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Head Injury: Metabolic, Nutritional, and Energy Considerations

  • Christine Charrueau
  • Béatrice Morio
  • Christophe Moinard
Chapter

Abstract

Head injury does not consist of the primary injury alone, it also includes secondary type injury. Although primary brain injury is irreversible, it is not necessarily the cause of death. Morbidity and mortality often result from secondary brain injury. Within the brain, head injury effects are mediated by deleterious neurotransmitters such as glutamate, reactive oxygen species (ROS), and inflammatory processes governed by complement and cellular immunity. These damaging processes result in cerebral edema, brain cell metabolic dysfunction, and ultimately cell death due to energy failure. At the systemic level, extensive adaptations immediately follow head injury. They include inflammatory cascade; increase in catabolic and counterregulatory hormones, such as catecholamines, glucagon, and cortisol; and alterations in the hypothalamic–pituitary feedback mechanism. The consequences are alterations in whole-body metabolism such as hypermetabolism, hypercatabolism, hyperglycemia, diminished immunocompetence, altered gastric functioning, and increased endothelial permeability. These metabolic disturbances (in particular protein wasting) lead to a dysimmunity, which compromises clinical outcome and thereby increases morbidity and mortality. So far little attention has been paid to nutritional intervention as a potential treatment of head injury. However, nutrition may have many interests, among which preventing the wasting syndrome, preserving the immune function, restoring the gastrointestinal function, and improving the neurological outcome. Despite promising experimental and clinical results, there are not yet sufficient clinical trials to make nutritional recommendations in head injury patients. Therefore, the development of large trials is mandatory to determine which nutrient, at which dose, would be the most appropriate to positively influence head injury patients’ outcome.

Key words: Head trauma, nutritional management, hypermetabolism, dysimmunity, resistance to renutrition

Keywords

Head Injury Enteral Nutrition Rest Metabolic Rate Glasgow Coma Scale Score Severe Head Injury 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

ATP

Adenosine triphosphate

DNA

Deoxyribonucleic acid

GCS

Glasgow coma scale

HI

Head injury

IED

Immune-enhancing diet

IGF-1

Insulin-like growth factor-1

IL1

Interleukin-1

IL6

Interleukin-6

IL8

Interleukin-8

IL10

Interleukin-10

RMR

Resting metabolic rate

RNA

Ribonucleic acid

ROS

Reactive oxygen species

Sir2α

Mammalian silent information regulator

TNFα

Tumor necrosis factor-α

3-MH

3-methylhistidine

Notes

Acknowledgments

The authors wish to thank Geneviève Arnaud-Vincent from the Paris Descartes University Language Center for proofreading the English version of this chapter.

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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Christine Charrueau
  • Béatrice Morio
  • Christophe Moinard
    • 1
  1. 1.Laboratoire de Biologie de la Nutrition EA 4466, Faculté des Sciences Pharmaceutiques et BiologiquesUniversité Paris DescartesParis Cedex 06France

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