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)

Summary:

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)

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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

Recommend:

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

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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

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