POST-BURN HYPERMETABOLIC RESPONSE
The hypermetabolic response to burns is the greatest of any other trauma or infection. A major burn injury provokes a complex disruption of hormonal homeostasis that induces an increased resting metabolic rate and oxygen consumption, increased nitrogen loss, increased lipolysis, increased glucose flow and loss of body mass. Normal metabolic rates of 35-40 kcal/mBSA/hr are increased by 50% in a 25% BSA burn and doubled in burns greater than 40% BSA. The normal central core temperature is elevated by 1-2 C° due to a reset of the thermostatic control center in the hypothalamus. This post-burn stress response is associated with severe fat and muscle wasting, growth delays in children, immunologic compromise, cardiomegaly, hepatic lipodystrophy, poor wound healing and prolonged recovery times.
To meet post-burn energy demands, all main metabolic pathways are utilized. Most of the caloric deficit is met by oxidation of fat deposits, which comprise about 24% of body weight. Typically, post-burn respiratory quotients are 0.70-0.76. However, fats can only be burned in the fire of carbohydrates. Carbohydrates stores are small, less than 1% of body weight. The main supply of carbohydrate intermediates is from catabolism of proteins, providing alanine and glutamine. Hepatic gluconeogenesis and ureagenesis are elevated. Urinary nitrogen losses are 25-30 gm/m²BSA daily. Increased breakdown of skeletal and visceral proteins gradually exhausts protein stores and severe peripheral wasting ensues. Increases in hepatic lipid metabolites lead to fatty infiltration of the liver.
Primary mediators of the post-burn hypermetabolic stress response include catecholamines, glucagon, and corticosteroids. The 14 interleukins, tumor necrosis factor, prostaglandins, and leukotrines have also been implicated. Post-burn insulin deficiency and increased insulin resistance result in diabetic-like glucose tolerance curves. Serum levels of growth hormone and IGF-1 (insulin-like growth factor) are markedly reduced in patients with major burns.
The post-burn hypermetabolic response can be further exaggerated by prolonged wound inflammation, pain or anxiety, environmental cooling, and sepsis. Unbalanced hormonal levels will not return to normal until the burn wound is closed. Perception of pain or suffering will dramatically increase levels of catecholamines and metabolic rate. Evaporation is a cooling process and reduces heat by 0.576 kcal/ml. In a burn patient with evaporative fluid losses of 350 ml/hr, evaporative heat losses are 3000-3500 kcal/day. If this heat energy is not provided by the environment, it must be supplied by the internal combustion of the patient.
The main principles for
successful management of the post-burn hypermetabolic response are :
Caloric requirements in burn patients have been calculated based on linear regression analysis of intake versus weight loss. The Curreri formula, which is the most popular estimation method, calculates caloric requirements of 25 kcal/kg/day plus 40 kcal/%BSA burned/day in a burned adult. For children, formulas based on body surface area rather than weight may be more appropriate. Our recommendation for caloric replacement in burned children is 1500 kcal/mBSA(total)/day for maintenance plus 1500 kcal/mBSA.
The composition of the nutritional supplement is also important. Caloric replacement should be based on non-protein calories only. Approximately 50% of the calories should be supplied as carbohydrates, 20% are protein, and approximately 30% of the calories should be supplied as fat. In adults, protein requirements are 100-150 gm/day, or about 1-2 gm/kg/day. In general, protein should be provided to achieve a calorie to nitrogen ratio of 100:1, which results in better immune function and survival in experimental and clinical burn trials than a ratio of 150:1. For a balanced daily diet, administration of vitamins C, A and E, zinc, iron, folate, and trace minerals are essential.
In burn patients, caloric support is best provided with enteral feedings. We recommend beginning nasogastric or nasoduodenal tube feedings within 6 hours following burn injury. Despite post-burn gastric hypomotolity, post-burn intestinal ileus rarely occurs. Early enteral feeding sustains intestinal mucosa, maintains caloric support in the resuscitation period, and may reduce the degree of the hypermetabolic stress response. Gastric residual volumes are checked hourly then returned. Rates of enteral infusion are gradually increased as tolerated, and intravenous infusion reduced to keep total fluid intake rate constant. By 48 hours, on-going fluid requirements are delivered enterally. Many commercial feeding solutions are available, but hypertonic solutions commonly caused diarrhea. For children 1 year and older, we prefer 3/4 strength Vivonex TEN (total enteral nutrition) providing 0.75 Kcal/ml. It is carbohydrate-based and raises endogenous insulin levels, which is postulated to increase endogenous insulin with the beneficial side-effect of reducing donor site healing time.
A good alternative where commercial feeds are not available is milk (0.66 Kcal/ml). Milk is nutritionally balanced, inexpensive, easily available, and well tolerated. The electrolyte composition of milk is such that potassium requirements are easily supplied, however the amount of sodium in milk (25 mEq/L) is insufficient to meet demands. Frequently during diuresis, sodium losses exceed intake and hyponatremia occurs. Sodium supplementation can be administered via milk in amounts of as much as 50 mEq/L. Such supplementation is usually necessary as long as milk is the only enteral foodstuff. With the introduction of a regular diet, sodium supplementation can usually be discontinued.
Infants under one year are normally fed an infant formula. Infant formula has even lower sodium and potassium than milk:
9.96 mEq/L Na
17 mEq/L K+
Ensure (vanilla, chocolate,
Resource Fruit (orange,
peach, wild berry)
Resource Just for Kids (JFK)
(strawberry cream, french vanilla, swiss chocolate)
Pediasure - general
purpose liquid food for children 1 to 10 years of age
Shriners patients should be ordered a regular diet as soon as it is tolerated. Patients do not receive any fluid other than milk (i.e. juice, cola, water) without a physician's order.
When the patient's wounds are virtually covered, the diet should transition from one in which the majority of the nutrition is supplied via tube feedings to a totally oral diet. The transition should be slow and may take several days. The following steps should be followed:
a. Reduce tube feedings to a rate
that, with the p.o. intake, equals 100% of goal.
Environmental control is a well-recognized part of appropriate burn care. Burn patients lose some of their thermo-regulatory abilities and are prone to hypothermia. An ambient room temperature of 28-33°C keeps the patient more comfortable and reduces the patient's heat loss from evaporation. The hypermetabolism is slightly diminished but not corrected to normal. Internally, the patient's body will still strive to maintain a temperature of 38-39°C. In order to accommodate this, we maintain patient care areas and operating rooms at elevated temperatures to minimize the amount of futile cycling required by the patient to generate the heat to achieve these elevated temperatures.
The value of appropriate pain management in acute burn management should not be underestimated. Pain is the most immediate concern of the burn patients. Suffering, a combination of physical discomfort and mental torment, increases the post-burn hypermetabolic stress response. The key to pain management is closure of the burn wound. In the interim, reduction in pain and suffering by sedatives, narcotics, and psychological support improves comfort and quality of life. It also reduces the hypermetabolic response. Treatment for a patient's suffering involves more than control of pain. Emotional support is essential. Uninterrupted sleep is very beneficial. Over-zealous use of narcotics alone provides a poor substitute, reduces GI mortality, and interferes with enteral nutritional support.
Hormonal manipulation of the post-burn hypermetabolic response may reduce morbidity from burn injuries. Continuous intravenous infusion of insulin and glucose reduces nitrogen and fat losses and maintains body weight, but is difficult to manage. Post-burn hypermetabolism is also reduced by anabolic steroids and adrenergic blockage. Propranolol reduces the hyperdynamic post-burn response and improves cardiac function, possibly protecting against post-burn cardiomyopathy. Recombinant human growth hormone reduces protein catabolism in the post-burn patient and increases the role of wound healing in donor sites. Oral oxandrolone is converted to testosterone upon metabolism by the liver. On-going clinical investigations are currently in progress. Check with the Fellows/Research Nurse/Faculty for information on the current protocols.
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