Hospital Medicine

Cholangitis

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Cholangitis

I. What every physician needs to know.

Cholangitis is an inflammation of the bile ducts. Types of cholangitis include the following:

  1. Acute cholangitis or ascending cholangitis

  2. Primary sclerosing cholangitis (PSC)

  3. Secondary sclerosing cholangitis (SSC)

  4. Recurrent pyogenic cholangitis (RPC)

Ascending cholangitis

Ascending cholangitis occurs when bacterial infection is superimposed on bile stasis from impeded bile drainage. Bacteria ascend from the duodenum into the common bile duct (CBD) causing infection. Gram-negative bacteria (e.g. Escherichia coli, Klebsiella, Enterobacter), gram-positive bacteria (e.g. Enterococcus, Streptococcus) and mixed anaerobes (Bacteroides, Clostridia) are the usual culprit organisms.

Blood cultures usually grow a single organism while bile cultures typically show polymicrobial infection (70%). Presence of biliary stents is a risk factor for Enterococcus. Pseudomonas infection is associated with previous biliary manipulation while Staphylococcus aureus is associated with transcutaneous biliary procedures.

Incomplete obstruction of the CBD as seen with CBD stones or strictures enables bacterial reflux from the duodenum more easily unlike complete obstruction as seen more often in neoplasms (e.g. ampullary and pancreatic head tumors). Only about 15-20% of patients with neoplastic obstruction develop cholangitis. Biliary obstruction, especially when chronic, raises intrabiliary pressure promoting movement of bacteria from the biliary tree to the portal circulation and subsequently into the systemic circulation causing sepsis.

Primary sclerosing cholangitis

PSC is an idiopathic condition likely of autoimmune origin that causes progressive inflammation and scarring of intrahepatic and extrahepatic biliary ducts resulting in progressive liver disease, which can lead to liver cirrhosis and be complicated by cholangiocarcinoma.

Most patients are asymptomatic at diagnosis. It is associated with inflammatory bowel disease (mostly ulcerative colitis) and other autoimmune conditions. Elevated alkaline phosphatase is typical. Transaminases are only mildly elevated.

Diagnosis is made following imaging studies such as magnetic resonance cholangiopancreatography/endoscopic retrograde cholangiopancreatography (MRCP/ERCP) or ultrasonography (US) which show an irregular beaded appearance of the biliary tract suggestive of multifocal strictures with associated segmental dilatations. Exclusion of secondary causes is needed. Definitive treatment is liver transplantation.

Secondary sclerosing cholangitis

SSC is a condition that mimics PSC morphologically. It is caused by specific conditions, unlike PSC, which is idiopathic. Causes include the following:

  • Chronic biliary obstruction by CBD stones

  • Following recurrent pyogenic cholangitis

  • Toxic damage following intra-arterial chemotherapy

  • Following ischemic damage

  • Chronic pancreatitis

Recurrent pyogenic cholangitis

Recurrent pyogenic cholangitis which may be seen in the literature as Oriental cholangiohepatitis or hepatolithiasis is an endemic disease in southeast Asia characterized by intrahepatic and extrahepatic biliary strictures with intrahepatic, pigmented soft stones in the biliary tree. Patients present with recurrent bouts of pyogenic cholangitis.

It is a complex syndrome thought to be from the interaction of malnutrition, exposure to biliary parasites and bacterial superinfection. Imaging studies assist in diagnosis. Management is difficult and requires a multimodality approach to clear hepatic stones and establish biliary drainage using transcutaneous or surgical methods. Acute episodes are treated with antibiotics.

II. Diagnostic Confirmation: Are you sure your patient has cholangitis?

The classic triad of fever, abdominal pain (mostly right upper quadrant (RUQ)) and jaundice (Charcot's triad) is present in only 50-70% of patients. A history of biliary tract manipulation, malignancy or previous choledocholithiasis is helpful.

Reynolds' pentad (confusion and hypotension added to charcot's triad) is present in less than 20% of patients.. It signifies high morbidity and mortality and is suggestive of suppurative cholangitis with sepsis.

The presence of predisposing conditions causing bile duct stasis or biliary manipulation is necessary for cholangitis.

CBD stones (choledocholithiasis) are the most common cause and are seen in approximately 80-85% of patients. Stones arising within the biliary duct are primary stones and are usually brown pigment stones unlike those derived from the gallbladder, which are secondary stones and composed of cholesterol. Retained stones are left behind following a cholecystectomy while recurrent stones are new CBD stones.

Bile duct trauma from a previous surgery such as cholecystectomy causing a benign postoperative stricture, neoplasms (cholangiocarcinoma, hepatoma, pancreatic tumors, gallbladder tumors, ampullary tumors, duodenal tumors), PSC associated extrahepatic or intrahepatic biliary strictures, and bile duct scarring due to chronic pancreatitis are other important causes.

Choledochal or biliary cysts, acquired immune deficiency syndrome (AIDS) related cholangiopathy, stenosis of the ampulla of Vater, postoperative states (sump syndrome post choledochoduodenostomy, post Roux-en-Y hepaticojejunostomy, and post Roux-en-Y choledochojejunostomy) are other causes.

Biliary manipulation (endoscopic or percutaneous) such as biliary drain insertion, biliary stents or endoscopic sphincterotomy with ERCP is increasingly a more common cause.

Hemobilia can occasionally cause transient biliary duct obstruction. Porta hepatis lymphadenopathy from lymphomas or metastatic tumors can cause extrahepatic biliary obstruction. Mirizzi's syndrome can present with cholangitis when an impacted gallbladder stone causes common hepatic duct obstruction.

Parasitic infestations such as Clonorchis sinensis, Opisthorchis viverrini and parasitic migration of adult Ascaris lumbricoides into the biliary tract can be seen in certain patient populations (e.g. immigrants from the far east, tropical and subtropical countries).

Recurrent pyogenic cholangitis (described above) is an endemic disease in Southeast Asia characterized by recurrent bouts of pyogenic cholangitis.

A. History Part I: Pattern Recognition:

Fever is present in many patients and may be associated with chills and rigors. RUQ pain can be transient and mild. Accompanying RUQ tenderness can be detected in about 80-90% of patients. Jaundice or icterus is seen in about 80% of patients. Confusion can indicate sepsis and could be the only presenting feature in the very elderly. Hypotension/shock can be seen in severe cases. Darkening of urine might be noticed by the patient or family members.

Accompanying clinical features of acute pancreatitis can be present in some cases.

Complications include sepsis, hepatic abscesses, acute renal failure, disseminated intravascular coagulopathy (DIC), and multiorgan failure.

B. History Part 2: Prevalence:

The prevalence of ascending cholangitis is linked to the prevalence of choledocholithiasis. Choledocholithiasis is seen in 5-10% and up to as high as 15% of some cholecystectomy populations. The elderly have a high incidence of CBD stones and cholangitis. Please also see other predisposing conditions associated with acute cholangitis above in “Diagnostic confirmation”.

C. History Part 3: Competing diagnoses that can mimic cholangitis.

Cholecystitis can present with fever, RUQ pain and often with nausea and vomiting. Physical examination reveals RUQ tenderness with a Murphy's sign. Diabetics and the elderly can have only minimal features on examination. Lab studies can reveal normal or mildly abnormal liver function tests (LFTs) with transient mild elevations in aminotransferases and bilirubin as well as leukocytosis on a complete blood count (CBC).

Right upper quadrant ultrasound reveals features typical of cholecystitis as well as a positive sonographic Murphy's sign. While gallstones are detected in most, acalculous cholecystitis needs to be kept in mind.

Liver abscesses also present with fever, chills and RUQ pain as well as abnormal LFTs. A RUQ US is usually the first test done and can detect abscesses in most. A computed tomography (CT) scan of the abdomen is more sensitive and can pick up lesions less than 1cm.

Mirizzi's syndrome can present with RUQ pain, jaundice and fever. Gallstones that become impacted in the cystic duct or the Hartmann's pouch cause extrinsic compression of the common hepatic duct causing obstructive jaundice with associated cholestatic LFT pattern.

Imaging studies (US/CT/MRCP/ERCP) can pick up a shrunken gallbladder with a dilated common hepatic duct that transitions to a normal CBD below an impacted gallstone in the gallbladder neck (the incomplete biliary duct obstruction here can also result in acute cholangitis as well).

Acute viral hepatitis A can present with non-specific symptoms including fever, as well as RUQ pain and jaundice. LFTs are often significantly elevated with the aminotransferases often more than 1000. Serology is diagnostic with elevated immunoglobulin M (IgM) anti-hepatitis A (anti-HAV) antibodies.

Acute alcoholic hepatitis can present with RUQ pain, jaundice, RUQ tenderness and a leukocytosis on the CBC.

Non-biliary sepsis can cause confusion with mild total bilirubin elevation although levels usually are in the range of 2-3.

D. Physical Examination Findings.

Icterus and RUQ abdominal tenderness can be noted. Icterus is often more pronounced in cases of neoplastic obstruction. Courvoisier's sign is present when an enlarged gallbladder is palpable in the presence of jaundice. It is suggestive of malignant obstruction of the CBD.

E. Diagnostic work up.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

A CBC shows leukocytosis with left shift in most patients. Leukopenia or a normal white blood cell count may also be seen.

Serum bilirubin level is elevated to more than 2-3mg/dl and usually more than 5mg/dl in most cases and can be up to as high as 10-15mg/dl. High levels can be suggestive of CBD stone impaction or Mirizzi's syndrome. Elevation to more than 20mg/dl in the absence of concomitant liver disease can indicate neoplastic obstruction. The serum alkaline phosphatase is often elevated as well.

The aminotransferases, aspartate transaminase (AST) and alanine transaminase (ALT) can be elevated by four to fivefold and up to tenfold, especially in acute obstruction. An elevated serum amylase or lipase level suggests coexisting pancreatitis. An impacted ampullary stone must be considered when bilirubin levels remain persistently elevated in the setting of acute pancreatitis. Prothrombin time (PT) can be elevated due to vitamin K deficiency from bile stasis causing poor vitamin K absorption. A low albumin can be indicative of underlying liver disease or be a negative acute phase reactant.

Blood cultures can become positive for enteric pathogens. This can guide antibiotic regimen. Bile cultures are typically not performed and often show a mixed flora. The significance of bacteria growing in biliary cultures is difficult to establish in each individual case (however, it is standard practice to include antimicrobial therapy against organisms growing in biliary cultures if and when obtained e.g. when obtained by interventional radiology (IR)).

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Transabdominal RUQ US is usually the first imaging study. It can detect CBD stones in about 25% to 50% of patients. A dilated CBD (more than 6mm) can be seen in about 70% of patients. Overlying bowel gas causes poor visualization of the distal CBD. A normal ultrasound study does not rule out cholangitis and further studies are needed if clinical suspicion for cholangitis is high.

Abdominal CT imaging cannot exclude CBD stones but can aid diagnosis by picking up other conditions or complications. A spiral CT has a sensitivity of 65% to 80% for detection of CBD stones. A MRCP has a sensitivity of 85% to 95% and can be indicated in more stable patients or when biochemical markers suggest that biliary obstruction has resolved such as when a CBD stone passes.

Endoscopic ultrasonography (EUS) has a sensitivity of 90 to 97%. In experienced hands, EUS can be more sensitive than ERCP. It is considered when patients have a low to moderate clinical probability of CBD stones or when risks of an ERCP are high or in pregnancy. An MRCP or EUS is often required to make sure one is not dealing with malignancy or choledocholithiasis.

ERCP is the standard test to diagnose CBD stones with a sensitivity and specificity of 95%. It can also decompress the biliary tract and establish drainage of infected bile. Risks include pancreatitis and post-sphincterotomy bleeding. It is generally indicated when there is clinical probability of choledocholithiasis and therefore the need for intervention is high. If an ERCP is unsuccessful, a percutaneous transhepatic cholangiography (THC) can be performed.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

III. Default Management.

  1. Intravenous fluids (IVF).

  2. Blood cultures.

  3. Intravenous (IV) broad-spectrum antibiotics.

  4. Close monitoring of vital signs.

  5. Vasopressors, if necessary, for septic shock.

  6. Correction of coagulopathy with vitamin K for prolonged PT/international normalized ratio (INR).

  7. Transabdominal US or abdominal CT.

  8. MRCP in stable patients or if cholestatic markers return to normal.

  9. ERCP plus sphincterotomy with stone extraction and/or plastic biliary stent placement (usually large bore 10F or larger) when cholestatic markers remain persistently high or in cases of poor response to treatment. A nasobiliary catheter placement without sphincterotomy is another option.

  10. IR guided percutaneous (transhepatic) biliary drainage and decompression in patients too unstable for an ERCP, those with a Roux-en-Y gastric bypass, hilar cholangiocarcinoma too high for a biliary stent, and intrahepatic stones.

  11. Antibiotic therapy is guided by blood culture results.

  12. Non-urgent ERCP in stable patients for definitive management.

  13. Definitive management can include cholecystectomy if the gallbladder is still present and ERCP plus endoscopic sphincterotomy with stone extraction. Pneumatic dilatation of the sphincter of Oddi is an option when coagulopathy is an issue. Mechanical endoscopic lithotripsy, endoscopic laser lithotripsy and non-endoscopic extracorporeal shock wave lithotripsy are options when dealing with large CBD stones.

    Plastic biliary stents tend to fall out themselves, but can be removed or replaced. Self-expanding metal stents might be needed for hilar tumors. High tumors might need percutaneous transhepatic biliary stents by IR when anatomy is surgically altered as in Roux-en-Y patients. Laparoscopic transgastric or transenteric ERCP, ERCP with special endoscopes such as spiral enteroscopes, laparoscopic (transcystic or choledochotomy approach) or open CBD exploration are different options available.

  14. Timely gastroenterology or IR consultations are usually required. Infectious disease consultation can be considered when choosing appropriate antibiotics is difficult.

A. Immediate management.

Immediate management usually includes general measures such as IVF, nil per os (NPO) status and correction of any coagulopathy such as by administering vitamin K intravenously. Blood cultures are drawn and antibiotic therapy is initiated immediately. Some antibiotic options are listed below. Antibiotic penetration into the biliary tract is usually poor secondary to elevated intrabiliary pressures. Antibiotics aimed at covering enteric organisms (gram negatives and anaerobes) are given empirically via parenteral route.

Penicillin/beta-lactamase inhibitors (ampicillin/sulbactam) or second-generation cephalosporins can be used in stable patients with low grade cholangitis. However, there is concern for E. coli resistance to ampicillin/sulbactam (usual dose: 3gm IV every 6 hours). Also, cefoxitin (1-2gm IV every 6-8 hours) has moderate but inadequate anaerobic coverage.

Extended spectrum penicillin/beta-lactamase inhibitors can be used as monotherapy. E.g. piperacillin/tazobactam/Zosyn (usual dose: 3.375/4.5gm IV every 6 hours), ticarcillin/clavulanate/Timentin (usual dose: 3.1gm IV every 4-6 hours).

Third and fourth generation cephalosporins have good gram-negative coverage. Third generation cephalosporins (e.g. ceftriaxone 1-2gm IV every 12/24 hours) except ceftazidime (1-2gm IV every 8 hours) have no anti-pseudomonal activity. Metronidazole (500mg IV every 8 hours) will need to be added for anaerobic coverage. Cephalosporins have no enterococcal coverage and this needs to be kept in mind especially in the presence of biliary stents. Cefepime (fourth generation) has anti-pseudomonal activity (2gm IV every 8-12 hours).

Fluoroquinolones (e.g. ciprofloxacin 400mg IV every 12 hours, levofloxacin 500-750mg IV every 24 hours) have good activity against Enterobacteriaceae, streptococci and Pseudomonas aeruginosa. Levofloxacin has very limited activity against enterococci. They must be combined with metronidazole for anaerobic coverage. Hospital antibiograms can identify communities with less than 90% E.coli or Klebsiella pneumoniae susceptibility to fluoroquinolones.

Carbapenems provide good gram-negative, gram-positive (including enterococci) and anaerobic coverage and can be used as monotherapy. They are usually reserved for severe infections or when bacterial resistance is suspected. For example, meropenem (Merrem, 1gm IV every 8 hours), imipenem with cilastatin (Primaxin, 500mg IV every 6 hours or 1gm IV every 8 hours), doripenem (Doribax, 500mg IV every 8 hours). Ertapenem is less active against Pseudomonas and Enterococcus.

Monobactams provide good aerobic gram-negative coverage. Aztreonam/Azactam (1-2gm IV every 8-12 hours) can be used in cases of penicillin or cephalosporin allergy. However, both gram-positive and anaerobic coverage need to be added.

Regimens such as ampicillin and aminoglycoside combinations used previously have fallen out of favor secondary to development of bacterial resistance to ampicillin and nephrotoxicity of aminoglycosides.

If a good clinical response is seen with antibiotic therapy (mild acute cholangitis), then definitive therapy can be performed less urgently (or semi-electively during the same admission). Failure to respond in about 12-24 hours with features of mild sepsis (moderately severe acute cholangitis) or the presence of severe acute cholangitis (e.g., with septic shock or severe sepsis) is an indication for early or immediate biliary decompression with either an ERCP with endoscopic sphincterotomy and stone extraction or biliary stent placement/nasobiliary drainage tube (without sphincterotomy when the situation is complicated by coagulopathy or severe sepsis) or IR guided percuatenous cholangiogram (PTC) with percutaneous biliary drainage.

Morbidity and mortality outcomes following endoscopic decompression are better compared to percutaneous drainage. Surgical drainage is usually not required and can include choledochotomy with decompression and T-tube insertion. Emergent surgical drainage has the worst morbidity and mortality scores.

Following biliary decompression, antibiotics are usually continued for another 3-5 days in an improving patient. An oral regimen (usually amoxicillin/clavulanic acid or a quinolone class medication with metronidazole) can be chosen, if feasible, based on culture results, antibiograms, patient allergies, and clinical situation. A total of about 7 days is appropriate in most situations. Many clinicians provide up to 7-10 days of antibiotics especially in severe acute cholangitis and from 7-14 days when complicated by enterococcal or gram-negative bacteremia.

Definitive management for acute cholangitis usually requires an ERCP with endoscopic sphincterotomy and bile duct clearance. This can be performed following about 5 days of antibiotic therapy after biliary decompression if needed. Subsequently, a laparoscopic cholecystectomy is pursued on an elective basis in the presence of a gallbladder when the patient is thought to be a reasonable candidate for the procedure.

B. Physical Examination Tips to Guide Management.

Vital signs including fever are closely monitored to guide therapy. Improving vital signs, including fever, are an indication that the chosen antibiotic regimen is right. Abdominal pain and tenderness on RUQ palpation should also improve with response. Failure to improve when accompanied by other markers of infection such as worsening or non-improving leukocytosis or worsening LFTs is an indication to expand antibiotic coverage or consider decompression.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Liver enzymes and CBC are usually monitored every day to monitor response to treatment. PT/INR is also followed-up every day or every other day until correction or stability. Basic metabolic panel (BMP) is also monitored every day or every other day especially when IVF are being given or if there is concern for renal function. Laboratory frequency checks can be decreased as the patient improves. Blood cultures can help guide antibiotic regimens.

D. Long-term management.

This involves the management of specific causes causing biliary drainage obstruction. Elective laparoscopic cholecystectomy is performed if the patient is a suitable candidate when CBD stones are thought to be derived from the gallbladder. Post-surgical biliary strictures need follow-up with gastroenterology (for ERCP placed biliary stents) or IR for percutaneous biliary drains.

Neoplasms often require follow-up with medical oncology, surgical oncology, radiation oncology, and IR. Plastic stents can be removed or replaced by larger stents if necessary. 10F plastic stents do a better job than 8F stents. However, stents may clog and need to be replaced either on a scheduled or as needed basis. Expandable metal stents have a longer patency rate but are also more expensive. Metal stents cannot be removed and stent obstruction is dealt with by placing another stent, either plastic or metal, inside the first stent.

Care of percutaneous biliary drains is usually required. Internal-external drains can be capped. External only drains require a bag for bile collection. Normal saline flushes usually about twice a day are performed as instructed by IR.

E. Common Pitfalls and Side-Effects of Management.

Delaying biliary decompression can worsen outcomes. Percutaneous biliary drainage should be considered when ERCP is not possible. Antibiotic resistance needs to be considered when patients fail to respond appropriately. Complications of ERCP with sphincterotomy include pancreatitis, CBD stone impaction, bleeding, and perforation.

A failed attempt to place an endoscopic biliary stent in hilar cholangiocarcinomas especially when involving multiple hepatic ducts can result in recurrent segmental cholangitis and a worse outcome. Transcutaneous hepatic drainage needs to be considered in such situations. MRCP guidance of ERCP placed stents can avoid such situations.

IV. Management with Co-Morbidities.

A. Renal Insufficiency.

Will require appropriate dose changes of various antibiotics. Acute renal failure is associated with a poorer prognosis.

B. Liver Insufficiency.

Patients do fairly well following endoscopic sphincterotomy via ERCP. Surgery such as choledocholithotomy with T tube placement increases morbidity and mortality significantly. Complications include liver failure, bleeding and sepsis. Liver cirrhosis worsens prognosis generally.

C. Systolic and Diastolic Heart Failure.

No change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease.

Use of antiplatelet agents can cause bleeding with endoscopic sphincterotomy.

E. Diabetes or other Endocrine issues.

No change in standard management.

F. Malignancy.

Neoplasms can cause biliary obstruction and thus enable cholangitis. Diagnostic ERCPs can introduce infection and result in cholangitis when biliary duct obstruction is present and must be followed by a decompressive procedure. Failure to relieve cholestasis by biliary stents or percutaneous drains might make patients poor candidates for chemotherapeutic agents that are cleared by the hepatobiliary system.

G. Immunosuppression (HIV, chronic steroids, etc).

AIDS cholangiopathy can be seen in advanced AIDS when cluster of differentiation 4 (CD4) lymphocyte counts are typically less than 100. It results in biliary tree obstruction from biliary stricture formation, from chronic infectious inflammation. The culprit organism is usually Cryptosporidium parvum. Cytomegalovirus, Microsporidia and Cyclospora have also been implicated among other opportunistic organisms.

Patients typically present with RUQ or epigastric pain, fever and watery diarrhea. Jaundice is uncommon. Serum alkaline phosphatase levels are significantly elevated (approximately 600-800 before patients present with related abdominal pain) with only minimal elevations in bilirubin and aminotransferases.

Imaging studies including US/MRCP can show intra and extrahepatic biliary strictures and dilatation as well as bile duct wall thickening (can be detected incidentally when imaging studies are performed for different reasons). ERCP can detect papillary stenosis in about 50% of cases.

Stool studies often detect Cryptosporidium and other opportunistic infections responsible for the diarrhea associated with this condition. Initiation of antiretroviral therapy aimed at improving immunocompetence is the only treatment. Endoscopic sphincterotomy can help relieve symptoms related to papillary stenosis, including abdominal pain.

There is otherwise no change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

Please refer to predisposing causes listed at the beginning of this chapter.

Chronic CBD obstruction can cause malabsorption of the fat soluble vitamins i.e. vitamins A, D, E, and K.

J. Hematologic or Coagulation Issues.

Correction of coagulopathy is sometimes necessary with either IV or subcutaneous vitamin K. Fresh frozen plasma might be occasionally necessary.

K. Dementia or Psychiatric Illness/Treatment.

Confusion can be a presenting complaint in the elderly and can be a sign of severe cholangitis when accompanied by hypotension.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

None

B. Anticipated Length of Stay.

For less severe cases responding well to IV antibiotics length of stay is usually 3-5 days. For more severe cases and those with issues related to antibiotic resistance or allergy, patients might be hospitalized for 5-7 days.

C. When is the Patient Ready for Discharge.

When the patient's vitals are stable, fever has resolved, abdominal pain has significantly improved, and the patient is tolerating an oral diet, then he/she can be discharged home. If further antibiotic therapy is necessary to complete a course, then an antibiotic regimen that the patient can be discharged home on should be feasible.

If definitive intervention has not been performed this hospitalization, then the patient's gastroenterologist should be involved in planning close outpatient follow-up and intervention before deciding on discharge

D. Arranging for Clinic Follow-up.

The discharging physician should discuss with the consulting gastroenterologist or with the interventional radiologist before discharging the patient home.

1. When should clinic follow up be arranged and with whom.

Time of follow-up is to be determined based on discussion with the gastroenterology or IR service. Specific interventions if needed should be discussed and arranged for before discharge. In the case of neoplasms, follow-up with medical oncology might be necessary as well.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

None

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Generally no tests are necessary. In certain situations, LFTs with serum bilirubin levels might be needed on the day of follow-up.

E. Placement Considerations.

Consider a physical therapy consult during the patient's hospitalization if the hospitalization has caused deconditioning. Subacute rehabilitation might be necessary sometimes in the elderly. A physical therapy evaluation can be performed about 3-4 days following hospitalization in an improving patient.

A social worker consult might be necessary for home visiting nursing services if the patient is to be discharged on a biliary drain especially if the patient or family are uncomfortable caring for the biliary drain.

F. Prognosis and Patient Counseling.

Prognosis depends on the cause of biliary obstruction (neoplasms have poorer prognosis), severity at presentation (Reynolds' pentad can increase mortality), underlying comorbid factors (cirrhosis with hypoalbuminemia and coagulopathy, malignancy), amenability to decompression (surgical decompression especially emergent has a higher morbidity and mortality), and advanced age (more than 80 years). Generally younger populations with no significant comorbidities who respond well to decompression have a mortality of less than 5%.

Factors predisposing patients to recurrence include biliary neoplasms causing incomplete obstruction, presence of biliary stents or percutaneous drains, hepaticojejunostomy, conditions with biliary strictures such as PSC, or postoperative strictures not amenable to stenting.

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.

None

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Pre-procedural (before ERCP or percutaneous procedures such as biliary drain change) prophylaxis with antibiotics is performed.

Occasionally, certain specific antibiotics might be necessary based on previous culture results (e.g. meropenem for a patient with a biliary drain that needs to be changed and previous cholangitis with extended spectrum beta-lactamases (ESBL) producing E. coli). This needs to be communicated to the appropriate physician before any procedure.

VII. What's the Evidence?

**The original source for this chapter was Dr Vijay Dev Lakkappa. The chapter was revised for this program by Dr Jason A. Ramirez.

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