Pancreatitis

GASTROENTEROLOGY 2007;132:2022–2044

AGA Institute Technical Review on Acute Pancreatitis

CME quiz on page 2002.

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cute pancreatitis remains a disease characterized by significant morbidity and mortality, with several reports noting an increasing annual incidence of disease.1 Clinical practice position papers, such as this one, are designed to educate and guide physicians in patientcare decisions. These guidelines attempt to summarize the best available data and to describe best clinical practice. It is worthwhile to state directly that this approach is somewhat limited in the area of acute pancreatitis, owing to the relative paucity of large randomized controlled trials. Guidelines such as these, in the absence of this type of supporting scientific proof, must include a healthymeasure of less solid evidence-based recommendations, including a wealth of expert opinion. It is certainly possible that future large randomized trials might lead to changes in yet-to-be-written guidelines similar to this one. Acute pancreatitis is a disease of such variability that it cannot be effectively managed by following blindly any set of recommendations, and these guidelines are notintended as tantamount to the legal standard of care. Rather, it is hoped this position paper can combine the available scientific studies and evidence base (or lack thereof) with expert opinion into a useful tool for clinicians.

Diagnosis
The diagnosis of acute pancreatitis is usually suspected based on compatible clinical features including abdominal pain, nausea, and vomiting. It has beenestimated that in 40%–70% of patients, the classic pattern of pain radiation to the back is present. Pain usually reaches its peak over 30 – 60 minutes and persists for days or weeks. It is clear that not all patients may experience pain, or alternatively that the presence of pain may not be appreciated by the clinician caring for the patient. Several retrospective analyses of fatal acute pancreatitishave noted that in 30%– 40% of patients, the diagnosis of acute pancreatitis was only made at autopsy.2– 4 The diagnosis of acute pancreatitis was not suspected in these patients because abdominal pain was not present or because other clinical symptoms (eg, coma or multiorgan system failure) dominated the clinical picture. In some of these patients, the serum amylase level was also normal or onlyminimally elevated. The clinical suspicion of acute pancreatitis is supported by the finding of elevations in serum amylase and/or lipase levels. Measurement of amylase is more widely used. The pancreas is responsible for about 40% of total serum amylase, with the rest originating primarily in the salivary

glands. Elevations in total serum amylase are therefore not specific for pancreatitis, anda number of other intra-abdominal conditions should be considered (Table 1). Most textbooks and most expert opinions suggest a level of at least 3 times the upper limit of normal as the most accurate cutoff. In one prospective analysis of 500 patients presenting to an emergency department with acute abdominal pain, the sensitivity of serum amylase estimation was 85%, with a specificity of 91%.5 Aretrospective analysis of 95 patients with nonpancreatic abdominal pain and 75 patients with acute pancreatitis estimated a sensitivity for serum amylase of 72% and specificity of 99%.6 A prospective analysis of serum amylase measurements at a single hospital over 3 years noted a sensitivity of 45% and a specificity of 97%, using a post-hoc diagnostic threshold of 176 U/L (about 2 times the upperlimit of normal).7 Serum amylase is hampered as a diagnostic tool by the fact that elevations may not occur (or be missed, depending on the timing of collection of serum) in mild attacks, in acute flares superimposed on chronic pancreatitis (especially chronic alcoholic pancreatitis), and in some patients with marked hypertriglyceridemia (elevated triglyceride levels can interfere with the assay)....