Nutrition in Intensive Care

Question 1

Stages in critical illness

Answer 1

1- Primary insult (surgery, trauma, burns, acute pancreatitis, IBD)
2- Hypermetabolic inflammatory catabolic state (hyper-metabolism, anorexia, neuroendocrine/cytokin mediated)
3- Sepsis, Recovery or Death

Question 2

Responses to critical illness

Answer 2

Failure of adaptation

Question 3

Response to critical illness: Simple fasting

Answer 3

Glycogen and protein mobilized–> provide glucose
Ketogenesis and ketosis increase, glucose needs fall
Metabolic rate slows
Energy needs fall
Protein and Energy conservation

Question 4

End result of simple fasting

Answer 4

Protein and energy conservation

Question 5

Response to critical illness: Severe stress

Answer 5

Glycogen & Prot mobilized for glucose and acute phase prots
Less or no ketogenesis and ketosis–> gluconeogensis from prot remains high
Metabolic rate rises
Energy needs increase
Accelerated protein and energy depletion

Question 6

End result of severe stress

Answer 6

Accelerated protein and energy depletion

Question 7

Systemic Increases in the hyper-metabolic state of critical illness

Answer 7

Metabolic rate
Body Temp
Water retention
Cardiac output
Blood volume
Tissue perfusion
Free radical production
NO production

Question 8

Skeletal Muscle Increases in the hyper-metabolic state of critical illness

Answer 8

Net proteolysis

Amino acid oxidation

Question 9

Liver Increases in the hyper-metabolic state of critical illness

Answer 9

AA oxidation/N excretion
Acute phase prot synthesis
Gbuconeogensis
Cori cycle

Question 10

Adipose Increases in the hyper-metabolic state of critical illness

Answer 10

Lipolysis/TG turnover

Question 11

Reduction during the hyper metabolic state of critical illness

Answer 11

Plasma albumin

Plasma IGF-1

Question 12

SIRS/hyper-inflammation of the hyper metabolic state

Answer 12

SIRS= systemic inflammatory response syndrome. Triggered by the injury, and activates CARS/immunosuppression, and leads to sepsis

  - CARS: Compensatory, Anti-inflammatory Response syndrome. Can increase SIRS or lead to Sepsis
 - Sepsis--> severe sepsis and MOF--> septic shock

Question 13

Septic shock

Answer 13

has 40-80% risk of mortality.

Metabolic acidosis and HoTN

Question 14

Immune-cytokine response to stress

Answer 14

Stress--> local rxns--> imunno-cytokine response of pro-inflame mediators:
TNFa
IL-1
IL-6
IL-8
PGE2
NO
ROS
These all lead to SIRS

Question 15

Endocrine response to stress

Answer 15

Stress–>local rxns–>
Increased catabolic hormones: E, glucagon, cortisol, GH
Reduced anabolic hormones: IGF1, T3. Insulin-Resistance.
Leads to SIRS

Question 16

Immunosuppression in trauma

Answer 16

Excess anti-inflam cytokines
Suppressed HLA expression and Ag presentation
Suppressed T-cell fxn

Question 17

Chemical intestinal barriers

Answer 17

Gastric acidity
Salivary lysozyme
Lactoferrin
Mucus secretion
Bile salts

Question 18

Inflammatory responses activated by compromised intestinal barrier

Answer 18

Complement activation: C3a, C3b, C3c, C3d
Decreased splanchnic blood flow
MOF/dysfxn
Cytokine release: IL-1, IL-6, TNF, PAF
Release of arachidonic acid metals PGE2, TXs, LKs
Acute-phase protein release

Question 19

EN v. TPN

Answer 19

EN is better than TPN
TPN increases the risk of infectious complications.
Either though reduce mortality by 70% in ICU pts.
Bowel rest (delayed EN) increased risk of systemic infection by 66%

Question 20

Why EN is needed?

Answer 20

enteral energy will stimulate CCK/gut trophic factors and maintain the immune fxn of the gut. TPN cannot do this, but can only provide energy.

Question 21

Aims of artificial nutrition

Answer 21

Maintain/restore body composition- with nutritionally rational and balanced intakes

To maintain/restore/modulate cell and organ fxn with us of specific AAs, antioxidants, micronutrients, and specific polyunsaturated FAs.Immunonutrition to optimize outcome

Question 22

Feeding objectives

Answer 22

3 options:

1- Minimization of losses (severely ill ICU pts)- provide as much E as is safe, prob TEE

Question 23

Refeeding syndrome

Answer 23

Metabolic complications of over feeding

Question 24

Total Energy Expenditure

Answer 24

TEE = BMR x Physical Activity Level

Question 25

How BMR is predicted

Answer 25

+/- 10% based on weight, age and gender

Question 26

Sustainable PAL values

Answer 26

Sedentary        1.4
Average           1.6
Active               1.8
Very Active     >/= 2
Elite Athlete     2.5

Question 27

Increased BMR

Answer 27

BMR increases in diseased states
Fever: 13% increase
Maintenance need will be similar to or greater than normal subjects

Greatest increases in BMR:
Burns > Sepsis > Blunt trauma > Pancreatitis > Cirrhosis etc…

Question 28

TEE aim

Answer 28

~30-35 kcal/kg per day in adults

For repletion aim for an additional 5kcal/kg

Question 29

Nitrogen losses

Answer 29

Surface: Skin/hair growth/sweat and secretions
UrineL urea, NH4+, creatinine
Feces

Catabolic states have increased N losses

Question 30

When protein needs increase

Answer 30

With catabolism assoc w SIRS
With tissue depletion in malnutrition

Intake ranges:

1. 3-1.5/kg with normal feeds (catabolic pts)
2. 9-2.2g/kg with high protein feeds (rehabilitation)

Question 31

Carbohydrates

Answer 31

Non-protein energy
Problems:
secondary lactose intolerance
osmolality/diarrhea
CO2 production
Has potential for respiratory failure and/or resp acidosis-- carb use should be limited

Question 32

Lipids

Answer 32

Non-prot E
Min requirement is small: 3-5% E
Potential Problems:
High plasma NEFA levels in catabolic pts.
Should limit to 20-30% of non-protein calories

Med-chain TGs are best- ease absorption/tissue consumption

long chain PUFAs have immune aspects

Question 33

n-6PUFAs

Answer 33

Linoleum acids
Create arachidonic acid metabs (PGs and LTs)–> inflammation and dysregulated immunity.

EPA from n-3FAs inhibit this production of PG and LT synthesis and cause less inflammation and improve immunity.

Question 34

n-3FAs

Answer 34

a-Linolenic acid
Creates EPA (in fish oil)
- can be converted to DHA
- can be broken down to 3-series PG and 5-Series LT by COX and 5-LOX respectively

EPA inhibits 2-series PG and 4-series LT production from n-6PUFAs which leads to less inflammation and improved immunity

Question 35

Increased vitamin and trace element requirements for catabolic patients

Answer 35

Thiamine, riboflavin and niacin: incr needs with incr metabolic rate

vits C, E, B6 and Se needed for increased antioxidant synthesis
- also riboflavin (cofactor for glutathione reeducates)

Trace elements needed: Fe, Cu, Mn, Zn

Question 36

Immunonutrition

Answer 36

Immunonutrients:

• AAs- glutamine, arginine, cysteine
• Antioxidants
• Fish oils (n-3 LC FAs)

Improved barrier fxn
Improved immune fxn
Decreased hyper inflammation
Improved wound healing

All improve clinical outcome