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Management of Patients withPancreatic Disease
Pancreatitis
Parenteral Nutritional (PN) Support
Spring 2012
Marjorie Miller MA RN
Timothy Frank MS RN1
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Key Questions What clinical manifestation occurs because the
pancreas lies retroperitoneally in the abdominalcavity?
What is the sphincter of Oddi? What common painmedication causes spasms of this sphinter?
Which digestive enzymes are secreted by thepancreas?
What is the hallmark lab abnormality in pancreatitis?
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Clinical SituationJT is a 48 year old, divorced business executive brought to
the emergency department by his buddies with a chiefcomplaint of abdominal & back pain and vomiting for 2
days.
As you approach him you observe that he is trying to sit up,and is almost in continuous movement on the bed. He is
alert and able to answer questions, but refuses to letanyone touch his abdomen or his back. He rates his painat 10/10. His skin is hot, dry and flushed with turgorand he complains of extreme thirst.
VS: BP 100/60, T-100F, P-120, R- 28 shallow, O2 sats-90%
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Sample questionBased on the information in the preceding
situation, place the following interventions
in priority?
1. Administer O2 @ 2L/nasal cannula
2. Administer pain medications
3. Complete the physical assessment
4. Initiate IV of Normal Saline at 125 ml/hour
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Headjoins Common Ductat Ampulla of Vater
BodyFormsshell for stomachto rest upon.
Tailshell forspleen to rest on
The Pancreas
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Acute Pancreatitis - PathophysiologyPremature Activation of Trypsin
Autodigestion of pancreatic tissue
ACTIVATION OF INFLAMMATORY RESPONSE
Inflammatory mediators
Vasodilation
SHOCK
ARDS MODS ATN
Extravascular movement
of serum albumin
3rdspacing Panc. edema
SHOCK 7
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Acute Severe PancreatitisPathophysiology
Injury or disruption of pancreatic ductsleakageof active pancreatic enzymes autodigestion
Breakdown of cell membranes edema vascular damage, hemorrhage, necrosis
inflammatory mediators Shock, MODS, .. 8
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Assessment - Clinical ManifestationsPhysiological Variable
abdominal painP
Q
R
S
T
None statedcomes on when recumbent
Deep, piercing (knife-like), continuous, twisting
LUQ or mid-epigastrium radiating to backPatient may flex spine to get reliefAggravated by eating & alcoholUnrelieved by vomiting
Aggravated by supine position or walkingRelieved by sitting up & leaning forward
Severe 10/10
Sudden onset
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Assessment -Physiological Variable
Clinical Manifestations O2
Nutrition
Skin
Flushed or cyanotic skin
Dyspnea, crackles, breath sounds
BP,
HR
N & V, or absent bowel sounds due toparalytic ileus; pain & distention rigidity,guarding
WBC, low grade fever (< 101 F.)
Jaundice: green-yellow-brown discoloration
Ecchymosis: Grey-Turner & Cullen signs
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Assessment
Physiological Variable
Diagnostic tests Serum amylase (25-125 U/L)
>200 U/L for 24-72 hours
starts to rise 2-6 hr after onset of pain
Peaks @ 24 hours
Return to normal @ 72 hr
Serum lipase (3-19 U/dL)
used with amylase; rises later than
amylase (48 hours)
return to normal 5-7 days
WBCs
glucose
lipids
calcium
magnesium
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Ranson-Imrie ScaleOn admission or dx
Age >55 years
WBC >16K/mm BG >200 mg/dl
LDH >400 IU/L
AST >250 IU/L
During first 48 hours
in HCT by 10%
IV Fluid needed > 6000 ml
Ca < 8 mg/dl PO2 < 60 mm Hg
BUN > 5 mg/dl after IVs
Serum albumin < 3.2 gm/dl
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Diagnostic Tests & Procedures Abdominal and chest films
CT scan
Ultrasound
Aspiration biopsy
Peritoneal lavage
Endoscopic Retrograde
Cholangio-pancreatography(ERCP)
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Acute PancreatitisSecondary Prevention -
Complications
Pulmonary
Coagulation
Immunological
Cardiovascular
Renal
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Acute PancreatitisComplications
Pulmonary Cardiovascular Coagulation Renall Immunological
Pleural Effusion(enzyme inducedInflammation of
Diaphragm)
AtelectasisAbdominal distention
& diaphragmaticmovement
3rdspacingBP, HR
Vasoconstriction d/tSNS activation
Trypsin activatesboth clotting
& lysing factorsDIC & PE
HypovolemiaGFR
Renal perfusionClots in renal
circulationATNARF
GI motilitybacteria outside GIPancreatic abscess
Necrosisinfection
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Acute PancreatitisSecondary Prevention -
Complications
Pulmonary
Enzyme induced inflammationof the diaphragm
Abdominal distention &diaphramatic movement
Pleural Effusion
Atelectasis
Pancreatic enzymes can injure the lungs directly
Watch for hypoxia PO 2 < 60 mm Hg 26
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Cardiovascular and Coagulation
ComplicationsCapillary permeability fluid shifts (3rdspacing) distributive shock
Vasodilationd/tinflammatory mediators distributive shock
Thrombus formation d/thypercoaguability DIC
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Acute PancreatitisSecondary Prevention
- Cardiovascular Complications
3rdspacing BP, HR,vasoconstriction (compensatorymechanisms) d/t SNS activation
Recall: compensatory mechanisms work for only a
short while before they begin to fail 28
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Acute PancreatitisSecondary Prevention -
Complications
Coagulopathy
Auto-digestion by Trypsin upon organ tissues:
activates prothrombin clotting
activates plasminogen lysing
This mechanism
Intravascular & pulmonary blood clots
DIC & pulmonary emboli
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Acute PancreatitisSecondary Prevention -
Complications
RenalHypovolemia GFR, renal
perfusion
development of clots in renalcirculation
Acute tubular necrosis & Acuterenal failure
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Acute PancreatitisSecondary Prevention -
Complications
Immunological
GI motility movement of bacteriaoutside GI tract due to pancreaticabscess &/or necrosis INFECTION
Peritonitis
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Collaborative Management
Pain
Rest the pancreas & GI tract
NPO
NG tube to suction
parenteral vs. enteral nutrition drug therapy
Manage Pain morphine
H2 antagonists
PPIs
Nursing Diagnosis: Acute Pain r/t inflammation ofpancreas and surrounding tissue, obstruction of biliarytree & interruption of blood supply to pancreatic tissue
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Nutritional management
When can the client
resume eating?
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Collaborative Management
Hemodynamic stability
Fluid volume replacement crystalloid, colloid or blood products
Hemodynamic monitoring (CVP or PA)
Monitor peripheral circulation, UOP
Nursing Diagnosis: Risk for fluid imbalance r/t vomiting &intake, fever & diaphoresis, fluid shifts, N/G suction
Vasoactive drugsdopamine
BP via vasoconstriction in high doses
renal perfusion in lower doses 34
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Collaborative Management
Respiratory Care
Supplemental O2@ 4L/NC (keep O2 Sat > 91%)
Positioning for adequate ventilation
Cough, deep breathe, IS with pain control Monitor ABGs, respiratory effort & breath sounds
Nursing Diagnosis: Ineffective Breathing Pattern r/tabdominal distention, ascites, pain or respiratorycompromise
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Collaborative Management
Maintain Metabolic Balance
Monitor labs for alterations, report significant alterations.
Nursing Diagnosis: Risk for Fluid Imbalance r/t
(same as previous dx)
K, Ca dysrhythmias
Ca neurologic changes
FBS hyperosmolar diuresis, electrolyte shifts
BUN, Creatinine indicates renal damage from perfusion
Amylase, lipase for return to normal
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Collaborative Management-
Alcohol Withdrawal SyndromeMonitor for withdrawal from alcohol
Clinical manifestations of hyperactive sympathetic
nervous system body temperature & VS
Diaphoresis
Anxiety/Aggitation
Tremors/Shakiness
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Care of patients withactual or risk for malnutrition
Nutritional Support
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Common Parenteral Nutrition (PN)
Preparations Water
Dextrose (20 - 50%)
Protein (amino acids) (3-15%) 1.5-2 g/kg/dayAvg. wt ofMale: 80 kg = 120-160 g/day
Recommended total intake of 25-35 cal/kg/day
Electrolytes (Na, K, Ca, Cl, Ph, Mg)
Trace elements (chr, cop, mang, zinc) individualized Multivitamins (fat and water soluble)
Lipids10-30% of calories
Other meds: heparin, insulin, H2blockers, albumin
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Lipid or IV Fat Therapy Purpose
to supply additional calories
to treat signs of fatty acid deficiency Supplied in 10% or 20% solutions
Composed of soy, safflower oils, egg yolk
Isotonic
Often added to PN (tri-mix or three-in-one)
May come with own tubing
IV Piggy back below PN filter
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Route of AdministrationPN requires central venous catheter access due to
the hypertonicity of solution 900 mOsm/liter
(20% dextrose)
Peripheral parenteral nutrition (PPN) orAugmented parenteral nutrition (APN)through aperipheral or midline catheter because it is lessconcentrated than PN
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Initiating TPNComponents of PN Order Sheet
Solution & rate of administration
Additives (trace elements, vitamins, insulin)
Lab work (baseline and ongoing)
Nursing responsibilities
Obtain the solution mixed by pharmacy Check contents with order/changes
Inspect bag & tubing for dates as bag &tubing changed Q 24 hours
MVI or trace elements 54
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Initiating PN(cont)Supplies
Correct solution, bag #
Tubing &/or Filter Infusion pump
Order sheet for rate
start slow and gradually
increase -ramping
Shared responsibilities Protocols for rate
Check orders for changes
Hang correct bag # Monitor lab work & report
FSBG protocols
Insulin coverage
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Nursing Responsibilities
(review)Nutrition
Daily Weight
Calorie Count
Monitoring Labs
FSBG & coverage
Reporting abnormal labs
PN Administration
Accurate I&O
Monitor infusion rate, start slowly
Never catch up if administrationruns behind
Bag & tubing changes per protocol
Patient Care
Oral care
IV site care Dressing changes per protocol
No blood draws, IVPB, IVP medsthrough same port as PN
No CVP readings
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Potential Complications of PNInfection
Fever & Chills
Glucose intolerance + blood/site cultures
(Gm + & - bacteria, fungi)
Fluid & Electrolyte Imbalance
Monitor & report
Replace in separate line
Abnormal Blood sugar
FSBG q6h with insulin coverage
Fatty intolerance
LFTs, bilirubin
Jaundice
Upper abdominal pain
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Additional procedure related
complications Air or Fat embolism Thrombosis of central
vein, Hemorrhage
Pneumothorax Catheter occlusion
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Refeeding Syndrome (RFS)
Electrolyte imbalance
BP, P, I & O
Monitor refeeding rate
Monitor ph, mg, K for 24-72
Monitor electrolytes
Correct prior to refeeding
Careful volume and Na replacement
Start slowly @ 15-20kcal/kg/day
Cardiac dysrhythmias, respiratory
arrest, neurological disturbances
http://www.nursingcenter.com/prodev/ce_article.asp?tid=789442
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Electrolyte Shifts in Refeeding Syndrome
GlucoseBloodstream
Ph, K, Ca, MgPancreas Insulin
Transportsglucose
Electrolytes shiftwith glucose
Cellular uptake Serum depletion
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Who Is at Risk for RFS? Chronic Alcoholics
Chronic Malnourished
Prolonged Vomiting and Diarrhea
Chemotherapy
Major Surgery
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Prevention of RFS Begin feeding at low dose, slowly
increasing rate of PN, avoid too rapid
an infusion initially Carefully monitor Phosphate Levels-
low serum level is hallmark of RFS
Patient Education: low carb high proteindiet, signs & symptoms of RFS
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References Phillips, R.Acute Pancreatitis inflammation gone
wild. Nursing Made Incredibly Easy! Sept/Oct 2006
www.nursingcenter.com/pdf.asp
Lewis, S., Dirksen, S., Heitkemper, M., et al.,Medical-Surgical Nursing, 8thEdition, 2011, Elsevier
Medical-Surgical Nursing, Clinical Management forPositive Outcomes, Black, J., Hawks, J., 8thEd., 2009Saunders
Mdcalc.com, retrieved 4/18/12
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