GI

s/sx of malnutrition

body habitus wasting (adipose tissue, somatic protein, or both)

low bmi

concomitant inflammatory disorders can be present

poorly healing wounds

decreased grip strength

actual body weight <90% of ideal body weight

lab changes that show malnutrition

low albumin, prealbumin and transferrin, elevated CRP

what risk calculations are used for malnutrition and what is considered high risk

NUTRIC score >5+

NRS-2002 score >3+

enteral nutrition

delivered into the gi tract

parenteral nutrition

delivered directly into the bloodstream

enteral/gi access routes

nasogastric, nasojejunal, gastrostomy/percutaneous endoscopic gastrostomy, jejunostomy/percutaneous endoscopic jujenostomy

which enteral access routes are good for short term use

nasogastric and nasojejunal

which enteral access routes are good for long term use

gastrostomy/percutaneous endoscopic gastrostomy, jejunostomy/percutaneous endoscopic jujenostomy

when is post-pyloric placement useful

high aspiration risk, pancreatitis, gastroparesis

risk factors for feeding tube clogging

suboptimal tube care or med administration

small bore feeding tubes

frequent aspiration of gastric residuals

prevention of feeding tube clogging

flush w/ 20-30 ml warm water, q4h during continuous feeding and before + after feeds/meds

medications tips for feeding tube clogging

use liquid formulations when possible, avoid mixing meds w/ enteral nutrition, do NOT flush w/ juice or carbonated bevs

management of feeding tube clogging

use pancreatic enzymes + sodium bicarb in ~5ml water, allow to dwell ~15 mins then flush

which drugs have dosage forms that are altered by crushing and what should you do to prevent this

drugs that are delayed release, extended release or enteric coated →

change the drug to an immediate release if possible!

which drugs are inactivated by exposure to cations w/in tube feedings and what should you do to prevent this

tetracyclines, fluoroquinolones (cipro, levo) → hold tube feeding for 1h before/after admin OR admin it IV

which drugs bind to proteins contained w/in tube feedings and what should you do to prevent this

phenytoin, warfarin → hold tube feedings 1-2h before/after admin OR increase dose OR admin IV

when should parenteral nutrition be used over enteral nutrition

if pts gut cannot be used, is inadequate, cannot be tolerated

which type of nutrition maintains gut integrity

enteral nutrition

which type of nutrition has a higher infection risk? (line related)

parenteral nutrition

which type of nutrition has a higher risk of aspiration or emesis!

enteral nutrition

which type or nutrition cost more and is used in longer hospital stays

parenteral nutrition

when is parenteral nutrition indicated

if there is a c/i to enteral nutrition

conditions where EN is not safe (requires bowel rest)

inability to meet nutritional needs through the gi tract

severe metabolic or clinical instability

contraindications to EN

failed EN trial or intolerance

nonfunctional / inaccessible gi tract (paralytic ileus, mesenteric ischemia, small bowel obstruction, high-output fistula)

conditions where EN is unsafe

ischemic bowel, gi perforation, severe gi bleeding

what constitutes an inability to meet a pts nutritional needs via gi tract

inadequate oral/enteral intake for >7d

preexisting malnutrition w/ anticipated prolonged NPO status

what constitutes severe metabolic or clinical instability

severe fluid or electrolyte disturbances

severe hyperglycemia or hyperosmolar state

encephalopathy limiting safe feeding

significant multiorgan system failure

if a pts nutritional risk is low, when should you initiate PN

after 7 days

if a pts nutritional risk is high or they are clearly malnourished, when should you initiate PN

as soon as posisble!

peripheral parenteral access routes

midline catheter

antecubital peripheral line

forearm peripheral line

hand peripheral line

central parenteral access routes

central venous catheter (CVC)

port a cath

peripheral inserted central catheter (PICC)

tunneled line

which type of parenteral nutrition is given through a central line/route

total parenteral nutrition (TPN)

which type of parenteral nutrition is given through a peripheral route

peripheral parenteral nutrition (PPN)

max osmolarity for peripheral access route

900 mOsm/L

max osmolarity for central access route

1300-1800 mOsm/L

which parenteral access route has a higher risk of infection

central! specifically central line associated bloodstream infection (CLABSI)

which parenteral access route is used for short term use

peripheral!

complications of peripheral lines

phlebitis, infiltration

complications of central lines

CLABSI, thrombosis, pneumothorax (placement-related)

3 ways to calculate calorie requirement

indirect calorimetry: based on o2 consumption / co2 production, most accurate but expensive

estimated energy requirement based on weight

total energy expenditure (TEE): specific to pts clinical status + body habitus, correction for stress!

calories per kg

25-35kcal/kg

maintenance: 20-25

moderate stress: 25-30

severe stress: >35

stress factor for pts confined to bed

1.2

stress factor for pts w/ sepsis

1.3

stress factor for pts w/ severe trauma

1.4

stress factor for pts w/ severe burns

2.0

ideal body weight equations

males: 50kg + 2.3kg (every in over 5 ft)

females: 45.5kg + 2.3 kg ( every in over 5 ft)

adjusted body weight equation

IBW + 0.4 (ABW-IBW)

when should ABW (actual body weight) be used

if bmi <30

or if it is less than IBW (to help maintain the current nutrition status)

when should adjBW be used

if bmi >30

protein requirement in general

1-2 g/kg

protein requirement for maintenance

0.8-1.2 g/kg

protein requirement for moderate stress

1.2-1.5 g/kg

protein requirement for severe stress

1.5-2 g/kg

protein requirement for renal insufficiency not on dialysis

0.6-0.8 g/kg

protein requirement for hemodialysis

1.2-1.3 g/kg

protein requirement for CRRT (continuous renal replacement therapy)

1.5-2.5 g/kg

protein requirement for overt encephalopathy

0.5-0.7 g/kg

fluid requirement

generally ~ 35 ml/kg

1000ml for first 10 kg, 500 ml for next 10 kg, and 20 ml/kg thereafter

maintenance: 1500ml + 20ml(pt wt in kg -20)

components of parenteral nutrition

macro: dextrose, amino acids, lipids

micro: electrolytes, vitamins, trace elements

use sterile water as vehicle!

additives (not required): insulin

calories of dextrose

3.4 kcal/g

max infusion rate of dextrose

5 mg/kg/min (25 kcal/kg/day)

max concentration of dextrose through a peripheral line (PPN)

dextrose 10%

max concentration of dextrose through a central line (TPN)

dextrose 25%

calories of amino acids

4 kcal/g

max concentration of AA through a peripheral line

2-5-5%

max concentration of AA through a central line

5-10%

calories of lipids

10 kcal/g

when are lipids contraindicated

pts w/ severe egg, soybean, and/or peanut allergy

ILE formulations

10% (1.1kcal/ml): only for premixed produces (ex: propofol)

20% (2 kcal/ml): used for direct iv lipid admin

30% (2.9-3 kcal/ml): used for compounding 3 in 1 mixture

intralipid

100% soybean!, higher omega 6 content and no omega 3 content, higher hepatotox risk

used in short term PN (<5-7d), institutional formulary limitation, cost constraints

SMOFlipid

contains soybean, medium chain TG, olive oil, fish oil

lower omega 6 content, and has omega 3 (fish oil)

lower hepatotox risk

used for long-term PN (wks - mon), in ICU pts requiring prolonged nutrition, pts at risk of liver dysfxn/cholestasis, hyperinflammatory states, critically ill

which electrolytes should be avoided

sodium bicarb, sodium lactate, calcium chloride

what does the calcium phosphate solubility curve show

the max allowable combos of calcium + phosphate that can safely remain dissolved in a 2 in 1 PN solution @ different AA concentrations

what is the standard dosing of multivitamins (ADEK + B1,2,6,12 + C + folic acid)

10 ml/bag

what is the standard dosing of trace elements (zn, cu, cr, mn, se)

1 ml/bag

insulin in TPN

use sliding scale! q6h

goal blood glucose while on TPN: 140-180 mg/dl

absorbed to plastic tubing + PVC (up to 50% loss)

add 1/2-1/3 of previous 24h ISS requirement

2-in-1 PN formulation

dextrose + AA only, lipids infused separately

max hang time: 24h

3-in-1 / total nutrient admixtures

dextrose, AA, lipids

decreases solubility of calcium + phosphate (increase risk for precipitation)

max hang time: 24h

multichamber bags

various formulations

2 in 1 or 3 in 1

convenient + cost effective`

max hang time for IV lipid emulsions (ILE)

12h

continuous TPN

infused continuously over 24h

provides stable, constant nutrient delivery

common in hospitalized pts

cyclic TPN

infused over 12-18h w/ daily “off” period

stepwise increase, steady infusion, then taper down

indicated for TPN associated cholestatic liver disease prevention, long term home TPN, improved pt qol

what additional info is important before initiating a TPN

max dextrose conc based on line status

osm limits based on line status

plans for change in line status

PMH/problem list

• DM, compromised resp fxn: low dextrose conc

• liver disease w/ ascites, CHF, HTN: minimize na

• pancreatitis: zero/low fat conc

• renal impairment: minimize k, mg, phos

• fluid restriction: concentrate formula, increase fat conc

diet (full nutrition support vs supportive)

current labs

0.22 micron filters

removes pathogenic microorganisms: staph epi, e.coli, candida albicans

1.22 micron filters

used for ILE containing PN

refeeding syndrome

neg consequences of metabolic + physiological shifts of fluid, electrolytes, vitamins, + minerals d/t aggressive nutrition repletion

driven mainly by insulin release after carb reintroduction (insulin increase → decrease phos, k, mg)

can occur during first 2-5 d after start of nutrition support

risk factors for refeeding syndrome

anorexia nervosa, prolonged periods of no nutrition, bmi <16

management for refeeding syndrome

initiate dextrose btwn 100-150g, titrate to nutrition goal every 1-2d

replace electrolytes according to protocols

if sudden electrolyte drop, decrease dextrose by 50%

metabolic complications

hypoglycemia: if infusion w/ >10% dextrose is stopped abruptly, must taper off + check blood sugar 1h after end of infusion

excess co2 production: d/t overfeeding w/ glucose cals, glucose oxidation produces more co2 than fat oxidation

TPN associated cholestatic liver disease: associated w/ prolonged, continuous feeding, increase in alkaline phosphatase + other liver enzymes as early as 7-10d following initiation of TPN

essential fatty acid deficiency: EFAs are substrates for other things (maintains integrity of skin + cell membranes, components of brain + retina, synthesis of prostaglandins + leukotrienes)

risk factors of TPN associated cholestatic liver disease

infxn, ongoing inflammatory process, alcoholism, obesity

management for TPN associated cholestatic liver disease

rule out other causes, decrease glucose intake (<25kcal/kg/day), cycle TPN

s/sx of EFA deficiency

dry, scaly rash

hair loss, hair depigmentation

poor wound healing

growth restriction in children

increased susceptibility to infxn

management of EFA deficiency

minimum requirement of lipid: 1g/kg/wk

monitoring parameters

endocrine hormone

insulin → regulates blood glucose

exocrine hormone

→ amylase, lipase, trypsin, others → secreted into duodenum to facilitate organic chemical breakdown

exocrine hormone secretion pathway

pancreatic acini → pancreatic duct → common bile duct → ampulla of vater → duodenum

need all parts of pathway to fxn normally to maintain normal physiology

pathophys

inability to excrete pancreatic exocrine enzymes into the duodenum → disrupted physiology

digestive enzyme buildup may lead to pancreatic inflammation + pancreatic cell death

can cause detectable levels of pancreatic enzymes in serum

etiology

blockage in pancreatic drainage system; may or may not have clear cause

B: biliary

A: alc

D: drugs

S: scorpion sting

H: hypertriglyeridemia

I: idiopathic

T: trauma/tumor

which drugs cause hypertriglyceridemia

estrogens, hctz

which drugs cause spasm of the sphincter of oddi

opioids