Nutrition in Critically Ill Flashcards
Multifactorial cause of catabolic state in critically ill (5)
- Systemic inflammatory response
- Hypermetabolism
- Multiple organ dysfunction
- Infectious complications
- Malnutrition
Physiologic adaptation to starvation
Pathologic adaptation to starvation in critically ill patients
Physiologic metabolism to starvation
1. Lowering blood glucose to near 3 mmol/L
- Suppresses insulin secretion
- Fat hydrolysis -> FFA release
2. Use of FFA - conversion to ketone bodies
- Theoretically: 15kg of fat can last for 67 days
(9kcal each g = 135,000kcal total)
- Conservation of glucose to feed the brain
4. Prolonged starvation - gluconeogenesis from amino acids -> protein catabolism
Pathologic metabolism in critically ill
1. Adrenal axis and system inflammation promotes protein breakdown and insulin resistance
2. Insulin fails to control blood glucose level and muscle catabolism
3. Poor mobilisation of FFA due to adipose tissue poor perfusion
4. Increased energy expenditure from baseline
History and shift to nutritional therapy in critically ill
Over past 20 years, there is a sift away from NBM to nutrition support to currently nutrition therapy
Nutrition support - nutrition as fuel to support critical illness
Nutrition therapy - nutrition intervention to modulate immunologic and inflammatory response
Goals of nutrition therapy in critically ill
- Nutrition consistent with patient’s condition
- Prevent nutrient deficiencies
- Avoid complications related to delivering nutrition
- Improve patient outcomes
Assessment of nutritional status in critically ill
- Historically
- Current practice
Historically: albumin and anthropometric measurements
–> Highly inaccurate - acute phase reactant, fluid resuscitation altered the levels
Current practice: ASPEN and SCCM guidelines (2016)
- NUTRIC score or NRS-2002
- Early enteral nutrition beneficial to critically ill (within 48 hours)
Enteral or parenteral nutrition?
RCTs meta-analysis: no difference in survival
However: enteral feeding is preferred unless absolute contraindications (ischaemic or bowel obstruction)
Reasons:
1. Reduction in infectious complications
2. Significantly less expensive
3. Prevents gut bacterial translocation - NBM rapidly causes gut luminal mucosa atrophy
(even small trophic feeds increase blood flow to guy and preserve GI structures)
4. Strengthens gut-associated lymphoid tissue
5. Lesser side effects compared to PN
When should enteral nutrition be initiated in critically ill patients?
Early enteral nutrition - within 48 hours of ICU admission
- Bowel sounds and flatus may not necessary be present for EN initiation
- Once resuscitated and haemodynamically stable with static or reducing vasopressors (no longer in shock)
(complications of ischaemic bowel due to EN in critically ill patients in shock) - Watch for feeding intolerance - abdominal distention, vomiting
RCTs meta-analysis:
1. Early EN reduces mortality and reduces infectious complications
2. Early EN does not affect duration of ventilation or ICU length of stay
NUTRIC Score
Quantify risk of critically ill patients developing adverse events that MAY BE MODIFIED by aggressive nutrition therapy
Comprises of:
- Age
- APACHE II score
- SOFA score
- Comorbids
- Days from hospital to ICU admission
- IL-6 levels
0-4 (0-5 with IL6): low score - low malnutrition risk
5-9 (6-10 with IL6): high score - worse outcome in mortality and ventilation, will benefit from aggressive nutrition therapy
How many calories should critically ill patients receive?
How to estimate energy expenditure?
Varies, and optimal calorie in unclear
Standard practice:
- Calories: 25-30 kcal/kg IBW
- Proteins: 1-1.2 g/kg per day IBW
(modified in severely obese - lower calories, more proteins)
Escalation:
Start within 48 hours of ICU admission
Acute phase - 70% TEE (hypocaloric)
Gradually increase to 100%
Methods of estimation
1. Indirect calorimetry - total energy expenditure (TEE)
2. Resting energy expenditure, multiplied by stress factor 1 to 2 -> estimate TEE
3. Equations: Harris-Benedict, Ireton-Jones, Weir
Composition of enteral nutrition in critically ill
A. Protein: 1-1.2 g/kg ABW (2-2.5g/kg IBW)
- More protein instead of total calories is associated with improved outcome
- Whole protein recommended instead of peptide based formula
B. Fat: 25-50% of calories
- Insufficient evidence on high fat or low fat feeding
C. Calories: 25-30 kcal/kg IBW
Choice of formulas
1. Arginine based - surgery, trauma (contraindicated in sepsis - increases mortality)
2. Anti-oxidants (Vit C, E) and minerals (selenium, zinc, copper) - burns, trauma, mechanical ventilation
3. Glutamine - RCTs no benefit, PN glutamine harmful -> avoided
4. Omega-3 FA - conflicting evidence
5. Low phosphate and potassium - CKD
Should critically ill patients in shock and/or receiving vasopressors receive enteral nutrition?
No.
Criteria to initiation of enteral feeding
1. Stabilised shock, adequately resuscitated
2. Stable or reducing vasopressors
3. Downtrending lactate
High risk of ischaemic bowel in critically ill patient in shock
Continuous or bolus enteral nutrition?
Continuous feeding preferred
(One pseudorandom study - aggressive early EN via bolus feeding harmful)
Continuous: small volume continuously over 24 hour period
Bolus: large volume over short period
Monitoring of enteral feeding tolerance
- Abdomen distention
- Bowel output
- Vomiting
- Pain (or haemodynamics)
- +/- gastric residual (aspirate) volume (GRV)
New guidelines: aspirate volume checks provide no clinical benefit
Positioning of patient during enteral feeding
Semi-recumbent (30-45 degree)
Evidence: conflicting results
1. Drakulovic 1999: significant reduction in pneumonia in semi-recumbent
2. Nieuwenhoven 2006: no statistical significance
Define high gastric output
Motility agents in critically ill
High gastric output > 500mL after 6 hours OR vomiting
- Start prokinetics
- Pause EN, restart at half rate
- If intolerance persists, KIV nasojejunal tube
- Attempt EN up to 7 days
Choice of motility agents
1. Metoclopramide 10mg Q8H
2. Erythromycin
3. Emerging: PO naloxone
(reverses side effects of opioid narcotics on GI tract - allows higher EN volume, reduced GRVs, reduce ventilator associated pneumonia)
