Acute pancreatitis is a disease characterized by acute inflammation of the pancreas, commonly as a result of excessive alcohol use or secondary to gallstones. Every year in the United States, it is responsible for over 200,000 hospital admissions leading to more than $2 billion in healthcare expenses. Patients usually present with rapidly escalating right upper quadrant or epigastric pain, often radiating to the back, accompanied by nausea and vomiting.

The pathophysiology of acute pancreatitis differs somewhat depending on the etiology and is still somewhat poorly understood. Alcoholic pancreatitis, the most important cause in males, is likely caused not only by the direct insult of the drug and its toxic metabolites of acetaldehyde and fatty acid ethyl esters (FAEEs), but the reactive oxygen species (ROS) produced by ethanol metabolism that can induce oxidative stress within the gland.

These factors help to stimulate acinar cells by increased trypsin activation and destabilize zymogen granules and lysosomes leading to autodigestion and necrosis. Once intrapancreatic inflammation is present, whatever the source or etiology, activation of inflammatory mediators may trigger extrapancreatic inflammation including systemic inflammatory response syndrome (SIRS) and acute respiratory distress syndrome (ARDS).

Continue Reading

Similarly, pancreatitis due to hypertriglyceridemia, the third leading cause, is thought by many to be triggered by free fatty acid and free radical production in the pancreas, albeit by excess triglycerides being hydrolyzed by pancreatic lipase. It has also been postulated that the pathogenesis is more likely related to local ischemia due to hyperviscosity from elevated levels of chylomicrons.

The etiology of the disease is extremely varied. It is difficult to discuss pathophysiology, diagnosis and treatment without first reviewing a fairly complete list of the causes. In general, most of them involve either direct or indirect toxic effects, partial or complete ductal obstruction or other causes of inflammation. The most common offenders are listed below; easily remembered by the mnemonic It Hurts Badle.

I. Infectious- the following have been implicated: (viral) mumps, rubella, hepatitis B, herpes simplex, coxsackie, echovirus, adenovirus, cytomegalovirus (CMV), Epstein-Barr virus (EBV), human immunodeficiency virus (HIV), (bacterial) Mycoplasma, Legionella, Leptospira, Salmonella, (fungal) Aspergillus, (parasitic) Toxoplasma, Cryptosporidium, Ascaris. Idiopathic.

T. Tumor

H. Hypercalcemia – see endocrine, Hereditary causes – mutations in cystic fibrosis transmembrane conductance regulator gene (CFTR), cationic trypsinogen gene (PRSS1) and serine protease inhibitor Kazal type 1 gene (SPINK1).

U. Ulcer (penetrating duodenal ulcer)

R. Renal failure (most commonly associated with peritoneal dialysis), remember Ranson’s Criteria (see section III. “Default management”).

T. Trauma – to midepigastrium

S. Stricture, Stent, Sphincter of Oddi dysfunction, Scorpion Sting

B. Biliary obstruction (gallstone pancreatitis)

A. Alcohol, Anatomic anomaly (pancreas divisum, annular pancreas, Autoimmune.

D. Drugs – (mnemonic FEAST) Furosemide, Estrogens, Etacrynic acid, angiotensin-converting enzyme (ACE) inhibitors, Azathioprine, Sulfa drugs, Thiazides, Tetracycline, and others such as metronidazole, mercaptopurine, valproate, and antiretroviral therapy are the most common.

L. Lipids – hypertriglyceridemia (triglycerides greater than 1000 (milligrams/deciliter [mg/dL])

E. Endoscopic retrograde cholangiopancreatography (ERCP)

The American College of Gastroenterology (ACG) recognizes three features essential to the diagnosis of acute pancreatitis. Two of the following three criteria should be met:

  • Characteristic epigastric pain
  • Abdominal computed tomography (CT) findings consistent with pancreatic inflammation
  • Elevation of serum amylase or lipase, or both, to three or more times the upper limit of normal

Of note, serum amylase levels may be falsely low or normal in those with significant hypertriglyceridemia as the cause of acute pancreatitis.

Many other laboratory tests including pancreatic isoamylase, trypsin, trypsinogen-2, pancreatitis-associated protein (PAP) and trypsinogen activation protein have been proposed as effective diagnostic tools, but have not been shown to be more cost-effective or a better predictor of disease.

The patient with acute pancreatitis typically presents complaining of rapid onset of epigastric pain associated with anorexia, nausea and vomiting. Many patients, especially males, will have a history of heavy alcohol use or recent binge drinking and may also be experiencing withdrawal symptoms secondary to inability to continue this excessive consumption.

Patients may also be experiencing shortness of breath from pleural effusion, pneumonia or diaphragmatic irritation. Those whose disease is secondary to gallstone obstruction and associated cholestasis may complain of a jaundiced appearance and scleral icterus.

The prevalence of the disease varies depending on the etiology of acute pancreatitis. Alcoholic pancreatitis is more common in men, while gallstones are more commonly the cause for women. Hypertriglyceridemia, the third most common cause overall, is much more prevalent in pregnancy. Hereditary causes should be considered in younger patients as the incidence overall increases with age.

The differential diagnosis for acute pancreatitis is broad as it includes most etiologies of diffuse abdominal pain. (See the chapter “Abdominal pain: generalized”.) As many patients present with abdominal distension, it is important to exclude an acute abdomen secondary to perforated viscus, cholecystitis, appendicitis, ectopic pregnancy, ischemic bowel, and small or large bowel obstruction. Other infectious causes that can mimic acute pancreatitis include pyelonephritis, perinephric abscess, psoas abscess, and viral gastroenteritis.

Classic epigastric pain is also seen in those with esophagitis or gastroesophageal reflux disease (GERD), esophageal rupture (Boerhaave syndrome), peptic ulcer disease, or even acute coronary syndrome. The severe pain and associated nausea and vomiting associated with nephrolithiasis can be mistaken for acute pancreatitis as well. Sharp, “tearing” pain that radiates to the back is pathognomonic of aortic dissection.

Acute gallstone pancreatitis can sometimes present with signs and symptoms of biliary obstruction. The differential diagnosis of these patients must include causes of hepatitis (including elevated liver enzymes). Similarly, hepatic etiologies should be considered in those that present with ascites or pleural effusion.

Although the differential diagnosis is often large, a complete history and physical together with appropriate laboratory and imaging studies can generally distinguish between them and confirm the diagnosis rapidly.

There are several physical examination findings that are important to recognize to help confirm the diagnosis of acute pancreatitis that vary widely depending on the severity of the disease at presentation.

The patient may have tachycardia and fever, as well as tachypnea if aspiration pneumonia or pleural effusion or ARDS is present. Altered mental status may be present, especially in those with concomitant alcohol withdrawal; encephalopathy or coma with shock with severe disease may be encountered.

On head and neck examination, the sclera may be icteric and parotid enlargement secondary to mumps should be ruled out. Most patients with acute pancreatitis are profoundly volume depleted and may have tacky or dry mucous membranes. Skin may be jaundiced in those with an obstructive cause including gallstone and tumor. The abdomen and back should be inspected for ecchymosis associated with hemorrhage.

Ecchymosis located at the flanks (Grey-Turner’s sign) and periumbilically (Cullen’s sign) have been described. In those patients with significant hypertriglyceridemia as the etiology of pancreatitis, eruptive xanthomas on the extensor surfaces may be the first clue.

Crackles may be auscultated on lung exam (especially right lower lung field), as pneumonia and atelectasis secondary to diaphragmatic irritation with shallow respiration are not uncommon. Additionally, decreased breath sounds with dullness to percussion and decreased vocal fremitus may be discovered, as right-sided or bilateral pleural effusions are relatively common. In those with severe acute pancreatitis, ARDS may be present.

The epigastrium is classically tender and sometimes accompanied by voluntary guarding with distension from ileus possible. Rarely, an epigastric mass from the formation of a pseudocyst may be palpable on careful examination. Hepatomegaly from alcoholic or viral hepatitis may be evident by palpation and percussion. Palpation of the left upper quadrant should be performed to evaluate for splenomegaly secondary to liver disease with portal hypertension.

Panniculitis, tender red-brown nodules, usually located on the lower extremities, secondary to subcutaneous fat necrosis, can rarely be seen and is often associated with pancreatic malignancy. Polyarthritis associated with panniculitis and pancreatitis has also very occasionally been described, dubbed the PPP (pancreatitis, polyarthritis, panniculitis) syndrome.

Physical examination findings most specific for the patient with acute pancreatitis include upper abdominal tenderness and diminished, but not absent, bowel sounds. Tenderness with voluntary guarding is classically described in the epigastric area, but may commonly be present in the right and left upper quadrants. The abdomen is commonly distended and may be tympanic on percussion with concomitant ileus, or conversely, shifting dullness may be demonstrated with pancreatic ascites.

See D. above for physical exam findings.

Measuring serum amylase and lipase levels is the most useful initial laboratory diagnostic step in making the diagnosis of pancreatitis. These tests, when levels are three or more times the upper limit of normal, have been recognized by the ACG as one of three features (along with characteristic abdominal pain and CT findings) essential to diagnosis. Of note, serum amylase levels may be falsely low or normal in those with significant hypertriglyceridemia.

Complete blood count should be ordered at presentation to evaluate for leukocytosis that may indicate cholangitis, cholecystitis, pancreatic abscess, or other potential etiology of diffuse abdominal pain including perforated viscus, appendicitis, pyelonephritis, and ectopic pregnancy. Hemoglobin and hematocrit should be followed serially for the possibility of hemorrhagic complications. Platelet count may be diminished in those with alcoholic liver disease or hepatitis or hepatic steatosis secondary to dyslipidemia in those with hypertriglyceridemia.

A complete metabolic profile is also recommended to evaluate renal and hepatic function. Serum calcium is important to monitor as it may precipitously drop during hospitalization, or if elevated, may represent the etiology of the disease. Depending upon the pattern, elevated transaminases will help diagnose viral or alcoholic hepatitis. Elevated alkaline phosphatase and bilirubin may also be associated with alcoholic hepatitis, but may also indicate biliary obstruction and gallstone pancreatitis.

Patients with acute pancreatitis present often with vague abdominal complaints making a diagnosis challenging. Often imaging studies are ordered based upon ascertaining the etiology of the symptoms with a large list of life-threatening differential diagnoses in mind.

Considering the degree of pain associated with the disease together with alarming physical exam findings, determining which patients have acute appendicitis, cholecystitis, ectopic pregnancy, aortic dissection, acute pancreatitis, acute coronary syndrome, or simple gastroenteritis can often be challenging in the emergency department. Of course the history and physical with point-of-care testing can narrow this differential substantially, but often imaging tests are ordered not to confirm acute pancreatitis, but to eliminate other etiologies of abdominal pain.

Abdominal plain films are helpful in assessing any patient with acute abdominal pain. It is important to rule out perforation and small or large bowel obstruction. Additionally, evidence of nephrolithiasis can sometimes be seen as well as foreign bodies or the telltale pancreatic calcifications of chronic pancreatitis. The liver size can often be estimated if hepatitis is considered. Patients with pancreatitis may display localized ileus of the small bowel or “sentinel loop”.

Chest films are important diagnostic tests in those with suspected pancreatitis as many patients will have pleural effusion, air space disease secondary to aspiration pneumonia, atelectasis, or even ARDS. The mediastinum and diaphragm can also be visualized for free air to exclude esophageal or bowel rupture.

If acute pancreatitis is suspected, abdominal ultrasound is usually indicated. This is especially important in those patients with the initial diagnosis to exclude biliary obstruction. Patients with a significant history of alcohol ingestion or abuse may erroneously be diagnosed with alcoholic pancreatitis and are still at risk for gallstone pancreatitis.

Most cases of biliary pancreatitis resolve as the stone has already passed at admission, but they are at significant risk of recurrence of pancreatitis within 6 weeks unless addressed. Additionally, those patients with elevated triglycerides are still statistically more likely to have gallstone pancreatitis.

Ultrasound is the test of choice to evaluate for biliary obstruction. However, as mentioned above, pancreatitis is often associated with functional ileus, or just increased bowel gas, and visualization can be limited on presentation without decompression. Although direct visualization of the pancreas is often compromised, the presence of gallstones or gallbladder thickening or sludge can usually be evaluated. Overall, the American College of Gastroenterology (ACOG) strongly recommends abdominal ultrasound imaging in patients presenting with signs and symptoms consistent with acute pancreatitis.

CT scan is an important tool to help not only in the diagnosis of acute pancreatitis, but also to assist in assessing prognosis and severity of disease. Abdominal CT is often performed initially to help delineate the cause of acute abdominal pain and eliminate other life-threatening etiologies that may include perforated viscus, appendicitis or even aortic dissection (see C. History part 3).

The CT scan, both unenhanced and contrasted, can be used in the Balthazar index to assess severity of disease. (See section III. “Default management”.) Determining the presence and percentage of pancreatic necrosis is essential in those with severe acute pancreatitis and is used by some to guide the decision to add antibiotic treatment. The most recent guidelines, however, do not recommend prophylactic antibiotics in those patients with necrotizing pancreatitis.

Although indicated if severe pancreatitis is suspected, most patients with pancreatitis do not require CT imaging as necrosis or pseudocyst formation is uncommon. Splenic vein thrombosis, a condition that often resolves with resolution of acute pancreatitis, or is associated with chronic pancreatitis, may be seen. Additionally, to best identify indicators of severity, the CT should ideally not be done for 48 to 72 hours after onset of symptoms.

Magnetic resonance imaging (MRI) and magnetic resonance cholangiopancreatography (MRCP) have some utility in the patient with pancreatitis in accurately identifying pseudocyst, abscess, or other fluid collections such as hemorrhage, as well as necrosis. MRCP is valuable for detecting the presence of cholelithiasis, especially if ERCP is contraindicated.

If gallstone pancreatitis is suspected, one may consider ERCP. Since most stones pass without intervention, this procedure should only be considered acutely in those with severe acute pancreatitis with persistent obstruction or cholangitis. In patients without evidence of acute cholangitis, MRCP or endoscopic ultrasound are preferred over ERCP.

Although serum amylase and lipase levels are routinely, and appropriately, ordered tests to help confirm the diagnosis of acute pancreatitis, they do not accurately predict severity of disease and daily monitoring of these laboratory tests is of little value.

The management of the patient with acute pancreatitis, of course, is somewhat determined by its cause, especially if ductal obstruction is suspected. Two phases of acute pancreatitis have been clearly identified with the first week after onset characterized by SIRS with the possibility of organ failure, followed thereafter by local complications. As the severity of the disease varies broadly from mild, isolated only to the pancreas, to severe cases with multiple organ failure and high mortality, the determination of appropriate level of care is of utmost importance. For this reason, several methods of risk stratification have been developed over the last decades, starting with Ranson’s criteria in 1974. Ranson’s criteria and Glasgow’s prognostic criteria are based on values obtained in the first 48 hours.

On admission

Age greater than 55 years

White cell count greater than 16 × 103/microliter

Lactate dehydrogenase (LDH) greater than 350 international units/liter (IU/L)

Aspartate aminotransferase (AST) greater than 250IU/L

Blood glucose greater than 200 milligrams/deciliter (mg/dL)

After 48 hours

Hematocrit fall greater than 10%

Urea increase greater than 5mg/dL

Serum calcium less than 8mg/dL

Oxygen partial pressure (PO2), 60 (millimeters mercury) mmHg

Base deficit greater than 4 milliequivalents/liter (mEq/L)

Fluid loss greater than 6 liters (L)

Within 48 hours

White cell count greater than 15 × 103/microliter

Blood glucose greater than 180mg/dL

Serum urea greater than 96mg/dL

PO2 less than 60mmHg

Serum calcium less than 8mg/dL

LDH greater than 600IU/L

Transaminases greater than 200IU/L

Serum albumin less than 3.2mg/dL

The Acute Physiology and Chronic Health Evaluation (APACHE) II scale offers a higher predictive value, and although it is a bit more cumbersome, it is the assessment scale most often currently recommended. Interestingly, it has been shown that the early warning score (EWS), a common scoring system that measures bedside parameters including blood pressure, urine output, pulse, respiratory rate, and level of consciousness, is similar to APACHE II in predicting mortality at 3 days.

The Balthazar CT severity index has also been widely used and is based on a scoring system that assigns points based on non-contrasted CT findings that include inflammation and presence and degree of fluid collection, as well as the degree of necrosis on contrasted views. CT scans have often already been obtained in the emergency department to rule out other etiologies of the patient’s symptoms.

Computed tomography grading (computed tomography without contrast)

A. Normal pancreas: points = 0

B. Pancreatic enlargement: points = 1

C. Pancreatic inflammation or peripancreatic fat: points = 2

D. Single peripancreatic fluid collection: points = 3

E. Two or more fluid collections or retroperitoneal air: points = 4

While patients with grades A, B, and C were observed to have a mortality rate of 4%, grades D and E had a mortality rate of 14% with a morbidity rate of 54%.

Contrast enhanced computed tomography
  • 0% necrosis: points = 0
  • Less than 30% necrosis: points = 2
  • 30 to 50% necrosis: points = 4
  • Greater than 50% necrosis: points = 6

In those patients without evidence of necrosis, there is a reported mortality rate of 0%, versus a mortality rate of 23% with necrosis.

A CT severity index built to integrate both CT grades and degree of necrosis was proposed to improve the prognostic value of this testing. A combined point total from both scores of 7 or more suggests severe pancreatitis with a 17% mortality rate.

Much research has been done to develop other methods of risk stratification to give prognostic information within the first 24 hours of presentation. The BISAP (scores 0-5 based on Blood, urea, nitrogen levels (BUN), Impaired mental status, SIRS, Age greater than 60 years, Pleural effusion) method predicted in-hospital mortality based on values obtained during the first day of hospitalization.

Most recently, BUN levels alone have been identified as a useful tool to assess early prediction of mortality in acute pancreatitis. As evaluation of renal function is key to many of the above criteria, its efficacy is a bit intuitive. An algorithm was developed that accurately predicted significantly increased mortality in those patients either with an admission BUN of 20mg/dL or higher or in those whose BUN increased by 2 or more at 24 hours. Other laboratory markers have also been proposed including procalcitonin and C-reactive protein levels.

In 2013 the Revised Atlanta Classification was published (recently updated from the longstanding guidelines from the 1993 Atlanta criteria) providing a different staging system based on disease severity.

The revised Atlanta Classification defines three severity criteria:

  • Mild acute pancreatitis (absence of organ failure and local complications)
  • Moderately severe acute pancreatitis (local complications and/or transient organ failure (<48 hours)
  • Severe acute pancreatitis (persistent organ failure > 48 hours)

Patient findings associated with a severe course can be divided into four main categories (patient characteristics, SIRS criteria [>2], and laboratory and radiologic findings). Risk factors for patients include age greater than 55 years, obesity, altered sensorium, and comorbid diseases. Laboratory values increasing risk include a BUN >20 mg/dL or rising (or elevated creatinine) and hematocrit >44% or rising. Pleural effusions or infiltrates and multiple or extensive extrapancreatic fluid collections on radiographic evaluation are also associated with severe disease.

Immediate management consists of aggressive IV hydration, analgesia, initial bowel rest, then early enteral nutrition, supplemental oxygen (O2) and determination of the need for ERCP. The patient should be risk stratified based on prognostic clinical scoring systems as described in more detail in the “Default management” section.

Fluid should be aggressively replaced as these patients are significantly intravascularly depleted from poor fluid intake, emesis and possible third spacing from inflammation. Patients often develop tachycardia and hypotension quickly, making them more susceptible to renal compromise and multi-organ failure.

Decreased pancreatic perfusion presents a higher risk of necrosis and subsequent hemorrhage. Initial infusion of 500 to 1000 milliliters (ml) of isotonic fluid per hour in those volume depleted patients, and 250 to 350 ml per hour in euvolemic patients is currently recommended. There is recent evidence that lactated Ringer’s solution may be preferred and this has a moderate recommendation from the ACOG. Of course, close monitoring for pulmonary edema or volume overload is paramount.

Additionally, since gut permeability has been implicated as a cause of infectious complications that have been shown to be responsible for significantly increased mortality, adequate perfusion is essential. For this reason, and in light of the fact that pancreatitis is a catabolic state, nutritional support with enteral, rather than parenteral, feeding, by nasojejunal or nasogastric tube if needed, should be initiated within the first 48 hours if possible. Probiotic treatment has not been shown to decrease infectious complications, however, and moreover increases the risk of bowel ischemia and mortality.

It has been shown that early enteral nutrition decreases disease severity and complications, such as prolonged ileus. Although emphasis in the past has been focused on reducing pancreatic stimulation, early feeding likely minimizes loss of gut permeability and subsequent exacerbation of SIRS.

Adequate parenteral analgesia should be administered. Secondary to significantly fewer side effects, risk of toxicity and a longer half-life, morphine is preferred over meperidine. There are currently no human studies that suggest increased sphincter of Oddi pressures by manometry of morphine over meperidine.

By convention, patients are initially kept nil per os to theoretically decrease secretion of pancreatic enzymes and prevent further inflammation. Nasogastric decompression may be required if the patient has evidence of ileus or has intractable nausea and vomiting.

Supplemental oxygen is additionally recommended initially to bolster oxygen delivery and minimize necrosis.

In those patients with acute gallstone pancreatitis and obstructive jaundice or acute cholangitis, ERCP with sphincterotomy in the first 24 hours of admission is recommended. No benefit has been shown with ERCP in mild acute biliary pancreatitis without cholangitis.

The management of acute pancreatitis varies somewhat depending on the cause, but most importantly on the severity of the disease. Multiple prognostic indicators have been mentioned here to assist the physician in determining the level of care required, but also to remind us of what clinical criteria to monitor in the first 48 hours. Vital signs need to be monitored for signs of SIRS. High or low temperature, tachycardia, tachypnea, and hypotension should therefore be anticipated.

The patient should be assessed daily for any changes in the severity of illness. Chest examination findings include development of crackles, decreased breath sounds and dullness to percussion associated with pneumonia or pleural effusion. Additionally, the abdomen should be assessed for evidence of ascites or hemorrhage (see section D. “Physical exam findings”).

Since alcohol abuse is often the initiating cause, monitoring for seizure, tremor and confusion secondary to alcohol withdrawal is recommended.

If biliary obstruction is suspected, the patient may develop hepatomegaly, Murphy’s sign, scleral icterus or jaundice. These findings are important to help guide decisions regarding antibiotic coverage in the setting of cholangitis, additional imaging with ultrasound or performing ERCP.

Routine lab tests include daily complete blood count, and a complete metabolic profile that includes BUN, creatinine, blood glucose, transaminases, bilirubin, and alkaline phosphatase should be obtained to assess for evidence of renal or hepatic failure and signs of SIRS.

Serum calcium should be followed to assess for acute decrease and as part of Ranson’s criteria. Serum sodium and potassium are also part of the APACHE II scoring system that should be assessed frequently on these patients. Arterial blood gas for PO2 or O2 saturation by pulse oximetry should be followed routinely.

Daily monitoring of serum amylase and lipase is of little value and is interestingly not included in any of the prognostic scoring systems.

Long-term management in general consists of eliminating or avoiding the causative insult. For example, abstinence from alcohol, discontinuation of causative medications, cholecystectomy, and treatment of hypertriglyceridemia are essential to prevent recurrence in those respective patients. Similarly, management of chronic or inherited medical conditions, such as autoimmune pancreatitis, chronic kidney disease or hypercalcemia can help prevent recurrence.

It has been estimated that over 60% of cases of biliary pancreatitis will recur within 6 weeks unless cholecystectomy is performed. It is recommended that cholecystectomy be done as soon as possible in cases of mild biliary pancreatitis either during the same admission or within 4 weeks after discharge.

If pancreatitis is complicated by the formation of a sterile pseudocyst, a repeat CT scan in the weeks following discharge should be ordered to assure resolution.

Acute pancreatitis patients should be monitored closely for signs of circulatory collapse, SIRS and multi-organ failure. Even with aggressive volume resuscitation, patients may continue to decline secondary to third spacing and proinflammatory factors. It has been estimated that 10 to 20% of patients develop SIRS secondary to various mechanisms mediated by cytokines and inflammatory cell activation that are poorly understood.

Aggressive volume replacement in severe pancreatitis may lead to respiratory compromise from the development of pleural effusions or pulmonary edema and ascites. Patients are also at increased risk of pneumonia from aspiration and from the introduction of nasogastric or nasojejunal tubes. Severe acute pancreatitis patients may develop ARDS.

Parenteral opioid analgesics, while recommended for management of pain, may also exacerbate hypotension, predisposing the patient to a greater risk of pancreatic necrosis and multi-organ failure.


Patients with chronic kidney disease should be monitored for signs of volume overload with initial fluid resuscitation. Care should be taken with administration of analgesic medications and electrolytes should be closely followed.

Caution should be exercised with the use of opiate analgesic medications in patients with significant liver disease.

Aggressive intravenous (IV) fluid administration is generally recommended at presentation to avoid circulatory collapse and shock. However, if the patient has coexisting systolic heart failure, fluids should be given judiciously with frequent reassessment for volume overload.

No change in standard management.

No change in standard management.

No change in standard management.

Patients diagnosed with human immunodeficiency virus (HIV) and on antiretroviral therapy should be evaluated for medication-induced pancreatitis.

No change in standard management.

No change in standard management.

Patients should be monitored for hemorrhage in the presence of severe pancreatitis with necrosis.

No change in standard management.

Depending on the etiology of pancreatitis, common sign out considerations include anticipation of development of alcohol withdrawal, and subsequent coverage with benzodiazepine administration as per the Clinical Institute Withdrawal Assessment (CIWA) protocol, and development of SIRS and multi-organ failure.

Two to five days for mild to moderate disease.

Typically, patients may be discharged when they are tolerating a low fat diet, are ambulatory or back to baseline mobility, are not requiring IV medication for pain control, and other comorbidities are well managed.


Most cases of acute pancreatitis can be managed at discharge by their primary care physician. In those who suffered severe pancreatitis requiring intensive care unit care, follow-up by gastroenterology and/or surgery (depending upon etiology and possible complications of abscess, pseudocyst or hemorrhage) is usually indicated.

Patients with hypercalcemia, familial hypertriglyceridemia, or who have development of diabetes secondary to pancreatic insufficiency may need endocrinology follow-up.

Infectious disease follow-up may be needed for those patients with HIV, or who developed pancreatitis secondary to an infectious cause (see 1. What every physician needs to know).

Recently described autoimmune pancreatitis should be followed by a rheumatologist.


Most patients will require no laboratory or radiologic testing prior to outpatient follow-up visits. As mentioned previously, the etiology of the pancreatitis dictates much of the testing and subsequent monitoring. Following serum transaminases, alkaline phosphatase and total bilirubin may be useful in patients who suffered biliary pancreatitis. A fasting lipid profile is indicated if pancreatitis was due to hypertriglyceridemia.

Patients with a history of excessive alcohol use should be counseled and offered treatment for alcoholism that may include inpatient treatment programs.

Patients with acute alcoholic pancreatitis should be warned of the consequences of repeated bouts of pancreatitis that will likely occur unless alcohol ingestion is reduced or eliminated. Chronic pancreatitis is complicated by chronic abdominal pain that is difficult to manage, diabetes and its complications, chronic diarrhea from malabsorption, and frequent hospitalizations.

In the same way, other etiologies of pancreatitis (listed in I. What every physician needs to know) if untreated or poorly managed can lead to the same fate.

All patients are candidates for the influenza vaccine during flu season and should be evaluated based on comorbidities whether pneumococcal vaccine should be administered.

Patients presenting with alcohol-induced acute pancreatitis should avoid future alcohol use. Smoking cessation is recommended for all patients as it has been identified as a risk factor for those patients. In those patients presenting with mild disease with gallstones present, a cholecystectomy prior to discharge has been shown to reduce incidence of recurrence.

Balthazar, EJ. “Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation”. Radiology. vol. 223. 2002. pp. 603-613.

Banks, PA, Freeman, ML. “Practice guidelines in acute pancreatitis”. Am J Gastroenterol. vol. 101. 2006. pp. 2379-2400.

Banks, P, Bollen, T, Dervenis, C, Gooszen, H, Johnson, c. “Classification of acute pancreatitis- 2012: revision of the Atlanta classification and definitions by international consensus”. Gut. vol. 62. 2013. pp. 102-111.

DiMagno, MJ, Wamsteker, E, DeBenedet, AT. “Advances in managing acute pancreatitis”. F100 Med Rep. vol. 1. 2009. pp. 1-8.

Mounzer, R, Langmead, C, Wu, B, Evans, A. “Comparison of existing clinical scoring systems to predict persistent organ failure in patients with acute pancreatitis”. Gastroenterology. vol. 142. 2012. pp. 1476-1482.

McClave, SA. “Nutritional support in acute pancreatitis”. Gastroenterol Clin North Am. vol. 36. 2007. pp. 65-74.

Pavlidis, TE, Pavlidis, ET, Sakantamis, AK. “Advances in prognostic factors in acute pancreatitis: a mini-review”. Hepatobiliary Pancreat Dis Int. vol. 9. 2010. pp. 482-486.

Riedel, DJ, Gebo, KA, Moore, RD, Lucas, GM. “A ten-year analysis of the incidence and risk factors for acute pancreatitis requiring hospitalization in an urban HIV clinical cohort”. AIDS Patient Care STDS. vol. 22. 2008. pp. 113-121.

Stevens, T, Parsi, MA, Walsh, RM. “Acute pancreatitis: Problems in adherence to guidelines”. Cleve Clin J Med. vol. 76. 2009. pp. 697-4672.

Tenner, S, Baillie, J, DeWitt, J, Vege, S. “American College of Gastroentrology Guideline: Management of Acute Pancreatitis”. American Journal of Gastroenterology. vol. 108. 2013. pp. 1400-1415.

Tonsi, AF, Bacchion, M, Crippa, S, Malleo, G, Bassi, C. “Acute pancreatitis at the beginning of the 21st century: The state of the art”. World J Gastroenterol. vol. 15. 2009. pp. 2945-2959.

Wang, GJ, Li, Y, Zhou, ZJ, Wang, C, Meng, WJ. “Integrity of the pancreatic duct-acinar system in the pathogenesis of acute pancreatitis”. Hepatobiliary Pancreat Dis Int. vol. 9. 2010. pp. 242-247.

Wu, BU, Bakker, OJ, Papachristou, GI, Besselink, MG, Repas, K, van Santvoort, HC, Muddana, V, Singh, VK, Whitcomb, DC, Gooszen, HG, Banks, PA. “Blood Urea Nitrogen in the Early Assessment of Acute Pancreatitis”. Arch Intern Med. vol. 171. 2011. pp. 669-676.