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Management of Patients with Pancreatic Disease
Pancreatitis Parenteral Nutritional (PN) Support
Spring 2012Marjorie Miller MA RN Timothy Frank MS RN
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Key Questions What clinical manifestation occurs because the
pancreas lies retroperitoneally in the abdominal cavity?
What is the sphincter of Oddi? What common pain medication causes spasms of this sphinter?
Which digestive enzymes are secreted by the pancreas?
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 chief complaint 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 let anyone touch his abdomen or his back. He rates his pain at 10/10. His skin is hot, dry and flushed with turgor and he complains of extreme thirst.
VS: BP 100/60, T-100°F, P-120, R- 28 shallow, O2 sats-90% 3
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Sample question
Based on the information in the preceding situation, place the following interventions in priority?
1. Administer O2 @ 2L/nasal cannula2. Administer pain medications 3. Complete the physical assessment4. Initiate IV of Normal Saline at 125 ml/hour
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Head – joins Common Duct at Ampulla of Vater
Body –Forms shell for stomach to rest upon.
Tail – shell for spleen to rest on
The Pancreas
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Acute Pancreatitis - Pathophysiology
Premature Activation of Trypsin →
Autodigestion of pancreatic tissue
ACTIVATION OF INFLAMMATORY RESPONSE
Inflammatory mediatorsVasodilation
SHOCK
ARDS MODS ATN
Extravascular movementof serum albumin
3rd spacing Panc. edema
SHOCK7
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Acute Severe PancreatitisPathophysiology
Injury or disruption of pancreatic ducts leakage of active pancreatic enzymes autodigestion
Breakdown of cell membranes edema vascular damage, hemorrhage, necrosis inflammatory mediators Shock, MODS, ….. 8
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Assessment - Clinical Manifestations Physiological Variable –
abdominal pain
P
Q
R
S
T
None stated – comes on when recumbent
Deep, piercing (knife-like), continuous, twisting
LUQ or mid-epigastrium radiating to back Patient may flex spine to get reliefAggravated by eating & alcoholUnrelieved by vomitingAggravated by supine position or walkingRelieved by sitting up & leaning forward
Severe “10”/10
Sudden onset11
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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 to paralytic ileus; pain & distention rigidity, guarding
WBC, low grade fever (< 101° F.) Jaundice: green-yellow-brown
discoloration Ecchymosis: Grey-Turner & Cullen
signs 17
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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 painPeaks @ 24 hoursReturn 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
WBC’s glucose lipids calcium magnesium
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Ranson-Imrie Scale
On admission or dx Age >55 years WBC >16K/mm³ 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 IV’s 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 Pancreatitis –Secondary 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& diaphragmatic
movement
3rd spacing BP, HR
Vasoconstriction d/tSNS activation
Trypsin activatesboth clotting
& lysing factors DIC & PE
HypovolemiaGFR
Renal perfusionClots in renal
circulationATNARF
GI motility bacteria outside GIPancreatic abscess
Necrosisinfection
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Acute Pancreatitis –Secondary Prevention -
Complications
Pulmonary
Enzyme induced inflammation of the diaphragm
Abdominal distention & diaphramatic movement
Pleural Effusion
Atelectasis
Pancreatic enzymes can injure the lungs directly
Watch for hypoxia – PO 2 < 60 mm Hg26
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Cardiovascular and Coagulation Complications
Capillary permeability fluid shifts (3rd spacing) distributive shock
Vasodilation d/t inflammatory mediators distributive shock
Thrombus formation d/t hypercoaguability DIC
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Acute Pancreatitis –Secondary Prevention - Cardiovascular Complications
3rd spacing BP, HR, vasoconstriction (compensatory mechanisms) d/t SNS activation
Recall: compensatory mechanisms work for only a short while before they begin to fail
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Acute Pancreatitis –Secondary Prevention -
Complications
Coagulopathy
Auto-digestion by Trypsin upon organ tissues:activates prothrombin clottingactivates plasminogen lysing
This mechanism
Intravascular & pulmonary blood clots
DIC & pulmonary emboli
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Acute Pancreatitis –Secondary Prevention -
Complications
RenalHypovolemia GFR, renal perfusion
development of clots in renal circulation
Acute tubular necrosis & Acute renal failure
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Acute Pancreatitis –Secondary Prevention -
Complications
Immunological
GI motility movement of bacteria outside GI tract due to pancreatic abscess &/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 PPI’s
Nursing Diagnosis: Acute Pain r/t inflammation of pancreas and surrounding tissue, obstruction of biliary tree & interruption of blood supply to pancreatic tissue
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Nutritional management
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Collaborative ManagementHemodynamic
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 drugs – dopamine BP via vasoconstriction in high doses renal perfusion in lower doses
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Collaborative ManagementRespiratory Care
Supplemental O2 @ 4L/NC (keep O2 Sat > 91%) Positioning for adequate ventilation Cough, deep breathe, IS with pain control Monitor ABG’s, respiratory effort & breath sounds
Nursing Diagnosis: Ineffective Breathing Pattern r/t abdominal distention, ascites, pain or respiratory compromise
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Collaborative ManagementMaintain 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
Syndrome
Monitor 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 with actual 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/day Avg. wt
of Male: 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) Lipids – 10-30% of calories Other meds: heparin, insulin, H2 blockers, 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 Administration
PN requires central venous catheter access due to the hypertonicity of solution 900 mOsm/liter ( 20% dextrose)
Peripheral parenteral nutrition (PPN) or Augmented parenteral nutrition (APN) through a peripheral or midline catheter because it is less concentrated 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
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Initiating PN – (con’t)
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 administration
runs behind Bag & tubing changes per
protocol
Patient Care Oral care
IV site care Dressing changes per protocol No blood draws, IVPB, IVP
meds through same port as PN No CVP readings
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Potential Complications of PN
Infection 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 LFT’s, 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 electrolytesCorrect prior to refeeding
Careful volume and Na replacement
Start slowly @ 15-20kcal/kg/day
Cardiac dysrhythmias, respiratoryarrest, neurological disturbances
http://www.nursingcenter.com/prodev/ce_article.asp?tid=789442
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Electrolyte Shifts in Refeeding Syndrome
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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 protein diet, 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, 8th Edition, 2011, Elsevier Medical-Surgical Nursing, Clinical Management for
Positive Outcomes, Black, J., Hawks, J., 8th Ed., 2009 Saunders
Mdcalc.com, retrieved 4/18/12
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