PANCREATITIS

Guide Questions:
1. What is Pancreatitis?
a. Acute pancreatitis
b. Chronic pancreatitis
2. What is the pathophysiology of Pancreatitis?
a. Acute pancreatitis
b. Chronic pancreatitis
3. What are the clinical manifestation of
Pancreatitis?
a. Acute pancreatitis
b. Chronic pancreatitis
4. What are the medical management of Pancreatitis?
a. Assessment and diagnostics findings
b. Pharmacological therapy
c. Surgical therapy
5. What are the nursing management of Pancreatitis?
a. Nursing care plan

What is Pancreatitis?
- Pancreatitis (inflammation of the pancreas) is a serious disorder.
- The most basic classification system used to describe or categorize the various stages and forms
of pancreatitis divides the disorder into acute or chronic forms.
o Acute pancreatitis can be a medical emergency associated with a high risk for life-
threatening complications and mortality, whereas chronic pancreatitis often goes
undetected until 80% to 90% of the exocrine and endocrine tissue is destroyed. Acute
pancreatitis does not usually lead to chronic pancreatitis unless complications develop.
o However, Chronic pancreatitis can be characterized by acute episodes. Typically,
patients are men 40 to 45 years of age with a history of alcoholism or women 50 to 55
years of age with a history of biliary disease (Hale et al., 2000).
- Although the mechanisms causing pancreatic inflammation are unknown, pancreatitis is
commonly described as auto-digestion of the pancreas. Generally, it is believed that the
pancreatic duct becomes obstructed, accompanied by hypersecretion of the exocrine enzymes
of the pancreas. These enzymes enter the bile duct, where they are activated and, together with
bile, back up (reflux) into the pancreatic duct, causing pancreatitis.

Acute Pancreatitis

What is acute pancreatitis?

- Acute pancreatitis ranges from a mild, self-limiting disorder to a severe, rapidly fatal disease
that does not respond to any treatment. Mild acute pancreatitis is characterized by edema and
inflammation confined to the pancreas. Minimal organ dysfunction is present, and return to
normal usually occurs within 6 months. Although this is considered the milder form of
pancreatitis, the patient is acutely ill and at risk for hypovolemic shock, fluid and electrolyte
disturbances, and sepsis. A more widespread and complete enzymatic digestion of the gland
characterizes severe acute pancreatitis. The tissue becomes necrotic, and the damage extends
into the retroperitoneal tissues. Local complications consist of pancreatic cysts or abscesses
and acute fluid collections in or near the pancreas. Systemic complications, such as acute
respiratory distress syndrome, shock, disseminated intravascular coagulopathy, and pleural
effusion, can increase the mortality rate to 50% or higher (Aronson, 1999).
 - (Gerontologic Consideration) Acute pancreatitis affects people of all ages, but the mortality
rate associated with acute pancreatitis increases with advancing age. In addition, the pattern of
complications changes with age. Younger patients tend to develop local complications; the
incidence of multiple organ failure increases with age, possibly as a result of progressive
decreases in physiologic function of major organs with increasing age. Close monitoring of major
organ function (i.e., lungs, kidneys) is essential, and aggressive treatment is necessary to reduce
mortality from acute pancreatitis in the elderly.

Pathophysiology
- Self-digestion of the pancreas by its own proteolytic enzymes, principally trypsin, causes acute
pancreatitis. Eighty percent of patients with acute pancreatitis have biliary tract disease;
however, only 5% of patients with gallstones develop pancreatitis. Gallstones enter the common
bile duct and lodge at the ampulla of Vater, obstructing the flow of pancreatic juice or causing a
reflux of bile from the common bile duct into the pancreatic duct, thus activating the powerful
enzymes within the pancreas. Normally, these remain in an inactive form until the pancreatic
secretions reach the lumen of the duodenum. Activation of the enzymes can lead to vasodilation,
increased vascular permeability, necrosis, erosion, and hemorrhage (Quillen, 2001).
- Long-term use of alcohol is commonly associated with acute episodes of pancreatitis, but the
patient usually has had undiagnosed chronic pancreatitis before the first episode of acute
pancreatitis occurs. Other less common causes of pancreatitis include bacterial or viral infection,
with pancreatitis a complication of mumps virus. Spasm and edema of the ampulla of Vater,
resulting from duodenitis, can probably produce pancreatitis. Blunt abdominal trauma, peptic
ulcer disease, ischemic vascular disease, hyperlipidemia, hypercalcemia, and the use of
corticosteroids, thiazide diuretics, and oral contraceptives also have been associated with an
increased incidence of pancreatitis. Acute pancreatitis may follow surgery on or near the
pancreas or after instrumentation of the pancreatic duct. Acute idiopathic pancreatitis accounts
for up to 20% of the cases of acute pancreatitis (Hale, Moseley & Warner, 2000). In addition,
there is a small incidence of hereditary pancreatitis.
- The mortality rate of patients with acute pancreatitis is high (10%) because of shock, anoxia,
hypotension, or fluid and electrolyte imbalances. Attacks of acute pancreatitis may result in
complete recovery, may recur without permanent damage, or may progress to chronic
pancreatitis. The patient admitted to the hospital with a diagnosis of pancreatitis is acutely ill and
needs expert nursing and medical care.

Clinical Manifestation
- Severe abdominal pain is the major symptom of pancreatitis that causes the patient to seek
medical care. Abdominal pain and tenderness and back pain result from irritation and edema of
the inflamed pancreas that stimulate the nerve endings. Increased tension on the pancreatic
capsule and obstruction of the pancreatic ducts also contribute to the pain. Typically, the pain
occurs in the mid-epigastrium. Pain is frequently acute in onset, occurring 24 to 48 hours after a
very heavy meal or alcohol ingestion, and it may be diffuse and difficult to localize. It is
generally more severe after meals and is unrelieved by antacids. Pain may be accompanied by
abdominal distention; a poorly defined, palpable abdominal mass; and decreased peristalsis. Pain
caused by pancreatitis is accompanied frequently by vomiting that does not relieve the pain or
nausea.
- The patient appears acutely ill. Abdominal guarding is present. A rigid or board-like abdomen
may develop and is generally an ominous sign; the abdomen may remain soft in the absence of
peritonitis. Ecchymosis (bruising) in the flank or around the umbilicus may indicate severe
pancreatitis. Nausea and vomiting are common in acute pancreatitis. The emesis is usually
gastric in origin but may also be bile-stained. Fever, jaundice, mental confusion, and agitation
also may occur.
 - Hypotension is typical and reflects hypovolemia and shock caused by the loss of large amounts
of protein-rich fluid into the tissues and peritoneal cavity. The patient may develop tachycardia,
cyanosis, and cold, clammy skin in addition to hypotension. Acute renal failure is common.
- Respiratory distress and hypoxia are common, and the patient may develop diffuse pulmonary
infiltrates, dyspnea, tachypnea, and abnormal blood gas values. Myocardial depression,
hypocalcemia, hyperglycemia, and disseminated intravascular coagulopathy (DIC) may also
occur with acute pancreatitis.

Assessment and diagnostic findings

- The diagnosis of acute pancreatitis is based on a history of abdominal pain, the presence of
known risk factors, physical examination findings, and diagnostic findings. Serum amylase and
lipase levels are used in making the diagnosis of acute pancreatitis. In 90% of the cases, serum
amylase and lipase levels usually rise in excess of three times their normal upper limit within 24
hours (Tierney, McPhee & Papadakis, 2001). Serum amylase usually returns to normal within 48
to 72 hours. Serum lipase levels may remain elevated for 7 to 14 days (Braunwald et al., 2001).
Urinary amylase levels also become elevated and remain elevated longer than serum amylase
levels. The white blood cell count is usually elevated; hypocalcemia is present in many patients
and correlates well with the severity of pancreatitis. Transient hyperglycemia and glucosuria
and elevated serum bilirubin levels occur in some patients with acute pancreatitis.
- X-ray studies of the abdomen and chest may be obtained to differentiate pancreatitis from other
disorders that may cause similar symptoms and to detect pleural effusions.
- Ultrasound and contrast-enhanced computed tomography scans are used to identify an increase
in the diameter of the pancreas and to detect pancreatic cysts, abscesses, or pseudocysts.
- Hematocrit and hemoglobin levels are used to monitor the patient for bleeding. Peritoneal
fluid, obtained through paracentesis or peritoneal lavage, may contain increased levels of
pancreatic enzymes.
- The stools of patients with pancreatic disease are often bulky, pale, and foul-smelling. Fat content
of stools varies between 50% and 90% in pancreatic disease; normally, the fat content is 20%.
ERCP is rarely used in the diagnostic evaluation of acute pancreatitis because the patient is
acutely ill; however, it may be valuable in the treatment of gallstone pancreatitis.

Activity

1. Present the medical management of Acute Pancreatitis by highlighting:

a. Nutritional therapy of patient with Acute Pancreatitis
b. Pharmacological therapy of patient with Acute Pancreatitis
c. Surgical management of patient with Acute Pancreatitis
2. Present nursing management of patient with Acute Pancreatitis
3. Make a nursing care plan of patient with Acute Pancreatitis.

Chronic Pancreatitis

What is chronic pancreatitis?

- Chronic pancreatitis is an inflammatory disorder characterized by progressive anatomic and
functional destruction of the pancreas. As cells are replaced by fibrous tissue with repeated
attacks of pancreatitis, pressure within the pancreas increases. The end result is mechanical
obstruction of the pancreatic and common bile ducts and the duodenum. Additionally, there is
atrophy of the epithelium of the ducts, inflammation, and destruction of the secreting cells of the
pancreas.
 - Alcohol consumption in Western societies and malnutrition worldwide are the major causes of
chronic pancreatitis. Excessive and prolonged consumption of alcohol accounts for approximately
70% of the cases (Clain & Pearson, 1999). The incidence of pancreatitis is 50 times greater in
alcoholics than in the nondrinking population. Long-term alcohol consumption causes
hypersecretion of protein in pancreatic secretions, resulting in protein plugs and calculi within the
pancreatic ducts. Alcohol also has a direct toxic effect on the cells of the pancreas. Damage to
these cells is more likely to occur and to be more severe in patients whose diets are poor in
protein content and either very high or very low in fat.

Clinical Manifestations
- Chronic pancreatitis is characterized by recurring attacks of severe upper abdominal and back
pain, accompanied by vomiting. Attacks are often so painful that opioids, even in large doses, do
not provide relief. As the disease progresses, recurring attacks of pain are more severe, more
frequent, and of longer duration. Some patients experience continuous severe pain; others have a
dull, nagging constant pain. The risk of dependence on opioids is increased in pancreatitis
because of the chronic nature and severity of the pain.
- Weight loss is a major problem in chronic pancreatitis: more than 75% of patients experience
significant weight loss, usually caused by decreased dietary intake secondary to anorexia or fear
that eating will precipitate another attack. Malabsorption occurs late in the disease, when as little
as 10% of pancreatic function remains. As a result, digestion, especially of proteins and fats, is
impaired. The stools become frequent, frothy, and foul-smelling because of impaired fat
digestion, which results in stools with a high fat content. This is referred to as steatorrhea. As
the disease progresses, calcification of the gland may occur, and calcium stones may form within
the ducts.

Assessment and diagnostic findings

- ERCP is the most useful study in the diagnosis of chronic pancreatitis. It provides detail about the
anatomy of the pancreas and the pancreatic and biliary ducts. It is also helpful in obtaining tissue
for analysis and differentiating pancreatitis from other conditions, such as carcinoma. Various
imaging procedures, including magnetic resonance imaging, computed tomography, and
ultrasound, have been useful in the diagnostic evaluation of patients with suspected pancreatic
disorders. Computed tomography scanning or ultrasound is helpful to detect pancreatic cysts.
- A glucose tolerance test evaluates pancreatic islet cell function, information necessary for making
decisions about surgical resection of the pancreas. An abnormal glucose tolerance test indicative
of diabetes may be present. In contrast to the patient with acute pancreatitis, serum amylase levels
and the white blood cell count may not be elevated significantly.

Scenario:
B.K. is a 63-year-old woman who is admitted to the medical-surgical unit from the emergency
department (ED) with nausea and vomiting (N/V) and epigastric and left upper quadrant (LUQ)
abdominal pain that is severe, sharp, and boring and radiates through to her mid-back. The pain started
24 hours ago and awoke her in the middle of the night. B.K. is a divorced, retired sales manager who
smokes a half-pack of cigarettes daily. The ED nurse reports that B.K. is anxious and demanding. B.K.
denies using alcohol. Her vital signs (VS) are as follows: 100/70, 97, 30, 100.2° F (37.9° C)
(tympanic), SpO2 88% on room air and 92% on 2 L of oxygen by nasal cannula (NC). She is in normal
sinus rhythm. She will be admitted to the hospitalist service. She has no primary care provider (PCP)
and hasn't seen a physician “in years.”
The ED nurse giving you the report states that the admitting diagnosis is acute pancreatitis of
unknown etiology. A computed tomography (CT) scan has been ordered, but, unfortunately, the CT
scanner is down and won't be fixed until morning. However, an ultrasound of the abdomen was
performed, and “no cholelithiasis, gallbladder wall thickening, or choledocholithiasis was seen. The
pancreas was not well visualized due to overlying bowel gas.” Admission labs have been drawn; a
clean-catch urine specimen was sent to the lab, and the urine was dark in color.
1. What are the possible causes of pancreatitis?
2. If a CT scan is planned for the morning, what orders would you expect?
3. What other information do you need from the ED nurse before you assume responsibility for
the patient?

Case study progress:

You complete your admission assessment and note the following abnormalities: B.K. is restless
and lying on her right side in a semifetal position. Cerebrovascular findings are: Skin is cool,
diaphoretic, and pale with poor skin turgor; mucous membranes are dry. Heart rate is regular but
tachycardic, without murmurs or rubs. Peripheral pulses are faintly palpable in four extremities.
Respirations are rapid but unlabored on 2 L O2/NC with SpO2 90%. Breath sounds are absent in lower
left lobe (LLL) posteriorly— otherwise, clear to auscultation throughout. She complains of nausea and
is having dry heaves. Bowel sounds are hypoactive. Abdomen is distended, firm, and tender in a
diffuse fashion to light palpation, with guarding noted.

Chart View
Admission Laboratory Test Results

 Lipase 3000 units/L

 Amylase 2000 units/L
 Alk phos (ALP) 350 units/L
 ALT (SGPT) 90 units/L
 AST (SGOT) 150 units/L
 Total bilirubin 2.0 mg/dL
 Albumin 3.0 g/dL
 BUN 24 mg/dL
 Creatinine 1.4 mg/dL
 WBC 17,500/mm3

4. Which specific laboratory results point to a diagnosis of pancreatitis?

5. Which labs are the most important to monitor in acute pancreatitis? Why are they significant?
6. What do the BUN and creatinine tell you about her renal function and volume status?
7. Why are the WBCs elevated?

Case study progress:

During your physical exam, you noted “respirations rapid but unlabored on 2 L O2/NC with
SpO2 90%. Breath sounds are absent in LLL posteriorly—otherwise, clear to auscultation throughout.”
The admission chest x-ray (CXR) report reads, “small pleural effusion in the left lower lobe (LLL).”
8. Identify three actions you could initiate to help correct this situation.
9. B.K. turns on her call light. She complains of thirst and demands something to drink. Her
orders indicate “NPO, except sips and chips.” What is your response to her request? What
nursing action would help her complaints?

Case study progress:

B.K. eventually falls asleep and seems to be sleeping peacefully. Several hours later, you hear
an alarm on her pulse oximeter and enter her room to investigate. You find B.K. moaning softly; her
oximeter reads 87%.
10. What will you do next?
 11. Your assessment findings are as follows: lung sounds absent in the LLL and very diminished
in the right lower lobe (RLL). You percuss a dull thud over the left middle lobe (LML) and
LLL up to the scapula tip. On percussion, you hear resonance over the entire right lung and left
upper lobe (LUL). What is the significance of your findings?
12. What actions should you take next?

Case study progress:

The physician orders a STAT CXR which shows a significant pleural effusion developing in
the LLL, with extension into the RLL.
13. Based on the evolving pleural effusion with evidence of decompensation (hypoxia) by the
patient, what treatment would the physician likely pursue, and what preparations would you be
responsible for?

Case study progress:

The physician removed 200 mL of slightly cloudy serous fluid. Antibiotics were adjusted to
provide broad spectrum coverage for an upper respiratory tract infection until culture and sensitivity
results return. B.K. is resting quietly with oxygen at 3 L per nasal cannula, and her respirations are
unlabored and regular. Her SpO2 reads 96%. It is now 72 hours after B.K.'s admission, and her labs
show improvement. An abdominal CT scan is completed and shows “a moderately severe pancreatitis,
but no local fluid collection or pseudocysts. No ileus or evidence of neoplasia was noted.” BUN is 9.0
mg/dL, and creatinine is 1.0 mg/dL. She has adequate urinary output. Her IV fluids are decreased to 75
mL/hr. Her amylase and lipase levels are decreasing toward normal levels. The physician writes an
order to advance B.K.'s diet to full liquids.
14. How would you know whether B.K. was not able to tolerate the advancement in diet?
15. If B.K. does not tolerate the advancement in diet, what physiologic need should be addressed at
72 hours?

Case study progress:

The afternoon of the third day of B.K.'s hospitalization, she becomes agitated with tremors,
some disorientation, and auditory hallucinations. Her pulse and blood pressure (BP) are elevated,
although her pain has not increased, and the pain medication schedule has not changed. B.K. has had
no visitors since being admitted.
16. What is B.K. most likely experiencing, and what actions will you take?

Case study progress:

You contact the physician with your observations, and he orders scheduled chlordiazepoxide
(Librium) and a social services consult to evaluate and treat for possible alcohol abuse. Three days
later, B.K. is lucid, tolerating clear liquids, and her pain is controlled with oral pain medications. As
she becomes oriented and calmer, B.K. eventually admits to drinking “3 or 4 scotch-on-the-rocks”
daily. You also discover that B.K. is estranged from her family because of her drinking. The physician
advances her diet to “low fat/low cholesterol” and writes orders to discharge that evening if she
tolerates the advancement in diet, which she does.
17. What will you include in your discharge teaching with B.K.?

Activity

1. Present the medical management of Chronic Pancreatitis by highlighting:

a. Pharmacological therapy of patient with Chronic Pancreatitis in a form of
MNEMONICS.
b. Surgical management of patient with Chronic Pancreatitis
2. Present nursing care plan of patient with Chronic Pancreatitis
3. Make a nursing care plan of patient with Chronic Pancreatitis.
4. Make your own pathophysiology of Chronic Pancreatitis.