Panc TPN InstructorSP09 (1)

8/13/2019 Panc TPN InstructorSP09 (1)

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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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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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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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Complications

RenalHypovolemia GFR, renal

perfusion

development of clots in renalcirculation

Acute tubular necrosis & Acuterenal failure

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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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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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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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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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http://www.nursingcenter.com/prodev/ce_article.asp?tid=789442http://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

Panc TPN InstructorSP09 (1)

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