AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland.

The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatitis. It can recur intermittently, contributing to the functional and morphologic loss of the gland. Recurrent attacks are referred to as chronic pancreatitis. Both forms of pancreatitis are present in the ED with acute clinical findings.

Pathophysiology

Because the pancreas is located in the retroperitoneal space with no capsule, inflammation can spread easily. In acute pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first. This process is known as acute edematous pancreatitis.

When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland, the inflammation evolves into hemorrhagic or necrotizing pancreatitis.

Pseudocysts and pancreatic abscesses can result from necrotizing pancreatitis because of enzymes being walled off by granulation tissue (ie, pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic tissue (ie, pancreatic abscess formation). Ultrasonography or, preferably, CT can be used to detect both.

The inflammatory process can cause systemic effects because of the presence of cytokines, such as bradykinins and phospholipase A. These cytokines may cause vasodilation, increase in vascular permeability, pain, and leukocyte accumulation in the vessel walls. Fat necrosis may cause hypocalcemia. Pancreatic B-cell injury may lead to hyperglycemia.

Frequency

United States

Acute pancreatitis has an incidence of approximately 40 cases per year per 100,000 adults.¹

International

The incidence of acute pancreatitis ranges between 5 and 80 per 100,000 population, with the highest incidence recorded in the United States and Finland.²

Mortality/Morbidity

• Although acute pancreatitis should be noted, chronic pancreatitis has a more severe presentation as episodes recur.
• Acute respiratory distress syndrome (ARDS), acute renal failure, cardiac depression, hemorrhage, and hypotensive shock all may be systemic manifestations of acute pancreatitis in its most severe form.
• Mild edematous pancreatitis occurs in about 80% of presentations, and the mortality rate is below 1%.
• Severe acute pancreatitis occurs in about 20% of presentations, with a mortality rate reaching 24%.

Race

The annual incidence of acute pancreatitis in Native Americans is 4 per 100,000 population; in whites, 5.7 per 100,000 population; and in blacks, 20.7 per 100,000 population.³

Sex

No predilection exists.

Age

The risk for African Americans aged 35-64 years is 10 times higher than for any other group. African Americans are at higher risk than whites in that same age group.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

• The main presentation of acute pancreatitis is epigastric pain or right upper quadrant pain radiating to the back.
• Nausea and/or vomiting
• Fever
• Query the patient about recent surgeries and invasive procedures (ie, endoscopic retrograde cholangiopancreatography) or family history of hypertriglyceridemia.
• Patients frequently have a history of previous biliary colic and binge alcohol consumption, the major causes of acute pancreatitis.

Physical

• Tachycardia
• Tachypnea
• Hypotension
• Fever
• Abdominal tenderness, distension, guarding, and rigidity
• Mild jaundice
• Diminished or absent bowel sounds
• Because of contiguous spread of inflammation (effusion) from the pancreas, lung auscultation may reveal basilar rales, especially in the left lung.
• Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcemia.
• Severe cases may have a Grey Turner sign (ie, bluish discoloration of the flanks) and Cullen sign (ie, bluish discoloration of the periumbilical area) caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis.

Causes

• The major causes are long-standing alcohol consumption and biliary stone disease.
  
  
  • In developed countries, the most common cause of acute pancreatitis is alcohol abuse.
    
    
    • On the cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release.
    • On the ductal level, ethanol increases the permeability of ductules, which allow enzymes to reach the parenchyma, resulting in pancreatic damage.
    • Ethanol increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the formation of protein plugs that block the pancreatic outflow and obstruction.
  • Another major cause of acute pancreatitis is biliary stone disease (eg, cholelithiasis, choledocholithiasis). A biliary stone may lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma.
• Minor causes of acute pancreatitis
  
  
  • Medications, including azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, nonsteroidal anti-inflammatory drugs (NSAIDs), mercaptopurine, methyldopa, and tetracyclines
  • Endoscopic retrograde cholangiopancreatography (ERCP)
  • Hypertriglyceridemia (When the triglyceride [TG] level exceeds 1000 mg/U, an episode of pancreatitis is more likely.)
  • Peptic ulcer disease
  • Abdominal or cardiopulmonary bypass surgery, which may insult the gland by ischemia
  • Trauma to the abdomen or back, resulting in sudden compression of the gland against the spine posteriorly
  • Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction
  • Viral infections, including mumps, coxsackievirus, cytomegalovirus (CMV), hepatitis virus, Epstein-Barr virus (EBV), and rubella
  • Bacterial infections, such as mycoplasma
  • Intestinal parasites, such as Ascaris, which can block the pancreatic outflow
  • Pancreas divisum
  • Scorpion and snake bites
• Vascular factors, such as ischemia or vasculitis

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Perforated viscus
Acute peritonitis
Choledocholithiasis
Macroamylasemia
Macrolipasemia
Intestinal obstruction
Pancreatic cancer
Malabsorption syndromes/processes

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• A complete blood count (CBC) demonstrates leukocytosis (WBC >12,000) with the differential being shifted toward the segmented polymorphs.
• If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and crossmatch.
• Measure blood glucose level because it may be elevated from B-cell injury in the pancreas.
• Obtain measurements for BUN, creatine (Cr), and electrolytes (Na, K, Cl, CO₂, P, Mg); a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids.
• Measure amylase levels, preferably the amylase P, which is more specific to pancreatic pathology. Levels more than 3 times higher than normal strongly suggest the diagnosis of acute pancreatitis.
• Lipase levels also are elevated and remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase levels may be elevated in the presence of a normal serum amylase level.
• Perform liver function tests (eg, alkaline phosphatase, serum glutamic-pyruvic transaminase [SGPT], serum glutamic-oxaloacetic transaminase [SGOT], G-GT) and bilirubin, particularly with biliary origin pancreatitis.

Imaging Studies

• Perform plain kidneys, ureters, bladder (KUB) radiography with the patient in the upright position to exclude viscus perforation (ie, air under the diaphragm). In patients with a recurrent episode of chronic pancreatitis, peripancreatic calcifications may be noted.



• Ultrasonography can be used as a screening test. If overlying gas shadows secondary to bowel distention are present, it may not be specific.
  


• CT is the most reliable imaging modality in the diagnosis of acute pancreatitis. The criteria for diagnosis are divided by Balthazar and colleagues into 5 grades⁴, as follows:
  
  • Grade A - Normal pancreas
    
  
  
  • Grade B - Focal or diffuse gland enlargement
    
  
  
  • Grade C - Intrinsic gland abnormality recognized by haziness on the scan
    
  
  
  • Grade D - Single ill-defined collection or phlegmon
    
  
  
  • Grade E - Two or more ill-defined collections or the presence of gas in or nearby the pancreas
    


• The use of contrast material intravenously is yet to be proved detrimental on the microcirculation of the pancreas in cases of severe necrotizing pancreatitis.

Other Tests

• Para-aminobenzoic acid test (ie, bentiromide [Chymex] test) for chronic pancreatitis

Procedures

• In the case of biliary pancreatitis where a dilated obstructed common bile duct is diagnosed by CT or any other imaging modality and an elevated plasma bilirubin (>5 mg/dL), an ERCP with a sphincterotomy is warranted within the first 72 hours.
• Biliary pancreatitis should always be treated eventually with a cholecystectomy after the process has subsided.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Emergency Department Care

Most of the cases presenting to the ED are treated conservatively, and approximately 80% respond to such treatment.⁵

• Fluid resuscitation
  
  
  • Monitor accurate intake/output and electrolyte balance of the patient.
  • Crystalloids are used, but other infusions, such as packed red blood cells (PRBCs), are occasionally administered, particularly in the case of hemorrhagic pancreatitis.
  • Central lines and Swan-Ganz catheters are used in patients with severe fluid loss and very low blood pressure.
• Patients should have nothing by mouth, and a nasogastric tube should be inserted to ensure an empty stomach and to keep the GI system at rest.
• Begin parenteral nutrition if the prognosis is poor and if the patient is going to be kept in the hospital for more than 4 days.
• Analgesics are used to relieve pain. Meperidine is preferred over morphine because of the greater spastic effect of the latter on the sphincter of Oddi.
• Antibiotics are used in severe cases associated with septic shock or when the CT scan indicates that a phlegmon of the pancreas has evolved.
• Other conditions, such as biliary pancreatitis associated with cholangitis, also need antibiotic coverage. The preferred antibiotics are the ones secreted by the biliary system, such as ampicillin and third-generation cephalosporins.
• Continuous oxygen saturation should be monitored by pulse oximetry, and acidosis should be corrected. When tachypnea and pending respiratory failure develops, intubation should be performed.
• Perform CT-guided aspiration of necrotic areas, if necessary.
• An ERCP may be indicated for common duct stone removal.

Consultations

Consult a general surgeon in the following cases:

• For phlegmon of the pancreas, surgery can achieve drainage of any abscess or scooping of necrotic pancreatic tissue. It should be followed by postoperative lavage of the pancreatic bed.
• In patients with hemorrhagic pancreatitis, surgery is indicated to achieve hemostasis, particularly because major vessels may be eroded in acute pancreatitis.
• Patients who fail to improve despite optimal medical treatment or patients who push the Ranson score even further are taken to the operating room. Surgery in these cases may lead to a better outcome or confirm a different diagnosis.
• In biliary pancreatitis, a sphincterotomy (ie, surgical emptying of the common bile duct) can relieve the obstruction. A cholecystectomy may be performed to clear the system from any source of biliary stones.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

The goal of pharmacotherapy is to relieve pain and minimize complications.

Drug Category: Antibiotics

These agents are used to cover the microorganisms that may grow in biliary pancreatitis and acute necrotizing pancreatitis. The empiric antibiotic regimen usually is based on the premise that enteric anaerobic and aerobic gram-bacilli microorganisms are often the cause of pancreatic infections. Once culture sensitivities are made, adjustments in the antibiotic regimen can be done.

Drug Category: Analgesics

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and has sedating properties, which are beneficial for patients who have sustained trauma or have painful lesions.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Inpatient Care

• Medical treatment consists of the following:
  
  
  • Fluid resuscitation and hydration: Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal area. These fluids have to be replaced promptly within the first 24 hours with both crystalline and colloid solutions, sometimes reaching 10 L.
  • Central venous pressure, pulmonary artery wedge pressure, and urine output (>0.5 mL/kg/h) can be followed up as markers of adequate hydration.
  • The previously followed rule of NPO has changed, and prospective randomized controlled trials have showed that enteral tube feeding is superior to parenteral nutrition to avoid malnutrition and reverse the catabolic state of these patients.
  • Adequate analgesia: Opiate derivatives and epidural analgesia can be added if needed.
  • Antibiotic coverage is needed to prevent gram-negative sepsis.
• Surgery is an option in cases with complications of pancreatitis such as acute necrotizing pancreatitis where the necrotic phlegmon is excised to limit the source of sepsis, or in cases of hemorrhagic pancreatitis where the process has eroded into one of the vessels supplying the pancreas and a surgical control of bleeding is warranted.

Further Outpatient Care

• The patient should be monitored routinely with physical examination and amylase and lipase assays.

Transfer

• Transfer patients with Ranson scores of 0-2 to a hospital floor.  
• Transfer patients with Ranson scores 3-5 to an intensive care unit.  
• Transfer patients with Ranson scores higher than 5 to an intensive care unit with emergency surgery as a possibility.

Complications

• Infected pancreatic necrosis may result from seeding of bacteria into the inflammation.
• An acute pseudocyst is an effusion of pancreatic juice that is walled off by granulation tissue after an episode of acute pancreatitis.
• Hemorrhage into the GI tract retroperitoneum or the peritoneal cavity is possible because of erosion of large vessels.
• Intestinal obstruction or necrosis may occur.
• Common bile duct obstruction may be caused by a pancreatic abscess, pseudocyst, or biliary stone that caused the pancreatitis.
• An internal pancreatic fistula from pancreatic duct disruption or a leaking pancreatic pseudocyst may occur.

Prognosis

• Ranson developed a series of different criteria for the severity of acute pancreatitis.⁶ This scoring system is still widely used:
  
  
  • Present on admission
    
    
    • Older than 55 years
    • WBC higher than 16,000 per mcL
    • Blood glucose level higher than 200 mg/dL
    • Serum lactate dehydrogenase (LDH) level more than 350 IU/L
    • SGOT level (ie, aspartate aminotransferase [AST]) greater than 250 IU/L
  • Developing during the first 48 hours
    
    
    • Hematocrit fall more than 10%
    • BUN level increase more than 8 mg/dL
    • Serum calcium level less than 8 mg/dL
    • Arterial oxygen saturation less than 60 mm Hg
    • Base deficit higher than 4 mEq/L
    • Estimated fluid sequestration higher than 600 mL
• A Ranson score of 0-2 has a minimal mortality rate.
• A Ranson score of 3-5 has a 10-20% mortality rate.
• A Ranson score higher than 5 has a mortality rate of more than 50% and is associated with more systemic complications.
• Other scoring systems are Glasgow, Imrie, and APACHE II.

Patient Education

• Educate patients about the disease and advise them to avoid alcohol in binge amounts and to discontinue any risk factor, such as fatty meals and abdominal trauma.
• For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education article, Pancreatitis.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

1. Granger J, Remick D. Acute pancreatitis: models, markers, and mediators. Shock. Dec 2005;24 Suppl 1:45-51. [Medline].
2. Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc. Dec 2002;56(6 Suppl):S226-30. [Medline].
3. Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in African-American and Hispanic patients. Pancreas. Nov 2004;29(4):291-7. [Medline].
4. Balthazar EJ. Staging of acute pancreatitis. Radiol Clin North Am. Dec 2002;40(6):1199-209. [Medline].
5. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. May 18 2006;354(20):2142-50. [Medline].
6. Imrie CW. Prognostic indicators in acute pancreatitis. Can J Gastroenterol. May 2003;17(5):325-8. [Medline].
7. Bernhardt A, Kortgen A, Niesel HCh, Goertz A. [Using epidural anesthesia in patients with acute pancreatitis--prospective study of 121 patients]. Anaesthesiol Reanim. 2002;27(1):16-22. [Medline].
8. Calleja GA, Barkin JS. Acute pancreatitis. Med Clin North Am. Sep 1993;77(5):1037-56. [Medline].
9. Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ. Jun 12 2004;328(7453):1407. [Medline].
10. Moscati RM. Cholelithiasis, cholecystitis, and pancreatitis. Emerg Med Clin North Am. Nov 1996;14(4):719-37. [Medline].
11. Plock JA, Schmidt J, Anderson SE, Sarr MG, Roggo A. Contrast-enhanced computed tomography in acute pancreatitis: does contrast medium worsen its course due to impaired microcirculation?. Langenbecks Arch Surg. Apr 2005;390(2):156-63. [Medline].
12. Schwartz Gr, et al. Acute pancreatitis. In: Principles and Practice of Emergency Medicine. Vol 2. 1992:1782-6.
13. Sharma VK, Howden CW. Metaanalysis of randomized controlled trials of endoscopic retrograde cholangiography and endoscopic sphincterotomy for the treatment of acute biliary pancreatitis. Am J Gastroenterol. Nov 1999;94(11):3211-4. [Medline].
14. Steer ML. Classification and pathogenesis of pancreatitis. Surg Clin North Am. Jun 1989;69(3):467-80. [Medline].
15. Taylor SL, Morgan DL, Denson KD, Lane MM, Pennington LR. A comparison of the Ranson, Glasgow, and APACHE II scoring systems to a multiple organ system score in predicting patient outcome in pancreatitis. Am J Surg. Feb 2005;189(2):219-22. [Medline].
16. Trede M, Carter DC. Acute pancreatitis. In: Surgery of the Pancreas. 1993:161-259.
17. Werner J, Feuerbach S, Uhl W, Büchler MW. Management of acute pancreatitis: from surgery to interventional intensive care. Gut. Mar 2005;54(3):426-36. [Medline].

Article Last Updated: Jul 16, 2007