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It is important to eat a protein rich, high calorie diet throughout recovery because:
Support immune system
Help wound/s to heal
Maintain muscle mass and strength
Minimise weight loss
Support rehabilitation

Nutritional requirements decrease and approach pre-injury levels as wound healing progresses. Research indicates that increased protein intake during the recovery phase increases body weight gain and muscle function.

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If child not tolerating oral fluids or is < 12 months old, and it is clinically indicated then commence IV maintenance fluids as follows:

For 1st 10kg = 4ml/kg/hr
For 2nd 10kg = 2ml/kg/hr
Every extra kg = 1ml/kg/hr

- Enteral feeds must commence as soon as possible and increased to maximise fluid allowance and decrease crystalloid (water, electrolytes and glucose)

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Main source of Vitamin D is from direct sunlight
If advised to stay out of sunlight it is important for patients to have a substantial intake of vitamin D to avoid a deficiency. Vitamin D supplements are often recommended- 10micrograms daily.

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Advised PROTEIN RICH foods following burns injury (NHS North Bristol)

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Advised PROTEIN RICH foods following burns injury (NHS North Bristol)

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High Protein Foods:
Meat, Fish, Eggs, Cheese, Milk

Vegetarian:
Beans, Nuts, Seeds, Soya

Drinks:
Milky drinks (hot chocolate/milkshakes), Milk

Snacks:
Custard, Rice pudding, Nuts, Yogurts, Cheese, Sausage rolls, Biscuits

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Consider reduced appetite and be creative in increasing nutritional intake

Strict fluid balance required, input and output

Nutritional support should be started within the first 24 hours of the injury, but within 6-8 hours for optimum recovery

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Vitamin D supplements are important while avoiding sun exposure

Protein rich diet aids faster wound healing

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INTRAVENOUS (IV) MAINTENANCE FLUIDS

Additional IV maintenance fluids is only required if clinically indicated, if the child is not tolerating oral fluids or the child is <12months old:

For 1st 10kg = 4ml/kg/hr
For 2nd 10kg = 2ml/kg/hr
Every extra kg = 1ml/kg/hr

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Hildreth formula for energy requirements

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Hildreth formula for energy requirements

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Children <12 1800kcal/m2 Total Body Surface Area (TBSA) + 1200kcal/m2 Burn Surface Area(BSA)

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Appropriate wound healing is achievable in children over 1 year receiving 2-3g protein/day

Children require 1,800 kilocalories per square meter of body surface plus 2,200 kilocalories per square meter of burn area per day to maintain body weight (NCBI, 2011)

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Insertion of a nasogastric tube and commencement of enteral feeds should be considered for children who sustain significant burn injuries and/or facial burns and are unable to tolerate adequate oral intake. Where possible feeds should commence within 6 - 8 hours of the burn injury.

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* FEEDING/NUTRITION

Start oral/enteral feed as soon as possible (post operatively) and increase as quickly as tolerated to maximum fluid allowance and decrease crystalloid accordingly (refer to dietitian). Monitor aspirates.

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Protein requirements are significantly increased in burned patients. Protein is necessary for wound healing, enhancement of host defence mechanisms and replacement of losses.

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Children require 1,800 kilocalories per square meter of body surface plus 2,200 kilocalories per square meter of burn area per day to maintain body weight (NCBI, 2011)

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Children with significant burn injuries are at risk of acute gastric ulceration and a H2 antagonist should be considered for these patients.

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Hourly fluid balance. Urine outputs > 2mls per kg per hour for more than two hours should result in a decrease in resuscitation fluid. Urine outputs < 0.5ml/kg/hr should result in clinical examination and serum urea and electrolytes should be checked

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3255093/

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METABOLIC CHANGES FOLLOWING SEVERE BURN INJURY

Severe burns covering more than 40% total body surface area (TBSA) are typically followed by a period of stress, inflammation and hypermetabolism, characterized by a hyperdynamic circulatory response with increased body temperature, glycolysis, proteolysis, lipolysis and futile substrate cycling. These responses are present in all trauma, surgical, or critically ill patients, but the severity, length and magnitude is unique for burn patients. Marked and sustained increases in catecholamine, glucocorticoid, glucagon and dopamine secretion are thought to initiate the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state. The response is characterized by supraphysiologic metabolic rates, constitutive muscle and bone catabolism, growth retardation, insulin resistance, and increased risk for infection. If untreated, physiologic exhaustion ensues, and the insult becomes fatal. This period is characterized by profoundly accelerated glycolysis, lipolysis, proteolysis, insulin resistance, liver dysfunction, and decreases of lean body mass and total body mass. A ten percent loss of total body mass leads to immune dysfunction; 20% leads to decreased wound healing; 30% leads to severe infections; and a 40% loss leads to death. Severely burned, catabolic patients can lose up to 25% of total body mass after acute severe burn injury.

The cause of this complex response is not well understood. However, it is hypothesized that interleukins 1 and 6, platelet-activating factor, tumor necrosis factor (TNF), endotoxin, neutrophil-adherence complexes, reactive oxygen species, nitric oxide and coagulation as well as complement cascades have also been implicated in regulating this response to burn injury. Once these cascades are initiated, their mediators and by-products appear to stimulate the persistent and increased metabolic rate associated with altered glucose metabolism seen after severe burn injury. The primary mediators of this response after severe burn injury are catecholamines, corticosteroids, and inflammatory cytokines. There is a 10 to 50-fold elevation of plasma catecholamines and corticosteroid levels that last up to 12 months post-burn. Inflammatory cytokine levels, serum hormones, acute proteins and constitutive proteins are altered immediately post-burn and remain abnormal throughout the acute hospitalization up to 2 months post-burn compared with normal levels.

Several studies have indicated that these metabolic phenomena post-burn occur in a timely manner, suggesting two distinct patterns of metabolic regulation following injury. The first phase occurs within the first 48 hours of injury and has classically been called the "ebb phase," characterized by decreases in cardiac output, oxygen consumption, and metabolic rate as well as impaired glucose tolerance associated with its hyperglycemic state. These metabolic variables gradually increase within the first five days post-injury to a plateau phase (called the "flow" phase), characteristically associated with hyperdynamic circulation and the above mentioned hypermetabolic state.

Multi-organ dysfunction is the hallmark of the acute phase response post-burn. Immediately post-burn, patients may have low cardiac values characteristic of early shock. However, by four days post-burn, at the onset of shock, they have cardiac outputs greater than 150% compared with non-burned, healthy volunteers. Heart rates of our patients approach 160% compared with non-burned, healthy patients. Post-burn, patients have increased cardiac work that lasts well into the rehabilitation phase. Myocardial oxygen consumption values far surpass values of marathon runners and are sustained well into the rehabilitation phase. Profound hepatomegaly occurs after burn injury. The liver increases its size by 225% by two weeks post-burn and remains increased at discharge by 200%.

Insulin release during this time period was found to be twice that of controls in response to glucose load and plasma glucose levels are markedly elevated, indicating the development of an insulin-resistance. Current understanding has been that these metabolic alterations resolve soon after complete wound closure. However, recent studies found that the hypermetabolic response to burn injury may last for more than 12 months after the initial event. We found in a recent study that sustained hypermetabolic alterations post-burn, indicated by persistent elevations of total urine cortisol levels, serum cytokines, catecholamines and basal energy requirements, were accompanied by impaired glucose metabolism and insulin sensitivity that persisted for up to three years after the initial burn injury.

Glucose metabolism in severely burned patients is dramatically deranged. In order to provide glucose, a major fuel source to vital organs, release of the above mentioned stress mediators oppose the anabolic actions of insulin. By enhancing adipose tissue lipolysis and skeletal muscle proteolysis, they increase gluconeogenic substrates, including glycerol, alanine and lactate, thus augmenting hepatic glucose production in burned patients. In healthy subjects glucose metabolism is tightly regulated, and under normal circumstances, a postprandial increase in blood glucose concentration stimulates release of insulin from pancreatic β-cells. Insulin mediates peripheral glucose uptake into skeletal muscle and adipose tissue and suppresses hepatic gluconeogenesis, thereby maintaining blood glucose homeostasis. In severe burns, however, metabolic alterations can cause significant changes in energy substrate metabolism. Hyperglycemia fails to suppress hepatic glucose release during this time, and the suppressive effect of insulin on hepatic glucose release is attenuated, significantly contributing to post-trauma hyperglycemia. Catecholamine-mediated enhancement of hepatic glycogenolysis, as well as direct sympathetic stimulation of glycogen breakdown, can further aggravate the hyperglycemia in response to stress. Catecholamines have also been shown to impair glucose disposal via alterations of the insulin signaling pathway and GLUT-4 translocation in muscle and adipose tissue, resulting in peripheral insulin resistance. Researchers have shown an impaired activation of Insulin Receptor Substrate-1 at its tyrosine binding site and an inhibition of AKT in muscle biopsies of children at seven days post-burn. There is a link between impaired liver and muscle mitochondrial oxidative function, altered rates of lipolysis, and impaired insulin signaling post-burn, attenuating the suppressive actions of insulin both on hepatic glucose production and on the stimulation of muscle glucose uptake. Another counter-regulatory hormone of interest during stress of the critically ill is glucagon. Glucagon, like epinephrine, leads to increased glucose production through both gluconeogenesis and glycogenolysis. The action of glucagon alone is not maintained over time; however, its action on gluconeogenesis is sustained in an additive manner by the presence of epinephrine, cortisol, and growth hormone. Similarly, epinephrine and glucagon have an additive effect on glycogenolysis. Pro-inflammatory cytokines contribute indirectly to post-burn hyperglycemia by enhancing the release of the aforementioned stress hormones. Other groups showed that inflammatory cytokines, including tumor necrosis factor (TNF), interleukin (IL) -6 and monocyte chemotactic protein (MCP) -1 also act via direct effects on the insulin signal transduction pathway through modification of signaling properties of insulin receptor substrates, contributing to post-burn hyperglycemia via liver and skeletal muscle insulin resistance. Alterations in metabolic pathways as well as pro-inflammatory cytokines, such as TNF, have also been implicated in significantly contributing to lean muscle protein breakdown, both during the acute and convalescent phases in response to burn injury. In contrast to starvation, in which lipolysis and ketosis provide energy and protect muscle reserves, burn injury considerably reduces the ability of the body to utilize fat as an energy source.

Skeletal muscle is thus the major source of fuel in the burned patient, which leads to marked wasting of lean body mass (LBM) within days after injury. This muscle breakdown has been demonstrated with whole body and cross leg nitrogen balance studies in which pronounced negative nitrogen balances persisted for 6 and 9 months after injury. Since skeletal muscle has been shown to be responsible for up to 80% of whole body insulin-stimulated glucose uptake, decreases in muscle mass may significantly contribute to this persistent insulin resistance post-burn. The correlation between hyperglycemia and muscle protein catabolism has been also supported by Flakoll and others, in which an isotopic tracer of leucine was utilized to index whole-body protein flux in normal volunteers. The group showed a significant increase in proteolysis rates occurring without any alteration in either leucine oxidation or non-oxidative disposal (an estimate of protein synthesis), suggesting that hyperglycemia induced increased protein breakdown. Flakoll and others further demonstrated that elevations of plasma glucose levels resulted in a marked stimulation of whole body proteolysis during hyperinsulinemia. Net loss of protein leads to loss of lean body mass, and severe muscle wasting leads to decreased strength and failure to rehabilitate fully. The resultant muscle weakness was further shown to prolong mechanical ventilatory requirements, and delay mobilization in protein-malnourished patients, thus markedly contributing to the incidence of mortality in these patients. This loss of protein is directly related to increases in metabolic rate and may persist up to 9 months after critical burn injury, often resulting in significantly negative whole-body and cross-leg nitrogen balances. Severely burned patients have a nitrogen loss of 20-25 g/m ² TBSA/day, and if unattended, lethal cachexia becomes imminent in less than 30 days. Persistent protein catabolism may also account for the delay in growth frequently observed in our pediatric patient population for up to 2 years post-burn.

Perturbations, such as sepsis, increase metabolic rates and protein catabolism up to 40% compared with patients with like-size burns that do not develop sepsis. A vicious cycle ensues, as patients that are catabolic are more susceptible to sepsis due to changes in immune function and immune response. The emergence of multi-resistant organisms have led to increases in sepsis related infections and death overall. Inflammatory cells, in response to burn wounds and burn wound infections metabolize glucose anaerobically to pyruvate and lactate. These are returned to the liver for gluconeogenesis which produces recycled energy for use by leukocytes and fibroblasts in the burn wound.

In past years, therapeutic approaches therefore, have, mainly focused on reversing the hypermetabolic response, with its ensuing catabolic state post-burn, using a large number of different strategies.

Nutritional Support of the Severely Burned Patient

The hypermetabolic response for a severely burned patient far surpasses that in any other disease state. Determinants of successful initial burn treatment include early aggressive resuscitation (including nutrition), control of infection, and early closure of the burn wound. Aggressive, early enteral feeding improves outcomes in the burned patient by mitigating the degree and extent of catabolism. Attempting to overcompensate by providing excess calories and/or protein is ineffective and likely to increase such complications as hyperglycemia, carbon dioxide retention (CO2), and azotemia. Thus, the primary goal of nutritional support in burn patients is to satisfy acute, burn-specific requirements, and not to overfeed.

Patients with 40% TBSA treated with vigorous oral alimentation alone can lose a quarter of their preadmission weight by 3 weeks after injury. Attempts to feed severely burned patients orally failed due to altered mental status, inhalation injuries that compromised pulmonary function, gastrointestinal dysfunction, and/or feeding intolerance. The amount of nutrition necessary to provide adequate support and prevent severe catabolism was intolerable for these patients. Inanition proved fatal as severely burned victims succumbed to severe systemic infections and respiratory failure. Thus, the primary goal of nutritional support, is to address the ever-evolving metabolic needs in severely burned patients. Nutrition should be tailored to promote wound healing, to increase resistance to infection, and to prevent persistent loss of muscle protein. During the acute hospitalization of severely burned patients, attempts to optimize nutrition are countered by immobility and evolving catabolic responses to injury; attempts to achieve a positive nitrogen balance are repeatedly thwarted.

Total parenteral nutrition (TPN) for the nutrition and rehabilitation of severely burned patients surfaced in the 1970's. TPN allows for the provision of elemental components that do not require digestion or a functioning alimentary tract. Dextrose is the main calorie source in TPN, and protein is supplied as crystalline amino acid solutions. Lipid emulsions can comprise a significant proportion of the calories in TPN. Use of TPN has now been largely replaced by enteral nutrition (EN) in burn patients.

Adults can maintain body weight after severe burn injury only with aggressive, continuous nutrition of 25 kilocalories per kilogram body weight per day plus 40 kilocalories per percent total body surface area burn per day. Children require 1,800 kilocalories per square meter of body surface plus 2,200 kilocalories per square meter of burn area per day to maintain body weight. The mechanism by which patients are fed affects outcomes. Research shows that parenteral nutrition alone or even in combination with enteral nutrition could lead to overfeeding, liver failure, impaired immune response and increased mortality by 3-fold. Enteral nutrition reduces translocation bacteremia and sepsis, maintains gut motility, and preserves `first pass' nutrient delivery to the liver. For these patients, parenteral nutrition should be reserved primarily for those who have enteral feeding intolerance or prolonged ileus.

Timing of Nutrition

Advances in burn care have altered the magnitude of the post-burn hypermetabolic response, but not the nature of the response. A major determinant of outcome for severe burn patients is time to treatment. Any delays in resuscitation lead to poorer outcomes. In the acute phase, in the unfed patient, there is significant gut mucosal damage and increased bacterial translocation that collectively lead to decreased nutrient absorption. Therefore, optimal nutritional support for the severely burned patient is best accomplished by early initiation of enteral nutrition. Moreover, multiple studies demonstrate that early institution of enteral feeding can significantly modulate the hypermetabolic response to severe burn. Laboratory studies showed significant decreases in metabolic rates by two weeks post-burn in animals enterally fed continuously by two hours post-burn compared with animals fed 3 days post-burn, indicating the benefits of early initiation. Significant modulation of catecholamine levels and support of gut mucosal integrity have been shown with early enteral nutrition. In human studies, early continuous enteral nutrition delivered calculated caloric requirements (resting energy expenditure) by post-burn day three, nearly prevented the hypermetabolic response, and significantly decreased circulating levels of catecholamines, cortisol and glucagon. Early enteral feeding preserved gut mucosal integrity, motility and intestinal blood flow. Intestinal hypoperfusion or ileus, secondary to delays in resuscitation can be reversed by reperfusion or adequate resuscitation. Post-burn ileus spares the small bowel and primarily affects the stomach and colon. Patients with severe burn injury can be safely enterally fed in the duodenum or jejunum 6 hours post-burn, whether or not they have total gastroduodenal function. Nasojejunal, or nasoduodenal feeding should be initiated as soon as possible to facilitate the full resuscitation of the severely burned patient.

The Nutritional Requirements

Actual caloric requirements can be accurately determined by measuring resting energy expenditures with bedside carts.. Preservation of lean body mass should be a nutritional goal for severe burn victims, as a major consequence of the hypermetabolic response is severe total body catabolism. Appropriate nutrient delivery can be accomplished by feeding 1.2 to 1.4 times the measured resting energy expenditures (in kilocalories per square meter per day). Goran et al found that by feeding patients 1.2 times the measured resting energy expenditures, body weight may be maintained, but with a loss of 10% of lean body mass. While others found an increase in body weight by feeding 1.4 times the resting energy expenditure, the gains, however, were in fat deposition, not lean body mass.

The major energy source for burn patients should be carbohydrates which serve as fuel for wound healing, provide glucose for metabolic pathways, and spare the amino acids needed for catabolic burn patients. It is estimated that critically ill, burned patients have caloric requirements that far exceed the body's ability to use glucose, which is approximately 7 grams per kilogram per day (gm/kg/day) (2,240 kcal for an 80 kilogram man). Providing a limited amount of dietary fat reduced requirements for carbohydrates and can improve glucose tolerance significantly.

The hypermetabolic, catabolic response to severe burns suppresses lipolysis and limits the extent to which lipids can be utilized for energy. Thus, fat should comprise no more than about 30% of non-protein calories, or about 1 gm/kg/day of intravenous lipids in TPN. Thirty percent may be overwhelming in burned patients. In an animal model, immune function was further compromised with diets containing more than even 15% lipids, advocating the use of low-fat diets in severely burned patients. The composition of administered fat is more important than the quantity. Most common lipid sources contain omega-6 free fatty acids (ω-6 FFA's) such as linoleic acid which are metabolized through synthesis of arachidonic acid, a precursor of pro-inflammatory cytokines such as Prostaglandin E2. Omega-3 fatty acids (ω-3 FFA's) are metabolized without provoking pro-inflammatory compounds. Diets high in ω-3 FFA's have been associated with an improved inflammatory response, improved outcomes, and reduced incidences of hyperglycemia.

Proteolysis is another hallmark of the hypermetabolic response after severe burn injury. Protein catabolism in burn patients can exceed 150 grams/day, or almost a half-pound of skeletal muscle. Increased protein catabolism leads to decreased wound healing, immuno-incompetence, and loss of lean body mass. There is some evidence that increased protein replacement for severely burned patients may be beneficial. Healthy individuals require 1 gram per kilogram body weight per day of protein intake. However, based on in vivo kinetics studies measuring oxidation rates of essential and non-essential amino acids, burn patients have 50% higher utilization rates than healthy individuals in the fasting state,. Thus, burn patients require a minimum of 1.5 to 2 grams per kilogram body weight per day protein intake. Any higher amount of supplementation in burned children, however, leads to increased urea production without improvements in lean body mass or muscle protein synthesis.

Amino acids have a key role in recovery following injury. Alanine and glutamine (GLU) are important transport amino acids, created in skeletal muscle to supply energy to the liver and to aid in wound healing. GLU serves as a primary fuel for enterocytes and lymphocytes, and aids in maintaining small bowel integrity, preserving gut-associated immune function, and limiting intestinal permeability following acute injury. GLU is rapidly depleted from both serum and muscle following severe burn injury, limiting visceral protein synthesis, and underscoring the importance of glutamine replacement after severe burn injury. When GLU was given at 25 gm/kg/day, severely burned patients had a decrease in incidence of infections, improved visceral protein levels, decreased length of stay, and reduced mortality. Replacement of branched-chain amino acids led to improvements in nitrogen balance, but no effect on survival.

Vitamins and other micronutrients are also profoundly affected by the hypermetabolic - catabolic response post-burn (). Decreased levels of Vitamins A, C, and D, iron, zinc, and selenium have been implicated in decreased wound healing and immune dysfunction post severe burn injury. Vitamin A replacement is important for wound healing and epithelial growth. Vitamin C is paramount for synthesis and the cross-linking of collagen post-burn, and burn patients often require up to 20 times the recommended daily allowance. Vitamin D is essential in the prevention of further bone catabolism post-burn. Iron is an important cofactor in oxygen-carrying proteins. Zinc supplementation contributes to improvements in wound healing, DNA replication, and lymphocyte function. Selenium replacement improves cell-mediated immunity. Collectively, replacement of these micronutrients has contributed to the improvement in morbidity of severely burned patients.

Milk, traditionally an isocaloric-isoprotein, but high fat diet, consisting of 44% fat, 42% carbohydrate and 14% protein, became standard of care for the pediatric burned patient,. Although it was well-tolerated, fat did not serve as the optimal energy source for these patients. There was continued protein degradation, and lean body mass gains paled in comparison with high carbohydrate diets - consisting of 3% fat, 15% protein and 82% carbohydrate. The high carbohydrate diet increased protein synthesis, increased effective endogenous insulin production, and improved lean body mass. Increased endogenous insulin levels, stimulated by high carbohydrate delivery, may have contributed to improved muscle protein synthesis. Parenteral formulas which are traditionally 70% dextrose, 15% amino acids and 20% lipids, can be manipulated and adjusted to meet patients' caloric needs. However, TPN is associated with increased pro-inflammatory cytokines, increased pulmonary dysfunction, and increased mortality. Thus, all TPN formulas containing currently available fat emulsions should be reserved for patients that cannot tolerate EN.

Overfeeding

The overfeeding of severely burned patients can lead to major complications. Overfeeding with carbohydrates results in elevated respiratory quotients, increased fat synthesis, and increased CO2 elimination. Ventilated patients become more difficult to manage and to wean from support. Excess carbohydrate or fat can also lead to fat deposition in the liver. Excess protein replacement leads to elevations in blood urea nitrogen (BUN), which could lead to acute renal failure, increased propensity to sepsis, and death. Overfeeding can lead to hypergycemia, which is already present in up to 90% of all critically ill patients - leading to increased morbidity and mortality. This iatrogenic hyperglycemia is even harder to treat as both endogenous and exogenous insulin effects are often countered by the surge of catabolic hormones. These complications are not specific to parenteral or entereal feedings, but are manifestations of attempts to over-compensate for the tremendous losses suffered by severely burned patients.

Positive changes in body weight are among the best predictors of overall nutritional status. Significant weight loss, particularly rapid and unplanned, is a predictor of mortality. However, it should be noted that resuscitation and maintenance fluid increases may mask ongoing loss of lean body mass so that patients can suffer significant inanition and still weigh more than they did at the time of admission. In addition, fluid shifts associated with infections, ventilator support, hypoptroteinemia, and elevations in aldosterone and antidiuretic hormone lead to wide fluctuations in weight that have little to do with nutritional status. Judicious monitoring of long-term trends is paramount in the clinical management of severely burned patients.

Determination of nitrogen balance, serum proteins, and abnormalities of immune function will also aid the assessment of nutritional supplementation post-burn. While no single laboratory test is fully reliable in nutritional monitoring, regular metabolic assessment is paramount in the ever-evolving physiologic response post-burn.

The Hormonal Response in Severe Burns

Elevated levels of catecholamines, cortisol, and glucagon perpetuate the profound changes in metabolic rates, growth, and physiology observed in the burn patient population. Anabolic agents such as recombinant human growth hormone (rhGH), insulin, insulin-like growth factor (IGF-1), and insulin-like growth factor binding protein-3 (IGFB-3) in combination with testosterone and oxandrolone have been shown to abate post-bun metabolism. To counter elevated levels of catecholamines, the adrenergic antagonist, propranolol, has been used with profound results. Other glucose modulators, besides insulin, have also been shown to attenuate post-burn metabolic derangements. The use of anabolic or anti-catabolic agents in severely burned children, in addition to standard of care, have led to significant decreases in protein catabolism.

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WHAT, HOW, AND HOW MUCH SHOULD BURN PATIENTS BE FED?

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Severe burns covering more than 40% total body surface area (TBSA) are typically followed by a period of stress, inflammation and hypermetabolism, characterized by a hyperdynamic circulatory response with increased body temperature, glycolysis, proteolysis, lipolysis and futile substrate cycling.

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Nutritional support is a critical aspect of the treatment of burn patients. The metabolic rate of these patients can be greater than twice the normal rate, and this response can last for more than a year after the injury.

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http://www.uhbristol.nhs.uk/for-clinicians/clinical-guidelines/

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For Clinicians | University Hospitals Bristol NHS Foundation Trust

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6998073/

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Abstract

Nutrition therapy during critical illness has been a focus of recent research, with a rapid increase in publications accompanied by two updated international clinical guidelines. However, the translation of evidence into practice is challenging due to the continually evolving, often conflicting trial findings and guideline recommendations. This narrative review aims to provide a comprehensive synthesis and interpretation of the adult critical care nutrition literature, with a particular focus on continuing practice gaps and areas with new data, to assist clinicians in making practical, yet evidence-based decisions regarding nutrition management during the different stages of critical illness.

Keywords: Critical illness, Intensive care, Nutrition therapy, Enteral nutrition, Parenteral nutrition

Background

In recent years, there has been much interest in the role of nutrition therapy in critical illness with an increase in publications and two updated international clinical guidelines [ 1, 2]. However, trial findings and guideline recommendations continue to be conflicting, making the translation of evidence into practice challenging. Further, it is becoming evident that the stage of critical illness and individual factors such as body composition may be important when considering how individuals might respond to nutrition interventions [ 3, 4]. This narrative review aims to provide a summary and interpretation of the adult critical care nutrition literature, with a particular focus on continuing practice gaps and areas with new data, to help clinicians make practical, yet evidence-based decisions regarding nutrition management during critical illness.

The metabolic response to critical illness and the role of nutrition therapy

It is recognised that 'one-size fits all' and 'set and forget' approaches to nutrition do not adequately address the complex metabolic, hormonal, and immunological changes that occur with critical illness [ 3, 5]. It is essential that clinicians understand these processes and the impact on nutrient metabolism [ 4]. In 1942, Cuthbertson described two distinct metabolic phases during acute illness-the 'ebb' or early shock phase, followed by the 'flow' or catabolic phase [ 6]. In brief, the 'ebb' phase is characterised by haemodynamic instability and hormonal changes (including insulin resistance) in order to prioritise the delivery of energy substrates to vital tissues [ 6, 7]. This survival mechanism results in endogenous glucose production as well as lower energy expenditure compared to pre-injury [ 4]. The 'flow' phase involves the breakdown of tissue (including lean muscle tissue) in order to provide substrates to cover the immediate needs for the 'fight or flight' response and to reduce the risk of bleeding and infection [ 4]. More recently, a third, anabolic recovery phase has been described [ 3]. It is during this recovery phase when resynthesis of lost tissue can take place and the body may be more metabolically able to process delivered nutrients [ 3, 4]. Currently, there is no known clinical marker to identify when an individual shifts from one phase of critical illness to another. For the purposes of this review which aims to provide practical recommendations, we have adapted the terminology from the 2019 European Society of Parenteral and Enteral Nutrition (ESPEN) critical care guideline to describe the different stages of critical illness: ICU day 1-2 (acute early phase), ICU day 3-7 (acute late phase), and after ICU day 7 (recovery phase) [ 2].

While it is considered that nutrition may be more physiologically available and hence more important in the later phase of illness, due to the average intensive care unit (ICU) length of stay (LOS), the majority of nutrition trials have provided nutrition interventions in the acute phases of illness (regardless of the intended trial intervention period). Traditionally, it was thought that aggressive nutrition in the early stages of critical illness may improve clinical outcomes. However, evidence from recent randomised controlled trials (RCTs) does not support this, finding no benefit or harm with early nutrition delivery [ 8- 11]. An explanation for this may be because a substantial amount of energy was provided in a period of critical illness where energy expenditure is decreased and endogenous production is enhanced [ 4]. Specifically, harm was observed in The Early Parenteral Nutrition Completing Enteral Nutrition in Adult Critically ill Patients (EPaNIC) trial, the largest nutrition trial in critical illness [ 10]. In a study of 4640 mixed ICU patients ( n = 2818 (61%) cardiac surgery patients) who were eligible to receive EN, late initiation of PN (started on day 8 of the ICU stay) led to an increase in the proportion of patients discharged alive and earlier from ICU and hospital (hazard ratio (HR) 1.06; 95% CI 1.00-1.13; p = 0.04 for both) when compared to PN commenced within 48 h of ICU admission [ 10]. Late initiation PN also led to a reduction in infectious complications (22.8% vs 26.2%, p = 0.008), cholestasis, duration of mechanical ventilation (MV), duration of renal replacement therapy, and health care costs [ 10]. Most recently, results from the largest enteral nutrition (EN) trial, The Augmented versus Routine approach to Giving Energy Trial (TARGET), support the theory that augmented energy delivery in the early phase of illness does not improve clinical outcomes compared to standard care [ 8]. This pragmatic prospective RCT of 3957 patients assessed 90-day mortality with augmented energy delivery (based on a predictive estimate of 1 ml/kg ideal body weight for height per day), compared to routine care [ 8]. Energy delivery was 50% higher in the intervention group (~ 30 kcal/kg ideal body weight/day) over the median 6-day nutrition delivery period (and approximated clinician estimated energy aims) but did not impact mortality or any secondary clinical outcomes [ 8]. However, it must be noted this study included a very 'general' (or unselected) population and that overfeeding may have occurred. Further post hoc work may increase the understanding and clinical implications of these results. Lack of benefit has also been observed with hypocaloric (low energy and adequate protein) and trophic (low energy and protein) feeding strategies compared to standard care, also provided early in critical illness and for short periods [ 9, 12]. The results of these trials support the hypothesis that for mixed ICU patients, nutrition interventions in the acute early and acute late phase of critical illness may not impact clinical outcomes and may cause harm in some groups. Therefore, less than 100% of energy expenditure should be targeted in this period due to endogenous glucose production. It remains unknown whether nutrition interventions continued for longer, impact functional recovery and quality of life [ 3].

Guidelines for nutrition therapy in critical illness

There are currently four international clinical practice guidelines available to inform the nutrition management of critically ill patients [ 1, 2, 13, 14]. Table summarises each guideline and outlines key recommendations and their level of supporting evidence.

Table 1

Guideline

Basis of recommendation

Energy requirements

Protein requirements

Commencement of ENa

Commencement of PN

ASPEN/SCCM (2016)

Observational studies, RCTs, and consensus opinion from topic experts

Use IC (quality: very low)

1.2-2 g/kg/day (quality: very low)

Early EN (24-48 h) (quality: very low)

Exclusive PN (when oral intake or EN contraindicated) for patients at low nutrition risk, withhold for the first 7 days (quality: very low)

For patients at high nutrition risk or severely malnourished start PN as soon as possible (EC)

Supplemental PN b should be considered after 7-10 days if unable to meet > 60% of energy and protein requirements by EN (quality: moderate)

Patients at low nutrition risk, well-nourished, and/or with low disease severity do not require specialised nutrition therapy over the first week in ICU (EC)

Patients at high nutrition risk or severely malnourished, EN should advance to goal as quickly as tolerated over 24-48 h in (while monitoring for refeeding) (quality: very low)

Obesity: high protein, BMI 30-40 = 2.0 g/kg IBW/day; BMI ≥ 40 = up to 2.5 g/kg IBW/day (EC)

In the absence of IC use 25-30 kcal/kg/day (EC)

Obesity: hypocaloric nutrition, 65-70% measured requirements by IC. If no IC, BMI 30-50 = 11-14 kcal/kg ABW/day; BMI > 50 = 22-25 kcal/kg IBW/day (EC)

Canadian Clinical Practice Guidelines (2015)

RCTs and consensus opinion from topic experts

Nil

Nil

Early EN (within 24-48 h) (based on 16 level 2 studies c)

Exclusive PN (when oral intake or EN contraindicated) should be considered early in nutritionally high-risk patients (based on 6 level 2 studies c)

For patients who are not malnourished, are tolerating some EN, or when PN is indicated for <10 days, low dose PN should be considered (based on 4 level 2 studies c)

Supplemental PN b should be assessed on case-by-case basis (based on 1 level 1 study and 7 level 2 studies c)

ESICM clinical practice guidelines (2017)

Observational studies, RCTs, and consensus opinion from topic experts

Nil

Nil

Early EN should be prescribed rather than delaying EN (low-quality evidence)

Nil

ESPEN (2019)

Observational studies, RCTs, and consensus opinion from topic experts

Use IC (grade B d)

1.3 g/kg/day delivered progressively (grade 0 d)

Early EN (within 48 h) (grade A d)

Exclusive PN (when oral intake or EN contraindicated) within 3-7 days (grade B d)

For severely malnourished patients, consider early and progressive PN (grade 0 d)

Supplemental PN b should be considered on a case-by-case basis (grade 0 d)

Hypocaloric nutrition (< 70% of EE) in the early acute phase (ICU day 1-3) (grade B d)

If using IC-isocaloric nutrition (80-100% EE) can be progressively implemented after day 3 (grade 0 d)

If using predictive equations-hypocaloric nutrition (< 70% of EE) for the first week (grade B d)

Obesity: 1.3 g/kg ABW/day (grade 0 d)

In the absence of IC use VO ₂ or VCO ₂ predictive equations (grade 0 d)

Obesity: if no IC, 20-25 kcal/kg ABW/day (grade 0 d)

Energy in critical illness

Determination of energy requirements is one of the most significant challenges in critical illness and is of vital importance as prescribed targets are used to guide nutrition delivery. Predictive equations that estimate energy expenditure are the most commonly used method due to their ease of application but are often inaccurate compared to measured energy expenditure using indirect calorimetry [ 15]. Table summarises why predictive equation estimates vary from measured energy expenditure [ 16, 17]. Importantly, inaccuracies increase at the extremes of weight, in the most severely unwell, and in older and more malnourished populations [ 16, 18]. Despite these failings, predictive equations continue to be widely used and are recommended in international clinical guidelines in the absence of indirect calorimetry [ 1, 2].

Table 2

Equation factors

Patient and system factors

* Sample size of the original equation

* Individual patient heterogeneity in the metabolic response to critical illness

* Differing body composition (fat-free mass and fat mass)

* Changes in medical management over time in elements that impact metabolism (like surgery, pain, and sedation practices)

* The characteristics of the original development population (including age, body composition, and disease state)

* The population characteristics in which the equation is used

* The addition of commonly used 'injury' or 'stress' factors

* Using an adjusted body weight with the equation

Estimating energy expenditure via VO₂ and VCO₂

Due to the persistent inaccuracies associated with the use of predictive equations, other methods (many of which have existed for some time) have been recently recommended in the 2019 ESPEN critical care guideline in the absence of indirect calorimetry [ 2]. Resting energy expenditure (REE) can be estimated via VCO ₂ (carbon dioxide production) from the ventilator and the rewritten Weir formula (REE = VCO ₂ × 8.19) or using VO ₂ (oxygen consumption) from a pulmonary artery catheter via the Fick method [ 19- 22]. A recent study in 84 critically ill patients reported a higher level of agreement between energy requirements estimated by the VCO ₂ method and measured REE compared to other predictive equations [ 20]. There are methodological limitations to note with this method: an assumed normal respiratory quotient (RQ) of 0.85 is used, which is the RQ of most nutritional products (with RQ = VCO ₂/VO ₂, normally ranging between 0.67 and 1.2 depending on the proportion of carbohydrate, fat, and protein being combusted) [ 23]. However, in critical illness, RQ may also be influenced by endogenous glucose production and by periods of hypo- and hyper-ventilation, and is likely to fluctuate between populations [ 19, 20].

Measuring energy expenditure in the critically ill-indirect calorimetry

Indirect calorimetry allows for the measurement of VO ₂ and VCO ₂ through the ventilator and is the gold standard method for measuring REE in critical illness when ideal test conditions are implemented [ 24]. Both the European (ESPEN) and American (ASPEN/SCCM) clinical practice guidelines recommend the use of indirect calorimetry to measure energy expenditure (Table ) [ 1, 2].

Despite the guideline recommendations, only three single-centre RCTs have investigated the impact of delivering energy according to a measured energy expenditure (via indirect calorimetry) compared to energy delivery using a 25-kcal/kg/day estimate (standard care) on clinical outcomes. The first, published in 2011, included 130 patients and observed a trend towards reduced hospital mortality (primary outcome) in the intervention group using intention to treat (ITT) analysis ( n = 21/65, 32.3%, vs 31/65, 47.7%, p = 0.058) [ 25]. However, infectious complications ( n = 37 vs 20, p = 0.05) and mean (± standard deviation) duration of MV (16.1 ± 14.7 vs 10.5 ± 8.3 days, p = 0.03) and ICU LOS (17.2 ± 14.6 vs 11.7 ± 8.4 days, p = 0.04) were increased in the intervention group compared to standard care [ 25]. In a more recent and slightly larger trial of 203 patients, no differences were observed in the primary outcome (self-reported physical component summary score of SF-36 at 6 months) between intervention and control in the ITT analysis ( n = 199, 22.9 vs 23.0, p = 0.99, respectively) or in any clinically important secondary outcomes [ 11]. However, in a post hoc analysis, a longer median (interquartile range) ICU LOS was observed in the intervention group (8 (5-25) vs 7 (4-12) days, p = 0.03) [ 11]. Lastly, in a pilot study ( n = 40), no statistically significant differences were observed between groups in the primary outcome of change in bioelectrical impedance phase angle (related to nutritional status and prognosis) from baseline to ICU discharge [ 26]. However, a declining trend in mean phase angle was observed in the standard care group (3.31 ± 1.34° to 2.95 ± 1.15°, p = 0.077), and a significantly shorter ICU LOS was reported in the intervention versus the standard care group (13 ± 8 vs 24 ± 20 days, p < 0.05) [ 26].

Consistently across all three RCTs, indirect calorimetry was feasible and energy targets were more closely met when using indirect calorimetry in place of fixed-energy prescription. Methodological characteristics must be noted in interpreting these results; all studies were unblinded and single-centre in design and were likely underpowered to demonstrate true differences in clinical and functional recovery outcomes. Further, these studies aimed to meet 100% of indirect calorimetry targets early in the ICU admission, which recent evidence suggests is not beneficial, and there was limited investigation into high-risk subgroups in which indirect calorimetry may have avoided harm by under- or overfeeding (i.e. obesity). Despite this, these studies do not suggest that indirect calorimetry to guide energy delivery is superior to using predictive equations with regard to improving clinical outcomes.

Measurement or estimation of energy expenditure?

Regardless if energy expenditure is measured or estimated, there is no consensus on how much energy should be provided. Based on current evidence, the most significant benefit of using indirect calorimetry is to personalise energy prescription and avoid under- or overdelivery of energy across the different phases of critical illness. For this reason, it is the opinion of the authors that if indirect calorimetry is available, it should be used primarily in patients where the clinicians are concerned about under- or overestimating energy needs (i.e. obese and underweight individuals) [ 27]. When used, clinicians should aim for high-quality tests by reaching a steady test state (defined as a variation in VO ₂ and VCO ₂ less than 10% over five consecutive minutes), conduct tests for ≥ 30 min, and repeat tests at least weekly (or more frequently if clinically indicated) [ 24].

For the majority of clinicians, current practice will continue to include the use of a predictive equation for estimation of energy needs. Clinicians must be aware that accurate estimation of energy expenditure with a predictive equation requires considerable knowledge of the underlying patient condition, the factors that alter the metabolic response to illness, and the limitations of the equation being used. It is also important to consider that delivery of calories to meet measured or estimated energy expenditure may not equate to what should be provided to improve outcomes. This may be particularly relevant in the acute early phase of critical illness where endogenous substrate mobilisation provides a substantial portion of the energy requirement and insulin resistance occurs, and therefore, a conservative energy target should be the aim [ 28]. Energy prescription and energy delivery (including non-nutritional sources such as dextrose and propofol) should be regularly reviewed in the context of the patient's clinical condition and metabolic phase to prevent considerable under- or overfeeding [ 29].

Protein in critical illness

In states of stress, such as in critical illness, the synthesis of acute phase proteins and those involved in immune function increase to support recovery [ 30]. Rapid and significant loss of skeletal muscle mass occurs to provide precursor amino acids to aid this process [ 31]. Despite a lack of definitive evidence, clinical guidelines recommend protein delivery of between 1.2 and 2 g/kg/day (Table ) based on the assumption that like energy, delivery of adequate protein will attenuate skeletal muscle wasting and improve clinical outcomes. The ASPEN/SCCM guidelines also make recommendations for higher protein provision in specific clinical conditions (i.e. burns, obesity, and multi-trauma), which again are based on limited, primarily observational data and expert opinion [ 1]. The variation in the clinical guideline recommendations for protein delivery reflects the lack of good quality trials investigating the role of protein provision on clinical outcomes.

Protein delivery and clinical outcomes

Higher protein provision has been associated with improved survival in a number of observational studies [ 32- 36]. Conversely, higher protein delivery during ICU admission has led to increased urea production and has been associated with increased muscle wasting in a small observational study [ 10, 11, 31, 37].

In RCTs aiming to compare high versus lower protein delivery in critical illness, no benefit has been shown with an increased protein dose, although most have been underpowered to demonstrate an effect on clinical outcomes [ 11, 37- 39]. The largest RCT ( n = 474) investigating intravenous protein provided at a dose of up to 100 g/day compared to standard care found no impact on the primary outcome of renal dysfunction [ 37]. A smaller RCT compared intravenous protein at a dose of either 0.8 g/kg ( n = 60) or 1.2 g/kg ( n = 59) delivered over ten days while controlling for energy intake [ 38]. While there was no difference in the primary outcome of handgrip strength, the group who received the higher protein dose had less fatigue and higher forearm thickness (using ultrasound) at day 7 [ 38]. However, these findings may be impacted by unadjusted confounders and must be interpreted with caution [ 40].

Timing of protein delivery may also influence clinical outcomes. Two observational studies have reported increased survival with early increased protein delivery (day 3-4) [ 32, 33]. In the largest study ( n = 2253), early protein delivery (> 0.7 g/kg/day versus ≤ 0.7 g/kg/day) was associated with increased survival (adjusted HR 0.83, 95% CI 0.71-0.97, p = 0.017) [ 33]. Contrary to these findings, in a post hoc secondary analysis of the EPaNIC trial, a cumulative protein dose, rather than the cumulative glucose dose, early during ICU stay was associated with delayed ICU discharge [ 41]. Further, a single-centre retrospective cohort study ( n = 455) reported a lower protein intake (< 0.8 g/kg/day) before day 3 and high protein intake (> 0.8 g/kg/day) after day 3 was associated with lower 6-month mortality (adjusted HR 0.609; 95% CI 0.480-0.772, p < 0.001) compared to patients with overall high protein intake [ 42]. Prospective, randomised data is required to inform the most appropriate amount and timing of protein to deliver to critically ill patients. Adequately powered RCTs are urgently needed to better understand the impact of both protein dose and timing on clinical outcomes in critical illness. Such trials should ideally control for energy delivery, by ensuring it is consistent across both the intervention and control groups.

How much energy and protein do patients get in clinical practice?

One of the most important pieces of information that clinicians should consider is that patients do not receive the energy and protein dose that is prescribed. In a recent retrospective observational study of 17,524 patients, the mean ± standard deviation energy and protein received was 56 ± 30% and 52 ± 30% of the intended aim, respectively [ 43]. This has consistently been shown across different time periods and geographical regions [ 44]. The reasons for this are multifactorial, including interruptions to EN for procedures, delayed initiation of nutrition, and gastrointestinal intolerance [ 45].

What energy and protein targets should clinicians aim for?

In light of the current evidence, the authors support the gradual introduction of nutrition therapy during the acute phases of critical illness, with energy and protein targets outlined in Fig. . In patients who are 'at risk' of refeeding syndrome, it is crucial that nutrition therapy is introduced slowly, and electrolytes are monitored closely and replaced as necessary [ 46]. If hypophosphatemia is present (e.g. < 0.65 mmol/l) in the first few days after starting nutrition therapy, then energy delivery should be restricted to ~ 50% requirements for 2-3 days [ 47].

Enteral nutrition

When to start?

Early provision of EN (within 48 h of ICU admission) in patients who are mechanically ventilated is an established standard of care and supported by all clinical guidelines [ 1, 2, 13, 14].

How should EN be delivered?

The most common method of delivering EN in ICU is via a gastric tube, with a continuous hourly infusion. However, this continuous supply of nutrients does not mimic normal volitional intake which is most commonly in the form of boluses followed by periods of fasting. Recently, it has been proposed that bolus (intermittent) feeding may be more physiologic and therefore superior to continuous feeding [ 48]. A systematic review was conducted as part of the recent ESPEN guidelines to investigate whether bolus EN has an advantage over continuously administered EN [ 2]. Including 5 small prospective studies and 236 patients, a significant reduction in diarrhoea was observed with continuous versus bolus administration of EN (RR 0.42, 95% CI 0.19-0.91, p = 0.03) [ 2]. No differences in gastric residual volume, rates of aspiration, or pneumonia were observed. It has also been suggested that muscle protein synthesis may be improved when EN is delivered via a bolus when compared to continuous delivery, and a phase II multicentre RCT has recently completed recruitment to investigate this question ( ClinicalTrials.gov NCT02358512) [ 5, 48]. Moving from continuous to bolus delivery of EN in the ICU is a significant change to practice in most countries, which would require a variation in feeding protocols and extensive education of clinical staff. Due to the considerable practice change associated, until definitive evidence is available to support one method of delivery over the other, it is reasonable that clinicians continue to deliver EN via a continuous infusion.

EN delivery-an ongoing challenge

International guidelines are unanimous in favouring EN delivery into the stomach or small bowel over parenteral nutrition (PN) [ 1, 2]. Due to continued and consistent recommendations to meet energy requirements over many years, many strategies to 'optimise' EN delivery closer to predicted targets have been tested, including the use of evidence-based feeding protocols, small bowel feeding tubes, prokinetic drugs, and increase of the acceptable gastric residual volume [ 49- 58]. Guideline recommendations to maximise EN delivery are summarised in Table . Despite the implementation of such interventions, these trials have observed modest to no increase in nutrition delivery and none have demonstrated a beneficial effect on clinical outcomes, potentially related to the disconnect between 'delivery' and 'utilisation' of nutrients.

Table 3

Strategy

Evidenced-based feeding protocol

GRV (minimum 500 ml cut-off)

Appropriate and timely use of prokinetics for EN intolerance

Post-pyloric tubes for EN intolerance

ASPEN/SCCM (2016)

Use an EN protocol (designed and implemented to increase the overall percentage of goal energy delivered) (quality: moderate to high)

Do not use GRVs as part of routine care to monitor ICU patients on EN

If GRVs are used, use 500ml cut-off (quality: low)

Use metoclopramide or erythromycin where indicated (quality: low)

Nil

Canadian Clinical Practice Guidelines (2015)

Use an EN protocol (that details strategies to improve delivery of EN) (based on 2 level 2 studies and 3 cluster RCTs a)

Use GRV of 250-500 ml every 4-6 h (based on 3 level 2 studies a)

Use metoclopramide where indicated (based on 1 level 1 study and 5 level 2 studies a)

Use post-pyloric tubes for patients at high risk for intolerance to EN or aspiration (based on 16 level 2 studies a)

ESPEN (2019)

Nil

EN should only be delayed when GRV is > 500 ml/6 h (grade 0 b)

Use IV erythromycin as a first line therapy (grade of recommendation B b) or use IV metaclopramide or combination therapy (grade 0 b)

Alternatively, combination therapy (IV metoclopramide and erythromycin) (grade 0 b)

Use post-pyloric feeding for EN intolerance not resolved with prokinetics (grade B b)

Parenteral nutrition

When to start?

PN is indicated when the delivery of nutrients via the gastrointestinal tract is contraindicated or insufficient. PN can be provided either as a full source of nutrition (exclusive PN) or as an additional nutrition source when full requirements are not able to be met by oral intake or EN (supplemental PN). Recent RCT evidence has indicated there are no differences in clinical outcomes, including mortality and infective complications, when PN is provided versus EN in a modern day ICU setting and when energy provided is comparable in both groups [ 59, 60]. Guideline recommendations for when to commence PN differ and are outlined in Table . Due to the potential harm with early PN, it is the opinion of the authors that if oral intake or EN is contraindicated, then PN should only be considered between ICU days 3 and 7 and that supplemental PN be considered on an individual case-by-case basis (Fig. ).

Body composition analysis

The measurement of weight and muscularity is important in the assessment of nutrition status and monitoring the effectiveness of nutrition interventions [ 61]. However, due to the extreme fluid shifts that critically ill patients experience, measured weight and/or muscularity assessed by traditional bedside methods (e.g., subjective physical assessment, mid-arm muscle circumference) may be inaccurate in this patient population [ 62- 64]. Table summarises the emerging tools for assessment of muscularity in the ICU setting: computed tomography image analysis, bioimpedance analysis, and ultrasound. Currently, these methods for assessing muscle mass and quality are mostly limited to research [ 64- 66]. There is an essential need to evaluate which bedside tools can accurately measure muscle mass, and identify those individuals with lower than normal muscularity, as well as to better understand the clinical importance of changes in muscle health and the interface with nutrition interventions in critical illness.

Table 4

CT image analysis at the abdominal (L3) area

* Muscle CSA (cm ²)

* Specialised software can be used to measure muscle area and density using a CT slice at L3

* Provides specific and precise results

* Limited for use in patients who have had a CT at L3 area

* Specialist training and time required for analysis

* Published cut-off values to identify patients with lower than normal muscularity

* Quantification of muscle CSA at L3 is highly correlated to whole body muscle (using scans performed for clinical purposes)

* Muscle quality (density) (Hounsfield units)

Bioimpedance analysis (multi-frequency or spectroscopy)

* Fat-free mass (kg)

* Involves application of a weak current at differing frequencies, through electrodes placed on the hands and feet

* Easy and quick to use

* Fat-free mass estimates are not likely to be reliable in critically ill patients who experience significant fluid shifts

* Positioning (separation in limbs) and electrode placement may be challenging in some ICU patients

* Safe (no radiation involved)

* Total body water, percentage body fat, and fat-free mass are estimated via regression equations (with assumed constants for estimating intra- and extracellular water)

* Raw data such as phase angle (which is independent of weight and related to cellular health) may be a predictor of outcome in critically ill populations

* Phase angle (50 kHz)

Ultrasound

* Muscle thickness (cm)

* Muscle thickness and CSA can be measured at different sites (i.e. quadriceps, upper arm)

* Readily available in most ICUs

* No consensus on the ideal sites to predict whole body muscle or to monitor changes over time

* Role of oedema on measurements is unclear

* No widely accepted cut-points to identify patients with low muscularity

* Easy, safe, and quick to use

* Muscle quality can also be assessed using specialist software

* Muscle CSA (cm ²)

* Muscle quality (echogenicity)

Nutritional management in critically ill subgroups

RCTs conducted to date have focused on key practice questions, but included heterogenic populations. These studies have not shown clinical benefit with nutrition interventions for reasons previously discussed though there are several patient subgroups that may still benefit from nutrition interventions. In an attempt to investigate such groups, a number of large RCTs have included pre-planned subgroup analysis (e.g. response to the intervention according to differing BMI category). However, results from these types of analyses must be interpreted with caution as the sample size may be small. Moreover, if a benefit or harm is observed in a subgroup, but the overall trial result suggests no difference, it must be considered that another subgroup hidden in the heterogeneous population may have experienced the opposite effect.

Malnourished

The diagnosis of malnutrition in critically ill patients is challenging. Diagnostic tools, such as the widely used Subjective Global Assessment (SGA) and criteria outlined in the recent Global Leadership Initiative in Malnutrition (GLIM) recommendations, rely heavily on obtaining accurate anthropometrical data, weight and diet history, and the assessment of muscle mass, all of which are difficult to acquire in the acute early phase of ICU admission [ 61]. For this reason, RCT evidence attempting to investigate if patients who may be malnourished respond differently to nutrition is limited to subgroup analysis in patients with differing BMI categories or nutrition risk scores [ 10, 12, 67]. To date, no benefit has been observed when more or less nutrition is provided in these subgroups although the numbers included are often small. Further, BMI is a poor surrogate measure for malnutrition, and commonly used nutrition risk scores have not been well validated, which limits any conclusions on how nutrition therapy may affect outcomes in this vulnerable subgroup [ 2]. Despite the lack of evidence in this area, the authors support minimising progression of malnutrition. Where possible, clinicians should use local hospital guidelines or the recent GLIM criteria, combined with clinical judgement to diagnose malnutrition. As outlined in Fig. , in severely malnourished patients, we encourage early low dose nutrition therapy in the acute early phase, with a slow progression to target during the acute late phase, while carefully monitoring for refeeding syndrome.

Obese

The unique and complex care needs of obese patients (BMI ≥ 30 kg/m ²) are amplified when they become critically ill and include a greater risk of insulin resistance and loss of lean muscle mass, and wide variations in macronutrient metabolism, which makes nutrition management complex [ 4, 68]. There is currently very limited, low-quality evidence to inform nutrition provision in the critically ill obese patient, and as a result, the latest clinical guidelines provide inconsistent recommendations regarding energy and protein targets (Table ).

In the TARGET trial, 1423 obese critically ill patients were included, representing the largest population of obese patients in an ICU nutrition study [ 8]. While not statistically significant, the obese subgroup was the only pre-specified subgroup where the point estimate sat on the side of benefit with greater energy delivery [ 8]. These results require formal evaluation in a robust, adequately powered and blinded clinical trial; however, they highlight that obese patients may respond differently to nutrition delivery than non-obese individuals and that there is a critical need for further research in this patient group.

In the absence of definitive evidence of the impact on functional recovery in particular, it is the opinion of the authors that obese patients should be managed like any other patient admitted to the ICU. If predictive equation estimates are used, a method to adjust body weight should be used in the nutrition prescriptions (not actual weight), and delivery monitored carefully with the knowledge that most predictive equations significantly underestimate requirements in this group [ 69]. It may be appropriate to consider a weight loss regime in the recovery phase once the acute illness has resolved.

The non-ventilated patient

Critically ill patients who are not intubated may have prolonged periods of inadequate oral intake. In a prospective observational study, 50 patients who were not receiving any EN or PN were studied for 7 days following endotracheal extubation [ 70]. The average daily energy and protein intake failed to exceed 50% of daily requirements on all 7 days for the entire population [ 70]. To prevent malnutrition, it is important that clinicians monitor the oral intake of awake patients and the authors support the ESPEN guideline recommendation that medical nutrition therapy should be considered for all patients staying in the ICU for > 2 days regardless of their ventilation status [ 2].

Post-ICU

The limited data available indicates that the predominant mode of nutrition following an ICU admission is via the oral route and nutrition intake in this period remains below clinician recommendations. In 32 patients from 2 centres, nutrition intake was assessed 3 times per week in the post-ICU phase [ 71]. Oral nutrition was the most common type of nutrition therapy (55% of study days) [ 71]. The median [interquartile range] energy and protein intake was 79% [41-108%] and 73% [44-98%], respectively; however, considerable variation was observed depending on the type of nutrition therapy provided, with energy and protein provision the lowest in patients who received no additional oral nutrition supplements (37% [21-66%] of target energy and 48% [13-63%] protein) [ 71]. A second single-centre study of patients with traumatic brain injury indicated poorer intake post-ICU compared to in ICU, and nutritional deficit was significantly greater in patients who consumed oral nutrition alone compared to those receiving artificial nutrition support [ 72]. Despite this, dietitians spent just 20% of their time managing patients receiving oral nutrition therapy and saw the patients a mean of 2.2 (1.0) times per week for 34 (20) min per occasion on the post-ICU ward [ 72]. The predominant issues impacting nutrition intake are reported as appetite, disinterest in food, and taste changes [ 73].

Unfortunately, non-individualised, 'one-size fits all' processes to the management of nutrition are likely impacting on nutrition adequacy in the post-ICU period. In one of the only studies investigating processes that impact nutrition in the post-ICU period, it was found that of nine patients transferred to the post-ICU ward, six had their gastric tube removed on the advice of the medical team without assessment of nutrition intake [ 73]. Early removal of gastric tubes may improve patient comfort and is encouraged by many post-surgical protocols, but has the potential to negatively impact nutrition intake [ 73]. The decision to remove a tube should be made on a case-by-case basis and after consultation with the patient, the treating team, and the dietitian [ 74]. Among other possible causes, it is plausible that inadequate nutrition following critical illness may result in significant energy and protein deficit and may explain the lack of benefit in long-term outcomes observed in nutrition studies that have delivered an intervention in the acute early and late phases. This is an important knowledge gap for investigation and to provide initial insights; a multicentre RCT is underway ( ClinicalTrials.gov NCT03292237).

Conclusion

Results from recent large-scale trials highlight that in heterogeneous groups of patients, full feeding in the acute phases of critical illness does not provide an advantage over trophic feeding and may be harmful. It remains uncertain what impact specific nutrition interventions have in the recovery phase of illness and in specific subgroups who may respond differently to nutrition interventions. The effect of nutrition delivery on other clinically meaningful outcomes, such as muscle health and physical function, is also insufficiently studied. We recommend nutrition prescriptions that tailor for pre-admission nutrition status, and severity and stage of illness. Particular attention should be paid to patients that are in (or likely to stay in) ICU for greater than a week, with ongoing monitoring of nutrition delivery and regular review of measured or estimated nutrition requirements.

Abbreviations

ASPEN/SCCM

American Society of Parenteral and Enteral Nutrition/Society of Critical Care Medicine

ESPEN

European Society of Parenteral and Enteral Nutrition

ICU

Intensive care unit

PN

Parenteral nutrition

RCT

Randomised control trial

Authors' contributions

EJR conceived of the idea. KJL and EJR drafted the manuscript. All authors reviewed and commented on the manuscript and approved the final draft.

Availability of data and materials

Not applicable.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

EJR has received an honorarium and has unrestricted, investigator-initiated grant funding from Baxter Healthcare Corporation for trial Clinicaltrials.gov NCT03292237. The other authors declare that they have no competing interests.

Footnotes
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References

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6. Cuthbertson DP. Post-shock metabolic response. Lancet. 1942;239(6189):433-437. [ Google Scholar]

14. Critical Care Nutrition . The Canadian clinical practice guidelines. 2015. [ Google Scholar]

33. Bendavid I, Zusman O, Kagan I, Theilla M, Cohen J, Singer P. Early administration of protein in critically ill patients: a retrospective cohort study. Nutrients. 2019;11(1):106. [ PMC free article] [ PubMed]

50. Heyland DK, Lemieux M, Shu L, Quisenberry K, Day AG. What is "best achievable" practice in implementing the enhanced protein-energy provision via the enteral route feeding protocol in intensive care units in the United States? Results of a multicenter, quality improvement collaborative. JPEN J Parenter Enteral Nutr. 2016;42(2):308-17. [ PubMed]

# data[].attributes.attachment_link.title
Nutrition therapy in critical illness: a review of the literature for clinicians

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Nutrition therapy during critical illness has been a focus of recent research, with a rapid increase in publications accompanied by two updated international clinical guidelines. However, the translation of evidence into practice is challenging due to the continually evolving, often conflicting trial findings and guideline recommendations.

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Appropriate wound healing is achievable in children over 1 year receiving 2-3g protein/day

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https://www.rch.org.au/rchcpg/hospital_clinical_guideline_index/Nursing_management_of_burn_injuries/

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Introduction Definition of Terms
Assessment - ABCD

Management - Fluids and Burn Dressings
Companion Documents Evidence Table References
Introduction

Children are vulnerable to sustaining a burn injury due to their physiological, psychological, and developmental differences.

Burn injuries have a significant impact on paediatric patients and may affect a range of body systems. The impact of these injuries on children and families is often long lasting. As the injury itself and required treatment often causes distress, pain and anxiety, appropriate management by nurses is essential in providing family centered care.

Ongoing care requirements are based on the size, depth, anatomical site and mechanism of injury.

Aim

The aim of this clinical guideline is to assist and support nursing staff at The Royal Children's Hospital to plan and deliver care to children with burn injuries, across all departments including: Emergency, Paediatric Intensive Care Unit, Inpatient Units, Theatres and Outpatients.

Definition of terms

Burns Multidisciplinary Team - consists of Burns Consultant/Fellow, Burns Clinical Nurse Consultant, Burns registrar/resident, Nurse Coordinator, Occupational Therapist, Physiotherapist, Dietitian, Social Work, Mental Health, Child Life Therapy (CLT), Specialist Clinics Team.

% TBSA - percentage of total body surface area burnt (not including erythema or superficial burns) calculated using theLund Browder chart.

Minor Burn - In paediatric burns a minor burn is considered to be less than 10% TBSA.

Major Burn - In paediatric burns a major burn is considered to be more than 10% TBSA.

Assessment

Burn injuries cause a significant insult on the body and a thorough ABCD assessment, followed by a full head to toe and focused assessment are vital to ensure clinical issues/deterioration are identified early and appropriate management initiated. See Burns- Acute management CPG for further details of burn injury assessment.

Assessment of the pediatric patient with a burn injury should occur on admission and regularly throughout care.

Detailed information regarding completion and documentation of ABCD, head to toe and focused assessments can be located on the Nursing Assessment Clinical Guideline.

Burns specific information is outlined below.

Airway and Breathing

Assessment and monitoring of airway patency and breathing should be carefully observed as patients at risk of inhalation burns can deteriorate up to 72 hours post burn injury, particularly if they have:

Sustained burns in an enclosed space (at risk due to smoke inhalation)

Have facial burns

Singed nasal hairs

Facial swelling

Blackened sputum

Stridor or hoarseness of voice

Respiratory distress/increased work of breathing

If inhalation burns are suspected high flow oxygen therapy via a Hudson mask should be administered to the patient and changes/abnormal findings reported to the treating team immediately for further assessment and management.

Circulation

Children who sustain burns injuries are at increased risk of circulatory compromise due to significant fluid loss and fluid shifts, these patients must be closely monitored for:

Signs and symptoms of hypovolemia.

Signs and symptoms of hypothermia.

Other circulatory concerns include:

Circumferential burns should be identified, monitored for circulatory compromise ( neurovascular observations nursing guideline) and the affected area elevated where ever possible.

Consider the need for an ECG and continuous cardiac monitoring if the burn is of electrical origin.

Pain assessment

Detailed information regarding paediatric pain assessment can be located on the Pain Assessment Nursing Clinical Guideline. Information regarding procedural pain management can be located on the Procedural Pain Management Clinical Guideline.

Wound assessment

Assessment of the burn injury should occur on the initial presentation to the Royal Children's Hospital as well as prior to completing wound care throughout the inpatient stay and outpatient visits. Burn injuries can take up to 10 days to truly present the depth and extent of injury so reassessment is vital. As burn injuries heal accurate wound assessment will ensure wound management is altered as needed to ensure appropriate wound care continues to be delivered to the patient.

Wound assessment of a burn injury includes (available on Electronic medical Records):

Assessment of Total Body Surface Area (TBSA) burnt, utilising the Lund Browder chart. Areas of erythema and superficial burns are not included in calculations of TBSA.

Assessment of depth of burn injury.

Assessment of wound healing.

Accurate documentation of wound assessment should be recorded.

Further information regarding wound assessment in a burn injury can be located on the Burns Clinical Practice Guideline as well as the Burns Unit: Clinical Information.

Further information regarding wound assessment and healing can be located on the Wound Care Clinical nursing guideline.

A thorough patient history should be collected on admission to hospital.
Specific information regarding the burn injury must be obtained from the patient, family and first responders as this will inform ongoing treatment. History taking should include:

Time of injury

Mechanism of injury: How the burn occurred/type of burn, including length of exposure and estimated temperatures of heat source.

Was first aid completed? If so, what type and for how long?

Tetanus status of the patient (if not up to date consider immunisation, see Immunisation of inpatients Clinical Guideline.)

In addition to this information a detailed patient and family history should also be obtained. Further information regarding this can be located on the Nursing Assessment Nursing Clinical Guideline.

Non accidental injuries must be considered when the history does not match with the injury or inconsistencies with the history/story occur. Refer to medical staff & social work. Victorian Forensic Paediatric Medical Service (VPFMS) can also be notified.
For further information regarding non accidental injuries refer to the Child Abuse Clinical Guideline.

Social history

Burn injuries are traumatic and life altering events which can significantly impact the patient and their family. Early support from social work, contact with CLT and chaplains should be offered to the child, siblings and family. It may also be appropriate to consider referrals to mental health/psychology.

Management

First Aid

Completion of first aid for a child who has sustained a burn injury is an important initial aspect of care as it assists with pain relief as well as minimising the progression of tissue damage. First aid is effective for up to three hours post time of injury. If appropriate first aid was not initiated and it is still within the 3 hour time frame post burn injury, first aid should be completed as outlined below, prior to any wound care:

The area of tissue damage should be cooled with cool running water for 20 minutes.

Ensure the unburnt areas of the patient are covered and warm to prevent hypothermia.

Further information regarding burn injury first aid including burns to the eye area and chemical burns can be found on the Burns Clinical Practice Guideline.

Fluids

For initial fluid management see Burns Acute Management CPG

Burn injuries greater than 10% TBSA and including the dermis result in circulatory compromise secondary to fluid loss via damaged tissue, widespread vasodilation as well as increase capillary permeability and fluid shifts (third spacing). This can result in hypovolemia leading to burns shock. Therefore it is vital that adequate fluid is administered to the patient in combination with ongoing circulatory and fluid balance assessment.

A Strict Fluid Balance must be maintained at all times, including all intake (both intravenous and oral) and strict measurement of all output (weigh nappies, weigh pans/bottle, measure IDC)

Fluid resuscitation is required in patients who have >10-15% TBSA.

Patients receiving fluid resuscitation may need two large bore Intravenous cannulas inserted

Fluid resuscitation is calculated utilising the modified parkland formula. For further information regarding this please see the Burns Acute management CPG.

An IDC is essential for patients receiving fluid resuscitation to allow close monitoring of fluid status and adjustment of IVT as necessary.

Expected urine output is 1ml/kg/hr unless otherwise stated by the medical team.

U&E's should be monitored 8 hourly while patient is receiving fluid resuscitation.

Fluid resuscitation rates will need to be adjusted to accommodate the patients urine output.

Burn pain can be extremely intense and distressing for paediatric patients and can also be challenging to manage due to the individual experience and its unique characteristics. Initial and ongoing pain management is vital to ensure patient comfort, maximise healing and minimise risk of mental trauma/post-traumatic stress.

Initial pain relief should be administered immediately following an accurate pain assessment, further information regarding initial pain management can be located on the Burns Clinical Practice Guideline.

Pre-emptive analgesia may be necessary prior to re-positioning, physiotherapy and follow up outpatient appointments.

Reassessment and evaluation of pain management is vital, referral to Children's Pain Management Service may be necessary.

Burn pain experienced by patients is likely to increase during procedures such as dressing changes. Management of pain during burn dressing changes is discussed in detail below ( preparing for a dressing change).

Preparation for Burns Dressing

Preparation of patient and family

Burn dressing changes can produce feelings of anxiety and distress in both patients and their families. It is very important that both patients and families are physically and emotionally prepared and well informed regarding the procedure and the pain management options.

Families/primary care givers should be given a thorough explanation of the procedure, where appropriate pictures could be used to visualise the procedure along with orientation to the treatment room/bathroom to be used.

Referral to CLT prior to the procedure may assist in explaining and preparing the patient for the dressing change.
CLT are also able to empower the child to identify distraction techniques, as well as provide support and distraction throughout the procedure.

Where possible and appropriate children should be given the opportunity to choose whether they want to participate in wound care for example assisting to remove dressings.

For further information, staff and families can access reducing children's discomfort during tests and procedures kids health info factsheet. Assessment

Assessment

Children who are planned to undergo a burns dressing change should have an ABCD assessment completed along with pain assessment prior to the dressing change commencing.
The child will require continuous ABCD monitoring and pain assessment throughout the procedure to ensure that analgesics provide are adequate and effective.

Pre Medication/ Pain Relief

Burns dressing changes can be painful and distressing for children.
Nursing staff should assess the child's pain prior to the procedure commencing and pre-emptive analgesia should be administered. Staff should re-evaluate the effectiveness prior to the procedure commencing and throughout the procedure.
Choice of analgesia is an individual process and staff should take into account the % TBSA, depth, amount of debridement required as well as the pain tolerance, distress and past experience of the child. Review of analgesia/sedation requirements for previous dressing changes is essential.
The Children's Pain Management Service (CPMS) may also be utilised to assist in planning procedural pain relief for burns dressing changes.
Options may include:

Simple analgesia such as Paracetamol and NSAIDs

Oral Analgesia such as Opioids (Oxycodone), Tramadol, Ketamine and Oral Sedatives such as Benzodiazepines e.g. Diazepam, Midazolam

Intravenous Sedation/Analgesics including infusions, PCA or intermittent bolus (Morphine/Fentanyl/Ketamine)

Nitrous Oxide (refer to the procedural sedation ward and ambulatory care procedure)

Intranasal medications such as Intranasal Fentanyl

Anaesthetics may be involved to provide sedation (Ketamine/Propofol) and continuous monitoring of the patient.

A combination of the above options may be ordered and utilised to provide pain relief. Further information regarding this can be located on the Procedural Sedation - ward and ambulatory care procedure or through consultation with CPMS or comfort kids.

Pain Assessment should occur continuously throughout the procedure by observing the behaviour and comfort level of the child as well as using an appropriate pain assessment scale.
If analgesia and sedative agents prescribed are not providing effective pain management/sedation then the procedure should be paused until appropriate analgesia/sedation is available and pain is manageable. Escalation to the children's pain management service or Burns resident can occur at any stage throughout the procedure.
As the patient's burn injury heals, analgesia and sedative agents utilised throughout the procedure should start to be slowly weaned with the support of CPMS, medical teams and senior nursing staff.
All sedative agents should be administered in line with the Sedation and Procedural Sedation Ward and Ambulatory Areas procedure.

Staffing Requirements

To complete a burns dressing change in a safe and time efficient manner which minimises patient and family distress, staffing requirements must be considered.

Simple analgesia: 1-2 nursing staff of which 1 is experienced in burns dressing changes.

Oral sedation agents: 2-3 nursing staff of which 1 monitors the patient, 1 is experienced in burns dressing and 1 staff member assists.

Nitrous Oxide: 2-4 nursing staff of which 1 is accredited in nitrous oxide administration, 1 is experienced in burns dressing and 1-2 staff members assists

IV agents: An Anaesthetist and Anaesthetic technician are required; 2-3 nursing staff of which 1 is experienced in burns dressing and 1-2 nursing staff members to assist

All roles must be designated prior to commencement of dressing change and the patient should remain in line of sight to staff at all times. For further information refer to the Sedation and Procedural Sedation Guideline Ward and Ambulatory Care Areas procedure.
Burn injuries which have a large TBSA percentage and patients with reduced mobility may require increased staff numbers to assist in dressing changes. For further information refer to the High Dependency and Special Nursing Care nursing guideline.

Preparation of environment and equipment

For children who have larger %TBSA burn injuries (>10%) consider using a treatment area where heaters can be utilised to minimise the risk of hypothermia. These heaters should be turned on prior to the dressing change commencing. (i.e. Platypus Burns Bathroom, Theatre)

Adequate preparation of the environment should be completed prior to the child being taken into the treatment room/bathroom.

Consider the need to organise:

Physiotherapy/Occupational therapy - to review patient mobility and splinting requirements.

Medical team - to review burn injury and wound healing.

Clinical photography

Staff Roles

Prior to the procedure a team leader should be allocated. Other team member's roles/responsibilities ie. Dressings nurse, sedationist, observations nurse, hygiene nurses should also be communicated.
An ISBAR handover should also occur; identifying patient name, age, weight, allergies, procedure, any pre procedure medication and staff roles.

Burns dressing

Staff should adhere to the aseptic technique procedure for all aspects of wound care outlined below.

Removal of previous dressing

Removal of the previous dressing should not damage the healing burn wound and should be as atraumatic as possible. The use of an adhesive remover, normal saline or water will assist with gentle removal of previous dressings.

Wound Management

Clean the wound using a soft wipe with water, normal saline, pH neutral soap or cetrimide (please note cetrimide is not to be used on face or scalp). Enough pressure should be applied to debride the damaged skin and remove exudate, loose skin and slough.
Consider the need for a wound swab and complete if necessary.
Debridement of any blisters present allows for wound bed assessment and appropriate dressing application.
The wound and surrounding skin should be dry before application of the dressing.

Personal Hygiene

Ensure the patient's personal hygiene is thoroughly attended to if the burns dressing change is occurring in the bath or shower. If the patient is not having a bath use a sponge to clean non dressed areas.

Application of Burns Dressing

A thorough wound assessment should occur with every dressing change and will determine the appropriate dressing required (see wound assessment above).

Dressings should cover all area where tissue damage has occurred but avoid unburnt skin as maceration may occur.

A crepe bandage/tubifast/tubigrip assists with securing dressings as well as absorbing some excess fluid. They also add pressure to support with scar management.

Oedema is common in the initial days post burn, therefore tight circumferential bandages should not be applied. Elevation of the limb in the immediate days post injury will limit swelling.

Dermal burns produce a large amount of exudate in the initial few days and changing of the outer bandage or tubifast may need to occur. Where possible retaping/securement of the dressing should occur unless a dressing change is scheduled.

Common burn dressing product

Acticoat™ -
Note - Acticoat™ is a 3 day application
Acticoat 7™ is a 7 day application
Acticoat Flex is a 3 or 7 day application

Commonly used on partial to full thickness burns as well as burns of indeterminable depth in initial stages of injury.

- Moisten Acticoat ™ with sterile water, not saline, to activate

- Wring out excess water from Acticoat ™ using forceps. Silver or blue side to wound.

- Cover Acticoat ™ with Intrasite Conformable ™

- Cover the 2 layers with cling wrap and cut to appropriate size, ensuring no overlap of cling wrap on healthy skin.

- Apply dressing to wound

- Secure with tape e.g. Hypafix ™ or Mefix ™

- Reinforce dressing with crepe and tubifast/tubigrip

- Please review the Burns Unit: Clinical Information for pictures of an Acticoat™ dressing ( Burns Dressings).

Mepilex Ag™
Commonly used on superficial, mid dermal or deep dermal to full thickness facial burns or on areas where it is difficult to secure acticoat.

- Self-adhesive
Secure with tape e.g. Hypafix ™ or Mefix ™ or tubifast.

Bactigras™
Commonly used on superficial dermal wounds and doner site.

- Use in conjunction with gauze.

- Secure with tape e.g. Hypafix ™ or Mefix ™ or tubifast.

Xeroform™
Commonly used on small areas of unhealed burn when Silver products are no longer required. Also used on areas of hypergranulation.

- Kenacomb™ ointment may be applied prior to xeroform™ to areas of hyper granulation.

- Use in conjunction with Melolin™

- Secure with tape e.g. Hypafix ™ or Mefix ™ or tubifast.

Additional products may be utilised on burns wounds at the discretion of medical and nursing staff.

For further information regarding the above and additional products please refer to the wound care guideline.

Specific body areas

Facial Burn's Care

Facial burns may require regular wound care including cleansing followed by application of paraffin cream. Parents should be encouraged to be involved in providing this care.

If dressings are utilised on the face balaclavas can be made from large tubifast and used to secure dressing products.

Additional information can be located on the Burns Medical Treatment.

Hand Burn's Care

Any dressing applied to fingers, should ensure fingers are taped individually. Padding must be applied to web spaces to prevent further friction/pressure area injury. Initially fingers which have circumferential burns should be dressed with the finger tips exposed to monitor neurovascular status. Once oedema has decreased the finger tips can be enclosed in the dressing.

Referral to hand therapy is vital.

Documentation

A summary post dressing change should be documented including: pain relief/ sedation and effect, non-pharmacological techniques and effect, parental involvement, wound assessment, dressing product utilised, staff present (including allied health, interpreter etc.) and plan of ongoing care. See Nursing Documentation Clinical Guideline for further information.

Nutrition

Nutrition plays a vital role in burn healing, minimising complications of care and meeting the increased metabolic demands associated with paediatric patients with burns. A diet high in protein, calcium, energy and micronutrients (in particular Zinc and Vitamin C) has been shown to be most beneficial for wound healing. Children should be encouraged to eat and drink foods high in these nutrients and nutritional supplements such as Sustagen™ may also be required.

Insertion of a nasogastric tube and commencement of enteral feeds should be considered for children who sustain significant burn injuries and/or facial burns and are unable to tolerate adequate oral intake. Where possible feeds should commence within 6 - 8 hours of the burn injury.

Referral to the Burns Team Dietician is recommended for all patients with significant burn injuries, facial burns, infants as well as patients who are not tolerating adequate oral intake.

Management of Itch

Itching is a common and debilitating issue in the healing phase of a burn injury.

The following may assist in reducing itch:

- Advise child and parent to avoid scratching - short finger nails will assist in this.

- Consider use of antihistamines i.e. Periactin or Certizdine

- Avoid overheating the child

- Fragrance free moisturiser (Sorbolene™) may assist.

- Distraction will play a big role in patient comfort

Scar management:

Strategies to reduce scar development post burn injury include:

Regular bathing and showering

Massage with fragrance free moisturiser (Sorbolene™) should be massaged into the healed skin at least twice daily to daily.

Pressure therapy in the form of tubifast/tubigrip, tapes, pressure garments and silicone may be prescribed by Physiotherapy (PT) or Occupational therapy (OT). It is often recommended that garments are worn continuously except during personal hygiene.

Physiotherapy / occupational therapy - splinting & positioning:

Physiotherapy (PT) and Occupational therapy (OT) may be necessary throughout both inpatient stay and outpatient management for patients who have sustained a burn injury.
Significant burn wounds and those over joints are at high risk of contracture development. This can have an impact on both growth and mobility. Prevention of contractures needs to occur early and to assist in this PT and OT will prescribe patients with a splinting and positioning regime. To aid PT/OT in assessing the patient's burn injury and range of movement it is often beneficial for them to attend changes of dressings.
It is vital that these regimes are adhered to by nursing staff. Paediatric patients may find the splints and positioning regimes uncomfortable and distressing. It is important to educate both patient and family on the importance of splints and the positioning regimes. Strategies to support splinting and positioning regimes include:

Regular and pre-emptive analgesia

CLT, distraction and rewards (i.e. sticker charts)

Concerns regarding splinting and positioning regimes should be documented and reported back to PT/OT so as appropriate alterations to regimes can be initiated.

Discharge planning

The decision for a patient to be discharged should have involvement from the burns multidisciplinary team and family meetings may be beneficial for planning purposes. Early discussion regarding discharge may facilitate a smoother transition home for the family.

Children may be ready for discharge when:

Pain is able to be appropriately managed at home

An appropriate plan for wound care and follow up has been made

Nutritional requirements are being met

Mobility, positioning and splinting are able to be managed at home

The following should be discussed with the family and child prior to discharge

Pain management and itch plan, including plan for procedures (outpatients dressing changes)

Home care of burn wound

Nutritional requirements

PT/OT recommendations

Medical review

When to return to hospital - ED/Specialist Clinics

Companion documents

Nursing competency workbook - burns dressing, assessment, and fluid management of burns.

Links

Evidence table

The evidence table for this nursing guideline can be found here.

Please remember to read the disclaimer.

The development of this nursing guideline was coordinated by Kate Glassford, Nurse Coordinator & Clinical Nurse Specialist Platypus Ward, and approved by the Nursing Clinical Effectiveness Committee. Updated July 2022.

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Introduction Definition of Terms Assessment - ABCD Management - Fluids and Burn Dressings Companion Documents Evidence Table References Children are vulnerable to sustaining a burn injury due to their physiological, psychological, and developmental differences. Burn injuries have a significant impact on paediatric patients and may affect a range of body systems. The impact of these injuries on children and families is often long lasting.

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https://jeccm.amegroups.com/article/view/4372/4984#:~:text=Protein%20need%20in%20burned%20children,lower%20than%2035%25%20of%20TEI.

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Introduction

Polytrauma (multi-trauma) is a short verbal equivalent to describe (mainly) blunt trauma patients whose injuries involve multiple body regions or cavities, compromise the patients' physiology and potentially cause dysfunction of uninjured organs. These patients are at risk of higher morbidity and mortality than the summation of expected morbidity and mortality of their individual injuries ( 1). Burns are the main example of polytrauma, as they affect the skin, as well as the cardiovascular, respiratory and renal systems. In polytrauma management a pivotal role is played by nutritional support.

Among children, burns are a serious injury and one of the main reasons of trauma, especially during the first 5 years of life. For these patients, the nutritional support has been acknowledged as one of the most significant aspects of the medical burns treatment in terms of mere nutrition and protection from infections.

Energy target

In burned children, a sound increase in caloric requirement is necessary, as much as in adults, because of a marked hypermetabolism immediately or early after burn. Hypermetabolism can be caused by burn injuries, by the release of catecholamines just after the injury, but also by pain, anxiety, surgical procedures, and metabolic requirements by tissues. Moreover, it can persist for up 2 years post burn.

Resting energy expenditure (REE) has a curvilinear increasing trend according to the total burned surface area (TBSA). Hence, children with burns affecting ≤10% of total body surface area have a percentage of REE very close to the normal, whereas children with burns affecting more than 40% of TBSA have an increase in REE, which becomes 1-1.5 times higher than standard by the first 2 weeks post burn.

Evidence shows that in sterile environments, at a temperature of 30 °C, the metabolic rates of the patients under consideration are around 150% REE, and they decrease to 135% upon wound healing ( 2).

The loss of weight and the various metabolic measurements lead to the development of the concept of "hyper-nutrition" that causes a massive over-nutrition of the patient, such as the uptake of 5,000 kcal/die, that is considered normal according to the equation of Curreri ( 3). The supply of too many calories has been, nevertheless, often associated to an acceleration of metabolism, hyperglycemia, liver failure and an increase in the production of carbon dioxide ( 4- 6). Most equations and mathematic formulas, developed to estimate energy requirements in burned patients, use, in fact, body weight, age, sex and burned surface area as the key determinants of the calories intake, and they do not consider the wide range of variations along the timeline.

Over the last years, several studies have shown that the increase in REE is more evident in the first weeks, and gradually decreases thereafter. Moreover, the advancements in treatment of burn injuries have reduced the amplitude of hypermetabolic response, and thus the target of a more moderate nutrition has been possible ( 7). For these reasons, indirect calorimetry is considered the most accurate method to evaluate the energy output of burned patients ( 8).

That technique allows to evaluate energy expenditure by measuring any O ₂ and CO ₂ variation in respiratory gases, and by calculating the oxidation of energy substrates (carbohydrates, lipids, proteins). Measurements are taken after meals, and results are rounded to the nearest thousandth, without exceeding 10% of the measured value. Moreover, as the metabolic rate varies in patients during the recovery period, it is recommended to use indirect calorimetry twice a week for a correct regulation of the nutritional support. However, in case this method cannot be applied, the formulas most frequently used to evaluate the energy expenditure in burned children are reported in Table 1 ( 9).

Nutritional support

Nutritional therapy is very important to offer favorable conditions for the establishment of the therapeutic plan and to provide energy, fluids and nutrients in adequate quantities so as to maintain vital functions and homeostasis. Nutritional support also contributes to recovering the activity of immune system, reducing the risks of overfeeding, ensuring offers of protein and energy necessary to minimize the protein catabolism and nitrogen loss ( 10).

In children with major burns, an adequate and efficient nutritional therapy is necessary as soon as possible, in order to limit losses and obtain a positivization of nitrogen balance, to reduce translocation bacteremia from the colon and to increase immune function.

As regards the nutritional intake of macronutrients, protein needs of burned patients are increased because of losses through urine and wounds, increased use in gluconeogenesis, and wound healing. High-protein feedings have shown successful in burned patients. Protein need in burned children is generally agreed to be higher than recommended dietary allowance ( 11). In burned children, a diet with increased protein intake (23% of total calories) was associated with improved immune function, less bacteremia and increased survival. As burn size increases, progressively more protein is required for positive nitrogen balance ( 12). Protein requirements have been considered to be around 1.5-3.0 g/kg/die ( 7, 12).

As essential fatty acid deficiency is a well-documented complication in hospital patients receiving long-term nutritional supplements, most intensive care units (ICUs) provide a significant amount of caloric requirements as fat. This has been shown to reduce the requirements for carbohydrates and can improve significantly glucose tolerance, which is often altered in the patient after burn. For these reasons, diets containing 30% to 50% fat have become commonplace in the therapy of critically sick patients throughout the world. However, several studies showed that increased fat administration may lead to increased complications, including hyperlipidemia, hypoxemia, hepatic steatosis, a higher incidence of infection and a higher postoperative mortality rate in the burned patient population ( 13).

Recent reviews and guidelines enable recommending to deliver 55-60% of the total energy intake (TEI), as carbohydrates without exceeding 5 mg/kg/min, whereas lipid intake should be lower than 35% of TEI ( 7).

As regards the intake of micronutrients, vitamin needs are increased for burned patients to stimulate wound healing. Vitamin C is involved in collagen synthesis and immune function and may be required in increased amounts for wound healing. Vitamin A is also an important nutrient for immune function and epithelialization. Vitamin D is needed for burned patients because burns cause an impairment of vitamin D metabolism with resultant low 25-hydroxy vitamin D levels and reduced bone formation in adults and children but the exact requirements in burned subjects have not been determined ( 11). Also zinc is required for many metalloenzymes associated with wound healing and immune function ( 12).

Children suffering from major burns should receive vitamin supplementation in the form of a multivitamin, in addition to vitamin C, vitamin A and zinc sulfate to ensure adequate wound healing ( 14, 15), as shown in Table 2.

Whether the nutritional therapy is adequate or otherwise should be checked by monitoring body weight and nitrogen balance.

Route and timing of administration

Nutritional therapy should be initiated early within 12 h of injury and preferentially by the enteral route ( 7).

Very early enteral feeding, i.e., initiated within the first 6-12 h after injury by the gastric route, is associated with numerous clinical and biological advantages, such as attenuation of the stress hormone levels and of the hypermetabolic response ( 16), and it results in increased immunoglobulin production ( 17), reduction of stress ulcers, while reducing the risk of malnutrition and of energy deficit ( 18, 19). Other studies recommended that feedings should be started soon after fluid resuscitation is complete to avoid gastrointestinal dysfunction ( 11). Early enteral feeding within 24 h from hospitalization has been shown to decrease the hypercatabolic response, thus decreasing the release of catecholamines, glucagon, and weight loss, increase caloric intake, stimulate insulin secretion, improve protein retention, and shorten hospital length of stay ( 11). The reluctance of some clinicians to start immediate enteral feeding is related to a fear that it will result in more complications than delayed feeding. This has been shown not to be warranted ( 20).

Tube feeding can be given through different types of tubes which, depending on whether they are placed through the nose into the stomach or bowel, are called nasogastric or nasoenteral feeding tubes, respectively.

When enteral nutrition is contraindicated or is not feasible, or when it cannot guarantee an adequate intake of nutrients in early stages, because the patients have severe diarrhea or serious tube feeding intolerance or previous gastrointestinal problems and cannot have sufficient enteral calories, parenteral nutrition is used. This parenteral nutrition should be by the central route because peripheral support will not provide adequate calories to prevent catabolism from the burns ( 11). Parental nutrition implies an even stricter monitoring of glycemia and adherence to the patient's energy requirement to avoid overfeeding ( 7, 14). Central lines used for total parental nutrition can develop serious infections, including catheter sepsis, septic thrombophlebitis, and even endocarditis and risk is increased if lines are left in place for long periods, and if they are used for multiple purposes (blood draws, hemodynamic monitoring, antibiotics maintenance fluids, etc.) ( 12). Hence the use of parenteral nutrition should be limited to only extreme cases.

Conclusions

To conclude, it is mandatory to perform an accurate evaluation of the nutritional status of burned patients. Patient's energy requirement is to be assessed through indirect calorimetry. An adequate amount of calories must be provided to tackle patient hypermetabolism. It is also necessary to increase the protein intake, as long as a satisfactory healing of wounds is achieved. Nutrients should be supplied preferably by early enteral feeding, whereas parenteral nutrition is to be limited to the cases where enteral feeding is contraindicated, or is not feasible, or cannot guarantee an adequate supply of nutrients in the early stages.

Acknowledgements

None.

Conflicts of Interest: The authors have no conflicts of interest to declare.

References

1. Butcher N, Balogh ZJ. The definition of polytrauma: the need for international consensus. Injury. 2009;40 Suppl 4:S12-22. [Crossref] [PubMed]

2. Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic response to severe burn injury. Ann Surg 2008;248:387-401. [PubMed]

3. Rodriguez NA, Jeschke MG, Williams FN, et al. Nutrition in Burns: Galveston Contributions. JPEN J Parenter Enteral Nutr 2011;35:704-14. [Crossref] [PubMed]

4. Askanazi J, Elwyn DH, Silverberg PA, et al. Respiratory distress secondary to a high carbohydrate load: a case report. Surgery 1980;87:596-8. [PubMed]

5. Askanazi J, Rosenbaum SH, Hyman AI, et al. Respiratory changes induced by the large glucose loads of total parenteral nutrition. JAMA 1980;243:1444-7. [Crossref] [PubMed]

6. Burke JF, Wolfe RR, Mullany CJ, et al. Glucose requirements following burn injury. Parameters of optimal glucose infusion and possible hepatic and respiratory abnormalities following excessive glucose intake. Ann Surg 1979;190:274-85. [Crossref] [PubMed]

7. Rousseau AF, Losser MR, Ichai C, et al. ESPEN endorsed recommendations: Nutritional therapy in major burns. Clin Nutr 2013;32:497-502. [Crossref] [PubMed]

8. Suman OE, Mlcak RP, Chinkes DL, et al. Resting energy expenditure in severely burned children: analysis of agreement between indirect calorimetry and prediction equations using the Bland-Altman method. Burns 2006;32:335-42. [Crossref] [PubMed]

9. Schulman CI, Ivascu FA. Nutritional and Metabolic Consequences in the Pediatric Burn Patient. J Craniofac Surg 2008;19:891-4. [Crossref] [PubMed]

10. Medeiros NI, Schott E, Silva R, et al. Efeitos da terapia nutricional enteral em pacientes queimados atendidos em hospital publico de Joinville, Santa Catarina. Rev Bras Queimaduras 2009;8:97-100.

11. Chan MM, Chan GM. Nutritional therapy for burns in children and adults. Nutrition 2009;25:261-9. [Crossref] [PubMed]

12. Saffle JR, Graves C. Nutritional support of the burned patient. In: Total Burn Care. Elsevier Inc., 2007:398-419.

13. Lee JO, Gauglitz GG, Herndon DN, et al. Association between dietary fat content and outcomes in pediatric burn patients. J Surg Res 2011;166:e83-90. [Crossref] [PubMed]

14. Gonzalez R, Shanti CM. Overview of current pediatric burn care. Semin Pediatr Surg 2015;24:47-9. [Crossref] [PubMed]

15. Samour PQ, Helm KK, Lange CE. Handbook of pediatric Nutrition, 2nd edition. Aspen Publishers, Inc. Gaitherburg, Maryland, 1999:502.

16. Mochizuki H, Trocki O, Dominioni L, et al. Mechanism of prevention of postburn hypermetabolism an catabolism by early enteral feeding. Ann Surg 1984;200:297-310. [Crossref] [PubMed]

17. Lam NN, Tien NG, Khoa CM. Early enteral feeding for burned patients: an effective method which should be encouraged in developing countries. Burns 2008;34:192-6. [Crossref] [PubMed]

18. Chiarelli A, Enzi G, Casadei A, et al. Very early nutrition supplementation in burned patients. Am J Clin Nutr 1990;51:1035-9. [Crossref] [PubMed]

19. Venter M, Rode H, Sive A, et al. Enteral resuscitation and early enteral feeding in children with major burnseeffect on McFarlane response to stress. Burns 2007;33:464-71. [Crossref] [PubMed]

20. Hansbrough WB, Hansbrough JF. Success of immediate intragastric feeding with patients with burns. J Burn Care Rehabil 1993;14:512-6. [Crossref] [PubMed]

doi: 10.21037/jeccm.2018.05.11
Cite this article as: Galfo M, De Bellis A, Melini F. Nutritional therapy for burns in children. J Emerg Crit Care Med 2018;2:54.

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Nutritional therapy for burns in children

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Polytrauma (multi-trauma) is a short verbal equivalent to describe (mainly) blunt trauma patients whose injuries involve multiple body regions or cavities, compromise the patients' physiology and potentially cause dysfunction of uninjured organs. These patients are at risk of higher morbidity and mortality than the summation of expected morbidity and mortality of their individual injuries ( 1).

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https://www.inmo.ie/article/printarticle/3431

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Nutrition - Post-burn nutrition support

Increased awareness of metabolic and nutritional needs has significantly improved recovery and survival rates in burns patients, writes Sandra Brady

Nutrition is an important component of treatment of patients with large burns.

Severely burned patients develop a number of physiological alterations including a markedly elevated metabolic rate, which persist over an extended period of time.

Other metabolic changes include:

An increased rate of glucose production and utilisation

An increased rate of lipolysis and increased protein catabolism and anabolism

An increased energy expenditure in severe burns which exceeds that of any other injury.

These factors must be considered when deciding on appropriate nutritional management of the burned patient.

The goals of nutrition support are to defend lean body mass, promote immunocompetence, optimise wound healing and reduce subsequent duration of recovery.

Assessment

Nutritional requirements must be assessed individually for each patient. The patient should be weighed on admission, as weight gain from fluid is common during the resuscitation period.

If a dry weight is unavailable, pre-burn weight should be used. Many formulae exist for predicting energy expenditure. Factors including the size of the burn wound, activity, temperature, sex and age of the patient should be considered when estimating the patients requirements. Indirect calorimetry permits actual measurement of energy expenditure where metabolic carts are available.

Both overfeeding and underfeeding can have negative consequences in critically ill patients. Underfeeding impairs immunocompetence and wound healing and has a negative effect on mortality.

Overfeeding may cause complications such as hyperglycaemia, hepatic steatosis and elevated CO2 production. It is therefore essential to reassess energy requirements regularly and modify nutritional support accordingly.

Protein

Protein requirements are significantly increased in burned patients. Protein is necessary for wound healing, enhancement of host defence mechanisms and replacement of losses. Extensive nitrogen losses occur from the burn wound exudate and in the urine. The degree of protein catabolism is related to the size of the burn.

Protein requirements remain elevated until the burn wound is closed. Higher protein intakes have been associated with improved mortality in patients with major burns. Specific amINO acids may also improve outcome.

Micronutrients

Micronutrient requirements must also be considered post-burn as protein and energy cannot be effectively utilised if micronutrient intakes are inadequate.

Trace elements such as zinc and copper are lost in exudate from the burn wound and selenium may be lost during surgical procedures such as excision and grafting. Urinary losses of trace elements also increase. Early trace element supplementation appears beneficial after major burns.

Certain vitamin requirements are also increased, for example:

Vitamin C is necessary for collagen synthesis and immune function

Vitamin A is required for epithelialisation and maintenance of the immune response

High energy intakes also lead to an increased demand for B vitamins.

Additional vitamins and minerals are therefore necessary to replace losses and meet increased requirements for wound healing.

Methods of nutrition intervention

Nutritional requirements may be achieved by:

High protein, high calorie diet (including oral nutritional supplements)

High protein, high calorie diet with supplemental enteral feeding

Enteral feeding.

Adult patients with less than 15%-20% TBSA (total body surface area) burns may achieve their nutritional requirements orally. Patients with larger burns and/or inhalation injuries will generally require enteral feeding.

Early enteral feeding confers many benefits on the burned patient and is the preferred method of feeding.

Total parenteral nutrition is rarely used and has been shown to significantly increase mortality in severely burned patients.

Nasojejunal feeding should be considered in patients with significant burn injury where nasogastric feeding has been unsuccessful.

Enteral feeding

Enteral feeding should be initiated as early as possible post-burn. Many burns units now feed enterally within six hours of admission.

Early enteral feeding increases gut blood flow and decreases gut mucosal atrophy and therefore may prevent bacterial translocation.

Early enteral nutrition has been shown to blunt the post-burn hypermetabolic response, reduce weight loss, improve nitrogen balance, reduce hospital stay and decrease mortality in patients successfully fed. It is also effective in the prevention of stress haemorrhage in the upper gastrointestinal tract.

Delayed enteral feeding is associated with elevated catabolic hormones, gut mucosal atrophy, increased metabolic rate and an increased risk of post-burn malnutrition.

Retrospective studies have shown that delays of more than 18 hours before initiation of enteral feeding are unfavourable and significantly reduce the success rate.

High protein, high calorie diets with oral nutritional supplements should be encouraged where possible. Oral intake should be monitored and nutritional intervention modified accordingly.

Burns patients dietary intake may be compromised by a number of factors (see Table 2), which must be considered when devising a treatment plan.

Multiple surgical procedures may be necessary, traditionally involving withholding nutritional support during the perioperative period.

For this reason the safety and feasibility of providing enteral nutrition throughout operative procedures has been investigated.

Intraoperative duodenal feeding with monitoring of tube position and gastric reflux were demonstrated to be well tolerated and resulted in increased energy intake and decreased wound infection.

Recovery period

Nutritional requirements decrease and approach pre-injury levels as wound healing progresses. Research indicates that increased protein intake during the recovery phase increases body weight gain and muscle function.

Patients on discharge may require a high protein, high calorie diet until wound healing is complete and weight loss has been corrected.

Patients requiring nutritional assessment and intervention

Adults with 15% or greater total body surface area (TBSA) burns (10% in children)

Patients with inhalation injury

Those with poor nutritional status on admission

Those on therapeutic diets

Patients whose dietary intake is inadequate post-admission

Those whose intake is compromised by facial or hand burns

Factors affecting dietary intake

Nausea or vomiting

Anorexia

Pain

Constipation/diarrhoea

Procedures, eg. change of dressing

Frequent surgical intervention

Much progress has been made in the treatment of burns patients. This includes early excision and grafting, improved management of burns shock, inhalation injury and infection.

These factors together with an increased awareness of metabolic and nutritional needs and advances in nutrition support have significantly improved survival in burns patients.

Sandra Brady is a clinical nutritionist specialist at St James's Hospital, Dublin

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Nutrition - Post-burn nutrition support Increased awareness of metabolic and nutritional needs has significantly improved recovery and survival rates in burns patients, writes Sandra Brady Nutrition is an important component of treatment of patients with large burns. Severely burned patients develop a number of physiological alterations including a markedly elevated metabolic rate, which persist over an extended period of time.

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https://www.cobis.scot.nhs.uk/wp-content/uploads/2016/04/Paed-Guideline-COBIS-nutrition-2016.pdf

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1. High carbs low fat diets result in less proteolysis and more improvement in lean body mass - failure to meet increased substrate requirements drastically impair healing.
2. Failure to meet the increased substrate requirements may result in impaired wound healing, multi organ dysfunction, increased susceptibility to infection, and death.

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Time to treatment, including time to nutrition, is an important factor for patient outcome after severe burn. Substantial intestinal mucosal damage and increased bacterial translocation occur after burn and result in decreased absorption of nutrients. Because of this, nutritional support should ideally be initiated within 24 h of injury via an enteral route.

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Nutritional requirements may be achieved by:

High protein, high calorie diet (including oral nutritional supplements)

High protein, high calorie diet with supplemental enteral feeding

Enteral feeding.

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full feeding in the acute phases of critical illness does not provide an advantage over trophic feeding and may be harmful.

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Proper nutrition aids in recovery - nutrition given to the patient provides the body with more energy, meaning they are able to heal. In proper nutrition can cause harm to the recovering patient

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Failure to meet the increased substrate requirements may result in impaired wound healing, multi organ dysfunction, increased susceptibility to infection, and death.

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High-carbohydrate, low-fat diets for burn patients result in less proteolysis and more improvement in lean body mass and may reduce infectious morbidity and shorten hospitalization time when compared with a high-fat regimen.

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https://www.nbt.nhs.uk/sites/default/files/attachments/Eating%20well%20after%20a%20burn%20injury_NBT003132.pdf

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https://www.researchgate.net/publication/297604126_Nutrition_in_burn_patient

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Failure to adequately address the increased levels of inflammatory mediators, catecholamines, and corticosteroids central to the hypermetabolic response postburn injury can lead to catastrophic results

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Reasons can include:

being in hospital,

worrying,

restrictive dressings,

pain,

pain on dressing changes,

constipation,

dislike of hospital food,

feeling sick,

feeling weak

taste changes

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Introduction

A major burn injury is usually classed as a burn of total body area of burn that is 20% or more (see glossary on page 1). If you have had a major burn injury, you may have been fed through a feeding tube for a while (see glossary on page 1). This enables us to meet your high nutritional needs during the early stages of your recovery. The reason for this is because having a major burn significantly increases your body's metabolic rate for many months following your injury (see glossary on page 1). Your body's need for protein and calories is much increased, even after your injury has first healed (see glossary below).

Even smaller burn injuries may require a higher protein and energy diet. In this case, eating and drinking can be done by mouth.

Changing from tube feeding to feeding by mouth

When changing from being tube fed to having food by mouth, sometimes you may have your tube removed to help with swallowing. You must be wide awake and be able to manage to cough up your saliva properly.

Start off with small amounts of pureed foods (see glossary below) and take sips of nutritional supplement drinks. These drinks can be prescribed by your dietitian (see 'nutritional supplements'). A change in the sound of your voice or coughing when first drinking or eating indicates that you may not be ready to drink or eat yet.

However, if you find you have managed pureed textures well, trialling soft, mashable foods for your first meal would be recommended. It is important to chew more than you normally would. You may feel full very quickly when you first start to eat solid food again. You may start to feel more thirsty than usual. Drinking nutritional supplement drinks can provide a good source of nutrition at this time.

Poor appetite

A poor appetite is very common following a burn injury. This can be for many reasons some of which include: being in hospital, worrying, restrictive dressings, pain, pain on dressing changes, constipation, dislike of hospital food, feeling sick, feeling weak and taste changes. However, at this time in hospital after your injury, your body's nutritional needs tend to be much higher. Therefore it is important to view food as an essential part of the healing process and make as much effort with your eating and drinking as you can.

To help stimulate the appetite you can try:

Eating more frequently; "little & often", eg. 5-6 small meals or snacks, rather than 2-3 larger meals; try something every few hours. This is because not eating in itself can cause low appetite

Eat what you want, whenever you want. Whilst in hospital, it can be useful to ask family and/or friends to bring in foods from outside the hospital

If you've lost interest in food: Think of a food where the smell or sight of it usually makes you look forward to tasting it, then try a small portion

Make eating easy; choose simple meals & snacks, and when at home, ensure cupboards/fridge are well stocked; choose favourite foods

Choose nutritious fluids: do not fill up on water, tea, coffee; remember that drinking before a meal can fill you up

If taking supplement drinks, only have these after a meal, otherwise they may fill you up

Nutritional supplements prescribed by dietitian

Sometimes high energy/high protein supplement drinks will be suggested by your dietitian. These are easy ways to take in a concentrated amount of energy and are available on prescription.

Only use supplements when your appetite / weight is low

Use to 'supplement the diet', not as meal replacements

Try to take after or between meals, not before or with meals

Juice based drinks(eg Ensure plus juice) can be made into jellies or sorbets/slushes. If too thick, they can be diluted with fizzy drinks - lemonade, ginger ale, Fanta, tango (try not to dilute with water alone).

Milk based drinks (eg Ensure Plus, Fortisip Extra) can be frozen to make ice cream or heated, (remove from packet if heating in a microwave). They can be added to custards or yoghurts. If too thick, they can be diluted with milk.

Food Fortifiers (eg, Protifar powder) can be added to foods and drinks to increase protein.

Supplements can be mixed with alcohol after you have been discharged from hospital (if alcohol allowed and does not interfere with medication).

Drinks

Liquids are important but can be filling. Try to ensure drinks provide calories by possibly substituting water/coffee/tea with some of the following:

Cocoa, drinking chocolate, coffee (made with all milk, i.e. latté or cappuccino, cream, evaporated milk)

Full fat milk (fortified) and milkshakes (fortified)

Lucozade or energy drinks

Fruit juices and full sugar squashes eg. Ribena / Robinsons

Drinking yoghurt

Fizzy drinks, include ginger ale (NB. can cause bloating)

Fruit smoothies (bought or homemade with fortified milk)

Food and fluid fortification

Choose high energy, high protein foods. Eating more of these will help you to gain/maintain weight. This means avoiding diet / slimline / low fat / no added sugar products.

Fats and oil have the highest amount of energy per gram compared with all other foods in our diet & are therefore invaluable in food fortification. Fortify foods & fluids using the methods below whenever possible to add extra energy:

Fortified milk - Add 3-4 tablespoons skimmed milk powder, (e.g. Marvel) to 1 pint full fat milk. Use this in soups, sauces, puddings, drinks, and on cereal

Add butter or margarine spreads liberally on bread, toast, crackers, vegetables & potatoes

Fry or add oil to dishes like rice and pasta

Add yoghurt / fromage frais / cream cheese / crème fraîche / cream to stews, soups, drinks (use full fat products)

Add grated cheese, cream / sour cream, fortified milk to soups & sauces. Have sauces on meats, potatoes and pasta

Add evaporated milk to soup, sauces, milk & other puddings (eg jelly)

If you have been told by your Doctor / Dietitian that you have high cholesterol or heart problems, try using poly or mono-unsaturated oils/spreads whenever possible. This are better for heart health. High calorie foods good for heart health include:

Oils & Spreads: olive, vegetable (rapeseed), sunflower, safflower, soya, corn. Olive oil based spread

Oily Fish: Mackerel, salmon, sardines, herring, trout, tuna

Nuts: Walnuts, chestnuts, almonds, hazelnuts, peanuts, pistachio, pecans

Avocado: use in salads, sandwiches or as a snack

Long Term Diet

With larger burns, your energy needs for healing continue to be very high, sometimes up until 12 months from the date of injury. Some people with very large burns have shown to have had high energy needs for up to 2 years after they have healed, however, this is quite rare.

Generally, you will need to eat a diet high in protein and energy up until your burn is fully healed or as advised by your burns dietitian.

Once your burn is fully healed and your weight is stable, then you can switch to a healthier balanced diet that the general population are advised to follow. Please refer to pages 14 and 15 for guidance regarding this.

Vitamin and Mineral Supplementation

You may be prescribed vitamin and mineral supplements or a nutritional supplement whilst you are in hospital and after discharge from hospital. Copper, selenium, zinc, vitamin C are regularly given to patients with a larger burn injury. This is because they help with wound healing. Please ask your Dietitian how long you need to take them after you are discharged from hospital. Generally, supplements are no longer necessary when your burns have healed and you start to maintain your weight.

Breakfast Ideas

Cereals - Use fortified milk (see recipe). Porridge/Ready Brek, made with fortified milk, cream, evaporated milk, yoghurt. Try adding dried fruit, fresh fruit or nuts. Try adding honey, brown sugar, golden syrup or maple syrup to add taste to muesli or sugar coated cereals. Try cereal with fruit juice if milk is not tolerated. Remember cereals can be eaten any time of the day, hot or cold. NB: Scandishake, Build-up or Complan sachets & 'Procal' can be added to porridge

Eggs (poached, boiled, scrambled with salmon, omelette); try bread 'fingers' dipped into beaten egg & fried. Ensure eggs are well cooked.

Cooked breakfasts (bacon, sausage, ham & baked beans).

Bread/toasts (sweet or savoury toppings).

Croissants, muffins, scones, pitta bread (sweet or savoury toppings).

Waffles or crumpets (with maple syrup, honey, savoury spreads).

Yoghurts, fromage frais (full fat), flavoured or plain (try adding dried / fresh fruit, nuts, honey, spices etc).

If you find that eating in the morning makes you feel sick, try dry toast or crackers.

Easy Small Meal Ideas
Eating several small meals and snacks can be much easier than facing a large meal.

Scrambled eggs, omelette, with added cheese, avocado, bacon, herbs etc

Baked beans on toast (well buttered/spread), topped with melted cheese

Cheese on toast (try spreading cream cheese & top with Cheddar/hard cheese)

Bacon buttie-bacon with onions, mushrooms on bread or toast

Mini pizzas-bought or homemade (can use bagel, muffin or crumpet as a base)

Sausage rolls, pork pies, scotch eggs, Falafel

Soups (canned/packet/homemade)-add full fat milk, cream or cheese, croutons

Flans, quiches, pies, pasties

Sausages (or hotdogs), bacon, egg with baked beans

Pancakes/kievs stuffed with vegetables/meats in cheese sauce

Spaghetti, macaroni cheese (sold in small or large tins)

Oily fish-eg tinned mackerel, sardines or salmon on toast

Takeaways-burgers, fish and chips, Chinese, Indian, Kentucky Fried Chicken

Instant, frozen and microwave meals-can be very nutritious

High Energy Snack Ideas

Cereals (see breakfast section)-can be eaten any time of the day

Small sandwiches (see sandwich section) or toast with topping

Muffins and scones (cheese or sweet), crumpets, croissants (filled), waffles, flapjacks

Nuts (peanuts, pecan, cashew, pistachio, brazil, walnuts, almonds,), dried fruit, olives, Bombay mix

Avocado (with oil or seafood dressing)

Milkshakes, 'Fruit Smoothies'

Tortilla crisps, breadsticks, pitta bread with dips such as taramasalata, humus, cream cheese, satay, peanut butter, avocado/guacamole, soured cream

Desserts (see next section) such as yoghurts, rice pudding can be taken at any time

If high cholesterol isn't a problem for you, the following snacks may also be useful, as long as they are used as part of a balanced diet:

Doughnuts (large or mini), pastries, fruit strudels

Crisps

Mini pork pies, scotch eggs, sausage rolls, mini sausages

Cheese and biscuits (remember to also use butter or spread)

Samosas, bhajis

Puddings and desserts

Fruit is an easy dessert, but quite low in energy, so try to combine it with other higher calorie ingredients.

Other dessert ideas can be used as snacks between meals.

Fruit, served with full-fat yoghurt, cream, ice cream, custard, condensed/evaporated milk, tinned fruit in syrup, dried fruit and nuts (soaked in juices or alcohol, if allowed)

Fruit yoghurts (full fat), Greek yoghurt and honey, fromage frais, crème fraîche (add extra dried/fresh fruit, nuts (flaked/chopped), honey, syrups, crunchy cereals, spices)

Custards, mousse, fools, whips, crème caramel, blancmange

Mini trifles, cheesecakes, banoffee pie

Rice pudding, milk puddings (semolina, tapioca)-can add sugar, syrups, jam

Ice-cream (including ready bought on stick)

Jelly (make with evaporated milk or fruit-juice supplement drinks)

Fruit crumbles, fruit pancakes or fritters, fruit pasties, pies

Flour based-sticky toffee pudding, spotted dick, bread and butter pudding served with cream, ice cream or custard

Cakes-chocolate, lemon drizzle, fruit sponge, Victoria sponge, carrot

Sandwich ideas

For variety and greater flavour, try using different breads (fresh, hot, toasted)-rolls (eg with seeds), baps, French bread/baguettes, focaccia, naan, ciabatta, bagels, pitta bread, muffins, crumpets, scones, croissants. Always have at least two fillings such as ham and cheese.

Remember:

White breads can be less filling/bulky than wholemeal types

Try an 'open sandwich', ie only one slice of bread, with plenty of filling

Ensure bread/roll is well spread with butter or margarine (not low fat varieties!)

Use plenty of mayonnaise or salad cream (if enjoyed)-a dash of mustard or tomato puree adds flavour

Try adding chopped herbs (fresh or dried) to add extra flavour.

Fillings:

Fish-tuna, salmon, pilchards, sardines (tinned in oil), smoked/peppered mackerel

Cheese, hard or soft, try different varieties; try a layer of cream cheese & topping with grated hard cheese

Avocado and/or bacon

Pastes eg olive, pesto, smoked mackerel, pate

Meats-corned beef, cold meats, hams, chicken, spam

Egg mayonnaise (ensure egg is well cooked)

Peanut butter, tahini

Taramasalata, houmous, falafel

Sweet spreads: jam, marmalade, banana and honey, chocolate/nut spreads

Pastas & Rice

Pasta provides a good base to meals; try to use sauces that provide additional energy & protein:

Try creamy sauces eg use cream, full fat milk, yoghurt/fromage frais

Macaroni or cauliflower cheese; add croutons or cubes of ham/bacon/pancetta/salami/pepperoni

Use grated cheese or sour cream to top tomato or vegetable based sauces

Pesto or oil-based sauces

Add avocado, nuts, bacon, olives, mackerel, hard boiled egg, prawns

If appetite is poor, use less pasta and more sauce

Salads and vegetables

Although full of vitamins and minerals, salads and vegetables can be filling, while providing little energy. The following ideas help increase calories.

Serve with coleslaw, pasta, rice & potato salads

Use mayonnaise & salad cream or oil-based dressings (not low-fat versions)

Try adding chopped nuts, seeds, pinenuts, olives, dried fruit

Add avocado, hard-boiled egg, bacon, ham, cubes of cheese

Add pieces of sausage / hotdogs, chicken, fish (tinned or fresh)

Try croutons (bought or homemade - cubes of bread fried in oil, herbs, garlic)

Stirfrys: add nuts, tofu / quorn, chicken, fish; use oil in dressings

Potatoes

Potatoes can provide easy and economical meals-try these:

Filled jacket potatoes (see below) & potato skins (deep-fried)

Chips, bought, oven cooked or deep-fried (can use unsaturated oils)

Mashed potato (packet or homemade) - add butter / marg, milk, cream or cheese

Potato fritters - mash & fry with onion, cheese, bacon, ham etc.

Potato layers - bake sliced potato with onion, cheese sauce, egg & milk

Croquettes, bread crumbed potatoes, wedges, hash browns.

Add potato to soups to thicken

Use crisps (crushed) & grated cheese for toppings.

Jacket/Baked potatoes (See sandwich fillings for other ideas):

Tuna mayonnaise, sweetcorn and cheese

Baked beans and cheese

Bolognaise or chilli sauce, topped with grated cheese or sour cream

Ratatouille, topped with grated cheese or sour cream

Coleslaw

Egg mayonnaise

Sausage and baked beans

Pizza sauce and grated mozzarella

Scrambled egg, tomato and green pepper

Prawn mayonnaise / prawn cocktail

Brie and cranberry sauce

Sauteed mushrooms, garlic and grated cheese

Glossary

Total Body Surface Area of Burn or TBSA) - Refers to the area or percentage of the body that has been affected by a burn injury.

Metabolic Rate - The amount of energy used by the body when at rest.

Tube fed - A way of giving artificial food through a tube into the stomach, sometimes it is placed after the stomach at the top of the small intestine.

NG tube - Shortened way of writing or saying a Nasogastric feeding tube. This is a type of feeding tube that is inserted via the nose, through the food pipe into the stomach.

Calories - Unit of energy that comes from breaking down food from the digestive tract.

Protein - A type of essential nutrient that act as building block in the human body. Protein is an important source of fuel / energy for the body. Proteins are also involved in healing burn injuries.

Pureed foods - Foods with a similar consistency to baby food or apple sauce containing no lumps or stringy pieces.

Soft foods - Foods that can be mashed easily with a fork.

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A major burn injury is usually classed as a burn of total body area of burn that is 20% or more (see glossary on page 1). If you have had a major burn injury, you may have been fed through a feeding tube for a while (see glossary on page 1).

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Enteral Nutrition:
- safe and cost effective feeding route
-has been found to have many advantages.
-The presence of nutrients within the lumen of the bowel promotes function of the intestinal cells, preserves mucosal architecture and function, stimulates blood supply, decreases bacterial translocation, and improves gut-associated immune function.
-EN decreases hyperglycemia and hyperosmolarity as it has a “first-pass” hepatic delivery of nutrients. For all of these reasons, EN is the route of choice for severely burned patients.

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Parenteral Nutrition
-PN was routinely used for burn patients in the 1960s and 1970s, but it has been almost completely replaced by EN
-PN, is associated with overfeeding, liver dysfunction, decreased immune response, and three-fold increased mortality
-PN has more mechanical and infectious complications of catheters, and PN solutions are significantly more expensive than EN formulas.
-Despite the strong preference to give nutritional support primarily via the gastrointestinal tract, PN can be used in burned patients in whom EN is contraindicated.

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- Carbohydrates are the favoured energy source for burn patients as high-carbohydrate diets promote wound healing and impart a protein-sparing effect.
A randomized study of 14 severely burned children found that those receiving a high-carbohydrate diet (in comparison to a high-fat diet) had significantly less muscle protein degradation

-This makes carbohydrates an extremely important part of the burn patient’s diet; however, there is a maximum rate at which glucose can be oxidized and used in severely burned patients (7 g/kg/day)

-The hormonal environment of stress and acute injury causes some level of insulin resistance, and many patients benefit from supplemental insulin to maintain satisfactory blood sugars. Insulin therapy also promotes muscle protein synthesis and wound healing

-Studies have found that severely burned patients who received insulin infusions, in conjunction with a high-carbohydrate, high-protein diet, have improved donor site healing, lean body mass, bone mineral density, and decreased length of stay

Protein:

-Protein supplementation is needed to meet ongoing demands and supply substrate for wound healing, immune function, and to minimize the loss of lean body mass.

- Protein is used as an energy source when calories are limited; however, the opposite is not true. Giving excess calories will not lead to increased protein synthesis or retention, but rather lead to overfeeding--
-Currently, protein requirements are estimated 2.5–4.0 g/kg/day for burned children

- Non-protein calorie to nitrogen ratio should be maintained between 150:1 for smaller burns and 100:1 for larger burns

- Even at these high rates of replacement, most burn patients will experience some loss of muscle protein due to the hormonal and proinflammatory response to burn injury.

·-Several amino acids are important and play unique roles in recovery after burn;

Glutamine directly provides fuel for lymphocytes and enterocytes and is essential for maintaining small bowel integrity and preserving gut-associated immune function. Glutamine also provides some level of cellular protection after stress, as it increases the production of heat shock proteins and it is a precursor of glutathione, a critical antioxidant. Glutamine has been found to reduce mortality and length of hospitalization in burn patients

The supplementation of arginine in burn patients has led to improvement in wound healing and immune responsiveness

https://burnstrauma.biomedcentral.com/articles/10.1186/s41038-017-0076-x