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Pancreatitis, which is the inflammation of the pancreas, can be acute or chronic in nature.
It may be caused by edema, necrosis or hemorrhage. In men, this disease is commonly
associated to alcoholism, peptic ulcer or trauma; in women, it’s associated to biliary tract
disease. Prognosis is usually good when pancreatitis follows biliary tract disease, but
poor when the factor is alcoholism. Mortality rate may go as high as 60% when the
disease is associated from necrosis and hemorrhage. (Schilling McCann, 2009)
Pancreatitis ranges from a mild, self-limited disorder to a severe, rapidly fatal disease that
does not respond to any treatment.
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Classification
The most basic classification system divides the disorder into acute and chronic forms.
Pathophysiology
Self-digestion of the pancreas caused by its own proteolytic enzymes, particularly
trypsin, causes acute pancreatitis.
Entrapment. Gallstones enter the common bile duct and lodge at the ampulla
of Vater.
Obstruction. The gallstones obstruct the flow of the pancreatic juice or causing
a reflux of bile from the common bile duct into the pancreatic duct.
Activation. The powerful enzymes within the pancreas are activated.
Inactivity. Normally, these enzymes remain in an inactive form until the
pancreatic secretions reach the lumen of the duodenum.
Enzyme activities. Activation of enzymes can lead to vasodilation, increased
vascular permeability, necrosis, erosion, and hemorrhage.
Reflux. These enzymes enter the bile duct, where they are activated and
together with bile, back up into the pancreatic duct, causing pancreatitis.
Pancreatitis affects people of all ages, but the mortality rate associated with pancreatitis
increases with advancing age.
Approximately 185, 000 cases of pancreatitis occur in United States each year.
150, 000 of these cases are the result of cholelithiasis or sustained
alcohol abuse.
The overall mortality rate of patients with pancreatitis is 2% to 10%.
Even though the frequency is about 5000 new cases per year in the United
States, with a mortality rate of about 10%, it is yet unknown about the number
clients who have recurrent acute pancreatitis or chronic pancreatitis. (Black,
2009)
The incidence of pancreatitis varies in different countries and also depends on
the cause (e.g., alcohol, gallstones, metabolic factors, drugs). In United States,
acute pancreatitis is related to alcohol consumption more commonly than to
gallstones (second most common); in England, the opposite is true. (Black,
2009)
Causes
Mechanisms causing pancreatitis are usually unknown but it is commonly associated with
autodigestion of the pancreas.
Alcohol abuse. Eighty percent of the patients with pancreatitis have biliary
tract disease or a history of long term alcohol abuse.
Bacterial or viral infection. Pancreatitis occasionally develops as a
complication of mumps virus.
Duodenitis. Spasm and edema of the ampulla of Vater can probably cause
pancreatitis.
Medications. The use of corticosteroids, thiazide diuretics, oral contraceptives,
and other medications have been associated with increased incidences of
pancreatitis.
Clinical Manifestations
Complications
Complications that arise in pancreatitis include the following:
Serum amylase and lipase levels. These are used in making diagnosis,
although their elevation can be attributed to many causes, and serum lipase
remain elevated for a longer period than amylase.
WBC count. The WBC count is usually elevated.
X-ray studies. X-ray studies of the abdomen and chest may be obtained to
differentiate pancreatitis from other disorders that can cause similar symptoms.
Ultrasound. Ultrasound is used to identify an increase in the diameter of the
pancreas.
Blood studies. Hemoglobin and hematocrit levels are used to monitor the
patient for bleeding.
CT scan: Shows an enlarged pancreas, pancreatic cysts and determines extent
of edema and necrosis.
Ultrasound of abdomen: May be used to identify pancreatic inflammation,
abscess, pseudocysts, carcinoma, or obstruction of biliary tract
Endoscopic retrograde cholangiopancreatography: Useful to diagnose
fistulas, obstructive biliary disease, and pancreatic duct strictures/anomalies
(procedure is contraindicated in acute phase).
CT–guided needle aspiration: Done to determine whether infection is present.
Abdominal x-rays: May demonstrate dilated loop of small bowel adjacent to
pancreas or other intra-abdominal precipitator of pancreatitis, presence of free
intraperitoneal air caused by perforation or abscess formation, pancreatic
calcification.
Upper GI series: Frequently exhibits evidence of pancreatic
enlargement/inflammation.
Serum amylase: Increased because of obstruction of normal outflow of
pancreatic enzymes (normal level does not rule out disease). May be five or
more times normal level in acute pancreatitis.
Serum lipase: usually elevates along with amylase, but stays elevated longer.
Serum bilirubin: Elevation is common (may be caused by alcoholic liver
disease or compression of common bile duct).
Alkaline phosphatase: Usually elevated if pancreatitis is accompanied by
biliary disease.
Serum albumin and protein: May be decreased (increased capillary
permeability and transudation of fluid into extracellular space).
Serum calcium: Hypocalcemia may appear 2–3 days after onset of illness
(usually indicates fat necrosis and may accompany pancreatic necrosis).
Potassium: Hypokalemia may occur because of gastric losses; hyperkalemia
may develop secondary to tissue necrosis, acidosis, renal insufficiency.
Triglycerides: Levels may exceed 1700 mg/dL and may be causative agent in
acute pancreatitis.
LDH/AST: May be elevated up to 15 times normal because of biliary and liver
involvement.
CBC: WBC count of 10,000–25,000 is present in 80% of patients. Hb may be
lowered because of bleeding. Hct is usually elevated (hemoconcentration
associated with vomiting or from effusion of fluid into pancreas or
retroperitoneal area).
Serum glucose: Transient elevations of more than 200 mg/dL are common,
especially during initial/acute attacks. Sustained hyperglycemia reflects
widespread cell damage and pancreatic necrosis and is a poor prognostic sign.
Partial thromboplastin time (PTT): Prolonged if coagulopathy develops
because of liver involvement and fat necrosis.
Urinalysis: Glucose, myoglobin, blood, and protein may be present.
Urine amylase: Can increase dramatically within 2–3 days after onset of
attack.
Stool: Increased fat content (steatorrhea) indicative of insufficient digestion of
fats and protein.
Medical Management
Surgical Management
There are several approaches available for surgery. The major surgical procedures are the
following:
Nursing Management
The patient who is admitted to the hospital with a diagnosis of pancreatitis is acutely ill
and needs expert nursing care.
Nursing Assessment
Diagnosis
Based on the assessment data, the nursing diagnoses for a patient with pancreatitis
include:
Nursing Interventions
Performing nursing interventions for a patient with pancreatitis needs expertise and
efficiency.
Evaluation
Evaluation of a successful plan of care for a patient with pancreatitis should include:
Documentation
Nursing documentation of the case of a patient with acute pancreatitis involves the
following: