Fig. 1
Phases of the response to injury
The ebb phase, also named acute phase, usually lasts 1–3 days. The clinical presentation of ebb phase is hypometabolism, decreased temperature, decreased energy expenditure and normal glucose production, but with insulin resistance, mild protein catabolism, increased blood glucose, increased catecholamines, increased glucocorticoids, decreased cardiac output, lowered total oxygen consumption, and vasoconstriction. All these metabolic changes would lead to muscle catabolism.
The ebb phase ends after adequate resuscitation and replaced by the flow phase. The metabolic response of the flow phase is characterized by high oxygen consumption, hypermetabolism, increased resting energy expenditure (REE), increased cardiac output, increased glucose production, profound protein catabolism, increased catecholamines, increased glucocorticoids, increased glucagon, increased potassium, and increased nitrogen losses. During this phase, four types of mechanisms regulate metabolic changes: the release of tissue factors, the synthesis of cytokines, endocrine changes and central nervous system functions.
3 Metabolic Response to Trauma
The typical metabolic response to trauma can be summarized in six points: increased energy expenditure, accelerated gluconeogenesis, increased lipolysis, increased water-sodium retention, increased nitrogen excretion as well as decreased muscle protein synthesis. The hypothalamus and the adrenergo-sympathetic system might play important roles in initiating these metabolic changes.
3.1 Increased Energy Expenditure
It has been shown that there is a moderate increase in the energy expenditure in patients after uncomplicated elective surgery. Only those patients with severe trauma, sepsis and burns would have a 50–100 % increase in energy expenditure. This increased energy demand can be met without problems by giving glucose and fat emulsions, but it may be necessary to measure the energy expenditure directly by indirect calorimetry in critically ill patients in order to prevent overloading of nutritional substrates, particularly in those with multiple organ failure (MOF).
3.2 Accelerated Gluconeogenesis
Hyperglycemia always follows injury. Hyperglycemia may be the result of rapid catecholamine-mediated mobilization of body carbohydrate stores in the early stage of trauma . The carbohydrate stores in the liver will last only 12–24 h without replenished. The body glucose requirement must be met with an increased hepatic production of glucose from protein precursors. While in the late stage, the hyperglycemia is always the result of an increased synthesis of glucose relative to an increased turnover rate. Injury and sepsis apparently do not impair the ability of the body to oxidize glucose, in turn, the glucose oxidation is actually increased in septic patients and gluconeogenesis cannot be suppressed even with intravenous glucose infusion. The study by Wilmore et al. [3] has demonstrated that wound is responsible for the increased glucose utilization instead of skeletal muscle.
3.3 Increased Lipolysis
The turnover rates of glycerol and free fatty acids are increased in postoperative patients, but the production of ketone bodies probably remains unchanged as skeletal muscle uses almost exclusively lipids as substrates.
3.4 Water-Sodium Retention
As is well known, trauma and sepsis would cause an increase in the muscle contents of water, sodium and chloride. Bergstrom et al. has revealed that, retained water is mainly distributed extracellularly in postoperative patients. Although potassium and magnesium are less affected, their concentrations in muscle are decreased after operation. And in the conditions of severe trauma and sepsis, these changes deteriorate more. For these reason, nutrition support may partly correct these water and electrolyte abnormalities.
3.5 Increased Nitrogen Excretion
Normally there is a balance between protein synthesis and breakdown, but the catabolic rate becomes much greater than synthetic rate in trauma patients. In most trauma patients, there is an increase in both synthesis and degradation. However, the enhancement of degradation is the more pronounced. As a result, the nitrogen balance becomes negative in the posttraumatic period. Skeletal muscle is the major source for the excreted nitrogen, leading to muscular fatigue and weakness. Therefore, it is very important to apply an appropriate nutrition formula to preserve the body proteins of the trauma patients. In addition to nutrition support, some adjuvant therapies such as insulin and growth hormone may also be necessary.
3.6 Decreased Muscle Protein Synthesis
O’Keefe et al. found that the total ribosome concentration per mg of deoxyribonucleic acid (DNA) and the proportion of polyribosomes decreased in postoperative patients, suggesting that the operative trauma would cause the decrease in ribosome utilization. The decrease in the concentration of polyribosomes is the same as that is observed during starvation, indicating that skeletal muscle is used as an important source of nutrients in trauma patients. Tissue analysis reveals a markedly decrease both in the activity of and the capacity for protein synthesis.
4 Nutrition Support in Trauma Patients
4.1 Rationale for Nutrition Support
Nutrition support is critical in the management of trauma patients. The rationale is 3-fold: First, to prevent acute protein malnutrition; Second, to modulate the immune response; Last, to promote gastrointestinal structure and function [4].
4.1.1 Prevent Acute Protein Malnutrition
Patients would always develop a systemic inflammatory response syndrome (SIRS), which resolves with recovery, after the initial traumatic insult. However, in the condition of patients with overwhelming SIRS, hypercatabolism would result in acute protein malnutrition and subsequent immune system impairment. This persistent hypercatabolism dominates the metabolic response to trauma . If exogenous amino acids were not supplied timely, the initial demand would be met by skeletal muscle proteolysis. Thereafter, there is depletion of visceral structural elements, as well as circulating proteins. The resultant acute protein malnutrition is associated with subclinical multiple organ dysfunction (MODS) .
4.1.2 Immune Response Modulation
SIRS, characterized by the localized and systemic production and release of multiple pro-inflammatory cytokines, is an acute condition following trauma. However, the traumatic insult also stimulates a parallel release of anti-inflammatory cytokines, called the compensatory anti-inflammatory response syndrome (CARS). Overwhelming CARS seems to be responsible for post-traumatic immunosuppression, leading to increased susceptibility to infections , sepsis and MODS . Compared to parenteral nutrition, the use of enteral nutrition has been shown to improve clinical outcomes, decreased infective complications and reduced the incidence of MOF in patients with SIRS and CARS. Previous studies to explain these effects suggest immunomodulatory effects of enteral nutrition on both the systemic and intestinal mucosal immune systems [5]. Our previous studies have also shown that early enteral nutrition could moderate the excessive immune response during the early stage in severe acute pancreatitis (SAP) patients [6]. The integrity of the intestinal epithelial and immune cells of the gut-associated lymphoid tissue and the intestinal barrier plays an important role in maintaining the intestinal homeostasis and preventing bacterial translocation. The intestinal epithelial cells (IEC)-derived cytokines secretion plays a major role both in maintaining intestinal mucosal functions and in the maturation and optimum functions of lymphocytes. While enteral nutrients play a major role in maintaining the integrity of IEC. As a result, enteral nutrition could modulate the intestinal mucosal immune systems.
4.1.3 Gastrointestinal Structure and Function Promotion
Gut dysfunction occurs in the majority of the critically ill patients. In trauma patients, gut dysfunction occurs for multiple reasons. First of all, trauma itself would cause an ischemia/reperfusion injury to the intestine. Subsequent therapies such as anesthesia and bowel manipulation would cause further injury to the intestine. Consequently, the dysfunctional gut becomes a reservoir for pathogens and leads to infection , sepsis as well as multiple organ failure (MOF). A series of animal studies have demonstrated that enteral nutrition could promote the protective effects of commensal bacteria, maintain the mass of gut-associated lymphoid tissue and preserve gastrointestinal mucosal structure and function [7–9]. Furthermore, clinical studies have shown these effects translate into better outcomes with respect to infection , organ failure and length of hospital stay [10, 11].
4.2 Route and Time of Nutrition Support
Despite the widespread use of nutrition in trauma patients, there still remains controversial in the aspect of the route and timing of nutrition support.
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