The clinical diagnosis of acute pancreatitis is considered after the typical presentation of severe epigastric pain radiating through the back. Associated nausea and vomiting are frequently seen. Low-grade fevers are common; high-grade fevers are unusual in the absence of localized or systemic infection. Depending on the causative etiology (i.e., gallstones), jaundice may be present.

Biochemical evidence of pancreatic injury helps to confirm the diagnosis of acute pancreatitis. In the unexaminable, obtunded patient, laboratory abnormalities may be the first clue of pancreatic injury. In acute pancreatitis a variety of digestive enzymes escape from acinar cells and enter the systemic circulation. Amylase and lipase are the most widely assayed to confirm the diagnosis. Amylase levels rise within several hours after the onset of symptoms and typically remain elevated for 3 to 5 days. However, because of the short serum half-life of amylase (2.5 to 3.0 hours), levels may normalize within 24 hours of disease onset. Lipase has a longer serum half-life and may be useful for diagnosing acute pancreatitis later in the course of an episode. It is important to remember that the magnitude of increases in amylase or lipase concentrations does not correlate well with the severity of pancreatitis. High levels do not predict worse disease. Other serum biomarkers such as C-reactive protein, neutrophil elastase, interleukin-6, procalcitonin, and urinary concentrations of trypsinogen-activating peptide (TAP) tend to correlate better with disease severity. However, because assays of these markers are not widely available they are of limited clinical utility to predict outcomes or triage patients for ICU admission.