgical or
endoscopic intervention, patient outcomes have significantly
improved, although there is still progress to be made. Objec-
tive of Review: The objective of this review is to provide an
emergency medicine centered approach to the risk factors,
presentations, and various diagnostic and treatment modal-
ities in cholangitis. Discussion: Early recognition and treat-
ment of cholangitis in the emergency department is
instrumental in ensuring a favorable outcome for patients.
Recognition of acute cholangitis can be challenging, as
many patients do not present with the classic symptoms of
Charcot’s triad. This article reviews the risk factors in chol-
angitis, as well as the typical presentations and necessary
diagnostic studies. Furthermore, once diagnosis is made, dis-
tinguishing those requiring emergent biliary decompression
from those who may tolerate a delayed procedure can also
be difficult. Scoring systems that attempt to identify patients
who may tolerate a delayed approach have yet to be vali-
dated. This review discusses the appropriate antibiotic ther-
apy based on most common pathogens, as well as the options
for achieving biliary decompression. Conclusions: Cholan-
gitis is a life-threatening infection that carries a high likeli-
hood of poor outcomes if not treated early and
aggressively in the emergency department. Appropriate
This review does not reflect the views or opinions of the
United States government, Department of Defense, United
States Air Force, or San Antonio Uniformed Services Health
Education Consortium Emergency Medicine Residency.
resuscitation are paramount, and in patients with severe dis-
ease, early biliary decompression will significantly reduce
mortality. Published by Elsevier Inc.
, Keywords—cholangitis; biliary obstruction; Charcot’s
triad; Reynold’s pentad
INTRODUCTION
Cholangitis, also referred to as ascending or acute cholan-
gitis, was first defined in 1877 by Jean-Martin Charcot, at
which time the pathognomonic triad of fever, right upper
quadrant pain, and jaundice was described (1). Today,
cholangitis is defined as the presence of increased hepatic
intraductal pressure with a concurrent infection of the ob-
structed bile (1–7).
Untreated, mortality from acute cholangitis ap-
proaches 100%, making identification and appropriate
management by emergency physicians imperative (1).
Since cholangitis was first described in 1877, diagnostic
and treatment modalities have improved significantly
(1). However, diagnosis of cholangitis remains a chal-
lenge, with no universally agreed upon gold standard
(8). Historically referenced symptom complexes, such
as Charcot’s triad and Reynold’s pentad, confer a dismal
sensitivity in diagnosis, making it important to be aware
of advances in diagnostic tools and guidelines. More
importantly, certain patients carry a higher risk of treat-
ment failure without emergent biliary decompression,

RECEIVED: 20 December 2016; FINAL SUBMISSION RECEIVED: 10 June 2017;

ACCEPTED: 29 June 2017

64
EM-Focused Review of Cholangitis
and identifying these patients represents a diagnostic
challenge without a clear solution to date (9).
Objective
Cholangitis continues to present a diagnostic challenge to
emergency practitioners, and the stakes in missing a sub-
tle case of cholangitis should not be understated. The
objective of this review is to provide an emergency med-
icine centered review of the risk factors, presentations,
and various diagnostic and treatment modalities in chol-
angitis.
METHODS
A PubMed and Google Scholar search was performed to
identify articles detailing the epidemiology, pathophysi-
ology, prognosis, diagnosis, and preliminary manage-
ment of cholangitis. The following key words were
used: cholangitis, ascending cholangitis, suppurative
cholangitis, Tokyo guideline, Charcot’s triad, and Rey-
nold’s pentad. These results were narrowed to include
English-language articles and, of those results, authors
reviewed articles to identify those relevant to the emer-
gency department (ED) management of suspected chol-
angitis. Excluded studies include those specifically
detailing surgical or endoscopic techniques of manage-
ment that are beyond the ED scope.
DISCUSSION
Definitions
Historically, symptom complex and pathophysiology of
cholangitis has been referred to by several different terms
with overlapping definitions. The term hepatic fever was
introduced by Charcot in 1887, and referred to a disease
characterized by right upper quadrant pain, rigors, and
jaundice (3). Reynolds and Dargan expanded the symp-
tom complex, adding mental status change and shock to
the hepatic fever definition and introduced the term acute
obstructive cholangitis (10). In 1971, Longmire intro-
duced the terms acute suppurative cholangitis, which
corresponded to Charcot’s hepatic fever, and acute
obstructive suppurative cholangitis, which corresponded
to Reynolds’ and Dargan’s acute obstructive cholangitis
(11). Multiple publications differentiate between acute
cholangitis, defined as bacterial proliferation and coloni-
zation of the bile duct, and acute suppurative cholangitis,
defined as a severe form of acute cholangitis in which pu-
rulence accumulates in the bile duct (5,12,13). The term
ascending is often used, and refers to the theory that
bacteria migrate or ascend from the duodenum into the
hepatopancreatic duct (2).
65
In 2007, the Tokyo Guidelines Working Group estab-
lished a set of standardized diagnostic criteria and
severity assessment in an attempt to improve diagnostic
uniformity and accuracy both for clinicians as well as
for research purposes (14).
Epidemiology
The most common characteristics that predispose pa-
tients to the development of cholangitis are bile duct
stones and previous manipulation of the biliary tree,
including stenting and biliary surgery resulting in stric-
ture. Gallstones are estimated to be responsible for
approximately 65% of cholangitis cases, followed by
24% as a result of malignant stenosis, 4% caused by
benign stenosis, 3% a result of sclerosing cholangitis,
and 1% caused by other or unknown factors (1,9). Of
those with asymptomatic gallbladder stones,
approximately 0.6%–1.3% will go on to develop
cholangitis over a 10-year period (3). Orthotopic liver
transplantation, primary sclerosing cholangitis, and ac-
quired immune deficiency syndrome related cholangi-
opathy are also etiologies to be considered in patients
presenting with cholangitis. Malignancy itself rarely pre-
sents with cholangitis without first presenting with signs
of obstruction; however, it is common to develop cholan-
gitis secondary to biliary stenting or manipulation after
malignant obstruction has been identified (2). Cholangitis
is a known complication of endoscopic retrograde chol-
angiopancreatography (ERCP), second only to pancrea-
titis in incidence after the procedure (1). However,
overall incidence is low, with estimates ranging from
0.5% to 5% of ERCPs resulting in cholangitis (15).
Risk of biliary sepsis after ERCP is increased by incom-
plete drainage of biliary obstruction, concomitant percu-
taneous drainage, and the presence of a hilar stricture
(16). Other phenomena that have been described include
Mirizzi syndrome, a result of mechanical pressure on the
common bile duct due to stones in the gallbladder neck or
cystic duct, and Lemmel syndrome, in which a divertic-
ulum near the duodenal papilla compresses the opening
of the bile duct and causes cholestasis and resultant infec-
tion (1). Acalculous cholangitis, which occurs in the
absence of bile duct stone or obstructive malignancy, is
typically observed in severely ill patients, often in the
intensive care unit (ICU), and was found to have an inci-
dence of approximately 0.6% in one large Japanese
observational study (17).
It is estimated that 15% of the U.S. population has
gallbladder stones, and 2%–3% of these patients are ex-
pected to develop complications related to these stones,
such as cholecystitis, pancreatitis, or biliary obstruction
(15). The factors surrounding entrance of stones into
the common bile duct and whether they pass silently is
66
unknown; approximately one-third are estimated to suc-
cessfully pass through the common bile duct without
symptoms of biliary colic or resultant obstruction (15).
Cholecystitis, an acute inflammatory process of the gall-
bladder, is most commonly a result of a stone obstructing
the gallbladder neck or cystic duct (3). Choledocholithia-
sis is defined by a stone present in the common bile duct
(3). The location, degree, and chronicity of obstruction
contribute to the potential development of pancreatitis,
cholangitis, or hepatic abscess (15).
Pathophysiology
The development of cholangitis is dependent on two key
factors: biliary obstruction and bacterial growth in bile
(1). Bacteria primarily enter the biliary system by
ascending from the duodenum into the common hepato-
pancreatic duct. The portal venous system and the peri-
portal lymphatic system are also potential routes of entry,
which is thought to occur less frequently (2). Biliary
obstruction results in increased intraductal pressures, re-
sulting in disruption of tight junctions between hepatic
cellular architecture. This disruption leads to the reflux
of bacteria into the bloodstream (2). Intrabiliary pressure
has been directly linked to incidence of bacteremia, sug-
gesting that the degree of biliary obstruction is directly
responsible for severity of illness at patient presentation
(18).
Microbiology
In healthy patients, bile is sterile (19). In cholangitis,
biliary obstruction creates a nidus first for bacterial colo-
nization, followed by infection. Bile cultures are positive
in 80%–100% of patients with cholangitis, and up to 70%
will have positive blood cultures, likely as a result of
cholangio venous reflux (1,2). The most common
bacteria identified in acute cholangitis are Escherichia
coli, Klebsiella species, and Enterococcus species (19).
Patients with prior biliary surgery, the elderly, and those
with severe disease are more likely to have anaerobic or-
ganisms such as Clostridium or Bacteroides species, and
polymicrobial infection in this population is more likely
as well (20). Anaerobic and polymicrobial infection are
typically associated with more severe disease (20). Pa-
tients with indwelling biliary stents or recent instrumen-
tation for the biliary tract are specifically more likely to
have infection with Enterococcus, Pseudomonas,
methicillin-resistant Staphylococcus aureus, or
vancomycin-resistant Enterococcus, and antibiotic
coverage should be selected accordingly (2,20). There
is no universally agreed upon recommendation for or
against the collection of blood cultures in suspected
cholangitis; however, bacteria isolated from blood
R. Ely et al.
cultures is often the same responsible for infection of
the biliary tract and can help guide antibiotic selection
once culture results are available (19,20).
Presentation
Though Charcot’s classic triad of fever, right upper quad-
rant pain, and jaundice remains pathognomonic for iden-
tifying cholangitis and carries a specificity of 85%, it
yields a sensitivity of approximately 25% (8,21).
Additionally, these three signs plus findings of
hypotension and altered mental status (Reynold’s
pentad) are seen in only 5%–7% of cases, but typically
represent more severe disease when present (2). Fever
in isolation has been reported to have a sensitivity be-
tween 40% and 100%, while abdominal pain alone carries
a sensitivity between 60% and 100%; however, lack of
specificity makes fever and abdominal pain alone poor
diagnostic criteria (6).
Diagnosis
Laboratory and imaging studies can support a suspected
diagnosis after a focused history and physical examina-
tion. Liver function testing results are most commonly
elevated, but the elevation can range from mild to severe.
Elevation of both g-glutamyl transpeptidase and alkaline
phosphatase elevation is approximately 90% sensitive for
acute cholangitis (4). Lipase elevation suggests the pres-
ence of a common bile duct stone causing obstruction.
Leukocytosis is observed in 82% of cases, and white
blood cell count > 15,000/mm3 has been reported as hav-
ing an odds ratio of 5.127 for the presence of systemic
disease, including sepsis (5). Elevated erythrocyte sedi-
mentation rate and C-reactive protein are common but
nonspecific findings. While not immediately useful in
the initial evaluation, blood cultures are positive in up
to 70% of patients with cholangitis and may help in se-
vere disease to guide antibiotic therapy once sensitivities
are available (2). There is some disagreement concerning
the utility of routinely obtaining blood cultures in patients
with suspected cholangitis (20,22,23). The Infectious
Disease Society of America (IDSA) does not
recommend routine collection of blood cultures in mild,
community-acquired intra-abdominal infection, but spec-
ifies that cultures may be helpful if obtained in septic or
toxic-appearing patients (23). A study by Schneider
et al. argues that the presence of bacteremia changes mor-
tality risk stratification and, for that reason, obtaining
routine blood cultures in all patients with cholangitis is
important (24).
Historically, ultrasound (US) has been the initial mo-
dality for evaluating for biliary obstruction in the setting
of suspected cholangitis (2). However, research and
EM-Focused Review of Cholangitis 67

Figure 1. Ultrasound demonstrates choledocholithiasis with dilated common bile duct. The threshold for biliary duct dilation on
ultrasonographic evaluation is 7 mm (25). However, the presence or degree of biliary dilation does not correspond well to the
severity of cholangitis; rather, severity of disease is more strongly associated with the amount of intraductal pressure (26,27).
CBD = common bile duct. Case courtesy of Radiopaedia.org (28).

recommendations published over the last decade have suspected cholangitis and conclude that CT is the most
challenged this approach, and data have become increas- effective imaging method for evaluating etiology and
ingly supportive of the use of computed tomography (CT) complications of cholangitis (32).
as the initial imaging study of choice to confirm biliary
obstruction and identify its source. Transabdominal US
is approximately 25%–60% sensitive for the detection
of common bile duct stones, which is modestly improved
with indirect evidence of obstruction, such as gallbladder
stones or biliary ductal dilation (2). Mosler’s 2011 algo-
rithm for approach to patients with suspected cholangitis
includes US as the initial imaging study, with other
confirmatory noninvasive studies, including CT, to follow
(4). US can identify dilated intrahepatic ducts, as well as a
dilated common bile duct to indicate common bile duct
stone or other distal obstruction (Figure 1) (28,29).
However, CT can identify dilated intrahepatic and
common bile ducts and may also identify a nearby mass
causing external compression on the biliary structures
(Figure 2) (30,31). Multidetector CT with i.v. contrast
demonstrates a sensitivity of 85%–97% and specificity
of 88%–96% in the identification of common bile duct
stones (2). Findings of papillitis and the presence of an
ampullary stone on CT can suggest the presence of sup-
purative cholangitis (13). Hepatic abscess, while identifi-
able on US, is also better characterized by CT (2). The Figure 2. Computed tomography demonstrating choledo-
cholithiasis and extra- and intrahepatic ductal dilation.
2013 Tokyo Guidelines (TG13) (Table 1) recommend CBD = common bile duct. Case courtesy of Dr. Roberto Schu-
contrast-enhanced dynamic CT be used in diagnosis of bert, Radiopaedia.org (30).
68
Table 1. Tokyo Guidelines 13 Diagnostic Criteria for Acute
Cholangitis (6)
Category* Threshold
A. Systemic Inflammation
Fever or shaking chills Body temperature > 38 C
Laboratory evidence of WBC < 4000 or > 10,000
inflammatory response CRP > 1
B. Cholestasis
Jaundice T-Bili $2 mg/dL
Abnormal LFT Alk Phos > 1.5  upper
limit normal
GGT > 1.5  upper limit
normal
AST > 1.5  upper
limit normal
ALT > 1.5  upper
limit normal
C. Imaging
Biliary dilatation
Evidence of etiology on imaging
Alk Phos = alkaline phosphatase; ALT, alanine aminotransferase;
AST = aspartate aminotransferase; CRP = C-reactive protein;
GGT, g-glutamyl transferase; LFT = liver function tests;
T-Bili = total bilirubin; WBC = white blood cell count.
Diagnosis is considered definite if one item from A, B, and C are
present.
* Diagnosis should be suspected if one item from A plus one item
from B or C are present.
Complicating the diagnosis of cholangitis are several
other biliary pathologies, with a great deal of overlap in
presentation and diagnostics. The differential diagnosis
includes acute cholecystitis, choledocholithiasis, gall-
stone pancreatitis, and acute hepatitis, among others
(2). Acute cholecystitis may present with right upper
quadrant pain and fever, but is also typically accompanied
by vomiting and rarely causes jaundice, unless advanced
in its course (33). Cholecystitis is readily identified on US
with a sensitivity approaching 94% (34,35). In most
cases, cholecystitis is not accompanied by a significant
rise in transaminases, as is typically found in
cholangitis (33). Choledocholithiasis may present with
right upper quadrant pain and jaundice similar to cholan-
gitis presentations, and will also have imaging findings
suggestive of obstruction (2). Serum alkaline phosphatase
and g-glutamyl transferase are elevated in 90% of symp-
tomatic patients with common bile duct stones (2). Chol-
edocholithiasis alone does not typically present with
rigors or fevers, and the presence of these findings should
prompt suspicion for cholangitis secondary to common
bile duct stone obstruction and should be investigated
and treated as such (36). Acute hepatitis, whether viral,
drug-induced, or ischemic in etiology, may present with
symptoms such as fever or right upper quadrant pain
that overlap with the presentation of cholangitis (37).
Differentiating factors include level of transaminases
and imaging findings. Acute hepatitis typically results
in much higher aspartate aminotransferase (AST) and
R. Ely et al.
alanine aminotransferase (ALT), with relatively normal
alkaline phosphatase, while cholangitis is expected to
demonstrate modestly elevated AST and ALT with
concurrently elevated alkaline phosphatase to indicate
an obstructive pattern (37). Imaging in acute hepatitis
may demonstrate hepatomegaly, increased periportal
echoes with decreased parenchymal echogenicity, or gall-
bladder wall abnormalities, or imaging may show no
particular abnormalities (38). Evidence of obstruction,
such as dilated intrahepatic or extrahepatic bile ducts,
should prompt the emergency physician to broaden the
differential beyond acute hepatitis and toward other
obstructive biliary processes (39).
There have been attempts to develop diagnostic
criteria in cholangitis. The Tokyo Guidelines have offered
improved sensitivity over two iterations. The most recent,
TG13, offers a sensitivity of 91.8% and specificity of
77.7% in derivation studies (8,32). This clinical tool
requires a criterion from three diagnostic categories for
diagnosis: systemic inflammation (fever/rigors or
evidence of inflammatory response on laboratory
evaluation), cholestasis (jaundice or abnormal liver
function tests), and imaging (biliary dilatation or
imaging evidence of etiology of obstruction) (Table 1)
(32). The criteria were derived from a broad literature re-
view of the most sensitive and specific clinical manifesta-
tions, laboratory abnormalities, and imaging findings in
cholangitis (6). Laboratory values were modified in the
2013 revision to increase the threshold of positivity for
liver function tests to 1.5 times the upper limit of normal
in an effort to improve specificity with the exclusion of
other biliary processes, such as cholecystitis, which
may cause a modest elevation in liver function tests
(21). The revised 2013 criteria were an improvement
over TG07, which offered a sensitivity of 72% and spec-
ificity of 39% with positive and negative likelihood ratios
of 1.17 and 0.72 in a Japanese validation study of sus-
pected and definitive cholangitis (8). TG13 itself has
yet to be externally validated (8,21).
Treatment
For all patients, early recognition of cholangitis, fluid
resuscitation, and i.v. antibiotics are imperative. Antibi-
otics should be given early and provide broad coverage.
There have been no experimental data to support the
consideration of biliary penetration in antibiotic selec-
tion, although the first iteration of the Tokyo Guidelines
supported using biliary penetration to guide antibiotic
choice (20). However, citing evidence suggests that
biliary obstruction will prevent secretion of antimicro-
bials into the biliary tree, and this recommendation to
choose antibiotics based on biliary penetration has since
been discarded (23).
EM-Focused Review of Cholangitis
Table 2. Tokyo 13 Severity Criteria for Acute Cholangitis (32)
Grade
Grade III: Severe, dysfunction in at least one of following systems
Cardiovascular
Neurologic
Respiratory
Renal
Hepatic
Hematologic
Grade II: Moderate, any two of the following
Abnormal WBC count
High Fever
Advanced Age
Hyperbilirubinemia
Hypoalbuminemia
Grade I: Mild
Does not meet criteria of severe or moderate at diagnosis
FiO2 = fraction of inspired oxygen; INR = international normalized ratio; PaO2 = arterial partial pressure of oxygen; WBC = white blood cell
count.
The IDSA recommends antimicrobial therapy based
on severity of disease, using the broad categories of
community-acquired infection, severe community-
acquired infection, cholangitis with bilio-enteric anasto-
mosis, and health care associated infection (40,41).
The Tokyo Guidelines also recommend a severity-
based antibiotic hierarchy, with severity of disease
defined as shown in Table 2. Per TG13, mild disease
(grade I) disease may be managed with a carbapenem,
fluoroquinolone, penicillin with beta-lactamase inhibi-
tor, or fourth-generation cephalosporin (2,23,40).
While fluoroquinolones are included in the IDSA
guidelines, increasing resistance to Escherichia coli in
certain regions make this a less favorable selection;
E. coli resistance to ampicillin/sulbactam is also
problematic in some regions and, therefore, has been
removed as a monotherapy recommendation from the
most recent Tokyo Guidelines (23). Many third-
generation cephalosporins have limited activity against
Enterobacteriaceae, and their use as monotherapy is
discouraged (23). Metronidazole should be added
when an anaerobic organism is suspected, such as
with known bilio-enteric anastomosis. When Pseudomo-
nal species are suspected, piperacillin/tazobactam is an
appropriate selection (20). For severe (grade III) disease
or suspected health care associated disease, vancomy-
cin should be added to the monotherapy for Entero-
coccus species coverage (23,40).
Many less-severe infections respond well to medical
therapy alone. However, early recognition of cases
requiring emergent surgical intervention is imperative,
as delayed biliary decompression after failure of medi-
cal therapy carries a mortality rate up to 80% (9).
Delayed ERCP beyond 24–48 h has been associated
with prolonged hospital stay, increased risk of death,
69
Criteria
Hypotension requiring dopamine $ 5 mg/kg/min, or any dose of
norepinephrine
Altered mental status
PaO2/FiO2 ratio < 300
Oliguria, or serum creatinine > 2.0 mg/dL
INR > 1.5
Platelet count < 100,000/mm3
> 12,000/mm3 or < 4000/mm3
$ 39 C
$ 75 years
Total bilirubin $5 mg/dL
< 70% lower limit normal
increased need for vasopressor support, persistent organ
failure, and increased ICU stay (42,43). Previous
scoring systems employed to quantify the severity of
infection used response to initial medical treatment
and end-organ dysfunction as quantifiers. Except for
the sickest of patients, this scoring system does not
adequately identify patients requiring surgical interven-
tion until medical therapy has already failed (29,43).
The TG07 and TG13 attempted to identify these
patients earlier and use prognostic factors, such as
age, laboratory abnormalities, fever, and end organ
dysfunction to stratify patients into one of three
grades of severity (Table 2) (32). Recommended man-
agement based on these severity criteria remains un-
clear, although there is consensus that grade III
disease requires near-immediate biliary decompression
(20,23). The TG13 recommend emergent or early
biliary drainage in patients with grade II (moderate)
and grade III (severe) disease, while patients with
grade I (mild) disease may require medical
management only or delayed surgical intervention to
relieve obstruction (32). A recent mortality prediction
risk model suggests that grade II disease can be surgi-
cally decompressed within 24 h without worsening out-
comes (24). On the horizon is the use of delta neutrophil
index, which quantifies the fraction of circulating imma-
ture granulocytes and has shown promise in identifying
patients at increased risk of 28-day mortality as a result
of severe cholangitis (44).
Mortality in cholangitis has significantly improved
since the development of ERCP in the 1970s; however,
this is only one of several methods of biliary decom-
pression (31). ERCP has lower morbidity and mortality
than open surgical biliary decompression in those pa-
tients with severe cholangitis, though this benefit is
70
blunted in the elderly population (2,9). Percutaneous
drainage of the gallbladder or biliary tree remains an
option when ERCP is unsuccessful or if open
decompression is not feasible. For the emergency
physician, the most important factor is recognizing
those patients who require emergent surgical or
gastroenterology evaluation in order to improve
outcomes in moderate or severe disease.
Prognosis
Early reports of cholangitis cited mortality approaching
100% despite medical therapy (45). In 1903, the first
attempt at surgical decompression of the biliary tree
was described (46). Despite surgical advances and the
introduction of antibiotics over the next decades, the
mortality rate remained at 50% through 1980 (1). Since
1980, mortality has improved to 10%–30%, likely as a
result of the introduction of ERCP in the late 1970s.
Death is most commonly a result of multi-organ
dysfunction with irreversible shock (1). A recent study
by Schwed et al. demonstrates increased risk of organ
failure and death in patients presenting with white blood
cell count > 20,000 cells/mL, or a total bilirubin >
10 mg/dL (47). Other risk factors for end-organ failure
in patients with confirmed bacterobilia are the presence
of extended-spectrum beta-lactamases organisms in
blood culture (odds ratio [OR] = 15.376), pre-existing
renal dysfunction (OR = 6.319), and presence of chole-
docholithiasis (OR = 3.573) (48). For those patients
who survive to discharge, those with delayed biliary
decompression (ERCP > 48 h from presentation)
had > 2-fold increased risk for readmission over the
next 30 days (49). This further supports the need for
early recognition of cholangitis and identification of pa-
tients requiring early surgical intervention.
CONCLUSIONS
Cholangitis is a life-threatening condition that occurs in
the setting of biliary obstruction and bacterial infiltra-
tion of the biliary tree. Diagnosis requires high suspi-
cion for the disease in the setting of previous biliary
manipulation or evidence of stone, stricture, or external
compression and can be confirmed with CT imaging
demonstrating dilated intra- and extrahepatic ducts. If
not aggressively treated with fluid resuscitation, appro-
priate broad-spectrum antibiotics, and biliary decom-
pression, cholangitis can progress quickly into multi-
organ dysfunction and death. Improvement in surgical
and endoscopic interventions have significantly
improved mortality in patients with cholangitis; howev-
er, emergency physicians must identify potential cases
early in order to ensure the best possible outcomes.
R. Ely et al.
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72 R. Ely et al.

ARTICLE SUMMARY
1. Why is this topic important?
Cholangitis results from obstruction of the biliary tract
that can be life-threatening without treatment. Early
recognition and appropriate treatment improves out-
comes.
2. What does this review attempt to show?
This review evaluates the risk factors, presentation, and
diagnostic and treatment modalities of cholangitis.
3. What are the key findings?
Rapid recognition and treatment of cholangitis is
imperative. Charcot’s triad of right upper quadrant
abdominal pain, fever, and jaundice occurs in 25% of pa-
tients and is not reliable. Fever is variable. Due to biliary
obstruction, patients require biliary decompression, and in
the emergency department, broad-spectrum antibiotics
and resuscitation are required. Several scoring systems
are available that may identify patients who may tolerate
delayed approach for decompression, but these require
validation.
4. How is patient care impacted?
This review focuses on the presentation and manage-
ment of cholangitis, a potentially life-threatening disease.
Early recognition, broad-spectrum antibiotics, and proce-
dural biliary decompression significantly reduce mortal-
ity.