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Chapter 35 Nursing Care of Patients With Liver, Pancreatic, and Gallbladder Disorders
Acute Pancreatitis
Pathophysiology
Inflammation of the pancreas appears to be caused by a
process called autodigestion. Recall that the pancreas
normally secretes digestive enzymes. For reasons not fully
understood, pancreatic enzymes can be activated while they
are still in the pancreas and be gin to digest the pancreas. In
addition, large amounts of enzymes are released by inflamed
cells. As the pancreas digests itself, chemical cascades occur.
Trypsin destroys pancreatic tissue and causes v asodilation.
As capillary permeability increases, fluid is lost to the
retroperitoneal space, causing shock. In addition, trypsin
appears to set off another chain of events that causes the con-
version of prothrombin to thrombin, so that clots form. The
patient may develop disseminated intravascular coagulation
(see Chapter 28).
Etiology
Acute pancreatitis is most commonly associated with heavy
alcohol consumption or gallstones. Alcohol appears to
act directly on the acinar cells of the pancreas and the
pancreatic ducts to irritate and inflame the structures.
Cholelithiasis (gallstones) or cholangitis (inflammation of
the bile ducts) can also trigger pancreatitis. Gallstones may
plug the pancreatic duct and cause inflammation from
excessive fluid pressure on sensiti ve ducts. The irritant
effect of bile itself may cause inflammation. Ele vated
triglycerides, pancreatic tumors, or, rarely, medications can
cause pancreatitis.
Prevention
Caution patients who drink alcohol to stop. P atients with
biliary disease need to seek medical treatment for these
conditions so that pancreatitis does not de velop as a
complication.
Signs and Symptoms
Patients with acute pancreatitis are very ill, with dull abdom-
inal pain, guarding, a rigid abdomen, hypotension or shock,
and respiratory distress from accumulation of fluid in the
retroperitoneal space. The abdominal pain usually is located
in the midline just belo w the sternum, with radiation to the
spine, back, and flank. The location and degree of pain indi-
cate the area of the pancreas involved and to some extent the
amount of involvement. Respirations are likely to be shallow
as the patient attempts to splint painful areas. Eating mak es
the pain worse.
The patient may have a low-grade fever, dry mucous mem-
branes, and tachycardia. If the primary cause is biliary , the
patient may report nausea and v omiting, and jaundice may
be evident. The islets of Langerhans in the terminal one-third
of the pancreas are usually not impaired.
Complications
It may be useful to think of acute pancreatitis as a chemical
burn to the organ. As with other severe burns, death is likely
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to occur from secondary causes. From the onset of symptoms,
cardiovascular, pulmonary (including acute respiratory dis-
tress syndrome), and renal failure are the most likely causes
of death. Hemorrhage, peripheral v ascular collapse, and in-
fection are also major concerns. A purplish discoloration of
the flanks (Turner’s sign) or a purplish discoloration around
the umbilicus (Cullen’s sign) may occur with e xtensive he-
morrhagic destruction of the pancreas.
Diagnostic Tests
Diagnosis of acute pancreatitis is made when tw o of these
are present: abdominal pain, serum amylase (normal: 8 0–
180 units/dL) and/or serum lipase (normal: 0 to 160 units/L)
more than 3 times normal, abdominal imaging is indicative
of it. Serum amylase rises quickly and then returns to
normal in 3 to 5 days. Serum lipase is thought to be more
specific for acute pancreatitis and ele vates and stays ele-
vated for a longer period of time. Glucose, bilirubin,
alkaline phosphatase, lactic dehydrogenase, ALT, AST,
cholesterol, and potassium are all ele vated. Decreases are
seen in serum albumin, calcium, sodium, and magnesium.
Ultrasonography may sho w pleural ef fusion from local
inflammatory reaction to pancreatic enzymes or a change
in the size of the pancreas.
Therapeutic Measures
Early aggressive IV hydration during the first 24 hours for
hypovolemia treatment is recommended. In asymptomatic
mild acute pancreatitis, oral nutrition is gi ven (“Nutrition
Notes”). In severe cases, enteral feeding is maintained (see
“Evidence-Based Practice”). A histamine (H 2) antagonist
can help decrease acid stimulation of pancreatic secretions
(Table 35.4). Additional drug orders include electrolytes
such as calcium and magnesium to replace losses, short-
acting insulin to combat hyperglycemia, and antibiotics to
treat sepsis (T able 35.5). Sur gery may be needed for
debriding necrotic tissue. Abscesses or pseudocysts may
need to be drained.
Nutrition Notes
Nourishing the Patient With Pancreatitis
Nutritionally, mild acute pancreatitis can be treated with
the following:
• Aggressive hydration with IV fluids
• Nothing by mouth for 48 hours to avoid stimulating
the pancreas
• Clear liquids after pain has been controlled and nau-
sea and vomiting end
• Low-fat, soft diet
• Soft to general diet over 3 or 4 days if satisfactory
progress
If the disease progresses to se vere pancreatitis,
the goal of nutritional support is to meet the ele vated