Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.173625
Source of Support: None, Conflict of Interest: None
Adequate nutritional therapy is essential for recovery from critical illness. Nutritional requirement varies in different patients and varies daily in a single patient. Both under and over feeding are associated with complications. Besides this, not all patients behave in a similar way to nutritional therapy. Appropriate nutritional therapy requires identification of patients “at nutritional risk” and providing aggressive nutritional support to them. The current article deals with nutritional support in critical illness with special emphasis on neurocritical care patients.
Keywords: Nutrition; nutritional risk; overfeeding; stress response; underfeeding
Nutritional support in critically ill patients is a complex issue and field of ongoing research. Nutritional requirement depends upon multiple factors including the patient's baseline nutritional status, severity of illness, temporal progression of illness, use of mechanical ventilation, use of sedatives/hypnotics, etc. Therefore 'one size does not fit all' and the nutritional support should be tailored according to the needs of individual patients.
Any patient who experiences insult in the form of surgery, trauma or critical illness shows certain metabolic and hormonal changes termed as stress response. The stress response to an insult evolves temporally with each phase manifesting changing needs. Researchers have attempted to classify metabolic response to insult into various stages. These stages also help in identifying changing nutritional needs of critically ill patient. Metabolic response to surgical stress was first described by Cuthberston in 1932. He classified the metabolic response into the early 'ebb' phase with decreased metabolic activity and oxygen consumption, followed by the 'flow' phase with exaggerated metabolic rate. The ebb phase is of limited clinical relevance due to its short duration (mostly <12 hrs). It is followed by a phase of hypercatabolism which requires appropriate nutritional support. These phases have been redefined. Recently Aller et al., attempted to classify the metabolic response to severe injury (surgical or accidental) into three phenotypes namely ischemic-reperfusion, leukocytic and angiogenic.,
By and large, the phased metabolic/inflammatory response to an insult can be divided into acute, chronic and recovery phases. Acute phase occurs immediately after the insult and lasts for hours to days during which the patient admitted in a modern intensive care unit (ICU) undergoes resuscitation and initial management. This phase is characterized by a surge in the inflammatory mediators and sympathetic nervous system activation [Figure 1]. In evolutionary terms, the metabolic response during the acute phase helps to maintain adequate supply of glucose to the vital organs via catabolism of the stored body fuels.
The acute phase is followed by the chronic phase during which patient becomes prone to secondary infections and other complications. The chronic phase is followed by the recovery phase which represents systemic rehabilitation and recovery of physical function.
In the authors' opinion, these demarcations proposed in the literature are “grey zones” as it is difficult to define the transition from one phase to another. A patient in chronic phase may go back to the acute phase if there is new onset hospital acquired infection. The best approach is to individualise one's therapy according to the individual patient's needs.
Nutrition is an easily neglected domain in a clinical setting. Frequently, other pressing issues like maintenance of hemodynamic parameters and optimization of metabolic milieu take precedence over nutritional support and monitoring. Research in the field of nutrition has highlighted the negative effects of both under and overfeeding.
Consequences of underfeeding
Over past two decades, numerous studies have reported worsening of outcome with increasing energy deficit., Malnutrition is associated with loss of lean body mass, poor wound healing, impaired immune function, poor diaphragmatic strength, increased risk of hospital acquired infection and organ dysfunction.
Badjatia et al., studied energy balance in 57 poor grade subarachnoid haemorrhage patients (SAH). They reported underfeeding (14 ± 5 kcal/kg/day) with a cumulative energy deficit of -117 ± 53 kcal/kg over the first 7 days. Negative energy balance was associated with increased infectious complications (P < 0.001). Another study on 229 SAH patients by the same author reported that older age, higher Hunt and Hess grade, lower caloric intake, and negative nitrogen balance were good predictors of the time required to develop the first hospital acquired infection.
Alberda et al., collected data on the nutritional status of 2772 mechanically ventilated patients from 37 countries. The average energy received by the patients was 14 kcal/kg/day, and the per day protein given was 47 g. The mean delivery of calories was 1,034 kcal/day. The authors reported an improved outcome in the form of reduced mortality and increase in ventilator free days with increased administration of proteins and a caloric intake of 1,000 kcal per day. The effect of increasing the calories on the mortality status was the largest in patients with extremes of nutritional status, that is, the most lean and most obese (BMI <25 and >35 kg/m 2) patients, with minimal benefit seen in patients with BMI between 25 to 35 kg/m 2.
Three randomised controlled trials (RCTs) were conducted under FOOD trial (Feed Or Ordinary diet) enrolling recent stroke patients from 131 hospitals in 18 countries from 1996 to 2003. Trial 1 compared the normal hospital diet with the normal hospital diet plus oral nutritional supplements (equivalent to 360 ml of 1.5 kcal/ml, 20 gm of protein per day). The supplemental diet was associated with a 0.7% absolute reduction in the risk of death. Trial 2 compared early enteral tube feeding versus no enteral tube feeding for at least 1 week in dysphagic stroke patients. Early enteral tube feeding was associated with a 5.8% absolute reduction in the risk of death. Trial 3 compared nasogastric tube (NG) feeding versus percutaneous endoscopic gastrostomy (PEG) feeding. PEG feeding was associated with a worse outcome with 1% increased absolute risk of death, the reason for which could not be established.
Malnutrition is associated with a poor outcome in stroke patients as they show a higher stress reaction, and an increased frequency of infections and bedsore. Observational data from FOOD trial showed that 37% of the undernourished patients were dead compared with only 20% of patients with normal nutritional status at a 6 month follow up indicating that a close association exists between the nutritional status of patients and the long term outcome after stroke. It has been shown in the animal models that protein energy malnutrition (PEM) worsens the outcome after ischemic brain injury. Various postulated mechanisms that have been proposed include upregulation of nuclear factor kappa B (a transcription factor responsible for increased production of inflammatory mediators), glutathione depletion and oxidative stress.,,
Consequences of overfeeding
Overfeeding is not without harm. Hypercaloric feeding is associated with hepatic dysfunction, hyperglycemia and increased risk of infections. In a multicentric study involving 725 patients, calculated energy >25 kcal/kg/day was found to be an independent predictor of hepatic dysfunction in the multivariate analysis, besides the role played by the use of total parenteral nutrition (TPN), sepsis and early use of artificial nutrition. Weijs et al., in a study on 843 critically ill patients (117 septic/736 non-septic) reported a higher mortality with early energy overfeeding and a lower mortality with early high protein intake in non-septic patients. There was no beneficial effect of early high protein intake in septic patients.
The common reasons for overfeeding include lack of nutritional monitoring, not including non-nutritional energy sources like propofol infusion, and not modifying the energy needs as per the changing physiology.
The refeeding syndrome
Initiating nutrition in patients after a prolonged fasting can result in the refeeding syndrome. Patient can develop cardiac failure, respiratory failure and death. The true incidence of refeeding syndrome is unknown as it is frequently an undiagnosed and under-reported condition.
The hallmark biochemical feature of this entity includes hypophosphatemia. Other features are hypokalemia, hypomagnesemia, thiamine deficiency as well as abnormal sodium and fluid balance. The pathogenesis responsible for the refeeding syndrome is the major fluid and electrolyte shift induced by metabolic and hormonal changes following institution of artificial feeding (enteral or parenteral) in a malnourished patient. During starvation, the body switches from using carbohydrates to fat and proteins for energy production, thereby making ketones and free fatty acids the preferred energy source instead of glucose. The basal metabolic rate decreases by 20-25%. Intracellular minerals (including phosphate) are depleted but their serum concentrations are maintained within the normal range. Refeeding these patients leads to secretion of insulin and synthesis of glycogen, fat and proteins. There is intracellular shift of potassium, magnesium and phosphate. As a result, these ions fall in the serum leading to the clinical manifestations of the refeeding syndrome. Thiamine is essential for carbohydrate metabolism and its deficiency results to Wernicke's encephalopathy or Korsakoff's syndrome. Refeeding syndrome can be prevented by identifying the high risk patients [Table 1] and starting the feeds slowly along with a close monitoring and replacement of electrolytes.
It is clear from the above discussion that appropriate nutritional strategy requires an understanding of the patient's pathophysiology and in maintaining a demand-supply balance. Some patients may require more aggressive nutritional support as compared to others due to their baseline nutritional status and/or the nature of illness. Therefore, the concept of nutritional risk stratification has evolved. Nutritional classification of patients is important to plan an appropriate nutritional strategy. Nutritional status assessment not only requires assessment of malnutrition [Table 2] at the time of admission but also an assessment of the severity of illness and the catabolic stress. A well nourished patient can rapidly deplete lean body mass and become malnourished in a short span of time if the illness induces a severe catabolic state. On the other hand, a patient with a chronic disease may develop severe malnutrition even with minimal amount of catabolic stress. Besides this, the patient's nutritional requirement evolves temporally with the disease progression/recovery. Therefore, the initial nutritional assessment should be followed by nutritional monitoring at regular intervals and strategy modulation as per the changing needs.
A nutritionally high risk subject is one who is likely to develop complications and adverse events that can be prevented by appropriate nutritional support. Currently, there is no consensus regarding the best method to identify these patients. Data from observational studies suggests that patients with extremes of BMI (i.e., <25 and >35 kg/m 2) and those with a prolonged intensive care unit (ICU) stay are most likely to benefit from aggressive nutritional support. It is the “long stayers” who require a well-planned nutritional intervention to prevent protein calorie deficit and associated complications.
Weight and body mass index (BMI)
Weight and BMI can be used for nutritional risk stratification. Weight measurement is a simple and easily available bedside tool to assess total body composition. It is more useful when used to construct percentage weight loss or BMI. An involuntary weight loss >10% in 6 months or >5% in 1 month is considered as a marker of severe malnutrition.
BMI uses the correlation of weight with height. BMI <18.5 kg/m 2 is indicative of malnutrition while BMI >30 kg/m 2 is considered obese.
The disadvantage of using BMI is that it does not take the body composition into consideration. Increased body weight or BMI can be due to increased muscle mass as well fat deposition. Researchers have highlighted that it is the lean muscle mass which might be more important than the BMI or the actual body weight in determining nutritional risk and survival after catabolic stress. In a retrospective study on 240 mechanically ventilated patients, Weijs et al., demonstrated that a low skeletal muscle area, as assessed by computed tomography of the abdomen, was an independent predictor of mortality while BMI was not.
Nutritional screening tools
There are at least 32 nutritional screening tools described in the literature for hospitalised patients but their utility in critically ill patients is limited. De van der Schueren et al., conducted a systematic review of studies dealing with construction and/or validation of nutritional screening tools in hospitalised patients. They reported a good performance of SGA (subjective global assessment), NRS-2002 (Nutrition Risk score) and MUST (Malnutrition Universal Screening Tool) in approximately half of the studies that reviewed adult patients, but not in studies dealing with older patients.
According to the European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines, MUST scoring should be used for patients coming from the community. NRS 2002 should be used for hospitalised patients and MNA (mini nutritional assessment) should be used for elderly patients in nursing homes or hospital settings.
Scores studied in critically ill are described below.
SGA is a nutritional assessment tool designed by Baker et al., in 1982. It uses 5 components of medical history (weight change, dietary intake, gastrointestinal symptoms, functional capacity and metabolic stress) and 2 components of clinical examination (features of fat loss and muscle wasting, alterations in fluid balance). These 7 components are together used to classify patients as normally nourished, moderately malnourished or severely malnourished.
Sheean et al., evaluated SGA in 57 mechanically ventilated medical patients and reported the excellent reliability of SGA as a nutritional assessment tool. Another retrospective study on mechanically ventilated medical ICU patients by Bector et al., used SGA for assessment of malnutrition. The prevalence of malnutrition at ICU admission was found to be 35%. Mortality was significantly higher in moderately and severely malnourished patients as compared to well nourished patients. The authors recommended the use of SGA as a valuable prognostic tool in critically ill patients.
Heyland et al., described the NUTRIC score for identification of the nutritional risk in critically ill patients. The score has six variables (age, Acute Physiology and Chronic Health Evaluation (APACHE) II, Sequential Organ Failure Assessment (SOFA), number of co-morbidities, pre-intensive care unit (ICU) length of stay and interleukin-6). The score does not use classical nutrition variables (BMI, recent weight loss, recent decreased intake) and therefore, requires more robust external validation data from randomized controlled trials before it can be used routinely in ICU patients.
NRS uses grading of disease severity along with nutritional components to construct the score. The score is calculated by adding nutritional status points with disease severity points as well as age points. The score is criticized for including all patients with APACHE II >10 as being at nutritional risk. By using this cut off, almost all ICU patients will qualify as having a nutritional risk. It has been recommended by experts that NRS 2002 requires an update on this point.
Biochemical parameters for risk stratification
Parameters like albumin, pre-albumin and transferrin retinol binding proteins are acute phase proteins and do not accurately reflect the nutritional status in acutely ill patients.
Assessment of nutritional requirement is difficult in hospitalized patients due to the interplay of multiple factors. Stress due to sepsis, trauma, surgery, seizures or fever leads to an increase in the nutritional requirements, while immobilization and the use of hypothermia, analgesics or sedative medications causes a decrease in the energy expenditure. Moreover, as has already been discussed, there can be a variability in the energy requirement depending upon the 'phase' of critical illness.
Under ideal circumstances, energy intake should match the energy expenditure. Indirect calorimetry is considered the accepted standard for measurement of energy expenditure but is not always available and feasible.
In the absence of indirect calorimetry, physicians rely on predictive equations for calculation of energy requirements [Table 3]. Walker et al., reviewed nine such equations available in the literature. The authors highlighted the importance of understanding the reference population on which the equation was generated. Critically ill patients form a heterogeneous group of patients; correct application of the predictive equations, therefore, requires clinical judgement and an understanding of the limitations of these equations.
The Harris- Benedict equation, which is one of the most commonly used equations for calculation of the caloric requirement, was originally derived from indirect calorimetry on 239 non-obese healthy volunteers.
The equation was generated from healthy individuals. An additional factor is often added to compensate for the elevated energy requirement due to injury/stress in hospitalized patients. It has been shown by various studies that accuracy of this equation ranges from 17 to 67% with a strong tendency to overestimate and under-estimate the caloric needs.,
The Penn state equation was initially derived from 169 ventilated patients in 1998. It was later modified in 2003. The accuracy of the 2003 Pen state equation has been reported to be 72%.
Indirect calorimetry is considered the accepted standard for measuring energy expenditure in critically ill patients. Its use is limited by the cost incurred and the difficulty in ensuring the availability of the sensitive equipment required. It is based on the physiological principle that energy expenditure can be calculated by measuring oxygen consumption and CO2 production. Indirect calorimetry should be done when steady state (stable acid base balance and CO2 production) is achieved. Higher levels of oxygen requirement, air leak around the endotracheal cuff or through the chest tube, fever with shivering, and changes in vasoactive drug requirements can alter the correct measurement of energy expenditure by indirect calorimetry.
In a recently conducted single centre study (the Tight Calorie Control Study, TICACOS), patients were randomized to receive enteral nutrition either by repeated indirect calorimetry measurements or as a fixed regimen of 25 kcal/kg/day. Patients in the indirect calorimetry group received higher mean caloric and protein intake and achieved a trend towards improved hospital mortality. The study highlights that individualized nutritional support can bring about clinical benefits in nutritionally compromised patients.
Calories (carbohydrates and fats)
According to the American Society for Parenteral and Enteral Nutrition (ASPEN) guidelines, the energy requirement should be calculated using simplistic formulas (25-30 kcal/kg/day), predictive equations or indirect calorimetry. In obese patients, calculation should be made with the ideal body weight. In malnourished patients, the first 7-10 day calculation should be done using the existing body weight due to the risk of developing the refeeding syndrome; thereafter, calculation should be according to the ideal body weight. In acute settings, weight becomes an unreliable marker due to changes in the fluid status of the patient.
Intentional underfeeding in the acute phase of illness is a subject of debate in literature and has been very well described in a recently published article by Wischmeyer. Currently, there are two schools of thoughts regarding the feeding goals in the acute phase of critical illness. For the chronic and recovery phase of illness, adequate provision of calories and proteins is supported by all the studies but for acute phase of illness, one school of thought supports intentional underfeeding while the other group favours full nutritional support. The supporters of intentional underfeeding argue that provision of artificial nutrition during the acute phase hampers the process of autophagy (orderly degradation and recycling of cellular components). Insufficient autophagy leads to accumulation of cellular debris and delays recovery.,,
The supporters of full feeding in acute phase of critical illness argue that the cumulative protein and energy deficit is directly related to mortality and morbidity. Underfeeding during the acute phase (the initial 5-7 days) of critical illness may aggravate this cumulative deficit.,
Hypocaloric feeding with adequate delivery of proteins has been shown to be of benefit in some studies.
Arabi et al., randomized 894 critically ill adults (118 of them suffering from a traumatic brain injury) from medical/surgical/trauma units to receive either underfeeding (40 to 60% of the calculated calories) or standard feeding (70 to 100%) while maintaining equal protein intake in both the groups for 14 days. There was a non-significant trend towards a reduced 28-day mortality in the trophic feeding group (18.3%) when compared with the standard feeding group (23.3%, P < 0.07). There was no difference in the 90-day mortality, hospital mortality or the ICU acquired infections in the two groups. In contrast to these findings, Wei et al., demonstrated that high risk ICU patients (mechanically ventilated >8 days) receiving a low nutritional intake during the first week of ICU stay had increased mortality as compared to patients receiving adequate nutrition (>80% of calorie needs). Härtl et al., studied 797 patients with severe traumatic brain injury (Glasgow coma scale <9) from 22 different trauma centres. They reported a 30 to 40% increase in mortality for every 10 kcal/kg decrease in the caloric intake. The amount of decrease in nutrition during the first five days was directly related to death. Wang et al., analysed 13 randomized control trials (RCTs) and 3 non-randomized prospective studies (NPS) on traumatic brain injury. The pooled data showed significant reduction in the mortality and in infectious complications with early feeding. Small bowel feeding was associated with a decreased rate of pneumonia as compared to nasogastric feeding. It has been repeatedly emphasized in literature that all ICU patients are not the same and using the same strategy for all patients might not be appropriate.
Protein should be given in the range of 1.2 to 2 gm/kg actual body weight/day. Protein supplements can be added to the standard enteral formula to achieve the target requirement.
In patients with a higher BMI (BMI >30 kg/m 2), however, protein should be provided in the range of 2 to 2.5 gm/kg of the ideal body weight/day.
Critically ill patients show a rapid protein loss due to the initiation of an inflammatory response caused by catabolic hormones and cytokines. This catabolic state is closely linked to the severity of inflammation. Enhanced protein breakdown and hampered protein synthesis lead to the loss of lean muscle mass. To what extend this loss of lean muscle mass can be prevented by aggressive nutritional support is at present not known. It has been shown in observational studies that the cumulative protein and energy deficit goes on increasing with increase in the duration of ICU stay. This cumulative deficit is associated with an increased mortality and morbidity. In the light of current evidence, a high protein intake (1.5 gm/kg/day) should be given to patients during the acute phase of critical illness, regardless of the caloric intake. This strategy may help in reducing muscle catabolism but strong evidence in this field is lacking. A high protein intake should be continued in the chronic and recovery phase along with adequate caloric provision to prevent proteolysis for fuel generation.
Enteral route is the preferred route of nutritional delivery in patients with an intact gastrointestinal tract. Both gastric as well as small bowel feeding are acceptable in the ICU setting. Patients at a high risk of aspiration can be administered small bowel feeding via the nasojejunal route. The enteral route, when compared to the parenteral route, is associated with significant reduction in the number of infectious complications and the length of ICU stay.
Enteral feeding should be started within 24 to 48 hrs of ICU admission. Initiation of early enteral feeding is associated with nutritional as well as non-nutritional advantages. Besides preventing protein-calorie deficit, early enteral feeding helps to maintain structural and functional integrity of the gut, attenuates metabolic response to injury, and decreases insulin resistance and oxidative stress. Studies in the settings of elective surgery and surgical intensive care unit have shown that starting enteral nutrition as soon as possible after surgery is associated with a reduced rate of infection as well as a decreased length of hospital stay and mortality when compared with patients in whom feeding was deferred until the return of bowel sounds.
Various strategies to optimize enteral feeding include small bowel feeding, prokinetics, tolerating higher gastric residual volumes and using concentrated feeds.
There is considerable discrepancy between various guidelines regarding the use of parenteral nutrition when enteral nutrition is not feasible or fails to achieve the desired target. Both American (A.S.P.E.N) and European (E.S.P.E.N) guidelines support an early (24 to 48 hrs) start of enteral nutrition but ASPEN suggested withholding parenteral nutrition for one week if enteral nutrition is not feasible, while ESPEN supported combining both the enteral and parenteral nutrition if the nutrition targets are not achieved within 3 days.,
Until more literature is available in this field, we suggest using aggressive nutritional support, that is, combining enteral and parental routes to achieve the target nutrition in nutritionally high risk patients (the likely long stayers, or those having extremes of BMI) while a more moderate approach can be used for less sick patients with an expected short span of ICU stay and mechanical ventilation [Table 4].
Glutamine is a metabolic substrate for enterocytes and immune cells. Critically ill patients frequently develop glutamine deficiency during the course of illness. A lower plasma glutamine level has been associated with increased mortality and immune dysfunction in critically ill patients. Glutamine replacement has been shown to be beneficial in severe sepsis, trauma and burn injuries.
Chen et al., published a meta-analysis of 18 trials comparing glutamine supplementation with placebo in ICU patients. They did not find any significant difference in the hospital mortality or the six month mortality between the glutamine group and the control group.
Eight trials used glutamine in the range of 0.3 gm/kg/day to 0.5 gm/kg/day. Four trials used glutamine <0.3 gm/kg/day while six trials used high dose glutamine (>0.5 gm/kg/day). Subgroup analysis based on the different glutamine dosages showed significantly higher mortality (33.5% vs 28.2% P = 0.03) in the high dose glutamine study subgroup. The other two subgroups did not show any difference in the mortality between the glutamine and control group. Fifteen trials reported a high infection rate associated with glutamine deficiency. Glutamine supplementation was associated with a decreased incidence of nosocomial infections in surgical patients.
Current insight into glutamine metabolism suggests that both low and high levels of glutamine can lead to increased mortality. Therefore, it is suggested that glutamine plasma concentration should be checked before giving glutamine to critically ill patients. Patients with level <420 micromol/l should receive glutamine in the dose of 0.3 gm/kg/day to 0.5 gm/kg/day.
Body's immune function is closely linked with arginine metabolism. Arginine is metabolized to ornithine by the enzyme arginase 1. Orthinine is a precursor for polyamines and proline which stimulate cell growth, proliferation and wound healing. Arginine is also a substrate for inducible nitric oxide synthetase (iNOS). Nitric oxide is a potent oxidant and helps in bacterial killing. Surgery/trauma causes release of immature myeloid cells in the circulation and lymphatic tissues. These cells produce arginase 1 causing rapid breakdown of arginine. Arginine deficiency is associated with deleterious effects on T cell proliferation and function.
A meta-analysis of 11 trials including 321 patients showed that L-arginine supplementation was associated with a significantly higher T cell proliferation response and decreased incidence of infections (OR 0.40; 95% CI 0.17, 0.95; P < 0.05) than controls.
Arginine supplementation has been found to be beneficial in surgical and trauma patients. The same effect has not been demonstrated in patients with severe sepsis. Arginine supplementation in patients with severe sepsis can lead to nitric oxide overproduction, vasodilatation and worsening of systemic inflammatory response syndrome (SIRS).
Omega-3 fatty acids
It has been demonstrated that dietary intake of certain oils can modulate the immune response by changing the cell membrane composition of immune cells. Arachidonic acid, found in the cell membranes of immune cells, acts as a precursor for inflammatory cytokines. Omega 3 fatty acids down-regulate the immune response by producing less inflammatory cytokines. Fish oil, borage oil and canola oil are rich in omega-3 fatty acids. They also act as precursors for resolvins and protectins which in turn help to reduce tissue injury.
Langlois et al., analysed 10 RCTs evaluating fish oil containing lipid emulsions and found a significant reduction in the rate of infection. Enteral formulae designed for specific patient populations (like the small peptide medium chain triglycerides for patients with gut dysfunction; a high protein - low caloric formula for obese patients; organ failure formulae for patients with a liver or a renal injury) can be used on a case-by-case basis. Outcome-benefit studies are lacking in this field. Probiotic agents have been found to be useful in certain patient populations like those undergoing a major abdominal surgery or organ transplantation as well as those sustaining a major trauma. The benefits of these agents are highly variable depending upon the species used, dose given and the population under study. Therefore, specific recommendations regarding use of probiotics in critically ill patients are lacking. Critically ill patients, especially the burn victims and trauma patients, should receive micronutrients in the form of trace elements, vitamins and antioxidants.
Neurocritical care patients differ from general ICU patients in several aspects. Various measures to control intracranial pressure like sedatives, analgesics, barbiturates, muscle relaxants and hypothermia cause decrease in the nutritional requirement. Neurocritical patients of traumatic aetiology show severe hypercatabolism which does not correlate with the Glasgow coma scale (GCS). As has already been discussed, patients with increased catabolic rate are at a higher nutritional risk. Foley et al., published a systematic review of 24 studies on hypermetabolism following moderate-to-severe traumatic brain injury. Six studies used indirect calorimetry to measure the energy expenditure while rest of the studies used other analytical methods for calculation of oxygen consumption and carbon dioxide production. They reported the mean energy expenditure (MEE) of 75% to 200% of the predicted value. Administration of paralysing agents, barbiturates/sedatives decreased energy expenditure by 12 to 32%. One study (n = 45) showed that energy expenditure was maximum with more severe injury. Patients with a Glasgow Coma Scale (GCS) of 4-5 had a MEE of 168 ± 53%, while those with a GCS 6-7 had a MEE of 129 ± 31% and those with a GCS of 8 had a MEE of 150 ± 49%. Without indirect calorimetry, bedside assessment of energy expenditure is very difficult due to the wide variation of values depending upon the disease severity, use of sedation and paralysis and changes in body temperature. Most of the patients who go on mechanical ventilation due to a neurological reason require prolonged ventilation and easily become nutritionally high risk. Except in the cases with a subarachnoid hemorrhage, most neurocritical patients are older and have multiple co-morbidities like diabetes and hypertriglyceridemia. Therefore, neurocritical care patients are more likely to develop nutrition-related complications when compared to other ICU patients.
Stress response to injury induces a state of severe catabolism and loss of lean body mass. Patients who are malnourished at admission and those who are likely to stay longer in ICU due to the nature of their illness are at a high nutritional risk. Aggressive nutritional strategy should be planned for these patients from the very beginning of their hospitalization. Enteral route is the preferred mode of feeding. Post pyloric feeding should be considered in patients at a high risk of aspiration.
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[Table 1], [Table 2], [Table 3], [Table 4]