What is new in Metabolic and Nutritional care?

Annika Blaser (Luzern, Switzerland)

Updates covered: ESPEN guidelines, GI Bleed prophylaxis, Future studies in GI dysfunction

ESPEN Guidelines

Recent evidence suggests Early Full nutrition (any route) is harmful

  • In health, glucose infusion suppresses endog. glucose production
  • NOT seen in crit illness e.g. burns, sepsis, trauma, pancreatitis etc –> ongoing endog. glucose production and energy expenditure. Early Full feeding results in OVERFEEDING

Autophagy: Evolutionary stress response which removes damaged organelles and degrades pathogens

  • In catabolic state, cells may be more effective at autophagy and more resilient to various stressors
  • Autophagy and catabolism likely inevitable in critical illness; nutrition suppresses autophagy   –>> Don’t be too afraid of catabolism in early phase of acute illness

All pts on ICU >48hrs with critical illness are at risk of malnutrition

* EN increases splanchnic blood flow and O2 demand, which may not be met early on in critical illness despite additional O2 delivery –> risk mesenteric ischaemia in early full EN (vs PN)


a. No specific feeding recommendation for specific pt sub-groups

b. Focus on Not causing harm through overfeeding, refeeding, underfeeding or GI complications

c. Nutritional support cannot be individualised using only clinical diagnosis / pt demographics without considering changes and adaptation in metabolism (however no metabolic monitor available)


GI Bleed Prophylaxis

BMJ rapid recommendations triggered by SUP-ICU trial showing no benefit of stress ulcer prophylaxis in pts at risk

Multitude of risk factors for GI bleed in ICU pts incl. mech ventilation, coagulopathy, shock sepsis, renal / hepatic failure etc… Enteral nutrition is the ONLY protective factor


a. Restrict acid suppression to pts with >4% GIB risk

b. PPI preferable, H2 antagonist also acceptable, NOT sucralfate

* Suggested mortality risk with PPI in severe illness – needs exploring, future SUP may be even further restricted


GI Dysfunction in Critical Illness

Proposed 32 studies to facilitate overview of GI dysfunction and plan future research

Areas needing consensus:

  • EN intolerance
  • core set daily monitoring of GI function
  • core set outcomes
  • US protocol to assess GI function
  • descriptive definition of non-occlusive mesenteric ischaemia
  • reference methods to measure gastric emptying / nutrient absorption / barrier dysfunction

Session: How to evaluate body composition in fluid-resuscitated patients

Bioimpedance can make it

Julius Grunow  (Berlin, Germany)


BMI does not reflect body composition

Obesity paradox: Decreased mortality in overweight and obese patients contrary to decreased survival in general population (excluding the underweight and morbidly obese) – ? related to greater nutritional reserve

Low skeletal muscle mass is a risk factor for mortality in mechanically ventilated pts – as measured on CT (practical limitations for ICU pts)

Bioimpedance analysis (BIA) – bedside tool, radiation-free, reflects physician estimated hydrations levels quite well in prospective clinician-blinded study

Muscle mass at L3 level on a CT is highly reflective of whole body muscle mass. Assessing muscle mass from equations using BIA values vs. CT – Talluri and Janssen equations overestimate / Kyle equation underestimates

BIA cannot accurately / directly calculate muscle mass, however the values CORRELATE well – the consistency in this ‘relative inaccuracy’ may be useful

Phase angle (PhA) correlates well with muscle density = a good marker for muscle quality


Bioimpedance should certainly not be used

Sandra Stapel (Amsterdam, The Netherlands)


Body composition analysis can identify pts with nutrition risk, limited physiological reserve and predict adverse outcome (in low muscle mass)

Estimation of different body compartments using Population-specific predictive equations (combination of electrical and anthropomorphic data)

  1. Not valid in critical illness
  2. Accuracy depends on two prerequisites
  • accurate body weight (rarely available in ICU pts – often guess/estimate)
  • normal fluid distribution (almost always abnormal in inflammation and after fluid resuscitation)

Within 1st week ICU admission, phase angle (PhA) and reactance (Xc) both decrease as hydration increases

Potential applicability of BIA in ICU if

1) use weight / height-independent parameters e.g. PhA

2) measuring early in admission  (PhA on Day 1 predictive of 28-d mortality in critical illness and several other pt groups; PhA on Day 5 no longer predictive, likely due to fluid resuscitation)

Low PhA associated with 90-d mortality

Further research should focus on methods to correct BIA equations for fluid imbalance and effects of nutrition / exercise on PhA.


Phase angle to predict ICU outcome

Mette Berger (Lausanne, Switzerland)


Lean body mass determines outcome; fat – energy reserves, muscle – defence

Increased pectoralis muscle area on CT – significant increase in 6-mth survival, decreased hospital mortality, more ICU-free days

Measuring LBM:

  • DEXA – not practical
  • CT – at L3 (well-validated) – not practical, radiation
  • MRI – not feasible in ICU
  • US thigh – operator variability, training required
  • BIA – precise values, portable, quick and easy to perform

Main determinants of PhA

  • In health: age, gender, BMI
  • In disease states: malnutrition (Pre-albumin, subjective global assessment), inflammation (CRP, IL-6), fluid accumulation

Lower PhA in pts with advanced cancer undergoing palliative follow-up –> worse overall survival 

Lower PhA on admission in pts who later died during ICU stay (PhA in combination with APACHE II / SAPS II scores provide multi-variable composite score for 28-d mortality)

PhA improves in pts receiving beta-hydroxy-beta-methylbutyrate (metabolite of leucine) vs placebo


Critical illness: Increased muscle catabolism and lung production of glutamine

  • whole body production of essential and branched-chain amino acids almost doubles
  • ICU pts low / high SOFA scores – increased glutamine production but decreased plasma [glutamine]

Pts with higher SOFA scores have significantly lower PhA

Currently ICU severity scores not specific for metabolic state

  • PhA provides additional info reflecting cell viability and possibly protein metabolism (as seen in glutamine study)
  • Pick pts who will benefit from nutritional support


*Phase Angle = Superior prognostic marker + most precise screening tool for impaired nutritional and functional status currently available*

Metabolic challenges: Ketogenic diet in General ICU patients

Zudin Puthucheary (London, UK)

Muscle wasting is rapid in critical illness

Muscle protein synthesis

  • Impaired (same rate as fasted controls) from Day 1 of critical illness despite feeding
  • Recovery rate is variable
  • Highly energy-dependent process, uses 40-60% of energy in cell


ATP content in muscle falls on Day 1 of critical illness

  • more marked in pts with pre-existing illness
  • continues over first week despite adequate feeding

Glucose  –> Pyruvate –> Acetyl CoA –> ATP production and further ATP via e-transport chain (total ~38ATP)

In critical illness (hypoxia + inflammation)

  • Pyruvate diverted to lactate (Pasteur effect inhibition of pyruvate dehydrogenase kinase) – very inefficient form of fuel
  • Mitochondrial beta-oxidation of fatty acids blocked (normally excellent source of energy ~125ATP / gram) –> build-up of fat in muscle, cannot be used for energy production
  • Amino acids unlikely to be useful (no human data for this to date)

–>> So energy-dependent protein synthesis greatly limited

Ketone bodies (Acetoacetate, beta-Hydroxybutyrate) can bypass 1) Pasteur effect  (pyruvate diversion to lactate) and 2) block on beta-oxidation of fatty acids

–>> forms basis of Alternative Substrates In the Critically ill Subject (ASICS) trial NCT04101071 – currently recruiting

Muscle strength as a proxy for frailty

Hans Flaatten (Bergen, Norway)

Fried criteria for frailty

  • weight loss 5kg / 1yr
  • weak grip
  • poor endurance
  • slowness (of gait)
  • low activity

Time to perform 5x sit/stand from chair correlates with grip strength and walking speed

Strong correlation between multiple dimensions of frailty: Physical, Cognitive (processing speed / memory / exec function) and Quality of Life (social, housekeeping, finances etc)


  • decreased muscle mass and muscle quality
  • normal phenomenon in ageing, can be partly prevented with exercise
  • often coexists with frailty in elderly

Clinical Frailty Scale 

  • pictographic – can be applied to ICU pts
  • 3 non-frail classes
  • 1 transition group ‘Vulnerable’
  • 4 frail classes – moderate to severe
  • Terminally ill (may not appear frail / elderly)


Detecting Sarcopenia

  • questionnaires, screening tools (SARC-FG)
  • muscle strength (e.g. normogram for grip)
  • skeletal muscle mass / quality (DEXA, BIA, Lumbar L3 cross-sectional CT / MR)
  • physical performance (e.g. walking speed)
  • Ultrasound – easy to use but inter-operator variability, non-standardised examination/ reporting

Presence / extent of sarcopenia can be used to risk-stratify ICU pts, individualise post-op intervention e.g. early mobilisation, optimise nutritional support, use of sedation and opioids

Sarcopenia (CT-Lumbar L3 score + SNAQ score) as a predictor of ICU mortality

Interventions for management and prevention of sarcopenia in the critically ill: A systematic review

  • 22 studies; 2792 pts
  • 3 main intervention gps  (neuromuscular electrical stimulation ; exercise-based; nutritional)
  • wide variation in intervention with heterogeneous outcomes

–>> NMES + exercise MAY preserve muscle mass; nutritional alone not useful