Pancreatic Necrosis and Pancreatic Abscess 

Updated: Jul 01, 2021
Author: Abraham Mathew, MD, MS; Chief Editor: BS Anand, MD 

Overview

Background

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 pseudocyst. 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.

Pathophysiology

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 the acinar cells; inflammation; and parenchymal cell death through apoptosis and necrosis.[2] The activated pancreatic enzymes cause autodigestion. These inflammatory processes lead to the 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.

Etiology

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.

Epidemiology

United States data

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.

Prognosis

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)

  • Recurrent pancreatitis

  • Bowel obstruction

  • Death

Patient Education

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.

 

Presentation

History

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.

Physical Examination

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.

 

DDx

Diagnostic Considerations

Important considerations

Obtain further imaging studies if a patient's pancreatitis is not improving.

Obtain sample fluid collection(s), if possible, for evidence of necrosis or abscess formation.

Consider surgery for definitive treatment.

Differential Diagnoses

 

Workup

Laboratory Studies

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.

Imaging Studies

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.

Contrast-enhanced CT scan of an infected pancreati 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.

Procedures

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]  See Guidelines.

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 the 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.

 

Treatment

Medical Care

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.

Surgical Care

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.[24] 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.[25] 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.[26]

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.

Diet and Activity

Diet

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.

 

Guidelines

WSES Guidelines

In June 2019, the World Society of Emergency Surgery (WSES) released updated guidelines for the management of severe acute pancreatitis.[27] Their strong recommendations are summarized below.

Severity grading

Grade 1C recommendations

Severe acute pancreatitis is associated with persistent organ failure (cardiovascular, respiratory, and/or renal), and high mortality. Both new classification systems, Revised Atlanta Classification and Determinant-based Classification of Acute Pancreatitis Severity, are similar in establishing the diagnosis and severity of acute pancreatitis.

Patients who have persistent organ failure with infected necrosis have the highest risk of death.

Patients with organ failures should be admitted to an intensive care unit (ICU) whenever possible.

Diagnostic laboratory parameters

The cut-off value of serum amylase and lipase is normally defined to be three times the upper limit.

A hematocrit level above  44% represents an independent risk factor of pancreatic necrosis (grade 1B recommendation).

Imaging

Grade 1C recommendations

On admission, perform ultrasonography (US) to determine the etiology of acute pancreatitis (biliary).

When doubt exists, computed tomography (CT) scanning provides good evidence of the presence or absence of pancreatitis.

Assess all patients with severe acute pancreatitis with contrast-enhanced CT (CE-CT) scanning or magnetic resonance imaging (MRI). Optimal timing for first the CE-CT assessment is 72-96 hours after symptomatic onset.

Consider MR cholangiopancreatography (MRCP) or endoscopic ultrasonography to screen for occult common bile duct stones in patients with unknown etiology.

Follow-up imaging (all grade 1C recommendations)

In severe acute pancreatitis (CT scan severity index ≥ 3), a follow-up CE-CT scan is indicated 7-10 days from the initial CT scan.

Additional CE-CT scans are recommended only if the patient's clinical status deteriorates or fails to show continued improvement, or when invasive intervention is considered.

Surgical intervention

The following are indications for surgical intervention (all grade IC recommendations):

  • As a continuum in a step-up approach after percutaneous/endoscopic procedure with the same indications

  • Abdominal compartment syndrome

  • Acute ongoing bleeding when an endovascular approach is unsuccessful

  • Bowel ischemia or acute necrotizing cholecystitis during acute pancreatitis

  • Bowel fistula extending into a peripancreatic collection

The following are indications for emergent endoscopic retrograde cholangiopancreatography (ERCP):

  • Routine ERCP with acute gallstone pancreatitis is not indicated (grade 1A recommendation).

  • ERCP in patients with acute gallstone pancreatitis and cholangitis is indicated (grade 1B recommendation).

Surgical strategies include the following:

  • Infected pancreatic necrosis: Percutaneous drainage as the first-line treatment (step-up approach) delays the surgical treatment to a more favorable time or results in complete resolution of the infection in 25-60% of patients; it is recommended as the first line of treatment (grade 1A recommendation).

  • Minimally invasive surgical strategies (transgastric endoscopic necrosectomy, video-assisted retroperitoneal debridement [VARD]): These result in less postoperative new-onset organ failure but require more interventions (grade 1B recommendation).

  • Mortality: There is insufficient evidence to support an open surgical, mini-invasive, or endoscopic approach (grade 1B recommendation).

Consideration of the timing of cholecystectomy includes the following:

  • Laparoscopic cholecystectomy during the index admission is recommended in mild acute gallstone pancreatitis (grade 1A recommendation).

  • When ERCP and sphincterotomy are performed during the index admission, the risk for recurrent pancreatitis is reduced; same admission cholecystectomy is still advised owing to an increased risk for other biliary complications (grade 1B recommendation).

Open abdomen

Considerations regarding open abdominal surgery include the following:

  • Clinicians should be cautious not to over-resuscitate patients with early severe acute pancreatitis and to measure intra-abdominal pressure regularly (grade 1C recommendation).

  • Avoid the open abdomen if other strategies can be used to mitigate or treat severe intra-abdominal hypertension (IAH) in severe acute pancreatitis (grade 1C recommendation).

  • It is recommended not to use the open abdomen after necrosectomy for severe acute pancreatitis (unless severe IAH mandates open abdomen as a mandatory procedure) (grade 1C recommendation).

  • It is recommend not to debride or undertake early necrosectomy if forced to undertake an early open abdomen due abdominal compartment syndrome or visceral ischemia (grade 1A recommendation).

  • The use of negative pressure peritoneal therapy is recommended for open abdomen management (grade 1B recommendation).

Timing for abdominal closure (grade 1B recommendation)

Early fascial and/or abdominal definitive closure should be the strategy for management of the open abdomen once any requirements for ongoing resuscitation have ceased, the source control has been definitively reached, no concern regarding intestinal viability persist, no further surgical reexploration is needed, and there are no concerns for abdominal compartment syndrome.

AGA Guidelines

2018 AGA guidelines (initial AP management)

In March 2018, the American Gastroenterological Association (AGA) released guidelines on the initial management of acute pancreatitis (AP).[28] These are outlined below.

The diagnosis of AP requires at least two of the following features: characteristic abdominal pain; biochemical evidence of pancreatitis (ie, amylase or lipase elevated >3 times the upper limit of normal); and/or radiographic evidence of pancreatitis on cross-sectional imaging.

Presentations of AP occur along a clinical spectrum and can be categorized as mild, moderately severe, or severe, based on the recent revised Atlanta classification.

Most cases of AP (around 80%) are mild, with only interstitial changes of the pancreas without local or systemic complications.

Moderately severe pancreatitis is characterized by transient local or systemic complications or transient organ failure (< 48 hours), and severe AP is associated with persistent organ failure.

Necrotizing pancreatitis is characterized by the presence of pancreatic and/or peripancreatic necrosis, and is typically seen in patients with moderately severe or severe AP.

There are two overlapping phases of AP, early and late. The early phase of AP takes place in the first 2 weeks after disease onset, and the late phase can last weeks to months thereafter.

In patients with AP, the AGA suggests against the use of hydroxymethyl starch (HES) fluids.

In patients with predicted severe AP and necrotizing AP, the AGA suggests against the use of prophylactic antibiotics.

In patients with acute biliary pancreatitis and no cholangitis, the AGA suggests against the routine use of urgent endoscopic retrograde cholangiopancreatography (ERCP).

In patients with AP, the AGA recommends early (within 24 hours) oral feeding as tolerated, rather than keeping the patient nil per os (NPO).

In patients with AP and inability to feed orally, the AGA recommends enteral rather than parenteral nutrition.

In patients with predicted severe or necrotizing pancreatitis requiring enteral tube feeding, the AGA suggests either nasogastric or nasojejunal route.

In patients with acute biliary pancreatitis, the AGA recommends cholecystectomy during the initial admission rather than after discharge.

In patients with acute alcoholic pancreatitis, the AGA recommends brief alcohol intervention during admission.

2015 AGA guidelines (pancreatic cysts)

As of 2015, the AGA recommends the following in the diagnosis and management of asymptomatic neoplastic pancreatic cysts[22] :

  • For asymptomatic mucinous cysts, a 2-year interval is recommended for a cyst of any size undergoing surveillance, with surveillance being stopped after 5 years if there is no change.

  • Perform surgery only if there is more than one concerning feature on MRI confirmed on endoscopic ultrasonography (EUS) and only in centers with high volumes of pancreatic surgery, and there should be no surveillance after surgery if there is no invasive cancer or dysplasia.

  • The risk of malignant transformation of pancreatic cysts is approximately 0.24% per year, and the risk of cancer in cysts without a significant change over a 5-year period is likely to be lower.

  • The small risk of malignant progression in stable cysts is likely outweighed by the costs of surveillance and the risks of surgery.

  • Positive cytology on EUS-guided fine-needle aspiration (FNA) has the highest specificity for diagnosing malignancy; if there is a combination of high-risk features on imaging, that is likely to increase the risk of malignancy even further. Similarly, if a cyst has both a solid component and a dilated pancreatic duct (confirmed on both EUS and MRI), the specificity for malignancy is likely to be high even in the absence of positive cytology.

  • There is lower immediate postoperative mortality, as well as long-term mortality, for patients who undergo surgery in high-volume pancreatic centers.

  • It seems sensible to offer screening even after the cyst has been resected, provided the patients have not undergone total pancreatectomy. Surveillance should continue as long as the patient remains a good candidate for surgery. MRI every 2 years may be a reasonable approach for these patients. The clinician may elect to offer more frequent surveillance in the case of invasive cancer resection, particularly if there is concern that the lesion has not been fully resected.

ACG Guidelines

In 2013, the American College of Gastroenterology (ACG) issued guidelines for the management of acute pancreatitis (AP), including the following[7] :

  • Because AP can usually be diagnosed based on clinical symptoms and laboratory testing, contrast-enhanced computed tomography (CT) scanning and/or magnetic resonance imaging (MRI) of the pancreas should be performed only in the absence of clinical improvement or if the diagnosis is unclear

  • Assessment of the patient’s hemodynamic status should occur immediately upon presentation, with resuscitative measures initiated as necessary

  • Patients with systemic inflammatory response syndrome (SIRS) and/or organ failure should, if possible, be admitted to an intensive care unit (ICU) or an intermediary care setting

  • All patients should receive aggressive hydration, unless this is precluded by cardiovascular and/or renal comorbidities; aggressive intravenous (IV) hydration is most effective within the first 12-24 hours, with possibly little benefit derived from its administration after this point

  • Within 24 hours of admission, patients with concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP); in high-risk patients, the risk of severe post-ERCP pancreatitis should be reduced through the use of postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories and/or pancreatic duct stents

  • The guidelines recommend against routinely using prophylactic antibiotics in cases of severe acute pancreatitis and/or sterile necrosis; however, intervention in patients with infected necrosis may be delayed through the use of antibiotics that do not penetrate the necrotic tissue

  • In mild cases of acute pancreatitis with no nausea and vomiting, oral feeding can be initiated immediately; enteral nutrition should be used in severe cases to prevent infectious complications, and parenteral nutrition should be avoided

  • Regardless of the lesion's size, location, and/or extension, intervention is not necessary for asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts

  • Surgical, radiologic, and/or endoscopic drainage in stable patients with infected necrosis should be postponed (for 4 weeks if possible) to permit a wall to develop around the necrosis

 

Medication

Medication Summary

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.

Antibiotics

Class Summary

Patients typically are bacteremic and/or septic.

Imipenem and Cilastin (Primaxin)

Drug of choice (DOC) because of broad coverage, excellent penetration, and best clinical data to support use.

Cefuroxime (Ceftin)

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.

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

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.

Ofloxacin (Floxin)

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.

Ticarcillin, clavulanate potassium (Timentin)

Extended-spectrum penicillin. Inhibits biosynthesis of cell-wall mucopeptide and is effective during the stage of active growth.

Piperacillin/Tazobactam (Zosyn)

An extended-spectrum penicillin. Inhibits biosynthesis of cell-wall mucopeptide and is effective during the stage of active multiplication.