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Trace elements and vitamins, named together micronutrients (MNs), are essential for human metabolism. Recent research has shown the importance of MNs in common pathologies, with significant deficiencies impacting the outcome. This guideline aims to provide information for daily clinical nutrition practice regarding assessment of MN status, monitoring, and prescription. It proposes a consensus terminology, since many words are used imprecisely, resulting in confusion. This is particularly true for the words "deficiency", "repletion", "complement", and "supplement". The expert group attempted to apply the 2015 standard operating procedures (SOP) for ESPEN which focuses on disease. However, this approach could not be applied due to the multiple diseases requiring clinical nutrition resulting in one text for each MN, rather than for diseases. An extensive search of the literature was conducted in the databases Medline, PubMed, Cochrane, Google Scholar, and CINAHL. The search focused on physiological data, historical evidence (published before PubMed release in 1996), and observational and/or randomized trials. For each MN, the main functions, optimal analytical methods, impact of inflammation, potential toxicity, and provision during enteral or parenteral nutrition were addressed. The SOP wording was applied for strength of recommendations. There was a limited number of interventional trials, preventing meta-analysis and leading to a low level of evidence. The recommendations underwent a consensus process, which resulted in a percentage of agreement (%): strong consensus required of >90% of votes. Altogether the guideline proposes sets of recommendations for 26 MNs, resulting in 170 single recommendations. Critical MNs were identified with deficiencies being present in numerous acute and chronic diseases. Monitoring and management strategies are proposed. This guideline should enable addressing suboptimal and deficient status of a bundle of MNs in at-risk diseases. In particular, it offers practical advice on MN provision and monitoring during nutritional support.

With extended life expectancy, the older population is constantly increasing, and consequently, so too is the prevalence of age-related disorders. Sarcopenia, the pathological age-related loss of muscle mass and function; and malnutrition, the imbalance in nutrient intake and resultant energy production, are both commonly occurring conditions in old adults. Altered nutrition plays a crucial role in the onset of sarcopenia, and both these disorders are associated with detrimental consequences for patients (e.g., frailty, morbidity, and mortality) and society (e.g., healthcare costs). Importantly, sarcopenia and malnutrition also share critical molecular alterations, such as mitochondrial dysfunction, increased oxidative stress, and a chronic state of low grade and sterile inflammation, defined as inflammageing. Given the connection between malnutrition and sarcopenia, nutritional interventions capable of affecting mitochondrial health and correcting inflammageing are emerging as possible strategies to target sarcopenia. Here, we discuss mitochondrial dysfunction, oxidative stress, and inflammageing as key features leading to sarcopenia. Moreover, we examine the effects of some branched amino acids, omega-3 PUFA, and selected micronutrients on these pathways, and their potential role in modulating sarcopenia, warranting further clinical investigation.

Zusammenfassung: Hintergrund: Schwerbrandverletzte (mehr als 20% verbrannter Körperoberfläche bei Erwachsenen) weisen in der ersten Phase (8-48h) einen durch das massive Kapillarleck bedingten Verbrennungsschock auf, der einer Infusionstherapie bedarf, um die Hämodynamik wieder herzustellen. Bis in die 80erJahre stellte eine unzureichende Flüssigkeitstherapie (Unterinfusion) die Haupttodesursache von Verbrennungspatienten dar. Seither ist die übermäßige Flüssigkeitstherapie (Überinfusion) zu einer beachtenswerten Quelle von Komplikationen geworden: abdominales Kompartmentsyndrom, Entlastungsschnitte (Escharotomie), Verschlechterung des Gasaustauschs, Verlängerung der künstlichen Beatmung und des Spitalaufenthalts. Die Überinfusion hat Ende der 90erJahre begonnen, wo innerhalb der ersten 24h Flüssigkeitsmengen zugeführt wurden, die weit über den 4ml/kg/%BSA ("burn surface area") der Parkland-Formel lagen. Ziel: Dieser Beitrag analysiert die Faktoren, welche zu einer Überinfusion führen können und zeigt Möglichkeiten, dem durch eine strikte Kontrolle der präklinischen Infusionstherapie sowie durch eine permissive Hypovolämie vorzubeugen

The feeding of critically ill patients has recently become a controversial issue, as several studies have provided unexpected and contradictory results. Earlier beliefs regarding energy requirements in critical illness-especially during the initial phase-have been challenged. In the current review, we summarize existing evidence about fasting and the impact of early vs. late feeding on the sick organism's responses. The most important points are the non-nutritional advantages of using the intestine, and recognition that early endogenous energy production as an important player in the response must be integrated in the nutrient prescription. There is as of yet no bedside tool to monitor dynamics in metabolism and the magnitude of the endogenous energy production. Hence, an early "full-feeding strategy" exposes patients to involuntary overfeeding, due to the absence of an objective measure enabling the adjustment of the nutritional therapy. Suggestions for future research and clinical practice are proposed.

Critically ill patients depend on artificial nutrition for the maintenance of their metabolic functions and lean body mass, as well as for limiting underfeeding-related complications. Current guidelines recommend enteral nutrition (EN), possibly within the first 48 hours, as the best way to provide the nutrients and prevent infections. EN may be difficult to realize or may be contraindicated in some patients, such as those presenting anatomic intestinal continuity problems or splanchnic ischemia. A series of contradictory trials regarding the best route and timing for feeding have left the medical community with great uncertainty regarding the place of parenteral nutrition (PN) in critically ill patients. Many of the deleterious effects attributed to PN result from inadequate indications, or from overfeeding. The latter is due firstly to the easier delivery of nutrients by PN compared with EN increasing the risk of overfeeding, and secondly to the use of approximate energy targets, generally based on predictive equations: these equations are static and inaccurate in about 70% of patients. Such high uncertainty about requirements compromises attempts at conducting nutrition trials without indirect calorimetry support because the results cannot be trusted; indeed, both underfeeding and overfeeding are equally deleterious. An individualized therapy is required. A pragmatic approach to feeding is proposed: at first to attempt EN whenever and as early as possible, then to use indirect calorimetry if available, and to monitor delivery and response to feeding, and finally to consider the option of combining EN with PN in case of insufficient EN from day 4 onwards.

Major burns are characterized by an initial capillary leak, which requires fluid resuscitation for hemodynamic stabilization. While under resuscitation was the major cause of death until the 1980s, over resuscitation has become an important source of complications, including abdominal compartment syndrome, escharosis, impaired gas exchange with prolonged mechanical ventilation and hospital stay. Fluid over infusion started in the 1990s with an increasing proportion of the fluid delivered within the first 24 h being well above the 4 ml/kg/% burn surface area (BSA) according to the Parkland formula. The first alerts were published in the form of case reports of increased mortality due to abdominal compartment syndrome and respiratory failure. This paper analyses the causes of this fluid over infusion and the ways to prevent it, which include rationing prehospital fluid delivery, avoiding early administration of colloids and prevention by permissive hypovolemia.