Nutrition of the Burned Patient and Treatment of the Hypermetabolic Response
Advances in therapy strategies, based on improved understanding of resuscitation, enhanced wound coverage, more appropriate infection control, and improved treatment of inhalation injury, improved the clinical outcome of burn patients over the past years
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Nutrition of the Burned Patient and Treatment of the Hypermetabolic Response Marc G. Jeschke
7.1
Introduction
Advances in therapy strategies, based on improved understanding of resuscitation, enhanced wound coverage, more appropriate infection control, and improved treatment of inhalation injury, improved the clinical outcome of burn patients over the past years [1, 2]. However, severe burns remain a devastating injury affecting nearly every organ system and leading to significant morbidity and mortality [2]. One of the main contributors to adverse outcome of this patient population is the profound stress-induced hypermetabolic response, associated with severe alteration in glucose, lipid, and amino acid metabolism [1, 3–5] (Fig. 7.1).
M.G. Jeschke, MD, PhD, FACS, FCCM, FRCS(C) Division of Plastic Surgery, Department of Surgery and Immunology, Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute, University of Toronto, Rm D704, Bayview Ave. 2075, M4N 3M5, Toronto, ON, Canada e-mail: [email protected] M.G. Jeschke et al. (eds.), Burn Care and Treatment, DOI 10.1007/978-3-7091-1133-8_7, © Springer-Verlag Wien 2013
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Burn Wound
↑↑Oxygen Consumption
↑↑20-fold Catecholamines
Heart
Serum
Intestine Alanine
Ammonia
↑↑Glucagon ↑↑Cardiac Output ↑↑Heart Rate
↑↑Cortisol ↑↓Insulin
Glutamine
Glutamine Nitrogen ↑↑ Wasting
Kidney Ammonia
Liver
Alanine
Urea Fat
Glycogen Stores
Glucose Glycolysis
↑↑Fatty Acids ↑↑Glycerol
Glutamine
Ammonia Muscle Glucose
Glucose
Lactate Glycolysis
Lactate
Pyruvate Lipid Complexes
Pyruvate ↑↑Lactate
Fig. 7.1 Complexity of the post-burn hypermetabolic response. From Williams FN JACS 2009 April 208(4):489–502
7.2
Post-Burn Hypermetabolism
A hallmark for severely burned patients is the hypermetabolic response that is not only very profound but also extremely complex and most likely induced by stress and inflammation [1, 3–5]. The cause of this response is not entirely defined, but it has been suggested that sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are involved in initiating the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state [6–15]. In addition, cytokines, endotoxin, neutrophil-adherence complexes, reactive oxygen species, nitric oxide, and coagulation as well as complement cascades have also been implicated in regulating this response to burn injury [16]. Once these cascades are initiated, their mediators and by-products appear to stimulate the persistent and increased metabolic rate associated with altered glucose, lipid, and amino acid metabolism seen after severe burn injury [17] (Fig. 7.1). The metabolic changes post-burn occur in two distinct patterns of metabolic regulation following injury [18]: 1. The first phase occurs within the first 48 h of injury and has classically been called the “ebb phase” [18, 19], characterized by decreases in cardiac output,
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Nutrition and Hypermetabolic Response Post-Burn
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