© Springer Nature Singapore Pte Ltd. 2017
Xiaobing Fu and Liangming Liu (eds.)Advanced Trauma and Surgery10.1007/978-981-10-2425-2_11Metabolic Changes and Nutrition Therapy in Burn Patients
(1)
State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Burn Injury, Southwest Hospital, Third Military Medical University, Chongqing, People’s Republic of China
Abstract
The metabolism pattern changes obviously after severe burn injury, the primary pathological phenomena are energy consumption and catabolism increased significantly, and nutrients utilize barriers. Severe burned patients will lead to autophagy metabolism, continuous consumption, and progressive emaciation. If the pathological process can not effectively block, it will lead to organ damage, immune dysfunction, wound healing delay and other adverse outcomes. Therefore, hypermetabolism after burn is one of the leading cause of multiple organ dysfunction and even death. After many years research, although there is certain understanding of hypermetabolism mechanism, but it is difficult to fully explain the causes of the hypermetabolism after burn, up to now. At the same time, the therapeutic measures of regulating hypermetabolism are still not perfect, and obstacle to burn comprehensive treatment level continuous progress.
Keywords
Metabolism patternCatabolismProgressive emaciationHypermetabolismThis chapter will introduce the mechanism of metabolic changes and the nutrition therapy strategy on severe burned patients. Focus on discussing the indication, dose, course of treatment, and supplement pathway of macronutrients and micronutrients.
1 Changes in Energy Metabolism After Burn Injury
Hypermetabolism after burn injury is characterized by increased metabolic rate, augmented protein metabolism, and energy consumption. Hypermetabolism reaction on severe burn patients could last several months even a few years. Previous studies have confirmed that the metabolic rates of burn patient maximum of up to 1.8 times the normal person [1]. With the development of the disease, the metabolic rate is gradually reduced, but the resting energy expenditure (REE) in the burn patient was still 10–20 % higher than that of the healthy people post burn 12 months [2].
There are two methods to detect the patient’s energy consumption, the indirect calorimetry and the energy consumption estimation formula. Indirect calorimetry is accurate but requires expensive instruments, and it is difficult to be popularized [3]. Therefore, there are many energy consumption estimation formulas used in burn clinical, but their common problem is more energy estimates than patient confirmed consumption [4, 5]. Assessment of the energy requirements is an ongoing process and modified according to the progress of the disease. No single formula can accurately assesses the true energy consumptions. Take the third military medical university (TMMU) formula as an example, although the formula is convenient and practical, it overestimates energy consumptions in severe burned patients. Our further investigation demonstrated that estimated values produced from the TMMU formula is more about 15, 23, and 40 % than measured REE values in patients with total body surface areas (TBSA) burned of 31–50, 51–70, and 71–100 %, respectively [6]. Other formulas have similar problems, they usually overestimate the caloric needs of burn patients when compared to metabolic expenditure requirements. The overestimation may be related to the progress in burn treatment since the formula was developed. Early wound closure, higher ambient temperature, improvements in infection control, and pain management all reduce the hypermetabolic response to the burn injury. it is now recognized that the value of energy consumption estimation on 1 % burn area should be decreased, from 25 to 10–15 kcal. As a result, lead the daily total energy consumption in severe burn patients from 3000–3500 kcal drop to 2500–3000 kcal.
The changes of energy metabolism on burned patients are complex and are regulated by many factors. Therefore, no formula can be estimated completely consistent patient’s energy consumption, and can only provide a rough range of energy consumption. Energy supply should be based on the specific conditions of the patient, in addition to considering the predicted energy consumption, the physician must also consider the patient’s metabolic capacity. In the early stage of burn, the energy demand is often lower than the energy consumption in patients with extensive burns.
2 Changes in Substance Metabolism After Burn Injury
After severe burn injury, pathophysiological conditions is complicated and highly related to material metabolism change significantly [7]. As a whole, glucose utilization disorders, gluconeogenesis increase, protein catabolism enhanced, and the anabolism is relatively lower, induce protein net release. Moreover, the long chain fatty acid transport is blocked, and fatty acid beta oxidation is partially inhibited. The metabolism pattern changes obviously after severe burn injury, the primary pathological phenomena is energy consumption and catabolism increased significantly [8].
2.1 Changes in Protein Metabolism
Daily nitrogen intake can be calculated from food tables, and fecal and exudate losses can be estimated using information derived from previous studies. If a normal individual consumes 12 g nitrogen in 75 g protein, he will excrete a similar amount, thus maintaining nitrogen equilibrium. Following injury, however, several factors occur which lead to a depletion of nitrogen. Nitrogen intake decreases and lose increases, resulting in a negative nitrogen balance [9]. The period of negative balance is called the catabolic phase. Its duration and the total loss of nitrogen are related to the severity of the trauma. In the burned patient the severity of the catabolic phase as well as its duration are related to the quantity of tissue destroyed and the degree of sepsis .
Therefore, skeletal muscle is the main source of fuel for burn patients, resulting in apparent lean body mass (LBM) lose for a long period after burn injury. This muscle decomposition has been shown in systemic and cross legged in nitrogen balance studies in which pronounced negative nitrogen balances sustained for 6 and 9 months after burn injury. Since skeletal muscle has been shown to be responsible for 80 % of glucose uptake into the systemic insulin stimulation, muscle mass decline may contribute to persistent insulin resistance after burn injury [10]. The relationship between hyperglycemia and muscle protein catabolism has also been supported by many studies, these researches showed that there are remarkable increased in proteolysis rates occurring without any alteration in either leucine oxidation or nonoxidative disposal, suggesting that hyperglycemia induced increased protein decomposition. This loss of protein is directly related to increases in metabolic rate and may persist up to 9 months after critical burn injury, often resulting in significantly negative whole-body and cross-leg nitrogen balances. These protein loss is directly related to an increase in metabolic rate, which may be sustained for up to 9 months after severe burns, often resulting in remarkably negative whole-body nitrogen balances. Daily nitrogen loss on severe burned patients could reach 20–25 g/m [2] TBSA, and if no effective treatment, lethal cachexia is imminent in less than 30 days [11].
Persistent proteolysis may also account for the delay in allografted skin growth, pressing immune functions. Eventually leading to the occurrence of various complications, such as sepsis. Patients with increase metabolic rates and protein catabolism up to 40 % of the same burned size who do not develop sepsis. Ensuing vicious circle, because patients who are more susceptible to sepsis since changes in immunity and immunologic response. The emergence of multi-resistant bacteria, leading to infections and sepsis-related death. Immunological cells, in response to burn infections , metabolize glucose anaerobically to pyruvate and lactate. These compounds are returned to the liver for gluconeogenesis, which produces recycled energy for use by immunocyte and fibroblasts in the burn wound.
2.2 Changes in Glucose Metabolism
Some studies have found that hepatic glucose synthesis disorder after burn injury, result in increasing the level of gluconeogenic hormones, for instance, catecholamine, glucagon, and cortisol. Further data indicate that there are notable disorder in major ATP consumption pathways such as increased protein turnover and urea production and gluconeogenesis. Hypermetabolic response after burn could lead to Glycolytic-gluconeogenetic cycling increased 250 % and triglyceride-fatty acid cycling raised 450 % [12]. All of these reactions could cause severe hyperglycemia and impair insulin sensitivity.
After burn injury, there was remarkably increased insulin level and fasting glucose and glucose clearance was significantly decreased. Glucose levels were increased by threefold, although glucose oxidation was restricted to glucose delivery to the peripheral tissues. Increased glucose production is aimed at burn wounds, in order to support the anaerobic metabolism of vascular endothelial cells, fibroblasts, and inflammatory cells . Lactic acid, the end product of glucose anaerobic oxidation, the cycle to the liver of the sugar production of different ways to produce more glucose. Serum glucose and insulin level were still significantly increased through the whole acute inpatient treatment. Insulin resistance appeared in the first week after the burn and continued at least until discharge.
2.3 Changes in Fat Metabolism
In addition to these changes of glucose and protein, fat metabolism is also significantly changed after burn injury. The total free fatty acid turnover and plasma glycerol concentrations are increased. Compared with control group, the change of plasma free fatty acid concentration was not obvious, but the glycerol concentration was elevated above normal for the first 20 days after burn injury [13]. Each intracellular triglyceride molecule, the hormone sensitive lipase promotes the release of a glycerol and three free fatty acids, whereas in muscle cells free fatty acids recovery may be responsible for the lack of increase in free fatty acids concentration. In spite of variable concentrations of free fatty acids, the free fatty acid flux is increased postburn [14]. The free fatty acids flux represents the futile cycle involving the breakdown of adipose and muscle triglyceride into free fatty acids, followed by reesterification into very low density lipoprotein and triglycerides in the liver, and eventually regenerating into adipocytes or muscle triglyceride. After burn injury, the rate of free fatty acids release far more than the required energy utilization, so that most of the free fatty acids is regenerating in liver and resecreted as very low density lipoprotein triglycerides. It appears that all parts of the regulator increase in trauma patients and may affect the effects of hormone sensitive lipase on the catecholamine.
3 Nutrition Therapy in Burn Patients
Nutrition therapy , also called nutrition supply therapy, is an important treatment method in the comprehensive management of severe burned patients. The aim of the nutrition therapy is to reduction in hypermetabolic response, maintenance cellular function, and improvement the prognosis.
3.1 Reasonable Energy Supplement in Burn Patients
The calorie of burn patient expenditure can be determined or estimated approximately by indirect calorimetry or energy expenditure equations. However, the energy expenditure is not entirely equal to energy requirement in the whole process of burn injury. The energy consumption is increased significantly, but the ability of nutrient absorption and anabolism is decreased remarkably in the early phase after burn injury, thus result in imbalance between energy demand and consumption. However, nutritional supplement as calculated according to energy consumption may lead to overfeeding. Supplement excessive nutrients can not be fully utilized, and it might aggravate metabolic disorder . Therefore, the nutrition administration should be lower than REE whether it is direct determination or by formula estimation. With the disease progresses, the internal environment gradually tends to be stable, ending in the balance between anabolism and catabolism. The amount of nutritional support should be increased gradually. During convalescence, anabolic metabolism outstrip catabolic metabolism, therefore the quantity of nutritional administration should be moderately higher than that of energy consumption. Therefore, in the whole treatment process, energy consumption and energy supplement may reach a balance point [15].
Assessment of the energy requirements is an ongoing process and modified according to the progress of the patient. There is no single formula accurately assesses the true energy needs and continued vigilance is required to prevent some complications induced by overfeeding or underfeeding. Assessment of nutritional supplement is divide into two distinct categories: the initial demand and continuous demand. The assessment of caloric require within the first 24 h is an initial goal so that nutrition support can be initiated. However, it should be necessary to make adjustments for the continue needs during the whole course of disease. The assessment of the energy demand need comprehensive of the following factors: Basal metabolic rate, Hypermetabolism, Percent of total body surface area (TBSA) burned, Ventilatory support, Infections, Sepsis, Multiple organ failure, Level of physical activity, Thermic effect of food. Many mathematical equations have been developed to estimate the energy demand of the burn patients. Avoidance of overfeeding minimizes the risks of hyperglycemia, fat accretion, and infections. However, most of the formulas overestimate the amount of calories required in burn patients. The overestimation may be related to the changes in burn care since the formula was developed. Early wound closure, higher ambient temperature, improvements in infection control, and pain management all reduce the hypermetabolic response to the burn injury [16]. it is now recognized that the daily total energy required in severe burn patients is from 2500 to 3000 kcal.
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