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emedicine.medscape.com

Cholangitis
Updated: Mar 11, 2020
Author: Homayoun Shojamanesh, MD; Chief Editor: Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS

Overview

Background
Cholangitis is an infection of the biliary tract with the potential to cause significant morbidity and mortality. Many
patients with acute cholangitis respond to antibiotic therapy; however, patients with severe or toxic cholangitis may not
respond and may require emergency biliary drainage. Jean M. Charcot recognized this illness in 1877 when he
described a triad of fever, jaundice, and right upper quadrant pain.[1] In 1959, Reynolds and Dargon described a more
severe form of the illness that included the additional components of septic shock and mental confusion, which is
referred to as the Reynolds pentad.[1]

Pathophysiology
Historically, choledocholithiasis was the most common cause of biliary tract obstruction resulting in cholangitis. Over
the past 20 years, biliary tract manipulations/interventions and stents have reportedly become more common causes
of cholangitis. Hepatobiliary malignancies are a less common cause of biliary tract obstruction and subsequent bile
contamination resulting in cholangitis.[2]

Etiology
The two main causes of cholangitis are common bile duct stones and biliary tract manipulation.[3] In patients with a
stent in situ, cholangitis indicates stent block and need for change. Other possible causes of biliary tract obstruction
that may lead to infection include strictures, tumors, choledochal/biliary cysts, or sump syndrome. Hepatolithiasis is
also a possible cause of cholangitis[4] and is observed more frequently in East Asia. More than 90% of patients with
hepatolithiasis have calcium bilirubinate stones, also referred to as brown pigment stones. Worms (eg Ascaris,
Clonorchis) in the biliary tract can also cause cholangitis. Cholangitis in patients with a biliary-enteric anastomosis (eg,
hepatico-jejunostomy or a bilio-biliary anastomosis) after liver transplant indicates anastomotic stricture.

Epidemiology
Race-, sex-, and age-related demographics

Cholangitis is reported in all races. One variant, Asian cholangitis (also referred to as Oriental cholangio-hepatitis
[OCH] or recurrent pyogenic cholangitis [RPC]), is observed with increased frequency in Southeast Asia.[5]

The condition is reported in both females and males and has no clear predominance in either.

It mostly occurs in adults, with a reported median age at onset of 50-60 years. In neonates, extrahepatic biliary atresia

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(EHBA) is a cause of cholangitis. In children and young adults, choledochal cyst can cause cholangitis.

Prognosis
The prognosis is usually guarded, although it improves with early antibiotic treatment and appropriate drainage and
decompression of biliary tract as needed. Factors reportedly associated with a poor prognosis include old age, female
sex, acute renal failure, preexisting cirrhosis, and malignant biliary obstruction.

Mortality/morbidity

The mortality rate of acute cholangitis ranges from 5-10%, with a higher mortality rate in patients who require
emergency biliary decompression or surgery.

Cholangitis has significant potential for mortality and morbidity, especially if left untreated. Reported mortality rates
have been as high as 88% for untreated cholangitis.

Complications

Complications include pyogenic liver abscess, cholangiolytic abscess (usually small and multiple) in the liver,
longstanding recurrent cholangitis (eg, Asiatic cholangitis), and acute renal failure. Longstanding recurrent cholangitis
can cause secondary biliary cirrhosis (SBC), portal hypertension, and liver failure.[6]

Presentation

History and Physical Examination

History
A history of choledocholithiasis or recent biliary tract manipulation associated with fever (often with chills and rigors),
abdominal (right upper quadrant) pain, and jaundice (the Charcot triad) is highly suggestive of cholangitis. Fever
reportedly occurs in nearly 95% of patients with cholangitis. Approximately 90% of patients have right upper quadrant
tenderness, and 80% have jaundice.

According to Fujii et al, the 2007 Tokyo guidelines for the diagnosis and treatment of acute cholangitis were mostly
acceptable.[7] However, classification into mild or moderate grade using the guidelines could be challenging, so it was
necessary for clinicians to carefully distinguish organ dysfunction associated with cholangitis itself from dysfunction
associated with the underlying disease in determining the severity of the disease.[7]

Similarly, Nishino et al found that the 2013 Tokyo guidelines for the diagnosis and treatment of acute cholangitis are
practical, but they may underestimate some cases that necessitate urgent/early biliary drainage as mild disease.[8]
The investigators developed a scoring system that took into consideration the following five predictors, which they
indicate may improve identification of patients at high risk of needing urgent/early biliary drainage[8] :

Age of 75 years or older

The presence of systemic inflammatory response syndrome (SIRS)

Blood urea nitrogen (BUN) level above 20 mg/dL

Platelet count below 120,000/µL

Serum albumin level below 3.0 g/dL

Physical Examination

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Physical examination may reveal fever, icterus, jaundice, and abdominal tenderness.

DDx

Diagnostic Considerations
Delay in diagnosis or treatment of cholangitis may result in a higher risk of death.[9]

Consider variants such as Asian (Oriental) cholangitis, primary sclerosing cholangitis, acquired immunodeficiency
syndrome (AIDS)-related cholangitis, immunoglobulin G4 (IgG4)-associated cholangitis (IAC), primary biliary
cholangitis (previously called primary biliary cirrhosis [PBC]).

Workup

Workup

Laboratory Studies
Note the following:

Obtain complete blood cell (CBC) count, liver function tests, coagulation profile, renal function tests, and blood
cultures.

Common laboratory findings include polymorphonuclear leukocytosis, hyperbilirubinemia (patients with a

malignant obstruction generally have a significantly higher bilirubin level than those with a benign obstruction),
and elevated alkaline phosphatase and gamma glutamyl transpeptidase (GGTP) levels.

Other possible laboratory findings include elevation of transaminases and serum amylase levels (due to
possible concurrent pancreatitis from stone impaction at the ampulla of Vater).

Blood culture findings are positive in nearly 50% of patients.

Bile (obtained at the time of biliary drainage—endoscopic or percutaneous) culture findings are positive in
nearly all patients.

Multiple organisms are identified in approximately 60% of patients. Commonly reported aerobic organisms
include Escherichia coli and Klebsiella and Enterococcus species. The most commonly reported anaerobic
organism is Bacteroides fragilis.

Imaging Studies
Imaging modalities include abdominal ultrasonography and abdominal computed tomography (CT) scanning.[10]

The diagnosis of the cause of cholangitis can be made on magnetic resonance cholangiography (MRC) as it is
noninvasive and involves no exposure to radiation, but diagnostic and therapeutic (drainage of the biliary system)
modalities include endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic
cholangiography (PTC).

MRC is preferred before ERC or PTC, as it indicates the level of the block (eg, high or low) and the patency of the
biliary ductal confluence; this helps in the selection of the therapeutic procedure for drainage of the biliary system (ie,
ERC for low blocks and PTC for high blocks with confluence but not patency).

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Treatment

Medical Care
Administration of broad-spectrum intravenous antibiotics and correction of fluid and electrolyte imbalances constitute
essential medical care for cholangitis.[11, 12] Patients should take nothing by mouth in the acute stage of cholangitis.
Accomplish hydration with intravenous fluids.

Vitamin K or fresh frozen plasma (FFP) may be used for correction of coagulopathy, when needed.

Note the following:

High biliary pressures caused by an obstruction may impair the biliary secretion of antibiotics; therefore,
treatment may require decompression and drainage of the biliary system.[13]

For patients with severe cholangitis, endoscopic biliary drainage (using a stent or endoscopic nasobiliary drain
[ENBD]) has replaced emergency surgical common duct exploration and T-tube drainage as standard
treatment. Data from a metaanalysis indicate that ENBD may cause fewer perioperative complications (eg,
preoperative cholangitis rate, postoperative pancreatic fistula rate) than endoscopic biliary stenting (EBS) in
patients with malignant biliary obstruction.[14] However, a limitation of the metaanalysis was that there were no
data from randomized controlled trials.

Endoscopic biliary drainage is relatively easy in the presence of common bile duct (CBD) stones, a lower CBD
block (eg, pancreatic or periampullary cancer), and choledochal cyst. This procedure may be difficult in patients
with a high block (eg, hilar cholangiocarcinoma or gall bladder cancer). In these patients, the primary (and,
sometimes, even the secondary) biliary ductal confluence may be blocked, and bilateral (or even multiple)
drainage is required to control cholangitis. This may be difficult or even impossible to achieve endoscopically,
and percutaneous transhepatic biliary drainage may be required.

Percutaneous transhepatic biliary drainage (PTBD) is another possible nonsurgical method of biliary drainage.
PTBD is required in patients with high block when endoscopic biliary drainage may not be possible. Bilateral
(even multiple) tubes may have to be placed.

Consultations
Obtain consultations with the following specialists in a timely manner:

Radiologists

Gastroenterologists

Surgeons

Prevention

Consider maintenance therapy/antibiotics (ie, sulfamethoxazole and trimethoprim [SMZ-TMP] or a fluoroquinolone) for
patients with recurrent cholangitis.

It has been reported that prophylactic antibiotics do not prevent endoscopic retrograde cholangiopancreatography
(ERCP)-induced cholangitis significantly in unselected patients, and these agents should not be routinely
recommended for this reason.[15]

Surgical Care
Endoscopic or percutaneous biliary drainage and decompression have usually replaced surgery as the initial treatment

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of severe cholangitis. Surgical decompression in the form of T-tube drainage of the common bile duct (CBD)
(choledochostomy) is appropriate for patients in whom endoscopic or transhepatic drainage is unsuccessful or
unavailable. This can be performed laparoscopically also.

Following adequate biliary drainage and decompression for acute cholangitis with bacteremia, Park et al found no
significant differences in the recurrence of acute cholangitis and 30-day mortality between early switch to oral antibiotic
therapy and standard 10-day intravenous antibiotic therapy.[16]

Definitive management depends on the underlying cause (eg, removal of CBD stones, resection of tumor, excision of
choledochal cyst, percutaneous balloon dilatation, and stenting of anastomotic stricture). Cholangitis, however, must
be controlled before the patient undergoes operative intervention. In the case of an unresectable cancer, definitive
palliation can be achieved with placement of self-expandable metal stents (SEMS) which remain patent over a long
period (eg, plastic stents).

Guidelines

Biliary Cholangitis
UK-PBC and the British Society of Gastroenterology

In March 2018, the British Society of Gastroenterology/UK-PBC released guidelines for the treatment and
management of primary biliary cholangitis.[17] These guidelines build from previous guidelines from the European
Association for the Study of the Liver (EASL) and the American Association for the Study of Liver Diseases (AASLD).

Recommend that any patient with persistently elevated cholestatic liver biochemistry (raised alkaline phosphatase
[ALP] or gamma-glutamyl transferase [GGT]) without an alternative cause should have autoantibodies checked for
anti-mitochondrial (AMA) and anti-nuclear (ANA) reactivity.

The presence of antimitochondrial antibodies (>1 in 40) or highly primary biliary cirrhosis (PBC)-specific antinuclear
antibodies, in the appropriate context of cholestatic liver biochemistry, without alternative explanation, is usually
sufficient for confidently reaching the diagnosis of PBC.

All patients with PBC should be offered structured life-long follow-up, recognizing that different patients have different
disease courses and may require different intensity of follow-up.

Risk assessment should evaluate disease severity and activity at baseline and on treatment. We recommend a
combination of serum liver tests (to identify those with an elevated bilirubin, a platelet count < 150, or biochemical
disease activity on treatment), imaging (liver ultrasound to identify overt cirrhosis and splenomegaly; transient
elastography (to identify increased liver stiffness), recognition of young age at disease onset (< 45 years), and male
sex.

To identify those at greatest risk of disease progression, we recommend that all patients have individualized risk
stratification using biochemical response indices following 1 year of ursodeoxycholic acid (UDCA) therapy. We suggest
that UDCA-treated patients with an ALP >1.67 × upper limit of normal (ULN) and/or elevated bilirubin < 2 × ULN
represent a group of high-risk patients in whom there is randomized controlled trial evidence for the addition of second-
line therapy.

Recommend oral UDCA at 13–15 mg/kg/day be used as the first-line pharmacotherapy in all patients with PBC. If
tolerated, treatment should usually be life-long.

In patients with inadequate response to UDCA (or UDCA intolerance) as defined by ALP >1.67 × ULN and/or elevated
bilirubin < 2 × ULN, the addition of obeticholic acid (OCA) has been associated with improvements in biochemical
surrogates of disease activity reasonably likely to predict improved outcomes. We therefore recommend, in keeping
with the National Institute for Health and Care Excellence (NICE) evaluation of OCA, that the addition of OCA for
patients with an inadequate response to UDCA, or intolerant of UDCA, is considered. We recommend dose adjustment
in patients with advanced liver disease as per the drug label.

Recommend that all patients be evaluated for the presence of symptoms, particularly fatigue and itch. Clinicians

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should recognize that severity of symptoms does not correlate with stage of disease.

True overlap with autoimmune hepatitis is probably rare, and we suggest that, when suspected, liver biopsy with
expert clinicopathologic review is needed to make the diagnosis and guide treatment.

Recommend that patients with PBC be offered the chance to seek support from patient support groups.

Resources
For more information, please see the following:

Primary Sclerosing Cholangitis Clinical Practice Guidelines (2019)

Primary Biliary Cholangitis Management Clinical Practice Guidelines (2018)

IgG4‐Related Sclerosing Cholangitis Clinical Practice Guidelines (2019)

See also the following Medscape articles:

Acute Cholangitis

Recurrent Pyogenic Cholangitis

Primary Sclerosing Cholangitis

Primary Sclerosing Cholangitis Imaging

Recurrent Pyogenic Cholangitis Imaging

Pediatric Primary Sclerosing Cholangitis

For more Clinical Practice Guidelines, please go to Guidelines.

Medication

Medication Summary
Possible antibiotic treatments include penicillin derivatives (eg, piperacillin) or a second- or third-generation
cephalosporin (eg, ceftazidime) for gram-negative coverage, ampicillin for gram-positive coverage, and metronidazole
for anaerobic coverage. Some researchers have reported use of fluoroquinolones (eg, ciprofloxacin, levofloxacin) as
effective therapy.

The selection and dosing of appropriate antibiotics and other medications listed below or from another source must be
performed by the patient's primary physician and gastroenterologist based on history and clinical presentation.

Antibiotics

Class Summary
Initial empiric antimicrobial therapy must be comprehensive and should cover both aerobic and anaerobic gram-
negative organisms.

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Piperacillin (Pipracil)
Inhibits biosynthesis of cell wall mucopeptides and the stage of active multiplication; has antipseudomonal activity.

Ceftazidime (Ceptaz, Fortaz, Tazidime)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive
organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-
binding proteins.

Ampicillin (Marcillin, Omnipen, Polycillin, Principen)

Bactericidal activity against susceptible organisms.

Metronidazole (Flagyl)
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.

Ciprofloxacin (Cipro)
Fluoroquinolone with activity against Pseudomonas species, streptococci, MRSA, Staphylococcus epidermidis, and
most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently,
growth.

Levofloxacin (Levaquin)
For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Beta lactam and beta lactamase inhibitor (BL + BLI) combinations (eg, ampicillin + sulbactam, amoxicillin + clauvulanic
acid, cefoperazone + sulbactam, piperacillin + tazobactam) may be indicated in the presence of extended-spectrum
beta lactamase (ESBL)-producing organisms.

Coagulants

Class Summary
Vitamin K or fresh frozen plasma (FFP) may be used for correction of coagulopathy when needed.

Phytonadione (AquaMEPHYTON, Konakion, Mephyton)

Promotes liver synthesis of clotting factors that in turn inhibit warfarin effects.

Fresh frozen plasma (FFP)

Plasma is the fluid compartment of blood containing the soluble clotting factors. Indications for using FFP include
bleeding in patients with congenital coagulation defects and multiple coagulation factor deficiencies (severe liver
disease).

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Questions & Answers

Overview

What is cholangitis?

What is the pathophysiology of cholangitis?

What causes cholangitis?

Which patient groups have the highest prevalence of cholangitis?

What is the prognosis of cholangitis?

What is the mortality and morbidity associated with cholangitis?

What are the possible complications of cholangitis?

Presentation

Which clinical history findings are characteristic of cholangitis?

What are the challenges of determining the grade of cholangitis?

Which factors are predictors of high-risk cholangitis?

Which physical findings are characteristic of cholangitis?

DDX

Which conditions are included in the differential diagnosis of cholangitis?

Workup

What is the role of lab tests in the workup of cholangitis?

What is the role of imaging studies in the workup of cholangitis?

Treatment

How is cholangitis treated?

Which specialist consultations are beneficial to patients with cholangitis?

How is cholangitis prevented?

What is the role of surgery in the treatment of cholangitis?

Guidelines

What are the British guidelines on the treatment of primary biliary cholangitis?

Medications

What is the role of medications in the treatment of cholangitis?

Which medications in the drug class Coagulants are used in the treatment of Cholangitis?

Which medications in the drug class Antibiotics are used in the treatment of Cholangitis?

Contributor Information and Disclosures

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Author

Homayoun Shojamanesh, MD Former Fellow, Digestive Diseases Branch, National Institutes of Health

Homayoun Shojamanesh, MD is a member of the following medical societies: American College of Gastroenterology,
American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Praveen K Roy, MD, AGAF Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine

Praveen K Roy, MD, AGAF is a member of the following medical societies: American Gastroenterological Association,
American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Victor C Nwakakwa, MD, MRCP Gastroenterologist, Watson Clinic, LLP

Victor C Nwakakwa, MD, MRCP is a member of the following medical societies: American Gastroenterological
Association, American Medical Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases,
American College of Gastroenterology, American Gastroenterological Association, American Society for
Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS Professor of HPB Surgery, Mahatma Gandhi Medical College
and Hospital (MGMCH), Jaipur, India

Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS is a member of the following medical societies: Association of
Surgeons of India, Indian Association of Surgical Gastroenterology, Indian Society of Gastroenterology, Medical
Council of India, National Academy of Medical Sciences (India), Royal College of Surgeons of Edinburgh

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Pfizer Sanofi.

Additional Contributors

Anil Minocha, MD, FACP, FACG, AGAF, CPNSS Professor of Medicine, Director of Digestive Diseases, Medical
Director of Nutrition Support, Medical Director of Gastrointestinal Endoscopy, Internal Medicine Department, University
of Mississippi Medical Center; Clinical Professor, University of Mississippi School of Pharmacy

Anil Minocha, MD, FACP, FACG, AGAF, CPNSS is a member of the following medical societies: American Academy of
Clinical Toxicology, American Society for Gastrointestinal Endoscopy, American Federation for Clinical Research,
American Association for the Study of Liver Diseases, American College of Forensic Examiners Institute, American
College of Gastroenterology, American College of Physicians, American Gastroenterological Association

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Disclosure: Nothing to disclose.

References

1. Zimmer V, Lammert F. Acute bacterial cholangitis. Viszeralmedizin. 2015 Jun. 31(3):166-72. [QxMD MEDLINE Link]. [Full
Text].

2. Lee JG. Diagnosis and management of acute cholangitis. Nat Rev Gastroenterol Hepatol. 2009 Sep. 6(9):533-41. [QxMD
MEDLINE Link].

3. Shojaiefard A, Esmaeilzadeh M, Ghafouri A, Mehrabi A. Various techniques for the surgical treatment of common bile duct
stones: a meta review. Gastroenterol Res Pract. 2009. 2009:840208. [QxMD MEDLINE Link]. [Full Text].

4. Li FY, Cheng NS, Mao H, et al. Significance of controlling chronic proliferative cholangitis in the treatment of hepatolithiasis.
World J Surg. 2009 Oct. 33(10):2155-60. [QxMD MEDLINE Link].

5. Lee KF, Chong CN, Ng D, et al. Outcome of surgical treatment for recurrent pyogenic cholangitis: a single-centre study. HPB
(Oxford). 2009. 11(1):75-80. [QxMD MEDLINE Link]. [Full Text].

6. Mattner J. Impact of microbes on the pathogenesis of primary biliary cirrhosis (PBC) and primary sclerosing cholangitis
(PSC). Int J Mol Sci. 2016 Nov 9. 17(11):1864. [QxMD MEDLINE Link]. [Full Text].

7. Fujii Y, Ohuchida J, Chijiiwa K, et al. Verification of Tokyo Guidelines for diagnosis and management of acute cholangitis. J
Hepatobiliary Pancreat Sci. 2012 Jul. 19(4):487-91. [QxMD MEDLINE Link].

8. Nishino T, Hamano T, Mitsunaga Y, et al. Clinical evaluation of the Tokyo Guidelines 2013 for severity assessment of acute
cholangitis. J Hepatobiliary Pancreat Sci. 2014 Dec. 21(12):841-9. [QxMD MEDLINE Link].

9. Sulzer JK, Ocuin LM. Cholangitis: causes, diagnosis, and management. Surg Clin North Am. 2019 Apr. 99(2):175-84. [QxMD
MEDLINE Link].

10. Pitchumon CS. Choledocholithiasis and cholangitis. In: Floch MH, Floch NR, Kowdley KV, Pitchumon CS, eds. Netter's
Gastroenterology. 2nd ed. Saunders; 2010. 534-6.

11. [Guideline] Miura F, Okamoto K, Takada T, et al. Tokyo Guidelines 2018: initial management of acute biliary infection and
flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci. 2018 Jan. 25(1):31-40. [QxMD MEDLINE Link]. [Full Text].

12. Lan Cheong Wah D, Christophi C, Muralidharan V. Acute cholangitis: current concepts. ANZ J Surg. 2017 Jul. 87(7-8):554-9.
[QxMD MEDLINE Link].

13. Navuluri R, Hoyer M, Osman M, Fergus J. Emergent treatment of acute cholangitis and acute cholecystitis. Semin Intervent
Radiol. 2020 Mar. 37(1):14-23. [QxMD MEDLINE Link].

14. Lin H, Li S, Liu X. The safety and efficacy of nasobiliary drainage versus biliary stenting in malignant biliary obstruction: A
systematic review and meta-analysis. Medicine (Baltimore). 2016 Nov. 95(46):e5253. [QxMD MEDLINE Link]. [Full Text].

15. Bai Y, Gao F, Gao J, Zou DW, Li ZS. Prophylactic antibiotics cannot prevent endoscopic retrograde
cholangiopancreatography-induced cholangitis: a meta-analysis. Pancreas. 2009 Mar. 38(2):126-30. [QxMD MEDLINE Link].

16. Park TY, Choi JS, Song TJ, Do JH, Choi SH, Oh HC. Early oral antibiotic switch compared with conventional intravenous
antibiotic therapy for acute cholangitis with bacteremia. Dig Dis Sci. 2014 Nov. 59(11):2790-6. [QxMD MEDLINE Link].

17. Hirschfield GM, Dyson JK, Alexander GJM, et al. The British Society of Gastroenterology/UK-PBC primary biliary cholangitis
treatment and management guidelines. Gut. 2018 Sep. 67(9):1568-94. [QxMD MEDLINE Link]. [Full Text].

18. Hanau LH, Steigbigel NH. Acute (ascending) cholangitis. Infect Dis Clin North Am. 2000 Sep. 14(3):521-46. [QxMD
MEDLINE Link].

19. Lai EC, Mok FP, Tan ES, et al. Endoscopic biliary drainage for severe acute cholangitis. N Engl J Med. 1992 Jun 11.
326(24):1582-6. [QxMD MEDLINE Link].

20. Kwan KEL, Shelat VG, Tan CH. Recurrent pyogenic cholangitis: a review of imaging findings and clinical management.
Abdom Radiol (NY). 2017 Jan. 42(1):46-56. [QxMD MEDLINE Link].

21. Ma CL, Wang LP, Qiao S, et al. Risk factors for death of elderly patients with acute obstructive suppurative cholangitis. West
Indian Med J. 2015 Dec 1. 65(2):316-9. [QxMD MEDLINE Link].

22. Copelan A, Kapoor BS. Choledocholithiasis: diagnosis and management. Tech Vasc Interv Radiol. 2015 Dec. 18(4):244-55.

https://emedicine.medscape.com/article/184043-print Page 10 of 11
 31/08/22 10.35

[QxMD MEDLINE Link].

23. [Guideline] Takada T, Kawarada Y, Nimura Y, et al. Background: Tokyo Guidelines for the management of acute cholangitis
and cholecystitis. J Hepatobiliary Pancreat Surg. 2007. 14(1):1-10. [QxMD MEDLINE Link]. [Full Text].

https://emedicine.medscape.com/article/184043-print Page 11 of 11