|
HOME
Page last
updated 2-22-07
© COPYRIGHT 2007 ALL RIGHTS RESERVED
TOTALBURNCARE.COM |
*
Advances in Burn Care
*
D.N. Herndon, M.D., Chief of
Staff
Shriners Burn Hospital - Galveston, Texas
(Click here for
layman's
version of this article)
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 change health
delivery in burns. The areas of advancement in burn care have been
resuscitation, early excision and grafting, hypermetabolic responses to burn
injury, and infection control. The mortality and length of hospital stay of
burned children have been greatly reduced over the last 25 years. In the
1960's, the likelihood of survival was only 50% for pediatric burns covering
35-44% of the TBSA (total body surface area), and few patients with burn
sizes above 45% TBSA survived. The average length of stay for the acutely
burned child was 103 days. Today, the LA50 (lethal burn size for
50% of the patients) for 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 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 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
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, combined with hypotensive anesthetic techniques
and other blood-conservation measures, allowed prospective, but
nonrandomized, 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 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,
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 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 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 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 to cover larger surface areas has been
described (16). Extremities and the trunk were more often grafted with mesh
graft. 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. 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
palmar burns that required skin grafting to compare the efficacy of
split-thickness versus full-thickness autografting (18). 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.
Back to
TOC
Metabolism and Nutrition
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
(glucose) 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, measured by indirect calorimetry, rarely exceeds
twice the basal metabolic rate as calculated by standard correlations.
Therefore, twice the basal energy expenditure 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). One of the more dramatic alterations
is that glucose uptake rates and glucogenesis 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 exceeds unity and causes
excess CO2 production and increases minute alveolar ventilation
requirements. The combination of diaphragmatic elevation and increases in
CO2 makes 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 mobilized peripherally 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 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,
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 or aerobic 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 compensatory 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 is the
administration of a compound that stimulates the incorporation of amino
acids into protein. Exogenously 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 burn
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. 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.
Back to
TOC
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 contractures. Therapists observed that burn patients rarely
developed hypertrophic 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 fiber deposition in non-hypertrophic
scars were parallel, whereas those of the hypertrophic scar formed
predominantly nodular or whorl-like patterns (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 and
hypertrophic 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 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. Failure to decompress extremities with elevated
pressures may lead to significant, but preventable, complications (44).
Back to
TOC
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).
Back to
TOC
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 survival of thermally
injured pediatric patients, decreasing mortality from renal failure from
100% before 1984 to 56% after 1984 (50). Studies have further shown that
patients with smoke inhalation injury require 2 cc per kg per percent TBSA
burn more fluid than equivalent size burns without smoke inhalation injury.
Investigations have shown that after thermal injury there was a massive
systemic vasoconstriction that occurred independent of sympathetic nervous
system activity (51). These studies implicated antidiuretic hormones and
the renin angiotensin systems 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 multiorgan failure (53).
Back to
TOC
Anesthetic Agents
Most surgical patients in the 1960’s were given halothane for anesthesia.
This agent was associated with liver damage and malignant hyperpyrexia (54,
55). During this same time, dissociative anesthetics were being released for
clinical trials and the use of ketamine in children became standard
worldwide (56,57). The salutary 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 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 induction agent 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 route
and is now considered when rapid, acute control of agitation is required
(67).
Back to
TOC
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. To test
this hypothesis, the gastrointestinal tract of a group of dogs was infected
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 (68).
Recently, the importance of bacterial translocation has been recognized
after cutaneous thermal injury, endotoxin administration, or an inhalation
injury (53,69). Bacterial translocation associated with reduced blood flow
was prevented by the use of vasodilators (70). These changes may be
clinically important since a reduction in blood flow to abdominal organs is
associated with the release of myocardial depressants (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 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 mediators (a thromboxane synthetase
inhibitor), 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 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 vasoconstriction and myocardial depression
observed with inhalation injury (79,80).
Back to
TOC
Mediators of Burn Injury
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-induced edema (83). Researchers demonstrated that the
blood flow to the renal papillae was remarkably reduced in burned dogs that
were treated with the materials which block the formation of prostaglandin
(83). Studies have also demonstrated that if prostaglandin synthetase
inhibition was combined with the osmotic diuretic mannitol, 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.
Back to
TOC
Inhalation Injury
Inhalation injury studies often follow two main pathways, one relating to
parenchymal injury and the other to damage of the airway of the
tracheobronchial tree (85-87). Inhalation injury was found to be associated
with a marked increase in a transvascular fluid flux across the lungs (88).
This fluid flux occurred as the result of changes in both microvascular
pressure and permeability to protein (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 flux (92, 93). These studies have resulted in an
enhancement of fluid resuscitation in patients with concomitant thermal and
inhalation injury. Techniques for measuring extravascular lung water by the
thermal dilution technique have been applied to patients to evaluate the
extent of their pulmonary edema (94).
Hyperemia (excessive amounts of blood) of the tracheobronchial tree 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
flux commonly associated with an inhalation injury.
There are several concomitant changes in the systemic circulation related
to an inhalation injury. The heart muscle is depressed, there is an
increase in the vasomotor tone of the gut, and systemic microvascular
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 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).
Back to
TOC
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, however, was shown not only unnecessary but also
detrimental (111, 112). Early enteral and continuous feeding has now
decreased mortality in burned children and is now accepted practice in burn
units around the world.
Back to
TOC
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 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 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).
Back to
TOC
References Cited
1.
Cope, O., Laugohr, H., Moore, F.D., Webster, R. Expeditious care of
full-thickness burn wounds by surgical excision and grafting. Annals of
Surgery 125: 1-22, 1947.
2.
Janzekovic, A. A new concept in the early excision and immediate
grafting of burns. Journal of Trauma 10:1103-1108, 1970.
3.
Burke, J.F., Bondoc, C.C., Quinby, W.C. Primary burn excision and
immediate grafting: A method of shortening illness. Journal of Trauma 14:
389-395, 1974.
4.
Engrav, L.H., Heimbach, D.M., Reus, J.L., Harnar, T.J., Marvin, J.A.
A randomized prospective study of early excision and grafting of
indeterminant burns less than 20 percent TBSA. Journal of Trauma 23:
1001-1004, 1983.
5.
Demling, R.H. Improved survival after massive burns. Journal of
Trauma 23: 179-184, 1983.
6.
Herndon, D.N., Parks, D.H. Comparison of serial debridement and
autografting and early massive excision with cadaver skin overlay in the
treatment of large burns in children. Journal of Trauma 26(2): 149-152,
1986.
7.
Herndon, D.N., Barrow, R.E., Rutan, R.L., Rutan, T.C., Desai, M.H.,
Abston, S. A comparison of conservative versus early excision: Therapies in
severely burned patients. Annals of Surgery 209(5): 547-553, 1989.
8.
Desai, M.H., Herndon, D.N., Broemeling, L., Barrow, R.E., Nichols,
R.J., Jr., Rutan, R.L. Early burn wound excision significantly reduces
blood loss. Annals of Surgery 211(6): 753-762, 1990.
9.
Burke, J.F., Quinby, W.C., Bondoc, C.C. Primary excision and prompt
grafting as routine therapy for the treatment of thermal burns in children.
Surgery Clinics of North America 56: 477-494, 1976.
10.
Heimbach, D.M. Early burn excision and grafting. Surgery Clinics of
North America. 67: 93-107, 1987.
11.
Bondoc, C.C., Burke, J.F. Clinical experience with viable frozen
human skin and a frozen skin bank. Annals of Surgery 174: 371-382, 1971.
12.
Burke, J.F., Yannas, I.V., Quinby, W.C., Bondoc, C.C., Jung, W.K.
Successful use of a physiologically acceptable artificial skin in the
treatment of extensive burn injury. Annals of Surgery 194: 413-428, 1981.
13.
Yannas, I.V., Burke, J.F., Orgill, D.P., Skrabut, E.M. Wound tissue
can utilize a polymeric template to synthesize a functional extension of
skin. Science 215: 174-176, 1982.
14.
Heimbach, D., Luterman, A., Burke, J., Cram, A., Herndon, D., Hunt,
J., Jordan, M., McManus, W., Solem, L., Warden, G., Zawacki, B. Artificial
dermis for major burns: A multi-center randomized clinical trial. Annals of
Surgery 208: 313-320,1988.
15.
Tompkins, R.G., Hilton, J.F., Burke, J.F., Schoenfeld, D.A., Hegerty,
M.T., Bondoc, C.C., Quinby, W.C., Behringer, G.E., Ackroyd, F.W. Increased
survival after massive thermal injuries in adults: a preliminary report
using artificial skin. Critical Care Medicine 17: 734-740, 1989.
16.
Archer, S.B., Henke, A., Greenhalgh, D.G., Warden, G.D. The use of
sheet autografts to cover extensive burns in patients. Journal of Burn Care
and Rehabilitation 19: 33-38, 1998.
17.
Greenhalgh, D.G., Barthel, P.P., Warden, G.D. Comparison of back
versus thigh donor sites in pediatric patients with burns. Journal of Burn
Care and Rehabilitation 14: 21-25, 1993.
18.
Schwanholt, C., Greenhalgh, D.G., Warden, G.D. A comparison of
full-thickness versus split-thickness autografts for the coverage of deep
palm burns in the very young pediatric patient. Journal of Burn Care and
Rehabilitation 14: 29-33, 1993.
19.
Wolfe, R.R., Burke, J.F. Effect of burn trauma on glucose turnover,
oxidation, and recycling in guinea pigs. American Journal of Physiology
233: E80-E85, 1977.
20.
Burke, J.F., Wolfe, R.R., Mullany, C.J., Mathews, D.E., Bier, D.M.
Glucose requirements following burn injury: Parameters of optimal glucose
infusion and possible hepatic and respiratory abnormalities following
excessive glucose intake. Annals of Surgery 190: 274-285, 1979.
21.
Kien, C.L., Young, V.R., Rohrbaugh, A.M., Burke, J.F. Increased
rates of whole body protein synthesis and breakdown in children recovering
from burns. Annals of Surgery 187: 383-391, 1987.
22.
Goodall, M.G. Sympathetic nerve and adrenal medullary response to
thermal burn. Clinical analysis of adrenaline and noradrenaline depletion.
American Surgeon;32:448-452, 1966.
23.
Goodall, M. Sympatho-adrenal medullary response to thermal burn.
Annals of the New York Academy of Science 150:685-689, 1968.
24.
Minifee, P.K., Barrow, R.E., Abston, S., Desai, M., Herndon, D.N.
Improved myocardial oxygen utilization following propranolol infusion in
adolescents with postburn hypermetabolism. Journal of Pediatric Surgery
24:806-810, 1989.
25.
Herndon, D.N., Barrow, R.E., Rutan, T.C., Minifee, P., Jahoor, F.,
Wolfe, R.R. Effect of propranolol administration on hemodynamic and
metabolic responses of burned pediatric patients. Annals of Surgery
208:484-492, 1988.
26.
Wolfe, R.R., Herndon, D.N., Peters, E.J., Jahoor, F., Desai, M.H.,
Holland, O.B. Regulation of lipolysis in severely burned children. Annals of
Surgery 206:214-221, 1987.
27.
Aarsland, A., Chinkes, D., Wolfe, R.R., Barrow, R.E., Nelson, S.O.,
Pierre, E.J., Herndon, D.N. Beta-blockade lowers peripheral lipolysis in
burned patients receiving growth hormone: Rate of hepatic VLDL triglyceride
secretion remains unchanged. Annals of Surgery 223(6): 777-789, 1996.
28.
Jahoor, F., Desai, M., Herndon, D.N., Wolfe, R.R. Dynamics of the
protein metabolic response to burn injury. Metabolism 37:330-337, 1988.
29.
Wolfe, R.R., Jahoor, F., Herndon, D.N., Miyoshi, H. Isotopic
evaluation of the metabolism of pyruvate and related substrates in normal
adult volunteers and severely burned children: Effect of dichloroacetate and
glucose infusion. Surgery 110:54-67, 1991.
30.
Gore, D.C., Honeycutt, D., Jahoor, F., Rutan, T., Wolfe, R.R.,
Herndon, D.N. Effect of exogenous growth hormone on glucose utilization in
burn patients. Journal of Surgical Research 51:518-523, 1991.
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.
45.
Hargest, T.S., Artz, C.P. A new concept in patient care: The
air-fluidized bed. Association of Operating Room Nurses Journal 10:50-53,
1969.
46.
Wilson, R.D., Nichols, R.J., Poth, R. A clinical and laboratory
evaluation of a "disaster mixture" in cardiovascular resuscitation. Southern
Medical Journal 60:875-881, 1976.
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.
Top↑
LINKS
DISCLAIMER
SITE SEARCH
|
