How can I be sure that the patient has post-ERCP complications?

According to the 1991 Consensus criteria formulated by selected experts and a comprehensive review of the literature, a complication is an adverse event, attributable to the procedure and requiring hospitalization for management and treatment.

In 2012, revised Atlanta classification developed consistent terminology and definition of acute pancreatitis, its severity and sequelae (See Table I).

Table I.
Complications Mild Moderate Severe
Pancreatitis Pancreatitis requiring hospitalization of 1-3 days Pancreatitis requiring hospitalization of 4-10 days Hospitalization for more than 10 days, or (for hemorrhagic pancreatitis, phlegmon, or pseudocyst) intervention (percutaneous drainage or surgery)
Bleeding Clinical (i.e., not just endoscopic) bleeding; hemoglobin drop less than 3 g, and no need for transfusion Transfusion (4 units or less), no angiographic intervention or surgery Transfusion of 5 units or more, or intervention(angiographic or surgical)
Perforation Possible, or only a very slight fecal fluid or contrast, treatable by fluids and suction for 3 days or less Any definite perforation treated medically for 4-10 days Medical treatment for more than 10 days, or intervention (percutaneous or surgical)
Infection(cholangitis) Temperature more than 38°C for 24-48 hr Febrile or septic illness requiring more than 3 days of hospital treatment or endoscopic or percutaneous intervention Septic shock or surgery
Basket impaction Basket released spontaneously or by repeat endoscopy Percutaneous intervention Surgery
Definition of most common post-ERCP complications

The 1991 consensus workshop defined the most common post-ERCP (endoscopic retrograde cholangiopancreatography) complications as follows (See Table II; see also Figure 1).

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Table II.
Increased risk? Procedure-related Patient-related Operator-related

Pancreatic duct injection

Pancreatic sphincterotomy

Difficult or failed cannulation

Balloon dilation of intact biliary sphincter

Precut sphincterotomy

Young age


Suspected SOD

Prior post-ERCP pancreatitis

Absence of chronic pancreatitis

Fecurrent pancreatitis


Therapeutic vs. diagnostic

Prior failed ERCP

Intramural contrast injection

Biliary sphincterotomy

SOD manometry (aspiration catheter)

Small CBD diameter

Periampullary diverticulum

Pancreas divisum

Gastrectomy with Billroth type II


Pancreatic acinarization

Pancreatic brush cytology

Absence of CBD stone

Normal serum bilirubin

Low endoscopist volume
Don’t know

Automated electrosurgical currents delivery system (ERBE) vs. pure-cut electrosurgical current

Use of papillotomes and guidewires for cannulation

Abbreviations: CBD, common bile duct; SOD, sphincter of Oddi dysfunction.

Source: Adapted from Freeman ML, DiSario JA, Nelson DB, et al. Risk factors for post-ERCP pancreatitis. Gastrointest Endosc 2001;54(4).

Figure 1

Severity and management of acute pancreatitis.

What signs and symptoms of post-ERCP pancreatitis are usually found?

Abdominal pain post ERCP

My patient is complaining of abdominal pain after ERCP. Is he suffering from post-ERCP pancreatitis?

According to the consensus criteria: post-ERCP pancreatitis is defined as “a clinical illness with typical pain, associated with at least a threefold increase in serum amylase (or lipase) at 24 hours, with symptoms impressive enough to require admission to hospital for treatment (or extension off and existing or on admission).”

Other widely accepted definitions include two of the following three criteria:

  • Abdominal pain suggesting acute pancreatitis,

  • Serum amylase and/or lipase more than or equal to 3 times the upper limit of normal, and

  • Characteristic findings of acute pancreatitis on CT scan.

Alternate classifications of pancreatitis include:

Mild or interstitial or edematous pancreatitis (focal or diffuse enlargement of pancreas gland with enhancement of parenchyma that is either homogeneous or slightly heterogeneous in response to IV contrast). It accounts for the majority of pancreatitis cases, and is self-limited, with very low mortality.

Severe or necrotizing pancreatitis (diffuse or focal area(s) of nonviable pancreatic parenchyma, typically associated with peripancreatic fat necrosis). This disease is a rare complication of ERCP, is associated with organ failure, and has a complicated course, with 20% mortality.

Abdominal bloating and discomfort post ERCP

Many patients experience abdominal bloating and discomfort following ERCP, which usually resolves within a couple of hours. This is often due to excessive air insufflation.

  • Encourage ambulation and/or left lateral decubitus position for expulsion of excessive air.

  • It has been suggested that CO2 insufflation instead of air might reduce post-ERCP abdominal distention and pain.

Escalated chronic pancreatic abdominal pain post ERCP

Sometimes patients with chronic pancreatic abdominal pain complain of escalated pain post procedure without any clear evidence of clinical pancreatitis. Management is often expectant with analgesia.

On the contrary, clinical pancreatitis usually becomes evident after a delay of 4-12 hours, and is characterized by typical pancreatic type pain, often associated with nausea and vomiting. On clinical exam, the patient may have tachycardia, epigastric tenderness, and absent or diminished bowel sounds. Serum levels of amylase and lipase are elevated (> 3 times upper limit of normal), with possible leukocytosis.

It is imperative to exclude perforation as the alternative diagnosis, especially if the patient has marked distress and abdominal tenderness, with nonsignificant elevation of serum amylase or lipase. A noncontrast CT scan of the abdomen is recommended or plain abdominal radiographs if perforation is suspected.

How can I confirm the diagnosis?


What other diseases, conditions, or complications should I look for in patients with complications of ERCP?

What are the risk factors for developing post-ERCP pancreatitis?

Post-ERCP pancreatitis can occur after an ERCP procedure; however, several factors (Table III), both patient- and procedure-related, have been known to increase the risks. These risk factors are synergistic.

Table III.
Increased risk? Procedure-related Patient-related Operator-related

Pancreatic duct injection

Pancreatic sphincterotomy

Difficult or failed cannulation

Balloon dilation of intact biliary sphincter

Precut sphincterotomy

Young age


Suspected SOD

Prior post-ERCP pancreatitis

Absence of chronic pancreatitis

Fecurrent pancreatitis


Therapeutic vs. diagnostic

Prior failed ERCP

Intramural contrast injection

Biliary sphincterotomy

SOD manometry (aspiration catheter)

Small CBD diameter

Periampullary diverticulum

Pancreas divisum

Gastrectomy with Billroth type II


Pancreatic acinarization

Pancreatic brush cytology

Absence of CBD stone

Normal serum bilirubin

Low endoscopist volume
Don’t know

Automated electrosurgical currents delivery system (ERBE) vs. pure-cut electrosurgical current

Use of papillotomes and guidewires for cannulation

Abbreviations: CBD, common bile duct; SOD, sphincter of Oddi dysfunction.

Source: Adapted from Freeman ML, DiSario JA, Nelson DB, et al. Risk factors for post-ERCP pancreatitis. Gastrointest Endosc 2001;54(4).

How can I reduce the risk of post-ERCP pancreatitis?

Some considerations for reducing risk factors of post-ERCP pancreatitis include the following.

Basic considerations

– Avoid marginally indicated ERCPs and ERCPs in high risk patients;

– Utilize other imaging modalities, such as EUS and MRI, and reserve ERCP for therapeutic purposes only;

– Know when to stop. Be cognizant of personal technical expertise level and limitations; and, finally,

– Consider referral to an ERCP expert for high-risk, complex cases.

Technical considerations

– Some recent data suggest that gentle wire-guided cannulation may have a lower incidence of post-ERCP pancreatitis compared to multiple contrast injections;

– Use an endoscopist-controlled contrast injection and wire manipulation;

– Reserve precutting for strong indications and for experts;

– Use aspiration catheter system for manometry;

– Avoid excessive coagulation near the pancreatic orifice; and, finally,

– Use/place a pancreatic stent for prophylaxis early in high-risk ERCP.

There are a variety of pancreatic stents available for this purpose. The type of stent inserted depends on availability, details of the procedure, personal preference, ductal anatomy, and wire caliber. The commonly used pancreatic stents for prophylaxis are short (3 or 5 cm) 5 French stent, straight or pigtailed, with or without internal flap for French stents and 3 French stents with pigtail and without internal flap, 3 Fr can only be deployed over 0.018-inch or 0.021-inch guidewire).

Follow-up abdominal radiograph is obtained 7-10 days post-deployment to ascertain spontaneous stent migration. In cases when stents fail to dislodge spontaneously or when stents with internal flap were deployed, a repeat endoscopy within 2 weeks of stent placement should be performed for stent removal.

Pharmacological prophylaxis

Several agents have been proposed for pharmacologic prophylaxis to prevent post-ERCP pancreatitis. Rectal NSAIDs (specifically diclofenac and indomethacin) prior to ERCP or immediately after ERCP have shown a statistically significant reduction in post-ERCP pancreatitis and their use should be considered, especially in high-risk patients.

What is the right therapy for the patient with post-ERCP complications?

How do I approach and manage the patient with acute post-ERCP pancreatitis?

Determination of severity

The basic principles of management of acute post-ERCP pancreatitis are the same as those for pancreatitis of other etiologies (Figure 1). Initially, the diagnosis can be established according to the definition provided earlier in the chapter.

Radiologic imaging – such as contrast-enhanced thin section, multidetector-row CT scan, or MRI – help establish the severity of pancreatitis and identify any pancreatitis-related complications.

A. Establish the risk factors for severity of your patient at admission. Older age (>55 years), obesity (BMI >30), organ failure at admission, and pleural effusion(s) and /or infiltrates are risk factors for severity. Patients with these risk factors should be monitored in ICU or the step-down unit.

B. Establish severity by clinical examination and laboratory tests at admission and at less than 48 hours. Several scoring systems and laboratory markers have been studied and have predicted severity of pancreatitis. Some of them can be used in the first 24 hours of admission to gauge severity (APACHE-II/capital APACHE-O, BISAP, serum creatinine, hematocrit levels), whereas others need 48 hours to predict severity (Ranson’s, CRP, CT SI).

1. The Acute Physiology and Chronic Health Evaluation Score (APACHE II) – based on an initial value of 12 routine physiological measurements, age, and previous health status (Figure 2). In general, an APACHE-II score that increases during the first 48 hour is strongly suggestive of the development of severe pancreatitis, whereas an APACHE-II that decreases within the first 48 hours strongly suggests a mild pancreatitis episode.

Figure 2

APACHE-II score.

The addition of an obesity score to the standard APACHE-II (so-called APACHE-O) appears to increase the accuracy of APACHE-II for severity. In this scoring system, a point is added to the APACHE-II score when the BMI is 26 to 30, and 2 points are added when the BMI is higher than 30.

2. Ranson score has been used for many years to assess the severity of acute pancreatitis but has the disadvantage of requiring a full 48 hours for complete evaluation. Severe pancreatitis is established by a total score of more than or equal to 3, with 1 point for each positive factor.

3. In several studies, a creatinine of higher than 2.0 mg/dL at admission and within 24 hours of admission was associated with a greater mortality.

4. Fewer studies report that a hematocrit higher than or equal to 44 at admission, and failure of the admission hematocrit to decrease at 24 hours is a reliable predictor of necrotizing pancreatitis. Other reports have not confirmed that hemoconcentration at admission or at 24 hours is a risk factor for severe acute pancreatitis. However, there is a general consensus that the likelihood of necrotizing pancreatitis is very low in the absence of hemoconcentration at admission or within first 24 hours.

5. BISAP score is calculated within the first 24 hours (blood urea nitrogen >25 mg/dL, impaired mental status, systemic inflammatory response system (SIRS), age >60 years, and pleural effusions) with a score of 3 or more suggesting severe pancreatitis, risk of organ failure, and necrosis.

6. C-reactive protein (CRP) is an acute phase reactant. Plasma levels higher than 150 mg/L within the first 72 hours of disease correlate with the presence of necrosis with a sensitivity and specificity of more than 80%. Because the peak is generally 36-72 hours after admission, this test is not helpful for assessing severity at admission.

7. CT severity index (CTSI) higher than or equal to 7 predicts necrotizing pancreatitis.

8. Several clinical findings – including polydipsia, oliguria (urine output <30 mL/hr), progressive tachycardia, tachypnea, hypoxemia, agitation, confusion, a rising hematocrit level, and a lack of improvement in symptoms despite resuscitation within the first 48 hours – are warning signs of severe disease. Consider a higher level of care in an intensive care unit with multidisciplinary care, including pulmonary/critical care, surgery, gastroenterology, and interventional radiology. Intensive care may also be warranted in patients at risk for rapid deterioration in their condition (elderly, obese), those who need ongoing volume resuscitation or invasive monitoring of fluid status (e.g., central venous pressure monitoring), or those with renal failure or respiratory compromise.

Management of acute pancreatitis

Supportive care

Supportive care that emphasizes measurement and prevention of hypoxemia and adequate fluid resuscitation is of utmost importance during the first 24 hours of admission.

Vital signs and oxygen saturation should be measured frequently (every 4 hours). Supplemental oxygen should be provided during the first 24-48 hours. Obtain blood gas analysis if pulse oximetry shows oxygen saturation less than 95% or if the patient has clinical manifestations suggestive of hypoxemia.

Aggressive fluid resuscitation (~250-500 cc of isotonic fluid per hour for 12-24 hours) is of critical importance to minimize the risk of necrotizing pancreatitis. The adequacy of fluid resuscitation should be monitored by vital signs, urine output (at least 30 mL/hour), and appropriate decline in hematocrit and BUN at 12 and 24 hours after admission. Watch for signs and symptoms of intravascular volume depletion, such as tachycardia, hypotension, oliguria, hemoconcentration (hematocrit >/=44), and prerenal azotemia.

Perform pain management with parenterally administered narcotic medication or patient controlled analgesia.


The initiation of oral intake in mild pancreatitis depends on improved abdominal pain and tenderness, absence of nausea and vomiting, presence of bowel sounds, and return of appetite. Generally, this is achieved within 3-7 days of hospitalization, and nutritional support is not required in these patients. It is safe to start the patient on either clear or full liquid diet prior to advancing the patient on a low-fat diet.

In severe pancreatitis, nutritional support should be started within the first week of illness. Enteral feeding (nasojejunal) is preferred to parenteral nutrition. In the patient who has sustained significant necrosis of head and/or body of the pancreas, it is advisable to initiate pancreatic enzymes and a proton pump inhibitor. The ongoing need for these can be addressed during the recovery phase by evaluation of the presence of pancreatic steatorrhea.

Role of prophylactic antibiotics

There is no role for routine antibiotics in patients with mild (interstitial) pancreatitis.

The use of prophylactic antibiotics for prevention of pancreatic infection is not recommended at this time in patients with severe (necrotizing) pancreatitis. The use of combined antifungal and antibacterial therapy for prophylaxis has not been validated in randomized trials.

Finally, clinical judgment should be used in every case. The majority of patients with necrotizing pancreatitis during the first week of illness may appear septic with fever, leucocytosis, and organ dysfunction. It is appropriate to initiate and keep them on antibiotics until infection is excluded, with proper imaging and appropriate cultures, including CT-guided fine-needle aspiration of pancreatic necrosis. If these measures are found to be negative, antibiotic therapy can be discontinued but with continued close surveillance of the patients.

What is the most effective initial therapy?

What are the complications of acute pancreatitis and how do I manage them?

The most common complication seen in more than half of the patients hospitalized with acute pancreatitis is the development of pancreatic and peripancreatic fluid collections. Early in the course of illness, these fluid collections are ill-defined, and evolve over 4-6 weeks. Usually, these are managed conservatively.

In the absence of any new or worsening symptoms, it is prudent to repeat cross-sectional imaging 2-3 months after the acute episode to ascertain resolution and/or stability of these fluid collections. On the contrary, if fluid collections continue to enlarge or they become symptomatic causing pain; gastric outlet obstruction leading to nausea; vomiting or oral nutrition intolerance; compression of adjacent organs; and with signs and symptoms of infection as suggested by fever, leucocytosis, and gas bubbles in the fluid collection on cross-sectional imaging, then medical/surgical/endoscopic/interventional radiological intervention may be needed.

Management of pancreatic and peripancreatic fluid collections depends on the availability of local expertise. These fluid collections often can be drained endoscopically with endoscopic ultrasound (EUS) and ERCP. Presence of high amylase in these fluid collections, pancreatic ascites, and left-sided high amylase pleural effusion suggests the presence of pancreatic ductal leak and/or disruption. ERCP is commonly performed in this scenario to confirm ductal compromise, for defining the anatomy and for transpapillary drainage or bridging the disruption or leak in conjunction with endoscopically accessible transgastric or transduodenal drainage of fluid collections.

The description of the endoscopic method of transgastric or transduodenal drainage of these fluid collections is beyond the scope of this chapter. Briefly, it involves carefully selecting the puncture site in the stomach or duodenum (good apposition of the fluid collection against the gastric or duodenal wall with less than 1-cm distance excludes the presence of major blood vessels either by EUS or a good quality CT). Entry into fluid collections is achieved either with an EUS FNA needle or needle knife. Successful entry is confirmed with contrast injection, a guidewire is advanced into the fluid collection, tract is dilated up to 10 mm and, finally, two 7Fr or 10Fr double pigtail plastic stents are deployed across the cystogastrostomy/duodenostomy.

The more perplexing and difficult to manage complication of pancreatitis is infected pancreatic necrosis. It is imperative to make the diagnosis promptly (algorithm 1). Infected necrosis is suspected when the patient’s clinical condition deteriorates with persistent or worsening fever and leucocytosis. This complication generally occurs in the second or third week of acute illness. Presence of gas bubbles within the necrotic tissue on CT scan signifies infection. In indeterminate clinical scenarios, diagnosis can be confirmed by CT-guided or ultrasound-guided percutaneous aspiration of necrotic material with the gram stain and bacterial and fungal culture. However, negative culture does not exclude infection since the false negative rate of percutaneous aspiration of necrotic collection is up to 20%.

For gram-negative organisms, choices for antibiotic treatment include a carbapenem, fluoroquinolone plus metronidazole, or third-generation cephalosporin plus metronidazole pending the results of culture and sensitivity. If gram stain reveals the presence of gram-positive bacteria , it is reasonable to add vancomycin until further culture and sensitivity results are available.

Severe acute and necrotizing pancreatitis requires a multi-disciplinary treatment strategy that must be individualized for each patient. Optimal treatment of infected necrotizing pancreatitis requires a staged, multi-disciplinary, minimally invasive “step-up” approach from less invasive to more invasive modality is recommended. Management of these patient requires algorithmic approach by a team of interventional radiologist, therapeutic endoscopist, and a surgeon.

An important distinction to make is between pseudocysts and walled-off necrosis (WON), as the interventions for each are different. WON is a mature, encapsulated collection of pancreatic /peri pancreatic necrosis which usually develops >4 weeks after onset of acute necrotizing pancreatitis. Therefore, endoscopic or other interventions should be delayed for at least 4 weeks for collections to encapsulate. Direct endoscopic necrosectomy (DEN) is an effective, minimally invasive option. Several variations in the technique, including the use of esophageal fully covered self-expanding metal stents (SEMS) and lumen-apposing SEMS have recently been described. The incremental effectiveness of these stents over conventional techniques utilizing plastic stents or nasobiliary drain needs to be studied. Dual-modality drainage with endoscopic transmural stent placement and aggressive lavage through interventional radiology guided percutaneous drains is also an effective option with low mortality and morbidity. Several minimally invasive surgical options, including video-assisted retroperitoneal debridement (VARD) and sinus tract endoscopy are available and may be preferable to open surgical necrosectomy.

Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.

What are the causes and risk factors of bleeding during ERCP and what is the treatment?

Bleeding has been reported to occur in up to 2% of ERCPs.

– Clinically significant bleeding is a rare occurrence and mainly occurs from sphincterotomy. Other causes include biopsy (intraductal and tumor biopsy); presence of coagulopathy; biliary varices; tumor-related bleeding; and therapeutic maneuvers such as ampullectomy or creation of transgastric or transduodenal fistula for management of pancreatic or peripancreatic fluid collections.

– Bleeding can occur immediately but can often be delayed up to a week. Delayed bleeding can present as melena, hematemesis, biliary-type pain, and cholangitis/jaundice due to occlusion of the bile duct from blood clots.

– Common risk factors include presence of coagulopathy, cholestasis, renal failure, and chronic liver disease complicated by portal hypertension.

Preventive measures

Some of the preventative measures include:

1. Correction of coagulopathy whenever possible.

2. Management of antiplatelet and anticoagulating agents, per American Association of Gastrointestinal Endoscopy (ASGE) guidelines. Stratify patient, according to the procedure needed (biliary sphincterotomy is considered high-risk procedure for bleeding, and ERCP without sphincterotomy is considered low risk) and the existing underlying comorbid condition causing thromboembolic risk (Figure 3 and Figure 4).

Figure 3

Anthrombotic drugs: duration of action and routes for reversal. (Adapted from ASGE Guidelines: management of antithrombotic agents for endoscopic procedures. Gastrointest Endosc 2009;70.)

Figure 4

Condition risks for thromboembolic event.

3. Use blended current for sphincterotomy.

4. Consider balloon sphincteroplasty instead of sphincterotomy for extraction of common bile duct stones in patients who need to be maintained on anticoagulation or have an irreversible coagulopathy.

Despite all these measures, we come across patients with either immediate or delayed bleeding, typically from a sphincterotomy site.

After initiating appropriate resuscitation measures, endoscopic management includes trial of following interventions either alone or in combination:

– Injection of dilute 1:10,000 epinephrine, using a standard sclerotherapy needle.

– Deploying hemoclips, taking care to avoid pancreatic orifice.

– Use of bipolar cautery, taking care to avoid pancreatic orifice.

– Balloon tamponade, whereby an occlusion balloon or CRE dilating balloon is over-inflated (12-15 mm, depending on the duct caliber) and positioned at the orifice (or intraductal for biliary varices) for up to 5 minutes.

– There have been some reports of deploying a fully covered biliary metal stent for tamponade. Needless to say, this is an off-label use of these stents and an act in sheer desperation.

– Finally, if a clinically profuse bleeding is obscuring the visual field, the patient should be promptly referred to interventional radiology for an angiogram and embolization of the bleeding vessel. Surgery is rarely needed and is reserved as a last resort when all else fails.

What are the causes of perforation during ERCP, and how should I approach this complication?

Perforation reportedly occurs in 1-2% of ERCPs. Four different sites and types of perforation have been described:

1. Retroduodenal perforation related to sphincterotomy. This is the most common cause of perforation. It is important to know that up to 10% of patients after uncomplicated sphincterotomy will have some retroperitoneal or periduodenal air on a routine CT scan performed post procedure for other indications. This does not need any intervention if the patient is clinically asymptomatic.

Perforation reportedly is more likely to occur in patients with SOD and who have had various endoscopic maneuvers like precutting or extension of previous biliary sphincterotomy. Suffice it to say that these maneuvers should not be undertaken without proper indication and training.

Diagnosis of perforation can be achieved either during the procedure itself upon viewing the retroperitoneum or with the aid of fluoroscopy, showing air around the right kidney and along the lower edge of the liver. However, in the majority of cases, diagnosis is suspected immediately after the procedure when the patient complains of significant abdominal pain and tenderness. Noncontrast CT scan is preferred over plain X-ray for the diagnosis of perforation.

Management includes the initiation of intravenous fluids, broad-spectrum antibiotics, nil per os status, and placement of nasogastric or nasoduodenal drainage tube. There have been some case reports of closure of perforation at sphincterotomy site with the help of hemoclips.

Sphincterotomy-related perforation can be managed conservatively if recognized early, and CT scan shows merely air, not fluid, in the retroperitoneum. However, it is prudent to obtain prompt surgical consultation and request continued daily evaluation, by surgical and medical teams, of patients who are managed conservatively.

2. Luminal perforation. This is a rather rare occurrence (<1%). This has been reported to occur more frequently in patients with altered surgical anatomy (Roux-en-Y, Billroth II), duodenal strictures, esophageal strictures, or diverticula. Management usually involves surgical intervention. Case reports of endoscopic closure of perforation with hemoclips followed by aggressive conservative treatment have been reported.

3. Guide wire or dilating-related perforation. This usually occurs when a stiff-tipped wire is used or an aggressive balloon dilation is performed for tight ductal strictures. It is wise to use hydrophilic tipped, less traumatic straight, or angled wires. Careful assessment of the native duct diameter should be made prior to choosing the dilating balloon or catheter size. This complication is easily recognized during the procedure by extravasation of contrast. It usually does not cause any significant morbidity. Management involves placement of a temporary stent to bridge the area of leak in the duct.

4. Stent-related perforation. This typically occurs when a straight, usually 10-french stent, is placed in the setting of generous sphincterotomy and/or long intraduodenal portion. These frequently migrate downward and can penetrate/perforate the opposite duodenal wall. This is managed by careful and gentle extraction. Hemoclips can be used to close an obvious stent-related perforation. If restenting is indicated, then stents with pigtails should be placed.

A listing of a subset of second-line therapies, including guidelines for choosing and using these salvage therapies

What are the other "technical" challenges or complications of ERCP?

Basket impaction

Impaction of the lithotripsy basket during endoscopic removal of a common bile duct stone is seen in up to 5% of cases. Nasobiliary or internal biliary drainage is temporarily used to decrease the risk of cholangitis. Rupture of the traction wire at the handle may be prevented by using baskets with a predetermined breaking point at the base or tip of the lithotriptor basket.

Although delayed spontaneous passage of an impacted basket has been reported, nonsurgical methods for basket retrieval are tried first. Impacted baskets located at the distal bile duct have been traditionally managed with the use of an extra-endoscopic mechanical lithotriptor (Soehendra lithotriptor).

In a case of traction wire fracture of a mechanical lithotriptor, successful continuation of the mechanical lithotripsy procedure can be achieved by replacing the long metal sheath stepwise with shorter ones (70 cm, 60 cm, and 50 cm, respectively).

An impacted Dormia basket can be disengaged from the stone with the help of a second basket by initially pulling the tip of the original basket proximally into the wider biliary lumen and subsequently flipping it downward.

ESWL has been used to disintegrate the captured stone within an impacted basket with subsequent basket removal. Intracorporeal electrohydraulic shock-wave lithotripsy has been successfully used for disimpaction of a basket after fragmentation of stone.

Stent migration

Migrated stents can be retrieved out of the papilla with inflation of either an occlusion/dilating balloon above or in tandem with the stent while gently dragging both down, grasping the stent with biliary or rat tooth forceps, snare, or a basket – cannulating the stent with a wire followed by inflation of an occlusion balloon within or insertion of appropriate caliber dilators over the wire within the stent and gently pulling them down across the papilla. Cholangioscopy-/pancreatoscopy-guided cannulation of the migrated stent and subsequent retrieval have been reported. Surgery may be necessary if all else fails.

Several newly developed through-the-scope lithotriptors have been introduced for the management of basket impaction in the common bile duct. Alternatively, a second through-the-scope mechanical lithotriptor can be used to crush the stone within the impacted mechanical lithotripsy basket.

Listing of these, including any guidelines for monitoring side effects.


How should I monitor the patient with complications of ERCP?


What's the evidence?

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