Enteral and Parenteral

Nutrition
 3 steps in managing nutritional disorders
1. Screening and diagnosis
2. Determination of severity and urgency of treating a diagnosed nutritional disorder
in its overall clinical context
3. Selection of the modality of specialized nutritional support
Nutrition Physiology
Total Energy Expenditure

 REE(~24 kcal/kg) + AEE (~12kcal/kg for sedentary

adult) + thermic effect of food (10% of TEE)
 REE
 Fever and critical illness can increase REE
 Prolonged semi-starvation can decrease REE
Protein and Amino Acids
 Proteins of nutritional interest usually 16% nitrogen by weight
 Excretion of 1g of nitrogen = loss of 6.25g formed protein and
~31 g body cell mass
 Minimum dietary protein intake for protein homeostasis and
zero nitrogen balance
 0.65g/kg
 Safe or recommended (2 SD from 0.65 g/kg)  0.8 g/kg
 Disease mechanism for increasing protein requirement
1. Increased Amino acid loss (malabsorption, diarrhea) or removal from
circulation (renal replacement therapy)
2. Increased muscle protein catabolism
Protein and Amino Acids

 Protein catabolic patients

 Excrete 15 g N/day in the urine = 94g muscle
protein = 1 lb of muscle lost from the body
everyday
 requiremore protein to minimize muscle
atrophy  recommended is 1.5g/kg
Protein Energy Interaction

 Energy Deficiency  amino acid loss from the muscle

hence increase dietary protein requirement
 To prevent this  generous protein provisions as long as protein
combined with exogenous energy source usually 50% of TEE (CHO
or fats)
 Energy provisions >50-70% of TEE  provide little protein sparing
effect (additional glucose and fluids have more adverse effects
than benefit in this case)
Micronutrients

 Hospitalized patients for more than a few days 

consume inadequate amount of food and micronutrients
 Na, K, Mg, PO4 and iron deficiencies occur frequently 
standard practice to monitor
 Drugs
 GI losses
 Wrong assumption  consumption of regular hospital diet
will protect patients from these deficiencies  esp if
nutritional status is borderline or deficiency at baseline
Protein Energy Malnutrition and its
variants
 PEM prolonged inadequate energy and protein
consumption—starvation—with consequent
depletion of body cell mass and body fat
 PEM vs physiologic process of starvation
 InPEM – BCM depleted enough to cause impairment in
specific physiologic function
 Cardinal Diagnostic Feature of PEM
 generalized muscle atrophy and subcutaneous
adipose tissue depletion
 ***too often undiagnosed  partly health care worker
unawareness and inattention, partly PEM overlap with
conditions causing muscle atrophy
Starvation-Related Malnutrition (SM)

 “uncomplicated” PEM due to PROLONGED STARVATION

 Adaptation  important feature of SM  increase likelihood of survival
 Reducing energy expenditure
 Reducing protein turnover
 Risk of complications/death increases when BCM depletion worsens (~50%)
 Patient feels unwell
 Lack of strength
 hypothermia
Starvation-Related Malnutrition (SM)

 Main causes
 Involuntary food deprivation  main cause worldwide
 Hospitalized patients:
 Inadvertent or physician ordered food deprivation
 Psychologic depression/distress
 Poorly controlled pain or nausea
 Badly presented unappealing food
 Communication barriers
 Anorexia
 Physical/sensory deficits
 thrush
 Dysphagia or other mechanical obstruction
 Intestinal angina
Chronic Disease-Related Malnutrition
and Cachexia (CDM)
 Starvation induced complicated by chronic systemic inflammation
 Both Causes and is Worsened by anorexia
Chronic Disease-Related Malnutrition
and Cachexia (CDM)
 Characteristics
 moderately increased rate of muscle protein catabolism,
 muscle atrophy and weakness,
 fatigue and reduced voluntary activity,
 and a subverted adaption to starvation
 Vicious cycle of worsening CDM
 Nutrient deficit on the INPUT side is the stronger driver than the OUTPUT side
 Inadequate intake more contribution than catabolism
Acute Disease-Related Malnutrition
(ADM)
 specific metabolic-nutritional environment that creates a very high risk of
severe PEM
 Intense SIRS + unable to take in food
 Synonym: “Catabolic critical illness”
 Patients frequently treated at ICU
 May not have ADM at onset, but will surely develop within days or weeks
unless medical or surgical disease is rapidly and effectively treated and SNS
appropriately provided
Nutritional Diagnosis
cardinal anatomic features of PEM—generalized muscle atrophy and
diminished body fat
Muscle Mass

 Generalized muscle atrophy  easy to identify and severity determinable at a

glance
 Problem is apart from inattention, MANY CAUSES
 Age related
 Disuse atrophy
 Steroid therapy
 Endocrine diseases
 Primary muscle or neuromuscular diseases
 Common misconception
 “necessary feature” of primary disease, IT IS MORE OF A REMEDIABLE COMPLICATION
Muscle Mass

 Muscle atrophy especially DANGEROUS in ADM  patients in this situation very

close to lethal BCM DEPLETION
 Reduced muscle mass not able to sustain amino acids for protein synthesis at sites
of injury and healing
Subcutaneous Adipose Tissue

 Sufficient to diagnose PEM

 NOT A NECESSARY CRITERION
 Obesity epidemic  muscle atrophy outpaces fat loss
ECF volume

 20% of BW
 Chronic starvation increases ECF  enough to cause edema, “starvation
edema”
 Patients with CDM also have other edema causing condition:
 Hypoalbuminemia
 Increased ECF can MASK THE TRUE EXTENT of PEM
BMI

 BMI >25 indicated increased body fat

 BMI <20 indicates decreased body muscle mass and fat
 BMI 11-13  generally incompatible with life
 BMI 17 – consistent with PEM, but >17 does not rule out PEM
 Due to residual obesity or expanded ECF
 ***BMI <16/17 as consistent with PEM is OVERSIMPLIFICATION OF THE PROBLEM
Visual BMI

 Acquired skill
 Can be used to estimate severity of PEM in obese or edematous patients
(where measured BMI is unreliable)
 Focusing on muscle architecture
 Discounting subcutaneous fat and edema
 Lab and Technical Assessment
 3 main purpose:

Muscle mass • via ultrasound,

• but not replaced by immediate and comprehensive clinical examination
Systemic inflammation - distinguishes SM from CDM/ADM
- Most useful lab indicators: low alb, high CRP
- Hypoalbuminemia DOES NOT INDICATED MALNUTRITION, it indicates
presence of systemic inflammation
- Hypoalb will not improve as long as there is systemic inflammation
- Once inflammation subsides  several weeks of optimal nutrition to
normalize ALB
Protein-catabolic • Defining feature: increase muscle amino acid catabolism
intensity • Measure rate of body N loss; 85% as urea
• Validated formula: g N in urinary urea/0.85+2
• Follows 1st order kinetics: proportional loss
• More muscle = more N loss; less muscle = less N loss
• Interpretation  consider existing muscle mass
Instrumental Nutritional Assessment

 Many instruments claim to identify “malnutrition”  enumerating and

summing a list of risk factors, labs and PE
 Hindered by
 Ambiguity about the intended meaning of “malnutrition”
 Failure to distinguish between screening and diagnosis

Diagnosis  identify known pathologic entity: SM vs CDM

Screening  application of test to identify patient at high risk for disease to warrant
carrying out definitive procedures to establish a diagnosis
Subjective Global Assessment

 best-validated and most useful formal bedside instrument for diagnosing SM

and CDM
 totality of
 (1) the patient’s history (for evidence of inadequate food intake, weight loss, and
the presence of factors, such as gastrointestinal disease, and systemic
inflammation, that strongly predict diminished ability consume enough food),
 (2) the patient’s current body composition (muscle mass, subcutaneous fat, and
ECF volume),
 (3) their functional status
 From these, form a clinical judgement whether: no SM or CDM, gray zone,
definitely SM or CDM
 3 Kinds of specialized nutritional support

Optimized voluntary nutritional support attention to detail how food is constituted,

prepared, served and consumption monitored
Forced Enteral Nutrition Liquid nutrient delivered via feeding tube
Parenteral nutrition Nutrients infused through bloodstream
 Advantage Disadvantage

Optimized voluntary - Patient centered - Time consuming

nutritional support  - Engages and empowers patient - Labor intensive
this is the SNS of - Encourages mobilization and reconditioning - Demands interest and attention to
choice - Risk free specific needs of patients

Enteral Nutrition - Relatively safe - Needs feeding tube placement  still

- Inexpensive has risks
- Maintains digestive/absorptive/immunologic
gut functions
- Delivery of accurately known nutrients

Parenteral nutrition - Complete nutritional regimen over the - Needs central vein infusion  high
bloodstream osmolarity and volume
- Allows precise protein and energy - Costlier
calculation - Riskier
- Resource intensive
- Requires more expertise
 Examples of EN products
Standard polymeric formula - Most widely used
- INTACT PROTEIN
- Requires normal pancreatic enzyme function
- Isotonic

Polymeric formula with fiber - Addition of dietary fiber – improve bowel function and tolerance
- Fermentable fiber  by bacteria to SCFA  colonocyte nutrition
- Nonfermentable fiber  stool bulk, improve diarrhea

Elemental and semi-elemental formula - Digested proteins

- For maldigestion and malabsorption
- Intolerant to standard polymeric formula

Immune-enhancing formulas - Contain nutrients to modulate inflammation  n3 FA, combination

of glutamate, nucleotides and antioxidants
- Benefit for perioperative GI surgery and TBI patients

Protein Enriched Formula - More protein

- For protein-catabolic patients, to prevent caloric over-feeding
 PN components
 Amino acids
 21 aa, 11 essential
 Hydrated status of aa in PN reduces caloric density from 4.0 to 3.3 kcal/g  17%
reduction in protein substrate
 100g aa = 83g protein and provides 340 kcal
 Carbohydrates
 Dextrose monohydrate : 3.4 kcal/g
 Lipids
 Emulsions containing essential n-3 n-6 FA
 Before  soybean based, now more mixed emulsions of MCT, n9-MUFA and n3 FA
 Higher n3 FA and lower n6 PUFA  lower pro-inflammatory n-6 derivatives
 Minerals, Macronutrients, Trace Elements
 Meet RDA
 MV mixtures are unstable  injected prior to delivery
Approach to Patients
 Initial consideration should always be for optimized
voluntary nutrition
 Invasive SNS if failure of or inappropriate for optimized
voluntary nutrition  4 factors to consider
 Inadequate nutrient ingestion likely to continue for many days;
 the patient has important muscle atrophy (of any cause) or fat
depletion
 the patient’s nutrient requirements are increased
 SNS has a reasonable prospect of improving the patient’s clinical
outcome or quality of life.
 EN Therapy
Indications - Cannot eat food
- GI tract functional
- Optimized nutrition therapy impossible/inadequate
CI Absolute Relative  increase risk of
• Intestinal ischemia, complication
• mechanical • Severe coagulopathy,
obstruction, • esophageal varices,
• peritonitis, • absent gag reflex,
• and gastrointestinal • hypotension,
hemorrhage • Adynamic ileus,
• pancreatitis,
• diarrhea,
• nausea and vomiting
EN therapy: initiation, progression and
monitoring
 NGT placement  ensure adequate gut function
 Gastric contractility (NGT output <1.2Lday)
 Intestinal contractility (no intestinal obstruction, no distension)
 Colonic contractility (passage of flatus/stools)
 Raise head by 30o prevent regurgitation
 Bolus vs drip feeding dependent on type of tube placed
 Intragastric feeding via PEG  can do bolus feeding
 Jejunal feeding  drip feeding
EN therapy Complications
 Aspiration

Cause/MOA - Delayed gastric emptying

- Impaired gag
- Ineffective cough
Preventions - Head elevation
- Mouth hygiene
- Gastrointestinal decontamination
- Formula advancement algorithms
- Post-pyloric feeding
Interventions - No need to withhold for gastric residuals of 300-400cc
without signs of GI intolerance
- Continuous EN better tolerated than bolus
 EN therapy Complications
 Diarrhea

Cause/MOA - Drugs or disease

- Infection/inflammation

Interventions - Fiber containing formula

- Anti-diarrheal agents
- H2RA or PPI  reduce net fluid in colon
- Continue if diarrhea is tolerable and moderate  has trophic
effects on intestinal mucosa (absorption not impaired)
- Can use elemental formula
 EN therapy Complications
 GI Intolerance
Symptoms - High gastric residual volume
- Abdominal distension, pain
- nausea
Preventions - Normal fluid balance and electrolytes
- Preventing severe hyperglycemia

Interventions - Anti-emetics and prokinetics on a regular basis

- Post-pyloric feeding for gastroparesis
 EN therapy Complications
 Fluid Volume, Electrolyte, and Blood Glucose Abnormalities
Cause/MOA - Variation in requirements by patients (EN is standardized
formulation)
Preventions - Monitor BGs, electrolytes, fluids, insulin

Interventions - Fluid volume requirements  alter EN osmolarity

 EN therapy Complications
 Failure to Reach the Nutritional Goal
Cause/MOA - Diagnostic tests and procedures
- PT or OT
- Clogged/pulled Tubes
- Intolerance to EN
- Tube clogging  dense formula, inadequate flushing,
inadequately homogenized solid meds
Interventions - High protein formula if EN is progressing to slowly (high
Protein: calorie ratio)
EN in the ICU

 2 goals
 Meet nutritional demands
 Maintain the intestinal mucosa
 Barrier and immune function
 Guidelines
 Start ASAP once resuscitated and stabilized
 Initial rate: 10-20 kcal/hr (~25g protein and ~500 kcal/d)  increased as tolerated
to goal
Parenteral Nutrition (PN)
Indications - Invasive SNS and EN is impossible
Risks - Central line insertion  high osmolarity, high volumes
- Allergies
- Glucose, electrolyte, magnesium, phosphate and acid-base
abnormalities
- Large fluid volumes
PN initiation

 Carbohydrates  maximum is 200g/day of dextrose  don’t go higher due to

risk of refeeding syndrome
 Increase in increment over the weeks
 Glucose infusion rate for a 70kg patient
 Not exceed 500g/day for noncritical ill patients
 Not exceed 350g/day for critical ill patients
 Amino acids  may start at full requirement dose
 Lipid emulsions  added after a week, for calorie shortfalls
PN monitoring

 Blood glucose monitoring

 Insulin added to PN to maintain BG at 80-140 mg/dl
 Added insulin based on CHO load
 Basal insulin ~ 30 units/day in normal individuals
 Non DM patients  10 units HR per 100g CHO
 Non insulin dependent DM  20 units HR per 100g CHO
 Non-catabolic insulin dependent DM  2x the daily dose of insulin
PN monitoring

 Chemistry monitoring  BUN, crea, electrolytes, Mg, PO4, Ca, Alb, Glucose
 Prior to starting
 Daily for first few weeks
 Then twice weekly or as required after
 Lipid
 Triglycerides at baseline prior  detect hypertrigly which is relative CI
 LFT at baseline
 Repeat after PN infusion to check if tolerated
 Nitrogen monitoring
 At the onset  check severity of protein catabolism
 During therapy  determine N balance improvement
PN monitoring

 Ferritin  measured every 2 months

PN Discontinuation
 ASAP once patient able to be fed enterally
 Reduce PN as food intake increases
 General rule: if tolerating ½ to 2/3 of food requirement by enteral route 
DC PN
 Some patients may require slow weaning off PN
 Stopping PN does not STIMULATE more food consumption and continuing PN does
not cause ANOREXIA
 Stopping too early  delay patient’s progression to full voluntary food consumption
 Successful weaning by
 Physical activity
 Optimizing voluntary nutrition
 Emotional support
 Patience
 Discharging to home  home made meals can be a potent stimuli
PN Complications
 Central Catheter related complications
Blood Stream Infections Risk Reduction by:
- Proper aseptic technique
- Meticulous dressing care
- One port dedicated solely to PN
Upper arm venous
thrombosis
PN Complications
 Hyperglycemia  most frequent metabolic complication
 In ADM  benefit of using lowest insulin dose (prevents
hyperinsulinemia and hypoglycemia) outweighs matching
caloric goal to patients EE

Cause - non-insulin dependent DM

- High dose steroid therapy
- Severe systemic inflammation
- Exacerbated by high rate of
glucose provision
Prevention - Hypocaloric amount of glucose to
keep BG <140mg/dl
- Meet the daily caloric
requirement via lipids
PN Complications
 Hyporglycemia

Causes Prevention
Reactive hypoglycemia due to - Slowing infusion rate to 50ml/h for 1-2hr
high dextrose, non-insulin prior to discontinuing PN
containing PN is rapidly - Replace PN with D10
discontinued - If oral route available, provide snack
Decreased metabolic stress - Frequent BG monitoring and medication
without adjusting insulin dose dose adjustment
PN Complications
 Artefactual Hyperglycemia and Hyperkalemia
 Intermixing blood with PN
 Suspect if K and glucose abruptly increases without reason and
out of sync from CBG monitoring
PN Complications
 Volume Overload
 Hypertonic IV dextrose  much potent insulin response
 Insulin promotes sodium and water retention
 Prevention

Fluid overload - Avoid overfeeding

- Use compounder to minimize glucose
infusion and avoid the need for
exogenous insulin
Fluid retention - Limit sodium delivery to 20-30
mmol/day
PN Complications
Hypertriglyceridemia

Cause • Rate of lipid infusion exceed plasma Tg

clearance
• Factors that decrease plasma Tg Clearance
- Renal failure, sepsis, excessive glucose,
diabetes mellitus, high-dose glucocorticoid
therapy, and multiple-organ failure
Complications - Impaired immune response
- Inc risk for pancreatitis
- Altered pulmonary hemodynamics
PN Complications
Hepatic Dysfunction
Mild elevations in LFT can occur in 2-4weeks of PN
Most case return to normal with DC of PN
Avoid energy overfeeding and resultant fatty liver
Intrahepatic cholestasis due to many weeks of
continuous PN
Prevented or reduce severity by cyclical PN: 12h
PN/day
PN in the ICU

 Start if after 7-10 of EN, nutritional goal not reached  amino acid rich PN
 Preferred
 High amino acids (85-140g protein/day for 70kg patient)
 Hypocaloric (1.2k-1.4kcal/day)
 Limits hyperglycemia and volume overload
 Avoid soy based emulsion during the 1st week of therapy
SNS in special situations
Old Age - High risk for PEM  plausible candidates for early SNS
- Age muscle atrophy + disuse atrophy confounds this risk
Inactivity - Reduced activity  reduced appetite
- Nutrition will not increase muscle mass, only maintain or normalize many
physiologic functions in bedridden patients
Renal failure - don’t withhold protein, unless RRT unavailable
- Increase protein and vit C if on RRT  removes large amount of amino acids and vit
C
Liver Failure - Relatively intolerant of starvation and usually have CDM
- Generous in calories and proteins despite inc risk for hep enceph
- Mitigate enceph  fluid balance and electrolyte status, spread protein provisions
over the entire day
Dementia - Optimized voluntary nutrition  key approach
- EN/PN no evidence that it improves QOL
SNS in special situations
Zinc - 1L secretory diarrhea = 12mg Zinc
- Chronic diarrhea or fistula needs additional 15mg Zinc on top
of RDA
- Low oral bioavailability: 30mg of oral zinc = 12mg parenteral
zinc
Cancer - Create conditions of starvation leading to SM or CDM
- General Rule: don’t give EN/PN to patients not undergoing
active cancer therapy  side effect and complications of
invasive SNS not counterbalanced by improved disease
trajectory
- BUT IF PATIENT WILL DIE FROM STARVATION FIRST DUE TO
SLOW GROWING TUMOR  EN/PN INDICATED
SNS in special situations: Peri-operative

PREOPERATIVE SNS
 Major surgery  7-10 days preop SNS if SM or CDN present
 Optimized voluntary nutrition is preferred
 Preop SNS benefits
 Improves Immunity
 Reduced postop complications
 DOES NOT INCREASE ALBUMIN
 Don’t delay surgery for starving patients if muscle mass is normal or mildly
depleted and don’t have systemic inflammation
 Urgency trumps need for preop SNS
SNS in special situations: Peri-operative

EARLY POSTOPERATIVE PN
 Patients who underwent urgent/emergent surgery who have indications for
preoperative SNS
 Other indications
 adequate feeding by mouth has not been achieved by day 5–7 after surgery
 there are indications that voluntary feeding will be further delayed
SNS in special situations: Iron and PN

 Iron deficiency common in acutely ill

 Risk factors
 Inadequate nutrition
 GI disease
 Frequent blood draws
 Frequently missed since ferritin is an acute phase reactant and is frequently
elevated in inflammation
 PN iron requirement: 1mg/day  not included in PN mixtures since highly
reactive
 Measure ferritin at commencement of PN and repeat at 8 weeks
 Falling MCV or intermediate ferritin (in systemic inflammation) suggests iron
deficiency
SNS in special situations: Iron and PN

 IRON REPLACEMENT AVOIDED during acute phase of critical illness 

substantial rise in serum iron = inc susceptibility to bacterial infections
Refeeding Syndrome

 Occurs in 1st week of nutrition therapy if CHO given too rapidly

 Caused by insulin
 Can have refeeding edema if too much salt given
 Due to insulin  glycogen synthesis, G6P  phosphate depletion
 Increased down regulated REE  N retention, cell synthesis, cellular
rehydration
 Acute thiamine deficiency when glucose given in a state of thiamine deficiency
 What to monitor
 Phosphate, zinc, magnesium, potassium

Refeeding Syndrome

Complications
 Left heart failure  abrupt increase in fluid volume (glucose, fluids, insulin),
increased cardiac demand on an atrophic left ventricle, myocardial
deficiencies of K, Mg, P
 Cardiac arrhythmias
 Acute wet beriberi