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Acute Pancreatitis Clinical Presentation

  • Author: Timothy B Gardner, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Apr 01, 2015
 

History

The cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically dull, boring, and steady. Usually, the pain is sudden in onset and gradually intensifies in severity until reaching a constant ache. Most often, it is located in the upper abdomen, usually in the epigastric region, but it may be perceived more on the left or right side, depending on which portion of the pancreas is involved. The pain radiates directly through the abdomen to the back in approximately one half of cases.

Nausea and vomiting are often present along with accompanying anorexia. Diarrhea can also occur. Positioning can be important, because the discomfort frequently improves with the patient in the supine position. The duration of pain varies but typically lasts more than a day. It is the intensity and persistence of the pain that usually causes patients to seek medical attention.

Ask the patient about recent operative or other invasive procedures (eg, endoscopic retrograde cholangiopancreatography [ERCP]) or family history of hypertriglyceridemia. Patients frequently have a history of previous biliary colic and binge alcohol consumption, the major causes of acute pancreatitis.

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Physical Examination

The following physical examination findings may be noted, varying with the severity of the disease:

  • Fever (76%) and tachycardia (65%) are common abnormal vital signs; hypotension may be noted
  • Abdominal tenderness, muscular guarding (68%), and distention (65%) are observed in most patients; bowel sounds are often diminished or absent because of gastric and transverse colonic ileus; guarding tends to be more pronounced in the upper abdomen
  • A minority of patients exhibit jaundice (28%)
  • Some patients experience dyspnea (10%), which may be caused by irritation of the diaphragm (resulting from inflammation), pleural effusion, or a more serious condition, such as acute respiratory distress syndrome (ARDS); tachypnea may occur; lung auscultation may reveal basilar rales, especially in the left lung
  • In severe cases, hemodynamic instability is evident (10%) and hematemesis or melena sometimes develops (5%); in addition, patients with severe acute pancreatitis are often pale, diaphoretic, and listless
  • Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcemia

A few uncommon physical findings are associated with severe necrotizing pancreatitis:

  • The Cullen sign is a bluish discoloration around the umbilicus resulting from hemoperitoneum
  • The Grey-Turner sign is a reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planes; more commonly, patients may have a ruddy erythema in the flanks secondary to extravasated pancreatic exudate
  • Erythematous skin nodules may result from focal subcutaneous fat necrosis; these are usually not more than 1 cm in size and are typically located on extensor skin surfaces; in addition, polyarthritis is occasionally seen

Rarely, abnormalities on funduscopic examination may be seen in severe pancreatitis. Termed Purtscher retinopathy, this ischemic injury to the retina appears to be caused by activation of complement and agglutination of blood cells within retinal vessels. It may cause temporary or permanent blindness.

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Complications

Acute fluid collections may occur, typically early in the course of acute pancreatitis. These are primarily detected by imaging studies rather than by physical examination. Because they lack a defined wall and usually regress spontaneously, most acute fluid collections require no specific therapy.

An acute pseudocyst is a collection of pancreatic fluid that is walled off by granulation tissue after an episode of acute pancreatitis; it requires 4 or more weeks to develop. Although pseudocysts are sometimes palpable on physical examination, they are usually detected with abdominal ultrasonography or computed tomography (CT).

Intra-abdominal infection is common. Within the first 1-3 weeks, fluid collections or pancreatic necrosis can become infected and jeopardize clinical outcome. From 3 to 6 weeks, pseudocysts may become infected or a pancreatic abscess may develop. A pancreatic abscess is a circumscribed intra-abdominal collection of pus, within or in proximity to the pancreas. It is believed to arise from localized necrosis, with subsequent liquefaction that becomes infected.

The intestinal flora is the predominant source of bacteria causing the infection. The usual suspects are Escherichia coli (26%), Pseudomonas species (16%), Staphylococcus species (15%), Klebsiella species (10%), Proteus species (10%), Streptococcus species (4%), Enterobacter species (3%), and anaerobic organisms (16%). Fungal superinfections may occur weeks or months into the course of severe necrotizing pancreatitis.

Pancreatic necrosis is a nonviable area of pancreatic parenchyma that is often associated with peripancreatic fat necrosis and is principally diagnosed with the aid of dynamic spiral CT scans. Distinguishing between infected and sterile pancreatic necrosis is an ongoing clinical challenge. Sterile pancreatic necrosis is usually treated with aggressive medical management, whereas almost all patients with infected pancreatic necrosis require surgical debridement or percutaneous drainage if they are to survive.

Hemorrhage into the gastrointestinal (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.

In the weeks (to months) following presentation, the physician’s attention shifts to developing signs of intra-abdominal infection, pancreatic pseudocyst, intra-abdominal hemorrhage, colon perforation, obstruction or fistulization, and multiorgan system failure.

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Contributor Information and Disclosures
Author

Timothy B Gardner, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of Pancreatic Disorders, Section of Gastroenterology, Dartmouth-Hitchcock Medical Center

Timothy B Gardner, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Pancreatic Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Brian S Berk, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of End Stage Liver Disease, Section of Gastroenterology, Dartmouth Hitchcock Medical Center

Brian S Berk, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center

Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Paul Yakshe, MD Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center

Paul Yakshe, MD is a member of the following medical societies: American College of Gastroenterology, American Pancreatic Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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