How Should Post-ERCP Pancreatitis Be Managed?

John Baillie, MB, ChB

Disclosures

September 14, 2012

Question

How does post-ERCP pancreatitis present, and how should it be managed?

Response from John Baillie, MB, ChB
Cartaret General Hospital, Cartaret Medical Group, Morehead City, North Carolina

The Most Feared Complication of ERCP

Acute pancreatitis is the most feared complication of endoscopic retrograde cholangiopancreatography (ERCP) because it has the greatest potential for causing prolonged hospitalization, major morbidity, and occasionally death.

When first used in the late 1960s, ERCP was largely a diagnostic tool, but in the past decade especially it has become almost exclusively a therapeutic intervention. Noninvasive cross-sectional imaging techniques such as helical CT scanning and MRI have displaced ERCP in the diagnostic arena. Endoscopic ultrasound offers a much less invasive endoscopic tool to investigate hepatobiliary and pancreatic pathology with minimal risk for acute pancreatitis and other ERCP-related complications.

Post-ERCP Pancreatitis: Presentation and Management

Typically, if a patient is going to develop post-ERCP pancreatitis, the probable diagnosis becomes apparent within a few hours of the procedure. It is characterized by severe abdominal pain and, frequently, back pain, nausea (with or without vomiting), and mild fever. Unfortunately, the usual 1-hour observation period after ERCP is often insufficient for post-ERCP pancreatitis to declare itself. If the patient can be kept under observation longer, or returns with symptoms, a 2-hour serum or urinary amylase level (> 1000 IU/L) is highly predictive of evolving post-ERCP pancreatitis.

Patients presenting with post-ERCP pancreatitis should receive adequate (narcotic) analgesia, treatment for nausea (if present), and copious intravenous fluids (starting with a 1-2 L bolus of Ringer's lactate solution and continuing with 250-300 mL/hr). A nasogastric tube should be placed only if the patient has unrelieved nausea or vomiting. Urine output should be monitored and charted, with the aim of at least 50 cc/hr of urine output (100 cc/hr is better). In patients unable or unwilling to spontaneously pass urine, placement of a urinary catheter is necessary to monitor urine output. Patients should be watched for signs of severe inflammatory response syndrome, which includes fever (> 38˚ C), tachycardia (> 90 beats/min), tachypnea (> 20 breaths/min), and low or high peripheral white blood cell count (< 4000/mm3 or > 12,000/mm3).

Fortunately, only a small percentage (2%-3%) of patients who develop post-ERCP pancreatitis have severe disease, which is life-threatening. Patients who present with or develop progressive multiorgan dysfunction in the setting of acute pancreatitis have a mortality rate in the range of 20%-40%. They should be managed by a multidisciplinary team in a high-dependency (eg, intensive care) hospital setting.

If the diagnosis of post-ERCP pancreatitis is in doubt, a contrast-enhanced abdominal CT scan should be performed in the first 24-48 hours. Earlier than this, important changes such as necrosis of pancreatic parenchyma and peripancreatic fluid collections may be missed. If contrast CT scanning cannot be performed because of renal impairment, magnetic resonance cholangiopancreatography is an acceptable alternative.

Minimizing the Risks and Severity

How can the risks and severity of post-ERCP pancreatitis be minimized?

First, ERCP should not be performed unless the benefit of doing so is clear. Experts spend much of their time talking patients out of having ERCP because it is "high risk/low yield" (eg, the study is not likely to produce diagnostic information or therapeutic benefit). ERCP should rarely, if ever, be the first-line investigation for abnormal liver serology (liver function tests) or unexplained dilated bile ducts. A particularly "dangerous" use of ERCP is in the investigation of obscure abdominal pain of possible biliary or pancreatic origin in young women. When laboratory testing is normal and cross-sectional imaging shows normal-caliber bile ducts, the unsuspecting endoscopist is entering the minefield of possible sphincter of Oddi dysfunction (SOD). Young women who have had their gallbladders removed (cholecystectomy) and have new or persistent abdominal pain without enzyme or imaging abnormality fall into SOD category type III, which carries the highest risk for post-ERCP pancreatitis in all patients undergoing ERCP. Such patients should be referred to specialist centers for management, which may include ERCP with sphincter pressure measurements (manometry).

Second, post-ERCP pancreatitis can be reduced by skilled use of the duodenoscope and its accessories, including a variety of catheters, guide wires, and stone retrieval devices (eg, balloons and baskets). Typically, ERCP training requires an additional (fourth) year of clinical fellowship in the United States, during which at least 200 mainly therapeutic procedures are performed under expert supervision, and trainees learn about the management of a spectrum of hepatobiliary and pancreatic disorders. Inexperienced endoscopists typically have difficulty cannulating; as a result, their patients often undergo long procedures with extensive manipulation of the duodenal papilla, which appears to be a potent trigger of post-ERCP pancreatitis. There is no substitute for proper training in ERCP.

Third, the use of 2 prophylactic measures in "high-risk" patients (eg, those undergoing needle knife papillotomy, ampullectomy, balloon dilation of the papilla) has been shown to reduce the risk for post-ERCP pancreatitis: placement of a prophylactic pancreatic duct stent, and administration of rectal indomethacin (100 mg) by suppository at the end of the procedure.

Small-caliber (3-5 French gauge) plastic pancreatic duct stents that bridge the pancreatic duct orifice have been shown to almost eliminate the risk for severe post-ERCP pancreatitis, provided that they are placed early enough in the procedure. These small-caliber stents are designed to migrate spontaneously out of the pancreatic duct and pass in the stool 3-7 days after placement. Those that fail to migrate are identified by plain abdominal x-ray or fluoroscopy and retrieved during a brief esophagogastroduodenoscopy.

Several studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the severity of post-ERCP pancreatitis. A recent prospective study published in the New England Journal of Medicine[1] showed a significant reduction in post-ERCP pancreatitis between those patients who received rectal indomethacin post-procedure and those who did not. Most of the patients in the study also received prophylactic pancreatic duct stents, so the jury is still out on the role of NSAIDs in preventing post-ERCP pancreatitis.

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