The guidelines for feeding critically ill humans are becoming less and less well defined (Preizer JC and van Zantem AR, Berger MM et al. Crit.Care 2015;19:35) (Maric PE, Rice TW AJRCCM2017;195:555-6). It is evident that critically ill patients demonstrate a tremendous catabolic and a moderate hypermetabolic milieu. There is, also, no doubt that this catabolism predisposes patients to myriad complications and poor outcome. The most significant problems are immune depression and muscular weakness. This muscular wasting and weakness arises from disuse atrophy, rapid catabolism and, the increasingly pervasive, critical illness neuro- myopathy(Plasma from septic shock opatients induces loss of muscle protein Crit. Care 2011:15:R233). These vulnerabilities ultimately lead to pneumo-sepsis (poor cough, swallowing, inspiratory muscle function and failure to wean from the ventilator), skin breakdown, wound infection, line and tube site infections and to long term immobility. These are the predominant processes leading to poor outcome or death.
It is also clear that, although fat is still well oxidized, carbohydrate is increasingly used, often purely for anaerobic glycolysis, with high lactate turnover. The route of feeding also seen to be clear. If the gut is available, enteral feeding should be started as soon as shock is adequately treated. The gut is dangerous when empty.
In a large study many years ago, John border (Ann. Surg 1987;206:427-448) demonstrated that neither complex antibiotics, complex surgical techniques nor an array of ventilator or circulatory support techniques altered outcome. Food intake was the only factor positively affecting outcome of his surgical patients. However, the questions of optimal quantity, protein, carbohydrate, fat and micro-nutrient substrate quality and balance continues to remain enigmatic.
In the recent Permit trial (Arabi et al. NEJM2015;372:2398-404), the provision of 60-70% of predicted caloric need did not reduce outcome in the critically compared to those receiving 80-100% of predicted caloric need. Secondary analysis of this trial also revealed that those patients receiving what was assumed to be optimal protein intake of 1.2-1.5 G/kg/day did not do any better than those receiving 0.8-1.0g/kg/d. The protein loss in the urine on day 1, was less in those receiving fewer amino acids, suggesting that the “optimal amount” initially suggested by Graham et al. was only producing expensive urine. This finding has also been demonstrated by the work of the group of van den Burgh (Casaer MP et al. Crit. Care 2013;187:247-55).
The physiological mechanism of autophagy seems to be an important mechanism that requires further clarification in both normal and the critically ill. This mechanism, by which cellular breakdown products are further digested and returned to the substrate pool, seems central to the optimal health of all cells and organelles. Autophagy is diminished by food intake, though which nutrient most fully diminishes this process is as yet unclear. Cell anabolism is determined by the size of the cell (Finn PJ et al. The Lancet1996;347:654-56) and it has long been known that branched chain amino-acids and glutamine are most active in enhancing cell size and, thus, anabolism. Insulin is also central to this anabolic and metabolic control as well as having an effect on inflammation. Whether the use of an enteral nutrition containing predominantly these amino acids, while avoiding excess calories and other substrates, perhaps supplemented by insulin or other adipokine hormones will be more effective in preventing muscle and immune breakdown in the critically ill is in need of urgent assessment.
Gwynne Jones has been an Intensive Care Specialist for the last 35 years. He has a special interest in the metabolic consequences of critical illness. He qualified in medicine from St. Mary’s hospital medical school, University of London in 1969. He completed his internal medicine residency in the UK with Fellowships in respiratory medicine in McMaster University, Canada and gastro-enterology in the Case Western University, Cleveland, Ohio, USA. He was a consultant physician in the NHS for 5 years before moving to Canada. Publications are related to Sepsis, pulmonary embolism and nutrition.