Optimal composition of intravenous lipids

The provision of energy from a lipid source is an essential component of any parenteral nutrition (PN) therapeutic regimen in the appropriate clinical setting. All available sources of intravenous lipid emulsions have a low osmolarity but they strongly differ in their immunologic effects and their effects on oxidative stress, liver injury and mitochondrial function. The ω-9/ω-6 lipid emulsion with its relative immuneneutrality and also the newer fish oil admixtures are lipid emulsions that can be used in most critically ill and non-critically ill patients. Despite extensive research and encouraging progress in the availability of such lipid emulsions, there is still need for a lipid emulsions that could be advantageous in patients with real hyperinflammation.

New developments in clinical practice guidelines

During the last four years revised clinical practice guidelines on nutritional support have been published by the major nutritional societies worldwide. The aim of these guidelines is to promote the safe and effective care of patients who need nutritional support as part of their overall management. All guidelines are based on the available “best evidence” in order to assist nutrition professionals in making decisions on the appropriate and cost-effective nutritional practices. Although such guidelines are a useful tool to patient management, they are meant to support, not replace, the clinical judgment and experience of nutrition professionals

Carbohydrates – Guidelines on Parenteral Nutrition, Chapter 5

The main role of carbohydrates in the human body is to provide energy. Carbohydrates should always be infused with PN (parenteral nutrition) in combination with amino acids and lipid emulsions to improve nitrogen balance. Glucose should be provided as a standard carbohydrate for PN, whereas the use of xylite is not generally recommended. Fructose solutions should not be used for PN. Approximately 60% of non-protein energy should be supplied as glucose with an intake of 3.0–3.5 g/kg body weight/day (2.1–2.4 mg/kg body weight/min). In patients with a high risk of hyperglycaemia (critically ill, diabetes, sepsis, or steroid therapy) an lower initial carbohydrate infusion rate of 1–2 g/kg body weight/day is recommended to achieve normoglycaemia. One should aim at reaching a blood glucose level of 80–110 mg/dL, and at least a glucose level <145 mg/dL should be achieved to reduce morbidity and mortality. Hyperglycaemia may require addition of an insulin infusion or a reduction (2.0–3.0 g/kg body weight/day) or even a temporary interruption of glucose infusion. Close monitoring of blood glucose levels is highly important

Energy expenditure and energy intake – Guidelines on Parenteral Nutrition, Chapter 3

The energy expenditure (24h total energy expenditure, TEE) of a healthy individual or a patient is a vital reference point for nutritional therapy to maintain body mass. TEE is usually determined by measuring resting energy expenditure (REE) by indirect calorimetry or by estimation with the help of formulae like the formula of Harris and Benedict with an accuracy of ±20%. Further components of TEE (PAL, DIT) are estimated afterwards. TEE in intensive care patients is generally only 0–7% higher than REE, due to a low PAL and lower DIT. While diseases, like particularly sepsis, trauma and burns, cause a clinically relevant increase in REE between 40–80%, in many diseases, TEE is not markedly different from REE. A standard formula should not be used in critically ill patients, since energy expenditure changes depending on the course and the severity of disease. A clinical deterioration due to shock, severe sepsis or septic shock may lead to a drop of REE to a level only slightly (20%) above the normal REE of a healthy subject. Predominantly immobile patients should receive an energy intake between 1.0–1.2 times the determined REE, while immobile malnourished patients should receive a stepwise increased intake of 1.1–1.3 times the REE over a longer period. Critically ill patients in the acute stage of disease should be supplied equal or lower to the current TEE, energy intake should be increased stepwise up to 1.2 times (or up to 1.5 times in malnourished patients) thereafter

Intensive medicine – Guidelines on Parenteral Nutrition, Chapter 14

In intensive care patients parenteral nutrition (PN) should not be carried out when adequate oral or enteral nutrition is possible. Critically ill patients without symptoms of malnutrition, who probably cannot be adequately nourished enterally for a period of <5 days, do not require full PN but should be given at least a basal supply of glucose. Critically ill patients should be nourished parenterally from the beginning of intensive care if they are unlikely to be adequately nourished orally or enterally even after 5–7 days. Critically ill and malnourished patients should, in addition to a possible partial enteral nutrition, be nourished parenterally. Energy supply should not be constant, but should be adapted to the stage, the disease has reached. Hyperalimentation should be avoided at an acute stage of disease in any case. Critically ill patients should be given, as PN, a mixture consisting of amino acids (between 0.8 and 1.5 g/kg/day), carbohydrates (around 60% of the non-protein energy) and fat (around 40% of the non-protein energy) as well as electrolytes and micronutrients

Prevention, diagnosis, therapy and follow-up care of sepsis: 1st revision of S-2k guidelines of the German Sepsis Society (Deutsche Sepsis-Gesellschaft e.V. (DSG)) and the German Interdisciplinary Association of Intensive Care and Emergency Medicine (Deutsche Interdisziplinäre Vereinigung für Intensiv- und Notfallmedizin (DIVI))

Practice guidelines are systematically developed statements and recommendations that assist the physicians and patients in making decisions about appropriate health care measures for specific clinical circumstances taking into account specific national health care structures. The 1st revision of the S-2k guideline of the German Sepsis Society in collaboration with 17 German medical scientific societies and one self-help group provides state-of-the-art information (results of controlled clinical trials and expert knowledge) on the effective and appropriate medical care (prevention, diagnosis, therapy and follow-up care) of critically ill patients with severe sepsis or septic shock. The guideline had been developed according to the “German Instrument for Methodological Guideline Appraisal” of the Association of the Scientific Medical Societies (AWMF). In view of the inevitable advancements in scientific knowledge and technical expertise, revisions, updates and amendments must be periodically initiated. The guideline recommendations may not be applied under all circumstances. It rests with the clinician to decide whether a certain recommendation should be adopted or not, taking into consideration the unique set of clinical facts presented in connection with each individual patient as well as the available resources

The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism

Increased intake of dietary carbohydrate that is fermented in the colon by the microbiota has been reported to decrease body weight, although the mechanism remains unclear. Here we use in vivo11C-acetate and PET-CT scanning to show that colonic acetate crosses the blood–brain barrier and is taken up by the brain. Intraperitoneal acetate results in appetite suppression and hypothalamic neuronal activation patterning. We also show that acetate administration is associated with activation of acetyl-CoA carboxylase and changes in the expression profiles of regulatory neuropeptides that favour appetite suppression. Furthermore, we demonstrate through 13C high-resolution magic-angle-spinning that 13C acetate from fermentation of 13C-labelled carbohydrate in the colon increases hypothalamic 13C acetate above baseline levels. Hypothalamic 13C acetate regionally increases the 13C labelling of the glutamate–glutamine and GABA neuroglial cycles, with hypothalamic 13C lactate reaching higher levels than the ‘remaining brain’. These observations suggest that acetate has a direct role in central appetite regulation

Incretins in patients with rheumatoid arthritis

Background: The precise mechanism linking systemic inflammation with insulin resistance (IR) in rheumatoid arthritis (RA) remains elusive. In the present study, we determined whether the incretin-insulin axis and incretin effect are disrupted in patients with RA and if they are related to the IR found in these patients. Methods: We conducted a cross-sectional study that encompassed 361 subjects without diabetes, 151 patients with RA, and 210 sex-matched control subjects. Insulin, C-peptide, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP), dipeptidyl peptidase 4 (DPP-4) soluble form, and IR indexes by homeostatic model assessment (HOMA2) were assessed. A multivariable analysis adjusted for IR-related factors was performed. Additionally, ten patients and ten control subjects underwent a 566-kcal meal test so that we could further study the postprandial differences of these molecules between patients and control subjects. Results: Insulin, C-peptide, and HOMA2-IR indexes were higher in patients than in control subjects. This was also the case for GLP-1 (0.49 ± 1.28 vs. 0.71 ± 0.22 ng/ml, p = 0.000) and GIP (0.37 ± 0.40 vs. 1.78 ± 0.51 ng/ml, p = 0.000). These differences remained significant after multivariable adjustment including glucocorticoid intake. Disease Activity Score in 28 joints with erythrocyte sedimentation rate (? coefficient 46, 95% CI 6?87, p = 0.026) and Clinical Disease Activity Index (? coefficient 7.74, 95% CI 1.29?14.20, p = 0.019) were associated with DPP-4 serum levels. GLP-1 positively correlated with ?-cell function (HOMA2 of ?-cell production calculated with C-peptide) in patients but not in control subjects (interaction p = 0.003). The meal test in patients with RA revealed a higher total and late response AUC for glucose response, a later maximal response of C-peptide, and a flatter curve in GIP response. Conclusions: The incretin-insulin axis, both during fasting and postprandial, is impaired in patients with RA.This work was supported by grants from the Spanish Ministry of Health, Subdirección General de Evaluación y Fomento de la Investigación, Plan Estatal de Investigación Científica y Técnica y de Innovación 2013–2016 Instituto de Salud Carlos III [ISCIII] PI14/00394) and by the Fondo Europeo de Desarrollo Regional (FEDER) (to IFA). The research of MAGG was supported by European Union FEDER funds and by the “Fondo de Investigación Sanitaria” (grants PI06/0024, PS09/00748, PI12/00060, and PI15/00525) of the Instituto de Salud Carlos III (ISCIII; Spanish Health Ministry). The research of MAGG was also partially supported by RETICS Programs RD12/0009 (RIER) and RD12/0009/0013 from the ISCIII (Spanish Health Ministry)