Acute Pancreatitis Clinical Presentation
- Author: Timothy B Gardner, MD; Chief Editor: BS Anand, MD more...
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.
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.
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.
Vege SS, Ziring B, Jain R, Moayyedi P, for the Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on the diagnosis and management of asymptomatic neoplastic pancreatic cysts. Gastroenterology. 2015 Apr. 148(4):819-22. [Medline].
Telem DA, Bowman K, Hwang J, Chin EH, Nguyen SQ, Divino CM. Selective management of patients with acute biliary pancreatitis. J Gastrointest Surg. 2009 Dec. 13(12):2183-8. [Medline].
Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan. 62(1):102-11. [Medline].
Haydock MD, Mittal A, van den Heever M, Rossaak JI, Connor S, Rodgers M, et al. National Survey of Fluid Therapy in Acute Pancreatitis: Current Practice Lacks a Sound Evidence Base. World J Surg. 2013 May 30. [Medline].
Ai X, Qian X, Pan W, Xu J, Hu W, Terai T, et al. Ultrasound-guided percutaneous drainage may decrease the mortality of severe acute pancreatitis. J Gastroenterol. 2010. 45(1):77-85. [Medline].
Li H, Qian Z, Liu Z, Liu X, Han X, Kang H. Risk factors and outcome of acute renal failure in patients with severe acute pancreatitis. J Crit Care. 2010 Jun. 25(2):225-9. [Medline].
Whitcomb DC, Yadav D, Adam S, et al. Multicenter approach to recurrent acute and chronic pancreatitis in the United States: the North American Pancreatitis Study 2 (NAPS2). Pancreatology. 2008. 8(4-5):520-31. [Medline]. [Full Text].
Granger J, Remick D. Acute pancreatitis: models, markers, and mediators. Shock. 2005 Dec. 24 Suppl 1:45-51. [Medline].
Singla A, Csikesz NG, Simons JP, Li YF, Ng SC, Tseng JF, et al. National hospital volume in acute pancreatitis: analysis of the Nationwide Inpatient Sample 1998-2006. HPB (Oxford). 2009 Aug. 11(5):391-7. [Medline]. [Full Text].
Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc. 2002 Dec. 56(6 Suppl):S226-30. [Medline].
Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible?. Pancreas. 2010 Jan. 39(1):5-8. [Medline].
Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in African-American and Hispanic patients. Pancreas. 2004 Nov. 29(4):291-7. [Medline].
Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. 2006 May 18. 354(20):2142-50. [Medline].
Suppiah A, Malde D, Arab T, Hamed M, Allgar V, Smith AM, et al. The Prognostic Value of the Neutrophil-Lymphocyte Ratio (NLR) in Acute Pancreatitis: Identification of an Optimal NLR. J Gastrointest Surg. 2013 Feb 1. [Medline].
Tenner S, Baillie J, Dewitt J, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis. Am J Gastroenterol. 2013 Jul 30. [Medline].
Imamura Y, Hirota M, Ida S, Hayashi N, Watanabe M, Takamori H, et al. Significance of renal rim grade on computed tomography in severity evaluation of acute pancreatitis. Pancreas. 2010 Jan. 39(1):41-6. [Medline].
Balthazar EJ, Ranson JH, Naidich DP, Megibow AJ, Caccavale R, Cooper MM. Acute pancreatitis: prognostic value of CT. Radiology. 1985 Sep. 156(3):767-72. [Medline].
Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990 Feb. 174(2):331-6. [Medline].
Balthazar EJ. Staging of acute pancreatitis. Radiol Clin North Am. 2002 Dec. 40(6):1199-209. [Medline].
Imrie CW. Prognostic indicators in acute pancreatitis. Can J Gastroenterol. 2003 May. 17(5):325-8. [Medline].
Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. 2007 Aug. 5(8):946-51; quiz 886. [Medline]. [Full Text].
Bakker OJ, van Brunschot S, van Santvoort HC, Besselink MG, Bollen TL, Boermeester MA, et al. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014 Nov 20. 371(21):1983-93. [Medline].
Maravi-Poma E, Gener J, Alvarez-Lerma F, Olaechea P, Blanco A, Dominguez-Munoz JE. Early antibiotic treatment (prophylaxis) of septic complications in severe acute necrotizing pancreatitis: a prospective, randomized, multicenter study comparing two regimens with imipenem-cilastatin. Intensive Care Med. 2003 Nov. 29(11):1974-80. [Medline].
Isenmann R, Rünzi M, Kron M, et al. Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial. Gastroenterology. 2004 Apr. 126(4):997-1004. [Medline].
Johnson CD, Kingsnorth AN, Imrie CW, et al. Double blind, randomised, placebo controlled study of a platelet activating factor antagonist, lexipafant, in the treatment and prevention of organ failure in predicted severe acute pancreatitis. Gut. 2001 Jan. 48(1):62-9. [Medline]. [Full Text].
Aboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B, Neville A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010 Apr. 251(4):615-9. [Medline].
van Santvoort HC, Besselink MG, Bakker OJ, Hofker HS, Boermeester MA, Dejong CH, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010 Apr 22. 362(16):1491-502. [Medline].