Open access peer-reviewed chapter

Emergency Management of Acute Pancreatitis

Written By

Rezan Karaali and Firdes Topal

Submitted: 17 December 2020 Reviewed: 13 January 2021 Published: 03 February 2021

DOI: 10.5772/intechopen.95986

From the Edited Volume

Recent Advances in Pancreatitis

Edited by Qiang Yan

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Acute pancreatitis (AP) is the sudden inflammation of the pancreas, and it may be confined to the pancreas, or more life-threatening, affecting all organs and systems. AP is a common gastrointestinal condition Worldwide and is associated with cost to the health care system. It progresses mildly in 80% of patients and resolves with treatment, but in cases of severe AP, with mortality of around 30% recorded. In this section, we will discuss the first management of the AP in the emergency department. Because this is the period when management decisions can change the course of the disease and the length of stay in the hospital. In the management AP, approaches regarding the utility and timing of antibiotics, the timing and type of nutritional support, endoscopic retrograde cholangiopancreatography (ERCP) and cholecystectomy approaches are constantly being updated. Treatment is mainly related to the severity of the disease. With early diagnosis and treatment, most of the patients can be discharged, and the development of complications and mortality can be reduced. Therefore, emergency management is important in acute pancreatitis.


  • acute pancreatitis
  • complications
  • diagnosis
  • emergency
  • management

1. Introduction

1.1 Definition and incidence

Acute pancreatitis (AP) refers to the sudden inflammation of the pancreas, and it may be confined to the pancreas, or more life-threatening, affecting all organs and systems [1, 2, 3, 4, 5]. Recurrence is experienced in 15–30% of patients, and 5–25% can develop chronic pancreatitis. It progresses mildly in 80% of patients and resolves with treatment, but in cases of severe AP, complications such as organ failure and pancreatic necrosis may develop, with mortality of around 30% recorded in this group [2, 4, 5]. AP is an acute gastrointestinal disease that requires hospitalization, and is the most common cause of admission to the emergency room worldwide [1, 6, 7]. Hospital admissions for AP in the United States are in the region of 270,000/year, with a mortality rate of 30% in severe cases. Death is due to systemic inflammatory response syndrome (SIRS) and organ failure in the first two weeks, while death after two weeks can be attributed to sepsis and complications [3, 6, 8, 9].

1.2 Etiology

Gallstones are the most common etiology of AP, being responsible for 40–70% of AP cases [10, 11, 12]. The ease at which small gallstones can pass into the bile duct make AP more common in this patient group [13]. Although alcohol is commonly blamed as the second most common cause, the link between alcohol and AP is unclear, as AP is seen in only a small number of alcoholics [2, 14, 15]. Recent studies have suggested that alcohol increases the oxidative metabolism in the acinar cells of the pancreas, thereby causing mitochondrial dysfunction and cell death. This increases also the production of acetaldehyde in the pancreatic stellate cells, and increases circulating lipopolysaccharide and tumor necrosis factor alpha (TNFα), leading to fibrosis in the pancreas [16, 17]. Alcohol has also been reported to increase the viscosity of pancreatic juice and to cause ductal obstructions. That said, it has also been suggested that genetic factors play a role in the development of AP,based on the low incidence of AP in people with chronic alcohol consumption [2, 15, 18]. Other causes have been identified as Hypertriglyceridemia (HTR), and diabetes, hypothyroidism, pregnancy and obesity that cause HTR [1]. Patients with a body mass index (BMI) >35 are at risk of both HTR and AP, while those with serum triglyceride levels >1000 mg/dl are at greater risk [19, 20, 21]. Following endoscopic retrograde cholangiopancreatography (ERCP) performed by inexperienced practitioners, patients with Sphincter of Oddi dysfunctions may develop AP following ERCP due to difficult cannulation [22].

AP can also occur due to drugs at a rate of 0.1–0.5% [2, 23, 24, 25]. Many drugs have been identified that cause acute pancreatitis. Drugs cause AP by different mechanisms. While some drugs cause direct toxicity to the pancreas (eg, diuretics, sulfonamides), some drugs cause acute pancreatitis by causing an immunological reaction (eg, 6-mercaptopurine, amino salicylates, sulfonamides). Diuretics and azothiopurine cause direct ischemia, while hormones such as steroids and estrogen cause vascular thrombosis or ischemic pancreatitis by decreasing the viskosity of the pancreatic juice. Toxic metabolites of drugs such as valproic acid and tetracycline may accumulate in the pancreas and cause pancreatitis [2, 26, 27].

AP cases have been reported associated with such infectious diseases as Mumps, Coxsackievirus, Hepatitis B, Cytomegalovirus, Varicella-Zoster, herpes simplex and human immunodeficiency virus (HIV) among the viruses; with Mycoplasma, Legionella, Leptospira and Salmonella among the bacteria; with Aspergillus among the fungi; and with Toxoplasma and Cryptosporidium among the parasites [2, 27, 28]. There have been reports of cases of AP with the recent SARS-CoV-2 infection at the heart of the current global pandemic [29, 30]. In a review of current literature, AP was found to be detected in 17% of patients hospitalized due to Covid-19 [29]. Although tests for specific infectious agents are not generally recommended in AP patients, Covid-19 infection should also be kept in mind in AP cases during the pandemic [30].

Concerning other rare causes, pancreatic injury following trauma is an extremely rare condition due to its retroperitoneal nature. Pancreatic duct injuries may occur due to blunt or penetrating traumas [31], while AP may occur due to gallbladder sludge, tumors, autoimmune pancreatitis, hypercalcemia, anatomical and physiological anomalies (pancreatic divisum, biliary cysts, pancreaticobiliary malunion, large juxta-ampullary diverticula, annular pancreas and Sphincter of Oddi dysfunction), and vasculitis [27, 32, 33, 34, 35, 36]. Ischemic AP can also be seen after major cardiovascular operations [27, 37, 38]. Patients with an unknown etiology after history-taking, physical examination, laboratory tests, imaging methods and advanced tests are classified as idiopathic. In the event of recurrent AP attacks in this patient group and AP at a young age, genetic factors should be investigated [27, 39].

1.3 Pathogenesis

As its main mechanism, AP blockades the secretion of enzymes while the synthesis of enzymes continues [2, 40]. Under normal conditions, trypsinogen is produced in the pancreas and secreted into the duodenum where it is converted into protease trypsin, but in cases where secretion is blocked, trypsin continues to be produced in pancreatic acinar cells. While activation continues, elimination is inhibited, and the active trypsin damages the vascular endothelium, interstitium and acinar cells [2, 40, 41]. As a result, autodigestion begins in the pancreas,and ischemia occurs at a tissue level in the pancreas due to the vasoconstriction and stasis of the capillary vessels. The activation of granulocytes and macrophages in response to these events causes a release of proinflammatory cytokines (tumor necrosis factor, interleukins 1, 6 and 8), arachidonic acid metabolites (prostaglandins, platelet activating factor and leukotrienes), proteolytic and lipolytic enzymes, and reactive oxygen metabolites [2, 27, 42, 43]. All of these factors together cause damage to the pancreatic tissue. In general, the inflammation is locally self-limiting, buton occasions, inflammatory agents may cause a systemic response, leading to the damage and failure of distant organs. This, in turn, may result in Acute Respiratory Distress Syndrome (ARDS), pleural effusion, acute renal failure, shock, and even death [2, 27, 44, 45].


2. Clinical features

Patients withAP present to the emergency room with sudden and severe abdominal pain that usually starts in the epigastric region. In patients with gallstones, the pain spreads to the right upper quadrant and is more sharply limited. In 50% of patients, the pain spreads to the back, and is felt around the entire abdomen, like a belt. Nausea and vomiting may accompany,and in rare cases there may be pain on the left side of the abdomen [2, 46, 47, 48, 49].

Physical examination findings can vary, depending on the severity of AP and any accompanying diseases. Initial findings typically include mild or generalized tenderness upon abdominal palpation, distension and diminished bowel sounds. In cases of obstruction due to gallstones, jaundice may be observed, while in severe AP, fever, hypotension, tachycardia, tachypnea and hypoxemia may be observed. In cases of pancreatic necrosis, ecchymotic lesions can be seen in the periumbilical region (Cullen’s sign) or on the flanks (Gray Turner’s sign) [2, 27, 50, 51].


3. Diagnosis

Diagnosis is established based on the presence of two of three criteria: 1) Presence of clinical findings consistent with AP, 2) serum lipase or amylase levels three times greater than normal, and 3) characteristic findings of AP on imaging [2, 27, 47, 48, 52].

3.1 Laboratory

In AP, enzymes pass from the basolateral membrane to the interstitial area, and then on to the systemic circulation due to the blockade of the secretion ofpancreatic enzymes, while the synthesis of enzymes continues, resulting in increased levels of pancreatic enzymes in the blood.

At the onset of AP, serum amylase starts to increase within 6–12 hours, peaks at 48 hours, and returns to normal within 3–5 days, although no increase in amylase levels will be observed in alcohol-induced pancreatitis and AP due to hypertriglyceridemia. Sensitivity and specificity in diagnosis are 67–83% and 85–98%, respectively [2, 27, 48, 53, 54]. Elevated amylase levels may also be seen in non-pancreatic diseases, such as renal failure, salivary gland diseases, acute appendicitis, cholecystitis, perforations, intestinal obstructions or intestinal ischemia, and gynecological diseases. For these reasons, amylase alone is not sufficient for a diagnosis of AP [2, 48, 49]. The increase in serum lipase levels in AP is more specific. Following the onset of symptoms, the levels begin to increase within 8–10 hours, peak at 24 hours, return to normal within 8–14 days, with a sensitivity of 82–100% [2, 48, 53, 55], and may increase in alcohol-induced AP and AP due to hypertriglyceridemia. It is useful in delayed patients who present 24 hours after the onset of pain [48, 55, 56]. Aside from amylase-lipase, liver and kidney tests,a complete blood count should also be made in AP, as this will allow the assessment of the patient’s clinical condition, the early identification of complications and the detection of organ failure, and will aid in a therapeutic evaluation. An alanine aminotransferase (ALT) liver function test value in excess of 150 U/L indicates gallstones [2, 47, 52]. There are also specific tests for AP that are not routinely used. Among the enzymes with early elevation are trypsinogen-activating peptide, urinary and serum trypsinogen and trypsin, phospholipase, carboxypeptidase, carboxyl ester lipase, colipase and pancreatic isoamylase [57, 58, 59], and an increase is also observed in inflammatory mediators such as C-reactive protein (CRP), interleukin IL-6, IL-8, IL-10, tumor necrosis factor (TNF) and PMN elastase. The elevation of inflammatory mediators is usually proportional to the severity of AP. A CRP level above 150 mg/dl within the first 48 hours has been associated with severe AP [60, 61].

3.2 Imaging

Imaging can aid in determining the etiology of AP, or complications due to AP. Abdominal and chest radiographs may reveal appearances of pleural effusion, atelectasis and ileus accompanying AP. Radiographs should be evaluated to rule out other causes of abdominal pain. Abdominal ultrasound should be performed on every patient with suspected AP, and USG can detect findings that support AP, if present, such as gallstones, obstructions in the common bile duct, intraabdominal free fluid and diffuse enlarged and hypoechoic appearance in the pancreas, as well as peripancreatic fluid, necrosis and abscesses. A normal USG cannot exclude AP [2, 27, 47, 48, 52, 62], while Contrast-Enhanced Computed Tomography (CECT) has a sensitivity of 90% in the diagnosis of AP. However, AP is not routinely recommended for diagnosis, since it is mild and uncomplicated in most patients [2, 47, 48, 52], but may be recommended in cases where other causes of acute abdomen cannot be excluded, or for patients who show no improvement within 48–72 hours [48, 63, 64].

Among the patients considered for CECT, MRI is recommended rather that CECT for those with renal failure, pregnant patients and those with allergies to IV contrast agents [48, 63].

Serum triglyceride levels must be examined in patients with normal test results, but with a strong suspicion of AP, in those with pancreatic tumors aged over 40 years, in the presence of genetic factors in patients under the age of 30 and in recurrent AP cases [39, 48].

3.3 Differential diagnosis

Other diseases that may cause abdominal pain should be excluded in a differential diagnosis. In particular, peptic ulcer disease, choledocholithiasis, cholangitis, biliary obstruction, cholecystitis, perforated viscus, intestinal obstruction, mesenteric ischemia and hepatitis should be considered in differential diagnosis due to their clinical similarities to AP [2, 27].


4. Initial management

AP can be classified into two groups as mild AP, in which patients have no accompanying organ failure, and recover and can be orally fed within 48 hours; and severe AP, which is accompanied by organ failure and a lack of response to treatment. Most patients with severe AP have not suffered organ failure at the time of admission to emergency room, and so may be evaluated as mild AP,but deteriorate rapidly due to inadequate hydration and inadequate treatment. As such, the severity of the disease should be determined along at the time of diagnosis in the emergency room, and treatment should be planned accordingly [47, 48, 52, 65].

According to the Atlanta classification, severe AP is characterized by resistant/persistent organ failure with no improvement within 48 hours, although in the absence of organ failure, the presence of local complications alone is an indicator of severe AP [66]. Patients who develop transient organ failure alongside local complications are classified as moderately severe AP (Table 1). The Atlanta classification evaluates the presence of organ failure based on Marshall’s organ failure criteria. Accordingly, the presence of shock (systolic BP <90 mmHg), pulmonary failure (PaO2 < 60 mmHg), renal failure (creatinine >2 despite adequate hydration), and/or the presence of gastrointestinal bleeding (>500 ml blood loss within 24 hours) should be evaluated as organ failure [48, 52, 67].

Mild APModerately APSevere AP
Absence of local complicationsLocal complications
Peripancreatic fluid collection
Pancreatic or peripancreatic necrosis(sterile or infected)
Gastric outlet disfunction
Splenic or portal vein thrombosis
Colonic necrosis
Persistent organ failure > 48 h
GI bleeding (>500 cc/24 hr)
Shock – SBP < 90 mmHg
PaO 2 < 60%
Creatinine >2 mg/d
Absence of organ failureTransient organ failure < 48 h
GI bleeding (>500 cc/24 hr)
Shock – SBP < 90 mmHg
PaO 2 < 60%
Creatinine >2 mg/d

Table 1.

Atlanta classification 2015.

Besides the Atlanta classification, several scoring systems have been proposed for the determination of the severity in AP. These include Ranson’s criteria,Acute Physiology and Chronic Health Examination-II, modified Glasgow score, Bedside Index for Severity in Acute Pancreatitis and the Balthazar CT Severity Index,none of which has been shown to be superior to any other, and they have only limited use in the emergency room, as they rely on too many parameters, and some give results only after 48 hours [68, 69]. The assessment of the patient in the emergency department is of utmost importance, with patient-related risk factors such as age, weight, comorbidities and vital signs as well as laboratory findings all being evaluated together (Table 2) [47, 52, 56, 65].

Patient characteristicsThe systemic inflammatory response syndrome (SIRS)Laboratory findingsRadiology findings
Age > 55 years
Obesity (BMI >30 kg/m2)
Altered mental status
Comorbid disease
  • pulse >90 beats/min

  • respirations >20/min or PaCO2 > 32 mmHg

  • temperature > 38°C or < 36°C

  • WBC count >12,000 or < 4,000 cells/mm3 or > 10% immature neutrophils (bands)

BUN >20 mg/dl
Rising BUN
HCT >44%
Rising HCT
Elevated creatinine
Pleural effusions
Pulmonary infiltrates
Multiple or extensive extrapancreatic collections

Table 2.

Initial assessment for risk of severe AP.


5. Treatment

5.1 Fluid replacement

The initial approach to AP involves aggressive fluid therapy, pain management and nutritional support. In AP, there is a large amount of fluid deficit due to losses from vomiting, reduced oral intake, passage of fluid into the third space, respiration and sweating. If the patient has no additional cardiovascular or renal disease, fluid replacement should be initiated at 5–10 ml/kg/hour. For patients presenting with evidence of hypovolemia and shock, 3 ml/kg of fluid should be given for 8–12 hours following a fluid bolus of 20 ml/kg in 30 minutes, with isotonic normal saline preferred as the fluid [47, 48, 52, 70, 71, 72]. A prospective study found hydration with Ringer’s lactate solution to be more beneficial, although Ringer’s lactate solution has been shown to activate trypsin in acinar cells, thereby making the patient more susceptible to injury due to its low pH. With normal saline, there is a risk of developing non-anion gap metabolic acidosis, and patients should be monitored accordingly during fluid replacement [2, 72]. An assessment should be made after 6, 24 and 48 hours to as certain whether the fluid administered is sufficient. With adequate hydration, the heart rate should drop below 120/min, mean arterial pressure (MAP) should be maintained between 65 and 85, and hematocrit (HCT) should be 35–44%. If the BUN value is initially high, a decrease upon hydration is an indicator of adequate hydration. Changes in blood urea nitrogen (BUN) values within the first 24 hours are particularly important [27, 47, 48, 73, 74]. If the BUN values continue to be high, or increase even further, acute tubular necrosis or resistant volume deficit should be suspected [27, 47, 52, 65, 75]. Another parameter that should be monitored during hydration is hematocrit. Continued hemoconcentration for more than 24 hours suggests the development of necrotizing pancreatitis, and so the patient’s urine output, BUN and HCT values should be closely monitored. The development of severe pancreatitis should be considered in patients who do not respond to aggressive hydration for 6–12 hours [47, 48, 52].

5.2 Pain management

Adequate hydration and the resolution of hypovolemia relieve ischemic pain secondary to hemoconcentration. Nevertheless, opioid analgesics are recommended for rapid pain management. Fentanyl can be used safely, especially in patients with kidney failure, in which intravenous (IV) fentanyl of 20–50 microgram is administered slowly over 10 minutes. Meperidine can be used as an alternative to morphine due to the spasm effect of morphine on the Sphincter of Oddi [2, 27, 76, 77].

5.3 Monitoring

AP patients should be followed closely for 24 hours, with continued monitoring of blood pressure, temperature, pulse, oxygen saturation and urine output. Blood tests should be monitored for hematocrit, BUN and electrolytes (calcium, magnesium), and blood glucose should be maintained between 180 and 200 mg/dl [2, 27, 52]. Intensive care follow-up is required for patients whose vital signs and laboratory values are unstable and / or continue (Table 3) [52].

Vital signsLaboratuary findingsPatient condition
pulse <40 or > 150 beats/min;
systolic arterial pressure < 80 mmHg (<10.7 kPa)
or mean arterial pressure < 60
or diastolic arterial pressure > 120 mmHg
respiratory rate > 35 breaths/min;
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 (>44.4 mmol/L); mmol/L);
serum calcium >15 mg/dl (>3.75
Furthermore, a patient with severe acute pancreatitis as defined by the revised Atlanta Classification (i.e. persistent organ failure)

Table 3.

Assessment for intensive care.

5.4 Nutrition

It is no longer recommended to stop oral intake until the AP has fully resolved and the enzymes have returned to normal limits in order to put the pancreas at rest. Patients ceasing oral intake may develop atrophy in the mucosa of gastrointestinal tract [27, 47, 48, 52, 78, 79], and so oral feeding should be initiated in patients without nausea, vomiting or ileus and with relieved pain, as soon as they can tolerate [47, 48, 52, 79, 80, 81]. Liquid, light and low-fat foods should be given at first [82]. In cases of severe AP, enteral feeding may be initiated in patients who are still unable to tolerate oral feeding after 5 days, and in those with complications. For enteral nutrition, a nasojejunal or nasogastric tube should be used for feeding. A nasogastric tube insertion may be easy, but there is a risk of aspiration, while a nasojejunal tube requires an operation. Depending on the conditions, both methods can help provide effective nutrition [47, 48, 82]. If the goal of enteral nutrition is not achieved within 48–72 hours, or if the patient cannot tolerate, parenteral nutrition should be initiated [80, 81, 83].

5.5 Antibiotics

20% of patients develop extrapancreatic infections that may be cholangitis, catheter infection, urinary tract infection or pneumonia. Prophylactic ABs, even if severe, are not routinely recommended in AP without an unidentified focus of infection or presence of infection. ABs for infective necrosis prophylaxis are not recommended, even for patients with sterile necrosis [2, 27, 47, 48, 52, 65, 84, 85].


6. Management of complicatıons

If, during the follow-up of moderately severe or severe AP patients, signs of sepsis appear, no improvement occurs within 72 hours or the condition deteriorates gradually, then complications should be suspected and a CECT should be performed.

6.1 Local complications

6.1.1 Acute peripancreatic fluid collection

Acute peripancreatic fluid collection occurs early, and has no specific wall. It resorbs spontaneously [27, 48].

6.1.2 Necrotizing pancreatitis

Necrotizing pancreatitis can involve both the pancreas and peripancreatic tissues. A variable amount of fluid and necrotic tissue may develop within the necrosis,and is known as Acute Necrotic Collection (ANC) when a clear wall cannot be defined, and as Wall-off Necrosis (WON) when there is a mature, encapsulated and well-defined wall. WON is a pancreatic pseudocyst that occurs around 4 weeks after an AP attack, and that has a noticeable wall, for which drainage may be required. In either case, the necrotic area may be sterile or infected, and the type of treatment is determined based on the presence or absence of infection [84, 86, 87, 88]. Infected necrosis

Infection should be suspected in patients with pancreatic or extrapancreatic necrosis upon clinical deterioration or a lack of improvement within 7–10 days of hospitalization. Infectious agents are usually of intestinal origin (such as Escherichia coli, Pseudomonas, Klebsiella and Enterococcus), and may be suspected with the emergence of clinical signs of infection in patients and the presence of gas around the pancreas on imaging [89, 90]. Empirical AB may be initiated in these patients, with ABs that can penetrate the pancreas well (carbapenem alone; or quinolone, ceftazidime, or cefepime combined with an anaerobic agent such as metronidazole)being recommended [27, 47, 48]. Fine needle aspiration (FNA) or sampling is not recommended in such patients. Necrosectomy may be scheduled for patients who show no improvement, but should be delayed as much as possible, since many patients respond well to AB therapy [48, 90, 91, 92]. Antibiotic therapy should have been completed 4 weeks prior to a decision of necrosectomy. For the necrestomy, endoscopic or invasive percutaneous procedures should be tried first, and if these fail, surgery should be scheduled [47, 48, 52, 91, 92, 93]. Sterile necrosis

In patients with necrotizing pancreatitis, sterile necrotizing pancreatitis should be suspected when there is no improvement despite treatment, and no clear clinical or imaging findings of infection. In such cases, FNA sampling is indicated, and if the collected material is sterile, there is no need to continue the ABs. Even ABs cannot prevent sterile necrosis from turning into infected necrosis [47, 52, 94]. In sterile necrosis in the absence of any sign of infection, interventions will be required in the following cases:

  • Continued obstruction of the gastric outlet, intestine or bile ducts, caused by mass effects after 4–8 weeks following the onset of acute pancreatitis.

  • Persistant symptoms (e.g. abdominal pain, nausea, vomiting, anorexia or weight loss) identified more than eight weeks following the onset of acute pancreatitis.

  • Disconnected duct syndrome (full transection of the pancreatic duct) with persistent symptomatic collections with necrosis (e.g., pain, obstruction) more than 8 weeks following the onset of acute pancreatitis.

Aside from these, CT and FNA should be repeated 5–7 days later in patients with sterile necrosis detected by CECT and FNA, but with signs of systemic toxicity [48, 52].

The much rarer complications include peripancreatic vascular complications, splanchnic vein thrombosis, abdominal compartment syndrome and pseudoaneurysm. Furthermore, patients may risk developing diabetes in the following periods [27, 52, 95].

6.2 Systemic complications

Respiratuar insufficiency includes pneumonia, atelectasis, and ARDS. Renal complications are prerenal azotemia, hypotansion and acute tubuler necrosis. Shock is caused by third space losses, vomiting and interstitial edema. Hypo-hyperglicemia, coagulation disorders, fat necrosis and pancreatic encphalophaty are other rare systemic complications of AP [27].


7. Management of predisposing underlying conditions

7.1 Nonsurgical management

The detection and treatment of the underlying diseases that cause AP are as important as AP itself. Most gallstones that pass into the common bile duct advance to the intestines, and are excreted with feces. However, stones that cause obstructions to the pancreatic duct and/or biliary ducts may result in severe AP and/or cholangitis. ERCP is recommended within the first 24 hours for AP patients with stones detected as causing an obstruction. The removal of stones by via a sphincterotomy with ERCP prevents both severe AP and the cholangitis and future development of biliary AP. ERCP should be performed within the first 24 hours in AP patients due to gallstones accompanied by acute cholangitis. A papillotomy, or the surgical removal of stones, with ERCP reduces the severity of AP [48, 52, 96, 97, 98]. It has been reported that mortality decreases with early ERCP in patients with no cholangitis, with biliary duct obstructions, and with elevated liver function test scores. That said, it is unnecessary to perform ERCP within the first 24 hours on patients with no increase in liver function tests, with therapeutic ERCP recommended for such patients before or during the cholecystectomy. It is recommended that EUS and MRCP be performed prior to ERCP in patients without cholangitis or jaundice, but with suspected choledocholithiasis, pregnant women and patients on whom ERCP cannot be performed anatomically [47, 48, 52, 65, 99].

7.2 Surgical managment

The removal of stones through the use of ERCP in patients without cholangitis can prevent the development of AP in the future, but it cannot prevent the development of biliary colic or cholecystitis. Accordingly, cholecystectomy is recommended prior to discharge in patients with mild AP and with gallstones [47, 48, 52, 65, 100, 101, 102, 103]. Preoperative MRCP or EUS, or intraoperative cholangiography may be carried out for the selection of patients with common bile duct stones who need to be treated through an operative bile duct exploration or endoscopic sphincterotomy during a cholecystectomy [48, 52, 99]. A cholecystectomy may be avoided in ineligible elderly patients (>80 years of age), particularly if a sphincterotomy has already been performed [48, 52, 96, 97]. A cholecystectomy should be performed in patients with gallbladder sludge and AP. In patients with necrotizing biliary AP, cholecystectomies should be delayed until the active inflammation subsides and fluid collections have resolved or stabilized. If collection takes longer than 6 weeks to resolve, the cholecystectomy should be delayed until it can be performed safely [47, 48, 52, 65]. Asymptomatic pseudocysts and pancreatic and/or extrapancreatic necrosis require no surgical intervention, regardless of the size, location and/or extension. In asymptomatic patients with infected necrosis, surgical, radiological and/or endoscopic drainage should be delayed for more than 4 weeks to allow for the liquefaction of the content and the development of a fibrous wall around the necrosis (WON). Minimally invasive necrosectomy methods are preferred in symptomatic patients with infected necrosis [47, 48, 52, 84, 87]. Percutaneous drainage and/or endoscopic drainage/debridement are minimally invasive alternatives to open surgery [104].

Percutaneous CT-guided catheter drainage: The procedure is performed under local anesthesia. Depending on the size and location of the necrosis, the catheter is placed under CT guidance. Irrigation with saline every several days after insertion [105, 106]. Although percutaneous catheter drainage was used for patients who are too unstable to undergo surgical debridement, approximately one third to one half of patients can be managed with this method alone [106, 107]. The only disadvantage of this method is the risk of persistent pancreatico-cutaneous fistula [108].

Endoscopic debridement: It is performed via transgastric or transduedonal [104, 105, 109]. Cystenterostomy is created using wire-guided balloon dilators. Mechanical debridement is performed using snares, baskets, and stone retrieval balloons. Following this, a stent is placed in the cavity. The flow of necrotic contents into the stomach or duodenum is provided [109]. Minimally invasive operative approaches are preferred to open surgical necrosectomy and given lower morbidity [110].


8. Conclusion

Although new guidelines have been published, there are several knowledge gaps identified in the initial management of the AP. Risk stratification of patients with AP is important to ensure the appropriate level of care. Therefore, there is a need to develop fast, easy and practical systems that can be used in the emergency room. There is also a need to define targeted therapies in AP. Future research will enable prevention of relapse, chronicity, and cancer development, improvement of quality of life and reduction of mortality.



No funding support.


Conflict of interest

The authors declare no conflict of interest.


  1. 1. Garg SK, Sarvepalli S, Campbell JP, Obaitan I, Singh D, Bazerbahi F et al. Incidence, admission rates and predictors and economic burden of adult emergency visits for acute pancreatitis data from the national emergency department sample 2006 to 2012. J Clin Gastroenterol 2019;53(3):220-225.
  2. 2. Besinger B, Stehman CR. Pancreatitis and Cholecystitis In Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM. editors. Tintinalli’s Emergency Medicine A Comprehensive Study Guide 8th ed. Mc Graw-Hill Education; 2016. p: 517-521 ISBN: 978-0-07-180913-9.
  3. 3. Singh VK, Bollen TL, Wu BU, et al: An assessment of the severity of interstitial pancreatitis. Clinical Gastroenterol Hepatol 2011;9(12):1098-103.
  4. 4. Lankisch PG, Breuer N, Bruns A, et al: Natural history of acute pancreatitis: a long-term population-based study. Am J Gastroenterol 2009;104(11):2797-805.
  5. 5. Yadav D, O’Connell M, Papachristou GI: Natural history following the first attack of acute pancreatitis. Am J Gastroenterol 2012;107(7):1096-103. doi: 10.1038/ajg.2012.126.
  6. 6. Peery AE, Dellon ES, Lund J et al. Burden of gastrointestinal diseases in the United States 2012 Update. Gastroenterology 2012;143:1179-87.
  7. 7. Fagenholz PJ, Fernandez-del Castillo C, Harris NS et al. Direct medical costs of acute pancreatitis hospitalizations in the United States. Pancreas 2007;35:302-7.
  8. 8. Gloor B, Müller CA, Worni M, et al. Late mortality in patients with severe acute pancreatitis. Br J Surg 2001; 88:975.
  9. 9. Mutinga M, Rosenbluth A, Tenner SM, et al. Does mortality occur early or late in acute pancreatitis? Int J Pancreatol 2000;28:91.
  10. 10. Cheon YK, Cho KB, Watkins JL, et al: Frequency and severity of post-ERCP pancreatitis correlated with extent of pancreatic ductal opacification. Gastrointest Endosc 2007;65(3):385-93.
  11. 11. Gullo I, Migliori M, Olah A et al. Acute pancreatitis in five European countries: etiology and mortality. Pancreas 2002;24:223-7.
  12. 12. Lowenfels AB, Maisonneuve P, Sullivan T. The changing character of acute pancreatitis: epidemiology, etiology, and prognosis. Curr Gastroenterol Rep 2009;11:97-103.
  13. 13. Venneman NG, Renooij W, Rehfeld JF, et al. Small gallstones, preserved gallbladder motility, and fast crystallization are associated with pancreatitis. Hepatology 2005;41(4):738-46.
  14. 14. Kristiansen L, Gronbaek M, Becker U, Tolstrup JS: Risk of pancreatitis according to alcohol drinking habits: a population-based cohort study. Am J Epidemiol 2008;168(8):932-7.
  15. 15. Ammann RW: The naturalhistory of alcoholic chronic pancreatitis. Intern Med. 2001;40(5):368-75.
  16. 16. Takahashi T, Miao Y, Kang F, Dolai S and Gaisano HY. Susceptibility Factors and Cellular Mechanisms Underlying Alcoholic Pancreatitis. Alcohol Clin Exp Res 2020;44(4):777-789.
  17. 17. Apte MV, Wilson JS, McCaughan GW, et al. Ethanol-induced alterations in messenger RNA levels correlate with glandular content of pancreatic enzymes. J Lab Clin Med 1995;125(5):634-40. PMID: 7738427.
  18. 18. Migliori M, Manca M, Santini D, et al. Does acute alcoholic pancreatitis precede the chronic form or is the opposite true? A histological study. J Clin Gastroenterol 2004;38(3):272-5.
  19. 19. Yadav D, Pitchumoni CS. Issues in hyperlipidemic pancreatitis. J Clin Gastroenterol 2003;36(1):54-62.
  20. 20. Nawaz H, Koutroumpakis E, Easler J, et al. Elevated serum triglycerides are independently associated with persistent organ failure in acute pancreatitis. Am J Gastroenterol 2015 ;110(10):1497-503.
  21. 21. Wan J, He W, Zhu Y, et al. Stratified analysis and clinical significance of elevated serum triglyceride levels in early acute pancreatitis: a retrospective study. Lipids Health Dis 2017 ;16(1):124.
  22. 22. Kahaleh M, Freeman M. Prevention and management of post-endoscopic retrograde cholangio pancreatography complications. Clin Endosc 2012;45(3):305-12.
  23. 23. Meczker A, Hanák L, Párniczky A, ET al. Analysis of 1060 Cases of Drug-Induced Acute Pancreatitis. 2020;159(5):1958-1961 DOI:
  24. 24. Trivedi CD, Pitchumoni CS: Drug-induced pancreatitis: an update. J Clin Gastroenterol 2005;39(8):709-16.
  25. 25. Badalov N, Baradarian R, Iswara K, Li J, Steinberg W, Tenner S: Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol 2007;5(6):648-61; quiz 644.
  26. 26. Gagnon AL, Lavoie A, Frigon MP, Michaud-Herbst A, Tremblay K. A Drug-Induced Acute Pancreatitis Retrospective Study. J Gastroenterol Hepatol 2020;2020:1516493.
  27. 27. Tenner S, Steinberg WM. Acute pancreatitis In Feldman M, freidman LS, Brandt LJ editors Sleisenger and Fordtrand’s gastrointestinal and liver disease: pathophihysiology, diagnosis and management book. 9th edition. Saunders-elsevier; 2010. p 959-983 ISBN: 978-1-4160-6189-2
  28. 28. Parenti DM, Steinberg W, Kang P. Infectious causes of acute pancreatitis. Pancreas 1996;13(4):356-71.
  29. 29. Inamdar S, Benias PC, Liu Y, Sejpal DV, Satapathy SK, Trindade AJ, Prevalence, risk factors, and outcomes of hospitalized patients with COVID-19 presenting as acute pancreatitis. Gastroenterology 2020;159:2226-2228
  30. 30. Bokhari SMMA, Mahmood F. Case Report: Novel Coronavirus—A Potential Cause of Acute Pancreatitis?Am. J. Trop. Med. Hyg 2020;103(3):1154-1155.
  31. 31. Wilson RH, Moorehead RJ. Current management of trauma to the pancreas. Br J Surg 1991 ;78(10):1196-202.
  32. 32. Ros E, Navarro S et al. Occult microlithiasis in idiopatic acute pancreatitis:prevention of relapses by cholecystecthomy or ursodeoxycholic acid theraphy. Gastroenterology 1991:101(6);1701-1709.
  33. 33. Uomo G, Manes G, Ragozzino A, et al. Periampullary extraluminal duodenal diverticula and acute pancreatitis: an underestimated etiological association. Am J Gastroenterol 1996; 91:1186. PMID: 8651168
  34. 34. Watts RA, Isenberg DA. Pancreatic disease in the autoimmune rheumatic disorders. Semin Arthritis Rheum 1989;19(3):158-65.
  35. 35. DiMagno MJ, Dimagno EP. Pancreas divisum does not cause pancreatitis, but associates with CFTR mutations. Am J Gastroenterol 2012;107(2):318-20.
  36. 36. SteinbergWM, Chari ST, Forsmark CE et al. Controversies in clinical pancreatology: management of acute idiopathic recurrent pancreatitis. Pancreas 2003;27(2):103-17.
  37. 37. Fernández-del Castillo C, Harringer W, Warshaw AL, et al. Risk factors for pancreatic cellular injury after cardiopulmonary bypass. N Engl J Med 1991;325(6):382-7.
  38. 38. Warshaw AL, O’Hara PJ. Susceptibility of the pancreas to ischemic injury in shock. Ann Surg 1978;188(2):197-201.
  39. 39. Jalaly NY, Moran RA, Fargahi F, et al. An Evaluation of Factors Associated WithPathogenic PRSS1, SPINK1, CTFR, and/or CTRC Genetic Variants in Patients With Idiopathic Pancreatitis. Am J Gastroenterol 2017;112(8):1320-1329.
  40. 40. Steer ML. Pathogenesis of acute pancreatitis. Digestion 1997;58 Suppl 1:46-9.
  41. 41. Halangk W, Lerch MM, Brandt-Nedelev B, et al. Role of cathepsin B in intracellular trypsinogen activation and the onset of acute pancreatitis. J ClinInvest 2000;106(6):773-81.
  42. 42. Prinz RA. Mechanisms of acute pancreatitis. Vascular etiology. Int J Pancreatol. 1991;9:31-8.
  43. 43. Kingsnorth A. Role of cytokines and their inhibitors in acute pancreatitis. Gut 1997;40(1):1-4.
  44. 44. Wang GJ, Gao CF, Wei D, Wang C, Ding SQ: Acute pancreatitis: etiology and common pathogenesis. World J Gastroenterol 2009;15(12):1427-30.
  45. 45. Sah RP, Dawra RK, Saluja AK: New insights into the pathogenesis of pancreatitis. Curr Opin Gastroenterol 2013;29(5):523-30.
  46. 46. Swaroop VS, Chari ST, Clain JE. Severe acute pancreatitis. JAMA 2004; 291:2865. JAMA 2004;291(23):2865-8.
  47. 47. Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AY;on behalf of American Gastroenterological Association Institute Clinical Guidelines Committee American Gastroenterological Association Institute Guidelineon Initial Management of Acute Pancreatitis. Gastroenterology 2018;154:1096-1101.
  48. 48. Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology Guideline:Management of Acute Pancreatitis. Am J Gastroenterol 2013; 108:1400-1415;
  49. 49. Kiriyama S, Gabata T, Takada T, et al: New diagnostic criteria of acute pancreatitis. J Hepatobiliary Pancreat Sci 2010;17(1):24-36.
  50. 50. Mookadam F, Cikes M. Images in clinical medicine. Cullen’s and Turner’s signs. N Engl J Med 2005;353(13):1386.
  51. 51. Meyers MA, Feldberg MA, Oliphant M: Grey-Turner’s sign and Cullen’s sign in acute pancreatitis. Gastrointest Radiol Winter 1989;14(1):31-7.
  52. 52. Working Group IAP/APA Acute Pancreatitis Guidelines IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 2013;13(4 Suppl 2):e1-15.
  53. 53. Yadav D, Agarwal N, Pitchumoni CS. A critical evaluation of laboratory tests in acute pancreatitis. Am J Gastroenterol 2002;97(6):1309-18.
  54. 54. Winslet M, Hall C, London NJM. Relation of diagnostic serum amylase levels to aetiology and severity of acute pancreatitis. Gut 1992;33(7):982-6. doi:10.1136/gut.33.7.982.
  55. 55. Gwozdz GP, Steinberg WM, Werner M, et al. Comparative evaluation of the diagnosis of acute pancreatitis based on serum and urine enzyme assays. Clin Chim Acta 1990;187(3):243-54.
  56. 56. Wu BU, Banks PA: Clinical management of patients with acute pancreatitis. Gastroenterology 2013;144(6):1272-81.
  57. 57. Kemppainen E, Hedström J, Puolakkainen P, et al. Increased serum trypsinogen 2 and trypsin 2-alpha 1 antitrypsin complex values identify endoscopic retrograde cholangiopancreatography induced pancreatitis with high accuracy. Gut 1997;41(5):690-5.
  58. 58. Huang QL, Qian ZX, Li H. A comparative study of the urinary trypsinogen-2, trypsinogen activation peptide, and the computed tomography severity index as early predictors of the severity of acute pancreatitis. Hepatogastroenterology 2010;57(102-103):1295-9. PMID: 21410075
  59. 59. Mayumi T, Inui K, Maetani I, et al. Validity of the urinary trypsinogen-2 test in the diagnosis of acute pancreatitis. Pancreas 2012;41(6):869-75.
  60. 60. Tian F, Li H, Wang L, Li B et al. The diagnostic value of serum C-reactive protein, procalcitonin, interleukin-6 and lactate dehydrogenase in patients with severe acute pancreatitis. Clinica Chimica Acta 2020;510:665-670. doi:10.1016/j.cca.2020.08.029.
  61. 61. Wang L, Qi X, Tian F, Li H et al. Diagnostic value of hematological parameters in acute pancreatitis. Ann Palliat Med 2020 Sep;9(5):2716-2722.
  62. 62. Johnson C, L é vy P. Detection of gallstones in acute pancreatitis: when and how? Pancreatology 2010;10(1):27-32.
  63. 63. Arvanitakis M, Delhaye M, Maertelaere VD et al. Computed tomography and MRI in the assessment of acute pancreatitis. Gastroenterology. 2004;126(3):715-23.
  64. 64. Fleszler F, Friedenberg F, Krevsky B, Friedel D, Braitman LE: Abdominal computed tomography prolongs length of stay and is frequently unnecessary in the evaluation of acute pancreatitis. Am J Med Sci 2003;325(5):251-5.
  65. 65. Vege SS, DiMagno MJ, Forsmark CE, et al. Initial Medical Treatment of Acute Pancreatitis: American Gastroenterological Association Institute Technical Review. Gastroenterology 2018 ;154(4):1103-1139.
  66. 66. Banks PA, Bollen TL, Dervenis C, et al: Classification of acute pancreatitis–2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62(1):102-11.
  67. 67. Marshall JC, Cook DJ, Christou NV et al. Multiple organ dysfunction score: a reliable descriptor of complex clinical outcome. Crit Care Med 1995;23(10):1638-52.
  68. 68. Papachristou GI, Muddana V, Yadav D, et al: Comparison of BISAP, Ranson’s, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis. Am J Gastroenterol 2010;105(2):435-41; quiz 442.
  69. 69. Singh VK, Wu BU, Bollen TL, et al: Early systemic inflammatory response syndrome is associated with severe acute pancreatitis. Clin Gastroenterol Hepatol 2009;7(11):1247-51.
  70. 70. Haydock, Mittal A, Wilms HR, et al. Fluid therapy in acute pancreatitis: anybody’s guess. Ann Surg 2013;257(2):182-8.
  71. 71. Zhao G, Zhang JG, Wu HS, et al. Effects of different resuscitation fluid on severe acute pancreatitis. World J Gastroenterol 2013 Apr 7;19(13):2044-52. doi: 10.3748/wjg.v19.i13.2044.
  72. 72. Wu BU, Hwang JQ , Gardner TH, et al. Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol 2011;9(8):710-717.e1.
  73. 73. Brown A, Orav J, Banks PA. Hemoconcentration is an early marker for organ failure and necrotizing pancreatitis. Pancreas 2000;20(4):367-72.
  74. 74. Wu BU, Johannes RS, Sun X, et al. Early changes in blood urea nitrogen predict mortality in acute pancreatitis. Gastroenterology 2009 Jul;137(1):129-35. doi: 10.1053/j.gastro.2009.03.056.
  75. 75. Brown A, Baillargeon JD, Hughes MD, Banks PA. Can fluid resuscitation prevent pancreatic necrosis in severe acute pancreatitis? Pancreatology 2002;2(2):104-7.
  76. 76. Basurto Ona X, Rigau Comas D, Urrútia G. Opioids for acute pancreatitis pain. Cochrane Database Syst Rev 2013;(7):CD009179.
  77. 77. Helm JF, Venu RP, Geenen JE, et al. Effects of morphine on the human sphincter of Oddi. Gut 1988;29(10):1402-7.
  78. 78. Yi F, Ge L, Zhao J, et al: Meta-analysis: total parenteral nutrition versus total enteral nutrition in predicted severe acute pancreatitis. Intern Med 2012;51(6):523-30.
  79. 79. Moraes JM, Feiga GE, Chebli LA, et al: A full solid diet as the initial meal in mild acutepancreatitis is safe and result in a shorter length of hospitalization: results from a prospective, randomized, controlled, double-blind clinical trial. J Clin Gastroenterol 2010;44(7):517-522.
  80. 80. Louie BE, Noseworthy T, Hailey D et al. 2004 MacLean-Mueller Prize enteral or parenteral nutrition for severe pancreatitis: a randomized controlled trial and health technology assessment. Can J Surg 2005;48(4):298-306. PMID: 16149365
  81. 81. Casas M, Mora J, Fort E et al. Total enteral nutrition vs. total parenteral nutrition in patients with severe acute pancreatitis.Rev Esp Enferm Dig 2007;99(5):264-9.
  82. 82. Singh N, Sharma B, Sharma M et al. Evaluation of early enteral feding through nasogastric and nasojejunal tube in severe acute pancreatitis. A non-inferiority randomized controlled trial. Pancreas 2012;41(1):153-159.
  83. 83. Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev 2010;2010(1):CD002837.
  84. 84. Freeman MF, Werner J, van Santvoort HC et al. Interventions for necrotizing pancreatitis. Summary of a multi-disciplinary consensus conference. Pancreas 2012;41(8):1176-94.
  85. 85. Wittau M, Mayer B, Scheele J, Henne-Bruns D, Dellinger EP, Isenmann R: Systematic review and meta-analysis of antibiotic prophylaxis in severe acute pancreatitis. Scand J Gastroenterol 2011;46(3):261-70.
  86. 86. Lenhart DK, Balthazar EJ. MDCT of acute mild (nonnecrotizing) pancreatitis: abdominal complications and fate of fluid collections. AJR Am J Roentgenol 2008;190(3):643-9.
  87. 87. Clancy TE, Ashley SW. Current management of necrotizing pancreatitis. Adv Surg 2002;36:103-21. PMID: 12465548
  88. 88. Jacobson BC, Baron TH, Adler DG, et al. ASGE guideline: The role of endoscopy in the diagnosis and the management of cystic lesions and inflammatory fluid collections of the pancreas. Gastrointest Endosc 2005;61(3):363-70.
  89. 89. Seewald S, Groth S, Omar S, et al. Aggressive endoscopic therapy for pancreatic necrosis and pancreatic abscess: a new safe and effective treatment algorithm (videos). Gastrointest Endosc 2005;62(1):92-100.
  90. 90. Runzi M, Niebel W, Goebell H et al. Severe acute pancreatitis: non surgical treatment of infected necrosis. Pancreas 2005;30(3):195-9.
  91. 91. van Brunschot S, van Grinsven J, van Santvoort HC, et al. Endoscopic or surgical step-up approach for infected necrotising pancreatitis: a multicentre randomised trial. Lancet 20186;391(10115):51-58.
  92. 92. Garg PK , Sharma M , Madan K et al. Primary conservative treatment results in mortality comparable to surgery in patients with infected pancreatic necrosis. Clin Gastroenterol Hepatol 2010;8(12):1089-1094.e2.
  93. 93. van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010;362(16):1491-502.
  94. 94. Dellinger EP, Tellado JM, Soto NE et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double blind, placebo controlled study. Ann Surg 2007;245(5):674-83.
  95. 95. Das S, Singh PP, Phillips A, et al. Newly diagnosed diabetes mellitus after acute pancreatitis: A systematic review and meta-analysis. Gut 2014;63(5):818-31.
  96. 96. Schepers NJ, Hallensleben NDL, Besselink MG, et al. Urgent endoscopic retrograde cholangiopancreatography with sphincterotomy versus conservative treatment in predicted severe acute gallstone pancreatitis (APEC): a multicentre randomised controlled trial. Lancet 202018;396(10245):167-176.
  97. 97. Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis. Cochrane Database Syst Rev 2012;(5):CD009779.
  98. 98. Moretti A, Papi C, Aratari A et al. Is early endoscopic retrograde cholangiopancreatography useful in the management of acute biliary pancreatitis? A meta-analysis of randomized controlled trials. Dig Liver Dis2008;40(5):379-385.
  99. 99. Arguedas MR, Dupont AW, Wilcox CM. Where do ERCP, endoscopic ultrasound, magnetic resonance cholangiopancreatography, and intraoperative cholangiography ft in the management of acute biliary pancreatitis? A decision analysis model. Am J Gastroenterol 2001;96(10):2892-2899.
  100. 100. Larson SD, Nealson WH, Evers BM. Management of gallstone pancreatitis. Adv Surg 2006;40:265-84.
  101. 101. Aboulian A, Chan T, Yaghoubian A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg 2010; 251:615. 2010;251(4):615-9.
  102. 102. Falor AE, de Virgilio C, Stabile BE, et al. Early laparoscopic cholecystectomy for mild gallstone pancreatitis. Arch Surg 2012;147(11):1031-5.
  103. 103. Trna J, Vege SS, Pribramska V, et al: Lack of significant liver enzyme elevation and gallstones and/or sludge on ultrasound on day 1 of acute pancreatitis is associated with recurrence after cholecystectomy: a population-based study. Surgery 2012;151(2):199-205.
  104. 104. Navaneethan U, Vege SS, Chari ST, Baron TH. Minimally invasive techniques in pancreatic necrosis. Pancreas 2009;38(8):867-75.
  105. 105. Papachristou GI, Takahashi N, Chahal P, et al. Peroral endoscopic drainage/debridement of walled-off pancreatic necrosis. Ann Surg 2007; 2007;245(6):943-51.
  106. 106. Traverso LW, Kozarek RA. Pancreatic necrosectomy: definitions and technique. J Gastrointest Surg 2005;9(3):436-9.
  107. 107. Mortelé KJ, Girshman J, Szejnfeld D, et al. CT-guided percutaneous catheter drainage of acute necrotizing pancreatitis: clinical experience and observations in patients with sterile and infected necrosis. AJR Am J Roentgenol 2009;192(1):110-6.
  108. 108. Gluck M, Ross A, Irani S, et al. Dual modality drainage for symptomatic walled-off pancreatic necrosis reduces length of hospitalization, radiological procedures, and number of endoscopies compared to standard percutaneous drainage. J Gastrointest Surg 2012;16(2):248-56; discussion 256-7.
  109. 109. Bradley EL 3rd, Howard TJ, van Sonnenberg E, Fotoohi M. Intervention in necrotizing pancreatitis: an evidence-based review of surgical and percutaneous alternatives. J Gastrointest Surg 2008;12(4):634-9.
  110. 110. BaronTH, DiMaio CJ , Wang AY, et al. American Gastroenterological Association Clinical Practice Update: Management of Pancreatic Necrosis Gastroenterology 2020;158(1):67-75.e1.

Written By

Rezan Karaali and Firdes Topal

Submitted: 17 December 2020 Reviewed: 13 January 2021 Published: 03 February 2021