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Advances in Burn Care

D. N. Herndon, M.D., Chief of Staff
Galveston SHC

Recent changes and new therapies have been incorporated into burn care throughout the world through the efforts of clinical and basic research. This article will summarize some of the important advances in treating burned children that were made possible through the support of the Shriners Hospitals for Children.

It is often difficult to determine what specific discoveries affect the delivery of healthcare in burns. The areas of advancement in burn care have been:

* Resuscitation – immediate lifesaving measures

* Early Excision and Grafting – removing burned tissue and covering it with skin or skin substitute

* Hypermetabolic Responses to Burn Injury – over-response of the whole body to the burn injury

* Infection Control – prevention of infection, or sepsis

The mortality and length of hospital stay of burned children have been greatly reduced over the last 25 years.

In the 1960’s, the survival rate was 50% for children with 35-44% total body surface area (TBSA) burns. Few patients with burns over 45% TBSA survived.

The average length of stay for the acutely burned child was 103 days.

Today, the survival rate is 50% for children with over 95% TBSA.

The average length of hospital stay for most serious burn injuries can be expected to be only 0.5 days per percent of TBSA that is burned.

This is truly a remarkable achievement and is striking testimony to the concentrated effort in personnel and resources that have been directed toward this problem. The Shriners Hospitals for Children have contributed in a major way to this remarkable achievement by their very sound and sustained investment of substantial resources toward this endeavor. Specific aspects of burn care that have dramatically improved in burn hospitals include: treatment of the wound with prompt eschar excision (burned tissue removal) and immediate wound closure, understanding and meeting the changes in metabolic and nutritional requirements, and the evolution of effective skin banks, infection control, and alternative wound-closure materials and strategies.

Prompt Eschar Excision and Immediate Wound Closure

Eschar is the dry scab that forms over skin that has been burned or exposed to corrosive agents.

Although as early as 1947 researchers (1) had recognized that prompt eschar removal and immediate wound closure could improve outcome in burn injuries, application of this approach to large burns had not been practical before the 1970’s because of an associated high rate of infection and bleeding complications. Many burn units adopted the excision technique (2), which was a single tangential slice that was intended to remove the superficial layer of second-degree injuries. The application of this tangential excision method to superficial injuries by most surgeons had been frustrated by the excessive blood losses that accompanied its use in large burns and those burns with full-thickness depths.

The development of effective topical antimicrobials and systemic antibiotics in the 1960’s to combat infection, combined with low-tension anesthetic techniques and other blood-conservation measures, allowed prospective, but nonrandomized (non-controlled), clinical trials to be conducted. In these studies (3), improvements in survival and length of hospital stay were seen, and as a result of these encouraging outcomes this surgical approach was promoted.

The exact contribution to the outcome of prompt eschar excision and immediate wound closure in large burns has largely remained unknown because prospective, randomized (controlled) clinical trials have not been conducted. A few prospective studies have been performed (4,5), which demonstrated that prompt excision improves hospital stay (6) and survival (7). Several centers have reported improvements in long-term function and cosmesis (concern for the patient’s appearance), leading to a decreased need for reconstructive procedures. Further developments have allowed safer operations and minimized blood losses (8). These advancements have allowed this method to be effectively used in burns of all sizes and make this approach the standard method of treating these injuries (9,10).

In order for prompt excision and immediate wound closure to be practical in massive burn injuries, alternative materials and approaches to wound closure became necessary in burns that covered more than 50% of the TBSA. A system of cryopreservation (freezing) and long-term storage of human skin for periods extending up to several months was developed (11). Although controversy surrounds the degree of viability of the cells within this preserved skin, the method has allowed greater flexibility in the clinical uses of autologous skin (from the patient) and allogenic skin harvested from cadavers.

Because a clear clinical need for a skin-replacement material was evident by 1981, a bilayer artificial skin for permanent wound closure was developed, and preliminary clinical results of its use were reported (12,13). This material has been studied in an 11-center clinical trial comparing the artificial dermis to conventional grafting techniques after the early excision of the burns in patients with major thermal injuries (14). This artificial skin provided a permanent wound cover that was at least as satisfactory as currently available skin-grafting techniques. The take of the “thin” epidermal grafts on the artificial skin was 80% successful, and at the completion of the study less hypertrophic (overgrown or enlarged) scarring was seen with artificial dermis. Furthermore, patients preferred the artificial skin to conventional grafting methods. Continued experience with this artificial skin has been extremely favorable, and a potential survival benefit has been associated with its use in massive burns (15).

The use of “sheet” autografts (skin from the patient) to cover larger surface areas has been described (16). Extremities and the trunk were more often grafted with mesh graft, which is graft with multiple slits to stretch over a large area. Sheet grafts were often the sole coverage in patients with burns up to 55%. With larger burns, sheet grafts were used to cover the face and hands. Because of its superior cosmetic and functional outcome, sheet autografting is now considered for covering moderately sized burns and is important in the cosmetic and functional areas, such as the face and hands.

To substantiate an observation that donor sites harvested from the back scar less than those harvested from thighs, donor sites from both areas were evaluated for the extent of scarring (17). From this study, it was concluded that back donor sites had significant improvement in scar height, color, and edema (fluid in the tissues). Thus, the back is now the preferred donor site for skin grafts in the pediatric burn population.

From 1984 through 1989, researchers studied 24 patients with 30 acute burns on the palm of the hand that required skin grafting to compare the efficacy of split-thickness versus full-thickness autografting (18). Split-thickness grafting uses portions of the skin, mostly the upper layer. Full-thickness grafting uses the skin and underlying tissue. The results demonstrated improved function and a decrease in the need for reconstructive procedures when full-thickness skin grafts are used for the treatment of deep palm burns in young pediatric patients.

Metabolism and Nutrition

Metabolism is the sum of physical and chemical processes that sustain the body. A large burn affects the whole body, and so it affects metabolism. Fundamental questions regarding the metabolic demands of the thermally injured patient have been evaluated, and several practical answers have emerged. The metabolic and nutritional questions include (1) how many calories do thermally injured patients require? (2) how many carbohydrate calories should these injured patients be given to avoid starvation and to promote protein synthesis? and (3) how many protein calories should these patients be given in order to achieve net protein synthesis? The solution to the first issue, as others have reported, is that the metabolic rate of thermally injured patients, measured by indirect calorimetry (measure of heat production), rarely exceeds twice the metabolic rate of a person at rest as calculated by standard measures. Therefore, twice the energy expenditure of a person at rest is a generous estimate of the total caloric requirement in burn patients.

Carbohydrate metabolism has been found to be greatly altered in these patients, and burn centers have pursued studies to consider how best to compensate for these changes (19,20).

Glucose is the end product of carbohydrate metabolism and is the chief source of energy for living organisms. One of the more dramatic alterations is that glucose uptake rates and glucogenesis (formation of glucose) are greatly increased after burn injury. Despite these increased rates, researchers have demonstrated 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 (20). The excess fat is stored in the liver and results in fatty livers, which elevate the diaphragm and compromise breathing. At glucose infusion rates above 5 mg/kg/min, the respiratory quotient, or ratio of carbon dioxide produced to oxygen consumed, exceeds normal balance and causes excess CO₂ (carbon dioxide) production and increases minute alveolar ventilation requirements. The combination of elevation of the diaphragm and increase in CO₂makes the respiratory failure frequently seen in these patients more severe.

Marked changes in organ and whole-body protein metabolism often accompany a severe thermal injury. Much of the knowledge about the nature of whole-body protein metabolism after trauma has been obtained from nitrogen-balance studies. These studies uncovered changes in total body nitrogen content without revealing the pathways in which these changes occurred. Many studies using stable isotopes and steady-state kinetic models have greatly contributed to understanding these changes in whole-body protein metabolism, and these studies have suggested how best to compensate for these changes in total body nitrogen content (21).

A source of energy is one of the most critical requirements to the patient recovering from a severe burn. The processes of wound healing, growing replacement tissue, and supporting normal metabolism require huge energy demands from the body. 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 unbalanced diet, therefore, can be extremely detrimental to the burn patient.

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 CO₂ production and further complicate the respiratory status. Unlike most research, these experiments do not use laboratory animals or in vitro studies but are performed on humans. This is research made possible through the use of nonradioactive isotopic tracers (stable isotopes) which are naturally occurring atoms that possess an extra neutron that distinguish them 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.

While the body of a burn victim undergoes many changes, the rampant acceleration of metabolism places an increased load on the heart, liver, kidneys, lungs and other vital organs that provide normal body stability. Massively burned children are similar in many aspects to long-distance runners, where both heart rate and catecholamine levels are two to three times elevated, resulting in the body digesting peripheral muscles in order to support the voracious need for building materials necessary to heal wounds. Part of this high metabolic rate is useful as it helps the body provide building materials for the wound-healing process. There are, however, some adverse effects where the elevated metabolic rate may complicate respiratory problems. In addition, not all of the increased energy moving around the body goes to wound healing. Burn patients show muscle wasting and become centrally fat as the liver is apparently unable to process the large amount of peripheral fuel presented to it. In many cases the metabolism in non-injured areas is so high that wound healing becomes retarded. Researchers have demonstrated a very high level of the hormone epinephrine (adrenaline) in thermally injured patients (22,23). This hormone can increase metabolism by stimulating the b-adrenergic receptors. Propranolol, a drug that is a competitive antagonist, or opponent, of b-adrenergic receptors, has been shown to lower heart rates in burned children from 200 beats per minute to 120, decrease the amount of oxygen needed to keep the heart pumping and reduce the anxiety caused by burn-released epinephrine without impairing the ability of the patient to respond to stresses (24,25). Fat is metabolized 2.5 times the normal rate in thermally injured patients, a process that is apparently the result of elevated catecholamines and b-adrenergic stimulation since it has been shown to be blocked by propranolol (26,27).

Researchers have also studied protein metabolism in which tissues, such as muscle, are constantly being built up and broken down into basic components or amino acids. After thermal injury, protein breakdown exceeds build-up, causing a net release of amino acids (28). When elevated in the serum, or fluid portion of the blood, these amino acids are converted in the liver to glucose, a process known as glucogenesis, and then broken down to smaller compounds in peripheral tissues by anaerobic (lacking molecular oxygen) or aerobic (having molecular oxygen) metabolism. When the energy-producing process is anaerobic, the smaller sugars are converted into lactate and pyruvate; this appears to be the process in thermally injured patients (29,30). The elevation of these substances can be detrimental to the patient. In addition to the acidosis created, other changes occur involving the utilization of glutamine, which is an essential fuel for the cells that line 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 in the administration of a compound that stimulates the incorporation of amino acids into protein. Exogenously (originating outside the body) administered growth hormone reverses the protein breakdown produced by thermal injury and stimulates the use of amino acids (31,32). This not only redirects metabolism away from glucogenesis but also causes an increased incorporation of amino acids into healing wounds. An increase in rate of donor site healing and a decrease in length of hospital stay have been shown when growth hormone is used to treat burned children. Patients with 60% burn wounds had a decrease in length of hospital stay from 46 to 32 days (33).

After a thermal injury there is also a reorganization of protein synthesis, or protein creation. Several enzymes and proteins involved in the body’s defense system, such as blood coagulation factors, proteolytic enzyme inhibitors, and enzymes involved in the destruction of bacteria are increased 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 prevention of edema. Investigators are now beginning to identify the genetic mechanisms responsible for these changes and have identified several factors that play a role in the regulation of these genes.

Pressure Garments and Scarring

Pressure garments, which are used to reduce scarring, were developed 30 years ago. Traditionally, elastic bandages were placed on the legs of the burn patients to improve venous return and decrease bruising or blood blister formation. These bandages were also applied to splints to reduce and prevent any contracture, which is the shortening or ‘bunching up’ of muscle tissue. Therapists observed that burn patients rarely developed hypertrophic (overgrown or enlarged) scars when these pressure garments were applied (34,35). Unsightly scars could be prevented if the pressure garments were continuously worn and if hypertrophic scars had already formed, they could be reversed if the pressure garments were applied. Investigators studying scar formation found that collagen fibers in non-hypertrophic scars were parallel, or all oriented in the same direction, whereas those of the hypertrophic scar formed predominantly nodular or whorl-like patterns, which look like knobby or twisted cells (35-38). With the application of pressure, these diffuse, disorganized fibers became parallel. The relationship of the whorl-like fibers was found to depend on the quantity of proteoglycan that make up the scar tissue. In hypertrophic scars, this material is more abundant. Several researchers concluded that the pressure application reduced the scar by limiting the blood supply to the wound. It has now been determined that the macrophages of patients with keloids (scar tissue, sometimes painful) and hypertrophic scars (overgrown or enlarged scars) produce elevated levels of the cytokines interleukin 6, b interferon, and tumor necrosis factor (39,40).

Contractions of the burn wound have produced orthopaedic deformities in some patients as a result of lack of pressure application. To prevent or treat these contractions, a practice of bone-pinning and skeletal traction was instituted (41). At the time, few surgeons would have placed bone pins into a thermally injured patient because of possible bone infections. A survey taken 17 years after the institution of the pinning procedures revealed that of the 626 patients that had been subjected to the procedure only 50 (8%) developed bone infections, and these were easily managed by removal of the pins and antibiotic therapy (42). In recent times the use of skeletal traction has been enhanced with the advent of the Ilizarov fixator (43). These procedures to reduce scarring and contractures are important developments in improving the quality of life of the thermally injured patient.

The frequency of inadequate decompression (release of pressure), and its complications have been studied and it was concluded that compartment pressures should be followed in burn patients since pressures may increase over time and pulses are not predictive of ischemia, which is the physical obstruction of the blood supply. Failure to decompress extremities with elevated pressures may lead to significant, but preventable, complications (44).

Air-Fluidized Bed

The first air-fluidized bed was developed in 1969. The introduction of this new concept in the care of burn patients has been especially important in treating posterior burns or massive burns where posterior donor sites are required (45).

Fluid Resuscitation

In the early 1960’s, formulas for fluid resuscitation for adults were already established. There was, however, a major controversy concerning the use of colloids as a part of the fluid resuscitation regimen (46). Studies led to the development of a resuscitation formula that was based upon body surface area and body weight (47), which proved to be more appropriate for the care of pediatric patients (48,49). This formula is now used around the world and has made a substantial contribution to the survival of thermally injured pediatric patients, decreasing the mortality due to renal failure from 100% before 1984 to 56% after 1984 (50). Studies have further shown that patients with smoke inhalation injury require more fluid than equivalent size burns without smoke inhalation injury. The additional fluid requirement is 2 cc per kg per percent TBSA burn.

Investigations have shown that after thermal injury there was a massive system-wide vessel constriction that occurred independent of sympathetic nervous system activity (51). These studies implicated antidiuretic hormones (lowers urine formation) and the renin angiotensin systems (regulates blood pressure) as probable vectors of this response (52). The changes discovered from these investigations bear an important relationship to bacterial translocation (the passage of bacteria from the intestine into the circulation) after thermal injury, which may contribute to the development of multi-organ failure (53).

Anesthetic Agents

Most surgical patients in the 1960’s were given halothane for anesthesia. This agent was associated with liver damage and malignant hyperpyrexia (exceptionally high fever) (54, 55). During this same time, dissociative anesthetics (not completely unconscious) were being released for clinical trials and the use of ketamine in children became standard worldwide (56,57). The beneficial cardiovascular actions of the drug were described (58,59), and the drug has been extremely useful in critically ill children (60,61). During anesthesia laryngeal reflexes are maintained intact and there is no respiratory depression. Ketamine can be used without intubation (breathing tube) in acute burns in children with contracted necks who need to have reconstructive surgery (61-63) and has little or no effect on the immune system when given multiple times (64). This drug was also shown to be an excellent agent for achieving surgical anesthesia in patients with unstable cardiovascular systems (65). Anesthesia, when given repeatedly, can result in some psychological trauma but it was demonstrated that ketamine was well tolerated by children (66).

The safe and effective use of haloperidol to treat severe agitation and delirium in the critically ill pediatric patient has also been described. The intravenous route appears to be more effective than the enteral (intestinal) route and is now considered when rapid, acute control of agitation is required (67).

Bacterial Translocation

The finding of a high incidence of gram-negative sepsis in thermally injured patients without an obvious source of bacteria led to the development of the hypothesis that the source was from the gastrointestinal tract. The concept that the burn wound became infected as a result of organisms from the gut entering into the circulation was proposed. This is called bacterial translocation. To test this hypothesis, the gastrointestinal tract of a group of dogs was infected with Pseudomonas labeled with a fluorescein tag to track its flow. 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 (68).

Recently, the importance of bacterial translocation has been recognized after cutaneous thermal injury, endotoxin (bacterial toxin) administration, or an inhalation injury (53,69). Bacterial translocation associated with reduced blood flow was prevented by the use of vasodilators (vessel dilators) (70). These changes may be clinically important since a reduction in blood flow to abdominal organs is associated with the release of myocardial depressants that affect the heart muscle (71-73). This could also explain the increase in mortality seen in patients with combined thermal and inhalation injury, since these two insults in combination produce a greater increase in abdominal vascular (blood vessel) resistance than either insult alone. The need to prevent “under-resuscitation” of burned patients has been well recognized (74-76). Most recently, a drug that inhibits the formation of one of the vasoconstrictive (vessel constricting) mediators, which was previously shown to be released by burn injury (77), has been shown to reverse the bacterial translocation of a thermal injury (78) and to reverse the myocardial (heart muscle) depression that occurs with the administration of endotoxin (79). Preliminary data also indicate that compounds with anti-thromboxane activities may also be effective in preventing the mesenteric (abdominal) vasoconstriction and myocardial depression observed with inhalation injury (79,80).

Mediators of Burn Injury

Prostaglandins affect such things as vasodilation (vessel dilation), vasoconstriction (vessel constriction), and stimulation of smooth muscle. Metabolites of arachidonic acid, known precursors to prostaglandins, are released after thermal injury (81, 82). Reducing the formation of these prostaglandins is known to reduce burn-caused edema, or swelling of the tissues (83). Researchers demonstrated that the blood flow to the renal papillae was remarkably reduced in burned dogs treated with the materials that block the formation of prostaglandin (83). Studies have also demonstrated that if prostaglandin synthetase inhibition was combined with the osmotic diuretic mannitol (promotes the elimination of water in the urine), the papillary blood flow could be restored. When this technique was added to the fluid resuscitation of the thermally injured patient, there appeared to be much less edema formation, and these patients required less fluid resuscitation (81). The early agent used for the blockade of prostaglandin synthesis was nicotinic acid. In laboratory investigations, nicotinic acid was shown to reduce the edema formation that resulted from thermal injury; however, the animals in the study developed liver damage (84). The latter work has led to more selective and successful inhibition of prostanoid vasoconstrictors, or prostaglandin-derived vessel constrictors.

Inhalation Injury

Inhalation injury studies often follow two main pathways, one relating to parenchymal injury, or injury to the functional elements of the lung, and the other to damage of the airway, or the tracheobronchial tree (85-87). Inhalation injury was found to be associated with a marked increase in a transvascular fluid flow across the lungs (88). This fluid flow occurred as the result of changes in both small-vessel pressure and ability of protein to pass through (88, 89). Later studies revealed that lung edema formation was associated with polymorphonuclear cells (90). These cells induced their injury to the lungs as the result of the release of proteolytic enzymes (91) and free oxygen radicals (90). It was determined that the amount of fluid resuscitation required after smoke inhalation was greater than that required for a burn alone and that appropriate fluid resuscitation would reduce, rather than enhance, transvascular fluid flow (92, 93). These studies have resulted in an enhancement of fluid resuscitation in patients with accompanying thermal and inhalation injury. Techniques for measuring extravascular (outside of the vessels) lung water by the thermal dilution technique have been applied to patients to evaluate the extent of their pulmonary edema (94).

Hyperemia, or excessive amounts of blood, of the tracheobronchial tree (airway) after an inhalation injury is a characteristic used for the diagnosis of an inhalation injury (95). Investigators have shown that hyperemia is associated with a 10-fold increase in bronchial blood flow (96-100) and an increase in the permeability of the tracheobronchial areas involved. Reducing the hyperemia has been shown to reduce the pulmonary edema seen after smoke inhalation (98,101). Treating animals with capsaicin, a compound that depletes sensory nerves of their neuropeptides, markedly reduced both the elevation in bronchial blood flow and transvascular fluid flow commonly associated with an inhalation injury.

There are several accompanying changes in the systemic circulation related to an inhalation injury. The heart muscle is depressed, there is an increase in the vasomotor (affects the diameter of the vessel) tone of the gut, and system-wide small-vessel permeability is elevated. Initial investigations have shown that the blockade of a potent arachidonic acid derivative, thromboxane A₂, could markedly reduce these changes (102). With inhalation injuries presently accounting for the majority of the deaths in thermally injured patients (103,104), research and clinical advances in these areas have become the new horizons for improved patient outcomes.

The association of the airway damage with the pulmonary changes noted with inhalation injury has changed just how patients with an inhalation injury are treated. It was first reasoned that the placement of an endotracheal tube (inside the windpipe) into a patient with existing damage to the airway would only aggravate the injury. Therefore, endotracheal tubes were not used in patients with bronchoscopic evidence of inhalation injury and the placement of tubes was avoided, even for anesthetic procedures. Endotracheal tubes are now used only if there is a marked reduction in arterial oxygen, an increase in carbon dioxide, or evidence of severe respiratory distress. The practice of avoiding endotracheal intubation has resulted in a decline in the number of ventilator days and a reduction in morbidity (unpublished data).

Early Enteral Feeding

Malnutrition and burn injuries have been associated with infection and death. Burn physicians in various cities began continuous feeding of milk to reduce the incidence of gastric and duodenal ulcers (105,106). As a result, stress ulcers rarely occurred in milk-fed patients. It was further shown that milk could 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 (107-110). The use of supplemental parenteral hyperalimentation (IV feeding), however, was shown not only unnecessary but also detrimental (111, 112). Early enteral (tube feeding) and continuous feeding has now decreased mortality in burned children and is now accepted practice in burn units around the world.

Rehabilitation and Psychosocial Adjustment

Models of burn treatment strongly emphasize the integration of basic science, clinical research, and clinical treatment that share information in a continuous feedback loop. It is customary for each clinical innovation to be based on empirical data from practical experience and to be evaluated for effectiveness through scientific study. Through research grants from Shriners Hospitals for Children, a database has been developed to follow patients longitudinally over a period of time on specific measures of physical and psychosocial recovery. Four hundred patients have been entered into a database, which includes longitudinal assessments of cardiopulmonary functions, physical growth and maturation, bone density, measures of functional capability, including range of motion and activities of daily living, scar formation, reconstructive needs, and several measures of the psychosocial adjustment of the child/patient and parent(s).

One important finding from these data is that the long-term successful psychosocial adjustment of burned children largely depends on the enduring qualities of the families in which they live (113-115). 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 percent of each sample have moderate behavior problems. These outcomes have been consistent even for survivors of the most massive injuries, many of who have now grown into young adults with careers and families of their own. In terms of physical impairment, the children, even those with the most severe injuries, are remarkably independent in their capabilities (116,117).

References Cited

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31. Gore, D.C., Honeycutt, D., Jahoor, F., Wolfe, R.R., Herndon, D.N. Effect of exogenous growth hormone on whole-body and isolated-limb protein kinetics in burned patients. Archives of Surgery 126: 38-43, 1991.

32. Cioffi, W.G., Gore, D.C., Rue, L.W., Carrougher, G., Guler, H-P., McManus, W.F., Pruitt, B.A. Insulin-like growth factor-1 lowers protein oxidation in patients with thermal injury. Annals of Surgery 220(3): 310-319, 1994.

33. Herndon, D.N., Barrow, R.E., Kunkel, K.R., Broemeling, L., Rutan, R.L. Effects of recombinant human growth hormone on donor-site healing in severely burned children. Annals of Surgery 212:424-429, 1990.

34. Linares, H.A., Kischer, C.W., Dobrkovsky, M., Larson, D.L. On the origin of the hypertrophic scar. Journal of Trauma 13:70-75, 1973.

35. Linares, H.A., Kischer, C.W., Dobrkovsky, M., Larson, D.L. The histiotypic organization of the hypertrophic scar in humans. Journal of Investigative Dermatology 59:323-331, 1972.

36. Linares, H.A., Larson, D.L. Early differential diagnosis between hypertrophic and nonhypertrophic healing. Journal of Investigative Dermatology 62:514-516, 1974.

37. Baur, P.S., Larson, D.L., Stacey, T.R., Barratt, G.F., Dobrkovsky, M. Ultrastructural analysis of pressure-treated human hypertrophic scars. Journal of Trauma 16:958-967, 1976.

38. Linares, H.A., Larson, D.L. Proteoglycans and collagenase in hypertrophic scar formation. Journal of Plastic and Reconstructive Surgery 62:589-593, 1978.

39. Xue, H., McCauley, R.L., Zhang, W., Martini, D. Altered interleukin-6 expression in fibroblasts from burn hypertrophic scars. Journal of Burn Care & Rehabilitation 19 (1): S189, 1998.

40. McCauley, R.L., Chopra, V., Li, Y.Y., Herndon, D.N., Robson, M.C. Altered cytokine production in black patients with keloids. Journal of Clinical Immunology 12:300-308, 1992.

41. Larson, D.L., Evans, E.B., Abston, S., Lewis, S.R., Artz, C.P. Skeletal suspension and traction in the treatment of burns and what's new in burns. Annals of Surgical Medicine Times 104:128-141, 1976.

42. Youel, L., Evans, E.B., Heare, T.C., Herndon, D.N., Larson, D.L., Abston, S. Skeletal suspension in the management of severe burns in children A sixteen-year experience. Journal of Bone and Joint Surgery [Am] 68:1375-1379, 1986.

43. Calhoun, J.H., Evans, E.B., Herndon, D.N. Techniques for the management of burn contractures with the Ilizarov fixator. Clinical Orthopedics and Related Research 280:117-124, 1992.

44. Brown, R.L., Greenhalgh, D.G., Kagan, R.J., Warden, G.D. The adequacy of limb escharotomies-fasciotomies after referral to a major burn center. Journal of Trauma 37(6): 916-920, 1994.

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47. Carvajal, H.F., Linares, H.A., Brouhard, B.H. Relationship of burn size to vascular permeability changes in rats. Surgical Journal of Gynecology and Obstetrics 149:193-202, 1979.

48. Carvajal, H.F. Fluid therapy for the acutely burned child. Comprehensive Therapy 3:17-24, 1977.

49. Carvajal, H.F. A physiologic approach to fluid therapy in severely burned children. Surgical Journal of Gynecology and Obstetrics 150:379-384, 1980.

50. Jeschke M.G., Barrow R.E., Wolf S.E., Herndon D.N. Mortality in burned children with acute renal failure. Archives of Surgery 134: 752-756, 1998.

51. Turner, R., Carvajal, H.F., Traber, D.L. Effects of ganglionic blockade upon the renal and cardiovascular dysfunction induced by thermal injury. Circulatory Shock 4:103-113, 1977.

52. Traber, D.L., Bohs, C.T., Carvajal, H.F., Linares, H.A., Miller, T.H., Larson, D.L. Early cardiopulmonary and renal function in thermally injured sheep. Surgical Journal of Gynecology and Obstetrics 148:753-758, 1979.

53. Morris, S.E., Navaratnam, N., Herndon, D.N. A comparison of effects of thermal injury and smoke inhalation on bacterial translocation. Journal of Trauma 30:639-643, 1990.

54. Wilson, R.D., Traber, D.L., Allen, C.R., Priano, L.L. Malignant hyperpyrexia: A re-examination. Southern Medical Journal 64: 411-414, 1971.

55. Wilson, R.D., Dent, T.E., Traber, D.L., McCoy, N.R., Allen, C.R. Malignant hyperpyrexia with anesthesia. Journal of the American Medical Association 202: 183-186, 1967.

56. Wilson, R.D., Traber, D.L., Barratt, E., Creson, D.L., Schmitt, R.C., Allen, C.R. Evaluation of CL-1848C: A new dissociative anesthetic in normal human volunteers. Anesthesia and Analgesia 49: 236-241, 1970.

57. Wilson, R.D., Nichols, R.J., McCoy, N.R. Dissociative anesthesia with CI-581 in burned children. Anesthesia and Analgesia 55: 719-724, 1976.

58. Traber, D.L., Wilson, R.D., Priano, L.L. Differentiation of the cardiovascular effects of CI-581. Anesthesia and Analgesia 46: 769-778, 1967.

59. Traber, D.L., Wilson, R.D., Priano, L.L. A detailed study of the cardiopulmonary response to ketamine and its blockade by atropine. Southern Medical Journal 63: 1077-1081, 1970.

60. Wilson, R.D., Traber, D.L., Priano, L.L., Evans, B.L. Anesthetic management of the poor risk pediatric patient. Southern Medical Journal 62: 767-772, 1969.

61. Wilson, R.D., Traber, D.L. Advances in anesthesia for plastic surgery in burns. Clinical Anesthesiology 3: 359-381, 1969.

62. Wilson, R.D., Knapp, C., Traber, D.L., Evans, B. Safe management of the child with a contracted neck: A new method. Southern Medical Journal 63: 1420-1425, 1970.

63. Wilson, R.D., Traber, D.L. Advances in anesthesia for plastic surgery. In: Decade of clinical progress. Fabian, L., Ed., F. A. Davis Company, Philadelphia, PA., pp. 359-381, 1971.

64. Wilson, R.D., Priano, L.L., Traber, D.L., Sakai, H., Daniels, J.C., Ritzmann, S.E. An investigation of possible immunosuppression from ketamine and 100 percent oxygen in normal children. Anesthesia and Analgesia 50:464-470, 1971.

65. Priano, L.L., Wilson, R.D., Traber, D.L. Comparison of ketamine and methohexital as induction agents for methoxyflurane anesthesia. Anesthesia and Analgesia 52:913-920, 1973.

66. Wilson, R.D., Traber, D.L., Evans, B.L. Correlation of psychologic and physiologic observations from children undergoing repeated ketamine anesthesia. Anesthesia and Analgesia 48:995-1001, 1969.

67. Brown, R.L., Henke, A., Greenhalgh, D.G., Warden, G.D. The use of haloperidol in the agitated, critically ill pediatric patient with burns. Journal of Burn Care and Rehabilitation 17: 34-38, 1996.

68. Howerton, E.E., Kolmen, S.N. The intestinal tract as a portal of entry of Pseudomonas in burned rats. Journal of Trauma 12:335-340, 1972.

69. Herndon, D.N., Morris, S.E., Coffey, J.A.J., Milhoan, R.A., Barrow, R.E., Traber, D.L., Townsend, C.M.. The effect of mucosal integrity and mesenteric blood flow on enteric translocation of microorganisms in cutaneous thermal injury. Progress in Clinical Biology Research 308:377-382, 1989.

70. Morris, S.E., Navaratnam, N., Herndon, D.N. Changes in mesenteric blood flow affect translocation in sheep. In: Shock, sepsis, and organ failure: First Wiggers Bernard conference. Schlag, G., Redl, H., Siegel, J.H., Eds., Springer-Verlag, New York, NY., pp. 548-557, 1990.

71. Redl, G., Abdi, S., Nichols, R.J., Traber L.D., Flynn J.T., Herndon D.N., Traber D.L. The effects of a selective thromboxane synthetase inhibitor on the response of the right heart to endotoxin in sheep. Critical Care Medicine 19:1294-1302, 1991.

72. Fujioka, K., Sugi, K., Isago, T., Flynn, J.T., Traber, L.D., Herndon, D.N., Traber, D.L. Thromboxane synthetase inhibition and cardiopulmonary function during endotoxemia in sheep. Journal of Applied Physiology 71:1376-1381, 1991.

73. Sugi, K., Theissen, J.L., Traber, L.D., Herndon, D.N., Traber, D.L. Impact of carbon monoxide on cardiopulmonary dysfunction after smoke inhalation injury. Circulatory Research 66:69-75, 1990.

74. Herndon, D.N., Thompson, P.B., Traber, D.L. Pulmonary injury in burned patients. Critical Care Clinicals 1:79-96, 1985.

75. Prien, T., Traber, D.L. Toxic smoke compounds and inhalation injury--a review. Burns Including Thermal Injuries 14:451-460, 1988.

76. Traber, D.L., Linares, H.A., Herndon, D.N., Prien, T. The pathophysiology of inhalation injury--a review. Burns Including Thermal Injuries 14:357-364, 1988.

77. Herndon, D.N., Abston, S., Stein, M.D. Increased thromboxane B2 levels in the plasma of burned and septic burned patients. Surgical Gynecology and Obstetrics 159:210-213, 1984.

78. Tokyay, R., Loick, H.M., Traber, D.L., Heggers, J.P., Herndon, D.N. Effects of thromboxane synthetase inhibition on postburn mesenteric vascular resistance and the rate of bacterial translocation in a chronic porcine model. Surgical Gynecology and Obstetrics 174:125-132, 1992.

79. Fujioka, K., Sugi, K., Traber, L.D., Herndon, D.N., Traber, D.L. The effect of thromboxane synthetase inhibition on cardiopulmonary function during endotoxemia in sheep. Journal of Burn Care and Rehabilitation 11:531-537, 1990.

80. Snapper, J.R., Hutchison, A.A., Ogletree, M.L., Brigham, K.L. Effects of cyclooxygenase inhibitors on the alterations in lung mechanics caused by endotoxemia in the unanesthetized sheep. Journal of Clinical Investigation 72:63-76, 1983.

81. Wells, C.H., Hilton, J.G., Larson, D.L., Sloan, D.F. Effects of nicotinic acid upon post-burn oedema: A preliminary report of clinical trials. Burns Including Thermal Injuries 2:152-157, 1976.

82. Hilton, J.G., Wells, C.H. Effects of nicotinic acid on plasma volume loss of experimental dysbarism. Undersea Biomedical Research 3:157-161, 1976.

83. Hayashi, M., Bond, T.P., Wells, C.H., Guest, M.M. Effect of mannitol and nicotinic acid on renal papillary blood flow in burned hamsters. Burns Including Thermal Injuries 2:245-249, 1976.

84. Traber, D.L., Bohs, C.T., Carvajal, H.F., Miller, T.H., Linares, H.A, Larson, D.L. Nicotinic acid mannitol supplements in postburn resuscitation a double-blind study in sheep. Burns 5: 299-307, 1979.

85. Herndon, D.N., Traber, D.L., Niehaus, G.D., Linares, H.A., Traber, L.D. The pathophysiology of smoke inhalation injury in a sheep model. Journal of Trauma 24:1044-1051, 1984.

86. Traber, D.L., Herndon, D.N., Stein, M.D., Traber, L.D., Flynn, J.T., Niehaus, G.D. The pulmonary lesion of smoke inhalation in an ovine model. Circulatory Shock 18:311-323, 1986.

87. Barrow, R.E., Wang, C.Z., Cox, R.A., Evans, M.J. Cellular sequence of tracheal repair in sheep after toxic smoke inhalation. Lung 170: 331-338, 1992.

88. Isago, T., Fujioka, K., Traber, L.D., Herndon, D.N., Traber, D.L. Derived pulmonary capillary pressure changes after smoke inhalation in sheep. Critical Care Medicine 19:1407-1413, 1991.

89. Isago, T., Noshima, S., Traber, L.D., Herndon, D.N., Traber, D.L. Analysis of pulmonary microvascular permeability after smoke inhalation. Journal of Applied Physiology 71:1403-1408, 1991.

90. Basadre, J.O., Sugi, K., Traber, D.L., Traber, L.D., Niehaus, G.D., Herndon, D.N. The effect of leukocyte depletion on smoke inhalation injury in sheep. Surgery 104:208-215, 1988.

91. Niehaus, G.D., Kimura, R., Traber, L.D., Herndon, D.N., Flynn, J.T., Traber, D.L. Administration of a synthetic antiprotease reduces smoke-induced lung injury. Journal of Applied Physiology 69:694-699, 1990.

92. Herndon, D.N., Traber, D.L., Traber, L.D. The effect of resuscitation on inhalation injury. Surgery 100:248-251, 1986.

93. Hilton, J.G. Effects of H-R upon post-burn plasma volume loss in the nonresuscitated dog. Burns Including Thermal Injuries 7:211-214, 1980.

94. Herndon, D.N., Barrow, R.E., Traber, D.L., Rutan, T.C., Rutan, R.L., Abston, S. Extravascular lung water changes following smoke inhalation and massive burn injury. Surgery 102:341-349, 1987.

95. Moylan, J.A., Alexander, L.G.J. Diagnosis and treatment of inhalation injury. World Journal of Surgery 2:185-191, 1978.

96. Abdi, S., Herndon, D., Mcguire, J., Traber, L., Traber, D.L. Time course of alterations in lung lymph and bronchial blood flows after inhalation injury. Journal of Burn Care and Rehabilitation 11:510-515, 1990.

97. Barrow, R.E., Morris, S.E., Herndon, D.N. Selective permeability changes in the airways of sheep. Respiratory Physiology 79:1-8, 1990.

98. Kramer, G.C., Herndon, D.N., Linares, H.A., Traber, D.L. Effects of inhalation injury on airway blood flow and edema formation. Journal of Burn Care and Rehabilitation 10:45-51, 1989.

99. Stothert, J.C.,Jr., Ashley, K.D., Kramer, G.C., Herndon, D.N., Traber, L.D., Ashley, K.D., Traber, D.L. Intrapulmonary distribution of bronchial blood flow after moderate smoke inhalation. Journal of Applied Physiology 69:1734-1739, 1990.

100. Abdi, S., Herndon, D.N., Traber, L.D., Ashley, K.D., Stothert, J.C., Jr., Maguire, J., Butler, R., Traber, D.L. Lung edema formation following inhalation injury: Role of the bronchial blood flow. Journal of Applied Physiology 71:727-734, 1991.

101. Montero, K., Lübbesmeyer, H.J., Traber, D.L., Kimura, R., Traber, L.D., Herndon, D.N. Inhalation injury increases systemic microvascular permeability. Surgical Forum 38:303-305, 1987.

102. Noshima, S., Fujioka, K., Isago, T., Traber, L.D., Herndon, D.N., Traber, D.L. The effect of a thromboxane synthetase inhibitor, OKY-046, on cardiopulmonary function after smoke inhalation injury. Journal of the Federation of American Societies for Experimental Biology 5:A371, 1991.

103. Thompson, P.B., Herndon, D.N., Traber, D.L., Abston, S. Effect on mortality of inhalation injury. Journal of Trauma 26:163-165, 1986.

104. Traber, D.L., Herndon, D.N. Pathophysiology of smoke inhalation. In: Respiratory Sequelae of Burns. Haponik, E.F., Munster, A.M., Eds., McGraw Hill, Inc., New York, NY., pp. 62-71, 1989.

105. Watson L.C., Abston S. Prevention of upper gastrointestinal hemorrhage in 582 burned children. American Journal of Surgery 132: 790-793, 1976.

106. Abston, S. Burns in children. Clinical Symposium 28: 1-36, 1976.

107. Hildreth, M.A., Herndon, D.N., Parks, D.H., Desai, M.H., Rutan, T. Evaluation of a caloric requirement formula in burned children treated with early excision. Journal of Trauma 27: 188-189, 1987.

108. Hildreth, M.A., Herndon, D.N., Desai, M.H., Duke, M.A. Reassessing caloric requirements in pediatric burn patients. Journal of Burn Care and Rehabilitation 9: 616-618, 1988.

109. Hildreth, M.A., Herndon, D.N., Desai, M.H., Duke, M.A. Caloric needs of adolescent patients with burns. Journal of Burn Care and Rehabilitation 10: 523-526, 1989.

110. Hildreth, M.A., Herndon, D.N., Desai, M.H., Broemeling, L.D. Current treatment reduces calories required to maintain weight in pediatric patients with burns. Journal of Burn Care and Rehabilitation 11: 405-409, 1990.

111. Herndon, D.N., Barrow, R.E., Stein, M., Linares, H., Rutan, T.C., Rutan, R., Abston, S. Increased mortality with intravenous supplemental feeding in severely burned patients. Journal of Burn Care and Rehabilitation 10:309-313, 1989.

112. Herndon, D.N., Stein, M.D., Rutan, T.C., Abston, S., Linares, H. Failure of TPN supplementation to improve liver function, immunity, and mortality in thermally injured patients. Journal of Trauma 27: 195-204, 1987.

113. Blakeney, P., Herndon, D.N., Desai, M., Beard, S., Wales-Seale, P. Long-term psychosocial adjustment following burn injury. Journal of Burn Care & Rehabilitation 19(6): 661-665, 1998.

114. Blakeney, P., Portman, S., Rutan, R. Familial values as factors influencing long-term psychological adjustment of children after severe burn injury. Journal of Burn Care & Rehabilitation 11(5): 472-475, 1990.

115. Meyer, W., III, Blakeney, P., Moore, P., Murphy, L., Robson, M. and Herndon, D.N. Parental well being and behavioral adjustment of pediatric burn survivors. Journal of Burn Care & Rehabilitation 15: 62-68, 1994.

116. LeDoux, J., Meyer, W., III, Blakeney, P., Herndon, D. Relationships between parental emotional states, family environment and the behavioral adjustment of pediatric burn survivors. Burns 24: 425-432, 1998.

117. LeDoux, J., Meyer, W., III, Blakeney, P., Herndon, D. Positive self-regard as a coping mechanism for pediatric burn survivors. Journal of Burn Care & Rehabilitation 17: 472-476, 1996.