Fluid and necrotic collections can occur as complications of acute pancreatitis. According to the latest classification, these can be divided into acute or delayed, depending on whether such a collection is of less than or more than 4 weeks' duration.[1]
In the acute period, the fluid collection is not well defined and is simply described as acute peripancreatic fluid collection. It is often associated with tissue edema. After 4 weeks, the fluid collection is much more organized with a definite wall and is described as a pseudocyt. A pseudocyst is a peripancreatic fluid collection containing high concentrations of pancreatic enzymes within a defined fibrous wall and lacking an epithelial lining. When a pseudocyst gets infected, it is called a pancreatic abscess.
Similarly, pancreatic necrosis is an acute necrotic collection in which there is a variable amount of fluid and necrosis. By around 4 weeks, a walled-off pancreatic necrosis (WOPN) may form, in which the collection is defined by a fibrotic and inflammatory wall. The term "infected necrosis" refers to bacterial invasion of the necrotic pancreatic tissue.
Pancreatic abscess is often a late complication of acute necrotizing pancreatitis (ANP), occurring more than 4 weeks after the initial attack. The mortality rate associated with pancreatic abscess is generally less than that of infected necrosis. The mortality rate of pancreatitis may exceed 20% or more in the presence of infected pancreatic necrosis and is largely related to sepsis and multiorgan failure.
A number of molecules mediating the inflammatory (NF-κB, cytokines/chemokines, adhesion molecules, and novel protein kinase C isoforms) and cell death responses (eg, caspases) play a role in the pathogenesis of acute pancreatitis.
Pancreatitis begins in acinar cells and leads to the premature, intra-acinar activation of digestive zymogens into their active forms (eg, trypsinogen to trypsin); accumulation of large vacuoles in acinar cells; inflammation; and parenchymal cell death through apoptosis and necrosis.[2] The activated pancreatic enzymes cause autodigestion. These inflammatory processes lead to collection of fluid in and around the pancreas. In addition, injury to the pancreatic duct or its branches leads to leakage of pancreatic enzymes into the lesser sac and the retroperitoneum. The enzyme rich fluid and necrotic collections if persistent will eventually develop fibrosis around its periphery leading to pseudocysts and WOPN. These processes often follow severe acute pancreatitis (SAP) as opposed to mild acute pancreatitis.
Acute necrotic pancreatitis is the most severe end of a spectrum of inflammation associated with pancreatitis. Inflammation in this situation may cause cell death. The resultant devitalized tissue becomes a potential bed for infection. The amount of necrotic tissue is the strongest predictor of mortality in necrotic pancreatitis. After necrotic pancreatitis three potential outcomes exist: resolution, persistent fluid collection (pseudocyst)/necrosis (WOPN), or formation of abscess or infected necrosis.
Pseudocysts and abscesses can be single or multiple and vary greatly in size and location. Approximately 3% of patients with acute pancreatitis develop pancreatic abscess.
The inciting events for pancreatitis are legion; however, cholelithiasis and alcohol account for more than 80% of cases in the developed world.
Peripancreatic fluid encased in a fibrinous capsule defines pseudocysts. It is often the result of a ductal leak or disruption.
Superinfection of pseudocysts leads to the development of pancreatic abscesses. Evidence suggests that colonic translocation of bacterial flora accounts for many cases of pancreatic infection.
The most typical organisms isolated from infected necrosis and abscesses are enteric bacteria and Candida species.
The incidence of pancreatitis is approximately 185,000 cases per year. At least 80% of cases are due to alcohol and cholelithiasis. Acute necrotic pancreatitis (ANP) is reported by some to occur in approximately 20% of all episodes of pancreatitis. Although sterile necrosis may occur, a variable percentage develops infection of the necrotic tissue. Depending on the time course and the host's ability to encase the necrotic tissue, the lesion is either infected necrosis or an abscess.
Sex-related demographics
Differences in sexual predilection are based on the difference in the frequency of causative factors of the pancreatitis and include the following:
Women are more likely to have gallstone pancreatitis than men.
Men have alcohol-induced pancreatitis more commonly than women.
A difference in the rate of abscess formation between men and women has not been clearly demonstrated.
Risk assessment of acute pancreatitis (AP) depends upon clinical indices (eg, Ranson, Imrie, or Apache I/II Scores), the presence of extrapancreatic complications, an elevated C-reactive protein or hematocrit, an elevated procalcitonin, and the finding of pancreatic necrosis on CT scanning.
The prognosis may be worse in obese patients, after trauma, after organ transplantation, after coronary artery bypass surgery, or in idiopathic AP.[3]
Morbidity/mortality
In the first 48-72 hours after the onset of acute pancreatitis using the Sepsis-Related Organ Failure Assessment (SOFA) score and contrast-enhanced CT scan (which has the highest diagnostic accuracy) one can predict the future development of infected necrosis, multiorgan failure syndrome (MOFS) and death. Balthazar and Ranson's radiographic staging criteria predict the formation of pseudocysts and, therefore, abscesses.
Note the following:
Grade A – Normal pancreas
Grade B - Focal or diffuse enlargement
Grade C - Mild peripancreatic inflammatory changes
Grade D - Single fluid collection
Grade E - Two or more fluid collections or gas within the pancreas or within the peripancreatic inflammation. In grade A, B, C, or D, the probability of abscess formation is less than 2%. With grade E disease (2 or more collections of peripancreatic fluid), the probability rises to 57%.
Patients are at risk for sepsis and, ultimately, even death. The mortality rate approaches 100% if intervention and drainage are not undertaken for the infected necrosis or abscess.
Pseudocysts and abscesses may result in prolonged abdominal pain, rupture leading to acute peritonitis, fistula formation, and erosion into vessels with acute hemorrhage. Pancreatic ascites or pleural effusion may result. Pseudocysts or abscesses may also cause hollow viscus obstruction by compression of the surrounding structures, including the colon, stomach, duodenum, and the common bile duct.
Even with aggressive intravenous fluid replacement, nutritional support, and early intervention of pancreatic necrosis or abscess, the hospital mortality rate of SAP is about 20%.
Overall, the mortality rate from acute pancreatitis is low (< 1% for acute edematous pancreatitis), but it depends upon the proportion of patients in the group with severe pancreatitis complicated by MODS, with or without associated sepsis.
The presence of pancreatic necrosis is associated with an overall increase in mortality. The mortality rate from sterile pancreatic necrosis is 10% and rises to 30% with infection in the necrotic area.[4] One meta-analysis concluded that when organ failure and infected pancreatic necrosis are present together, it portends an even worse prognosis, with mortality reaching 43%.[5]
Complications
Complications include the following:
Fistula formation (eg, enterocutaneous following surgery, entero-entero, enterovascular)
Inform patients about the common causes of pancreatitis.
Offer cholecystectomy to patients with gallstone pancreatitis if they are surgical candidates.
Provide counseling for patients to abstain from alcohol use.
Monitor patients for steatorrhea, and inform them about the potential for pancreatic insufficiency and the potential need for pancreatic enzymes and fat-soluble vitamin supplementation.
For patient education resources, see Digestive Disorders Center, as well as Pancreatitis.
Patients with pancreatic necrosis and pseudocysts will have definitive history of pancreatitis (often with a prolonged course), hemodynamic instability, fever, failure of medical therapy, or the presence of peripancreatic fluid collections on computed tomography (CT) scan.
Acute infection can set in in the pancreatic bed and lead to infected pancreatic necrosis and sepsis. When this occurs, it usually presents 10-12 days into the course of severe pancreatitis. Pancreatic abscess formation takes weeks to develop, as does WOPN. WOPN can then later become infected.
Patients with WOPN may be asymptomatic (50%) or present with symptoms (50%) such as abdominal pain, malaise, relapsing or recurrent pancreatitis, feeding intolerance, and/or weight loss.[1, 6] In severe cases, WOPN can obstruct the gastrointestinal tract, fistulize to adjacent anatomic structures, and compress or erode into blood vessels or the bile duct.
Abdominal pain with or without a mass on palpation of the epigastrium is suggestive of parietal peritoneal irritation.
Classic physical examination findings, such as Grey-Turner sign or Cullen sign, are supposedly characteristic of pancreatitis but rarely are noted in clinical practice.
Other physical findings are nonspecific and include abnormal vital signs consistent with sepsis, abdominal guarding, and rebound tenderness.
No specific hematologic studies define infected necrosis or pancreatic abscess. A persistently elevated white blood cell count with a left shift and positive blood cultures is suggestive of this diagnosis.
The degree of pancreatic enzyme elevation does not directly indicate the degree of necrosis.
The presence of air in necrotic tissue in a pseudocyst on imaging studies is specific for infection. The absence of a communication with the gut (often by spontaneous drainage into the gut lumen) is also a sign of infection.
Abdominal computed tomography (CT) scanning with intravenous (IV) contrast; ultrasonography, either endoscopic or transabdominal; and magnetic resonance imaging (MRI) (with gadolinium) are potential modes for imaging pancreatic necrosis or abscess.
MRI is becoming the imaging study of choice due to concerns regarding the use of iodinated contrast, which is said, by some, to devitalize marginal tissue, increasing the burden of necrotic tissue.
CT scanning and MRI
The current criterion standard for initial evaluation is contrast-enhanced CT scan (see the following image), which may reveal ischemic pancreatic tissue as evidenced by the lack of uptake of contrast. There is some suggestion that early CT scan may be detrimental in ANP, with IV contrast worsening the ischemia.
View Image
Contrast-enhanced CT scan of an infected pancreatic pseudocyst.
Consider repeat imaging in all patients with ANP who develop worsening abdominal pain, develop signs or symptoms of obstruction, or have a prolonged clinical course.
MRI may be of some additional benefit in the acute evaluation of ANP; gadolinium does not cause a worsening of ischemia in experimental models.
Splenic vein thrombosis is seen in 40% of patients with WOPN.
Pancreatic necrosis appears as devitalized tissue with decreased IV contrast present on CT scan or MRI. A pancreatic pseudocyst has a rim of fibrous tissue surrounding a pocket of peripancreatic fluid.
Earlier accumulations of fluid without the fibrous capsule, or peripancreatic fluid collections, and the surrounding inflammatory tissue were referred to as a phlegmon, but this term is now obsolete.
Demonstrable necrotic tissue in the pseudocyst may exist. Typically, this develops more than 3 weeks after the initial bout of pancreatitis.
In the absence of cholangitis or jaundice, the 2013 American College of Gastroenterology (ACG) guidelines recommend magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasonography, rather than diagnostic endoscopic retrograde cholangiopancreatography (ERCP) to screen for choledocholithiasis as the suspected etiology of acute pancreatitis.[7]
Endoscopic drainage
EUS-guided transgastric drainage of a pancreatic abscess, with the insertion of 2 double-pigtail catheters has also been reported to be useful.[8] The introduction of fully covered self-expandable metallic stents (FCSEMS) with their larger diameters has facilitated drainage and endoscope insertion into the cavities of walled-off pancreatic necroses for direct endoscopic necrosectomy.[9, 10]
Endoscopic necrosectomy and drainage may give impressive and immediate symptom relief.[6, 11]
No randomized trials have evaluated the minimally invasive techniques for infected pancreatic necrosis, and not all guidelines from professional organizations show "consensus to recommend this minimally invasive management of pancreatic abscess."[12, 13]
This lack of agreement likely relates to the fact that successful treatment of symptomatic, sterile or infected walled-off pancreatic necrosis with transoral/transmural endoscopic drainage needs to be followed by percutaneous drainage in 40% or by operative interventions in 20%.[14, 15, 16]
In cases of WOPN, creating multiple gateways for drainage of necrotic debris improves treatment success.[17]
Endoscopic drainage of pancreatic fluid collections in persons with acute or chronic pancreatitis is an accepted alternative treatment option to surgical intervention; it provides a successful drainage of the fluid and relief of symptoms in almost 90% of patients.[18] Complications occur in 11% of patients, including death in 5%. Not removing the transmural stents decreases the recurrence of pancreatic fluid collection.[17]
Endoscopic ultrasound-guided drainage is also the mainstay for symptomatic and/or enlarging chronic pancreatic fluid collections (which require intervention).[19] It is also the mainstay for drainage of walled-off pancreatic fluid collections, with similar efficacy to surgical and percutaneous management but with lower morbidity and expense.[9]
In general, pseudocysts require only transmural drainage, but adjunctive direct endoscopic necrosectomy may be necessary for walled-off pancreatic necrosis.[9] More recently, endoscopic ultrasound-guided drainage has been combined with a transduodenoscope cyclic irrigation technique for walled pancreatic necrosis, with treatment success in 16 of 17 patients (94.1%) and without the need for subsequent surgery; no complications such as perforation, bleeding, or multiorgan failure were reported.[20]
The use of fully covered biflanged metal stents appears to be superior to the placement of multiple plastic stents for the endoscopic ultrasound-guided drainage of walled-off pancreatic necrosis in terms of greater clinical success (94% vs 73.7%), fewer direct endoscopic necrosectomies (1.46 vs 2.74) and less frequent salvage surgeries (2.7% vs 26.2%) required; fewer adverse events (5.6% vs 36.1%), and shorter hospital stays (4.1 vs 8 days).[21]
In persons with SAP having intervention because of infection or abscess, 20% will develop an external pancreatic fistula (EPF).[22]
Spontaneous closure of the EPF occurs in 88% of persons in a median of 70 days. Of these 88% whose EPF closes, approximately 24% develop a pancreatic pseudocyst requiring surgical management.
CT-guided or ultrasonography-guided needle aspiration
The presence of either bacterial or fungal flora in pancreatic fluid collections usually aspirated via CT-guided needle biopsy is the sine qua non of pancreatic abscess. The presence of organisms on either Gram stain or culture is essential to establish a diagnosis of abscess.
Pancreatic fluid collections are frequent sequelae of pancreatitis, and endoscopic drainage of these collections is gaining acceptance as an alternative to surgical drainage. Endoscopic ultrasound (EUS)-guided drainage should be reserved for prepancreatic fluid collections located at the pancreatic tail. These fluid collections should be evaluated by EUS before attempts at endoscopic drainage.
In the last two decades, the indications for surgery have become less aggressive, focusing more on the treatment of complications such as necrosis, abscess, and pseudocyst.[23]
Surgical drainage
Even with aggressive intravenous fluid replacement, nutritional support and early intervention of pancreatic necrosis or abscess, the hospital mortality rate of SAP is about 20%.
Sterile necrosis may be followed with serial CT-guided drainage and continued antibiotics.
Surgical drainage of infected necrosis or an abscess is the procedure for cure. Placement of indwelling drains after the initial procedure may be necessary for complete resolution.
In the acute phase of pancreatitis, the medical care of patients with evidence of pancreatic necrosis is no different from that of those without necrosis. Intravenous hydration aimed at maintaining the patient's intravascular volume and perfusion pressures is the mainstay of treatment of all cases of acute pancreatitis.
The 2013 American College of Gastroenterology (ACG) guidelines include the following recommendations for the initial management of acute pancreatitis[7] :
Administer aggressive hydration, defined as the administration of isotonic crystalloid solution at a rate of 250–500 mL per hour, except in patients with cardiovascular, renal, or other related comorbidities. The greatest benefit of aggressive intravenous hydration is in the first 12–24 hours; there may be little benefit beyond this period.
In patients with severe volume depletion presenting as hypotension and tachycardia, it may be necessary to administer a bolus.
Lactated Ringer solution may be the preferred isotonic crystalloid replacement fluid.
Frequently reassess fluid requirements within 6 hours of admission and for the next 24–48 hours with the goal of reducing blood urea nitrogen levels.
Moreover, the ACR recommends the following for antimicrobial/antifungal management of acute pancreatitis[7] :
The routine use of prophylactic antibiotics and the routine use of antifungal agents along with prophylactic or therapeutic antibiotics in patients with severe acute pancreatitis are not recommended. In addition, it is not recommended to use antibiotics in patients with sterile necrosis to prevent infected necrosis.
Administer antibiotics for extrapancreatic infections (eg, cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia).
Consider infected necrosis in patients with pancreatic or extrapancreatic necrosis whose condition deteriorates or who fail to improve after 7–10 days of hospitalization. Obtain initial CT-guided fine-needle aspiration (FNA) for Gram stain and culture, or administer empiric antibiotic therapy after obtaining cultures for infectious agents, without CT FNA.
In patients with infected necrosis, administer antibiotics known to penetrate pancreatic necrosis (eg, carbapenems, quinolones, metronidazole), which may delay or avoid intervention, thereby decreasing morbidity and mortality.
Consultations
Obtain consultations with a gastroenterologist, general surgeon, and interventional radiologist.
Transfer
Patients usually should be in an ICU setting because they may decompensate quickly and require aggressive treatment, including mechanical ventilation.
A paradigm shift is occurring in the treatment of pancreatic necrosis and peripancreatic infections. In most tertiary care centers, open surgical procedures are being replaced by endoscopic or percutaneous procedures. Surgery is now reserved for cases in which an endoscopic or percutaneous approach is not feasible (ie, infection of the pancreatic bed before a well-formed, walled-off collection is formed; abdominal compartment syndromes). Open procedures, especially early on, carry significant mortality and morbidity and should be delayed until the patient's clinical situation is stable.
Transluminal drainage/necrosectomy by NOTES (natural orifice transluminal endoscopic surgery) approach is evolving as the preferred strategy for the management of pancreatic necrosis and abscesses. This procedure is ideally performed under endoscopic ultrasonographic (EUS) guidance.
EUS-guided necrosectomy
EUS-guided necrosectomy in specialized centers is the standard treatment for pancreatic necrosis and abscess. CT-guided drainage is the next best strategy when a good transluminal window is not available for EUS-guided transgastric drainage, if the need for drainage is very early in the course of pancreatitis, or if the patient is too sick to undergo an endoscopic procedure, which often requires at least deep sedation.
Under EUS, an ideal site for access into the peripancreatic collection is identified. An area of adherence of the wall of the stomach or the intestine to the wall of the WOPN or infected pseudocyst is required. Endoscopic access is best performed when the wall is mature, usually 4 weeks or more after the episode of pancreatitis. An endoscopic transgastric access can be created even as early as 2 weeks following pancreatitis, but intervention other than placement of stents may be high risk, with the possibility of dehiscence into the peritoneum.
If a mature collection is accessed by EUS, a cystgastrostomy is created by dilating a tract up to 20 mm over a wire passed into the collection usually via a 19-gauge needle. This is accomplished with a wire-guided dilating balloon.
Once a large enough cystgastrostomy is made, a regular upper endoscope can be passed under direct vision into the necrotic or abscess cavity. The cavity is then debrided if necrotic material is present. The necrosum is pulled back and either removed or discarded in the gut lumen. At the end of the necrosectomy, two double pigtail stents are placed to prevent premature closure and to allow further drainage. Note that placement of the transmural stents decreases the recurrence of pancreatic fluid collection.[17]
Complete necrosectomy may be accomplished in one or more sessions on the basis of the available time, amount of necrosum and ease of necrosectomy. One or more cystgastrostomies can be made for multiple gateways.[17]
The most recent technique is that of placing a transluminal fully covered metal stent, which is specifically designed to be stationed across the cystgastrostomy and maintains a wide opening to allow drainage, with or without necrosectomy.
Endoscopic intervention leads to immediate symptomatic relief, especially abdominal pain caused by a tense or infected collection.[6, 8, 11]
A Dutch randomized trial has evaluated minimally invasive techniques for infected pancreatic necrosis and favors their use.[24] The endoscopic approach results in lower morbidity rates, a faster recovery, and a shorter hospital stay.
Darrivere et al conducted a single-center observational study and concluded that minimally invasive drainage, such as percutaneous radiological drainage and endoscopic necrosectomy, was associated with improved outcomes compared to open surgery in critically ill patients with infected pancreatic necrosis.[25]
If the interventionalist does not complete the necrosectomy, additional intervention may be needed. In earlier studies, sterile or infected walled-off pancreatic necrosis with transoral/transmural endoscopic drainage required percutaneous drainage in 40% of cases or operative intervention in 20%.[14, 15, 16] These days, primary drainage involving an open procedure should be avoided, if at all possible.
Minimally invasive alternatives for endoscopic drainage
Percutaneous drainage followed by percutaneous or sinus tract endoscopy with necrosectomy is an option and a potential minimally invasive alternative for endoscopic drainage, but there may be an associated higher risk of forming a pancreaticocutaneous fistula.
Alternative minimally invasive approaches include retroperitoneal laparoscopic necrosectomy and drainage, in which the entire necrosectomy is performed via percutaneous access without entry into the abdominal cavity.
Another surgical strategy involves establishing percutaneous access into the stomach using a laparoscopic approach and then performing a laparoscopic transgastric necrosectomy using rigid devices.
Other considerations
Even in the setting of infection, one should implement medical management with antibiotics and delay any surgical intervention as much as possible.
An ERCP is needed in most patients with pancreatic necrosis to evaluate and establish continuity of the pancreatic duct if there is ductal discontinuity. Endoscopic sphincterotomy plays a role in patients with gallstone pancreatitis, as well as for those with infected pancreatic necrosis, pancreatic abscess, pseudocysts, and traumatic pancreatitis with a ruptured duct system.
The 2013 American College of Gastroenterology (ACR) guidelines include the following recommendations regarding nutritional management for patients with acute pancreatitis[7] :
For patients with mild disease, start oral feedings immediately in the absence of nausea/vomiting and with the resolution of abdominal pain. A low-fat solid diet appears to be as safe as a clear liquid diet.
For patients with severe pancreatitis, use enteral nutrition to prevent infectious complications. Avoid parenteral nutrition unless the enteral route is not available, is not tolerated, or caloric requirements are not being met.
Nasogastric delivery and nasojejunal delivery of enteral feeding appear to be equally safe and effective.
Activity
Patients generally are hospitalized and unable to perform usual activities.
Antibiotics are the primary medical therapy in pancreatic abscess, used for the control of bacteremia and sepsis. Supportive care with fluids is needed, and the use of vasopressors may be required.
Clinical Context:
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against P mirabilis, Haemophilus influenzae, E coli, K pneumoniae, and Moraxella catarrhalis. The condition of the patient, severity of infection, and susceptibility of microorganism determines the proper dose and route of administration. Shown in clinical trials to decrease mortality rates in ANP. Whether antioxidant effect may play a role in efficacy is questionable.
Clinical Context:
Third-generation cephalosporin with broad coverage and better gram-negative coverage than cefuroxime. Has antipseudomonal activity; however, resistance to ceftazidime is as high as 15%. Some data support use in combination with amikacin and metronidazole in ANP.
Clinical Context:
A pyridine carboxylic acid derivative with broad-spectrum bactericidal effect. All quinolones have good activity against common flora found in pancreatic abscess, with the exception of Candida species.
Clinical Context:
An extended-spectrum penicillin. Inhibits biosynthesis of cell-wall mucopeptide and is effective during the stage of active multiplication.
Abraham Mathew, MD, MS, Professor of Medicine, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Hershey Medical Center, Pennsylvania State University College of Medicine
Disclosure: Received ownership interest from Hershey Endoscopy Center for partner of ambulatory surgery center, practice site; Received consulting fee from Boston Scientific for consulting.
Specialty Editors
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.
Douglas M Heuman, MD, FACP, FACG, AGAF, Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.
Chief Editor
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Jose A Perez, Jr, MD, MBA, MSEd, Residency Director, Internal Medicine Residency Program, Vice Chair of Education, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College
Disclosure: Nothing to disclose.
Acknowledgements
Eric R Frizzell, MD
Instructor of Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Department of Medicine, Division of Gastroenterology, Walter Reed Army Medical Center
Eric R Frizzell, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada
Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada
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