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            Advances in Burn Care


David. N. Herndon, M.D., Chief of Staff and Director of Research
Shriners Hospitals for Children-Galveston



   Recent discoveries and new therapies resulting from clinical and basic research are continually being incorporated into burn care worldwide. As a result, the mortality of burned children and length of the hospital stay have been greatly reduced over the last 25 years. In the 1960s, the likelihood of survival was only 50% in children with burns covering 35 – 44% of the total body surface area (TBSA), and few patients with burn sizes exceeding 45% TBSA survived. The average length of stay for the acutely burned child was 103 days. Today, the lethal burn size for 50% of children exceeds 95% TBSA, and the average length of hospital stay for most serious burn injuries can be expected to be only 0.5 days per percent of burned TBSA.

   Given the fact that most burn victims now survive, current research directions at SHC-G have shifted to focus on developing and innovating ways to enable faster, more complete recoveries from burns and to improve overall quality of life. During the last funding period, researchers have made important discoveries and progress in a myriad of areas. These are described below with an emphasis on achievements in infection control, metabolism and nutrition, inhalation injury, and scar development and rehabilitation.

Infection Control

   Infections in severely burned children are the main cause of mortality. Recent studies from our center have found that 30 to >50% of deaths in burned children are due to sepsis and infections with antibiotic-resistant microorganisms. Studies conducted at SHC-G have shown that early excision and grafting not only improves scarring and cosmesis, but also decreases the incidence of infections and sepsis. Removal of the burn scar dramatically decreases colonization of bacteria and fungi that can lead to systemic infection or sepsis. Bacterial and fungal colonization of the burns can also be decreased by soaks developed at SHC-G. Shrine studies have demonstrated that these antimicrobial anti-fungal soaks are of great benefit in preventing tissue infection, systemic infection, or sepsis. Mafenide acetate, silver sulfadiazine, and 0.5% Dakins solution are current topical treatments and have shown to greatly improve graft take and prevent infections.

   A high incidence of gram-negative sepsis exists in thermally injured patients without an obvious source of bacteria. This led to the hypothesis that the gram-negative bacteria were derived from the gastrointestinal tract. The concept that the burn wound became infected as a result of microorganisms from the gut entering the circulation was proposed. This idea has been tested in dogs by infecting the gastrointestinal tract with Pseudomonas labeled with a fluorescein tag. Bacteria crossing the mucosal barrier in burned animals were identified from fluorescence tags in the plasma. Later, this tagged material was found in the burn wound itself.

   Recently, the importance of bacterial translocation after cutaneous thermal injury, endotoxin administration, or inhalation injury has been recognized. Bacterial translocation associated with reduced blood flow can be prevented with vasodilators. These events may be clinically important since a reduction in blood flow to abdominal organs is associated with the release of myocardial depressants. This could explain the increase in mortality seen in patients with combined thermal and inhalation injury, since the combination of these two insults produces a greater increase in abdominal vascular resistance than either insult alone. The need to prevent “under resuscitation” of burned patients is well recognized. Most recently, a drug (a thromboxane synthetase inhibitor) that inhibits the formation of a vasoconstrictive mediator that is released after burn injury (thromboxane) has been shown to reverse bacterial translocation following thermal injury and myocardial depression following administration of endotoxin. Preliminary data indicate that compounds with anti-thromboxane activities may also be effective in preventing the mesenteric vasoconstriction and myocardial depression that occurs following inhalation injury.

   Burn patients are immunocompromised and unable to fight off infections. Research from the Shrine centers is focused not only on the treatment of infections, but also on the improvement of patient defenses against infections. New pathways, receptors, cell populations, drugs, and interventions are currently being investigated to change the immune compromised patient into an immune competent patient to improve survival. Examples of ongoing research include studies determining the effects of propranolol (a non-selective ß1/ß2 receptor antagonist) on the immune system. Researchers at our hospital have shown that propranolol is able to change immune incompetent macrophages and monocytes to functional cells that increase bacterial clearance. This exciting finding suggests that we may have a new treatment to reverse the devastating immune compromised state of severely burned children.

  Other research performed at our hospital has shown that dendritic cell enhancement may increase resistance to infections. Dendritic cells are severely depleted in burn patients, and restoration of dendritic cells positively correlates with resistance to sepsis; conversely, a lack of dendritic cell repopulation correlates with sepsis and, ultimately, death. Our researchers have discovered that treatment with a dendritic cell growth factor after burn injury can restore dendritic cells and increase resistance to infections. This year we have also found that this same growth factor promotes the healing of burn wounds, which decreases the risk for wound-derived infections. Therefore, pharmacological dendritic cell enhancement may improve patient outcome both by improving immune function and promoting wound healing.

  Other investigators at our institution have identified a human protein, cystatin, as a novel immunomodulator that restrains damaging inflammation during infection and trauma. Ongoing investigations of this multi-faceted human protein may lead to new therapies to minimize systemic infection, stabilize intestinal integrity/microbiome and damaging inflammation following thermal injury.

  Another discovery that originated from research performed at SHC-G is the finding that severe burn injury triggers a remarkable upregulation of the inflammatory response in the immune system. Studies have shown that a dramatic upregulation of many cytokines, inflammatory markers, hormones, stress hormones, and stress markers persists for a prolonged time, leading to alterations in the immune system and the body’s metabolic response. Therefore, the immune system and the inflammatory response play a major role as mediators of the post-burn response. More recent work by our group has revealed that, in non-survivors of burn injury, plasma levels of many of these factors have a unique “profile” that markedly differs from that seen in survivors, suggesting that these can be used to predict poor outcomes and help provide personalized care. Moreover, interventions to alter these “mediators” would be expected to improve outcomes in severely burned children.


Metabolism and Nutrition

   Fundamental questions regarding the metabolic demands of the thermally injured patient have been investigated. These questions include the following. 1) How many calories do thermally injured patients require? 2) How many carbohydrate (glucose) calories should these injured patients be given to avoid starvation and to promote protein accretion? 3) How many protein calories should these patients be given to achieve net protein synthesis? 4) What treatments should be given to reduce diabetic-like symptoms such as insulin resistance? As discussed below, studies conducted at SHC-G have yielded several practical answers.

  In light of the above events, choosing the proper level and source of energy is one of the most critical aspects of helping patients recover from a severe burn. Large amounts of carbohydrates and fat must be converted to energy to satisfy the requirements needed to nourish the traumatized body and fuel the rapid growth of new cells. An insufficient diet can be extremely detrimental to the burn patient. On the other hand, excess calories can also be harmful. One major cause of mortality in burn patients is respiratory failure. Decreased respiratory and peripheral muscle mass reduces the ability to breathe and exercise. Excessive carbohydrate administration may increase carbon dioxide production and further complicate the respiratory status. Therefore, determining the optimal caloric intake requires giving sufficient, but not excess, calories. This has been an intense area of research funded by Shriners.

  Carbohydrate metabolism is greatly altered in burn patients, and burn centers have investigated how to best compensate for these changes. One of the more dramatic burn-induced alterations is the increase in glucose uptake rates and gluconeogenesis. Despite these increased rates, researchers have identified a practical limit in the glucose infusion rate (5 mg/kg/min), beyond which the excess glucose is not oxidized for energy but simply becomes stored as fat. Excess fat is stored in the liver. The resulting fatty liver elevates the diaphragm and compromises breathing. At glucose infusion rates above 5 mg/kg/min, the respiratory quotient exceeds unity, causing excess carbon dioxide production and increasing minute alveolar ventilation requirements. The combination of diaphragmatic elevation and increases in carbon dioxide exacerbates respiratory difficulties in burn patients.

  Malnutrition and burn injuries have been associated with infection and death. Burn physicians in various cities began continuously feeding patients milk to reduce the incidence of gastric and duodenal ulcers. As a result, stress ulcers rarely occurred in milk-fed patients. Milk was also shown to prevent weight loss in children who were recovering from severe burns. This led to the practice of milk feeding up to one hour before any surgical procedure. Accurate formulas for the precise amount of calories required to maintain weight in burned children of different ages have continued to develop. However, the use of supplemental parenteral hyperalimentation has been shown to be not only unnecessary, but also detrimental. Early enteral and continuous feeding has now decreased mortality in burned children and is an accepted practice in burn units around the world. Because giving fat rather than carbohydrate can exacerbate fatty liver, there has been a recent shift away from providing high-fat formulations such as milk toward high-carbohydrate formulations.

  Marked changes in organ and whole-body protein metabolism often accompany a severe thermal injury. Much of our knowledge about the nature of whole-body protein metabolism after trauma has been obtained from nitrogen-balance studies. These studies uncover changes in total body nitrogen content, though they do not reveal the pathways through which these changes occur. Many studies using stable isotopes and steady-state kinetic models have greatly contributed to our understanding of changes in whole-body protein metabolism after burn injury, and they have helped us to understand how to best compensate for burn-induced changes in whole-body nitrogen content. Unlike most studies, these studies do not involve laboratory animals or in vitro environments. Instead, they are performed on patients using nonradioactive isotopic tracers (stable isotopes). Stable isotopes are naturally occurring atoms that possess an extra neutron, allowing them to be easily distinguished from their more abundant natural form. By collecting expired air, blood, or tissue samples containing these stable isotopes, research scientists can track the transformation of amino acids into protein used to build muscle tissue.

   Protein metabolism is the process by which tissues (such as muscle) are constantly being built up and broken down. After thermal injury, protein breakdown exceeds synthesis, causing a net release of amino acids (the basic building blocks of protein). When elevated in the serum, these amino acids are converted to glucose in the liver, a process known as gluconeogenesis. Glucose is then broken down to smaller compounds in peripheral tissues through anaerobic or aerobic metabolism to generate energy. During anaerobic metabolism, the smaller sugars are converted into lactate and pyruvate. This appears to be the primary energy-producing process in thermally injured patients. The elevation of lactate and pyruvate can be detrimental to the patient. The resulting acidosis (generated by lactate build-up) is accompanied by compensatory changes in the utilization of glutamine, an essential fuel for cells lining the gastrointestinal tract and of the immune system. Depletion of this amino acid causes the starvation of these cells, allowing toxic materials and bacteria from the gut to enter the systemic circulation. A potential therapy to combat this is being tested and involves the administration of compounds that stimulate the incorporation of amino acids into protein. Administration of treatments such as oxandrolone and human recombinant growth hormone reverse the net protein breakdown produced by thermal injury and stimulate the use of amino acids for muscle synthesis. This not only redirects metabolism away from gluconeogenesis, but also increases incorporation of amino acids into healing wounds. An increase in the rate of donor site healing and a decrease in the length of the hospital stay have been shown to occur when burned children are treated with growth hormone and other anabolic agents. Patients with 60% burn wounds experience a decrease in the length of the hospital stay from 46 to 32 days.

  After thermal injury, a reorganization of protein synthesis occurs. Several enzymes and proteins involved in the body’s defense system are increased. These factors include blood coagulation factors, proteolytic enzyme inhibitors, and enzymes involved in the destruction of bacteria. At the same time, other proteins such as albumin are reduced. A reduction in albumin can be detrimental since this plasma protein plays an important role in preventing edema. Investigators are now beginning to identify the genetic and proteomic mechanisms responsible for these changes and have identified several factors that participate in regulating these genes and proteins.

  Optimizing the hormonal milieu is also a critical area of burn care that is undergoing important advances. Researchers have demonstrated that very high levels of the hormone epinephrine (adrenaline) are present in thermally injured patients. This hormone can increase metabolism by stimulating ß-adrenergic receptors. Propranolol, a competitive antagonist of ß-adrenergic receptors, has been shown to lower heart rates in burned children, decrease the amount of oxygen needed to keep the heart pumping, and reduce anxiety caused by burn-induced epinephrine release, without impairing the ability of the patient to respond to stress. In thermally injured patients, the rate of fat metabolism is 2.5 times higher than that in normal individuals. This appears to be due to elevated catecholamines and ß-adrenergic stimulation, since this increase can be blocked by propranolol. The deposition of excess fat in the liver causes fatty liver, which is thought to induce insulin resistance in burned children. Accordingly, burned children display many symptoms similar to those seen in diabetic patients. Importantly, SHC-G researchers have shown that reducing fatty liver in burned children with treatments such as propranolol and fenofibrate improves insulin sensitivity. In recent years, these initial investigations with propranolol have progressed into a large trial. Propranolol has now been shown to have a host of benefits in recovering burn patients, including improvements in cardiac work, muscle strength, lean mass, bone growth, sepsis and infection rates, and survival. This agent is now being investigated in multicenter trials, a final stage before incorporation into the standard of care for burns.

   Finally, one of the recent contributions of SHC-G to burn care is the discovery that the hypermetabolic response produces effects at the cellular level. Hypermetabolism is associated with cell death (apoptosis) in skeletal muscle, fat, liver, kidney, lung, heart, and gut. These detrimental cellular events are associated with dysfunction of cellular organelles such as the mitochondria and endoplasmic reticulum. New studies clearly show that a burn injury is not limited to the skin. Rather, it causes dysfunction of almost every cell in the body, leading to alterations in cellular functions and cellular signaling pathways. New strategies to alter these pathways may restore cellular function and productivity. This, in turn, may lead to improved energy metabolism, cell survival, morbidity, and mortality not only during acute hospitalization, but also long term. In the past, burn patients typically lost 40 – 50% of lean body mass, an occurrence that almost always resulted in death. Several new approaches have been successfully used to alter hypermetabolic responses, including use of adequate nutrition, ventilation, and fluid resuscitation; early excision and grafting; growth factors; air beds; and a warm environment. These approaches have decreased the loss of lean body mass, muscle, fat, and bone to 5 – 8%. This is a dramatic improvement given that loss of 5 – 8% lean body mass is associated with a dramatic increase in survival. Decreasing loss of lean body mass also improves strength, endurance, rehabilitation, and reintegration into society. These findings as well as others from SHC-G clearly show that the hypermetabolic response to burns plays a key role in burn injury and is a major determinant of survival. Research originating from all four centers at Shriners Hospitals for Children has advanced knowledge of how to attenuate and reverse the hypermetabolic response as well as of how to improve patient outcomes, including quality of life.


Inhalation Injury

   Traumatized acute lung injury greatly contributes to mortality in thermally injured patients. Within the past 5 years, the Cardiopulmonary Research Program has made great strides in advancing our current state of knowledge of the pathophysiologic cascade. Our findings have been published in more than 300 peer-reviewed, high ranked journals and major textbooks (burn and pulmonary disease), such as Total Burn and Fishman’s Pulmonary Disease and Disorders that are used around the world. Most recently, we have accumulated new evidence that airway dysfunction plays a critical role in pathophysiology of acute lung injury. We have characterized airway changes such as airway hyperemia with severe mucosal edema, airway obstruction, and bronchospasm. These studies demonstrate that treatment of airway dysfunction is crucial for prevention of life-threatening changes that occur in the lung parenchyma. We have proposed various effective and safe treatment options for these airway changes. Many of them have either been translated to clinical trials or used for treatment of burn patients with smoke inhalation.

Acute Lunge Injury

   The SHC-G group has significantly advanced our understanding of the pathophysiology of smoke inhalation or sepsis-induced acute lung injury and treatments. A description of our discoveries are as follows:

   Recent smoke inhalation studies have focused on airway damage as the major contributing factor to lung injury. These studies have revealed that airway dysfunction results from factors that narrow airway lumen, thus partially or completely blocking airflow to the alveoli causing severe hypoxia. These factors are described below.

  1. Airway hyperemia
    We have proven that increased airway blood flow plays a crucial role in airway mucosal edema as well as lung parenchymal edema. We have demonstrated that, following smoke inhalation, airway blood flow increases about 20-fold. As result, severe airway mucosal hyperemia and edema occur, narrowing the airway lumen. Most importantly, the augmented airway blood flow increases both flux of fluid and inflammatory mediators to the lung parenchymal circulation, thus significantly contributing to the pulmonary edema and inflammation. A series of studies conducted in sheep with ablated bronchial blood flow provided direct proof of this concept. We found that lung function in smoke-injured sheep was significantly improved through ligation of the bronchial artery because of reduced lung parenchymal edema and suppressed pro-inflammatory mediators. Since this technique (bronchial artery ligation) is not feasible in patients, we have offered an effective, safe, and cheap therapeutic option—nebulized epinephrine—that would exert similar effects as ablated bronchial blood flow. We have published data showing the efficacy of nebulized epinephrine in ovine models of acute lung injury induced by smoke only or combined smoke + burn in a major critical care journal “Critical Care Medicine.” Our findings in preclinical large animal studies have been successfully translated to a clinical trial at SHC-G. Nebulized epinephrine has multiple beneficial effects: 1) it reduces/prevents airway wall edema, 2) reduces/prevents airway exudate containing procoagulants that form solid airway obstructive casts, and 3) causes bronchodilation. We have demonstrated that nebulized epinephrine is superior to standard therapy—nebulized albuterol (translated to clinical practice form our team)—because it not only antagonizes the bronchospasm, but it also attenuates increases in airway blood flow and edema in both the airway mucosa and lung parenchyma. The use of nebulized epinephrine is increasingly attractive because it is FDA-approved, cost effective, and readily available.

  2. We have characterized the pathophysiological changes associated with airway obstruction—debris of injured airway epithelial cells, inflammation (neutrophils), mucus secretion, and plasma exudate containing procoagulants that form fibrin casts. Based on these pathological factors, we have developed efficient (preclinical) therapeutic strategies, such as nebulized or intravenously administered anticoagulants, nebulized fibrinolytic agents (to lyse fibrin clot in airway), mucolytic agents, intravenously administered and nebulized mesenchymal stem cells. Among these, nebulized heparin (anticoagulant) and mucomist (mucolytic) are currently used as a standard therapy in burn centers. In the future, we would like to translate the use of nebulized fibrinolytic agents (i.e., tissue plasminogen activator for fibrin breakdown) and mesenchymal stem cells or other cellular therapies to restore damaged airway epithelium.

  3. Bronchospasm
    We have translated the use of continuously nebulized albuterol to clinical practice for its bronchidilation effects as a standard of care. Recently, we have discovered a very important phenomenon. That is, we have found that it is effective only when it nebulized continuously. Our finding was recently confirmed by failure of a large clinical trial on use of nebulized albuterol for treatment of patients with ARDS, where albuterol was nebulized intermittently. As mentioned, our group has already put forth a better strategy with nebulized epinephrine.

   Our group has also extensively focused on the role of coagulopathy in the pathophysiology of lung injury following smoke inhalation. We have found (chest CT scan and pathology) that various size pulmonary vessels are clotted 24 hours following smoke inhalation. This finding is of particular interest because it clearly indicates that burn patients with smoke inhalation should receive adequate therapy with systemic anticoagulants. We have demonstrated the efficacy and safety of intravenously administered antithrombin, which is the most potent endogenous anticoagulant. We plan to translate our findings to clinical studies (perhaps multi center).

  Another challenging aspect of smoke inhalation injury is difficulty diagnosis this condition and grading its severity. There is no consensus among investigators on how best to do this. Consequently, no world-accepted guidelines exist. Recently, we have proposed using magnetic resonance imaging for diagnosis and grading of smoke inhalation injury in addition to existing but controversial criteria. We would like to organize a summit (Shriner-initiated) among clinicians and researchers to reach consensus on diagnosis, grading, and treatment of smoke inhalation injury.

  Our group has developed a novel strategy for treatment of acute lung injury during sepsis. We have demonstrated intravenously administered bone marrow-derived mesenchymal stem cell have beneficial effects in preclinical model of smoke-induced sepsis. Our safety and efficacy data were reviewed by the FDA, and the study was approved to be translated to the first clinical trial on use of stem cells for treatment of acute lung injury. Currently, a clinical trial phase II is being carried at University of California San Francisco under the leadership of Dr. Michael Matthay.

   We have recently discovered that there is considerable structural brain damage present following smoke inhalation. We have found that brain damage is associated with substantial neuronal and astrocytic death and is accompanied by micro and macro hemorrhage. These findings strongly indicate an urgent need for careful neurological examination of burn patients with smoke inhalation, as those symptoms can be masked by anesthesia, burn shock, or other accompanying morbidities. Burn survivors should also routinely undergo neurological follow up studies, as the chronic symptoms of brain structural damage can be masked under general diagnoses such as posttraumatic distress syndrome and/or depression. Our group is continuing to investigate pathophysiologic mechanisms underlying these changes and to develop effective therapies (possibly with mesenchymal stem cells).

   Finally, our group has translated the following therapeutics for treatment of acute lung injury:

  1. Continuously nebulized albuterol
  2. Nebulized epinephrine (ongoing clinical trial at SHC, Galveston)
  3. Oral Vitamin E supplementation (ongoing clinical trial at SHC, Galveston)
  4. Intravenously administered mesenchymal stem cells (phase II clinical trial at UFCU)
  5. Arginine vasopressin V1a agonist (selepressin; ongoing phase III clinical trial).
    This therapy has the potential to be the only drug approved for treatment of
    septic patients as it has successfully passed phase IIa & b clinical trials.
    We have discovered that selepressin reduces/prevents lung edema as well as systemic
    fluid retention in addition to maintaining adequate blood pressure during sepsis.


Scar Development and Rehabilitation

   One of the major issues that burn victims face once they survive the acute phase is the formation of hypertrophic scars. Current research performed at several centers is focused on how the development of the hypertrophic scar can be attenuated and altered. One of the goals of this research is to determine whether hypertrophic scars result from a genetic predisposition, a proteomic predisposition, or a surgical technique. These answers are extremely relevant because hypertrophic scarring requires repeated operations for burn patients. The debilitating appearance of hypertrophic scars limits the reintegration and rehabilitation of burn patients. It also diminishes the patient’s self perception. These research endeavors funded by Shriners Hospitals for Children are relevant not only for burn patients, but also for other surgical patients who develop hypertrophic scars or keloids. Major advances are expected over the next decade. One of the main achievements that has already taken place is the use of pressure garments to attenuate hypertrophic scar development.

   Pressure garments, which are used to reduce scarring, were developed 20 years ago. Traditionally, elastic bandages were placed on the legs of burn patients to improve venous return and decrease bruising or blood blister formation. These bandages were also applied to splints to reduce and prevent contractures. Therapists observed that burn patients rarely developed hypertrophic scars when these pressure garments were applied. Unsightly scars could be prevented if the pressure garments were continuously worn, and they could be reversed if the pressure garments were applied. Investigators studying scar formation have found that collagen fiber deposition in non-hypertrophic scars is parallel, whereas fibers in hypertrophic scars predominantly form nodular or whorl-like patterns. With the application of pressure, these diffuse, disorganized fibers become parallel. The relationship of the whorl-like fibers depends on the quantity of proteoglycan that makes up the scar tissue. In hypertrophic scars, this material is more abundant. Several researchers have concluded that pressure application reduces the scar by limiting blood supply to the wound. Other studies have shown that the macrophages of patients with keloids and hypertrophic scars produce elevated levels of interleukin 6, ß interferon, and tumor necrosis factor, suggesting that these inflammatory cytokines participate in scar formation.

   Although compression has beneficial effects on scar formation, pressures may increase over time and decompression of burn wounds is often necessary. Failure to decompress extremities with elevated pressures may lead to significant, but preventable, complications. These complications can be avoided by monitoring compartment pressures in burn patients. Interestingly, monitoring pulse is not an acceptable substitute, as it is not predictive of ischemia. Models of burn treatment strongly rely on the integration of basic science, clinical research, and clinical treatment that share information in a continuous feedback loop. Clinical innovations are usually based on empirical data and then evaluated for effectiveness through scientific study.

  In the last 5 – 7 years, advances in multiple aspects of burn care have improved the quality of life of burned victims. Quality of life has been improved by attenuating the hypermetabolic response as well as by increasing the patient’s physical function, performance, and well-being. A 12-week exercise training regimen developed by SHC-G has been shown to improve body composition (lean mass and muscle content), strength, rehabilitation, reintegration, and life quality of the burned patient. It has also decreased the need for reconstructive surgery by lessening scarring. This is a significant achievement since we have not only decreased mortality and hypermetabolism in burned patients acutely, but also improved the rehabilitation and reintegration of patients. We have also completed a study which shows that such 12-week exercise rehabilitation program can be implemented in hospitals or in community-based centers or gyms, with similar benefits.

   Other findings are also expected to lead to improvements in the quality of life of burn patients. Research support through Shriners Hospitals for Children has enabled development of a database to follow patients longitudinally on specific measures of physical and psychosocial recovery. Four hundred patients have been entered into this database, which includes longitudinal assessments of cardiopulmonary functions, physical growth, maturation, and bone density; measures of functional capability, including range of motion and daily living activities, scar formation, and reconstructive needs; and several measures of the psychosocial adjustment of the child/patient and parent(s).

  One important finding from the collected data is that the long-term successful psychosocial adjustment of burned children largely depends on the enduring qualities of the families with which they live. Based on these data, a treatment program has been developed that centers on strengthening the welfare of the family/patient unit. We emphasize the importance of having at least one parent/guardian available. Studies consistently indicate that, regardless of burn size, the majority of the children eventually function satisfactorily as socially integrated, behaviorally well-adjusted individuals with positive self-regard. Only about 20 – 30% of each sample has moderate behavior problems. These outcomes have been consistent. This is true even for survivors of the most massive injuries, many of whom have now grown into young adults with careers and families of their own. In terms of physical impairment, children are remarkably independent in their capabilities, even those with the most severe injuries.


Psychological Adjustment

   Recently, we measured the impact of exercise therapy on the recovery and quality of life of the children. We examined the effects of a 12-week Wellness and Exercise program on the quality of life of children with large burns using the Child Health Questionnaire (CHQ). We believed that this comprehensive regimen would improve physical and psychosocial outcomes. Seventeen children participated in the Wellness and Exercise program and 14 children received the Standard of Care. Significant differences were not evident between the groups; however, the parents of children who participated in the Wellness and Exercise program reported significant improvements with their children’s physical and emotional functioning. We also compared an in-hospital exercise program to a community based home exercise program. Significant differences were not found between the groups; however, both groups reported experiencing physical and psychosocial improvements one year-post burn.

   In another study, we compared the long-term quality of life of pediatric burn survivors with and without inhalation injuries using two measures: the World Health Organization Disability Assessment Scale II (WHODAS II) and the Burn Specific Health Scale-Brief (BSHS-B). Inhalation injury didn’t appear to significantly impact participants’ scores on the majority of the domains. However, increased burn size was associated with difficulty completing tasks. Another study compared the long-term psychological distress and quality of life in adult pediatric burn survivors using the WHODAS II to the BSHS-B. We found that quality of life was affected by burn size. Females and children burned prior to school entry reported better quality of life. The WHODAS II appears to be a more sensitive measure for identifying individuals with distress and lower quality of life.


Pain Control

   Excessive pain during medical procedures is a worldwide problem. Pain control is especially challenging for severe burn patients during wound debridement. Although Shriners is a world leader in prescribing the most effective pain medication regimens, even the most powerful pain meds are often not enough to control the pain experienced by children during severe burn wound debridement in the ICU tubroom. Side effects of the pain medications and habituation limit effectiveness of narcotic pain medications.

   Recently a powerful new non-drug psychological distraction analgesic has been developed that can be used in addition to traditional pain medications. Shriners Psychiatrist Walter Meyer, MD and colleagues at Shriners are spearheading the development and testing of this new technology at Shriners Galveston: Virtual Reality pain distraction.

   Shriners Hospitals for Children in Galveston Texas is now the world leading research center exploring the use of immersive virtual reality pain distraction as a non-drug psychological pain control technique that can be used in addition to traditional pain medications. A randomized controlled clinical trial is currently underway at Shriners Galveston, in collaboration with the researchers who originated the use of VR for pain distraction, Hoffman and Patterson from the Univ. of Washington in Seattle. Although the ICU tubroom is a very challenging environment, results from this Shrine funded study are already showing large reductions in pain and large increases in fun when patients play virtual reality during wound debridement in the ICU Tubroom at Shriners Galveston (used in addition to the patinet’s usual pain medications).

   Although this Shrine-funded study is still collecting data from this randomized control trial at Shriners Galveston, a preliminary analysis of our results presented at the American Burn Association earlier this year showed large, clinically meaningful, and statistically significant reductions in pediatric patients pain during burn wound care in the ICU tubroom at Shriners Galveston (see Figure 1 below). This Shrine study is using a custom Virtual Reality pain distraction system created at the University of Washington by modifying commercially available equipment, and integrating commercially available components. So although it is an original combination of commercially available components, there is no intellectual property. The VR software we have been using for this project (SnowWorld) was designed specifically for treating severe burn patients, and has been made available to Shriners Galveston free of charge by the University of Washington in Seattle. None of the researchers has any financial conflicts of interest.



   One of our focuses has been on identifying modifiable risk factor to prevent burns with young children. We know from the literature that they are at risk for injury due to their dependence on caregivers. At this pediatric burn center, we provide medical care to children with large, severe burns. In one study, we compared the nature of scald burns for children age 5 and younger from the U.S. and Mexico. The primary cause of burns for children from the U.S. was spills, pulling hot substances, and bathing. The primary cause for children from Mexico was falling into containers of food or hot water placed on the ground to cool. The median age at burn for children from the U.S. was 1.5 years and for children from Mexico. 2.5 years. Another study identify causes of burns in children five and younger from Mexico who received medical care at this center to identify modifiable risk factors and use the information as a guide for prevention. The primary cause of flame burns was due to explosions followed by house fires. The primary cause of scald burns was falling into containers of hot substances. The median age for flame injuries was 3.0 years and scalds 2.5 years. Mortality rate was low (5.4%).
A subsequent study examined the geographic distribution of burns in young children from Mexico who received medical care at this facility. We were interested in identifying the incidence of flame burns as opposed to scald burns in each state with relation to population density and poverty percentage. We found that the proportion of flame burns decreases with increasing poverty. Conversely, the proportion of scald burns increases with increasing poverty. This finding is striking in that the measure of poverty is by community and region and not the families’ socioeconomic status. We know from the literature that southern states in Mexico have higher poverty rates compared to northern states. Therefore, we suggest that safety and prevention programs can highlight flame burns for the Northern states of Mexico and scald burns for the Southern states of Mexico. Results of these studies will be shared with agencies that can implement prevention campaigns.


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