to pancreatic secretion.72 Also, the rising ethanol
concentration in acinar cells causes an increase
in cytosolic calcium, which is required for vesicular
zymogen activation. This relationship between cytosolic calcium and zymogen activation may also
help to explain the association between hypercalcemia and acute pancreatitis.71
DIAGNOSIS
The classic presentation of acute pancreatitis
includes mild to severe epigastric abdominal pain
(often radiating to the back) as well as nausea and
vomiting. The pain is typically constant in nature
and is not aggravated by coughing, movement, or
respiration. The pain tends to be more severe in a
supine position and may lessen if the patient leans
forward in a sitting position. On presentation, jaundice or tachycardia may be present, and patients
may appear pale and distressed, be febrile, and
have a distended abdomen.73 Turner’s sign (flank
bruising) or Cullen’s sign (bruising surrounding
the umbilicus) may be present in severe cases.
Some patients may have a more florid presentation that includes hypotension or shock due to
intravascular volume depletion and third spacing of
fluids.
Commonly accepted criteria for a clinical diagnosis of acute pancreatitis necessitate the presence
of 2 of the 3 following features: serum amylase and
lipase elevated at least 3 times above the upper
limit of normal; characteristic eipigastric abdominal
pain as described above; and typical radiologic
features as found on computed tomography (CT),
magnetic resonance imaging (MRI), or transabdominal ultrasound (US). Other clinical findings that
can be present in acute pancreatitis include dehydration, which may manifest with elevated blood
urea nitrogen and hematocrit and decreased urine
output. Findings that may be seen in more severe
presentations include hypotension despite volume
replacement and a corresponding rise in hematocrit
secondary to hemoconcentration, metabolic acidosis, acute respiratory distress syndrome/respiratory
failure, renal failure, and fluctuation in serum calcium
levels.74,75
Classification systems are currently being revised, including a 4-tier system with a moderate
severe acute pancreatitis category defined as pancreatitis with complications but without multi-organ
system dysfunction.76
BIOCHEMICAL DIAGNOSTIC PARAMETERS
Elevation of serum amylase and lipase to at least
greater than 3 times the upper limit of normal in
conjunction with the appropriate clinical history are
mainstays in the diagnosis of acute pancreatitis.
Prospective studies comparing the selective evaluation of lipase versus amylase demonstrate a slight
diagnostic advantage to lipase because amylase
may have a lower sensitivity (ie, it may be normal
in patients with acute pancreatitis).77–79 In general,
amylase and lipase levels do not correlate with
either the severity of the attack or with overall prognosis. In addition, serum amylase and lipase levels
neither assist in generating an overall prognosis
nor in predicting complications of acute pancreatitis.80–82 Most practicing physicians do not follow
serum amylase and lipase levels beyond the first
few days once the diagnosis has been established.
A fall in enzymes, however, accompanied by clinical improvement often adequately demonstrates
a resolving acute pancreatitis in most patients.
Persistent elevation of serum amylase and lipase
may suggest pancreatic ductal disruption and/or
necrosis. Finally, amylase and lipase assays do
not need to be ordered simultaneously as this may
incur higher health care costs.83
