Acute pancreatitis

is acute inammation of the pancreas that can also involve surrounding tissues and
remote organs. gallstones and excessive alcohol use account for 70% to 80% of
cases.
Acute pancreatitis is self-limiting and mild in 80% to 90% of patients, resolving
spontaneously within 5 to 7 days. However, 10% to 20% of patients will develop
severe acute pancreatitis, which is associated with local and systemic complications
and a signicantly higher mortality rate.
Pathophysiology
The acinar cells of the pancreas synthesize and secrete digestive enzymes to assist
in the breakdown of starch, fat, and proteins. Normally, these enzymes remain
inactive until they enter the duodenum.
In acute pancreatitis, pancreatic enzymes become prematurely activated in the
pancreas, resulting in autodigestion of the pancreas and the peripancreatic tissue.
Major Causes of Acute Pancreatitis
Biliary disease (gallstones or microlithiasis, common bile duct obstruction, biliary
sludge)
Chronic alcohol use
Medications (thiazide diuretics, furosemide, pro- cainamide, tetracycline,
sulfonamides, azathioprine, 6-mercaptopurine, angiotensin-converting enzyme
inhibitors, valproic acid)
Hypertriglyceridemia
Hypercalcemia
Abdominal trauma (pancreatic injury)
Endoscopic retrograde cholangiopancreatography (ERCP)
Infectious processes (mumps, staphylococcal and viral infections)
Pancreas divisum
Abdominal surgery
Gynecologic disorders (eg, ectopic pregnancy, ovarian cyst)
Total parenteral nutrition (TPN)
Idiopathic
Pancreatic tumors
Systemic Effects of Acute Pancreatitis
Pulmonary
Atelectasis
Acute respiratory distress syndrome (ARDS)
Pleural effusions
Cardiovascular
Hypotensive shock
Septic shock
Hemorrhagic shock
Renal

 Acute kidney failure

Hematological
Disseminated intravascular coagulation (DIC)
Metabolic
Hyperglycemia
Hypertriglyceridemia
Hypocalcemia
Metabolic acidosis
Gastrointestinal
Gastrointestinal bleeding
Ileus
Mild acute pancreatitis (called interstitial or edematous pancreatitis) is
characterized by areas of fat necrosis in and around pancreatic cells and localized
interstitial edema.
In severe acute pancreatitis (called hemorrhagic or necrotizing pancreatitis),
pancreatic enzymes, vasoactive substances, hormones, and cytokines released from
the injured pancreas cause a cascade of events that can lead to local and systemic
edema, vascular damage, hemorrhage, and necrosis.
Systemic inammatory response syndrome (SIRS) may develop and can result in
distant organ damage and multisystem organ failure. This systemic response is
responsible for most of the morbidity and mortality associated with severe acute
pancreatitis
Death during the rst 2 weeks of severe acute pancreatitis usually results from
pulmonary or renal complications (eg, acute respiratory distress syndrome [ARDS],
acute renal failure ARF). Local complications from acute pancreatitis resulting from
inammation of the peritoneum and uid accumulation in the peritoneal cavity
include pancreatic pseudocyst and pancreatic abscess:
Pancreatic pseudocyst is a collection of inammatory debris and pancreatic
secretions enclosed by epithelial tissue. Signs and symptoms of pancreatic
pseudocyst include persistent abdominal pain with nausea and vomiting, a
prolonged fever, and elevated serum amylase. A pancreatic pseudocyst can rupture
and hemorrhage or become infected, causing sepsis.
Pancreatic abscess is a walled-off collection of purulent material in or around the
pancreas thatusually occurs 6 weeks or more after the onset of acute pancreatitis.
Signs and symptoms of pancre- atic abscess include an elevated white blood cell
(WBC) count, fever, abdominal pain, and vomiting.
RED FLAG! Infections after the onset of pancreatitis (eg, due to abscess,
pseudocyst, or infection of necrotic tissue), if untreated, are often fatal.
Assessment
Clinical manifestations of acute pancreatitis are given in Box 25-8. o

RED FLAG! A persistent or high fever may indicate complications, such as

peritonitis, cholecystitis, or abscess.
Clinical Manifestations of Acute Pancreatitis

History and Physical Examination Findings

Abdominal pain
Nausea or vomiting without pain relief
Tachycardia
Hypotension
Low-grade fever
Diffuse abdominal tenderness and guarding
Hypoactive or absent bowel sounds
Abdominal distention
Grey Turners sign (ank ecchymosis)
Cullens sign (umbilical ecchymosis)
Jaundice (with biliary disease)

Laboratory Findings
Elevated serum and urine amylase
Elevated serum lipase
Elevated WBC count
Hypokalemia
Hypocalcemia
Elevated bilirubin, aspartate aminotransferase (AST), and prothrombin time (PT)
(with liver disease)
Elevated alkaline phosphatase (AP) level (with b iliary disease)
Hypertriglyceridemia
Hyperglycemia
Hypoxemia

Ransons Criteria for Acute Pancreatitis

Evaluate on Admission or on Diagnosis
Age greater than 55 years
Leukocyte count greater than 16,000/mL
Serum glucose greater than 200 mg/dL
Serum lactate dehydrogenase (LDH) greater than 350 IU/mL
Serum aspartate aminotransferase (AST) greater than 250 IU/dL

Evaluate During Initial 48 Hours

Decrease in hematocrit greater than 10%
Increase in blood urea nitrogen (BUN) greater than 5 mg/dL
Serum calcium less than 8 mg/dL
Base de cit greater than 4 mEq/L
Estimated uid sequestration greater than 6 L
Arterial oxygen saturation (PaO2) less than 60 mm Hg
Laboratory studies ordered in the evaluation of a patient with acute pancreatitis
include those used to evaluate pancreatic and liver function and a serum electrolyte
panel.

Imaging studies ordered to conrm the diagnosis, evaluate severity, and identify
potential causes
computed tomography (CT)
abdominal ultrasound,
magnetic resonance cholangiopancreatography (MRCP),
and endoscopic retro- grade cholangiopancreatography (ERCP)
An important aspect of assessment is identifying those patients who are likely to
develop severe acute pancreatitis. Early identication permits aggressive treatment
and surveillance, which can decrease complications and mortality. Ransons criteria
are widely used to assess the severity of acute pancreatitis. Three or more signs
identied at the time of admission or during the initial 48 hours are predictive of
severe acute pancreatitis, with an associated mortality rate of 10% to 20%.6 Six or
more have a corresponding mortality rate of 39%.6

Management Care of the patient with acute pancreatitis focuses on uid

and electrolyte replacement, pain management, resting the pancreas to prevent the
release of pancreatic secretions, and maintaining the patients nutritional status. A
collaborative care guide for the patient with acute pancreatitis is given in Box 25-10.
Fluid replacement.
The goal of uid replacement is to administer enough uid to obtain a circulating
volume sufcient to maintain organ and tissue perfusion and prevent end-stage
shock. Patients with severe acute pancreatitis may require 5 to 10 L of uid
replacement within the rst 24 hours of hospitalization. Hypovolemia and shock are
major causes of death early in the disease process when aggressive uid
resuscitation fails to reverse the shock process.
Electrolyte replacement
. Replacement of electrolytes (calcium, magnesium, potassium) is also part of the
initial management of patients with acute pancreatitis. Patients with severe
hypocalcemia are placed on seizure precautions with respiratory support equipment
on hand. Serum magnesium deciency usually needs to be corrected before calcium
and potassium levels can return to normal.
Pain management.
Acute pancreatitis is extremely painful. In addition, pain increases pancreatic
enzyme secretion. For these reasons, pain control is a nursing priority for patients
with acute pancreatitis.
Although meperidine has traditionally been the analgesic of choice because of the
potential for sphincter of Oddi spasm that can accompany opioid use, if meperidine
is not effective, other analgesics (including morphine) should be used as necessary
for pain control.
Pancreatic rest.

Gastric distention, food in the stomach, and chyme in the duodenum can all
stimulate the pancreas to secrete, further exacerbating the pancreatitis.
Interventions include placing the patient on NPO status; placing a nasogastric tube
connected to low wall suction to relieve gastric distention; administering protonpump inhibitors to decrease acid production; and administering octreotide,
somatostatin, or sandostatin to decrease pancreatic secretion of digestive enzymes.
Nutritional support.
Patients with acute pancreatitis who are on prolonged NPO status with nasogastric
suction require nutritional support. Total parenteral nutrition (TPN) has been
traditionally used because it provides nutrients with- out stimulating the pancreas.
Increasing evidence suggests that enteral nutrition delivered past the ligament of
Treitz to the distal duodenum or jejunum is safe for patients with acute pancreatitis;
an added bene t is that enteral nutrition may reduce bacterial translocation by
maintain- ing intestinal barrier function. Supplementation with TPN is appropriate if
oral and enteral nutrition cannot provide enough calories to prevent catabolism.
Hyperglycemia, which is often seen in acute pancreatitis, is managed by insulin
protocol.
Surgery.
Surgery for acute pancreatitis is indicated if massive pancreatic necrosis is present
in a patient with a worsening clinical status. Pancreatic resection or debridement
can be performed to remove dead or infected pancreatic tissue and pre- vent
systemic complications in patients with acute necrotizing pancreatitis. Broadspectrum antibiotics are administered following surgical debride- ment of necrotic
tissue.
ADDITIONAL Notes

CAUSES
Three factors cause premature enzyme activation.
Mechanical causessuch as pancreatic duct damage and obstructionmay result
from gallstones migrating into the duct, bile reux from the duodenum into the
duct, tumors, radiation therapy, ulcer disease, or inammation.
Metabolic causes result from changes in the secretory processes of the acinar cells
in condi- tions such as alcoholism (90% of the cases), diabetic ketoacidosis,
hyperlipidemia, hypercalcemia, and drugs (acetaminophen, estrogen).
Miscellaneous causes include infectious dis- eases (mumps, hepatitis B, coxsackie
viral infections) and ischemic injury as a result of lupus erythematosus,
cardiopulmonary bypass surgery, post-transplantation complications, or shock.
GENETIC CONSIDERATIONS
Mutation in the trypsinogen gene PRSS1 or mutations in the cystic brosis gene
(CFTR) have been associated with heritable forms of pancreatitis. Since genetic

testing for the PRSSI gene produces many false negatives, persons considered
vulnerable are often instructed to make those lifestyle adaptations, such as avoiding
alcohol and smoking and being vigilant about follow-up and screening, that will
protect the pancreas. Mutations in other genes regulating pancreatic enzyme
secretion have been seen in patients with chronic pancreatitis.
GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONS
The main cause of pancreatitis in adult males is alcohol abuse and dependence and
in adult females is cholelithiasis and biliary tract disturbances. Overall incidence is
approximately the same in males and females. The principal cause in children is
cystic brosis. Because pancreatic secretions decrease with age, elderly persons
have decreased ability to tolerate dietary fat and have an increased risk of
gallstones that may lead to pancreatitis. The risk for middle-age African Americans
is 10 times higher than that of whites and Native Americans, and the racial/ethnic
differences are more pronounced in me than in women. As people age, hospitalization rates increase for females in particular.
ASSESSMENT
HISTORY. Obtain a detailed history of alcohol use and ingestion patterns. Assess for
a family history of pancreatitis or a history of external abdominal trauma, surgery,
cancer, recent bacterial infections, and biliary or gastrointestinal disease. Obtain a
complete medication prole of prescribed and over-the-counter drugs. Determine
the onset and severity of symptoms. Patients often seek medical attention for
severe upper abdominal pain they describe as knifelike, twisting, and deep in the
midepigastrium or umbilical region. The pain may radiate to the dorsal area of the
back or around the costal margins. Pain begins 12 to 48 hours after excessive
alcohol intake or, with gallstone-related pancreatitis, can occur after a large fatty
meal. Nausea and vomiting are present in up to 90% of the cases.
PHYSICAL EXAMINATION. The patient appears acutely ill with restless, apprehensive,
and agitated behavior. Some become confused and, if shock or hypoxemia is
impending, unresponsive. Respirations are often rapid and shallow. The patient may
assume a fetal position with legs drawn upward to relieve abdominal pain. You may
note mottled or jaundiced skin. You may see a bluish discoloration in the anks
(Grey-Turners sign) and around the umbilicus (Cullens sign), which indicates blood
accumulation in these areas. Skin may be cold and diaphoretic. You may also note
coarse tremors of the extremities as a sign of low calcium. Other ndings include
tea-colored or foamy urine (indicating the presence of bile) and gray, foul-spelling,
foamy stools that indicate the presence of undigested fat. Ascultate the abdomen
before palpation and percussion to check for decreased bowel sounds, which is a
common nding in patients with pancreatitis. On palpation, note extreme abdominal
tenderness, distension, guarding, and rigidity. Ascites and rebound tenderness are
present in severe disease. When you percuss the abdomen, you may nd abdominal
tympany. The patient often has labile vital signs. During periods of pain, the patient
may be hypertensive, but as hypovolemic shock progresses to late stages, blood
pressure may fall. Patients usually have rapid heart rates; rapid, thready pulses; and

decreased breath sounds in the lower lobes because of shallow respirations, pain,
and increased abdominal size.
PSYCHOSOCIAL. Assess the patients anxieties and coping abilities related to the
demands of an acute care environment and a sudden illness. The patient with
chronic pancreatitis needs assistance with feelings of hopelessness and apathy that
may result from chronic pain and gen- eral debilitation. Assess the familys coping
with role changes and responsibilities. Alcohol abuse counseling may be necessary.
PRIMARY NURSING DIAGNOSIS
Pain (acute or chronic) related to inammation, edema, peritoneal irritation
OUTCOMES. Comfort level; Pain control behavior; Pain level; Symptom severity
INTERVENTIONS. Analgesic administration; Anxiety reduction; Environmental
management: Comfort, Pain management; Medication management; Patientcontrolled analgesia assistance
PLANNING AND IMPLEMENTATION Collaborative The immediate goal of therapy is to
control and decrease the inammation of the pancreas. The uid lost into the
retroperitoneal space can be as much as 4 to 12 L with severe disease. Volume
replacement with uids such as lactated Ringers injection or normal human serum
albumin is used to restore blood volume and prevent hypovolemic shock. Normal
human serum albumin is often used if low albumin levels lead to a loss of osmotic
pressure in the vascular system. Urinary output is monitored hourly to measure
volume status: less than 1 mL/kg per hour is a sign of hypoperfusion. The physician
may insert a pulmonary artery catheter for hemodynamic monitoring to assess the
adequacy of the volume replacement and cardiac output. Patients who develop
sepsis and shock may not respond to uid volume replacement and remain
hypovolemic. This complication requires vasoactive parenteral medications.
Hypocalcemia is a common electrolyte imbalance that accompanies pancreatic
necrosis and requires calcium replacement. It may cause tetany, seizures,
respiratory complications, and
695Pancreatitis 695
Abnormality with Test Normal Result Condition Explanation Diagnostic Highlights
Serum amylase
Serum calcium
Computed tomography
Serum lipase
Serum glucose
50180 units/dL
8.610.3 mg/dL

Normal pancreas
31186 units/L
75105 mg/dL
180 units/dL
8.6 mg/dL
Pancreatic enlargement, inammation, uid collection 186 units/L
105 mg/dL
Enzyme produced by pancreas that aids digestion of complex carbohydrates;
increases 12 24 hr after acute inammation Necrosis of fat from release of
pancreatic enzymes leads to binding of free calcium Inammation, necrosis,
swelling, uid collection changes the con- guration of the pancreas Enzyme
produced by pancreas that aids digestion of fat; specic marker for inammation of
pan- creas; begins to elevate within 2 hr of the inammation Interference with
insulin release and B cell injury leads to hyper- glycemia in some patients
Other Tests: Complete blood count (generally leukocytosis occurs), serum
electrolytes, blood urea nitrogen, creatinine, serum bilirubin, alkaline phosphatase,
abdominal ultrasound
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myocardial changes. Magnesium decits often accompany hypocalcemia and need
replacement as well. Loss of potassium through vomiting, uid loss in the third
spaces, acidosis, and renal insufficiency can lead to ventricular dysrhythmia. The
blood glucose is monitored as a part of the renal prole and by nger sticks every 6
hours to determine the need for exogenous insulin replacement. Respiratory
support involves administering oxygen by a variety of routes, which may include
mechanical ventilation. Because of inadequate breathing patterns and the risk of
laryngospasm, the patient may require endotracheal intubation; also, position endexpiratory pressure, pressure control ventilation, and inverse inspiratory-toexpiratory ratio ventilation (increasing inspiratory time) may be used. The goal of
therapy is to reduce the secretion of pancreatic enzymes, which stops the inammatory process. The inammation leads to nerve irritation and pain. Obtain a
baseline pain assessment, and reassess every 4 hours using a pain-rating scale;
provide narcotic analgesia as needed. Bedrest is important to decrease the basal
metabolic rate, which, in turn, decreases pan- creatic secretions. Insertion of a
nasogastric tube for intermittent suction also contributes to this goal by preventing
the release of secretion in the duodenum. Nothing-by-mouth (NPO) status is strictly
maintained, with no ice chips or sips of water during the acute phase. Nutritional
support to restore the damaged pancreatic cells is provided by initiating total
parenteral nutrition within 3 days of the onset of the acute phase. Surgical
interventions may be indicated for managing the complications that are associated

with pancreatic necrosis. The procedures include pancreatic drainage, pancreatic

resection or dbridement, and removal of obstructions (biliary stones).
The current therapy for removal of stones is early endoscopic retrograde
cholangiopancreatography and endoscopic sphincterotomy. Peritoneal lavage is
used for patients who do not respond to intensive treatment after 3 days; it has
signicantly decreased the incidence of complications and the mortality rate.
696 Pancreatitis
Medication or Drug Class Dosage Description Rationale Pharmacologic Highlights
Antibiotics
Opiates
Varies with patient
Varies with drug
Ceftriaxone (Rocephin), ampicillin
Meperidine (Demerol); fentanyl (Sublimaze)
For microorganisms causing biliary pancreatitis and acute necrotizing pancreatitis;
therapy is based on idea that enteric anaerobic and aerobic gram-bacilli
microorganisms are often the cause of pancreatic infections. Relieve pain; narcotic
analgesics that do not cause spasms of the sphincter of Oddi may falsely elevate
amylase level, so amylase levels need to be drawn before the pain therapy begins;
meperidine thought to produce less muscle spasm than other opiates
Other Drugs: Antacids to neutralize gastric secretions; histamine antagonists to
decrease gastric acid production; dopamine to improve myocardial contractility,
increase cardiac output, and decrease inammation by reducing permeability in
pancreatic ducts. Chronic therapy may include a low-fat diet and oral pancreatic
enzyme supplements. Insulin may be needed to control hyperglycemia.
Independent
During the acute phase of pancreatitis, focus on continued monitoring and teaching.
Monitor the patients pain to determine intensity, location, characteristics, and
factors that aggravate or relieve the pain. Frequent doses of analgesics are
required.
Other measures to provide comfort include positioning the patient in a knee-chest
posture, stress reduction, and relaxation exercises. Provide a restful environment,
but also initiate diversional activities.
Monitor the patients respi- ratory status continually.
Place the patient in high Fowler position to improve lung expansion, and use other
mechanisms to enhance gas exchange. If the patient is not intubated, keep

emergency intubation equipment close by in case tetany and laryngospasm occur.

The risk of tetany is enhanced if the patient hyperventilates.
Maintain a calm environment, a constant presence, and medications to assist the
patient with quiet breathing. After the removal of the nasogastric tube, the diet
progresses slowly from liquids to a diet high in calories and low in fat.
During the immediate recovery period, arrange for small, frequent meals. Explain
the need to avoid food and drinks with caffeine, spicy foods, and heavy meals that
stimulate pancreatic secretion.
Develop a realistic weight gain goal. Assist with dietary teaching by planning a
weeks menu, incorporating the patients specic dietary needs and restrictions.
DOCUMENTATION GUIDELINES
Patients description of pain and response to medications and alternative comfort
measures Physical ndings: Respiratory rate and rhythm, use of accessory
muscles, character of breath sounds, mentation, pertinent laboratory ndings,
presence of fever
Intake and output, uid balance, weight changes, vital signs, results of renal
prole laboratory studies
Presence of nausea and vomiting, nasogastric tube, weight loss to 20% under
ideal
Presence of complications: Hemorrhage, sepsis, shock, respiratory distress
syndrome, tetany, hyperglycemia
DISCHARGE AND HOME HEALTHCARE GUIDELINES
Prevention involves correcting the initiating events. If the disease is related to
alcohol use, rein- force the importance of abstaining and provide appropriate
referrals.
Teach the patient to recognize early symptoms that may indicate recurrence and
when to contact the physician.
Emphasize the importance of follow-up care.
Teach the rationale, action, dosage, and side effects of all pre- scribed medications
Instruct the patient to take prescribed pancreatic enzyme replacements with or
immediately after meals and to swallow them whole and not with hot liquids that
would disrupt the protective coating
If the patient is being discharged with the requirement for continued insulin
injections, the patient and family should demonstrate the injection technique and
the procedure for blood glucose self-monitoring. Provide a log and show them how
to keep a record of glucose levels and insulin dosages.

The patient with a loss of pancreatic endocrine function requires extensive ongoing
diabetic teaching after discharge; refer for additional counseling if necessary.
Encourage the patient to seek nutritional follow-up with clinic or physician visits,
especially for hyperglycemic management.