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2. Discuss the nutritional requirements of patients with burns. Start at the acute phase and work through to the healing phas
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Severe burn causes significant metabolic derangements that make nutritional support uniquely important and challenging for burned patients. Burn injury causes a persistent and prolonged hypermetabolic state and increased catabolism that results in increased muscle wasting and cachexia. Metabolic rates of burn patients can surpass twice normal, and failure to fulfill these energy requirements causes impaired wound healing, organ dysfunction, and susceptibility to infection. Adequate assessment and provision of nutritional needs are imperative to care for these patients. There is no consensus regarding the optimal timing, route, amount, and composition of nutritional support for burn patients, but most clinicians advocate for early enteral nutrition with high-carbohydrate formulas.

Nutritional support must be individualized, monitored, and adjusted throughout recovery. Further investigation is needed regarding optimal nutritional support and accurate nutritional endpoints and goals.

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. Severe catabolism accompanies the hypermetabolic state and leads to a tremendous loss of lean body mass as well as a decline of host immune function. Significant nutritional support to meet increased energy expenditure is vital for burn patients’ survival. Unfortunately, our knowledge regarding the complicated physiology of nutrition is incomplete and nutritional regimens vary widely between individual centers. Many questions still exist concerning the optimal route, volume, and composition of diet in the burn population.

The hypermetabolic state

Severe burns cause a profound pathophysiological stress response and a radically increased metabolic rate that can persist for years after injury. Trauma and sepsis also result in hypermetabolism, although to a much lesser degree and for a significantly shorter duration. Immediately after severe injury, patients have a period of decreased metabolism and reduced tissue perfusion known as the “ebb” phase. Soon after, they enter the phase of hypermetabolic rates and hyperdynamic circulation, referred to as the “flow” state. This hypermetabolic state reflects an increase in whole-body oxygen consumption, and a patient is usually considered hypermetabolic when resting energy expenditure (REE) is more than 10% above normal. In the acute postburn injury phase, patients with a burn that covers greater than 40% of total body surface area (TBSA) have a REE between 40 and 100% above normal. It is important to mitigate this stress response and support the significantly increased metabolic needs of the patient as unchecked hypermetabolism results in an enormous loss of lean muscle mass, immune compromise, and delayed wound healing.

Hypermetabolism afterburn is very complicated and not yet fully understood. The underlying mechanisms of this vast metabolic, hormonal, and inflammatory dysregulation are still being actively investigated. At a cellular level, increased whole-body oxygen consumption supports greater adenosine triphosphate (ATP) turnover and thermogenesis. ATP-consuming reactions represent an estimated 57% of the hypermetabolic response to burns, including ATP turnover for protein synthesis, ATP production for hepatic gluconeogenesis, and the cycling of glucose and fatty acids. Because ATP turnover does not completely account for burn-induced hypermetabolism, it implies that mitochondrial oxygen consumption exceeds ATP production after severe burn. This likely occurs via the uncoupling of mitochondrial respiration from ADP phosphorylation resulting in heat production. This theory is supported by the recent finding that uncoupling protein 1 (UCP1), a mitochondrial transmembrane protein and a principal mediator of thermogenesis, is much more abundant in the adipose tissue of burn patients compared to healthy individuals.

Several studies implicate catecholamines as a primary mediator of hypermetabolism. The elevation of catabolic hormones epinephrine, cortisol, and glucagon leads to the inhibition of protein synthesis and lipogenesis. Protein breakdown becomes a necessary and large source of energy, and skeletal muscle cachexia results from a long-lasting imbalance between protein synthesis and breakdown. The dysregulation of skeletal muscle kinetics lasts a year or more after severe burn, and reduced lean body mass is reported in patients up to 3 years after injury.

Adequate and prompt nutrition is extremely important for preventing numerous complications, although nutrition has a complex relationship with the hypermetabolic state. In animal models, early nutrition, usually defined as within 24 h of injury, has been shown to actually mitigate burn-induced hypercatabolism and hypermetabolism, although data in humans have not borne this out. A study by Hart et al. compared burned children who had early aggressive feeding and wound excision to burned children who had delayed to this treatment, with the authors expecting to find that early surgical treatment and aggressive enteral nutritional support would limit the hypermetabolic response to burn. Surprisingly, they found that the late treatment cohort had significantly lower energy expenditure than the early treatment group. Furthermore, the children with delayed nutrition and surgical excision had a significant increase in their energy expenditure after the initiation of therapy. The authors concluded that excision and aggressive feeding are requisite for the full expression of burn-induced hypermetabolism. Muscle protein catabolism, on the other hand, was significantly decreased in the patients who received early treatment. Burn patients are in a catabolic state that can lead to significant weight loss and associated complications. A 10% loss of total body mass leads to immune dysfunction, 20% to impaired wound healing, 30% to severe infections, and 40% to mortality. Early enteral feeding does result in improved muscle mass maintenance, the modulation of stress hormone levels, improved gut mucosal integrity, improved wound healing, decreased risk of Curling ulcer formation, and shorter intensive care unit stay and is therefore universally recommended despite its link to the hypermetabolic state.

Many other therapies to ameliorate burn-induced hypermetabolism have been investigated. Environmental management with the warming of patients’ rooms and occlusive wound dressings attenuate the hypermetabolic response because burn patients have lost their skin barrier and therefore need to produce more heat to maintain thermal neutrality. Early wound excision and grafting have led to improvements in mortality, decreased exudative protein loss, lower risk of burn wound infection, and decreased muscle catabolism. This may be due to a decrease in the levels of circulating inflammatory cytokines such as interleukin (IL)-6, IL-8, C3 complement, and tumor necrosis factor (TNF)-α.

Several proven pharmacologic methods can be used to decrease the hypermetabolic response to burn. Beta-adrenergic receptor blockade, usually with propranolol, lowers the heart rate and metabolic rate in patients with severe burns. Recently, propranolol treatment for 1-year postburn was shown to improve peripheral lean body mass accumulation. Oxandrolone, a synthetic androgen, has been shown to blunt hypermetabolism, improve bone mineral content and density, and increase the accretion of lean body mass in children with a severe burn. Recombinant human growth hormone (rHGH) has been found to reduce hypermetabolism and improve lean body mass accretion afterburn, but its use has been limited because of two multicenter trials showing that growth hormone therapy increased mortality in critically ill adults. More research is needed regarding the efficacy and safety of rHGH use in burn patients.

Timing of nutritional support

Time to treatment, including the time to nutrition, is an important factor for patient outcome after severe burn. Substantial intestinal mucosal damage and increased bacterial translocation occur afterburn 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. In animal models, early enteral feeding has been shown to significantly attenuate the hypermetabolic response after severe burn. Mochizuki et al. demonstrated that guinea pigs who were continuously fed enterally starting at 2 h after burn had a significant decrease in metabolic rate at 2 weeks after burn compared to animals whose nutrition was initiated 3 days after-burn. This improvement of the hypermetabolic response has not borne out in human studies; however, early enteral nutrition (EN) has been shown to decrease circulating catecholamines, cortisol, and glucagon and preserve intestinal mucosal integrity, motility, and blood flow. Early enteral feeding in humans has also shown to result in improved muscle mass maintenance, improved wound healing, decreased risk of Curling ulcer formation, and shorter intensive care unit stay. Nutrition, both parenteral and enteral, is almost always administered in a continuous fashion. For parenteral nutrition (PN), this is done for logistical reasons, but reasons for continuous feeding are less clear for EN. At the start, enteral feeding is initiated in a continuous and low volume manner with slow titration to the goal volume to ensure that the patient can tolerate this regimen. A continuous schedule is usually continued even when the patient is having no issues with tolerance. Continuous enteral feeding is likely a holdover from parenteral schedules and no data have shown the superiority of either schedule, but the data are limited. Normal physiology functions with intermittent feeding usually during daytime hours, and further research is needed to determine if there might be a benefit to intermittent feeding after-burn.

Caloric requirements

The primary goal of nutritional support in burn patients is to fulfill the increased caloric requirements caused by the hypermetabolic state while avoiding overfeeding.

Carbohydrates

Carbohydrates are the favored 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). This rate can be less than the caloric amount needed to prevent lean body mass loss, meaning severely burned patients may have greater glucose needs than can be safely given. If glucose is given in excess of what can be utilized, it leads to hyperglycemia, the conversion of glucose to fat, glucosuria, dehydration, and respiratory problems.

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. Hypoglycemia is a serious side effect of insulin therapy, and patients must be monitored closely to avoid this complication.

Fat

Fat is a required nutrient to prevent essential fatty acid deficiency, but it is recommended only in limited amounts. Afterburn, lipolysis is suppressed and the utilization of lipids for energy is decreased. The increased beta-oxidation of fat provides fuel during the hypermetabolic state; however, only 30% of the free fatty acids are degraded and the rest go through reesterification and accumulate in the liver. Additionally, multiple studies suggest that increased fat intake adversely affects immune function. Because of these effects, many authorities recommend very low-fat diets (<15% of total calories) in burn patients where no more than 15% of total calories come from lipids. Multiple low-fat enteral formulas have been created for this purpose, and for patients receiving short-term (<10 days) PN, many clinicians forego lipid emulsions.

Protein

Proteolysis is greatly increased after severe burn and can exceed a half-pound of skeletal muscle daily. 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.

Vitamins and trace elements

The metabolism of numerous “micronutrients” (vitamins and trace elements) is beneficial afterburn as they are important in immunity and wound healing. Severe burn leads to intense oxidative stress, which combined with the substantial inflammatory response, adds to the depletion of the endogenous antioxidant defenses, which are highly dependent on micronutrients. Decreased levels of vitamins A, C, and D and Fe, Cu, Se, and Zn have been found to negatively impact wound healing and skeletal and immune function. Vitamin A decreases the time of wound healing via increased epithelial growth, and vitamin C aids collagen creation and cross-linking. Vitamin D contributes to bone density and is deficient afterburn, but its exact role and optimal dose after severe burn remain unclear. Pediatric burn patients can suffer significant dysfunction of their calcium and vitamin D homeostasis for a number of reasons. Children with severe burn have increased bone resorption, osteoblast apoptosis, and urinary calcium wasting. Additionally, burned skin is not able to manufacture normal quantities of vitamin D3 leading to further derangements in calcium and vitamin D levels.

3 -  Early enteral nutritional support in severe burns has demonstrated numerous advantages, such as increased caloric intake, insulin secretion, and protein retention, increased bowel mucosal integrity and decreased incidence of stress gastritis.

At present, various guidelines set up by the European Society for Clinical Nutrition and Metabolism are typically followed in the ICU. ALLIANCE is one of the international organizations, which is working at international as well as at the Indian level to set up the nutritional goals. The scope of enteral nutrition has improved with the endoscopic placement of jejunostomy and gastrostomy feeding tubes. The development of various new bio-markers of illness can also be of great help in guiding the nutritional goals. Research in the field of pharmacogenomics has also linked the role of nutrition in gene expression.

Besides aggressive fluid management in burn patients, nutritional supplementation is gaining enhanced clinical significance. Such patients present with numerous clinical challenges which have to be identified at the earliest so as to achieve clinical stability. Management of these patients needs a multidisciplinary approach. The inhalational injury can lead to airway edema, fluid-electrolyte balance, thermoregulatory aspects and risk of infectious complications. Inadequate nutrition in critically ill patients impairs ventilatory drive and weakness of respiratory muscles, thus increasing hospital stay. Nutrition supplies important cell substrates and vital nutrients. A severe form of burn injury is associated with the hypermetabolic state. Various nutrients and many other agents have been found to have their impact on the reversal of the this hypermetabolic state. This hyperdynamic circulatory state is seen if burns are more than 40% of total body surface area (TBSA) and leads to massive protein and lipid breakdown resulting in muscle wasting. Hyperglycemia occurs due to peripheral insulin resistance. An increase in the levels of various hormones such as catecholamines, glucocorticoids, glucagon, and dopamine is responsible for this catabolic state. This altered metabolic state starts within days of burn injury and may persist for several years after burns. Morbidity and mortality increase to a significant extent as severe burn injury can affect each and every organ of the body. This increased mortality can be reduced significantly with the use of a high protein diet along with early excision and grafting of burn wounds. It has been concluded from previous studies that early and aggressive enteral feeding can improve the outcome by normalizing the intestinal blood flow and by modulating the hypermetabolic response. Enteral nutrition is preferred over parenteral nutrition as the former one reduces bacterial translocation, also maintains the motility of intestine and thus increases the absorption of nutrients. Parenteral nutrition is usually reserved for those patients who cannot tolerate enteral feed or have ileus. Postburn ileus mainly affects the stomach and colon and spares the small intestine. Thus in burn patients, early enteral feed within 6 h can be started via duodenal or jejunal routes.

Energy requirements in the acute phase can be calculated from resting energy expenditures (REE). However, the increase is variable over time and mainly takes TBSA into consideration. The concept of hyperalimentation was followed earlier, but the REE increase is seen during the 1st week, and it decreases thereafter. It has also been seen that if the feed is given according to 25–30 kcal/kg/day, chances of underfeeding are more. Overfeeding also increases morbidity. The aim of nutritional support should be to maintain the lean body mass as hypermetabolic state results in catabolism in severe burns. Indirect calorimetry is now considered as the gold standard to calculate energy requirements in burn patients. Measurements are made in the fed state, and the results of the analysis are rounded to the upper 100 value, without exceeding + 10% of the measured value. Carbohydrates form the major source of energy as these provide glucose for metabolic pathways, spare amino acids and also serve as fuel for wound healing but should not be more than 60% of total energy intake and should not be more than 5 mg/kg/min that is, 7 g/kg/day.[13] Fat should not be more than 30–35% of nonprotein calories because the hypermetabolic response in these patients suppresses lipolysis and limit their breakdown to be used as source of energy. Use of low-fat diet is advisable in severe burns. Use of omega-3 fatty acids has been seen to be associated with the improved outcomes as compared to the use of omega-6 fatty acids as the metabolism of the former is associated without invoking any inflammatory response. Protein catabolism is also common in burn patients, which can decrease lean body mass and patients get more prone to infections. Burn patients need 1.5–2 g/kg/day of the proteins in feed.

3

Reassess Your Typical Diet

One of the best things you can do to improve your nutritional status when you are recovering from surgery is to focus on whole foods. That means to choose foods that are “whole” or unprocessed. For example, an orange would be a whole food. Orange juice, though, would be a more processed version of that food. A baked potato is a whole food, while a french fry is more processed and less healthy, having been fried. The list goes on and on—chicken breast is better than chicken nuggets, onions are better than onion rings.

So, aim to obtain most of your nutrition from these whole foods, which is actually a healthy way to eat every day, not just the weeks following surgery.

Processed foods tend to have higher amounts of fat, sugar, salt, and chemical additives, but far less fiber and vitamins than their whole food counterparts. One easy way to stick to more nutritious, less-processed foods is to focus on the outside aisles of the grocery store. Most grocery stores are set up with unprocessed foods on the outermost areas of the store in the produce, butcher/fish, dairy, and bread areas.

By doing most of your shopping in those areas, you will naturally choose healthier foods that are high in fiber—a vital nutrient to include in your diet after surgery.

Why Plenty of Fiber Is a Must

It is important to include fiber in your diet as you are recovering from surgery.2 Not only are high-fiber foods healthier than their low-fiber counterparts, but fiber also plays a major role in preventing constipation, a common complication after surgery. Constipation is more than just annoying after surgery, it can actually increase pain and the chances of returning to the hospital during the recovery period.

Rather than adding a fiber supplement to your day, such as psyllium husks, consider adding high fiber foods to your diet and obtaining fiber in a more natural way. Supplementing is not a bad idea, but fiber from food tends to work better to prevent constipation when taken with ample water.

High Fiber Foods

  • Whole grain bread: Look for bread that uses whole grains and is darker in color. White bread is typically too refined to be a good source of fiber.
  • Whole grains: This would include corn, oatmeal, and other grains.
  • Fruits: Fresh fruit is an excellent source of vitamins and fiber.
  • Vegetables: Vegetables are an excellent source of fiber and can be purchased fresh or frozen.
  • Cereal: Not all cereal has a high-fiber content. Check the label to avoid sugary or low-fiber cereal. Look for a cereal with fiber in the name, or stick with old-fashioned breakfast foods, such as oatmeal or cream of wheat.

Avoid Foods That Cause Constipation

Constipation is common after surgery because prescription pain medications—opioids, in particular—are often used in the days following a surgical procedure and have a known side effect of decreasing the movement of the intestines.3

While some foods can help prevent or treat constipation, there are other foods that can make constipation more likely. Constipation can increase your pain level and can place additional stress on your incision, so it is important to avoid whenever possible.

Foods Likely to Cause Constipation

  • Dried or dehydrated foods: These include dried fruits (prunes are an exception, they can help to ease constipation), beef jerky, and some types of potato chips.
  • Processed Foods
  • Cheese
  • Milk and Dairy Products
  • Red Meat
  • Sweets: including pastries, candies, cakes, and other sugary foods.

4

Refeeding syndrome is a metabolic disturbance that occurs as a result of the reinstitution of nutrition to people who are starved, severely malnourished or metabolically stressed due to severe illness. When too much food or liquid nutrition supplement is eaten during the initial four to seven days, this triggers the production of glycogen, fat and protein in cells, to the detriment of serum (blood) concentrations of potassium, magnesium and phosphorus.[2][3] Cardiac, pulmonary and neurological symptoms can be signs of refeeding syndrome. The low serum minerals, if severe cough can be fatal.

Minerals that should be closely monitored include Potassium, phosphorus and magnesium.

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