1. Description of the problem

What every clinician needs to know

Majority of acute pancreatitis is mild to intermediate in severity; however, almost 20% can be severe with multi-system organ dysfunction within hours to days of presentation, with upward of 30% mortality for infected necrotizing pancreatitis.

Key to management is early identification of those patients who are at risk to develop systemic failure and complications. Aggressive resuscitation, end organ support, avoidance of infection, adequate nutrition, and vigilance for complications are important components of care.

There is no standard model for prognosticating the severity and outcome for acute pancreatitis. Older patients, obese patients, patients with more rapid onset of end organ dysfunction and larger fluid requirements tend to do worse.

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Severity prediction tools vary, being based on age, lab findings, evidence of organ dysfunction, and CT scan findings. None are exceedingly accurate and all have significant drawbacks.

Ranson’s criteria includes age, evidence of systemic inflammatory response, and end organ dysfunction. However, the criteria are spread over 48 hours so it is not helpful in triaging patients on presentation.

The APACHE II score, which includes several criteria, can be used to judge severity on initial evaluation; however, it has been noted to be cumbersome.

Other scoring systems have been suggested as well. The Bedside Index of Severity in Acute Pancreatitis (BISAP) uses less variables and can be used on presentation. The Ballthazar criteria is based on CT scan findings so is not available for many on initial presentation.

Below are the criteria and associated mortality.

Ranson’s Criteria

Initial evaluation

Age > 55yrs

White blood cell count > 16,000/mm3

Blood glucose > 200 mg/dl (11.1 mmol/L)

Lactate dehydrogenase > 350 U/L

Aspartate aminotransferase > 250U/L

48 hours

Hematocrit Decrease by > or equal to 10%
Blood urea nitrogen Increase by > or equal to 5 mg/dl (1.8 mmol/L)
Serum calcium < 8 mg/dl (2 mmol/L)
pO2 < 60 mmHg
base deficit > 4 mEg/L
Fluid sequestration > 6 L
Positive criteria Mortality
<3 0-3%
3 or > 11-15%
6 or > 40%


<8 Mortality 4%
8 or > Mortality 11-18%


Blood urea nitrogen 25 mg/dl (8.9 mmol) or > 1 point
Abnormal mental status Glasgow Coma Score < 15 1 point
Evidence of SIRS
(Two or more of the following are present – temp < 36C or > 38C; respirations >20/min; heart rate > 90/min; WBC < 4,000 or > 12,000 or more than 10% bands)
1 point
Age > 60yrs 1 point
Pleural effusion 1 point
0-2 points < 2% mortality
3-5 points > 15% mortality
5 points 22% mortality

Balthazar CT scoring

A – normal

B – enlargement

Figure 1

Figure 1.
Acute interstitial pancreatitis – Balthazar grade B

C – peripancreatic inflammation

D – single fluid collection

E – multiple fluid collections

Figure 2

Figure 2.
Multiple fluid collections

Grades A and B – close to zero chance of infection and death. Increasing chance of infection with Grade C-E, with E having almost 50% chance of infection and 15% mortality.

Whichever severity score is used, consideration for admission to intensive care unit should be considered with scoring that reveals higher mortality such as a Ranson score of 3 or greater, APACHE II 8 or greater or BISAP score of 3 or greater.

Clinical features

Severe acute pancreatitis is a classic example of systemic inflammatory response. All the hallmarks of severe sepsis without evidence of infection.

Fever, tachycardia, leukocytosis, and end organ dysfunction can all be seen as result of the inflammatory cascade and cytokine mediators; however, no actual infection of the pancreas is initially present.

Because there can be concomitant biliary infection or obstruction, one needs to be mindful that although there is no pancreatic infection, there may be another site that needs antimicrobial treatment.

Severe acute pancreatitis results in sequestering of large amounts of third space fluid. This translates to a need for often massive fluid resuscitation, similar to burn resuscitation.

Complications such as pancreatic necrosis, hemorrhagic conversion, and infection can occur and need to be monitored for rigorously.

Intra-abdominal hypertension and abdominal compartment syndrome have been associated with acute severe pancreatitis.

Bladder pressures should be monitored in these patients as decompressive maneuvers have trended toward improved outcomes.

Perforation of bowel can also occur and should be keep in mind.

2. Emergency Management

The basis of care of the acute pancreatitis patient is airway, breathing, and circulation. Most pancreatitis patients, including severe pancreatitis, will require fluid resuscitation. Pain control, bowel rest, and treatment of concurrent problems such as biliary obstruction and/or infection are cornerstones of therapy.

In severe cases, fluid resuscitation of 250-350 cc per hour for first 48 hours has been suggested in order to keep the perfusion of both pancreas and end organs adequate.

Pulse oxymetry and frequent vital signs are mandatory.

Close monitoring of urine output is necessary.

Observation for complications of vigorous fluid administration such as pulmonary edema should also be provided.

Bladder pressure should be measured to assess for intra-abdominal hypertension.

Measurement of electrolytes, glucose, calcium, hematocrit, lactate and bicarbonate should be considered on a serial basis to assess resuscitation and monitor for complications such as hypocalcemia, hyperglucosemia, and hemorrhage.

Antibiotics are not routinely recommended in early acute severe pancreatitis unless there is evidence of concomitant infectious process such as biliary tree disease or suspected infected pancreatic necrosis or abscess.

Imaging in severe cases or where the diagnosis is questioned should include:

  • Chest x-ray (upright) – assess for pleural effusion, atelectasis and free air.
  • Ultrasound of right upper quadrant – to assess for concomitant biliary tree disease.
  • CT scan of abdomen and pelvis – preferably with oral and IV contrast; however, intravenous contrast maybe detrimental in patients with acute renal injury.
  • EUS/ERCP – If patient has evidence of choledocolithiasis or obstruction.

Nasogastric suction is not necessary unless patient is vomiting, has signs of marked ileus or is obtunded with inability to protect airway from vomitus.

Routine prophylaxis should be used such as stress ulcer and DVT unless contraindicated

Surgical consultation early for severe pancreatitis especially with biliary disease, abdominal hypertension, or complications such as necrosis or hemorrhage.

3. Diagnosis

Diagnostic criteria

Hallmark of acute pancreatitis is abdominal pain classically described as sudden in onset, constant in nature, epigastric in location with radiation to the back. Nausea and vomiting are often associated with it.

Abdominal tenderness with guarding and distention are usually present.

Fever and tachycardia accompany the syndrome.

Rarely, discoloration or ecchymosis is noted on flank (Gray Turner sign) or peri-umbilical (Cullen’s sign) reflecting retroperitoneal hemorrhage.

Diagnostic tests

Labs are useful in helping diagnose acute pancreatitis but also help determining the etiology and help use the information in determining severity and possible prognostication. Below are the labs that should be obtained in suspected pancreatitis.

Elevated serum amylase (greater than three times normal values), and serum lipase. Amylase and lipase levels do not correlate with severity of disease.

Liver enzymes such as alkaline phosphatase, total bilirubin, aspartate aminotransferase, and alanine aminotransferase will help determine biliary etiology and possible simultaneous disease process.

Cholesterol and triglycerides should be measured to rule out for cause of pancreatitis.

Complete blood count with hematocrit and white blood cell count with differential.

Blood urea nitrogen and creatinine to assess renal function.

Bicarbonate level to determine acid/base.

Electrolytes should be monitored as baseline and followed with resuscitation.

Calcium should be checked as possible etiology of pancreatitis (elevated) as well as prognostication with hypocalcemia.

Glucose should be monitored for gauge of pancreas endocrine function with elevation being criteria for more severe disease.

Arterial blood gas if patient with signs of respiratory distress or if markedly abnormal bicarbonate.

C reactive protein has been used for prognostication at 24-48 hrs, CRP > 10 mg/dl suggests severe pancreatitis.

Imaging should be obtained for diagnosis, etiology of pancreatitis, assessment for simultaneous disease, and prognostication.

Plain abdominal radiographs may reveal non-specific gas pattern or sentinel loop of bowel. Mostly useful to assess for free air which would go against a diagnosis of only acute pancreatitis.

Upright chest x-rays are useful to assess for presence of pleural effusion as well as baseline.

The ultrasound of the abdomen and specifically the biliary tree is important to not only help assess for biliary etiology for pancreatitis but also to help evaluate for biliary tree abnormalities such as acute cholecystitis and choledocolithiasis. In most patients with pancreatitis, the ultrasound does not assess the pancreas well.

CT scan of abdomen and pelvis is the tool of choice for both diagnosis and assessment of the retroperitoneum. It also assess other intra-abdominal structures such that many other etiologies for abdominal pain can be ruled in or out, such as gastric or bowel perforation, diverticulitis or appendicitis. It is also quickly obtained.

MRI/MRCP: although it does not use iodinated contrast and can evaluate the common bile duct and the pancreas, it is lengthy and may not be tolerated as well as CT scan.

Confirmatory tests

The history and physical findings along with increased amylase and lipase are in general sufficient enough for diagnosis of pancreatitis. However, if in doubt, CT imaging is generally confirmatory.

Differential diagnosis

Pathology of the upper abdomen should be considered in the differential along with acute pancreatitis.

Biliary colic, acute cholecystitis, choledocolithiasis, and ascending cholangitis.

Hepatic or splenic trauma.

Gastric outlet obstruction, gastritis, peptic ulcer disease, especially perforation.

Renal colic and pyelonephritis.

Ruptured abdominal aortic aneurysm.

Aortic dissection.

Acute coronary syndrome.

Bowel obstruction.

Inflammatory bowel disease.

Boehaave yndrome (esophageal tear).

4. Specific Treatment

Fluid resuscitation with isotonic fluid, with goal to keep end organs perfused with normal urine output and blood pressure is mainstay of care of the acute pancreatitis.

Bowel rest is instituted as well initially.

Pain control is important and classically should avoid morphine in favor of other opiates because of possible Sphincter of Oddi spasm.

Nutrition however should be considered as soon as patient is resuscitated. Early enteral nutrition should decrease infectious complications and mortality. Although post-pyloric jejunal feeds have been the mainstay, studies have shown that if gastric ileus is not present, gastric feeds also have a positive outcome.

Parental nutrition should be begun if enteral nutrition has not established after 5 days. Starting parental nutrition prior to 5 days, has been shown to have worsen outcomes.

No specific drug to decrease pancreatic enzyme function are used, such as octreotide. Stress ulcer prophylaxis should be used however.

If need for antibiotics for infected pancreatic necrosis, most common organisms are enteric flora such as E. coli, Klebsiella pneumoniane, and Enterococcus faecalis. Antibiotic with broad spectrum and good pancreatic penetration such as imipenem/cilastatin or meropenem should be considered.

Supportive care is keystone to the outcome of the severe pancreatitis patient.

Provision of thiamine,folate, and delirium tremens in the alcoholic pancreatitis patient should be included.

Consideration for therapeutic plasma exchange in hyperlipidemia pancreatitis has also been described.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

In a patient with severe pancreatitis, expect a prolonged hospital stay. With mortality at 10-15% for severe pancreatitis, which rises to 40% with infected necrosis, these patients have multiple opportunities for complications during the disease course.

Early, up to one week, most deaths are from multisystem organ failure. After this, the incidence of infectious complications, and hemorrhage rise.

Incorrect diagnosis

If the clinical diagnosis is in doubt, CT scan of abdomen and pelvis is usually the diagnostic test of choice. However, the myriad of possible complications, including hemorrhage, infection, bowel perforation and obstruction can hinder the patient’s course.

Looking for these complications with additional imaging such as CT scan is important if a seemingly stable patient worsens.


Patients with severe pancreatitis often develop fluid collections which organize into pseudocysts, usually at 4-6 weeks after presentation. This should be considered as if they become symptomatic with pain or obstruction, surgical or endoscopic intervention is required.

If the patient’s etiology was biliary, the gallbladder should be removed as soon as the patient is stable and inflammation as resolved.

Pancreatic insufficiency can result from severe necrosis or surgical necrosectomy.


Acute pancreatitis is inflammation of the pancreas which can extend beyond the organ itself.

Whatever the inciting event, there is damage to the acinar cells and essentially autodigestion. The resultant cascade is a complex interaction of inflammatory cells and cytokines with resultant vascular permeability, edema, and necrosis.

The systemic inflammatory response from this process may result in multi-system organ failure.


Depending on the population studied either ethanol use or gallstone disease is the leading cause of pancreatitis in approximately 80% of patients. Other causes such as viral infection, medications, traumatic, post procedural, and idiopathic make up the remaining 20%.


The overall mortality of patients with acute severe pancreatitis is 10-15%. Concomitant organ failure raises the mortality to 30%. Organ failure is the cause of most mortality in the first week with infection and other complications more prevalent later on.

Special considerations for nursing and allied health professionals.


What’s the evidence?

Nathens, AB, Curtis, JR, Beale, RJ, Cook, DJ, Moreno, RP, Romand, JA, Skerrett, SJ, Stapleton, RD, Ware, LB, Waldmann, CS. “Management of the critically ill patient with severe acute pancreatitis”. Crit Care Med. vol. 32. 2004 Dec. pp. 2524-36. (Nathens et al provides an in depth consensus statement of critical care experts from several societies on the evidence based care of the patient with severe acute pancreatitis.)

Taylor Bryce, R, Hall, JB, Schmidt, GA, Wood, LDH. “Acute Pancreatitis in the Critically Ill””. Principles of Critical Care. (Overview of the general care of the critically ill patient with acute pancreatitis, includes diagnosis, management and outcome.)

Banks, PA, Freeman, ML. “Practice guidelines in acute pancreatitis”. Am J Gastroenterol. vol. 101. 2006 Oct. pp. 2379-400. (Dr Banks provides an in depth review of prognostication in acute pancreatitis, methodology for diagnosis with summary of management, general care flowchart included.)

Whitcomb, DC. “Clinical practice. Acute pancreatitis”. N Engl J Med. vol. 354. 2006 May 18. pp. 2142-50. (A concise discussion of diagnosis, prognosis and management of acute pancreatitis including severe acute pancreatitis.)