Appropriate nutrition is integral to patient care (Nestle Health Science sponsored session)

Smart nutrition not more nutrition

(Zudin A. Puthucheary)

Muscle wasting is common in critical illness, significantly greater in the sickest pts 

Intramuscular hypoxia in critical illness

  • unlikely to use glucose as fuel
  • fat can be used but decreased mitochondrial beta-oxidation leads to build up of fat within muscle
  • Increasing CHO / lipid delivery unlikely to be useful in acute critical illness

In ALL pts, ATP levels decreased in 1st week of critical illness, but chronic illness depletes ATP more quickly than in previously well individuals

ASICS trial: considers if ketogenesis can provide alternative substrate for energy

 

Altered protein homeostasis in critical illness: body attempts to increase anabolism but fails.  Can pts exercise to stimulate protein homeostasis? –> low tolerance for exercise during critical illness

 

Smarter use of protein is required

  • with continuous amino acid provision, protein synthesis drops off after 2 hours
  • not all proteins created equally – 10g leucine per 100g whey protein
  • no other amino acid stimulates muscle protein synthesis like leucine, but despite muscle growth, strength is not improved without exercise

 

In practice, cannot separate energy requirement from protein requirement

  • both are necessary
  • the ability of nutritional protein or calories to modulate muscle metabolism is likely to depend on quality and type of nutrition rather than quantity

 

Relevance of outcome measures: only 1% of trials since 2000 measure muscle function as a primary outcome – more trials needed which focus on functional outcome

 

Can nutrition be used to target mitochondrial dysfunction?

(Mervyn Singer)

Mitochondria are important

 

Lactate becomes important fuel source in critical illness – autocannibalism to feed other organs: is muscle wasting adaptive?

Long term Rodent model of critical illness (faecal peritonitis) – rats do not restore diurnal rhythm of metabolism by day 7

 

Strict blood glucose control using insulin- protects hepatocyte mitochondrial structure and function in critically ill pts

 

Fatty acids stimulate production of uncoupling protein –> more heat generated, but mitochondrial membrane potential decreases –> decreased ATP, decreased ROS generation

Oleic acid induces fatty acid oxidation and decreases organ dysfunction and mortality in experimental sepsis (raised IL-6 production in septic mice, but decreased upon addition of oleic acid)

Coenzyme Q10: No difference in clinical outcomes between ubiquinol (reduced Coenzyme Q10) and placebo in pts with severe sepsis / septic shock. No difference in vascular endothelial biomarkers, inflammatory biomarkers, or biomarkers related to mitochondrial injury.

Succinate: in septic rats, succinate increases mitochondrial oxygen consumption –> buildup of succinate during ischaemia causes reperfusion injury through mitochondrial ROS

Supplementing with antioxidants: if the pt is in MOF and damage has already been done, have we missed the boat?

  • Multiple means of modulating mitochondrial function via nutrition with no clear guide on what to do, but one-size-fits-all approach unlikely to benefit anyone

 

Update 2018 ESPEN guidelines

(Mette Berger)

Nutritional Risk Screening tool – quick scoring, screen within first 48 hours of admission

Exact timing of phases of critical illness is less important than the concept of Varying nutritional needs with each phase

  • If oral intake is not possible, early enteral nutrition (EN) is better than delayed EN
  • If EN / oral intake both not possible, implement PN within 3-7 days
  • If pt is very sick, the gut will be affected – don’t give full dose EN in septic shock pts –> risk of severe complications including vomiting, diarrhoea, bowel ischaemia, acute colonic pseudo-obstruction
  • Hypocaloric nutrition (not exceeding 70% energy expenditure) should be administered in early phase of acute illness

 

No strong evidence for high protein delivery – 1.3g protein / kg / day should be given progressively + physical activity may improve the beneficial effects

 

In healthy individuals, consuming breakfast will stop endogenous glucose production

  • this process carries on in sick pts, resulting in a protein loss of ~ 120g / day to generate 1200kcal /day

 

Slow progression in feeding may allow early detection of refeeding syndrome which can be treated

 

Increased protein delivery while decreasing carbohydrate loads

(Juan B. Ochoa)

 

Paradigm: Substitute for what the patient is unable to eat

  • but even 10% hyper caloric overfeeding will worsen outcomes in sick pt

 

No benefit to meeting caloric goals in the first 7 days, and in fact this will have undesirable consequences

 

Belief that 50% of caloric intake should be from carbohydrates is an outdated concept – it is a method of cheap food provision in 19th century prisons

  • regrettably most commercial formulae consist of mostly simple sugar, without complex CHO

 

Ideally use indirect calorimetry to estimate requirements; predictive equations tend to result in overfeeding

 

Protein delivery is affected by choice of feeding formula; hypocaloric high-protein nutrition is safe metabolically and clinically