C h a p t e r 3 0
Disorders of Hepatobiliary and Exocrine Pancreas Function
749
that cause pancreatic injury, resulting in an intense
inflammatory response. The acute inflammatory response
itself causes substantial tissue damage and may progress
beyond the pancreas to produce a systemic inflammatory
response syndrome and multiorgan failure (see Chapter
20). Although a number of factors are associated with
the development of acute pancreatitis, in the United
States alcohol abuse and gallstones account for 70% to
80% of all cases.
47–51
The precise mechanisms whereby
alcohol exerts its action are largely unknown; however,
alcohol is known to be a potent stimulator of pancreatic
secretions, and it also is known to cause partial obstruc-
tion of the sphincter of the pancreatic duct. In the case
of biliary tract obstruction due to gallstones, pancreatic
duct obstruction or biliary reflux is believed to activate
the enzymes in the pancreatic duct system. Acute pan-
creatitis also is associated with hyperlipidemia, hyper-
calcemia, infections (particularly viral), abdominal and
surgical trauma, and drugs such as thiazide diuretics.
Clinical Manifestations.
The manifestations of acute
pancreatitis can range from mild with minimal organ
dysfunction to severe and life-threatening. Overall,
about 20% of persons with acute pancreatitis have a
severe course, and 10% to 30% of those with severe
pancreatitis die.
49,50
The diagnosis of acute pancreatits is
made by the presence of 2 of the 3 following symptoms:
(1) abdominal pain;which is usually severe, located in
the epigastric or left upper quadarant and may radiate
to the back, chest, or flank areas; (2) serum amylase
or lipase greater than 3 times the upper limit of nor-
mal; and (3) classic signs on abdominal imaging. Serum
lipase may remain elevated slightly longer than amylase.
However, the level of elevation of the serum amylase or
lipase does not correlate with the severity of the disor-
der. The white blood cell count may also be increased,
and hyperglycemia and an elevated serum bilirubin level
may be present. Abdominal ultrasonography is usually
performed to assess for gallstones. Both CT scans and
dynamic contrast-enhanced CT of the pancreas are used
to detect necrosis and fluid accumulation.
Physical examination findings are variable and include
fever, tachycardia, hypotension, severe abdominal ten-
derness, respiratory distress, and abdominal distention.
Recognized markers of severe disease include laboratory
values that measure the inflammatory response (e.g.,
C-reactive protein), scoring systems that assess inflam-
mation or organ failure, and findings on imaging studies.
Clinical findings such as thirst, poor urine output, pro-
gressive tachycardia, tachypnea, hypoxemia, agitation,
confusion, a rising hematocrit level, and lack of improve-
ment in symptoms within the first 48 hours are warn-
ing signs of impending severe disease. Complications
include the systemic inflammatory response, acute respi-
ratory distress syndrome, acute tubular necrosis, and
organ failure. An important disturbance related to acute
pancreatitis is the loss of a large volume of fluid into
the retroperitoneal and peripancreatic spaces and the
abdominal cavity. Signs of hypocalcemia may develop,
probably as a result of the precipitation of serum calcium
in the areas of fat necrosis.
Treatment.
Determination of the cause is important
in guiding the immediate management and preventing
recurrence. Treatment measures depend on the severity
of the disease. Persons who present with persistent or
severe pain, vomiting, dehydration, or signs of impend-
ing severe acute pancreatitis require hospitalization.
Treatment measures are directed at pain relief, “putting
the pancreas to rest” by withholding oral foods and flu-
ids, and restoration of lost plasma volume. Meperidine
rather than morphine usually is given for pain relief
because it causes fewer spasms of the sphincter of the
pancreatic duct. Gastric suction is instituted to treat dis-
tention of the bowel and prevent further stimulation of
the secretion of pancreatic enzymes. Intravenous fluids
and electrolytes are administered to replace those lost
from the circulation and to combat hypotension and
shock. Intravenous colloid solutions are given to replace
the fluid that has become sequestered in the abdomen
and retroperitoneal space.
Complications.
Sequelae in persons surviving an episode
of severe acute pancreatitis include fluid collections and
infection.
49
In 40% to 60% of persons with acute necro-
tizing pancreatitis, the necrotic debris becomes infected,
usually by gram-negative organisms from the alimentary
canal, further complicating the condition.
47
Fluid collec-
tions with a high level of pancreatic enzymes are usually
associated with pancreatic duct disruptions and may even-
tually form pseudocysts (a collection of pancreatic fluid
enclosed in a layer of inflammatory tissue). A pseudocyst
most often is connected to a pancreatic duct, so that it
continues to increase in mass. The symptoms depend on
its location; for example, jaundice may occur when a cyst
develops near the head of the pancreas, close to the com-
mon duct. Pseudocysts may resolve or, if they persist, may
require surgical intervention.
Chronic Pancreatitis
Chronic pancreatitis is characterized by progressive and
permanent destruction of the exocrine pancreas, fibro-
sis, and, in the later stages, destruction of the endocrine
pancreas.
3,4,52,53
Most factors that cause acute pancre-
atitis can also cause chronic pancreatitis. However, the
chief distinction between the two conditions is the irre-
versibility of pancreatic function that is characteristic
of chronic pancreatitis. By far the most common cause
of chronic pancreatitis is long-term alcohol abuse. Less
common causes are long-standing obstruction of the
pancreatic duct by pseudocysts, calculi, or neoplasms,
autoimmune disorders, primary sclerosing cholangitis,
inflammatory bowel disease, cystic fibrosis (discussed in
Chapter 23), and hereditary pancreatitis, a rare autoso-
mal dominant disorder.
Chronic pancreatitis is manifested by episodes that
are similar, albeit of lesser severity, to those of acute
pancreatitis. Patients have persistent, recurring episodes
of epigastric and upper left quadrant pain; the attacks
often are precipitated by alcohol abuse or overeating.
Anorexia, nausea, vomiting, constipation, and flatulence
are common. Eventually the disease progresses to the
