Pancreatitis in Children Pediatric Care

Pediatric Care
Pancreatitis in Children
CHRIS KRAMER, RN, BSN, CCRN
ALVIN JEFFERY, RN-BC, MSN, CCRN, FNP-BC
Although the incidence of acute pancreatitis among children is less than that in adults, the physical and
psychosocial impact on children and their families can be overwhelming. Pancreatitis is manifested as pain
accompanied by a host of other complex issues. These issues are manifested more markedly when the patient
has additional concomitant diagnoses. Pain management, liver function tests, amylase and lipase levels,
endocrine and exocrine functionality, and recognition of systemic inflammation are especially important.
Management after discharge from the hospital is often an ongoing stress for these patients and families, and
multiple admissions to the intensive care unit may be necessary for feeding and pain complications. Presented
in the context of an actual clinical case at a 500-bed tertiary care pediatric hospital, this patient’s scenario
illustrates the importance of ensuring adequate nutrition, maintaining hydration, providing appropriate pain
management, and preventing infection and thromboembolic events. (Critical Care Nurse. 2014;34[4]:43-53)
haracterized by localized edema and systemic inflammation, pancreatitis is a
potentially life-threatening disease that has long-term consequences for many
patients. Clinicians who primarily care for adults most likely see patients with pancreatitis far more often than do those who primarily care for children. Because of the
lower incidence among children, little has been published on pancreatitis in this age
group. In this article, we address the scarcity of available information by discussing pancreatitis in
the context of a case review. We also illustrate key concepts and current trends in the management
of pancreatitis in children.
C
CNE Continuing Nursing Education
This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article,
which tests your knowledge of the following objectives:
1. Describe the common etiologies and diagnostic criteria for a child with pancreatitis
2. State common nursing and medical interventions for the child with pancreatitis
3. List complications experienced by the child with pancreatitis
©2014 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2014533
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Vol 34, No. 4, AUGUST 2014
43
Table 1
Overview of cell types contained in the pancreasa
Type of
cell
Type of
gland
Components secreted
Acinar
Exocrine
Enzymes and fluids
Promotes digestion
Duct
Exocrine
Enzymes and fluids
Promotes digestion
Endocrine
Insulin
Decreases blood glucose levels by promoting glucose uptake into
cells and conversion to glycogen
Endocrine
Glycogen
Increases blood glucose levels by promoting glycogenolysis and
gluconeogenesis
Endocrine
Somatostatin
Helps regulate digestion and absorption of nutrients and regulates the
secretion of other pancreatic hormones
F
Endocrine
Pancreatic polypeptide
Inhibits exocrine secretions of pancreas and contractions of gallbladder
a Based
Function
on information from Stanfield.1
Overview of Pancreatic Function
The pancreas is positioned in the middle of the
abdomen near the stomach, left kidney, and parts of the
small intestine. Rich in bicarbonate and several digestive enzymes, the pancreas is responsible for producing
pancreatic amylase (which breaks down starch and
glycogen) and pancreatic lipase (which breaks down
fats). Relative to its weight, the pancreas secretes more
protein than any other tissue in the body. The pancreas
functions as both an endocrine and an exocrine gland
with many different cell types1 (Table 1).
Table 2
Category
Gallstones, sludge in gallbladder
Medications
Valproic acid, prednisone,
L-asparaginase
Systemic diseases
Sepsis, hemolytic uremic syndrome,
systemic lupus erythematosus
Trauma
Transplants
Alvin Jeffery is an education specialist in the Center for Professional
Excellence/Education at Cincinnati Children’s Hospital Medical
Center.
Corresponding author: Chris Kramer, RN, BSN, CCRN, Pediatric Intensive Care Unit,
Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 11017,
Cincinnati, OH 45229 (e-mail: [email protected]).
To purchase electronic or print reprints, contact the American Association of CriticalCare Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949)
362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected]
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Solid organs, bone marrow
Systemic infections
Metabolic disorders
Authors
Chris Kramer is a registered nurse in the pediatric intensive care unit
at Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio.
Examples
Biliary diseases
Acute Pancreatitis in Children
The annual incidence of acute pancreatitis is 3.6 to
13.2 per 100000 for children2,3 and 4 to 45 per 100000
for adults.4 The most common causes in children include
biliary diseases, complications from medications, systemic diseases, systemic infections, trauma, and organ
transplant (Table 2). Regardless of the cause, the pathophysiology of pancreatitis starts with injury to acinar
cells and the release of proteases and other enzymes
Causes of pancreatitis in childrena
Diabetic ketoacidosis, hypertriglyceridemia, hypercalcemia
Hereditary causes
Idiopathic causes
a Based
on information from Bai et al5 and Srinath and Lowe.6
(eg, trypsin, elastase, lipase) that destroy cells and tissues.5 This process results in pancreatic edema and local
inflammation. Inflammatory mediators and large
amounts of trypsin are released, which can then lead to
systemic inflammatory response syndrome (SIRS) and
pancreatic necrosis5-7 (see Figure). The SIRS is the pathological reaction responsible for pulmonary complications and renal failure.8 In acute episodes of pancreatitis,
damage to the pancreas itself is reversible.7
The median hospital length of stay for children with
pancreatitis is 5 to 8 days.6 Treatment focuses on ensuring adequate nutrition, maintaining hydration, providing
appropriate pain management, and preventing infection
and thromboembolic events.
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Injury
Decreased
oral intake
Pain
Dehydration
Thrombosis
Acinar cell releases...
Systemic inflammatory
response syndrome
Pulmonary complications
Renal failure
Sepsis/shock
Pancreatic edema
Local inflammation
C
(tum ytoki
ne
Trypsin
o
plat r nec prod
elet ros ucti
acti is fa on
vati ctor
ng
fact and
or)
Proteases
Enzymes
e
tissu
Cell/ ction
u
r
dest
Ileus of bowel loops
Hematuria from left kidney
Infection
Figure Pathophysiology and sequelae of acute pancreatitis.
Case Review: First Admission
Initial Signs and Symptoms
TN is a 13-year-old, 120-kg boy with allergies to fentanyl and clindamycin and a history of obesity, sleep
apnea, and Angelman syndrome. Angelman syndrome
is a neurogenic disorder that is often misdiagnosed as
cerebral palsy or autism. The syndrome is characterized
by developmental delay, seizures, aphasia, and gait
instability.9 TN is developmentally similar to a 3-yearold child except that he is nonverbal.
TN initially was brought to the emergency department because he had epigastric abdominal discomfort
(as evidenced by his localization of pain to the affected
area), constipation, dehydration, oral intake less than
240 mL (8 ounces), and urine output less than 0.5 mL/kg
per hour in the preceding 12 hours. Vital signs at the
time of admission indicated tachycardia, tachypnea,
slight oxygen desaturation, hyperthermia, and slight
hypotension (see First time vital signs in Table 3).
While in the emergency department, TN received a
total of 40 mL/kg of physiological saline for dehydration, two 5-mg doses of morphine sulfate for pain, and
one 1200-mg dose of oral acetaminophen (Tylenol) for
fever. The pancreas was not well visualized during
abdominal sonography because of the patient’s inability
to cooperate and gaseous distention. Consequently,
contrast-enhanced computed tomography (CT) was
performed and showed a mildly edematous pancreas
with a small amount of peripancreatic fluid and inflammation reflecting pancreatitis. No evidence of necrosis
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or abscess was detected. Transient oxygen desaturations
to 86% to 89% were noted in the emergency department,
and administration of supplemental oxygen was efficacious. While TN was still in the emergency department,
blood samples were obtained for various laboratory
studies, including complete blood cell count, renal and
liver function tests, and venous blood gas analysis
(Table 3). Serum levels of amylase (734 U/L) and lipase
(9453 U/L) were the most abnormal values during the
first admission to the emergency department (to convert amylase and lipase values to microkatals per liter,
multiply by 0.0167).
The clinical features, elevated levels of pancreatic
enzymes, and CT results suggested acute pancreatitis,
and TN was admitted to the gastrointestinal unit for
further management of dehydration, pain, and diet.
Maintenance intravenous fluids consisting of 5% dextrose and physiological saline were started at 1.5 times
greater than basal need. Oral oxycodone for the epigastric pain and intravenous piperacillin-tazobactam (Zosyn)
for prophylactic antibiotic coverage were ordered. After
4 days, a repeat CT showed an edematous pancreas with
no fluid collection and no evidence of necrosis or abscess.
The lipase level had also decreased to 198 U/L. TN was
showing marked clinical improvement, with decreased
pain, minimal oxygen requirement (0.5 L/min by nasal
cannula), and vital signs within the reference range. A lowfat diet for pancreatic rest was started, and although oral
intake was returning to baseline values, low urine output
(<1 mL/kg per hour) and constipation continued to be
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Table 3
Relevant clinical findingsa
Visit to
emergency department
Clinical finding
First time
Second time
Admission to
intensive care unit
Body temperature, °C (normal value: 36-38)
38.7 (High)
39.5 (High)
39.8 (High)
Heart rate, beats per minute (normal value: 70-110)
142 (High)
150 (High)
145 (High)
Respiratory rate, breaths per minute (normal value: 12-20)
22 (High)
25 (High)
30 (High)
100/60 (Low)
98/56 (Low)
85/44 (Low)
Mean arterial pressure, mm Hg (normal value: 80-95)
78 (Low)
69 (Low)
55 (Low)
Oxygen saturation as measured by pulse oximetry, % (normal value: >93)
89 (Low)
90 (Low)
85 (Low)
Amylase, serum, U/L (normal value: 50-150)
734 (High)
908 (High)
Lipase, serum, U/L (normal value: 10-140)
9453 (High)
>15 000 (High)
Blood pressure, mm Hg (normal value: 110-120/70-80)
Aspartate aminotransferase, serum level, U/L (normal value: 15-45)
30
52 (High)
Alanine aminotransferase, serum level, U/L (normal value: 10-45)
32
120 (High)
14 100 (High)
15 400 (High)
15.3
15.9
White blood cells, blood level, /μL (normal value: 4500-13 500)
Hemoglobin, blood level, g/dL (normal value: 13-16)
Hematocrit, blood level, % (normal value: 37-49)
43
45.5
222 000
297 000
Sodium, serum level, mmol/L (normal value: 136-145)
143
144
Potassium, serum level, mmol/L (normal value: 3.6-5.0)
4.9
3.8
118 (High)
134 (High)
Platelets, blood level, /μL (normal value: 135 000-466 000)
Glucose, serum level, mg/dL (normal value: 75-110)
pH, venous blood gas analysis (normal value: 7.35-7.45)
7.18 (Low)
Pco2, venous blood gas analysis, mm Hg (normal value: 37-47)
72 (High)
Base excess, venous blood gas analysis (normal value: -2 to +2)
-8 (High)
a
Blank cells indicate that value was not measured.
SI conversion factors: to convert amylase, lipase, alanine aminotransferase, and aspartate aminotransferase to μkat/L, multiply by 0.0167; to convert glucose to
mmol/L, multiply by 0.0555.
problems. TN was discharged after 11 days in the
hospital. Discharge planning focused on adequate
hydration, pain management, maintenance of a strict
low-fat diet, improvement of defecation with milk of
magnesia, and oxygen at night to maintain oxygen
saturations greater than 91%.
Discussion
A diagnosis of acute pancreatitis can be made
once 2 of the following 3 criteria are present: abdominal pain, serum level of amylase or lipase or both at
least 3 times the upper value of the reference range,
and imaging results consistent with pancreatitis.10
TN met all 3 of these criteria. Although diagnosis of
acute pancreatitis could have been made simply on the
basis of pain and altered serum levels of pancreatic
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enzymes, sonography is often used to rule out
obstructive causes such as cysts or tumors, trauma,
or stones.10
Acute pancreatitis in children most commonly is
manifested as abdominal pain or irritability (either
occurs in as many as 91% of cases), epigastric tenderness (86% of cases), and nausea or vomiting (74% of
cases).6,11 For patients who are nonverbal because of
developmental age (such as TN), irritability is more
common.7 Causes of pain associated with pancreatitis
may be more complex than previously thought but
most likely are due to a combination of inflammation
(increased pressure), inflammatory mediators, cell
death, and genetic expression.5,12 In TN’s case, most
likely severe pain resulted in decreased oral intake,
which eventually led to constipation and dehydration.
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Serum levels of amylase and lipase are commonly
determined when pancreatitis is suspected. Although
lipase is a more sensitive indicator (ie, more likely to be
elevated in pancreatitis) than is amylase,10,11 some investigators6 have found elevations in serum levels of amylase without concomitant increases in lipase.
As in this case, transabdominal sonography is routinely the first imaging study used in children with suspected pancreatitis.10 Transabdominal or endoscopic
sonography, contrast-enhanced CT, and magnetic resonance imaging or magnetic resonance cholangiopancreatography are all acceptable forms of diagnostic imaging.10
Findings suggestive of acute pancreatitis include pancreatic or peripancreatic edema, necrosis, inflammation,
hemorrhage, abscess, and fluid collections.10
Based primarily on guidelines for adults, treatment
for children with pancreatitis focuses on correcting
dehydration, managing abdominal pain, ensuring nutritional intake, and preventing adverse events (ie, thromboembolism and infection). Alleviating the cause of
pancreatitis, if known, is also a priority.
Correcting Dehydration Although initial management in the emergency department of children with
dehydration includes rehydration with intravenous
fluids,13 the presence of a profound inflammatory
response makes such rehydration particularly important
in patients with acute pancreatitis.6 The optimal type,
rate, and volume of fluid have not been determined for
children or adults,6 but maintenance fluids should be
administered at a sufficient volume to result in urine
output of at least 0.5 to 1 mL/kg per hour.13 Frequently
assessing urine output and ensuring adequate vascular
access are key nursing interventions that will affect
patients’ outcomes. Because TN had no renal or cardiac
disease, a liberal amount of intravenous fluids (40 mL/kg
bolus followed by 1.5 times the continuous basal rate)
was administered.
Managing Pain Because of the intense pain associated with acute pancreatitis, analgesia is best achieved
with opiates.7 TN was given morphine because of his
allergy to fentanyl; however, morphine is typically avoided
because it might cause spasms of the sphincter of Oddi14
(even though occurrence of this complication has yet to
be proven in studies in humans).14,15 Meperidine should
be avoided in children because of its potential neurotoxic
effects, such as seizures.16 When a patient has allergies
to medications, finding an appropriate pharmacological
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intervention for pain relief may be difficult. Nurses
should promptly report the presence of pain to the
patient’s prescribing provider.
Ensuring Nutritional Intake Because of a presumed need for pancreatic rest,6 adults with pancreatitis
were previously expected to take nothing by mouth for
at least 5 to 7 days.17 Current evidence in adults, however, suggests that during an episode of acute pancreatitis, early initiation of enteral nutrition (especially
through a nasojejunal tube) is beneficial. This early initiation has resulted in a reduction in both infections and
hospital
Current guidelines on sepsis recommend
length of
prophylaxis for deep vein thrombosis in
stay.18 Oral
children with acute pancreatitis who are
feeding can
be resumed past puberty.
once the pain
begins to subside.7 No conclusive studies on the use of
early enteral nutrition in children with pancreatitis have
been done.6,7 In addition, a survey10 indicated that pediatricians are not likely to order enteral tube feedings in
children with acute pancreatitis, most likely because of
the hypothetical need for pancreatic rest. In patients
receiving enteral nutrition, resumed pancreatic activity
may cause the return of pain, and nurses should assess
patients for pain associated with these changes in diet.
Preventing Adverse Events If a patient has
pancreatic infection and/or necrosis, other measures,
including antibiotic prophylaxis, are needed.7,19 Additionally, current guidelines20 on sepsis recommend prophylaxis for deep vein thrombosis in children with
acute pancreatitis who are past puberty. The similar
systemic inflammatory effects of sepsis and pancreatitis
provide sufficient rationale for many clinicians to start
chemical prophylaxis, such as administration of enoxaparin (Lovenox).
Potential Complications
Additional sequelae of acute pancreatitis may include
recurrence of acute pancreatitis (known as acute recurrent pancreatitis), formation of pseudocysts, and necrotizing pancreatitis.
Acute recurrent pancreatitis is defined by the diagnostic criteria previously listed for acute pancreatitis plus
either an interval of at least 1 pain-free month between
diagnoses of acute pancreatitis or completely normal
serum levels of amylase and lipase with no pain,
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regardless of time between episodes.10 Although previous studies21 supported this nomenclature, more current recommendations refer to this recurrence as a
complication of acute pancreatitis rather than as acute
recurrent pancreatitis itself.10 Acute recurrent pancreatitis can occur in up to 15% to 36% of children who have
acute pancreatitis.22,23
A pseudocyst, one of the more common complications
of acute pancreatitis and acute recurrent pancreatitis, is
defined as “a collection of amylase-rich pancreatic fluid
that lacks an epithelial lining”19(p417) and includes nonnecrotic tissue. A more heterogeneous collection of fluid
with necrotic tissue present is identified as postnecrotic
collection or necrotizing pancreatitis.19 Differentiating
between a pseudocyst and a postnecrotic collection is
important for guiding further treatment. A more conservative (watch and wait) approach may be taken in a
patient with a pseudocyst, or antibiotic therapy and surgical intervention may be necessary when necrotic tissue
is the source of infection.19 Surgical options vary widely
and depend on the resources available at the institution.
Case Review: Second Admission
Approximately 7 months after his first admission,
TN was again brought to the emergency department.
At the time of admission and according to his family,
he had diaphoresis, abdominal and lower back pain, 3
incidents of loose stools, and 8 episodes of vomiting.
Vital signs
A more conservative (watch and wait) approach were even
may be taken in a patient with a pseudocyst,
more
or antibiotic therapy and surgical intervention
abnormal
may be necessary when necrotic tissue is the than those
source of infection.
at the first
admission.
TN had tachycardia, tachypnea, oxygen desaturations,
increased hyperthermia, and hypotension (Table 3).
While in the emergency department, TN received a
1-L bolus of physiological saline, 20 mg of intravenous
promethazine (Phenergan) for the nausea and vomiting,
and one 2-mg dose of hydromorphone (Dilaudid) for
pain. Once again, abdominal sonography could not be
done because of TN’s recent oral intake. A CT scan
showed a prominently edematous pancreas with possible necrotizing pancreatitis. Additionally, an area of
localized fluid 7.4 6.1 10.7 cm in size was noted at
the lesser sac near the pancreatic body, suggestive of a
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pancreatic pseudocyst. TN’s serum levels of amylase
(908 U/L) and lipase (>15000 U/L) were markedly elevated (Table 3). TN’s clinical features, CT results, and
elevated enzyme levels led to a diagnosis of acute pancreatitis complicated by a pseudocyst.
Because of treatments received in the emergency
department and the clinical signs and symptoms,
physicians decided to admit TN to the pediatric intensive care unit (PICU). Admission to the unit was warranted because of respiratory distress related to fluid
overload during correction of dehydration and the
increasing need for sedation. TN’s escalating aggression and agitation most likely were due to confusion
(a result of his neurological disorder) and pain. Table 3
highlights significant clinical findings present on
admission to the PICU.
TN’s clinical features in the PICU included further
hemodynamic instability, respiratory distress, persistent
hyperthermia, and a combined respiratory-metabolic
acidosis. The pseudocyst was the assumed culprit for
all of the complications; however, TN’s condition
needed to be stabilized before the pseudocyst could be
addressed. A chest radiograph showed atelectasis and
pulmonary edema. The radiographic findings, results
of blood gas analysis, and the clinical signs and symptoms were enough for elective intubation to provide
better airway management. TN was treated with adultdosage intravenous infusions of midazolam (Versed),
hydromorphone (Dilaudid), and dexmedetomidine
(Precedex) for sedation and airway management. He
remained consistently febrile and was treated with cooling blankets and scheduled doses of acetaminophen
(Tylenol) to achieve a temperature goal of less than
38ºC. TN had blood glucose levels from 100 to 350
mg/dL (to convert to millimoles per liter, multiply by
0.0555), so a continuous infusion of insulin was started
and glucose levels were assessed hourly.
In the PICU, 2 nontunneled central venous catheters
were placed, 1 in the intrajugular vein and 1 in the left
femoral vein. Central venous access was needed for continuous sedation, antibiotic therapy, parenteral nutrition,
and sporadic use of inotropes. Because of TN’s weight (>40
kg) and prolonged bed rest, sequential compression
devices were applied to prevent thromboembolic events.
However, after the femoral venous catheter was removed,
TN’s left lower extremity began to swell. Sonography
revealed a nonocclusive thrombus that was managed
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Table 4
Outline of patient’s progress
after insertion of external drain
Extubated 4 days after drain insertion
Urinary catheter removed 6 days after drain insertion
No central catheters except double-lumen peripherally inserted
central catheter
Glucose levels persistently <250 mg/dL
Table 5
Discharge instructions
Remain on insulin regimen of Lantus (insulin glargine) 20 units
every night at bedtime
Use Novolog (insulin aspart) correction factor to 1:35>120 mg/dL
Remain on continuous feedings of Vivonex (enteral feeding
formula) 60% at 150 mL/h for 20 hours
Transferred to gastrointestinal unit 13 days after drain insertion
Check blood glucose levels every 4 hours while receiving
continuous feedings
SI conversion factor: to convert glucose to mmol/L, multiply by 0.0555.
Check blood glucose level 30 minutes after feedings have stopped
No insulin correction 30 minutes before discontinuation of
feedings
with administration of enoxaparin. Urinary elimination
continued to be a problem because an anatomical false
passage had been created when an indwelling urinary
catheter was initially placed during TN’s first admission
to the emergency department. A urinary catheter that
was correctly placed while the patient was in the PICU
helped with urination and healing of the anatomic false
passage. Hypotension associated with the continuous
need for sedation and the SIRS was managed by using
norepinephrine. TN was unable to tolerate oral feedings, necessitating placement of a postpyloric nasal
tube and continuous, low-rate (5-10 mL/h) feedings.
A nasogastric tube was also placed for continuous gastric decompression. After 15 days of the aforementioned
treatments, TN’s condition finally became stable.
Care providers from the institution’s interventional
radiology, gastroenterology, and critical care medicine
were consulted about the pseudocyst. Because severe
pancreatitis and its complications are not often problems at pediatric institutions, the gastroenterology team
at a neighboring hospital for adults was also consulted.
After much debate, the teams agreed to use interventional
radiology to place an external drain in the pseudocyst/
pancreas. After placement of the drain, TN’s persistent
fevers, abdominal distention, pain and agitation, and
hyperglycemia markedly decreased (Table 4).
After 28 days in the PICU, TN was transferred to the
gastrointestinal unit, and a transcutaneous gastrojejunal
tube was placed for the continuation of a low-fat diet.
TN was discharged to home after 71 days of inpatient
treatment for acute pancreatitis complicated by pseudocyst formation. He still had the external pancreatic drain,
the gastrojejunal tube, and a peripherally inserted central catheter in place. Discharge teaching focused on
pain management, drain monitoring, maintaining a
strict feeding regimen, and hydration (Table 5).
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SI conversion factor: to convert glucose to mmol/L, multiply by 0.0555.
Additional Complications of
Pancreatitis in Children
The rationale for many of the interventions used for
TN during his stay in the PICU are described in the
Discussion section following the description of his first
admission to the emergency department. Additional
anomalies that may further complicate acute pancreatitis
in children are endocrine dysfunction, effects of SIRS,
and long-term considerations.
Endocrine Dysfunction
TN did have some endocrine dysfunction, as indicated by hyperglycemia. Although intuitively hyperglycemia is due to dysfunction of cells in pancreatic
islets and decreases in insulin levels, pancreatic cells
are also affected, and gluconeogenesis may be impaired.1
When determining the frequency of serum glucose
assessments, nurses should consider the possibility of
unexpected and counterintuitive changes in glucose levels
in children with acute pancreatitis. Regardless, hyperglycemia associated with acute pancreatitis can be treated
with oral antihyperglycemic agents; although, up to 30%
of adults with this complication require insulin therapy.19
Effects of SIRS
TN’s persistent fevers most likely were due to a severe
form of SIRS (due to trypsin release with subsequent
cytokine production). Inflammatory states are associated
with temperature dysregulation,24 and a wide variety of
nursing and medical interventions may be used to bring
a patient’s temperatures to equilibrium. Another effect
of SIRS is pulmonary edema, which TN experienced.
The mixed respiratory-metabolic acidosis most likely
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49
was due to this combination of SIRS, dehydration,
atelectasis, and pulmonary edema.
Long-Term Considerations
Although many health care providers use the term
chronic pancreatitis when a patient has recurrent episodes
of pancreatitis over a prolonged period, some experts
disagree. Some define chronic pancreatitis as a state of
irreversible changes in the pancreas that can occur without a previous episode of acute pancreatitis. They recommend that
Nurses must maintain an active role in ensuring the diagthat the families of children with pancreatitis
nosis of
obtain the resources needed.
chronic
pancreatitis not be made until imaging studies show chronic
changes to the pancreas, such as ductal and parenchymal changes.10
Because of the high incidence of pancreatitis in
patients with cystic fibrosis25 (and other genetic disorders), additional testing may include a genetic workup
and stool fat assessments to detect fat malabsorption.7
Case Review: Subsequent Admissions
During the next 3 months, TN required 3 more admissions to the PICU. Each admission lasted between 6 and 14
days. The main clinical problems in each readmission were
pain, increased output from the external pancreatic drain,
agitation, insulin maintenance, and diet management. Difficulty in diet management (feeding through a gastrojejunal
tube) was a marked problem mainly because of TN’s developmental level; he could not comprehend why he could no
longer consume food by mouth. He constantly wanted the
oral satisfaction of eating food. His family managed the
problem by keeping TN on a strict feeding regimen via the
gastrojejunal tube while allowing minimal oral intake. The
pseudocyst continued to produce output for 3 months after
insertion of the drain. The drain was subsequently removed
via interventional radiology during the second readmission;
it had been in the pseudocyst for 56 days. TN’s last CT scan
was performed 5 days after removal of the pseudocyst
external drain. The size of the pseudocyst had decreased; it
now measured 8 13 mm compared with 8 20 mm previously. The scan also showed minor atrophy of the pancreatic tail. Surrounding mesenteric edema and inflammatory
changes were revealed, including a poorly defined fluid collection inferior to the pseudocyst, which was similar in size
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but more well-defined, suggestive of continuing but unremarkable pancreatic edema. After the third readmission,
TN’s family was able to manage his home hydration, pain
management, and low-fat diet regimen adequately.
To date, TN continues to be fed through the gastrojejunal tube and is receiving oral antihyperglycemics daily for
control of the diabetes associated with chronic pancreatitis
and pseudocyst formation. However, TN’s hospital admissions have decreased in frequency, suggesting that the
disease process is being successfully managed at home.
Additional Considerations
Consultation with a gastrointestinal service is appropriate in managing children with pancreatitis, not only
because of the limited evidence available on the management of this condition in children but also because of the
common occurrence of comorbid conditions (eg, cystic
fibrosis), especially in infants and younger children.11 Critical care nurses will play a key role in coordinating these
services and ensure that patients and patients’ family
members are involved in care decisions.
Nurses are instrumental in ensuring that a holistic
approach is used every time a child with pancreatitis is
treated. The multifaceted and interdisciplinary approach to
the wide array of problems associated with pancreatitis can
potentially leave these children and their families feeling
overwhelmed. Therefore, nurses must maintain an active
role in ensuring that the families obtain the resources
needed. Normality and consistency are essential for continued success in the home setting; hence, accurate care plans
allow for appropriate streamlined care for these patients (see
Table 6 for a sample nursing care plan for TN). Families and
patients need to feel comfortable with their chosen health
care institutions, and as pancreatitis becomes more prevalent in children, education becomes more important. CCN
Financial Disclosures
None reported.
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To learn more about pediatric care, read “The KIDS SAFE Checklist
for Pediatric Intensive Care Units” by Ullman et al in the American
Journal of Critical Care, January 2013;22:61-69. Available at
www.ajcconline.org.
www.ccnonline.org
Table 6
Treatment focus, related to
Sample nursing care plan
Subjective/objective data
Nutrition assurance
Interventions
Nursing diagnosis: imbalanced nutrition (less than body requirements)
Inability to ingest food (because of pain)
Inability to digest food (because of pancreatic
exocrine dysfunction)
Increased metabolic needs (because of acute
illness and fever)
Dehydration correction
Presence of pain
Constipation
Hypoactive bowel sounds
Hyperthermia
Assess pain (refer to acute pain diagnosis)
Assess temperature (refer to hyperthermia diagnosis)
Assess bowel sounds
Maintain parenteral and/or enteral nutrition
If enteral tube present, assess and maintain patency
Encourage oral intake once diet is resumed
Assess tolerance of oral intake
Nursing diagnosis: fluid volume, deficient
Decreased fluid intake (because of pain)
Increased insensible fluid loss (because of
acute illness and fever)
Pain management
Tachycardia
Hypotension
Decreased urine output
Monitor vital signs and urine output
Assess and maintain patency of intravenous catheters
Administer intravenous fluids, including boluses
Report abnormal serum concentrations of sodium,
creatinine, and pH
Encourage oral intake once diet is resumed
Nursing diagnosis: acute pain
Pancreatic edema, inflammation, and irritation
Pain scales (verbal and/or
nonverbal cues)
Assess pain routinely, after interventions for pain
relief, and after changes in oral intake
Administer routine and as-needed analgesics, as
prescribed
Notify prescribing provider of unmanageable pain
Provide nonpharmacological pain interventions
(eg, play and/or distraction)
Nursing diagnosis: risk for ineffective family therapeutic regimen management
Coordination of care
Complexity of care regimen
Excessive demands on patient’s family members
Multiple prescribed
medications
Patient’s unique diet regimen
Frequent clinic visits
Assess knowledge of medication use and administration, teaching when appropriate
Assess knowledge of and skill at enteral tube feeding,
teaching when appropriate
Assess financial and transportation resources of
patient’s family (if assistance needed, explore
available social programs)
Combine multiple clinic visits into the same day
Interventions for adverse events and other complications
Nursing diagnosis
Intervention
Hyperthermia (associated with systemic inflammatory response
syndrome)
Assess body temperature
Maintain cool environment through use of fans, cooling blankets,
ice packs, etc
Administer antipyretics, as ordered
Risk for ineffective breathing pattern (related to hyperventilation
associated with pulmonary edema)
Assess respiratory rate, breath sounds, and ease of respiration
Monitor pulse oximetry
Administer oxygen, as ordered
Risk for ineffective tissue perfusion (related to venous
thromboembolism)
Assess pulses and capillary refill in all extremities
Assess respiratory rate, breath sounds, and ease of respiration
Encourage and assist with ambulation and range-of-motion activities
Administer antithrombotic medications, as ordered
Risk for infection (related to pancreatic inflammation)
Assess body temperature
Report abnormal serum white blood cell counts
Administer antibiotics, as ordered
References
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Boston, MA: Pearson; 2013:504-530.
2. Nydegger A, Heine RG, Ranuh R, Gegati-Levy R, Crameri J, Oliver MR.
www.ccnonline.org
Changing incidence of acute pancreatitis: 10-year experience at the Royal
Children’s Hospital, Melbourne. J Gastroenterol Hepatol. 2007;22(8):
1313-1316.
3. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute
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Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of
acute pancreatitis: a systematic review. Pancreas. 2006;33(4):323-330.
Bhatia M, Wong FL, Cao Y, et al. Pathophysiology of acute pancreatitis.
Pancreatology. 2005;5(2-3):132-144.
Bai HX, Lowe ME, Husain SZ. What have we learned about acute pancreatitis in children? J Pediatr Gastroenterol Nutr. 2011;52(3):262-270.
Srinath AI, Lowe ME. Pediatric pancreatitis. Pediatr Rev. 2013;34(2):79-90.
Meyer A, Coffey MJ, Oliver MR, Ooi CY. Contrasts and comparisons
between childhood and adult onset acute pancreatitis. Pancreatology.
2013;13(4):429-435.
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Morinville VD, Husain SZ, Bai H, et al; INSPPIRE Group. Definitions of
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Park AJ, Latif SU, Ahmad MU, et al. A comparison of presentation and
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di Sebastiano P, di Mola FF, Bockman DE, Friess H, Büchler MW.
Chronic pancreatitis: the perspective of pain generation by neuroimmune interaction. Gut. 2003;52(6):907-911.
Carcillo J, Tasker R. Fluid resuscitation of hypovolemic shock: acute
medicine’s great triumph for children. Intensive Care Med. 2006;32(7):
958-961.
Helm JF, Venu RP, Geenen JE, et al. Effects of morphine on the human
sphincter of Oddi. Gut. 1988;29(10):1402-1407.
Wu B, Conwell D. Acute pancreatitis, I: approach to early management.
Clin Gastroenterol Hepatol. 2010;8(5):410-416.
Benner KW, Durham SH. Meperidine restriction in a pediatric hospital.
J Pediatr Pharmacol Ther. 2011;16(3):185-190.
Martindale RG, McClave SA, Vanek VW, et al; American College of Critical Care Medicine; A.S.P.E.N. Board of Directors. Guidelines for the
provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine and American Society
for Parenteral and Enteral Nutrition: executive summary. Crit Care Med.
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Dellinger RP, Levy MM, Rhodes A. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012.
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CriticalCareNurse
Vol 34, No. 4, AUGUST 2014
www.ccnonline.org
CNE Test Test ID C1442: Pancreatitis in Children
Learning objectives: 1. Describe the common etiologies and diagnostic criteria for a child with pancreatitis 2. State common nursing and medical interventions
for the child with pancreatitis 3. List complications experienced by the child with pancreatitis
1. Which of the following laboratory tests best reflect pancreatic function?
a. Trypsin and elastase
b. Amylase and lipase
c. Total bilirubin and lipase
d. Direct bilirubin and lipase
8. At the time of the second admission for TN, CT findings were
suggestive of what complication?
a. Transaminitis
c. Hydronephrosis
b. Hypersplenism
d. Pancreatic pseudocyst
9. Which laboratory value illustrates endocrine dysfunction experienced
by TN?
a. Blood glucose level of 300 mg/dL
b. Sodium level of 140 mmol/L
c. Lipase level of 10 U/L
d. Aspartate aminotransferase level of 30 U/L
2. Which medication is associated with causing pancreatitis?
a. Clindamycin
c. Regular insulin
b. Lasix
d. Valproic acid
3. The diagnosis of pancreatitis could be made for which patient?
a. 8 year old reporting abdominal pain
b. 14 year old with jaundiced sclera and elevated lipase level
c. 6 year old with an elevated amylase level, abdominal pain, and pancreatic
edema on computed tomography (CT) scan
d. 17 year old with abdominal pain and elevated white blood cell count
10. What was the most likely cause of TN’s persistent fevers?
a. Urinary tract infection
b. Systemic inflammatory response syndrome
c. Lack of trypsin release
d. Pancreatic-cell function
4. The most common symptom of pancreatitis in children is what
manifestation?
a. Vomiting
c. Fever
b. Jaundice
d. Pain or irritability
11. The authors contend that the multiple readmissions were most
likely attributable to which of the following?
a. Inadequate discharge planning
b. Insulin resistance
c. Poor oral intake
d. Developmental level
5. Pain management would be best achieved with what medication?
a. Fentanyl
c. Demerol
b. Morphine
d. Tylenol
12. What nursing intervention would be part of the nursing care plan
for TN?
a. Pain assessment and management
b. Intracranial pressure assessment and management
c. Wound assessment and management
d. Assessment and management of external drain
6. Clear liquids have been prescribed for a child with pancreatitis; as the
nurse caring for the child, you would report what symptom of concern?
a. Normal blood glucose level, as would expect hypoglycemia
b. Abdominal pain, as this can recur from pancreatic stimulation
c. Normoactive bowel sounds, as you would expect hypoactive bowel sounds
d. Normal lipase level, as would expect it to be elevated
13. Assessment findings indicating that TN has a fluid volume deficit
would include which of the following?
a. Urine output of 2 mL/kg per hour and hypotension
b. Urine output of 1 mL/kg per hour, fever, and hypotension
c. Urine output of 0.3 mL/kg per hour, hypotension, and tachycardia
d. Pulmonary edema, tachycardia, and hypotension
7. Which symptoms indicate recurrent pancreatitis?
a. Abdominal pain with elevated amylase and lipase levels 2 weeks after the
initial diagnosis
b. Abdominal pain with elevated amylase level following a pain-free month
c. Vomiting with elevated lipase level 3 weeks after the initial diagnosis
d. A child experiencing 2 weeks of no abdominal pain with pain recurrence
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. a
b
c
d
2. a
b
c
d
3. a
b
c
d
4. a
b
c
d
5. a
b
c
d
6. a
b
c
d
7. a
b
c
d
8. a
b
c
d
9. a
b
c
d
10. a
b
c
d
11. a
b
c
d
12. a
b
c
d
13. a
b
c
d
Test ID: C1442 Form expires: August 1, 2017 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 10 correct (77%)
Synergy CERP Category A Test writer: Sarah A. Martin, RN, MS, CPNP-AC/PC, CCRN
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