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Are we making an impact? A review of a burn prevention program in Israeli schools.

In an attempt to challenge the immense toll of burn and scald injuries among children in Israel, a structured educational program was developed by our university center for plastic surgery in Beer-Sheva. Since 1986, more than 250,000 children and 10,000 teachers, in more than 460 elementary schools nationwide, have been exposed to our program. This article reviews the design of the program, the implementation procedures, and the studies evaluating its effectiveness. The studies revealed significant improvements in children's risk-related knowledge and injury-control beliefs. Both teachers and principals assessed the program as important, and the in-training workshops and intervention activities won high approval. An overall trend of reduction in the number of patients hospitalized with burn injuries in the southern part of Israel was found also. Although it is clear that the project is instructive, further comprehensive efforts are needed to make a dramatic nationwide impact. Some of the efforts already underway target the most vulnerable group of the non-Jewish population in Israel.

Adolescent↗

Profile of an abused burned child.

It is well recognized that child abuse is a common mechanism of injury to burned children. A profile of an abused burn child was constructed by analyzing 321 consecutive pediatric admissions to our burn center during a 24-month period starting in April 1993. Variables collected for analysis were age, race, insurance status, family structure, burn size, type, whether child abuse reports were filed, and the results of those reports. Of the 321 admissions, 93 were reported for abuse or neglect. From the 93 reported cases, 26 were taken into temporary custody, 56 were indicated for abuse, but returned to the home, and 14 were "unfounded" cases. Our analysis indicated burned children aged 3 years and under, from single-parent, impoverished homes, admitted with a scald or thermal-contact burn are at highest risk for abuse or neglect and warrant careful assessment.

Age Distribution↗

Thermal injury-induced enhancement of oxidative metabolism by mononuclear phagocytes.

C57BL/6 female mice were subjected to full-thickness scald thermal injuries covering 25% of their total body surface areas, and thioglycollate-elicited peritoneal macrophages were isolated 4 days later. Macrophages from burned mice displayed a 2-fold increase in phorbol ester-stimulated superoxide production, whereas superoxide production in response to zymosan or immune complexes was unaltered. Maximal levels of superoxide production by thermal injury macrophages were comparable for all stimuli. Reduction of injury size to 12.5% total body surface area abrogated the enhancement of superoxide production. Protein kinase C activity and protein phosphorylation was not altered after thermal injury. These results indicate that the enhancement of macrophage-oxidative metabolism after thermal injury is independent of changes in reduced nicotinamide adenine dinucleotide phosphate oxidase or protein kinase C activity and may in part explain the increased susceptibility to multiple organ failure after this form of trauma.

Animals↗

Pediatric burn patients with respiratory failure: predictors of outcome with the use of extracorporeal life support.

Extracorporeal life support (ECLS) for pediatric burn patients is a viable option for respiratory failure that is unresponsive to maximal conventional therapy. No criteria have been identified that are predictive of the success of the use of ECLS for these patients. This article presents a retrospective review of the pediatric burn patients placed on ECLS at a single pediatric medical center. It was found that 12 patients (mean age, 30.3 months; range 6 to 69 months) were placed on ECLS because of profound pulmonary failure that was unresponsive to aggressive ventilatory support. The mean size of the burns of these patients was 50.2% of the total body surface area (average size of full-thickness burns, 41.8% total body surface area), with 6 patients having scald burns and 6 having flame burns. The overall survival was 67% (8 of 12). Nonsurvivors had greater positive end-expiratory pressure, mean airway pressure, peak inspiratory pressure, and oxygenation index before ECLS. It is felt that ECLS is a life-saving therapy for pediatric patients with thermal injury. Greater ventilator requirements before ECLS are associated with nonsurvival. Early institution of ECLS in pediatric burn patients with severe respiratory failure may prevent excessive barotrauma and thus discourage the onset of irreversible lung injury.

Burns↗

The effect of leukocyte infiltration on apoptosis in an in vitro thermal injury bioartificial living skin equivalent model.

An in vitro bioartificial skin construct (BSC) model was studied to see how inflammatory infiltration affects apoptosis in skin that has been thermally injured. The BSC was used as a target organ. Control BSCs without leukocytes (CON) were burned (BCON) by scalding with phosphate-buffered saline heated to 70 degrees C for 6 seconds, and they were then cooled with room temperature phosphate-buffered saline for 15 seconds. Human alloimmunocytes were added to CON to create rejection cultures (REJ) and to BCON to create burned rejection cultures (BREJ). Slides were stained with hematoxylin and eosin and anti-Lewis antibody. In situ labeling of apoptosis was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Those sections that were immunostained for Lewis Y were analyzed for intensity stain index (ISI = [sigma P0 x I0]/ total tissue area in pixels). TUNEL was quantified with the following equation: no. of total apoptotic cells / total tissue area. Necrosis and blister formation in the epidermal layer were evident in BCON and BREJ. Pyknosis and nuclear fragmentation-indicators of apoptosis-were also present. Phagocytosis of keratinocytes by leukocytes was seen in REJ and BREJ. Immunostaining showed greater expression of Lewis Y antigen, as determined by ISI, in REJ as opposed to CON (58.2+/-2.3 vs. 36.4+/-2.3, respectively, P<.001), but no significant difference was found between BCON and BREJ (55.0+/-5.7 vs. 60.5+/-3.4, respectively) and REJ and BREJ (58.3+/-2.3 vs. 60.5+/-3.4, respectively). TUNEL staining indicated the presence of apoptosis as follows: REJ versus CON (0.0015+/-0.0002 vs. 0.0003+/-0.0001, respectively, P<.001); BREJ versus BCON (0.0031+/-0.0006 vs. 0.0018+/-0.0004, respectively, P<.05); REJ versus BREJ (0.0015+/-0.0002 vs. 0.0031+/-0.0006, respectively, P = .007). The presence of leukocytes and thermal injury induces apoptosis in BSC. The combination of these two variables results in increased apoptosis as determined by TUNEL. These findings suggest that a common pathway for skin injury may include inappropriate regulation of apoptosis exacerbated by a mechanism that includes inflammatory cellular infiltration.

Animals↗

The 1999 Moyer award. Burn injury induces skeletal muscle apoptosis and the activation of caspase pathways in rats.

Burn injury induces many metabolic disorders, including altered protein kinetics with muscle weakness. The skeletal muscle weakness that occurs as a result of the loss of muscle mass causes hypoventilation and dependence on respirators, a condition that increases morbidity and mortality. The presence or absence of apoptosis in muscle, which can be a cause of the loss of muscle mass, was studied in rats after they had received scald burns to 40% of their body surface areas. The potential pro-apoptotic pathways that were activated were also examined. The burn injury produced did not directly destroy the muscle beneath; muscles just beneath the burned surface showed dramatic apoptotic changes according to assessments with the cell death enzyme-linked immunosorbent assay and in situ TdT-mediated dUTP-X nick-end labeling staining. The extent of apoptosis reached a peak on postburn days 3 and 7. Of note is that apoptosis was also confirmed in muscles at sites distant from the burn injury (eg, tibialis anterior) on both postburn days 3 and 7, a condition that is suggestive of the systemic effects of pro-apoptotic factors. To show that heat itself causes the initiation of the pro-apoptotic signaling, muscle-derived C2C12 cells were subjected to heat treatment at 55 degrees C. Ceramide, a key apoptotic second messenger, was observed to increase in the caveolae fraction but not in non-caveolae fraction of these muscle cells. In muscle tissue from burned rats, stress-activated protein kinase (a downstream-signaling kinase of ceramide) was activated soon after burn injury; this finding is consistent with the hypothesis that ceramide plays a role in burn-induced apoptosis. Caspase-1, -3, and -9, important final apoptotic enzymes involved with the downstream signaling of stress-activated protein kinase, were also activated after burn injury in muscle tissue from burned rats. These findings confirm the hypothesis that apoptosis occurs in skeletal muscle and that major apoptotic pathways are activated after a burn injury. Further characterization of these apoptotic signaling cascades may provide new therapeutic targets for the prevention of burn-induced muscle wasting.

Animals↗

Macrophage mediated suppression of granulocyte and macrophage growth after burn wound infection reversal by means of anti-PGE2.

The production and release of granulocytes and macrophages, crucial elements of the host defense system, are significantly impaired after burn injury and sepsis. Prostaglandin E2 (PGE2) is known to be myelosuppressive. We hypothesized that the macrophages contributed to myelopoietic suppression by means of increased PGE2 production, which is induced by thermal injury and sepsis. In this study, peritoneal macrophages were elicited at day 3 from normal mice and from mice who underwent a 15% total body surface area dorsal scald burn with or without Pseudomonas aeruginosa burn wound infection. The macrophages were incubated with or without endotoxin and with or without PGE2 polyclonal antiserum (anti-PGE2) for 18 hours. Macrophage supernatants were then used in co-cultures of bone marrow cells in a clonogenic assay of granulocyte-macrophage colony-forming cells (GM-CFCs) to determine the effect of burn wound infection on the alteration of the proliferative status of the GM-CFCs. Burn wound infection and endotoxin both caused marked reductions in GM-CFC growth in culture (20%-40% as compared with normal, P < .05-.01). The inhibition of GM-CFC growth induced by burn, burn plus infection, or endotoxin was significantly reversed by the addition of anti-PGE2 to the cultures (30%-40% increase in GM-CFC colony growth as compared with cultures without anti-PGE2). These results suggest that PGE2 is a key mediator in the gram-negative sepsis-induced macrophage suppression of granulocyte and macrophage production. The ability of anti-PGE2 to neutralize PGE2 activity may provide a useful means of mitigating myeloid depression that follows postburn sepsis.

Animals↗

Pain and anxiety with burn dressing changes: patient self-report.

Pain and anxiety are integral parts of burn dressing care. Descriptions of pain and anxiety from the patients' perspectives enhance our understanding of their experiences. This descriptive study measured relationships between self-reported pain and anxiety. Twenty-four patients who had an uncomplicated flame or scald wound reported scores immediately before, immediately after, and 1/2 hour after dressing changes. Results indicated that pain and anxiety increased until day 4. Pain correlated with anxiety. Self-report scores showed that pain and anxiety are perceived by patients in a similar manner. Self-report scores are of great value because they indicate the degree of relief achieved with medication. Through the descriptive study, we found that the pain score immediately after dressing changes was greater than 3 on all study days. This finding indicates a need to further examine the way pain is managed with dressing changes.

Adolescent↗

Burn injury in kitchen workers: a cause for prevention.

Preventable thermal injuries in professional kitchen workers have been identified, and we have introduced a protective garment. Because of the nature of their occupation, kitchen workers are prone to thermal injuries. It has been our experience that the majority of these injuries are scald injuries on the ankles and dorsum of the feet. We propose that a protective garment, such as a waterproof shoe and garter, could reduce the incidence of these injuries.

Accident Prevention↗

The expression of cyclooxygenase and the production of prostaglandin E2 in neutrophils after burn injury and infection.

Recent studies have demonstrated that neutrophils have the capacity to produce a variety of cytokines after stimulation. The synthesis and release of prostaglandin E2 (PGE2) via the cyclooxygenase (COX) pathway has been reported to occur in activated neutrophils. In the present study, we sought to determine the status of COX protein synthesis and PGE2 production in murine neutrophils after burn injury. The effect of burn injury on neutrophil COX and PGE2 response to infection or lipopolysaccharide (LPS) was also examined. Peritoneal neutrophils were obtained from BDF1 mice at 4, 18, 24, and 36 hours after a 15% TBSA full-thickness scald burn or sham burn. We found that neutrophils from healthy mice express a low level of COX-2 protein. Neutrophil COX-2 protein expression in burn animals was significantly increased at 4 hours and dramatically decreased at 36 hours after burn injury. Animals 36 hours after burn and topically infected with Pseudomonas Aeruginosa had neutrophil COX-2 expression almost identical to burn injury only. Neutrophils harvested from healthy mice cocultured with LPS (1 microg/ml) had a marked induction of COX-2 protein. Neutrophils 24 hours after burn were unresponsive to LPS-stimulated COX-2 enhancement. COX-1 protein was strongly expressed constitutively and not affected further by burn injury or LPS. The production of PGE2 corresponded with the changes in COX-2 expression for all groups of mice. Our data suggested that neutrophils express both COX-1 and COX-2 and produce PGE2. The effects of burn injury on neutrophil COX-2 protein synthesis and PGE2 production suggest that after burn there is a time-dependent response. Insights into not only the global cellular response to injury and infection but also temporal nature of the response are important in the development of the therapeutic treatment strategies for burn patients.

Analysis of Variance↗

An analysis of 550 hospitalized pediatric burn patients in Hong Kong.

A total of 550 acute burn patients under the age of 15 years were admitted to the Burns Unit of Prince of Wales Hospital, Hong Kong between March 1993 and February 1999. There were 337 males and 213 females with a male to female ratio of 1.58:1. The median age was 2.5 years and the median burn size was 5% total body surface area (TBSA). Toddlers of age < 2 years accounted for 235 (42.7%) of admission. Domestic burns resulted in 481 (87.5%) injuries followed by play-related burns that caused 34 (6.2%) admissions. Scalding was the most common cause of injury, which accounted for 497 (90.4%) admissions, followed by flame burns, which resulted in 45 (8.2%) injuries. Nine patients (1.6%) had inhalation injury requiring intubation and ventilatory support. The median hospital stay was 8 days and there was no seasonal variation in admission. The majority of patients (80.2%) had their wounds healed without any operation. Only 19 out of 550 patients (3.5%) had burns of 30% TBSA or larger, and only nine patients (1.9%) had inhalation injuries. Only one patient died in this series, which yielded a mortality rate of 0.2%.

Adolescent↗

Burns and injuries resulting from the use of gel candles.

Scented gel candles are common decorative household items composed of gelled mineral oil, fragrances, and dye. Like traditional wax candles, they have an open flame. Because of defective design, there have been several burns and injuries caused by these products. Here we report our experience with a scald burn from a gel candle and describe 34 additional injuries attributed to gel candles previously unreported in the medical literature.

Adolescent↗

Epidemiology of childhood burn injuries in Fars province, Iran.

Childhood burn injuries are a major environmental agent responsible for significant morbidity and mortality in Iran. Thus, the objective of this study was to analyze the epidemiology and current causative factors of hospitalized burn injuries among the approximately 1.6 million children between the ages of birth through 15 years residing in the Fars province of Iran. These data will be used as a basis for developing a targeted preventive program to protect children from burns. Epidemiologic data for 760 children, aged 0 to 15 years, admitted to the two burn centers of Shiraz University of Medical Sciences, over a 4-year period, 1994 to 1998, were collected and analyzed. The overall hospitalization rate was 11.8 per 100,000 person-years (PY). The sex ratio (boys/girls) was 1.38. About 60% were children aged 7 years or younger. Children aged 2 years had the highest burn incidence rate (36.9/100,000 PY). A total of 77.4% of the children had body surface area burns less than 40%. Scalds accounted for 46.2% of the burns, whereas 42.9% were caused by flame. Most of the burn injuries occurred at home (93%). There were 31 burns from suicide attempts among children aged 11 to 15 years (1.4/100,000 PY), showing a major public health problem for these children in our society. During the period of the study, 131 children died of the consequences of burns (2/100,000 PY). The epidemiology of childhood burn injuries in the Fars province is similar to that reported in other economically developing countries. It is suggested that a public health education campaign on this issue would help to reduce the incidence of childhood burn injuries in this region.

Adolescent↗

Diabetes and burns: retrospective cohort study.

Burn injuries are often associated with multisystemic complications, even in otherwise healthy individuals. It is therefore intuitive that for the diabetic patient, the underlying pathophysiologic alterations in vascular supply, peripheral neuropathy, and immune function could have a profoundly devastating impact on patient outcome. The effects of diabetes on morbidity and mortality of the burn-injured patient have not been examined in great detail. The purpose of this retrospective study was to compare clinical outcomes between diabetic and nondiabetic burn patients. We reviewed the charts of 181 diabetic (DM) and 190 nondiabetic (nDM) patients admitted with burns between January 1996 and May 2000, matched by sex and date of admission. Burn cause and size, time to presentation, clinical course, and outcomes were evaluated. Because age was a factor, the analysis was done by three age groups: younger than 18 years, 18 to 65 years, and older than 65 years. Of patients 18 to 65 years, 51% (98/191) were diabetic, whereas 84% (81/96) of those older than 65 and only 4% (3/85) of patients younger than 18 were diabetic. Because of the disproportion in numbers of diabetics compared with nondiabetics in the younger than 18 and older than 65 years-old groups, these patients will not be discussed. Diabetics were more likely to incur scald injury from tub or shower water rather than hot fluid spills (33% DM vs 15% nDM; P < or = 0.01), and have a delayed presentation (45 vs 23%; P = 0.00001). There was no difference in total burn size in all groups. Diabetics in the 18 to 65 years group had a higher rate of full-thickness burns (51 vs 31%; P = 0.025), skin grafts (50 vs 28%; P = 0.01) and burn-related procedures (57 vs 32%; P = 0.001), infections (65 vs 51%; P = 0.05), and longer lengths of stay (23 vs 12 days; P = 0.0001). Although there was no statistically significant difference in incidence of specific infections, the rates of cellulitis, wound infection, urinary tract infection, line infection, and osteomyelitis, were consistently higher in the diabetic population. Partial graft slough was 6% in diabetics 18 to 65 years with a 3% regraft rate, whereas nondiabetics had a 1% regraft rate. Comparing diabetics with controlled vs uncontrolled glucose levels, diabetics with uncontrolled glucose had higher rates of infection (72 vs 55%; P < or = 0.025), all burn-related procedures (68 vs 45%; P < or = 0.025), and longer ICU stays (24 vs 10 days; P = 0.048). Mortality rate was 2% for diabetics and for nondiabetics. In summary, presence of diabetes in the burn patient was associated with a worse outcome. A predilection for burn injuries in the diabetic was noted in the older adult population. Deeper burns, delayed presentation, higher rates of infection, graft failure and operations, and longer lengths of stay translate into an increased cost to society both economically and in lives. This data would suggest a need for better burn education for diabetics and health care professionals, recognizing the elderly population as a "high-risk" group. We believe that targeted prevention measures and treatment strategies, emphasizing earlier and more aggressive intervention for this population, may have a favorable effect on morbidity and mortality.

Adult↗

Serious occupational burn injuries treated at a regional burn center.

This article will present the epidemiology of occupational burn injuries among patients admitted to a regional burn center. Patients admitted to University of Alabama at Birmingham University Hospital Burn Center between November 1994 and December 1999 for occupational burn injuries were studied. Descriptive statistics were generated for demographic, clinical, and outcome characteristics. Approximately one-quarter of all burn center admissions had sustained occupational burn injuries. The most common burns were flame, electrical, and scald burns. The most heavily represented occupations were "manufacturing" (19.1%), "electrician" (16.2%), and "laborer" (16.2%). Burn type varied with occupation. Over $16 million in hospital charges was accrued by patients sustaining occupational burn injuries. Understanding the epidemiology of serious burn injuries in the workplace is crucial to directing prevention efforts toward worker groups at highest risk.

Accidents, Occupational↗

Accelerated tumor growth following experimental burns.

When mice are given a 30% scald burn, the growth of subsequently inoculated Ehrlich ascites tumor is markedly accelerated. This effect, which parallels the well documented suppression of cell-mediated immunity occurring postburn, disappears 10 days postinjury. Possible clinical implications are discussed and an illustrative case report is presented.

Animals↗

Acute leukopenia associated with silver sulfadiazine therapy.

A patient with a 30% scald burn was treated with topical silver sulfadiazine (Silvadene). On two occasions, within 48 hours of treatment, the patient developed acute leukopenia. Bone marrow aspiration revealed cell maturation arrest. The possible mechanisms of this leukopenia are discussed. It is recommended that daily leukocyte counts be done in burn patients being treated with silver sulfadiazine.

Acute Disease↗

Adenylate cyclase after burn injury: resistance to desensitization by catecholamines.

In vivo injection of isoproterenol(IPR) (4 mg/kg) in normal rats caused fat cell adenylate cyclase to become desensitized to stimulation by IPR in vitro. In contrast, adenylate cyclase from tissues of burn-injured rats (20% body surface, full-thickness scald) remained fully responsive to stimulation by IPR for several days after injury even though catecholamine excretion was elevated more than twofold. Furthermore, fat cell adenylate cyclase from burn-injured animals was not desensitized after acute in vivo IPR injections, whereas adenylate cyclase from the shams did become desensitized after acute IPR injections. To determine whether the apparent resistance to desensitization in burn-injured rats might be an adaptation to the chronic elevation of catecholamines that follows burn injury, two other rat models in which catecholamines are chronically elevated were studied: one was produced by a twice daily schedule or IPR (1 mg/kg) injections for 3 weeks; the other by 3 weeks' cold exposure (0--4 degrees C). As had been observed in burn injury, adenylate cyclase remained fully responsive to IPR in both models, and adenylate cyclase from the cold-acclimated rats was resistant to desensitization by acute injections of IPR. It therefore seems likely that chronic elevations of catecholamines evoke regulatory mechanisms in target cells to circumvent the desensitizationwhich would otherwise occur consequent to acute exposures to catecholamines. In burn injury this may result in an inadvertent adaptation which contributes to hypermetabolism.

Adenylyl Cyclases↗