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Santhi Swaroop Vege, MD
David C Whitcomb, MD, PhD
Shilpa Grover, MD, MPH
INTRODUCTION — Acute pancreatitis is an acute inflammatory process of the pancreas. Mortality ranges from 3 percent in patients with interstitial edematous pancreatitis to 17 percent in patients who develop pancreatic necrosis [1,2].
This topic reviews the management of acute pancreatitis. Our recommendations are largely consistent with the American Gastroenterological Association (AGA), the American College of Gastroenterology (ACG), and the International Association of Pancreatology/American Pancreatic Association guidelines for the treatment of acute pancreatitis [3-5]. The etiology, clinical manifestations, diagnosis, and assessment of severity of acute pancreatitis are discussed separately. (See "Etiology of acute pancreatitis" and "Clinical manifestations and diagnosis of acute pancreatitis" and "Predicting the severity of acute pancreatitis".)
CLASSIFICATION — According to the Atlanta classification, acute pancreatitis can be divided into two broad categories [6]:
●Interstitial edematous acute pancreatitis, which is characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues, but without recognizable tissue necrosis.
●Necrotizing acute pancreatitis, which is characterized by inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis.
According to the severity, acute pancreatitis is divided into the following:
●Mild acute pancreatitis, which is characterized by the absence of organ failure and local or systemic complications
●Moderately severe acute pancreatitis, which is characterized by no organ failure or transient organ failure (<48 hours) and/or local complications
●Severe acute pancreatitis, which is characterized by persistent organ failure (>48 hours) that may involve one or multiple organs
ASSESSMENT OF DISEASE SEVERITY — At initial evaluation, the severity of acute pancreatitis should be assessed by clinical examination to assess for early fluid losses, organ failure (particularly cardiovascular, respiratory, or renal compromise) (table 1), measurement of the APACHE II score (calculator 1), and systemic inflammatory response syndrome (SIRS) score (table 2) [7].
Although measurement of amylase and lipase is useful for diagnosis of pancreatitis, serial measurements in patients with acute pancreatitis are not useful to predict disease severity, prognosis, or for altering management.
Routine abdominal computed tomography (CT) scan is not recommended at initial presentation in patients with acute pancreatitis unless there is diagnostic uncertainty because there is no evidence that CT improves clinical outcomes and the complete extent of pancreatic and peripancreatic necrosis may only become clear 72 hours after the onset of acute pancreatitis [5]. Several other scoring systems also exist to predict the severity of acute pancreatitis based upon clinical, laboratory, radiologic risk factors, and serum markers but can be used only 24 to 48 hours after disease onset and have not been shown to be consistently superior to assessment of SIRS or the APACHE II score. The assessment of disease severity in acute pancreatitis is discussed in detail, separately. (See "Predicting the severity of acute pancreatitis".)
Indications for monitored or intensive care — Admission to an intensive care unit setting is indicated in the following patients [5,7,8]:
●Patients with severe acute pancreatitis
●Patients with acute pancreatitis and one or more of the following parameters:
•Pulse <40 or >150 beats/minute
•Systolic arterial pressure <80 mmHg or mean arterial pressure <60 mmHg or diastolic arterial pressure >120 mmHg
•Respiratory rate >35 breaths/minute
•Serum sodium <110 mmol/L or >170 mmol/L
•Serum potassium <2.0 mmol/L or >7.0 mmol/L
•PaO2 <50 mmHg
•pH <7.1 or >7.7
•Serum glucose >800 mg/dL
•Serum calcium >15 mg/dL
•Anuria
•Coma
In patients with severe acute pancreatitis, intensive care unit monitoring and support of pulmonary, renal, circulatory, and hepatobiliary function may minimize systemic sequelae [7]. Transfer to a monitored or intensive care unit should also be considered in the following patients [9]:
●APACHE II score >8 in the first 24 hours of admission (calculator 1)
●Persistent (>48 hours) SIRS (table 2)
●Elevated hematocrit (>44 percent), blood urea nitrogen (BUN) (>20 mg/dL), or creatinine (>1.8 mg/dL)
●Age >60 years
●Underlying cardiac or pulmonary disease, obesity
INITIAL MANAGEMENT — Initial management of a patient with acute pancreatitis consists of supportive care with fluid resuscitation, pain control, and nutritional support.
Fluid replacement — We provide aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (eg, normal saline or lactated Ringer’s solution) to all patients with acute pancreatitis, unless cardiovascular, renal, or other related comorbid factors preclude aggressive fluid replacement. In patients with severe volume depletion that manifests as hypotension and tachycardia, we provide more rapid repletion with 20 mL/kg of intravenous fluid given over 30 minutes followed by 3 mL/kg/hour for 8 to 12 hours. In rare patients with acute pancreatitis due to hypercalcemia, lactated Ringer’s is contraindicated because it contains 3 mEq/L calcium. In these patients, normal saline should be used for volume resuscitation. Several other approaches to fluid replacement have also been reported in patients with acute pancreatitis [10,11].
Fluid requirements should be reassessed at frequent intervals in the first six hours of admission and for the next 24 to 48 hours. The rate of fluid resuscitation should be adjusted based on clinical assessment, hematocrit and blood urea nitrogen (BUN) values [12]. Adequate fluid replacement can be assessed by an improvement in vital signs (goal heart rate <120 beats/minute, mean arterial pressure between 65 to 85 mmHg), urine output (>0.5 to 1 cc/kg/hour) and reduction in hematocrit (goal 35 to 44 percent) and BUN over 24 hours, particularly if they were high at the onset [5,13]. Monitoring the BUN may be particularly important, as both the BUN at the time of admission and the change in BUN during the first 24 hours of hospitalization predict mortality [14]. Increased fluid resuscitation should be considered in patients whose BUN levels stay the same or increase. It is important to note that a low urine output may reflect the development of acute tubular necrosis rather than persistent volume depletion. In this setting, aggressive fluid replacement can lead to peripheral and pulmonary edema without improving the urine output. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure)".)
In the initial stages (within the first 12 to 24 hours) of acute pancreatitis, fluid replacement has been associated with a reduction in morbidity and mortality [5,15-17].
There is some evidence that fluid resuscitation with lactated Ringer’s solution may reduce the incidence of SIRS as compared with normal saline [12]. In one small randomized trial of 40 patients, patients who received lactated Ringer’s had significantly lower mean C-reactive protein (CRP) levels compared with patients who received normal saline (52 versus 104 mg/dL) and a significant reduction in systemic inflammatory response syndrome (SIRS) after 24 hours (84 versus 0 percent).
Inadequate hydration can lead to hypotension and acute tubular necrosis. Persistent hemoconcentration at 24 hours has been associated with development of necrotizing pancreatitis [18]. Necrotizing pancreatitis results in vascular leak syndrome leading to increased third space fluid losses and worsening of pancreatic hypoperfusion [19]. However, it is important to limit fluid resuscitation mainly to the first 24 to 48 hours after onset of the disease. Continued aggressive fluid resuscitation after 48 hours may not be advisable as overly-vigorous fluid resuscitation is associated with an increased need for intubation and increased risk of abdominal compartment syndrome.
Pain control — Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics. Uncontrolled pain can contribute to the hemodynamic instability.
●Attention to adequate fluid resuscitation should be the first priority in addressing abdominal pain, as hypovolemia from vascular leak and hemoconcentration can cause ischemic pain and resultant lactic acidosis. (See 'Fluid replacement' above.)
●Opioids are safe and effective at providing pain control in patients with acute pancreatitis [20]. Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given both as a bolus as well as constant infusion. The typical dose for the bolus regimen ranges from 20 to 50 micrograms with a 10-minute lock-out period (time from the end of one dose infusion to the time the machine starts responding to another demand). Patients on patient-controlled analgesia should be carefully monitored for side effects. (See "Pain control in the critically ill adult patient", section on 'Opioid side effects'.)
Meperidine has been favored over morphine for analgesia in pancreatitis because studies showed that morphine caused an increase in sphincter of Oddi pressure. However, there are no clinical studies to suggest that morphine can aggravate or cause pancreatitis or cholecystitis [21]. In addition, meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite normeperidine that causes neuromuscular side effects and, rarely, seizures.
Monitoring — Patients with acute pancreatitis should be monitored closely in the first 24 to 48 hours. Patients with organ failure will need ongoing monitoring for other complications that might arise. (See 'Management of complications' below.)
●Vital signs including oxygen saturation should be monitored and supplemental oxygen administered to maintain arterial oxygen saturation of greater than 95 percent. Blood gas analysis should be performed if oxygen saturation is less than 90 percent or if the clinical situation demands. Hypoxia may be due to splinting, atelectasis, pleural effusions, opening of intrapulmonary shunts, or acute respiratory distress syndrome (ARDS). Patients with persistent or progressive hypoxia should be transferred to an intensive care unit (ICU) for ventilatory support. (See "Acute respiratory distress syndrome: Clinical features and diagnosis" and "Supportive care and oxygenation in acute respiratory distress syndrome" and 'Indications for monitored or intensive care' above.)
●Urine output should be measured hourly and fluids should be titrated to maintain urine output (>0.5 to 1 cc/kg/hour) [5]. (See 'Fluid replacement' above.)
●Electrolytes should be monitored frequently in the first 48 to 72 hours and especially with aggressive fluid resuscitation. Hypocalcemia should be corrected if ionized calcium is low or if there are signs of neuromuscular irritability (Chvostek's or Trousseau's sign). Low magnesium levels can also cause hypocalcemia and should be corrected. (See "Treatment of hypocalcemia", section on 'Intravenous calcium'.)
●Serum glucose levels should be monitored hourly in patients with severe pancreatitis and hyperglycemia (blood glucose greater than 180 to 200 mg/dL) should be treated as it can increase the risk of secondary pancreatic infections. Hyperglycemia may result from parenteral nutritional therapy, decreased insulin release, increased gluconeogenesis, and decreased glucose utilization. The management of hyperglycemia is discussed in detail, separately. (See "Glycemic control and intensive insulin therapy in critical illness", section on 'General approach'.)
●Patients in the intensive care unit should be monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures [22]. (See 'Abdominal compartment syndrome' below.)
Nutrition — Patients with mild pancreatitis can often be managed with intravenous hydration alone since recovery occurs rapidly, allowing patients to resume an oral diet within a week. Nutritional support is often required in patients with moderately severe pancreatitis and almost invariably needed in patients with severe pancreatitis as they are unlikely to resume oral intake within five to seven days. Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to total parenteral nutrition (TPN).
Oral — The time to reinitiate oral feedings depends on the severity of the pancreatitis. (See 'Assessment of disease severity' above.)
●In mild pancreatitis, in the absence of ileus, nausea or vomiting, oral feeds can be initiated as soon as the pain is decreasing and inflammatory markers are improving [5]. This usually occurs 24 to 48 hours after the onset of pancreatitis. We usually start with a low residue, low fat, soft diet, provided there is no evidence of ileus or significant nausea and/or vomiting. We then advance the diet cautiously as tolerated. Traditionally, patients have been advanced from a clear liquid diet to solid food as tolerated. More recent data suggest that early refeeding when patients are subjectively hungry, regardless of resolution of abdominal pain and normalization of pancreatic enzymes, may be safe [23,24]. In addition, starting first with a solid, low fat diet may also be safe, although it does not necessarily decrease length of stay [23,25-27].
●In moderately severe to severe pancreatitis, oral feeding is frequently not tolerated due to postprandial pain, nausea or vomiting related to gastroduodenal inflammation and/or extrinsic compression from fluid collections leading to gastric outlet obstruction. Patients usually require enteral or parenteral feeding. However, when the local complications start improving, oral feeds can be initiated and advanced as tolerated. (See 'Local complications' below.)
Enteral — Enteral feeding rather than parenteral nutrition is recommended in patients with moderately severe and severe acute pancreatitis who cannot tolerate oral feeding [3,28]. Early enteral nutrition (within 24 to 48 hours) should be initiated upon transfer to an intensive care unit, development of organ failure, or systemic inflammatory response syndrome (SIRS) persisting for 48 hours [29-32]. Enteral feeding requires radiologic or endoscopic placement of a jejunal feeding tube beyond the ligament of Treitz.
If placement of a nasojejunal feeding tube is not possible, nasogastric feeding should be initiated. Two controlled trials comparing nasogastric with nasojejunal feedings found no significant differences in APACHE II scores, CRP levels, pain, or analgesic requirements [33-35]. However, another small study comparing nasogastric feeding with TPN noted increased pulmonary and total complications in the nasogastric group [36]. Further studies are needed before nasogastric feeding can be routinely recommended.
We use high protein, low fat, semi-elemental feeding formulas (eg, Peptamen AF) because of a reduction in pancreatic digestive enzymes. We start at 25 cc per hour and advance as tolerated to at least 30 percent of the calculated daily requirement (25 kcal/kg ideal body weight), even in the presence of ileus. Signs that the formula is not tolerated include increased abdominal pain, vomiting (with nasogastric feeding), bloating, or diarrhea (>5 watery stools or >500 mL per 24 hours with exclusion of Clostridium difficile toxin and medication-induced diarrhea) that resolves if the feeding is held.
Enteral nutrition helps maintain the intestinal barrier and prevents bacterial translocation from the gut. Another advantage of enteral nutrition is the avoidance of the complications associated with parenteral nutrition including those secondary to venous access and blood stream infections. Consistent with prior meta-analyses, a 2010 meta-analysis of eight trials demonstrated that enteral nutrition significantly reduced mortality, multiple organ failure, systemic infections, and the need for surgery as compared with those who received parenteral nutrition [37-40].
The presence of fluid collections or elevated pancreatic enzymes is not necessarily a contraindication to oral or enteral feeding. However, in a subgroup of patients there is clear correlation of pain, recurrence of pancreatitis, or worsening of fluid collections with feeding, either oral or enteral. These patients often have disrupted pancreatic ducts with fluid collections. Drainage of fluid collections may allow resumption of oral intake. If the fluid collections are not considered suitable for drainage, or if the target rate of enteral feeding is not achieved within 48 to 72 hours, supplemental parenteral nutrition should be provided. The diagnosis and management of pancreatic duct disruptions is discussed in detail, separately. (See "Overview of pancreatic stenting and its complications", section on 'Pancreatic duct disruptions'.)
Parenteral — Parenteral nutrition should be initiated only in patients who do not tolerate enteral feeding as the use of parenteral nutrition as an adjunct to enteral feeding may be harmful [41,42].
●An observational study that included 2920 mechanically ventilated, critically ill adults compared 60-day mortality in patients who received enteral nutrition alone, enteral nutrition plus early parenteral nutrition, and enteral nutrition plus late parenteral nutrition [42]. Enteral nutrition plus either early or late parenteral nutrition was associated with increased mortality as compared with enteral nutrition alone (35 versus 28 percent).
●In a randomized trial, 4640 critically ill adults receiving enteral nutrition were assigned to supplemental parenteral nutrition initiated early (within 48 hours of ICU admission) or late (after the eighth day of ICU admission) [41]. Compared with the early-initiation group, patients in the late-initiation group had lower rates of ICU infections (23 versus 26 percent), and fewer mechanical ventilation and renal replacement therapy days (relative risk reduction 10 percent). (See "Nutrition support in critically ill patients: An overview", section on 'Parenteral nutrition'.)
Antibiotics — Up to 20 percent of patients with acute pancreatitis develop an extrapancreatic infection (eg, bloodstream infections, pneumonia, and urinary tract infections) [43]. Extrapancreatic infections are associated with an increase in mortality [44]. When an infection is suspected, antibiotics should be started while the source of the infection is being determined. However, if cultures are negative and no source of infection is identified, antibiotics should be discontinued.
Prophylactic antibiotics are not recommended in patients with acute pancreatitis, regardless of the type (interstitial or necrotizing) or disease severity (mild, moderately severe, or severe) [4]. The use of antibiotics in patients with suspected infected pancreatic necrosis is discussed separately. (See 'Classification' above and 'Acute necrotic collection and walled-off necrosis' below.)
Other
●Antifungals – Administration of prophylactic antifungal therapy (eg, fluconazole) along with prophylactic or therapeutic antibiotics is not recommended [4]. Fungal infections occur in approximately 9 percent of necrotizing pancreatitis. However, it is not clear if they are associated with higher mortality [45].
●Protease inhibitors – The role of protease inhibitors in the treatment of acute pancreatitis remains unclear as evidence from clinical trials and a meta-analysis demonstrated only marginal reduction in mortality in patients with severe pancreatitis. Intra-arterial administration is another disadvantage [46-50]. We do not recommend them at the current time.
MANAGEMENT OF COMPLICATIONS — Patients with moderately severe or severe acute pancreatitis, signs of sepsis, or clinical deterioration 72 hours after initial presentation should undergo a contrast-enhanced computed tomography (CECT) scan to assess the presence of pancreatic or extrapancreatic necrosis and local complications. Patients with persistent organ failure and extensive local complications should be transferred to centers of expertise [9]. (See 'Classification' above.)
Local complications — Local complications of acute pancreatitis include acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection, and walled-off necrosis (table 3) [51]. While acute peripancreatic fluid collections and acute necrotic collections may develop less than four weeks after the onset of pancreatitis, pancreatic pseudocyst and walled-off necrosis usually occur more than four weeks after the onset of acute pancreatitis.
Acute peripancreatic fluid collection — Fluid collections usually develop in the early phase of pancreatitis. Acute peripancreatic fluid collections (APFC) do not have a well defined wall, usually remain asymptomatic, and resolve spontaneously without the need for drainage (image 1). In a longitudinal study of patients with interstitial pancreatitis, most acute fluid collections resolved within 7 to 10 days with only 6.8 percent of APFCs persisting beyond four weeks as pancreatic pseudocysts [52].
Pancreatic pseudocyst — A pancreatic pseudocyst is an encapsulated collection of fluid with a well defined inflammatory wall usually outside the pancreas with minimal or no necrosis (image 2). Pancreatic pseudocysts usually occur more than four weeks after the onset of interstitial edematous pancreatitis. The management of pancreatic pseudocysts is discussed in detail, separately. (See "Diagnosis and management of pseudocysts of the pancreas".)
Acute necrotic collection and walled-off necrosis — Necrotizing pancreatitis most commonly manifests as necrosis involving both the pancreas and peripancreatic tissues. Necrosis may result in an acute necrotic collection (ANC) that contains a variable amount of fluid and necrosis but lacks a definable wall (image 3) or walled-off necrosis (WON), which consists of a mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well defined inflammatory wall. Both ANC and WON are initially sterile but may become infected. The management of walled-off pancreatic fluid collections is discussed in detail, separately. (See "Diagnosis and management of pseudocysts of the pancreas".)
●Infected necrosis – The occurrence of pancreatic infection is a leading cause of morbidity and mortality in acute necrotizing pancreatitis (image 4). Approximately one-third of patients with pancreatic necrosis develop infected necrosis [28]. There is no correlation between the extent of necrosis and the risk of infection. Although infection can occur early in the course of necrotizing pancreatitis, it is more often seen late in the clinical course (after 10 days) [53,54]. The majority of infections (approximately 75 percent) are monomicrobial with gut-derived organisms (eg, Escherichia coli, Pseudomonas, Klebsiella, and Enterococcus).
Infected necrosis (image 4 and image 5) should be suspected in patients with pancreatic or extrapancreatic necrosis who deteriorate (clinical instability or sepsis physiology, increasing white blood cell count, fevers) or fail to improve after 7 to 10 days of hospitalization.
Management of patients with suspected pancreatic necrosis is controversial and is outlined in the algorithm (algorithm 1). These patients should either undergo initial CT-guided fine needle aspiration (FNA) for Gram stain and culture to guide use of appropriate antibiotics or empiric antibiotics may be started without CT-guided FNA [55,56]. If empiric antibiotics are initiated, antibiotics known to penetrate pancreatic necrosis (eg, carbapenems or quinolones and metronidazole) should be used.
In patients undergoing CT-guided FNA, we initiate antibiotics while awaiting microbiologic confirmation. If culture results are negative, antibiotics are discontinued. In patients with evidence of an infection on CT-guided FNA, antibiotics should be tailored to the culture and sensitivity results. If there is evidence of a bacterial infection, we consider debridement of pancreatic necrosis (necrosectomy) [48,53]. However, in stable patients with infected necrosis, we attempt to delay necrosectomy by continuing antibiotics for at least four weeks. Continued conservative management of necrotic fluid collection allows a minimally invasive debridement to be performed at a later date to clear necrotic debris [57-60]. In addition, some patients with infected necrosis clinically improve to an extent that no intervention is necessary.
Necrosectomy should be accomplished initially by a minimally invasive approach (endoscopic or percutaneous radiologic). Open surgical necrosectomy should be used if minimally invasive methods are not possible or fail [5,61]. In a randomized controlled trial, compared with open necrosectomy, a minimally invasive step-up approach consisting of percutaneous drainage followed, if necessary, by open necrosectomy, reduced the rate of the composite end point of major complications or death among patients with necrotizing pancreatitis and infected necrosis [62]. The technique, efficacy, and complications associated with percutaneous, endoscopic, and surgical necrosectomy are discussed in detail, separately. (See "Diagnosis and management of pseudocysts of the pancreas" and "Endoscopic management of pseudocysts of the pancreas: Technique" and "Endoscopic management of pseudocysts of the pancreas: Efficacy and complications" and "Pancreatic debridement".)
●Sterile necrosis – If the aspirated material on CT-guided FNA is sterile, we discontinue antibiotics and continue conservative treatment for four to six weeks. The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended. Sterile necrosis does not require therapy.
Indications for intervention (radiological, endoscopic, or surgical) in a patient with sterile necrosis with no signs of an infection (eg, fever, hypotension, leukocytosis) include [3,5]:
•Ongoing gastric outlet, intestinal, or biliary obstruction due to mass effect four to eight weeks after onset of acute pancreatitis
•Persistent symptoms (eg, abdominal pain, nausea, vomiting, anorexia or weight loss) >8 weeks after the onset of acute pancreatitis
•Disconnected duct syndrome (full transection of the pancreatic duct) with persisting symptomatic collections with necrosis (eg, pain, obstruction) >8 weeks after the onset of acute pancreatitis
In patients with sterile necrosis and signs of systemic toxicity (eg, fever, hypotension, leukocytosis), we repeat CT-guided FNA in five to seven days [49].
Peripancreatic vascular complications
Splanchnic venous thrombosis — Splanchnic vein thrombosis (splenic, portal, and/or superior mesenteric veins) is incidentally found on imaging in 1 to 24 percent of patients with acute pancreatitis, depending on the disease severity and the imaging modality [63].
Treatment should focus on the underlying pancreatitis as effective treatment may result in spontaneous resolution of the thrombosis. Despite the theoretical possibility of hemorrhage into pancreatic necrosis or fluid collections, anticoagulation should be initiated if there is extension of the clot into the portal or superior mesenteric vein resulting in hepatic decompensation or compromise of bowel perfusion. In contrast with patients who have splanchnic vein thrombosis due to chronic pancreatitis, complications such as variceal bleeding are rare and therefore prophylactic splenectomy is not recommended [64]. (See "Acute portal vein thrombosis in adults: Clinical manifestations, diagnosis, and management", section on 'Management'.)
Pseudoaneurysm — Pseudoaneurysms are a rare but serious complication of acute pancreatitis that should be suspected when patients with acute pancreatitis have unexplained gastrointestinal bleeding, an unexplained drop in hematocrit, or sudden expansion of a pancreatic fluid collection. The diagnosis and management of pancreatic pseudoaneurysms are discussed separately. (See "Diagnosis and management of pseudocysts of the pancreas".)
Abdominal compartment syndrome — Abdominal compartment syndrome is defined as sustained intra-abdominal pressure >20 mmHg with new onset organ failure [5]. Patients with severe pancreatitis are at increased risk for intra-abdominal hypertension and abdominal compartment syndrome due to tissue edema from aggressive fluid resuscitation, peripancreatic inflammation, ascites, and ileus [65]. Patients in the intensive care unit should be monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures [22]. The clinical presentation, diagnosis, and management of abdominal compartment syndrome are discussed in detail, separately. (See "Abdominal compartment syndrome", section on 'Clinical presentation'.)
Systemic complications — Patients with acute pancreatitis are at increased risk for exacerbation of underlying comorbidities (eg, coronary artery disease, chronic lung disease). In addition to treating these exacerbations, patients should be treated for other complications including alcohol withdrawal and hyperglycemia. (See "Management of moderate and severe alcohol withdrawal syndromes" and "Glycemic control and intensive insulin therapy in critical illness", section on 'General approach'.)
MANAGEMENT OF UNDERLYING PREDISPOSING CONDITIONS — In addition to treating pancreatic inflammation and its associated complications in patients with acute pancreatitis, it is important to address the underlying predisposing factors.
Gallstone pancreatitis — In patients with gallstone pancreatitis, most stones pass into the duodenum. However, in a small proportion of patients, obstructive stones in the biliary tract or ampulla of Vater can cause persistent biliary and pancreatic duct obstruction leading to acute pancreatitis and cholangitis. (See "Etiology of acute pancreatitis" and "Clinical manifestations and diagnosis of acute pancreatitis".)
Endoscopic retrograde cholangiopancreatography — Endoscopic retrograde cholangiopancreatography (ERCP) should be performed early in the course (within 24 hours of admission) for patients with gallstone pancreatitis and cholangitis. Other indications for ERCP include patients with common bile duct obstruction (visible stone on imaging), dilated common bile duct, or increasing liver tests without cholangitis.
In the absence of common bile duct obstruction, ERCP is not indicated for (mild or severe) gallstone pancreatitis without cholangitis. When in doubt about bile duct obstruction in the absence of cholangitis, liver tests can be rechecked in 24 to 48 hours to determine if they improve or a magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS) could be performed to determine if there are stones in the common bile duct.
●Indications for EUS/MRCP prior to ERCP – EUS or MRCP should be performed to determine the need for ERCP in the following patients:
•Persistent elevation of liver tests and/or dilation of common bile duct without overt cholangitis
•Pregnant patients
•Altered anatomy that would make an ERCP technically challenging
In patients who are found to have stones on EUS or MRCP, ERCP with sphincterotomy and stone extraction is necessary and will prevent future attacks of biliary pancreatitis. However, in the absence of a cholecystectomy, these patients remain at risk for acute cholecystitis, biliary colic, and gallbladder complications of cholelithiasis.
In patients with acute cholangitis and persistent obstruction, urgent (<24 hours) ERCP with papillotomy or surgical intervention to remove bile duct stones may lessen the severity of gallstone pancreatitis [5,66-69].
In patients with gallstone pancreatitis and persistent obstruction without cholangitis, although an ERCP may be needed, urgent ERCP is controversial [5]. Three meta-analyses and one multicenter study reached different conclusions [68-71]. Two meta-analyses found that early ERCP in patients without cholangitis did not lead to a significant reduction in the risk of overall complications and mortality regardless of the predicted severity [69,71]. In another meta-analysis of five prospective randomized trials that included 702 patients, early ERCP reduced pancreatitis-related complications but not mortality in patients predicted to have severe pancreatitis; no benefit was observed in patients predicted to have mild pancreatitis [70]. (See "Prophylactic pancreatic stents to prevent ERCP-induced pancreatitis: When do you use them?", section on 'Pancreatic sphincterotomy' and "Endoscopic management of bile duct stones: Standard techniques and mechanical lithotripsy", section on 'Safety of outpatient sphincterotomy'.)
Cholecystectomy — Cholecystectomy should be performed after recovery in all patients with gallstone pancreatitis including those who have undergone an endoscopic sphincterotomy [72]. In patients who have had mild pancreatitis, cholecystectomy can usually be performed safely within seven days after recovery and in the same index hospitalization [73,74]. In patients who have had severe necrotizing pancreatitis, cholecystectomy should be delayed until active inflammation subsides and fluid collections resolve or stabilize [73].
Failure to perform a cholecystectomy is associated with a 25 to 30 percent risk of recurrent acute pancreatitis, cholecystitis, or cholangitis within 6 to 18 weeks [75]. The risk of recurrent pancreatitis is highest in patients who have not undergone a sphincterotomy. (See "Endoscopic management of bile duct stones: Standard techniques and mechanical lithotripsy", section on 'Cholecystectomy following sphincterotomy'.)
If the clinical suspicion of common bile duct stones is high (eg, in those with persistent or worsening liver test abnormalities or cholangitis), a preoperative ERCP is the best test as there is a high likelihood that therapeutic intervention (sphincterotomy, stone extraction) will be required. If the suspicion of persistent common bile duct stones is low (eg, if liver tests normalize), an intraoperative cholangiogram during cholecystectomy is preferable to avoid the morbidity associated with ERCP. In patients with low to moderate likelihood, MRCP or EUS should be performed preoperatively to exclude common bile duct stones [76]. A preoperative ERCP can then be performed in those with stones or sludge in the common bile duct. (See "Magnetic resonance cholangiopancreatography" and "Endoscopic ultrasound in patients with suspected choledocholithiasis".)
Biliary sludge — Most patients with biliary sludge are asymptomatic. However, biliary sludge is commonly found in 20 to 40 percent of patients with acute pancreatitis with no other obvious cause. On ultrasound, sludge appears as a mobile, low amplitude echo that layers in the most dependent part of the gallbladder and is not associated with shadowing. We recommend cholecystectomy in patients who have had an episode of pancreatitis and have biliary sludge [23,27]. (See "Etiology of acute pancreatitis", section on 'Biliary sludge and microlithiasis'.)
Although there are no randomized trials demonstrating that cholecystectomy in patients with pancreatitis and biliary sludge or microcrystals prevents further attacks of pancreatitis, studies suggest that biliary sludge can lead to pancreatitis and that these patients may benefit from intervention [77,78].
●In one prospective study of 86 patients with acute pancreatitis of whom 31 were idiopathic, and 23 (74 percent) had either biliary sludge on ultrasonography (11 patients) and/or cholesterol monohydrate or calcium bilirubinate crystals on biliary microscopy [78]. Of the 21 patients in whom biliary sludge was the only finding (two patients also had dilated bile ducts when re-studied), the 10 patients treated by cholecystectomy or papillotomy had fewer recurrences of acute pancreatitis during follow-up (up to seven years) as compared with the 11 untreated patients.
●Another report evaluated the efficacy of biliary drainage in 51 patients recovering from an attack of acute "idiopathic" pancreatitis [77]. Clusters of cholesterol monohydrate crystals, calcium bilirubinate granules, and/or calcium carbonate microspheroliths were found in 67 percent. Examination of the gallbladder bile at cholecystectomy or serial ultrasonography of the gallbladder for up to 12 months demonstrated that 73 percent of the patients with unexplained pancreatitis had biliary sludge or microlithiasis. Dissolution of gallstones by ursodeoxycholic acid (UDCA) or cholecystectomy prevented further attacks, while those with a delay in surgery or failed UDCA therapy continued to have episodes of pancreatitis.
Hypertriglyceridemia — The treatment of hypertriglyceridemic pancreatitis is discussed separately. (See "Hypertriglyceridemia-induced acute pancreatitis".)
Hypercalcemia — Hypercalcemia is a rare cause of acute pancreatitis. If present, treatment should be directed at normalizing serum calcium levels and determining the underlying etiology. (See "Etiology of acute pancreatitis", section on 'Hypercalcemia' and "Etiology of hypercalcemia" and "Diagnostic approach to hypercalcemia" and "Treatment of hypercalcemia".)
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●Beyond the Basics topics (see "Patient information: Acute pancreatitis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Acute pancreatitis is an acute inflammatory process of the pancreas. Acute pancreatitis can be divided into two broad categories: edematous, interstitial acute pancreatitis and necrotizing acute pancreatitis. Mild acute pancreatitis is characterized by the absence of organ failure and local or systemic complications. Moderately severe acute pancreatitis is characterized by no organ failure or transient organ failure (<48 hours) and/or local complications. Severe acute pancreatitis is characterized by persistent organ failure (>48 hours) that may involve one or multiple organs. (See 'Classification' above.)
●At initial evaluation, the severity of acute pancreatitis should be assessed by clinical examination to assess for early fluid losses, organ failure (table 1), measurement of the APACHE II score (calculator 1), and systemic inflammatory response syndrome (SIRS) score. Routine abdominal computed tomography (CT) scan is not recommended at initial presentation in patients with acute pancreatitis unless there is uncertainty about the diagnosis. (See 'Assessment of disease severity' above and "Predicting the severity of acute pancreatitis".)
●Admission to a monitored or intensive care unit is indicated in patients with severe acute pancreatitis and in patients with acute pancreatitis who meet one or more of the following parameters (see 'Indications for monitored or intensive care' above):
•Pulse <40 or >150 beats/minute
•Systolic arterial pressure <80 mmHg or mean arterial pressure <60 mmHg or diastolic arterial pressure >120 mmHg
•Respiratory rate >35 breaths/minute
•Serum sodium <110 mmol/L or >170 mmol/L, serum potassium <2.0 mmol/L or >7.0 mmol/L, serum glucose >800 mg/dL, serum calcium >15 mg/dL
•PaO2 <50 mmHg
•pH <7.1 or >7.7
•Anuria
•Coma
●Acute pancreatitis is treated with supportive care including pain control, intravenous fluids especially during the first 24 hours, and correction of electrolyte and metabolic abnormalities. The majority of patients with mild pancreatitis require no further therapy, and recover within three to seven days. Patients with moderately severe and severe pancreatitis require more intensive monitoring as they have transient (<48 hours) or persistent (>48 hours) organ failure and local or systemic complications.
●Abdominal pain is often the predominant symptom in patients with acute pancreatitis. Adequate pain control requires the use of intravenous opiates, such as morphine and fentanyl, usually in the form of a patient-controlled analgesia pump. (See 'Pain control' above.)
●In patients with mild pancreatitis, recovery generally occurs quickly, making it unnecessary to initiate supplemental nutrition. A soft diet can be started as soon as the pain is decreasing and inflammatory markers are improving. We usually start with a low residue, low fat, soft diet, provided there is no evidence of ileus or significant nausea and/or vomiting.
In patients with severe pancreatitis, we recommend early enteral nutrition in the first 72 hours through a nasojejunal tube placed endoscopically or radiologically rather than initiating parenteral nutrition (Grade 1B). If the target rate is not achieved within 48 to 72 hours and if severe acute pancreatitis is not resolved, supplemental parenteral nutrition should be provided. (See 'Oral' above and 'Enteral' above and 'Parenteral' above.)
●Patients with moderately severe or severe acute pancreatitis, signs of sepsis, or clinical deterioration 72 hours after initial presentation, should undergo a contrast-enhanced CT scan to assess the presence of pancreatic or extrapancreatic necrosis and local complications. Patients with persistent organ failure and extensive local complications should be transferred to centers of expertise. (See 'Management of complications' above.)
●Patients with pancreatitis may develop local or systemic complications. Local complications of acute pancreatitis include acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection (ANC), and walled-off necrosis (WON) (table 3). While acute peripancreatic fluid collections and acute necrotic collections may develop less than four weeks after the onset of pancreatitis, pancreatic pseudocyst and walled-off necrosis usually occur more than four weeks after the onset of acute pancreatitis. (See 'Local complications' above.)
●Both ANC and WON are initially sterile but may become infected. The occurrence of pancreatic infection is a leading cause of morbidity and mortality in acute necrotizing pancreatitis. Infected necrosis (image 4) should be suspected in patients with pancreatic or extrapancreatic necrosis who deteriorate (clinical instability or sepsis physiology, increasing white blood cell count, fevers) or fail to improve after 7 to 10 days of hospitalization. In patients with suspected infected necrosis, we suggest empiric antibiotics rather than CT-guided fine needle aspiration (Grade 2C). (See 'Acute necrotic collection and walled-off necrosis' above.)
●In patients with infected necrosis who fail to respond to antibiotics or who are clinically unstable, we recommend pancreatic debridement rather than continued conservative management (Grade 2B). Where possible we attempt to delay intervention until four weeks after initial presentation to allow the infected necrosis to become walled off. We perform necrosectomy with minimally invasive methods and reserve open surgical debridement for patients who are clinically unstable or if minimally invasive debridement is not possible or fails. (See 'Acute necrotic collection and walled-off necrosis' above.)
●In patients with gallstone pancreatitis, we recommend urgent (<24 hours) endoscopic retrograde cholangiopancreatography (ERCP) and sphincterotomy for patients with cholangitis (Grade 1B). Cholecystectomy should be performed after recovery in all operable patients with gallstone pancreatitis. (See 'Gallstone pancreatitis' above.)
REFERENCES
Wolters Kluwer Health
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+1.781.392.2000 (all other countries) tel.
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