Running head: CLINICAL CASE STUDY: ACUTE PANCREATITIS
Allison Tayloe
Clinical Case Study: Acute Pancreatitis
Managing Common Acute and Emergent Health Problems I, NUR 7201
WSU, CONH
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CLINICAL CASE STUDY
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Clinical Case Study: Acute Pancreatitis
Source: patient, reliable source
Chief Complaint: “Abdominal pain, nausea and vomiting x six hours”
History of Present Illness: D.M. is52 year old year old female who presents to the emergency
department with complaints of left upper quadrant abdominal and epigastric pain radiating to the
back, nausea, and vomiting that began approximately six hours ago. She reports she woke up at
6:00 AM this morning with severe abdominal pain 8/10 that began in the left upper abdominal
quadrant with radiation to her epigastric area and around to her back. She describes the pain as a
constant sharp and burning pain that is aggravated by movement or lying down and is somewhat
improved when she leans forward sitting up. She attempted to take TUMS tablets x 4 this
morning without relief thinking the pain was due to an ulcer as she has had one in the past. She
also admits to nausea and vomiting three times this morning with the onset of abdominal pain
and states she has not eaten since last night. By 9:00 am, three hours after the onset of symptoms,
the patient reports the pain became more severe increasing to rate 10/10, thus she decided to call
911. She denies any fevers, chills, diarrhea, constipation, bloody emesis or stools in addition to
reported symptoms.
Medical History: Anxiety, depression, hypertension, peptic ulcer disease
Surgical History: cholecystectomy 1998, cesarean section 1984, 1986
Social History: The patient currently lives at home with her boyfriend. She is currently
unemployed. She denies any current exercise program. She admits to smoking 1PPD of
cigarettes x 20 years and consuming two-three 24 oz. beers nightly with two 4 oz. shots of vodka
or rum x 10 years. She denies any illicit drug use such as cocaine, heroin, or marijuana. She did
CLINICAL CASE STUDY
not receive the flu vaccine for the past three years and she does not recall ever receiving the
pneumococcal vaccine. She is up to date on all childhood vaccines.
Family History: Her paternal grandmother died at age 88 from unknown causes and paternal
grandfather died at age 50 in a car accident. Her maternal grandmother lived to age 85 and died
from lung cancer. Her maternal grandfather died at age 68 from chronic obstructive pulmonary
disease. Her mother died at age 72 from cirrhosis of the liver due to alcoholism and she is
estranged from her father. She has one living sister who has a history of hypertension and
diabetes. She has two living sons who are in their late twenties and have no known chronic
medical condition.
Medications: Alprazolam (Xanax®) 0.5 mg three times a day, Fluoxetine (Prozac®) 40 gm
daily, amlodipine (Norvasc®) 5 mg daily, hydrochlorothiazide 25 mg daily
Allergies: No known allergies
Review of Systems
ROS is positive for nausea, vomiting, and abdominal pain with radiation to back. Otherwise
negative as listed below.
General: Denies weight loss, malaise/fatigue, fever/chills, or decreased appetite
Neuro: Denies weakness, dizziness, syncope, or near syncope, headaches, seizures, or loss of
consciousness
HEENT: Denies sore throat, changes in hearing or vision, nasal drainage, ear pain, or blurry
vision.
Respiratory: Denies cough, sputum production, hemoptysis, or shortness of breath
Cardiovascular: Denies chest pain, PND, orthopnea, leg swelling, or palpitations.
Gastrointestinal: Denies diarrhea, constipation, or bloody stools.
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Genitourinary: Denies vaginal discharge, hematuria, or dysuria.
Musculoskeletal: Denies joint or bone pain/tenderness. Denies any recent falls.
Skin: Denies rashes, lesions, or scars.
Psychosocial: +history of depression and anxiety, denies any recent depressive or anxious
episodes while taking home medications. Denies suicidal thoughts or ideations. Denies any
domestic violence.
Physical Exam:
Vitals: (in ED) B/P 138/82, RR 32, and HR 102 bpm, O2 sat: 96 % on room air, temp: 99.4 ᵒF
General: Appears older than stated age, anxious, pale, restless in bed gripping abdomen
HEENT: Head normocephalic. Eyes, conjunctivae clear with no drainage. External ears
symmetrical bilaterally. Mouth, nose, and throat, no significant lesions. No palpable tenderness
over lymph nodes or sinuses. Mucous membranes dry, pink, no lesions or edema noted. No
thyromegaly, trachea midline on palpation. No jugular venous distention.
Skin: Diaphoretic, pale, warm. No appreciable rashes, lesions, or skin discoloration. No hair
thinning.
Neurological: Awake, alert, oriented x 3. Cranial nerves II-XII intact.
Cardiac: The apex is nonpalpable. Pulses are 2+ in carotid, radial, femoral, posterior tibialis and
dorsalis pedis bilaterally. Regular rhythm, tachy rate with no appreciable murmurs, rubs, or
gallops. S1, S2 present. No carotid bruits. No palpable thrills. No tenderness on palpation of
chest wall.
Pulmonary: Shallow breathing, tachypenic. Symmetric thoracic expansion. No wheezing or
rhonchi, or crackles. CTAB.
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Gastrointestinal: Hypoactive bowel sounds in all 4 quadrants. Mild distension. Unable to
palpate pancreas. Liver size approximately 8 cm in length. Voluntary guarding to upper right
quadrant. Tenderness to epigastric area and right upper quadrant on palpation. Mild tenderness to
left upper quadrant, no tenderness to bilateral lower quadrants. No peritoneal signs. No Cullen or
Grey Turner’s sign.
Genitourinary: Urinary meatus normal, no edema or erythema
Musculoskeletal: Deep tendon reflexes intact any symmetrical bilateral upper extremities (BUE)
and bilateral lower extremities (BLE). Motor and sensory function intact. Full range of joint
motion to BUE and BLE and 5/5 muscle strength bilaterally.
Table 1: Diagnostic Lab results
Diagnostic Lab Results
Glucose (70-100 mg/dL)
K (3.5-5 mEq/L)
Na (135-145 mEq/L)
Creat (< 1.2 mg/dL)
CO2 (22-28 mmol/L)
Cl (96–107 mEq/L)
BUN (5–18 mg/dL)
Ca (8.5–10.5 mg/dL)
GFR ( >70 mL/min)
Amylase (0-100 U/L)
Lipase (0-160U/L)
Trig (<150 mg/dL)
LDH
ABG: pH (7.35-7.45)
PaO2 (80-100 mm Hg)
CO2 (35-45 mm Hg)
BE (±2)
HCO3 (22-26 mm Hg)
O2 saturation
Result
248 mg/dL
3.8 mEq/L
137 mEq/L
1.0 mg/dL
23mmol/L
98 mEq/L
18 mg/dL
8.2 mg/dL
72 mL/min
468 U/L
2, 387 U/L
329 mg/dL
248mg/dL
7.42
82 mm Hg
33 mm Hg
0
24 mm Hg
96%
Diagnostic Lab Results
WBC (k/mm3)
RBC: (4.2-5.7 m/mm3)
Hgb (12.0-14.8 g/dL)
Hct (37.8-43.9%)
Plt (150 -450 k/mm3)
Troponin I (< 0.05 ng/mL)
Alkaline Phophatase (25–160 IU/L)
ALT (1–45 IU/L)
AST (7–42 IU/L )
Alkaline phosphatase (40-117 U/L)
Urinalysis: Color/clarity (clear/yellow)
pH (5.0-9.0)
Specific gravity (1.005-1.030)
Glucose (neg)
Nitrates (neg)
WBC (0)
RBC (0)
Protein (neg)
Ketones (neg)
Result
14.4 k/mm3
4.8 m/mm3
14.2 g/dL
43.9 %
237 k/mm3
0.01 ng/mL
IU/L
78 IU/L
63 IU/L
264 U/L
(clear/yellow)
6.0
1.025
neg
neg
0-1
neg
neg
neg
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Table 2: Additional diagnostic tests
EKG
Chest x-ray
Abdominal x-ray
Rhythm: ST
Rate: 110 bpm
PR interval: 0.12
QRS: 0.08
QT: 420 msec
No ST-T wave
abnormalities, no q waves,
normal axis
Cardiac silhouette is
unremarkable. No active
cardiopulmonary process,
no pleural effusions or
infiltrates visible.
Minimal small bowel
dilation concerning for
possible ileus
Abdominal CT with IV
contrast
Diffuse pancreatic
inflammation consistent
with pancreatitis. No fluid
collection, peripancreatic
fat infiltration or
pseudocysts visible.
Differential Diagnosis
The differential diagnosis for this patient could include various causes of sudden and
severe abdominal pain and physical exam findings listed above such as: acute cholecystitis, acute
cholangitis, acute pancreatitis, ruptured duodenal ulcer, pneumonia, acute myocardial infarction,
renal colic, perforated viscous, small bowel obstruction, mesenteric ischemia, dissecting aortic
aneurysm or diabetic ketoacidosis (Wu & Conwell, 2012).
Probability of various diagnoses, presentation of symptoms, past medical and surgical
history, physical exam findings, and diagnostic tests can all assist in differentiating appropriate
diagnoses for patients who present to the emergency department. As noted in the surgical history
of this patient, she has already had her gall bladder removed, helping to eliminate the diagnosis
of acute cholecystitis as a cause of symptoms. Diabetic ketoacidosis is also a consideration with
abdominal pain associated with nausea and vomiting, however, this patient describes a sudden
onset of symptoms and has no history of diabetes, making this diagnosis less likely. Although
this patient is hyperglycemia on presentation to the emergency department, anion gap is normal
and there were no ketones present in the urine, also lessening the chance of diabetic ketoacidosis
as a cause for her symptoms (Tierney, McPhee & Papadakis, 2014). Renal colic is also a
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consideration, but is unlikely given that renal calculi typically don’t cause elevations in serum
amylase, lipase, and triglycerides, pain with renal colic is typically located in the flank area with
radiation to the abdomen and groin, and urinalysis in this patient doesn’t show signs of infection,
hematuria, or crystals concerning for urolithiasis (Kasper et al., 2012). Pneumonia is also an
unlikely diagnosis, given the sudden onset of symptoms and absence of complaints of upper
respiratory infection or shortness of breath on admission. Acute cholangitis, an infection in the
biliary tract, is another possibility based on this patient’s presentation. Patients with acute
cholangitis frequently present with symptoms known as Charcot triad, which includes fever,
abdominal pain, and jaundice (Baillie, 2012). Although this patient did have a severe and sudden
onset of abdominal pain and has a low grade fever with an elevated white blood cell count, she
did not present with jaundice, which is almost always present in the sclera or sublingual area in
patients with acute cholangitis (Baillie, 2012). Endoscopic ultrasound is considered the gold
standard for diagnosing bile duct stones and may show dilation of biliary tree > 8 cm in patients
with acute cholangitis, however magnetic resonance imaging (MRI) and computed tomography
(CT) scan may give similar information if further testing is needed (Tierney, McPhee &
Papadakis, 2014). This patient had no such findings noted on her CT scan or abdominal
ultrasound, making acute cholangitis an unlikely diagnosis. Small bowel obstruction and
mesenteric ischemia are also diagnoses that should be considered based on the patient’s
presentation of symptoms, but can most likely be ruled out based on CT results not showing any
areas of bowel dilation, or heterogeneous/homogenous low attenuation areas of bowel (Mortele,
2012). Mesenteric ischemic is more likely to occur in patients with a history of congestive heart
failure, atrial fibrillation, unexplained weight loss, postprandial abdominal pain, or a recent
myocardial infarction, none of which is mentioned in this patient’s presentation (Lo, 2010). This
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patient is also not noted to be anemic, which typically occurs from blood loss in patients with
mesenteric ischemia related to coagulopathies causing lower GI bleeding and melena (Lo, 2010).
This patient does have a history of previous history of peptic ulcer disease, as well as
continued alcohol and tobacco use, further increasing her chances of having a ruptured duodenal
ulcer (Kasper et al., 2012). However, a ruptured duodenal ulcer is typically associated with mild
serum amylase elevation (< 2 times normal) and can be diagnosed with use of CT scan showing
free air located in the abdominal cavity or below the left and right hemi diaphragm on chest xray, neither of which was noted to be present in this patient’s testing (McQuaid, 2014). In
addition, perforated duodenal ulcers are rarely precipitated by nausea and vomiting and
abdominal pain with radiation to the back is an uncommon finding, further decreasing the
probability that this patient is experiencing a perforated ulcer (Doherty & Way, 2010).
Although this patient did not present with symptoms of chest pain, syncope, or focal
neurologic changes, an aortic dissection can present as severe abdominal pain with radiation to
the back depending on the location of the dissection (Johnson & Prince, 2011). Chest x-ray in
this patient did not show widening of the mediastinum or abnormal aortic contour which can
frequently be seen in thoracic aortic dissection, but the diagnosis can’t be excluded based on the
absence of this finding alone. Due to the severity of morbidity and mortality as well as
hemodynamic instability associated with this diagnosis, a CT of the chest and abdomen should
be performed with and without contrast to assess for aortic dissection if this diagnosis remains a
concern (Johnson & Prince, 2011). An acute myocardial infarction, typically inferior, also
needs to be considered as a possible diagnosis in a patient presenting with the above stated
symptoms. In addition, women are more likely than men to present with atypical symptoms for
acute myocardial infarction, such as epigastric pain (Boyle, 2014). To complicate matters more,
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conditions such as acute pancreatitis can mimic inferior myocardial infarctions for reasons
thought to be related to increased vasovagal responses, electrolyte abnormalities, coronary
vasospasm, or coagulopathy (Tejada et al., 2008). Therefore, electrocardiogram (EKG) findings
alone may not be indicative of acute myocardial infarction. This patient was not noted to have
any EKG ST-T wave abnormalities and troponin level was < 0.01, making the diagnosis of acute
myocardial infarction unlikely (Tierney, McPhee & Papadakis, 2014). Troponin is a specific
cardiac biomarker typically elevated within four to eight hours after initial injury and has a high
sensitivity and specificity for cardiac ischemia and necrosis (Boyle, 2014). It is possible for a
patient to be experiencing acute non ST elevated MI or unstable angina without subsequent EKG
changes, but an acute ST elevated myocardial infarction can be ruled out based on the absence of
EKG changes on this patient’s EKG (Boyle, 2014). This patient would need an additional one to
two troponin levels checked eight hours apart to completely rule out myocardial ischemia or
necrosis (Tierney, McPhee & Papadakis, 2014).
The most likely diagnosis for this patient is acute pancreatitis related to alcohol
consumption. The two most common causes of acute pancreatitis are alcohol exposure and
biliary tract disease (Lippi, Valentino, & Cervellin, 2012). Furthermore, acute pancreatitis due to
alcohol consumption is typically associated with chronic alcohol use of 5-15 years, which is
described in this patient’s social history. This patient has had her gallbladder removed over a
year prior to the onset of symptoms, lessening the chance of gallstones in the bile duct as a cause
for her AP, and has no known vasculitis disorders that would cause acute AP (Kasper et al.,
2012). Epigastric and left upper quadrant pain with radiation to the back with associated nausea
and vomiting are the most common presenting symptoms in acute pancreatitis, which this patient
is also described as experiencing (Atilla & Oktay, 2011). According to the American College of
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Gastroenterology, acute pancreatitis (AP) is diagnosed based on presence of two of the three
following criteria: abdominal pain consistent with the disease, serum amylase and/or lipase
elevations greater than three times upper normal limit, and findings characteristic of AP on
abdominal imaging (Tenner, Baillie, DeWitt, & Swaroop Vege, 2013). This patient not only has
characteristic abdominal pain as well as amylase and lipase levels three times upper limit of
normal, but also has CT abdominal results revealing pancreatic inflammation consistent with
acute pancreatitis. In addition, this patient is also noted to have elevated triglycerides,
hyperglycemia, hypocalcemia, and elevated liver enzymes which are often seen in certain types
of acute pancreatitis and help to classify the severity of acute pancreatitis diagnosis (Atilla &
Oktay, 2011).
Diagnostic Testing
Patients admitted to the emergency department with complaints of severe abdominal pain
should include laboratory testing and abdominal imaging in an effort to properly diagnose and
treat the patient presenting with these symptoms. In cases of acute pancreatitis, like many other
causes of acute abdomen, laboratory testing should include basic metabolic panel (BMP),
complete blood count (CBC), amylase, lipase, liver function tests (LFT) including aspartate
aminotransferase, serum alkaline phosphatase, and bilirubin levels, lactate dehydrogenase,
triglyceride levels, urinalysis, and C-reactive protein levels (Atilla & Oktay, 2011). CBC is
helpful in identifying leukocytosis often present in acute abdomen disorders, including acute
pancreatitis. In addition, CBC revealing low hemoglobin may help differentiate diagnoses such
as mesenteric ischemia, whereas patients with AP who yield high hematocrit levels above 44%
have higher predictive value for pancreatic necrosis related to hemoconcentration and overall
poorer prognosis (Tierney, McPhee & Papadakis, 2014). Serum amylase is primarily produced
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by the pancreas and salivary glands and rises rapidly (within 3-6 hours) with the onset of acute
pancreatitis, making it an important diagnostic laboratory value for acute pancreatitis (Lippi,
Valentino, & Cervellin, 2012). Even though amylase levels can be elevated in other disorders
affecting pancreatic or salivary gland production or renal excretion such as renal failure, chronic
alcoholism, pregnancy, appendicitis, and hepatitis, amylase levels elevated greater than three
times the upper limit of normal with associated abdominal pain increased specificity of acute
pancreatitis of ~95%, but sensitivity remains low at ~60% (Atilla & Oktay, 2011). Although
lipase can also be affected by some abdominal processes and renal failure, lipase is solely
produced by the pancreas and not salivary glands and stays elevated longer than amylase levels,
making it a more accurate diagnostic test for the diagnosis of acute pancreatitis (Tierney,
McPhee & Papadakis, 2014). Elevated fasting triglyceride levels ( > 1000 mg/dL) is associated
with acute pancreatitis due to hypertriglyceridemia, a poor prognosis for patients with acute
pancreatitis, and can inhibit serum amylase elevation in patients with acute pancreatitis masking
elevated levels Tenner et al., 2013). Thus, fasting triglyceride levels are important diagnostic lab
value when diagnosing acute pancreatitis, especially when gallstones or alcohol seems unlikely
as potential cause (Tenner et al., 2013). On the same note, lactate dehydrogenase levels > 500
U/dL are also associated with a poorer prognosis (Atilla & Oktay, 2011). Elevated liver function
tests and hyperbilirubinemia should be checked for degree of elevation and possibly underlying
liver disease, although these levels are often mildly elevated in patients with AP and return to
normal in approximately seven days (Kasper at al., 2012). In this patient, who is thought to have
AP caused from continued alcohol use, liver enzymes are also useful for assessing chronic
elevated liver enzymes which would occur with hepatitis or cirrhosis of the liver (Tierney,
McPhee & Papadakis, 2014). C-reactive protein is an important inflammatory marker both in
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acute and chronic AP and should be checked within the first 72 hours to make assess for levels >
150 mg/L, which is associated with higher rate of pancreatic necrosis and increased severity of
AP (Williamson & Williamson, 2010).
Many other electrolyte and lab values such as calcium levels, blood urea nitrogen levels,
and serum creatinine are not sensitive or specific for acute pancreatitis, but helpful in assessing
severity of disease in those with AP to help guide appropriate treatment, thus should be obtained
on all patients with AP (Kasper et al., 2012). For example, elevated creatinine > 1.8 mg/dL 48
hours after diagnosis of acute pancreatitis is associated with higher rates of pancreatic necrosis,
whereas hypocalcaemia, for unknown reasons, is associated with poorer prognosis in those with
acute pancreatitis (Tierney, McPhee & Papadakis, 2014). In patients diagnosed with acute
pancreatitis that present with hypotension and elevated creatinine on admission, guidelines for
treatment include more intense intravenous fluid volume management and admission to the
intensive care unit for closer observation (Tenner et al., 2013).
Diagnostic testing for acute pancreatitis also includes various forms of abdominal
imaging. Abdominal x-ray is useful in identifying free air consistent with perforated peptic ulcer,
but typically adds little assistance in diagnosing AP (Kasper et al., 2012). According to the
American College of Gastroenterology guidelines, all patients presenting with AP should have a
trans-abdominal ultrasound (Strong recommendation, low quality of evidence) (Tenner et al.,
2013). Trans-abdominal ultrasound is useful in identifying cholelithiasis, but is often not helpful
in diagnosing AP due to intervening bowel gas, therefore was not performed in this patient due
to previous cholecystectomy (Tierney, McPhee & Papadakis, 2014). Contrast enhanced
computed tomography (CECT) has > 90% sensitivity and specificity for diagnosing acute
pancreatitis (Tenner et al., 2013). However, routine use of CECT is not necessary in mild AP
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cases due to typical exam and laboratory findings aiding in diagnosis. Rather, CECT should be
completed in 48-72 hours after admission if patient does not improve to evaluate for pancreatic
necrosis or initially if abdominal ultrasound is not completed or serum amylase levels are less
than three times the upper limit of normal (Tenner et al., 2013). Magnetic resonance imaging
(MRI) is comparable to CECT and can be used as an alternative to identify necrosis in patients
who fail to improve within 48-72 hours after admission (Kasper et al., 2012). CECT imaging is
also useful in assessing the severity of acute pancreatitis three to five days after diagnosis
(Tenner et al., 2013). CECT images on admission in patients with mild AP can’t always predict
the progression to severe AP in these patients and are often reserved for AP patients who fail to
show improvement in 48-72 hours, therefore, CT images of this patient would need to be
repeated in three days in order to assess severity index and associated mortality for AP based on
CT results (Tierney, McPhee & Papadakis, 2014).
There are also several severity scoring systems for severity of AP based on presenting
signs and symptoms and whether or not there is improvement in 48 hours of admission. Such
scoring systems include the Atlanta classification scoring system and the Ranson criteria. The
Ranson criteria are especially useful in patients who present with acute alcoholic pancreatitis.
Ranson criteria includes factors such as age> 55 years and presenting white blood cell count (>
16, 000/mm3), blood glucose levels (>200 mg/dL), LDH levels (>350 U/L), and AST levels
(>250 U/L) and is associated with higher mortality if score ≥ 3or if other factors such as drop in
hemoglobin (>10%), BUN rise (>5 mg/dL), PaO2drop (<60 mm Hg), serum calcium (<8
mg/dL), increased base deficit (> 4 mEq/L) or increased fluid restoration (> 6L) develops within
48 hours (Sargent, 2006). Atlanta scoring system divided into mild AP, moderately severe AP or
severe AP. Severe AP is diagnosed based on findings of organ failure in at least one organ
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which would be defined as systolic blood pressure < 90 mm Hg, PaO2 < 60 mm Hg, creatinine >
2mg/dL, > 500 mL blood loss related to gastrointestinal bleeding within 24 hours, or local
complications such as peripancreatic fluid collections or pseudocysts (Tierney, McPhee &
Papadakis, 2014). Moderately severe AP includes definitions of severe AP, but with only
transient organ failure < 48 hours. Mild AP, associated with the best prognosis and typically
only requiring a short hospital stay of 72-96 hours, is defined by absence of organ failure or local
complications on abdominal imaging (Tenner et al., 2013). The Bedside Index for Severity in
Acute Pancreatitis (BISAP) and Acute Physiology and Chronic Health Evaluation (APACHE II)
assess mortality risk of AP patients within the first 24 hours of admission. BISAP score includes
levels of BUN (> 25 mg/dL), mental status impairment, systemic inflammatory response
syndrome (SIRS) criteria , evidence of pleural effusion, and age (> 60 years) as criteria with
scores ≤ 2 associated with mortality < 2% (Tierney, McPhee & Papadakis, 2014). Based on the
above findings, this patient is classified as having mild AP. However, review of the literature
regarding various scoring systems notes that severity scores usually take greater than 48 hours to
become accurate and may not be able to accurately predict patients with mild AP who can
quickly progress to severe AP (Tenner et al., 2013). Therefore, clinicians caring for these
patients need to continue to assess diagnostic labs such as amylase and lipase and daily renal
function panels to appropriately assess for hemodynamic stability and improvement of symptoms
over the first 48-72 hours (Tierney, McPhee & Papadakis, 2014).
Prioritized plan
Prioritized plan for the patient with acute pancreatitis includes assessing for level of
severity, intravenous fluid resuscitation and early oral diet/enteral feeding initiation, analgesic
medication administration, and treatment of underlying cause. In this patient’s case, treatment of
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AP would include all of the above as well as monitoring and treatment for alcohol withdrawal.
Thus, this patient will be admitted to the hospital in a ICU-step down bed with continuous
cardiac and pulse oximetry monitoring and receive treatment for acute pancreatitis.
Treatment of the patient presenting with AP always includes early aggressive intravenous
(IV) fluid hydration within the first 12-24 hours (strong recommendation, moderate quality of
evidence) due to the underlying inflammatory processes of AP causing decreased pancreatic
blood flow, as well as volume losses through nausea/vomiting, poor oral intake, and third
spacing (Tenner et al., 2013). Although IV fluid replacement hasn’t shown to be effective with
late AP presentation, this patient presented within six hours of symptom onset and therefore will
be given an initial bolus of two liters lactated ringers (LR) solution (20 ml/kg over 1-2 hours)
while in the emergency department (Marino, 2014). LR is the isotonic solution of choice for
patients with AP due to several studies showing decreased risk of systemic inflammatory
response syndrome with LR versus normal saline administration and overall decreased morbidity
(Tenner et al., 2013). Thus, following initial two liter fluid bolus, the patient will be continued
on LR on a continuous rate of 150 mL/hr up to 250 mL/hr to maintain mean arterial pressure >
65 mm Hg and urine output of 0.5 mL/kg/hr since this patient does not have any known
underlying cardiac or renal disorders (Marino, 2014). A BMP will be checked every six hours
with pancreatic enzyme levels including amylase and lipase every 24 hours with the goal of
hydration to decrease BUN and hematocrit levels while maintaining normal creatinine levels
(strong recommendation, moderate quality of evidence) (Tenner et al., 2013). As states above,
CT scans are unnecessary and not cost effective in patients with mild AP, but if patient fails to
improve within 47 hours ( low urine output < 0.5 mL/kg/hr or MAP < 65 mm Hg despite
adequate fluid resuscitation), a CT scan should be performed to evaluate for possible pancreatic
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necrosis or pseudocyst formation. If necrosis is discovered, surgical intervention may be needed
and antibiotic therapy may be warranted (Tierney, McPhee & Papadakis, 2014).
Pain in AP is caused by leakage of inflammatory exudates into retroperitoneal spaces
(Sargent, 2006). Furthermore, generalized pain with any illness increases metabolic activity
which in turn increases production and secretion of pancreatic enzymes, thus increasing pain for
patients with AP. Meperidine used to be the drug of choice for analgesia in acute pancreatitis
due to thoughts that other narcotics caused spasm in the sphincter of Oddi, but morphine is now
the analgesic of choice due to harmful metabolites of meperidine that can accumulate and
potentiate seizures (Tierney, McPhee & Papadakis, 2014). Patient controlled analgesia (PCA)
has also showed improved pain control in patients with acute pancreatitis, therefore, this patient
will be given 4 mg morphine IV in the emergency department every one-two hours and started
on a morphine PCA with demand dose of 1 mg every 15 minutes with a lockout of 4 mg every
hour and 20 mg lockout in four hours (Lexi-comp, 2014). Continuous end pulse oximetry and
cardiac monitoring will be applied to this patient as well as every four hour full nursing
assessments to monitor for central nervous system depression. If the PCA is ineffective at
controlling the patient’s pain, consideration of increasing morphine to 2 mg every 15 minutes or
a bolus of morphine 2 mg every two hours through the PCA should be considered (Sargent,
2006). Once the patient is pain free, usually in 48-72 hours with mild AP, IV pain medications
can be weaned. Non-steroidal anti-inflammatory agents have been shown to be ineffective in
treatment of AP (Doherty & Way, 2010). This patient will also be given an antiemetic, such as
zofran, 4 mg IV every four hours as needed for nausea and vomiting in the initial acute period of
AP (Lexi-Comp, 2014).
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Based on current recommended guidelines, patients admitted with AP no longer are
required to have nothing by mouth (NPO) to allow the pancreas to “rest” (Williamson &
Williamson, 2010). Furthermore, patients being maintained on an NPO diet causes bowel
atrophy due to nonuse (Tenner et al., 2013). Because this patient only shows mild AP on
admission to the hospital, a low-fat solid diet should be initiated within 12-24 hours as early oral
nutrition is associated with decreased hospital stay and overall morbidity and mortality
(Willamson & Williamson, 2010). Current evidence supports idea that initiation of solid low fat
diet is just as safe as initiation of clear liquid diet in patients with mild AP (conditional
recommendation, moderate quality of evidence) (Tenner et al., 2013). However, oral nutrition
should not be started until nausea/vomiting has abated and the patient’s pain has subsided
(Tierney, McPhee & Papadakis, 2014). In addition, if pain or vomiting reoccurs after starting an
oral diet, the patient should be made NPO again and may require placement of an oral gastric
tube for ileus release and control of symptoms (Kasper et al., 2012). Should this patient fail to
show improvement within 48-72 hours, enteral nutrition through placement of a nasojejunal or
even nasogastric tube with usual enteral nutritional formulas should be considered (Williamson
& Williamson, 2010). Enteral nutrition should include 25-35 kilocalories/kg, 1-2g fat/kg, 3-6
g/kg of carbohydrate and 1.2-1.5grams of protein/kg (Holcomb, 2007). Parenteral nutrition
should only be used if enteral nutrition is not tolerated or not meeting caloric requirements
(strong recommendation, high quality of evidence) (Tenner et al., 2013). Patients who present
with AP are frequently hyperglycemic on admission and treatment of AP should include blood
glucose levels as well as insulin therapy to maintain adequate glucose control. Current
recommendations of the American Diabetes Association includes blood glucose monitoring
every four hours in non-ICU hospitalized patients who are NPO admitted and noted to have
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18
hyperglycemia (Magaji & Johnston, 2011). Blood glucose monitoring should be changed to
prior to meals and at bedtime when the patient is eating. Current recommendations also support
basal and sort acting insulin for goal of blood glucose control of ≤ 140 mg/dL premeal glucose
and random blood glucose goal of ≤180 mg/dL (Marino, 2014). Therefore, this patient will be
started on basal insulin and short acting insulin in the dose of 0.3 units/kg/ day to be divided up
as 50% basal insulin once daily subcutaneously and the other 50% divided up into three doses of
short acting insulin to be given prior to meals subcutaneously (Magaji & Johnston, 2011). In
addition, the patient will be placed on sliding scale coverage for addition short acting insulin to
be given subcutaneously premeal and before bedtime or every four hours for blood glucose
levels ≥ 140 mg/dL. A fasting hemoglobin A1C should be obtained during the hospital
admission to assess for underlying insulin resistance or diabetes (Magaji & Johnston, 2011). As
the patient recovers from acute pancreatitis, basal insulin may need to be reduced as blood
glucose levels return to normal, but blood glucose monitoring should continue while the patient
is hospitalized. If the patient requires transfer to the intensive care unit, an insulin drip with
regular insulin should be initiated for blood glucose levels > 180 mg/dL (Magaji & Johnston,
2011). Although this patient is noted to have leukocytosis on admission, prophylactic antibiotic
treatment is not recommended due to the lack of evidence showing improved outcomes on
patients with AP, even when pancreatic necrosis develops, therefore antibiotics will not be
started (strong recommendation, moderate quality of evidence (Tenner et al., 2013).
Treatment of this patient with suspected alcoholic acute pancreatitis will include
management of alcohol withdrawal while in the hospital to prevent possible seizures. Thus, this
patient will be monitored with the clinical institute withdrawal assessment protocol (CIWA) with
Ativan IV in increments of 0-4 mg every two hours will be ordered based on CIWA scores
CLINICAL CASE STUDY
19
(Kasper et al., 2012). Doses will then be tapered over three-five days. A behavioral assessment
consult will also be placed to assess for underlying chronic alcohol abuse as well as
depression/anxiety medication adjustments needed on discharge. Chronic alcohol use is
associated with multiple vitamin deficiencies, therefore this patient will be treated with thiamine
100 mg IV daily for three days followed by 50 mg per day by mouth as this is the
recommendation for any patient with acute alcohol withdrawal (Lexi-Comp, 2014). Due to the
patient’s chronic alcohol use, it would not be inappropriate to draw a hepatitis panel, especially if
the liver enzymes remain elevated (Kasper et al., 2012). Scheduled alprazolam, which the
patient was taking prior to admission, should be continued as soon as the patient is able to
tolerate oral diet with 0.5 mg twice daily by mouth. As such, the patient’s Fluoxetine (40 mg
daily by mouth), hydrochlorothiazide (25 mg daily by mouth), and amlodipine (5 mg daily by
mouth) should be restarted when the patient is able to tolerate oral intake. Blood pressure will be
monitored every one-two hours in the first twenty four hours with goal blood pressure < 140/90
mm Hg and mean arterial pressure > 65 mm Hg (Marino, 2014). Treatment for this patient
should also include measures to aide in smoking cessation and nicotine replacement, if needed
while in the hospital, which could be accomplished with Nicoderm CQ transdermal patch 21
mg/day which should be continued after discharge for a total of six weeks, then tapered down to
14 mg/day for two weeks and 7 mg/day for two weeks (Lexi-Comp, 2014). This patient will be
counseled during the hospitalization regarding the importance of smoking cessation and
readiness to quit will be assessed.
Health Promotion/Follow-up
In follow-up for patients admitted with acute pancreatitis, management focuses on
prevention of recurrent AP as well as managing complications of the disease (Wu & Conwell,
CLINICAL CASE STUDY
20
2012). In this patient with presumed alcoholic acute pancreatitis, alcohol cessation and
abstinence will help prevent future AP occurrences as well as development of chronic
pancreatitis. Therefore, this patient will be given contact information on outpatient treatment
centers and outpatient group therapy sessions such as alcoholics anonymous (AA), which have
been shown to decrease alcohol consumption in as little as one to four sessions (Williamson &
Williamson, 2010). Follow-up with this patient’s primary care physician should include
assessment for continued alcohol use through questionnaires such as CAGE (cutting down,
annoyed by drinking, feel guilty, eye opener) (Kasper et al., 2012). Follow-up should also
include continued appointments with the patient’s primary care physician to assess smoking
cessation progress and if the patient has relapsed. The patient’s willingness to quit should be
reassessed at every visit if the patient continues to smoke. Furthermore, holistic care, in the form
of counseling should be used in addition to medical treatments such as bupropion or varenicline
if patient is willing to quit (Lexi-Comp, 2014). The patient should be encouraged to continue a
low fat diet, as well as continue his medications for management of underlying chronic
conditions with yearly vaccinations and diagnostic labs including fasting lipid levels,
hemoglobin A1C, and baseline BMP and CBC. Following discharge from the hospital, the
patient should follow-up with his PCP within a week to discuss hemoglobin A1C results if
greater than 6.5% for potential treatment options as well as assess liver enzymes, BMP, and
amylase to ensure return to normal levels. If the patient’s hepatitis panel comes back positive for
hepatitis C or liver enzymes remain elevated, further treatment may be recommended (Kasper et
al., 2012). Measures such as yearly vaccinations (influenza and pneumococcal), continued diet,
and daily rigorous exercise of 30 minutes or more should be encouraged in this patient in
CLINICAL CASE STUDY
addition to smoking and alcohol cessation to decrease this patient’s chance of recurrent AP
episodes.
21
CLINICAL CASE STUDY
22
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