eMedicine Specialties > Radiology > Gastrointestinal

Pancreatitis, Acute

Author: , Staff Physician, Staff Physician, Department of Radiology, Harbor Medical Center, University of California at Los Angeles
Coauthor(s): Jeffrey Phillips, MD, Associate Clinical Professor of Radiological Sciences, University of California at Los Angeles School of Medicine, Chief of Diagnostic Radiology, Associate Chair, Department of Radiology, Harbor-University of California at Los Angeles Medical Center
Contributor Information and Disclosures

Updated: Mar 18, 2008

Introduction

Background

According to the 1992 International Symposium on Acute Pancreatitis, acute pancreatitis is defined as an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.¹ Acute pancreatitis is classified further into mild and severe forms. Mild acute pancreatitis is associated with minimal organ dysfunction and uneventful recovery. Severe acute pancreatitis is associated with pancreatic necrosis and may lead to organ failure and/or local complications.^2,3,4

Local complications of acute pancreatitis include fluid collections, pseudocyst formation, abscess, pancreatic necrosis, hemorrhage, venous thrombosis, and pseudoaneurysm formation (see Images 1-4).⁵ A pseudocyst is defined as a collection of pancreatic juice enclosed by a wall of fibrous or granulation tissue. A pseudocyst lacks a true epithelial lining and often communicates with the pancreatic duct. A pancreatic abscess is a circumscribed intra-abdominal collection of pus. The development of both pseudocyst and abscess usually requires 4 or more weeks from the initial clinical onset of acute pancreatitis.⁶ Pancreatic necrosis is defined as focal or diffuse areas of nonviable pancreatic parenchyma; it usually is associated with peripancreatic fat necrosis. Necrosis usually develops early in the course of acute pancreatitis.⁷

Gallstones and alcohol abuse are the most common causes of acute pancreatitis, accounting for 60-80% of cases. Other causes include blunt trauma to the abdomen, iatrogenic trauma (postoperative trauma, endoscopic retrograde cholangiopancreatography), hypertriglyceridemia, hypercalcemia, drug-induced, infectious etiologies (eg, mumps, cytomegalovirus), congenital anomalies (pancreas divisum, choledochocele), ampullary or pancreatic tumors, vascular abnormalities (atherosclerotic emboli, hypoperfusion, vasculitis), cystic fibrosis, and Reye syndrome. These miscellaneous causes account for approximately 10% of cases of acute pancreatitis. In approximately 10-25% of patients, no underlying cause is found.^8,9,10

For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education article Pancreatitis.

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Pathophysiology

The pathophysiology of acute pancreatitis is not understood clearly. Steinberg and Tenner note that a number of factors can initiate the inflammation; these factors include but are not limited to obstruction or overdistention of the pancreatic duct, exposure to ethanol and other toxins, hypertriglyceridemia, and hypercalcemia.¹¹ The end result is a release of activated pancreatic destructive enzymes into the pancreas and surrounding tissues. As stated by Steinberg and Tenner, "an unpredictable cascade of events" ensues that results in mild localized interstitial pancreatitis or in severe necrosis.¹¹ Furthermore, release of toxic factors (resulting from inflammatory response) into the systemic circulation may result in systemic complications such as shock, renal failure, or acute respiratory distress syndrome.

Frequency

United States

Frequency of acute pancreatitis increases with age. According to Go, the rate is 270 cases per 100,000 in the United States in persons aged 15-44 years. The rate is 540 cases per 100,000 in persons older than 65 years.¹²

Mortality/Morbidity

The clinical severity of acute pancreatitis varies from a mild disease with an uneventful course to a severe life-threatening illness associated with multisystemic organ failure (eg, shock, renal failure, acute respiratory distress syndrome). Multiple clinical systems have been devised to assess the severity of acute pancreatitis and to predict the prognosis. These include the Ranson criteria, the modified Glasgow criteria, and acute physiology and chronic health evaluation (APACHE II) criteria.

Acute pancreatitis takes a mild course in approximately 70-80% of patients. According to Beger et al, most patients with acute pancreatitis suffer edematous interstitial pancreatitis, which is a mild self-limited disease.¹³ In approximately 20-30% of patients, the disease follows a more severe clinical course. Pancreatic infection and multisystemic organ failure are the primary contributors to morbidity and mortality. More than 80% of deaths resulting from acute pancreatitis are from septic complications as a consequence of bacterial infection of pancreatic necrosis.

Race

For unknown reasons, the rate of pancreatitis is 3 times higher in black Americans than in white Americans. Maxson et al have reported that the prevalence of acute pancreatitis among patients with AIDS is approximately 4-22 per 100 patients.¹⁴ This is believed to result from increased infections of the pancreas and from HIV/AIDS medications.

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Sex

The frequency of pancreatitis is approximately equal in men and women. In female patients, pancreatitis tends to be caused by biliary stones, whereas alcohol abuse is the usual cause of pancreatitis in men.

Age

Pancreatitis is uncommon in children, with a rate of 2.7 cases per 100,000 in children younger than 15 years. The leading cause of acute pancreatitis in children is blunt trauma, which occasionally is associated with child abuse.¹⁵

Anatomy

The pancreas is a retroperitoneal organ and is positioned in the anterior pararenal space. It is posterior to the stomach and lesser sac and anterior to the abdominal aorta and upper lumbar vertebrae. The pancreas is divided descriptively into 4 parts including, (1) head (which includes the uncinate process), (2) neck, (3) body, and (4) tail.

The head of the pancreas is nestled in the duodenal C-loop. The uncinate process curves around the superior mesenteric vein. The neck, body, and tail extend obliquely and superiorly; the tail is associated closely with the splenic hilum. The splenic vein is applied to the posterior border of the pancreas. The splenic vein merges with the superior mesenteric vein behind the pancreatic neck to form the portal vein confluence. The splenic artery and the gastroduodenal artery run along the superior and anterior surfaces of the pancreas, respectively. The common bile duct extends inferiorly through or behind the pancreatic head on its course to the duodenum. The pancreas also may have an ectopic location within the duodenal or gastric wall that can become inflamed as well.

The pancreatic exocrine secretions/enzymes primarily are drained by the duct of Wirsung, which extends the length of the gland. The duct of Wirsung may empty into the duodenal papilla separately or be joined by the common bile duct to form a common channel, which then empties into the duodenal papilla. An accessory duct of Santorini, located in the pancreatic head and neck, also is present and normally drains into the duodenum (just proximal to the duct of Wirsung).

Presentation

Typical symptoms include the sudden onset of epigastric abdominal pain that radiates to the back and flanks. The pain usually is constant and boring. Nausea and vomiting are commonly associated symptoms. The symptoms may begin after a heavy meal or after a drinking binge.

On physical examination, the abdomen may be distended and tenderness may exist over the upper abdomen. Rarely, the skin overlying the flank or abdominal wall may have a purple hue from hemorrhage (Grey Turner/Cullen sign). Common laboratory abnormalities include elevated serum amylase and lipase levels, hyperglycemia, hypocalcemia, decreased lactic dehydrogenase levels, elevated serum glutamic-oxaloacetic transaminase levels, and leukocytosis.

Preferred Examination

Contrast-enhanced computed tomography (CECT) is the standard imaging modality for the evaluation of acute pancreatitis and its complications. Using non–contrast-enhanced CT, clinicians can establish the diagnosis and demonstrate fluid collections but cannot evaluate for pancreatic necrosis or vascular complications.

CECT allows complete visualization of the pancreas and retroperitoneum, even in the setting of ileus or overlying bandages from a recent surgical procedure. CECT can help detect almost all major abdominal complications of acute pancreatitis, such as fluid collections, pseudocysts, abscesses, venous thrombosis, and pseudoaneurysms. In addition, CECT can be used to guide percutaneous/interventional procedures such as diagnostic fine-needle aspiration or catheter placement. CECT may be performed on severely ill patients including intubated patients. Lastly, CECT can be used as a prognostic indicator of the severity of acute pancreatitis.

Other adjunctive imaging modalities include ultrasound (US), MRI, and angiography. US is especially useful in the diagnosis of gallstones and follow-up observation of pseudocysts. US also can be used to detect pancreatic pseudoaneurysms. The diagnostic efficacy of MRI is comparable to that of CECT, although MRI examination is more time consuming and costly.^16,17 Angiography is primarily used to help diagnose the vascular complications of acute pancreatitis.^{18,19,20,21,22}

Limitations of Techniques

The usefulness of CECT is limited in patients who are allergic to intravenous (IV) contrast or have renal insufficiency. Patients who have severe acute pancreatitis often require multiple scans to assess progress and/or complications. This necessitates significant radiation doses.

In addition, CECT is far less sensitive than US in detecting gallstones or biliary duct stones, a common cause of acute pancreatitis. Therefore, if gallstones or an impacted common bile duct stone is not seen on CT, US is necessary to document the presence or absence of gallstones.

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Differential Diagnoses

Abdominal Aortic Aneurysm, Rupture

Other Problems to Be Considered

Acute epigastric abdominal pain
Peptic ulcer disease
Gastritis
Perforated viscus
Esophageal spasm
Intestinal obstruction
Leaking aortic aneurysm

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