Recommendations

Key Recommendations

The diagnosis of acute pancreatitis is made in patients presenting with acute epigastric pain. In most patients the diagnosis can be confirmed by the presence of at least two of the following three criteria:[8][47]

  • Pain consistent with the disease (e.g., epigastric pain of acute onset)

  • Elevated serum lipase or amylase if lipase is unavailable (>3 times the upper limit of normal)

  • Imaging study (computed tomography [CT] or magnetic resonance imaging/magnetic resonance cholangiopancreatography [MRI/MRCP]) consistent with acute pancreatitis

Physical findings vary according to the severity of acute pancreatitis, ranging from a generally well patient to a seriously ill patient with abnormal vital signs such as tachycardia and fever.[48]

An urgent assessment of hemodynamic status (looking for early signs of fluid loss) and for signs of organ dysfunction (to look for systemic inflammatory response syndrome [SIRS] and/or multi-organ failure) should be undertaken to identify patients requiring immediate resuscitation.[8][47]

  • Signs of hypovolemia may include hypotension, oliguria, dry mucous membranes, and decreased skin turgor. The patient may appear tachycardic, tachypneic, and sweating, particularly in more severe cases.

  • The definition of SIRS is met by the presence of at least two of the following:[49]

    • Pulse >90 beats per minute

    • Respiratory rate >20 per minute or partial pressure of carbon dioxide (PaCO₂) <32 mmHg

    • Temperature >100.4°F or <96.8ºF

    • WBC count >12,000 or <4000 cells/mm³, or >10% immature neutrophils (bands)

History

Most patients with acute pancreatitis present with severe epigastric pain. The pain usually begins suddenly and progresses over a short period of time (e.g., hours).

In patients who misuse alcohol, a more gradual progression may be reported if alcohol consumption was used to ease the pain.[1][5][19] Such patients may present with more advanced disease (e.g., with renal insufficiency and/or pancreatic necrosis) several days after symptom onset.

Typically, abdominal pain is localized to the epigastric region or left upper quadrant, and radiates to the back (sometimes band distribution, often straight through middle back; many patients describe it as being stabbed with a knife). The pain usually worsens with movement, and is alleviated when assuming the fetal position (bent over, with spine, hips, and knees flexed).[5][19]

Age and sex are important demographic variables, because the two most common causes of acute pancreatitis differ. Gallstone pancreatitis is seen most commonly in patients with gallbladder disease - typically women over the age of 40 years, with obesity and a positive family history.[50][51] Alcoholic pancreatitis is seen more frequently in men, generally younger than those with gallstone pancreatitis. The condition usually manifests after an average of 4-8 years of alcohol intake. Patients may present with agitation and confusion, and in severe distress. People who misuse alcohol, or those with a tumor, may give a history of anorexia, nausea, and vomiting with poor oral intake.[52]

Physical exam

The abdominal exam typically reveals marked tenderness in the epigastric region and distended abdomen, with diminished bowel sounds (if an ileus has developed), and voluntary guarding to palpation of the upper abdomen. Signs of hypovolemia (decreased skin turgor, dry mucous membranes, hypotension, and sweating) are usually found. In more severe cases, patients may be tachycardic and tachypneic. The pulse acutely is thin and thready, consistent with intravascular volume depletion. Fever may indicate a complicated pancreatitis or may simply represent cytokine release as part of the inflammatory process. Decreased breath sounds may be detected if there is a pleural effusion (more common on the left side); this is seen in up to 50% of patients with acute pancreatitis.[6]

Signs of complicated hemorrhagic pancreatitis are very rare: they include ecchymotic discoloration of the periumbilical skin (Cullen sign), both flanks (Grey-Turner sign), or the skin over the inguinal ligament (Fox sign).[9][12]

Laboratory workup

Most patients with acute pancreatitis will have a serum amylase and/or lipase greater than 3 times the upper limit of normal, typically over 1000 IU/dL. Levels of both of these enzymes increase soon after the onset of symptoms. Serum amylase levels usually peak at around 48 hours, and decrease to normal or near normal over the next 3-7 days. Serum lipase may remain elevated for up to 14 days.[28] Although serum lipase appears to be more specific than amylase and remains elevated for longer, the predictive value of both these tests may be reduced in certain patient populations (e.g., people with macroamylasemia or macrolipasemia); it is therefore important to have a low threshold for admitting and further assessing patients whose symptoms are suggestive of acute pancreatitis, even if these tests are normal.[8][53]

Serum lipase (if available) should be used in preference to serum amylase due to its higher sensitivity and larger diagnostic window.[8][28][54]​ Amylase can be normal in patients with acute pancreatitis caused by long-term alcohol misuse; in these patients, serum lipase is more sensitive. Serum lipase is also more sensitive than amylase in patients with lipemic serum, such as those with hypertriglyceridemia-induced acute pancreatitis. Lipemic serum can interfere with the amylase assay leading to a false normal amylase result. In general, serum lipase and/or amylase can be used to establish the diagnosis of acute pancreatitis when greater than 3 times normal in a patient with severe acute epigastric pain.[8]

In patients with a slightly elevated lipase the diagnosis of acute pancreatitis should be questioned. It is possible to have a slightly elevated serum amylase and lipase with little clinical significance, and people with diabetes may have significantly raised lipase levels without acute pancreatitis.[55] If the epigastric pain is not characteristic and the amylase and/or lipase are not more than 3 times normal, clinicians should also refer to imaging results to help establish the diagnosis of acute pancreatitis.

Leukocytosis with left shift is common in patients with acute pancreatitis. Sometimes this is due to unrelated infections, such as urinary tract infections. Patients should be evaluated for alternative causes of leukocytosis and managed as appropriate. When an infection is suspected, antibiotics should be given while the source of the infection is being investigated. However, once blood and other cultures are found to be negative and no source of infection is identified, antibiotics should be discontinued.[8]

Acute pancreatitis may be associated with hemoconcentration (elevated hematocrit) due to the reduction of intravascular volume as fluid moves into the peritoneum. Development of hemoconcentration is associated with an increased risk of developing necrotizing pancreatitis and organ failure.[56] As a result of decreased intravascular volume, there is decreased renal perfusion, and thus prerenal azotemia, manifested by an elevation of blood urea nitrogen. These patients need early rehydration with close monitoring. An elevation in creatinine is a warning sign that the patient may develop severe disease with renal failure, while urea >20 mg/dL is an independent predictor of mortality.[8][28]

Liver function tests are important in the early evaluation of acute pancreatitis. Elevation of aspartate aminotransferase/alanine aminotransferase (AST/ALT) is specific for gallstone pancreatitis.[57] However, most patients with gallstone pancreatitis will have a normal AST and/or ALT. In patients with elevations of the alkaline phosphatase and bilirubin, the possibility of a retained common bile duct stone must be considered (choledocholithiasis). While most gallstones that cause acute pancreatitis pass from the common bile duct into the duodenum, the possibility of a retained stone exists in a minority of patients.[8] If a patient with an elevated bilirubin develops signs of sepsis, early endoscopic retrograde cholangiopancreatography (ERCP) should be performed (within 24 hours).

The severity of acute pancreatitis is often not established in the first 24-48 hours, and serial laboratory testing at 6- to 12-hour intervals is needed for 48 hours from admission before severe disease can be excluded. Any patient with evidence of biliary obstruction or organ insufficiency requires close monitoring. Early, serial C-reactive protein (CRP) testing has been used in acute pancreatitis as an indicator of severity and progression of inflammation to necrosis.[58] CRP level ≥15 mg/dL at third day has been proposed as a prognostic factor for severe acute pancreatitis.[28] However, most patients with acute pancreatitis do not develop pancreatic necrosis, and the need for serial CRP testing for the diagnosis of pancreatic necrosis in people with acute pancreatitis has not been established.[59]

Other abnormal laboratory results may be present later in the clinical course (e.g., hypocalcemia as a marker for severe pancreatitis).[60] Triglycerides should be checked as part of the investigation into causative factors. An acute increase in circulating triglycerides in the range of a few hundred mg/dL is often seen in patients with acute pancreatitis; however, true hypertriglyceridemia-induced acute pancreatitis manifests a substantial increase in circulating triglycerides, commonly over 1000 mg/dL and as high as 9000 mg/dL.[27][28]

Severe acute pancreatitis is associated with SIRS and persistent organ dysfunction, which will require additional monitoring including regular assessment of oxygen saturations and arterial blood gas measurement (including pH and base deficit). Measurement of arterial blood gases should be considered if the patient shows signs of deterioration to assess both oxygenation and acid-base status; PaO₂ <60 mmHg is a sign of organ failure.[5][8][28]

Imaging

In most patients the diagnosis is based on clinical symptoms and laboratory testing. Abdominal imaging is not needed to confirm a diagnosis, but once a diagnosis of acute pancreatitis has been made, transabdominal ultrasound is required to rule out gallstones as the etiology.[8] Finding gallstones in a patient with acute pancreatitis is important because a cholecystectomy will prevent recurrent attacks. If the initial exam is inconclusive, a repeat ultrasound is recommended to improve accuracy.[8] The finding of a dilated biliary tree on transabdominal ultrasound is a sign that a retained common bile duct stone may be present. Such patients need to be monitored closely, and if biliary sepsis develops, an early ERCP is recommended.[8]

Early CT or MRI (magnetic resonance cholangiopancreatography [MRCP]) should be reserved for patients in whom the diagnosis of acute pancreatitis is not established.[8] Early CT will not identify most anatomic complications of acute pancreatitis, such as pseudocysts and necrosis. American College of Gastroenterology guidelines recommend CT or MRI/MRCP after 48 hours in patients who do not improve or whose symptoms worsen.[8] Other guidelines recommend a delay of 72-96 hours after symptom onset before contrast-enhanced CT or MRI to assess for necrosis.[28][47]​ Do not order unenhanced CT alongside intravenous contrast-enhanced CT because the addition of unenhanced CT does not provide additional diagnostic information and exposes patients to unnecessary radiation.[61][62]​

In patients needing CT or MRI/MRCP to confirm a diagnosis of acute pancreatitis (e.g., those with atypical pain or slightly raised lipase/amylase level), the imaging results require skilled interpretation. The characteristic findings in acute pancreatitis are: inflammatory stranding of the peripancreatic fat; peripancreatic fluid; and/or loss of the pancreatic border. However, a swollen pancreas is a nonspecific finding that does not confirm the diagnosis. MRI/MRCP has the advantage of not requiring intravenous contrast or radiation, although intravenous gadolinium enhances images as compared with noncontrast MRI. In addition, MRCP allows better visualization of common bile duct stones and the pancreatic duct. It can more readily distinguish solid from cystic in dealing with peripancreatic collections.[62]

Plain x-rays are not needed for the diagnosis of acute pancreatitis. A chest x-ray may show pleural effusion and basal atelectasis.[63]​​

In patients with acute pancreatitis and evidence of biliary obstruction without signs of sepsis, MRCP may be useful to exclude obstructing common bile duct stones.[62][64]​​ Endoscopic ultrasound (EUS) can be used as an alternative to MRCP to identify choledocholithiasis if it is highly suspected in the absence of cholangitis and/or jaundice.[8][37] CT, MRI/MRCP, or EUS may be considered at a later stage for patients with persistent symptoms or idiopathic disease to evaluate for possible tumors, pancreatic fluid collections, cystic neoplasm, or pseudoaneurysm.[65]

Emerging tests

Procalcitonin appears to be sensitive for detection of pancreatic infection, with low serum levels a strong negative predictor of infected necrosis.[66] Its use is supported by some international guidelines.[28]

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Venepuncture and phlebotomy: animated demonstration
Venepuncture and phlebotomy: animated demonstration

How to take a venous blood sample from the antecubital fossa using a vacuum needle.

Radial artery puncture animated demonstration
Radial artery puncture animated demonstration

How to obtain an arterial blood sample from the radial artery.

Femoral artery puncture animated demonstration
Femoral artery puncture animated demonstration

How to perform a femoral artery puncture to collect a sample of arterial blood.

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