optimal Safe Nutrition in Intensive care Richard D Griffiths School of Clinical Science, University of Liverpool, and Intensive Care Unit, Whiston Hospital, Merseyside, UK Email: rdg@liverpool.ac.kr Optimal Nutrition General malnutrition or a specific nutrient deficiency has profound effects on outcome and death. Outcome measured by morbidity (such as infection or wound healing) and death are all increased in the ICU patient who is severely malnourished on admission [1] and even in patients with multiple organ failure the survival curves start to diverge after 20-30 days [2] indicating that outcome should be measured over a longer time frame (e.g six months). Furthermore an increasing nutrition deficit during a long ICU stay is associated with increased morbidity [3]. Why might nutrition be so important to the critically ill patient? The traumatic or septic stressed ICU patient is characterised by increased substrate turnover of carbohydrates, lipids and amino acids, altered inter organ flux coupled with peripheral insulin resistance. This process linked to inflammation has many features similar to the cytokine signaling of metabolic syndrome of obesity and its role in type 2 diabetes. Optimising the particular increased substrate requirements and over coming insulin resistance is considered central to affect outcome. The landmark Leuven study improved outcome with tight glycaemic control on the background of an intensive nutrition programme [4]. Recognising the altered and sometimes increased metabolic requirements is central to understanding why nutrition becomes so important. All the processes of inflammation, cell maintenance, healing and repair are dependent on substrate provision that can come from mobilising limited stores or degrading existing structures in the absence of external provision. The myriad of lipid inflammatory mediators for instance are in part dependent on the character and potency of the long chain lipids previously ingested and incorporated into existing cell membranes. Therefore even the content of prior nutritional intake may affect the disease state. The provision of new lipid mixtures that perhaps better reflect substrate demands of our 10,000 year old genome is an exciting area of disease modification and nutritional genomics. The catabolism of structural proteins occurs specifically to mobilize important amino acids to meet these altered requirements and occurs, unlike in starvation, with increased protein synthetic demands in many tissues particularly the immune system, liver and those involved in healing. The increased demand for glucose and glutamine for instance must come from protein breakdown and the huge increase in skeletal muscle catabolism is the most evident. Nutrient provision is therefore struggling merely to keep pace with consumption and limit endogenous loss. With protein synthesis already stimulated amino acid and insulin provision has little ability to stimulate further and therefore there is on opportunity to catch up for missed feeding as in health and starvation? Consistency of nutrient delivery in this situation appears the most optimal and starting as soon as practical and continued for as longer as needed is important to give enough but not too much. Is enteral nutrition always best? Routes of delivery that can safely use the gastrointestinal tract will maintain intestinal organ function and the gut associated immunity. Studies of enteral nutrition (EN) consistently show in the less ill patients a reduced infectious morbidity compared with using parenteral nutrition (PN). Not delaying the start of enteral feeding in many patients appears advantageous but the overall risk and benefit is dictated by the presence of GI dysfunction which not only limits enteral nutrition delivery but increases morbidity and mortality of EN. However giving a patient only parenteral nutrition when the GI tract is completely functional prevents them from obtaining the advantages of enteral nutrition and at the same time exposes them to the risks of PN. Making an either or decision over EN or PN ignores the variability in GI dysfunction that occurs and ignores the metabolic requirement to delivery enough but not too much of the appropriate nutrients. Evidence shows that EN invariably results in underfeeding while PN carries the risk of overfeeding. The former often does not matter in the majority of well nourished patients in the short term but in the malnourished patient underfeeding may impact on survival over a long ICU stay. Overfeeding also must be avoided since it will only exacerbate the complications of the ICU form of metabolic syndrome and further increase insulin demand. Is there any evidence that following good nutrition practice will improve outcome? A 14 hospital cluster study from Canada, the ACCEPT study, showed that survival from intensive care was improved when an evidence based guideline for nutrition was followed and more nutrition was delivered more consistently. This was achieved by earlier introduction and more complete enteral nutrition delivery without any decline in the use of PN alone or in supplementation [5].