Background. Nutritional support is an important part of the treatment of critically ill patients. However, there are no specific recommendations for patients in a long unconscious state after brain damage to determine their energy needs. Aim. To determine the role of indirect calorimetry in assessing the energy expenditure of patients in prolonged unconsciousness after brain damage. Methods. Prospective cohort study included 81 patients with brain damage who were treated in the intensive care unit. All patients with prolonged unconsciousness had stayed in the intensive care unit for more than 30 days. Mean age of patients was 48.4 16.3 years. Men were predominant (58%). Almost all patients had normal body mass index (BMI) (mean 22.8 6.2 kg/m2). The main cause of brain damage was severe traumatic injury (42%). There were also patients with consequences of subarachnoid hemorrhage (35%), stroke (19%) and hypoxic damage (4%). Results. According to indirect calorimetry, mean energy requirements in patients in prolonged unconsciousness was 25.12 8.8 kcal/kg/day (1595.3 560 kcal/day). Variability of this value was high in this sample (10.661.6 kcal/kg/day, 6733514 kcal/day). According to urine nitrogen loss, mean protein requirement was 0.83 0.46 g/kg/day that was lower than the recommended values for critically ill patients. Variability of data obtained by indirect calorimetry was higher than that of the calculated values despite statistically similar energy requirements of patients. Variability of data obtained by Harris-Benedict equation ranged from 15.4 kcal/kg/day (1023 kcal/day) to 37.3 kcal/kg/day (2065 kcal/day). There was no relationship between energy expenditure and causes of brain damage. Moreover, significant correlation between metabolic rate, urine nitrogen loss and outcomes of disease was also absent. Conclusion. Indirect calorimetry alone is not enough to prescribe optimal nutritional support in patients with prolonged unconsciousness if function of the gastrointestinal tract and other factors affecting energy expenditure are not considered.

Critically ill patients often develop hyperglycemia because of the metabolic response to trauma and stress. In response to any form of damage to the organism, it reacts by increasing its own glucose production which subsequently causes hyperglycemia. This adaptive reaction of the organism is directed to aid in the rapid restoration after the damage. Therefore, glucose is an indispensable substrate in the critically ill which aids the reparation process. Severe and persistent hyperglycemia is associated with unfavorable outcomes and is considered to be an independent predictor of in-hospital mortality. The discussion remains on whether hyperglycemia is just a marker of increased stress which makes it a surrogate indicator of disease severity or if it is the reason for the unfavorable outcome. A few years ago, several published articles suggested that a tight glycemic control within the normal range improves treatment outcome. Over time, researchers have changed their point of view and currently there is a discussion on this matter in the scientific literatures. At the same time, the question of what glycemic level should be maintained for patients in the Neurological Intensive Care Unit is a matter of discussion. In this review, the authors analyzed the latest guidelines on treatment of critical patients with neurosurgical and neurological pathologies, specifically the glycemic control in this category of patients.