Introduction: Severe brain injury, either from trauma or stroke, induces a hypermetabolic (increased energy expenditure and oxygen consumption) and hypercatabolic (increased protein degradation) response. This hypermetabolic response lasts for 5-12 days and generally resolves thereafter, unless persistent seizure activity, decerebrate posturing, corticosteroid administration or infectious complications occur.
The pathophysiological mechanisms of this hypermetabolic response are poorly defined. Primary mediators are the catecholamines, glucocorticoids, glucagon and cytokines. Circulating insulin levels are elevated but tissue responsiveness is blunted by the counterregulatory hormones . In contrast to starvation, the metabolically stressed patient continues to catabolize muscle protein to provide substrate for gluconeogenesis. Adipose tissue is mobilized at an accelerated rate, with free fatty acids providing fuel for liver and skeletal muscle [2-5].
A concomitant increase in nitrogen excretion reflects the breakdown and mobilization of amino acids from skeletal muscle to meet increased demands for tissue fuel and synthesis of acute phase proteins. If no nutrition is provided or no metabolic adaptation occurs a progressive erosion of lean body mass and circulating proteins, the protein potential, will be the result. Loss of body weight of 15% is accompanied by protein loss of 20% and results in significant impairment of vital organ mass and function.
Besides this state of autocannibalism, most patients with acute neurological pathology develop an acute phase response (fever with/without infection, increase of acute-phase proteins), immunological dysfunction, altered gastric function and are initially at risk for hyperglycaemia [6, 7]. Nutrient administration alone cannot completely override the metabolic response to severe brain injury.
By exception some patients may present with decreased energy expenditure (e.g. associated quadriplegia, paraplegia, etc.) although urinary nitrogen loss remains increased.
The goals for nutritional support in comatose patients are:
a. to minimize the deleterious effects of the early and sometimes ongoing hypermetabolic and hypercatabolic phase;
b. to support the body defence mechanisms;
c. to create an optimal'milieu' for the recovery of the nervous system.
Nutritional assessment and requirements: Comatose patients admitted to the neurological critical care unit are generally of two types. A first group of previously healthy individuals admitted without any nutritional deficit but with an acute neurological injury. The second group includes individuals who have had previously an impaired macro- or micronutrient intake or utilization (e.g. neurodegenerative disease, brain tumours) or increased nutritional demands (alcohol, drug abuse, etc.). The last group will often present with some degree of protein-calorie malnutrition and eventually vitamin or trace element deficiency. Anthropometric parameters and laboratory data for nutritional assessment are rarely of any use in acute critical illness, because many interfering factors affect their validity.
Caloric requirements: These should ideally be determined by means of indirect calorimetry (IC) [8, 9]. The respiratory quotient (R = VCO2/VO2 or carbon dioxide production in ml min−1/oxygen consumption in ml min−1) gives important information of the quality of nutritional support (RQ < 0.7 = inadequate feeding; RQ > 1 = overfeeding; RQ ∼ 0.8-0.9 = adequate feeding). If IC is not available the Harris Benedict formula (see below) can be used to calculate the patient's basal energy expenditure (BEE). To estimate the total caloric requirements, BEE has to be multiplied by a factor (on average 1.4-1.6) accounting for the stress of critical illness. Hypermetabolic comatose patients may need up to 2.0 × BEE. The third and worse possibility is to estimate caloric needs based on weight alone (35-40 kcal kg−1 bodyweight). Patients with persistent motor posturing may need up to 50 kcal kg−1. Patient with spinal cord injuries or disease have been shown to have lower energy requirements because of reduced metabolic activity of denervated muscle.
Many factors may either increase (fever, seizure activity, steroid administration) or decrease (barbiturate coma, sedative drugs, beta-blockers) caloric requirements, by influencing cerebral and total body cellular metabolic demands.
Protein requirements: These can be deducted from nitrogen balance studies in patients with stable renal function. Metabolically stressed patients often require a minimum of 1.2 g kg−1 body weight protein (or amino acids). Starting with 1.2-1.5 g kg−1 body weight as a goal will be safe. If nitrogen excretion exceeds the 2.5 g kg−1 protein equivalent, further increase of protein administration only increases ureagenesis. Again patients with denervation of skeletal muscle will have an obligatory phase of negative nitrogen balances due to muscle atrophy. Protein requirements can also be calculated from the ratio calories to nitrogen (mild stress = 150 kcal:1 g nitrogen to severe stress= 100 kcal:1 g nitrogen).
Provision of nutrition: enteral or parenteral?: Practically there is no real controversy between the enteral or parenteral route of feeding, they are complementary. Comatose patients with severe malnutrition (loss of > 5% of usual bodyweight) should have immediate nutritional support after hemodynamic stabilization, while in patients with normal nutritional status a period of 5-7 days without any vigorous efforts to achieve the appropriate goals is acceptable.
Oral feeding is rarely applicable to comatose patients. Early enteral (EN) nutrition through a nasoduodenal or nasojejunal tube will overcome the problem of delayed gastric emptying. Patients requiring enteral feeding on a long-term basis should have a gastrostomy or gastrojejunostomy tube placed . Percutaneous endoscopic methods are preferable in intensive care patients. Isotonic enteral formulas are recommended for post-pyloric feeding. Continuous pump-assisted administration is best tolerated.
Parenteral nutrition (PN) is indicated when a patient's gastrointestinal tract does not tolerate full enteral feeding or when the access to the GI tract is difficult after head and neck trauma. Parenteral nutrition may be administered as central venous nutrition(expected duration of PN > 7 days) or as peripheral venous nutrition (short-term PN < 7 days). Hyperglycaemia has to be avoided specifically after acute brain injury. Gradual build-up of the EN and/or PN and regular glycaemia controls are advocated. Fluid and electrolyte balances should be carefully monitored and corrected. Several approaches of nutritional modification (glutamine, arginine, omega 3 fatty acids, etc.) to optimize the 'milieu' for recovery of the nervous system, need further investigation before introduction to the clinical arena.
Ethical and legal considerations in nutrition support of comatose patients: Ethical issues in the use of nutrition support in the comatose patient include justification for the decision to withhold or withdraw treatment and the principle of equality of access to the treatment. Parenteral and enteral nutrition are to be considered as a mode of medical treatment. If the imposed burdens are greater than the anticipated benefits, nutrition support may be discontinued in accordance with the principles and practices of governing the withholding and withdrawing of other forms of medical treatment .
Four objections are commonly encountered as moral constraints on withholding or withdrawing nutrition support. The health-care providers perceive it as an obligation:
a. to provide ordinary versus extraordinary care;
b. to continue treatment once started;
c. to avoid causing death;
d. to provide symbolically significant treatment.
The obligation to promote the good of the patient is a basic professional duty of the health-care provider. This obligation underlies the requirement to evaluate the benefit and burdens of a treatment from the patient's perspective. If from the incapacitated patient's perspective the burden of a treatment outweighs the benefits it is ethically permissible to withhold the treatment. The treatment should be provided when, from the patient's perspective the benefits outweigh the burdens. When it is unclear whether the benefits or burdens are greater than it is advisable to continue treatment as a time-limited trial.
Harris-Benedict equation to estimate Basal Energy Expenditure (BEE): Equation 1 where W = weight (kg); H = height (cm); A = age (years)
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The publication of this supplement has been supported by an eductional grant from Abbott Pharmaceuticals
Session I: Update on neurological ICU disorders