Abstract

The results of recent large-scale clinical trials have led us to review our understanding of the metabolic response to stress and the most appropriate means of managing nutrition in critically ill patients. This review presents an update in this field, identifying and discussing a number of areas for which consensus has been reached and others where controversy remains and presenting areas for future research. We discuss optimal calorie and protein intake, the incidence and management of re-feeding syndrome, the role of gastric residual volume monitoring, the place of supplemental parenteral nutrition when enteral feeding is deemed insufficient, the role of indirect calorimetry, and potential indications for several pharmaconutrients.

Highlights

  • Nutritional support in the acutely ill is a complex subject

  • The role of inflammation in the metabolic response to stress has been recognized for a long time and is currently under increased scrutiny after the results of the trials from Leuven University [6,7], in which the magnitude of the inflammatory response was attenuated in patients who received intensive insulin therapy (IIT) [6] and increased in patients who received no parenteral nutrition during the first week of critical illness [7]

  • The expression of adhesion molecules on the endothelium was reduced as was the transcription of Preiser et al Critical Care (2015) 19:35 inducible nitric oxide (NO) synthase gene in the liver and muscle of patients randomly assigned to IIT [15]

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Summary

Introduction

Nutritional support in the acutely ill is a complex subject. Several recent studies have led to considerable changes in our understanding of the metabolic response to critical illness and of various aspects of nutritional management, including monitoring of the metabolic response and the determination of caloric, protein, and micronutrient requirements. The expression of adhesion molecules on the endothelium was reduced as was the transcription of Preiser et al Critical Care (2015) 19:35 inducible nitric oxide (NO) synthase gene in the liver and muscle of patients randomly assigned to IIT [15]. These effects in patients treated with IIT could be related to the anti-inflammatory effects of insulin or to an attenuation of the pro-inflammatory effects of hyperglycemia or both [16]. The available clinical data suggest that prevention of severe hyperglycemia may reduce cell damage; preventing hyperglycemia by using high doses of insulin, as required in cases of high intake of carbohydrates, can blunt the early inflammatory response

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