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[An experimental study on large fragment deletion of rat myocardial mitochondrial DNA during early postburn stage].

OBJECTIVE: To investigate the influence of peroxidative injury in rat myocardium on the mitochondrial DNA (mtDNA) during early postburn stage. METHODS: Thirty-six Sprague-Dawley (SD) rats were employed in the study and were randomly divided into sham scald (SS) and scald groups. The rats in scald groups were inflicted with 30% TBSA III degree scalding and were further divided into 1, 3, 6, 12 and 24 post-scald hour (PSH) groups. The mtDNA deletion was determined by semi-quantitative PCR. The rat myocardial tissue samples were harvested and homogenized and the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) were determined. RESULTS: There was no mtDNA deletion in the rat myocardium in SS group. Partial or complete large fragment (4.8 kb) mtDNA deletion in the rat myocardium was identified at 1, 3 and 24 PSHs (P < 0.05 or 0.01). The SOD activity in the rat myocardium significantly decreased at 1 PSH, reaching the lowest level (76.90 +/- 8.30 U/mg) at 6 PSH, but the MDA content increased evidently at 1 PSH, peaking [(3.17 +/- 0.80) nmol/mg] at 6 PSH (P < 0.05). CONCLUSION: Peroxidative injury to the rat myocardium during early postburn stage might be the principal cause of the 4834 bp deletion of mtDNA in rat myocardium.

Animals↗

[Effects of ethyl pyruvate on splenocyte proliferation and apoptosis in burn rats with delayed resuscitation].

OBJECTIVE: To investigate the effects of ethyl pyruvate (EP) on splenocyte proliferation and apoptosis in burn rats with delayed resuscitation, and its potential underlying mechanism. METHODS: Seventy two male Wistar rats were randomly divided into sham-scalded control group (n=24), scald group (n=24), and scald with EP treatment group (n=24). Animals were sacrificed on days 1, 3, and 5 postburn, and spleen samples were collected to determine splenocyte proliferation and apoptosis. RESULTS: Splenic lymphocyte proliferation response to T cell mitogen, concanavalin A (Con A), as significantly depressed from 1 to 5 days after burn injury (all P<0.05). Meanwhile, burn injury resulted in a marked increase in splenic CD3(+)CD4(+)T lymphocyte apoptosis in comparison with that in sham-scalded controls on day 1 postburn (P<0.05). Treatment with EP after burns resulted in a dramatic restoration of lymphocyte proliferation response and reduction of splenic CD3(+)CD4(+)T lymphocyte apoptosis compared with scald group (P<0.05). CONCLUSION: Administration of EP can markedly improve the splenocyte proliferation response and inhibit splenic CD3(+)CD4(+)T lymphocyte apoptosis in thermally injured rats.

Animals↗

[Changes in the expression of rat hepatic lipid metabolism related genes in response to burn wound sepsis as assessed by DNA arrays].

OBJECTIVE: To examine the expression profile of lipid metabolism-related genes in liver of scalded rats with wound sepsis, and to analyze its significance. METHODS: Sixty male Wistar rats with 30% TBSA full-thickness scald wound on the back were enrolled in the study and randomly divided into wound sepsis group (n = 30) and control group (n = 30, with scald). Pseudomonas aeruginosa was inoculated to the wounds in sepsis group. Corresponding indices were determined to verify the diagnosis of wound sepsis. The rats were sacrificed and fresh liver tissues were obtained at 96 post-scald hours (PSH). Total RNA of liver was isolated with Trizol and the different expression of lipid metabolism related genes in response to burn wound sepsis was assessed by DNA microarray. RESULTS: By comparing expression profile of the two groups, totally 47 genes were observed to be differentially expressed in rat hepatic tissues, among them 9 genes were related to lipid metabolism. Among them, those which were upregulated were genes in relation with transportation and activation of fatty acid, and those downregulated were genes related in providing energy for fatty acid oxidation in mitochondria. CONCLUSION: The occurrence of wound sepsis in scalded rats can induce changes in the expression of hepatic lipid metabolism related genes in hepatic tissues, and aggravate

Animals↗

Local renal ischemia during burn shock in rat effected by thromboxane A2 and serotonin.

Intermittent patchy ischemia in the renal cortex during traumatic shock has previously been observed in dogs and rats. In recent experiments on rats a high rate of abrupt changes in local blood flow was observed after scalding. To try to reveal endogenous factors causing such ischemic episodes, we scalded six series of anesthetized rats (50% of body surface for 30 s in 80 degrees C water) and measured arterial pressure (AP), hematocrit (Hct), and local renal cortical blood flow (RCF). RCF was recorded by the local H2 washout technique. After scalding, RCF decreased markedly in all series whereas AP was relatively well preserved. In accordance with previous experiments, 11% of the washout curves recorded 0-75 min after scalding showed abrupt changes in local blood flow, rising to 27% during the next 60 min in drug-untreated rats. In contrast, blocking of serotonin S2 receptors with Ketanserin abolished the phenomenon. However, in rats treated with the prostaglandin synthesis blockers, indomethacin (general) or 3-ethyl pyridin (thromboxane A2 blocker), the phenomenon was observed in only 2-3% of the washout curves. Furthermore, after blocking the AngII receptors by saralasin or alpha receptors by phentolamine in separate series, the frequency of abrupt flow shifts was reduced in comparison to the frequency in untreated rats. The results indicate that intermittent, patchy vasoconstriction is mediated by serotonin and thromboxane A2 (TxA2), probably released from platelets. The occurrence of ischemic episodes also depends on the local AngII and alpha-adrenergic tonus present after scalding.

Animals↗

Scanning electron microscope studies of some normal and diseased conditions of mammalian skin as revealed in leather manufacture.

Sheep, goat and bovine skins, as leather, were examined. The surface contours of dermal response to sunburn, facial eczema, rape scald, and demodicosis are illustrated. In sunburn, demodicosis and rape scald, finger-like and ridge pattern projections had developed. In the photo-sensitive condition of rape scald and facial eczema distension was apparent, and in addition in rape scald reactions of contrasting nature involving hair follicles indicated a considerable disorientation of the skin. The transition from str. basale to str. corneum in bovine epidermis has been examined in leather from which the epidermis had unintentionally been incompletely removed in the course of manufacture, during attack on the keratinous tissue by hydrosulphide ions at high hydroxyl ion concentration. A "pore" presumably related to the position of the nucleus was observed in the outer surface of each of the cells in each layer exposed by the attack. The walls of the basal and adjacent cells appeared remarkably sturdy. As judged from the basal cells the intercellular cement (cell coating) disappeared before the cell wall degraded, but intercellular bridges remained clearly visible in the prickle cell layer, while towards the exterior, adjacent cell walls appeared more closely knit and the str. corneum (residues of which were observed around the follicles) appeared to lie in sheets. Discrete and fibrous cell components were exposed. At the latest degree of degradation observed in the basal cells the wall had reduced to a fibrous network.

Animals↗

Burn edema reduction by methysergide is not due to control of regional vasodilation.

To determine the extent to which edema modulation by methysergide is due to a blunting of the regional vasodilator response to scald and/or local reduction of transvascular fluid flux, a canine hind limb lymphatic was cannulated. Femoral blood flow (Qa; ml/min), lymph flow (QL; microliter/min/100 g), and lymph-to-plasma protein ratios (CL/CP) were monitored in groups of five dogs before and 4 hr after 5-sec, 100 degrees C foot paw scald; high (1.0 mg/kg) or low (.5 mg/kg) dose of methysergide 30 min before scald. The compression on a clamp placed around the femoral artery in other dogs was adjusted after scald to simulate the blunting effect on Qa observed in methysergide treated dogs. Hind leg venous pressure was elevated to approximately = 40 mm Hg before experimentation until steady state QL and (CL/CP)min were reached. Protein reflection coefficient (sigma d; 1-C1/ CP) and fluid filtration coefficient (Kf) were calculated. Compared to preburn values, all groups showed significant (P < 0.002, analysis of variance) increases in CL/CP and Kf. Contrasted with the burn only group, methysergide blunted increases in Qa, Kf and paw weight gain in a dose-dependent fashion, with no effect on the reflection coefficient. Compression clamp control of femoral Qa caused no effects on permeability. Methysergide limits burn edema in a dose-related fashion, though not due to a blunting of the regional vasodilator response. Local, not regional, mechanism(s) likely mediate this response.

Animals↗

Effects of diabetes and of injury on muscle protein in the mouse, and their interaction.

The effects of a 20% dorsal scald injury and of different severities of streptozotocin diabetes on hindquarter muscle protein have been studied in the mouse. Ten days after scald injury muscle protein contents were generally unaffected, whereas moderate diabetes (200 mg streptozotocin/kg body weight; plasma glucose concentrations 17--46 mmol/1; normal 11 mmol/l) led to net loss of muscle protein. Production of scald injury in the moderately diabetic mouse caused significant additional loss of muscle protein, especially from the extensor digitorum longus Milder diabetes (maximum plasma glucose concentration 15 mmol/l) did not lead to loss of muscle protein. However, scald injury in the mildly diabetic mouse caused significant loss of protein from all muscles studied. The effects of diabetes and of injury on loss of muscle protein were at least additive and in some muscles probably synergistic.

Animals↗

Systemic thermal injury in anesthetized rabbits causes early pulmonary vascular injury that is not ablated by lazaroids.

PURPOSE: To study the effects of a systemic thermal injury on the pulmonary vasculature with and without inhibitors of lipid peroxidation (U74389G). METHODS: In a prospective, placebo control, randomized, and blinded multi-group study, burn shock was induced by scalding thermal injury (65C) to 35% body surface area in rabbits (n = 28). Hemodynamics and gas exchange were followed for 240 min post burn in four groups: No Burn, Burn-Control, Burn-U74 (10 mg.Kg-1 U74389G), No Burn-U74 (10 mg.Kg-1 U74389G). RESULTS: Scald resulted in early pulmonary injury as measured by increased pulmonary vascular resistance in the pooled Burn group compared with the No Burn groups (942 +/- 358 vs 605 +/- 255 dynes.sec-1.cm-5 respectively, P < 0.05). These pulmonary changes were associated with alveolar sequestration of leukocytes (4.8 +/- 2.9 vs 17.7 +/- 6.0 cells x 10(9).L-1, P < 0.05) in the No Burn and Burn groups respectively. Histological evidence of decreased neutrophil sequestration after scald injury was present in U74 treated animals (3+ vs 2+, P < 0.05 in the Burn and No Burn groups respectively and 2+ vs 2+, P > 0.05 in the Burn-U74 and No Burn-U74 groups respectively) although bronchial alveolar lavage still demonstrated neutrophil sequestration (5.3 +/- 2.5 vs 12.2 +/- 3.3 cell 10(9).L-1, P < 0.05 in No Burn-U74 and Burn-U74 groups respectively). Similarly, circulating white blood cells were increased in the Burn group but not Burn-U74 group four hours post burn. The increase in pulmonary vascular resistance after burn was not altered by administration of U74. CONCLUSIONS: Systemic burn results in early pulmonary vascular changes associated with leukocyte sequestration. After scald injury administration of lazaroids (U744389G) did not lessen pulmonary vascular resistance changes but did reduce neutrophil sequestration.

Analysis of Variance↗

A study of the prevention of hot tapwater burns.

A 4-year retrospective study of hot tapwater scalds admitted to Mount Vernon Hospital Burns Unit suggested that the three high-risk groups are young children, the elderly and the mentally and physically handicapped. A household survey was conducted of 60 homes inhabited by people over 70 years of age and 60 homes inhabited by families with toddlers to identify what measures could be taken to prevent hot tapwater scalds. The survey showed that over half of the old people did not have adequate bathing aids and that one-third of all the homes visited had a hot tapwater temperature greater than 60 degrees C, which is the temperature recommended by British Building Services Engineers. The survey also revealed that 50 per cent of the immersion heaters and 25 per cent of the gas boiler central heating systems produced an excessively high hot tapwater temperature. The study thus indicated that both the wider provision of bathing aids to the elderly and a nationwide programme to update old inefficient immersion heater and gas boiler central heating systems would reduce the risk of hot tapwater scalds. The installation of a 'thermoscopic' mixing valve, pre-set and locked at 43 degrees C, at bath and shower outlets can totally eliminate the risk of hot tapwater scalds. At present it is not a feasible option to install these valves in every household, but there is a strong case for installing them in hospitals and residential homes for paediatric, geriatric and mentally/physically handicapped patients.

Accidents, Home↗

Prevalence of Arcobacter and Campylobacter on broiler carcasses during processing.

Broiler carcasses (n=325) were sampled in a U.S. commercial poultry processing plant for the prevalence of Arcobacter and Campylobacter at three sites along the processing line: pre-scald, pre-chill and post-chill. Samples (75-125 broilers per site) were collected during five plant visits from August to October of 2004. Arcobacter was recovered from pre-scald carcasses more frequently (96.8%) than from pre-chill (61.3%) and post-chill carcasses (9.6%). Campylobacter was isolated from 92% of pre-scald carcasses, 100% of pre-chill carcasses, and 52% of post-chill carcasses. In total, Arcobacter was isolated from 55.1% (179 of 325), while Campylobacter was isolated from 78.5% (255 of 325) of the carcasses from the three collection sites. For Arcobacter identification, a species-specific multiplex PCR showed that A. butzleri was the most prevalent species (79.1%) followed by A. cryaerophilus 1B (18.6%). A. cryaerophilus 1A was found at low levels (2.3%). PCR identified the most common Campylobacter species as C. jejuni (87.6%) followed by C. coli (12.4%). Overall, significant contamination of broiler carcasses by Arcobacter was observed, although less than that found for Campylobacter. From pre-scald to post-chill, a far greater reduction in Arcobacter numbers was observed than for Campylobacter. Our results for Arcobacter, obtained from the same environment as the closely related pathogen Campylobacter, will aid in the development of control measures for this emerging pathogen.

Animals↗

Electric water heaters: a new hazard for pediatric burns.

The electric water heater has recently become a popular household appliance replacing the hot water dispensing jug. This device provides hot water and potable cool water directly from the faucets thus removing the need to refill the container or boil water separately in a kettle. Along with the convenience of dispensing hot water immediately has come an increased incidence of pediatric burns. This paper presents a 6-year retrospective study of such pediatric scald burns from 1996 to 2001. Computer database records revealed that the incidence of pediatric scald burns caused by the electric water heater during the past 6 years was 6.4% (66/1028). The age of victims ranged 0-6 years (mean 1.5+/-1.1 years), most of the victims were in the 1-2-year-old group. In most common cases burn location was the trunk. The accidents often occurred during the cold months and in the living room of the house. From this retrospective study, it was seen that the etiology and incidence of scald burns among children have changed as people have modified their household practice for obtaining hot water in our country. This study aims to increase public awareness to the problem and suggest some prevention measures to reduce this type of scald injury.

Accidents, Home↗

Inhibitory effects of tachykinin receptor antagonists on thermally induced inflammatory reactions in a rat model.

Recent studies have proposed that activation of the sensory nervous system after thermal injury induces the release of vasoactive neuropeptides, including tachykinins which contribute to the local inflammatory reaction as well as to the nociceptive transmission at the spinal cord level. Effects of the tachykinins substance P and neurokinin A are mediated by the neurokinin 1 and 2 (NK1, NK2) receptors. The aim of the present study was to investigate the modulatory role of NK1 and NK2 antagonists on edema formation, and on hindpaw withdrawal latency to experimentally asses nociception. Thermal injury was inflicted on the anaesthetized rat by dipping the right hindpaw into hot water at 60 degrees C for 20 s. The amount of edema formation was calculated by measuring the hindpaw volume with a plethysmograph before and during 420 min after scalding. In other studies scalding was inflicted under brief anesthesia, and hindpaw withdrawal latencies (HWL) to mechanical stimulation were recorded before injury and at 180 min after. The effect on edemic reactions of rats treated locally with NK1 and NK2 receptor antagonist were studied, as well as the effect of the same compounds on HWL after intrathecal injection. Scalding induced a progressive edema formation which was reduced significantly in rats treated with local injection of 100 nmol of NK1 and NK2 antagonists 45 min after the injury. The thermally induced inflammation was followed by significant decrease of the latency of hindpaw withdrawal response to mechanical stimulation. Intrathecal injection of 30 nmol of the same drugs 180 min after scalding was followed by significant increase in HWL. The results indicate that SP and NKA contribute to the inflammatory reactions after thermal injury and that the tachykinin receptor antagonists possess the ability to reduce both the local edemic reaction as well as the nociceptive transmission at the spinal cord level.

Animals↗

Epidemiology of childhood burns in the critical care medical center of Kinki University Hospital in Osaka, Japan.

The objective of the present study was to describe the characteristics of pediatric burns in order to prepare a program for the prevention of severe burn injuries in children. We conducted a retrospective study of burn victims aged 15 years or younger who were hospitalized in our Critical Care Medical Center between 1982 and 1997. There were 73 children with burn injuries hospitalized in our center during the study period. The greatest number were children 1 year old. The average % body surface area burned was 21. 5+/-20.5%. The most important causes of pediatric burns were found to be hot bath water and other hot liquids. Hot bath scalds accounted for about half of the pediatric burns occurring in all age groups, and they were often extensive. Non-bath scalds accounted for about one-third of the pediatric burns and were most frequent in children 2 years and younger. All the injuries sustained at home occurred when a family member was in the house. Similar to many reports from overseas, non-bath scalds were one of the most common causes of burns in this study; however, hot bath scalds were the most important cause. These data are being used to develop a prevention program. We also consider it necessary to educate children and their family members about the dangers of burn injuries.

Accidents, Home↗

Preventing medical errors by designing benign failures.

BACKGROUND: One way to successfully reduce medical errors is to design health care systems that are more resistant to the tendencies of human beings to err. One interdisciplinary approach entails creating design changes, mitigating human errors, and making human error irrelevant to outcomes. This approach is intended to facilitate the creation of benign failures, which have been called mistake-proofing devices and forcing functions elsewhere. USING FAULT TREES TO DESIGN FORCING FUNCTIONS: A fault tree is a graphical tool used to understand the relationships that either directly cause or contribute to the cause of a particular failure. A careful analysis of a fault tree enables the analyst to anticipate how the process will behave after the change. EXAMPLE OF AN APPLICATION: A scenario in which a patient is scalded while bathing can serve as an example of how multiple fault trees can be used to design forcing functions. The first fault tree shows the undesirable event--patient scalded while bathing. The second fault tree has a benign event--no water. Adding a scald valve changes the outcome from the undesirable event ("patient scalded while bathing") to the benign event ("no water") LIMITATIONS: Analysis of fault trees does not ensure or guarantee that changes necessary to eliminate error actually occur. Most mistake-proofing is used to prevent simple errors and to create well-defended processes, but complex errors can also result. CONCLUSIONS: The utilization of mistake-proofing or forcing functions can be thought of as changing the logic of a process. Errors that formerly caused undesirable failures can be converted into the causes of benign failures. The use of fault trees can provide a variety of insights into the design of forcing functions that will improve patient safety.

Causality↗

Influence of ethylene action, storage atmosphere, and storage duration on diphenylamine and diphenylamine derivative content of Granny Smith apple peel.

The application of diphenylamine (DPA) to prevent the apple peel disorder superficial scald can result in accumulation of a number of DPA derivatives resulting from C-nitration, C-hydroxylation, O-methylation, and N-nitrosation during fruit storage. As the presence of these compounds may be indicative of metabolic processes leading to superficial scald development, the contents of DPA and DPA derivatives were determined in fruits treated at harvest with DPA or DPA plus the ethylene action inhibitor 1-methylcyclopropene (1-MCP), which also prevents scald development. Influences of fruit maturity, storage environment, storage duration, and a 14 day poststorage ripening period on accumulation of DPA metabolites were also assessed. Poststorage ripening, 1-MCP treatment, and controlled atmosphere storage had varied effects on DPA derivative contents suggesting that reactive oxygen and nitrogen species, such as *OH, *NO, and *NO2, or enzyme-catalyzed reactions may be present during certain ripening and senescence-related physiological processes. Definitive correlations between superficial scald incidence and contents of specific derivatives were not observed.

Diphenylamine↗

Serotonin receptors regulate canine regional vasodilator responses to burn.

OBJECTIVE: To determine which serotoninergic receptor subtype(s) mediates the regional vasodilator response to scald injury. DESIGN: Prospective, randomized trial. SETTING: Microcirculation research laboratory. SUBJECTS: Anesthetized dogs. INTERVENTIONS: Mechanically ventilated dogs underwent cannulation of a brachial artery and placement of an ultrasonic flow probe around one femoral artery. All animals received a 2% to 3% body surface area partial thickness scald injury by immersing the paw ipsilateral to the instrumented femoral artery into 100 degrees C water for 5 secs. In one group of dogs, BMY 7378 (a serotoninergic1A receptor antagonist) was given by the peripheral intravenous route before burn. These results were compared with those findings obtained from a group of animals that received a burn only, and groups of animals given a peripheral intravenous injection of methysergide (a serotoninergic receptor antagonist) or ritanserin (a serotoninergic2 receptor blocking agent) before burn. Experiments were conducted for two postburn hours. MEASUREMENTS AND MAIN RESULTS: Burn injury caused a marked and persistent increase in regional (e.g., femoral artery) blood flow, an effect that was significantly blunted by preburn administration of the serotoninergic receptor antagonist, methysergide. Preburn administration of BMY 7378 increased baseline femoral blood flow by 13%, reflecting its known serotonin agonist properties. However, when compared with the mean postscald increases in femoral blood flow over baseline seen in scald only dogs and in animals given the serotoninergic2 receptor blocking agent, ritanserin (before scald), the BMY 7378-treated group demonstrated a significant (p < .001 by analysis of variance) 2-hr-postscald blunting of this femoral vasodilator response. CONCLUSION: These data suggest that serotoninergic1A-like receptors play an integral, albeit not an exclusive, role in blood flow regulation to the site of burn injury.

Animals↗

Burn resuscitation: crystalloid versus colloid versus hypertonic saline hyperoncotic colloid in sheep.

OBJECTIVES: The present study was undertaken to assess the fluid balance and hemodynamic effects during the first 8 hrs of resuscitation in animals with a large body surface area burn, using lactated Ringer's solution, 6% hetastarch, and hypertonic saline dextran. DESIGN: A prospective, blinded, controlled, terminal study, using anesthetized animals. The initial baseline period was followed by scald injury, and three different treatment regimens were administered from coded bags to achieve a physiologic end point. SETTING: University laboratory. SUBJECTS: Eighteen female sheep (35 to 45 kg) were anesthetized with isoflurane. INTERVENTIONS: Test solutions (10 mL/kg of either lactated Ringer's solution, hetastarch, or hypertonic saline dextran) were infused 30 mins after the scald injury at a rate to restore and maintain the baseline oxygen delivery (DO2) value. MEASUREMENTS AND MAIN RESULTS: Cardiovascular hemodynamics, plasma sodium concentration, plasma colloid osmotic pressure, and fluid balance were measured before and after scalding and resuscitation. After the initial 10-mL/kg test solution dose was given, lactated Ringer's solution was infused to achieve the same end point of baseline DO2 for the remainder of the 8 hrs. The scald caused an initial 30% reduction in cardiac output, a 20% reduction in mean arterial pressure, and 10% to 15% increase in hematocrit. All three test solutions restored and maintained baseline DO2 within 1 hr. However, hetastarch and hypertonic saline dextran reduced the net fluid volume over 8 hrs by 48% and 74%, respectively, compared with lactated Ringer's solution. Edema in the burn wound was not affected by treatment, while hypertonic saline dextran reduced edema in nonburned skin compared with both lactated Ringer's solution and hypertonic saline dextran. Plasma colloid osmotic pressure was significantly higher in the hetastarch and hypertonic saline dextran groups. A continuous decrease in plasma sodium concentrations from baseline values (140 to 145 mmol/L) was measured in the lactated Ringer's solution and hetastarch groups (130 to 133 mmol/L) over 8 hrs. Plasma sodium concentrations in the group receiving hypertonic saline dextran were increased (150 to 155 mmol/L) at 4 hrs, but returned toward baseline by 8 hrs. CONCLUSIONS: Net volume loading can be reduced markedly by initial resuscitation of large body surface area burn injury using a colloid (hetastarch), and can be further reduced by use of hypertonic saline colloid. Hyponatremia was apparent in the isotonic crystalloid- and colloid-treated animals, but not in those animals treated with hypertonic saline colloid.

Animals↗

Pediatric patients in a regional burn center.

Because scald burns are reported to be the leading cause of burn injuries to children, little is written about other etiologies of burn injury in the pediatric literature. To test the hypothesis that burns from other etiologies are more serious and require longer hospitalizations than scald burns, a retrospective chart review was undertaken. The charts of all patients less than 16 years of age who were admitted to Harborview Medical Center Burn Unit in the years 1979 to 1984 were reviewed. Four hundred sixty-four children were admitted to the regional burn center during that time. We found that children under four years of age are at greatest risk for being hospitalized for thermal injury, that the burn most commonly occurs inside the home between 6 PM and midnight, and that scalds are the most common etiology for thermal injuries in children (54%). However, 46% of the burns resulting in admission to our burn center were from etiologies other than scald injury. There was no significant correlation between etiology of the burns and length of hospital stay, rate of infection, or need for excision and grafting. Thermal injuries to children from any etiology are serious; pediatric health care providers should be aware that children may be burned in a variety of ways and should direct some of their well-child visit time to the topic of burn prevention in the home.

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