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Rogobete, A.F.;  Grintescu, I.M.;  Bratu, T.;  Bedreag, O.H.;  Papurica, M.;  Crainiceanu, Z.;  Popovici, S.;  Sandesc, D. Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients. Encyclopedia. Available online: (accessed on 13 June 2024).
Rogobete AF,  Grintescu IM,  Bratu T,  Bedreag OH,  Papurica M,  Crainiceanu Z, et al. Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients. Encyclopedia. Available at: Accessed June 13, 2024.
Rogobete, Alexandru Florin, Ioana Marina Grintescu, Tiberiu Bratu, Ovidiu Horea Bedreag, Marius Papurica, Zorin Crainiceanu, Sonia-Elena Popovici, Dorel Sandesc. "Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients" Encyclopedia, (accessed June 13, 2024).
Rogobete, A.F.,  Grintescu, I.M.,  Bratu, T.,  Bedreag, O.H.,  Papurica, M.,  Crainiceanu, Z.,  Popovici, S., & Sandesc, D. (2022, July 08). Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients. In Encyclopedia.
Rogobete, Alexandru Florin, et al. "Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients." Encyclopedia. Web. 08 July, 2022.
Nutritional Imbalance in Mechanically Ventilated Multiple Trauma Patients

The critically ill polytrauma patient is characterized by a series of metabolic changes induced by inflammation, oxidative stress, sepsis, and primary trauma, as well as associated secondary injuries associated. Metabolic and nutritional dysfunction in the critically ill patient is a complex series of imbalances of biochemical and genetic pathways, as well as the interconnection between them. Therefore, the equation changes in comparison to other critical patients or to healthy individuals, in which cases, mathematical equations can be successfully used to predict the energy requirements. Recent studies have shown that indirect calorimetry is one of the most accurate methods for determining the energy requirements in intubated and mechanically ventilated patients. Current research is oriented towards an individualized therapy depending on the energy consumption (kcal/day) of each patient that also takes into account the clinical dynamics. By using indirect calorimetry, one can measure, in real time, both oxygen consumption and carbon dioxide production. Energy requirements (kcal/day) and the respiratory quotient (RQ) can be determined in real time by integrating these dynamic parameters into electronic algorithms. In this manner, nutritional therapy becomes personalized and caters to the patients’ individual needs, helping patients receive the energy substrates they need at each clinically specific time of treatment.

nutrition sepsis indirect calorimetry metabolism inflammation

1. Molecular and Pathophysiological Aspects of Metabolism

From a clinical point of view, the critically ill polytrauma patient is characterized by a series of primary traumatic injuries, as well as by a multitude of trauma-associated secondary injuries such as hemorrhagic shock, tissue hypoxia, generalized inflammation, oxidative stress, and infections. All of these subsequently lead to a multiple organ dysfunction syndrome (MODS) and to a significant increase in mortality rates [1][2][3][4][5].
From a molecular point of view, the above-mentioned events lead to the activation of a series of molecular systems and mechanisms, such as coagulation [6][7][8][9], complement [10], fibrinolysis, and an immense quantity of pro- and anti-inflammatory mediators released from macrophages, granulocytes, and lymphocytes [11][12][13][14][15][16]. Among these, the most researched are interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), interleukin 17 (IL-17), and tumor necrosis factor alpha (TNF-α) (Figure 1) [13][14][15][16].
Figure 1. The entire metabolic process in the critical patient and the correlation with continuous gas exchange monitoring (VO2 and VCO2).
Redox balance is significantly affected, with significant quantities of free radicals being released. In this case, the metabolic imbalance is strongly affected at a molecular level, with the free radicals being involved in a series of protein and lipid denaturation reactions [17][18][19][20]. Moreover, the redox protein and lipid denaturation reactions lead to the release of other reactive species, leading to augmentation of the pro-oxidative cascade [21][22].
An important aspect in the pathophysiology of critically ill polytrauma patients is represented by the negative nitrogen balance [23][24][25]. One of the main responses to severe injury is represented by the accentuation of protein catabolism and by the loss of urinary nitrogen and phosphorus. The process of nitrogen loss is very complex, and recent studies have shown that it correlates significantly with a change in metabolic rate, with a maximum peak a few days after the injury, and a gradual return to baseline after a few weeks. Hence, it has been concluded that if the mobilization of amino acids from metabolized proteins is not rapidly corrected through adequate and personalized nutrition, the consequences are dramatic, manifested through a rapid loss of muscular mass, and a very long and difficult recovery [26][27][28].
Regarding the metabolic answer to trauma, a series of articles described the following three phases of the event: the ebb phase, the catabolic phase, and the anabolic phase [29][30][31]. One very important aspect is the different biological and biochemical characteristics of each phase. From a clinical point of view, each of these phases needs a different therapeutic intervention from a nutritional viewpoint. From a clinical point of view, the ebb phase lasts for 12 h to 36 h, depending on the severity of the injuries, whereas the flow phase lasts between seven days and three weeks [32][33][34][35]. A therapeutic decision with high accuracy cannot be made without adequate monitoring of the metabolic changes and associated energy requirements.
From a biochemical, molecular, and cellular point of view in trauma, the researchers distinguish the ebb phase during the first 8 h to 24 h post-trauma, a phase characterized by important hemodynamic changes. From a clinical point of view, during this phase, volemic resuscitation through fluid and blood products is the basis of the therapy. Afterwards, during the next three days, patients are characterized by an aggressive production of cytokines and inflammatory molecules. During this phase, the metabolic disaster continues at a cellular level, with the redox imbalance being augmented and extensive. The last phase, described as an anabolic phase, is considered to be the one in which molecular and metabolic mechanisms are oriented towards recovery [32][36][37][38].
The existence of an inflammatory response without the clear presence of bacterial sources leads to an alarming activation of the immune system a short time after the traumatic event. These underlying signaling events are also called alarmines and influence the metabolic status of these patients considerably. The most researched endogenous signaling pathways responsible for the excessive augmentation of the immune response are represented by defensins, heat shock proteins (HSPs), cathelicidin, high-mobility group box 1 (HMGB1), and eosinophil-derived neurotoxin (EDN). Moreover, post-traumatic coagulopathy is responsible for a series of other side effects that lead to a metabolic imbalance [15][39][40][41][42].
In this manner, we can frame these molecular mechanisms in the so-called acute phase response, through which the liver’s protein synthesis is redistributed depending on the severity of trauma. In these situations, adapting the nutrition becomes an impossible task without adequate and correct monitoring of each individual patient.
Although enteral nutrition is recommended by the majority of clinical studies, it was concluded that in certain patients, the desired enteral nutrition cannot be ensured because of digestive intolerance. In the case of critically ill polytrauma patients, this aspect is present in the majority of the situations [43][44][45]. Fully enteral nutrition is impossible to achieve because of the intolerance manifested in the first three to five days post trauma. In this situation, parenteral nutrition should be applied. There are no clear guidelines regarding the exact time when the nutrition should be initiated and there have been important debates on the subject in the literature, but there are important differences between different guidelines on the topic in certain situations.
The European Society of Parenteral and Enteral Nutrition (ESPEN, recommends early initiation of enteral nutrition, in the first 24 h after admission to the ICU. On the other hand, The Canadian Society for Nutritional Science (CSCN, recommends initiation of enteral nutrition in the 24–48 h interval after admission to the ICU.
A critically ill polytrauma patient with sepsis also presents with changes, as well as specific interactions caused by plasmatic cholesterol and proteins. Recent studies have shown that hypercholesterolemia can be an important index for negative prognosis in these patients, especially because of the complex interactions that cholesterol has with protein fragments in plasma. Moreover, it has been noticed that hypercholesterolemia interfaces with the augmentation of the systemic inflammatory response [46]. Chiarla et al. conducted a study in order to identify correlations between plasmatic cholesterol levels and a series of metabolic changes in septic patients. Following this study, they reported that there are strong correlations between hypercholesterolemia and changes in the expression of amino acids in plasma [47].

2. Genetic and Epigenetic Expressions Associated with Hypermetabolism


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