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PubMedDate not supplied

The burn unit experience at Grady Memorial Hospital: 844 cases.

Between February 20, 1987 and July 13, 1990, 844 patients were admitted to the Grady Memorial Hospital Burn Unit. Mean age was 25.5 years, mean burn size 16.5% total body surface area, mean survivor hospital length of stay 15.9 days, and an overall survival 90.5%. Seventy-three percent were male. One half of the burns were less than 10% total body surface area. Almost half (48.5%) of the patients had flame burns, which accounted for 88.8% of the 80 deaths. The peak burn incidence occurred in infants and children as a result of scalds. If those with toxic epidermal necrolysis (n = 5), those without skin injury (n = 13), and those who were allowed to die (n = 16) are excluded, survival was 92.2%. Survival in 62 patients with inhalation injury (55.23%) was significantly less than that in 474 patients without inhalation injury (98.10%) (p less than 0.0001). The three variables--age, burn size, and inhalation injury--each influenced survival significantly but appeared to be dependent on each other; all three tended to increase or decrease together. Logistic regression equations to predict survival were developed.

Adolescent↗
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Efficacy of leupeptin, superoxide dismutase, and verapamil in modulating delayed reperfusion damage after burn injury.

Reperfusion damage has been identified as an important factor in multiorgan failure after severe burn injury. We wondered if leupeptin, a protease inhibitor, superoxide dismutase (SOD), a scavenger of free oxygen radicals, or verapamil, a calcium antagonist, would protect the cellular energy metabolism when they were given with fluid resuscitation that was delayed 6 hours after a severe burn injury. Fifty male rats weighing 280 to 300 gm received a 50% third-degree scald burn. Ten of these received fluid resuscitation at 30 minutes and 1 1/2 hours after injury, and 40 received delayed fluid resuscitation at 6 and 7 hours after injury. Thirty of these 40 rats were given leupeptin (n = 10), SOD (n = 10), or verapamil (n = 10). Heart, liver, and kidney tissue samples were obtained 8 hours after injury; adenosine triphosphate, adenosine diphosphate, and adenosine monophosphate were measured; and the energy charge potential was calculated. Tissue water content (TWC) in lung and skeletal muscle was also determined. The adenine nucleotide pool and the energy charge potential in heart, liver, and kidney tissue were all significantly decreased (p < 0.01) in rats receiving delayed fluid resuscitation compared with those receiving early resuscitation. Leupeptin was effective in protecting the heart against reperfusion damage, and verapamil and leupeptin showed some efficacy in protecting kidney tissue. Liver tissue, however, showed no protective response with therapy. TWC was significantly decreased (p < 0.01) in skeletal muscle with SOD treatment, and though all treatments appeared to keep lung water content reduced, none was significant at p < 0.01. We thus conclude that both the decreases in heart and kidney adenine nucleotides and the increase in TWC that are caused by delayed fluid resuscitation can be attenuated with appropriate pharmacologic agents.

Adenine Nucleotides↗
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Effects of rat interleukin-2 and rat interferon on the natural killer cell activity of rat spleen cells after thermal injury.

The natural killer cell activity of splenocytes from rats with scald injury was observed to be significantly suppressed at 7 days after injury compared with that of normal nonburned controls. Incubation of splenocytes from normal rats or rats with burn injury with either rat interleukin-2 or rat interferon (IFN-alpha and IFN-beta) significantly increased the natural killer cell activity. Addition of a rabbit anti-rat interferon antibody to spleen cells incubated with interleukin-2 did not produce any significant alteration in interleukin-2-related enhancement of natural killer cell activity. These results suggest that enhancement of natural killer cell activity after incubation of splenocytes with interleukin-2 is not due to interferon production but is an independent event. Preincubation of spleen cells with a mouse monoclonal antibody to rat interleukin-2 receptor was observed to abolish the interleukin-2-related enhancement of natural killer cell activity completely, whereas it partially blocked the interferon-related enhancement. These results were also confirmed by enhancement of natural killer cell activity of burned rats after in vivo administration of interleukin-2. Our studies thus indicate that after thermal injury, the observed decrease of natural killer cell activity can be enhanced by both interleukin-2 and interferon independently of each other. The decreased natural killer cell activity may be due to a decrease in interleukin-2 production or availability and not to an interleukin-2 receptor defect. These studies thus point toward a potential therapeutic significance of interleukin-2 in enhancing immune function after thermal injury.

Animals↗
PubMedDate not supplied

Core body temperature responses immediately after cutaneous thermal injury in rats.

Internal temperatures were continuously measured in rats that received 20% or 40% body surface area cutaneous scald injuries in 25 degrees C and 38.5 degrees C environments. In animals that received thermal injuries in the 25 degrees C environment, intraperitoneal, intraesophageal, and intrarectal temperatures rapidly rose to 40 degrees C within 5 minutes but returned to normal values within 15 minutes after injury. When 20% body surface area injuries were induced in a 25 degrees C environment, all of the animals survived. In the 25 degrees C environment, neither acute core body temperature elevations nor use of fluid resuscitation predicted survival. In contrast, in a 38.5 degrees C environment core body temperatures rapidly exceeded 41 degrees C with the 20% injury, and all of the animals died within minutes in spite of fluid resuscitation. These studies suggest that the ambient environmental temperature may significantly influence a thermally injured animal's ability to rapidly eliminate absorbed heat of injury and result in an elevated core body temperature, which may contribute to the immediate lethality of the injury.

Animals↗
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Burn care in Africa: reducing the misery index: the 1993 Everett Idris Evans Memorial Lecture.

Burn care in Africa is hampered by inadequate facilities, inadequate infrastructure, and inadequately trained staff. Burn units with burn teams are few. Burn injuries carry a high mortality rate with delayed healing and high complication rates among survivors. Most burns occur in the home from flame and scalding, and children are more affected than adults. Burn sepsis is mostly from staphylococci and pseudomonas. Various studies on epidemiology, sepsis, protein metabolism, and repigmentation indicate methods of prevention and improved care, including greater resort by surgeons to skin grafting, which speeds healing and both prevents and treats scarring, contractures, and depigmentation. Governments, industries, and entrepreneurs are exhorted to promote burn prevention, research, improved care, and rehabilitation, particularly through the establishment of burn units with burn teams, to reduce the misery and suffering caused by the high mortality and morbidity from burns in Africa.

Adult↗
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Effects of propranolol administration on cardiac responses to burn injury.

Previous studies showing that propranolol upregulates beta-adrenergic receptors and protects against myocardial ischemia led us to hypothesize that preburn propranolol would protect against postburn cardiac dysfunction. Guinea pigs were treated with propranolol 3 mg/kg/day for 14 days, then deeply anesthetized and subjected to a 45% 3 degrees scald burn; eight guinea pigs treated with propranolol served as the control group (group 1). Burned guinea pigs were resuscitated with Ringer's lactate given as either 4 ml (group 2, N = 8), 6 ml (group 3, N = 10), or 8 ml (group 4, N = 6) per kg/% burn. Guinea pigs treated for 14 days with vehicle (water) were subjected to either sham burn (non-propranolol control, group 5, N = 10) or burn and treatment (group 6, N = 10) as described for group 2. Fluid resuscitation in non-propranolol-treated guinea pigs failed to overcome burn-induced cardiac deficits, as indicated by significantly lower left ventricular pressure, 86 +/- 2 versus 62 +/- 3 mm Hg; +dP/dt max, 1365 +/- 43 versus 1110 +/- 44 mm Hg/sec; -dP/dt max, 1184 +/- 31 versus 881 +/- 40 mm Hg/sec, p < 0.001. Burn-mediated cardiac defects occurred in all propranolol-treated guinea pigs regardless of the fluid volume given. Our data show that (1) propranolol did not protect against burn-induced cardiac dysfunction, and (2) chronic beta-adrenergic blockade increases postburn fluid requirements for maintenance of cardiodynamic stability and for survival.

Animals↗
PubMedDate not supplied

Dysfunctional metabolism induced by the systemic effects of burn trauma: the role of rates of polyinositol and glycerophosphate formation in diaphragm.

Common complications among patients with burns are respiratory problems. Inspiration for breathing normally is facilitated by diaphragmatic contractility. However, in burn trauma numerous factors impose on skeletal muscle activity and chest wall function. These present limitations to surgical procedures requiring anesthesia. The hypothesis of this study was that the systemic effects of increasing burn size may result in metabolic changes in the polyinositol part of the phosphatidyl inositol signal transduction system in diaphragm. In this report, rate changes in polyinositol phosphates (i.e., inositol triphosphate (IP3), inositol 1,4 biphosphate (I1,4P2), inositol 1 phosphate (I1P), and inositol) that occurred in diaphragm subjected to the systemic effects of burn trauma were examined. Third-degree burn injury was applied by scalding predefined areas (i.e., 0%, 20%, and 50% body surface area) on the dorsal and ventral surfaces of mice. At postburn day 21 tissues were harvested and the levels of the polyinositol phosphates were measured by incorporation of myo-[2-3H]-inositol with separation of the phosphates by anion-exchange chromatography. All actual levels and rates of formation were analyzed with standard statistical tests and curve-fitting routines. Rate changes of the labelled [3H]-polyinositol phosphates were determined for the control, 20%, and 50% groups. These data show that rate changes occur in the polyinositol part of the phosphatidyl signal transduction system and are caused by the systemic effects of large percent body surface area burns. The changes that occur in the polyinositol phosphates provide insight into dysfunctional processes that can affect skeletal muscle physiology. The long-term goal of these studies is that they will lead to therapeutic advancements in the treatment of respiratory dysfunction in patients with burns.

Animals↗
PubMedDate not supplied

Superoxide dismutase and leupeptin prevent delayed reperfusion injury in the rat small intestine during burn shock.

Delayed fluid resuscitation during burn shock is thought to compromise the integrity of gut mucosa and allow enteric bacteria to cross the luminal wall and infect other sterile organ systems. Superoxide dismutase, a free-oxygen radical scavenger; leupeptin, a protease inhibitor; and verapamil, a calcium channel blocker, were studied to evaluate their efficacy in maintaining cellular integrity in the gut of thermally burned rats whose fluid resuscitation had been delayed. Fifty male rats weighting 280 to 320 gm were given a full-thickness scald burn covering 50% total body surface area. Ten received early fluid resuscitation beginning half an hour after burn, and 40 received fluid resuscitation delayed by 6 hours. Those receiving delayed resuscitation were given superoxide dismutase (n = 10), leupeptin (n = 10), verapamil (n = 10), or a placebo of normal saline solution (n = 10) at the time of fluid resuscitation. Ileal mucosa samples were harvested, and adenosine triphosphate, diphosphate, and monophosphate were measured. Adenosine triphosphate, total nucleotides, and energy charge potential were significantly lower in the placebo group without therapy compared with those of the early resuscitation group. Superoxide dismutase and leupeptin therapy prevented this drop in cellular energy. Total water content was significantly increased in the placebo group compared with that of the early resuscitation group; superoxide dismutase was able to prevent this increase. Data indicate that intestinal reperfusion injury in burned rats can be effectively modulated with superoxide dismutase or leupeptin therapy.

Adenosine Diphosphate↗
PubMedDate not supplied

Beneficial wound healing and metabolic effects of clenbuterol in burned and nonburned rats.

Clenbuterol is known to increase muscle mass in nonburned and burn-injured subjects. The effects of clenbuterol on wound healing and the postburn response were examined in both nutritionally matched and free-feeding groups of rats. Rats received either a sham or 30% total body surface area scald burn and then a dorsal incision. Clenbuterol (2 mg/kg/day) was administered subcutaneously via a miniosmotic pump. The burn injury resulted in a sustained non-temperature-dependent hypermetabolism that was not altered by clenbuterol. Clenbuterol induced muscle anabolism and body growth in sham and burned-injured animals. Treated sham animals demonstrated increased wound breaking strength. Matched nutritional intake attenuated the body weight gain, although muscle anabolism was still evident in treated animals. Clenbuterol elevated RNA concentration in the tibialis muscle and reduced it in the liver. There was no statistical difference in wound strength when nutritional intake was matched. Clenbuterol's actions appear to be dependent on substrate availability. Clenbuterol may prove beneficial in patients with severe prolonged catabolic state, such as that associated with burn injury, by promoting protein anabolism and enhancing wound healing.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Accelerated healing and reduced need for grafting in pediatric patients with burns treated with arginine-glycine-aspartic acid peptide matrix. RGD Study Group.

Arginine-glycine-aspartic acid (RGD) peptide matrix is designed to promote dermal healing by providing a molecular scaffold that facilitates cell ingrowth and establishment of normal tissue architecture. This study investigated the effectiveness and safety of RGD peptide matrix in the treatment of partial-thickness scald burns in pediatric patients. Either topical RGD peptide matrix or control treatment with silver sulfadiazine was applied to matched burn sites daily for up to 21 days. With RGD peptide matrix application under synthetic occlusive dressing, the incidence of healing was nearly threefold higher, average time to healing 2.5 days shorter (regression estimation), extent burn closure at all treated sites 37% greater, and number of needed grafting procedures fourfold lower compared with control treatment. All these differences were statistically significant. RGD peptide matrix was well tolerated. RGD peptide matrix promoted and accelerated healing in this study and thus may be able to reduce morbidity and treatment costs of partial-thickness burns in pediatric patients.

Administration, Topical↗
PubMedDate not supplied

Self-inflicted patient burns: suicide versus mutilation.

Though suicide by burning is well-described, little information is available regarding patients who mutilate themselves by burning without suicidal intent. We reviewed 31 patients admitted from 1980 to 1991 with self-inflicted burns to describe differences between self-mutilation and attempted suicide (AS). In 16 patients who had mutilated themselves, mean burn size was 1.6% TBSA (range 0.3% to 9.0% TBSA) compared with 35.4% TBSA in the 15 patients who had attempted suicide (range 11.5% to 90% TBSA; p < 0.0001). Twelve of 15 patients who had attempted suicide used flammable liquids for self-immolation, whereas patients who had mutilated themselves often used techniques that they could control, including scalding, chemicals, and contact injuries. Most patients in both groups and previous histories of psychiatric disorders. Self-mutilators had a high incidence of personality disorders (56%), whereas the AS group more frequently suffered from depression (47%). Nine (56%) patients who had mutilated themselves had previous self-inflicted burns, compared with only one patient in the AS group. Mean lengths of stay, number of surgeries, and hospital and physician charges were higher for the AS group. Case examples of both types of injuries are presented. Burn care professionals should be familiar with syndrome of self-mutilation by burning. Patients often present with puzzling injuries and require psychiatric treatment in addition to burn care.

Adult↗
PubMedDate not supplied

Lazaroids--not nitric oxide synthetase inhibitors--improve hemodynamics after thermal injury in anesthetized guinea pigs.

Our objective was to study the effects of a lipid peroxidation inhibitor (U74389G) and nitric oxide synthetase inhibitor (NG-methyl-L-arginine) on hemodynamic stability in burn shock. The design was a prospective, placebo control, randomized, and masked multigroup study in a research laboratory of a university hospital. We used 24 guinea pigs (N = 24), and induced burn shock by a scalding thermal injury (75 degrees C) to 35% of their body surface area. Hemodynamics and gas exchange were observed for 90 minutes after the burn injury in the four groups: no burn, burn-control, burn-U74 (10 mg/kg U74389G), and burn-LNMA (20 mg/Kg NG-methyl-L-arginine). The percentage of mean arterial pressure, normalized for the initial value at 30 minutes after the burn injury, decreased in all groups over time but was not significantly different in any group. The normalized percentage of flow also decreased over time in all groups with the slope of the linear regression significantly less in the burn-U74 group (-0.32 95% CI, -0.05, -0.15) and the no burn group (-0.37 95% CI, -0.48, -0.26), compared with the burn-control group (-0.66 95% CI, -0.77, -0.56) and the burn-LNMA group (-0.66 95% CI, -0.77, -0.56). The slope of the linear regression for the normalized percentage of systemic vascular resistance was significantly more marked in the burn-control group (2.45 95% CI, 1.35, 3.54) and the burn-LNMA group (1.22 95% CI, 0.89, 1.55) compared with the no burn group (0.16 95% CI, 0.11, 0.44) or the burn-U74 group (0.34 95% CI, 0.06, 0.74). The burn shock resulted in hemodynamic instability as measured with increased systemic vascular resistance, decreased cardiac output, and mean arterial pressure. Use of a lazaroid (U74389G), not a nitric oxide synthetase inhibitor (NG-methyl-L-arginine), altered the clinical course after thermal injury. These data suggest the importance of lipid peroxidation and free radicals as secondary mediators in the evolution of burn shock.

Analysis of Variance↗
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Effects of recombinant bactericidal, permeability-increasing protein on bacterial translocation and pulmonary neutrophil sequestration in burned mice.

Burn injury induces bacterial translocation (BT) from the gut in multiple animal models. Etiologic factors contributing to BT may be an ischemia-reperfusion injury to the gut, the release of inflammatory cytokines, oxygen metabolites and other mediators, and cytotoxic effects mediated by endotoxin (lipopolysaccharide). Bactericidal, permeability-increasing protein is a neutrophil granule protein with potent bactericidal and lipopolysaccharide-neutralizing activities. The use of this protein has not been previously reported in a burn-injury model. The purpose of this study was to determine whether recombinant bactericidal, permeability-increasing protein (rBPI23) affects the incidence of BT and myeloperoxidase content in lung tissue (a measure of leukocyte sequestration) in a burn-injury model. Mice received a 32% total body surface area, full-thickness, scald burn, and 10 mg/kg body weight rBPI23 in saline solution was given by intraperitoneal injection at 0, 3, and 6 hours after the burn. Control animals received intraperitoneal saline solution only. All animals received a total of 1 ml saline solution intraperitoneally immediately after burn injury for fluid resuscitation. At 24 hours after burn injury, mesenteric lymph nodes (MLN) were harvested, homogenized, and plated. Lung tissue was harvested and assayed for myeloperoxidase. Burned mice treated with rBPI23 had significantly (p = 0.005, Fisher's Exact Test, two-tailed) decreased incidence of BT, compared to burned mouse controls. Leukosequestration into lung tissues was not affected by rBPI23. Postburn administration of rBPI23 reduces but does not abolish the incidence of BT after burn injury in mice, perhaps by reducing intestinal injury during burn shock and the ischemia-reperfusion period by inhibiting the effects of lipopolysaccharide. An alternate explanation may be that rBPI23 could increase clearance and killing of bacteria by host defenses.

Animals↗
PubMedDate not supplied

Insulin-like growth factor-I liposomal gene transfer and systemic growth hormone stimulate wound healing.

Many of the anabolic effects of growth hormone (GH) act through insulin-like growth factor-I (IGF-I). Systemic administration of GH in combination with IGF-I has been shown to stimulate wound reepithelialization, however, it causes hyperglycemia or hypoglycemia, respectively. We hypothesize that very low doses of IGF-I in a liposome form will have the same positive wound-healing effect when administered locally as the higher doses of GH plus IGF-I given systemically. To test this hypothesis, rats were given a 40% TBSA full-thickness scald injury and received either placebo IGF-I (5.0 mg/kg/day, subcutaneously), IGF-I liposome (0.9 microgram/kg/week, subcutaneously), or a combination of GH and IGF-I, or IGF-I liposomes for 8 weeks. GH in combination with IGF-I showed a significant increase in postburn weight. Wound reepithelialization, measured by computerized planimetry as percentage original wound area, was significantly increased in rats receiving GH plus IGF-I, GH plus IGF-I liposomes, and IGF-I liposomes when compared to sham, or IGF-I (p < 0.05). Results indicate that small doses of IGF-I, delivered in the form of liposomes, are equally effective in increasing burn wound reepithelialization as the higher doses of GH plus IGF-I, or GH plus IGF-I liposomes.

Animals↗
PubMedDate not supplied

Childhood burns in camping and outdoor cooking accidents: a focus for prevention.

We have seen increasing numbers of children who present with serious burns related to camping and outdoor cooking, prompting this 5-year review. Of 34 children (21 boys and 13 girls), with an average age of 5.2 years (4 months to 17 years) and average burn size of 15% (1% to 98%) cared for (4 as outpatients and 30 as inpatients), there was one fatality (3%). Mechanisms of injury included falling into free pits, throwing flammables into grills or pits, placing hands on hot objects in or near a fire, walking or falling into hot embers from an extinguished fire, spills from insect repellant candies, tent fires, burning of paper eating utensils, and cooking scalds. We have initiated a directed prevention program with the regional state park systems.

Accident Prevention↗
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Pathogenesis of fever in a rat burn model: the role of cytokines and lipopolysaccharide.

We investigated the possible causal relationship between interleukin-6 (IL-6) and increased body temperature (T(B)) in a rat burn model. Transmitters for measuring core temperature and estimating activity were implanted in the abdominal cavity. Animals in the burn group were clipped and received full-thickness scald burns to 45% to 55% of the body surface area, and control animals were clipped. T(B) and activity were measured continuously through the tenth postburn day. Carotid lines were placed, and serial blood samples obtained for lipopolysaccharide, IL-6, and tumor necrosis factor-alpha assay. From the third through the tenth postburn day, the burn group had a consistently significantly higher T(B) during light hours than the control group did (average, 0.45 degrees C +/- 10 degrees C, p = 0.0001). Differences in activity during light hours were not significant between the two groups, therefore, do not account for the observed significant difference in T(B). The average IL-6 serum levels were 3.5-fold higher for the burned animals. In this study, burn and control serum levels of IL-6 demonstrated positive correlation with T(B). These data suggest, but do not prove, a causal relationship between IL-6 and fever in the rat burn model, and make it unlikely that circulating systemic lipopolysaccharide is the cause.

Animals↗
PubMedDate not supplied

The role of interstitial starling forces in the pathogenesis of burn edema.

The formation and sustainability of burn edema require substantial change in net microvascular forces. We directly measured interstitial hydrostatic pressure (Pi) and total interstitial absorptive pressure (Pi + IIi), in dermis of anesthetized sheep, before and after a 70% to 85% total body surface area scald and during fluid resuscitation. The most rapid change occurred in Pi in the burn wound, which rapidly decreased from its baseline value of approximately -2 mm Hg to -11 mm Hg in the first 5 minutes, and thereafter increased but remained approximately -4 mm Hg through 4 hours of resuscitation. Pi in nonburned skin slowly increased from its preburn level -2 mm Hg, to become positive +1 mm Hg after 4 hours of resuscitation. The total interstitial absorptive pressure, Pi + IIi, slowly declined similarly from 15 to 16 mm Hg to approximately 10 to 11 mm Hg over 6 hours of resuscitation in both burned and nonburned dermis. Taken together, these data suggest that the rapid formation of burn edema is the result of development of a negative Pi in the burn wound, and its sustainability is the result of a large increase in interstitial compliance. Edema in nonburned skin did not start until after fluid resuscitation was initiated, and then developed as the plasma oncotic pressure declined from 21 to 10 mm Hg.

Animals↗
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Burn area color changes after superficial burns in childhood: can they be predicted?

Pigmentation changes after superficial burn injuries are often difficult to predict. We analyzed a sample of patients with burn injuries, looking for clinical indicators of predictable color changes in burn wounds. A sample of 50 children, predominantly those with pigmented skins, who had sustained superficial partial-thickness, (second degree) thermal, scald, or friction burns, were retrospectively grouped. Chemical and electric burns, and those needing skin grafts were excluded. Forty-one patients returned for interview and examination, an average of 63 months after injury (range, 3 to 276 months). All patients had their skin color graded in terms of the Fitzpatrick scale--a numeric scale that combines innate skin color plus reported history of skin response to sun exposure, to assign a value from 1 to 6, where white skin that reddens but does not tan on sun exposure is 1 and heavily pigmented black skin is 6. The burn site, as well as unburned areas of control skin, were tested for reflectance and luminance with use of a well-validated spectrophotometric technique. As an addendum, clinical photographs of a further 50 patients were similarly analyzed. During the first 3 years after injury, burn site color changes were variable. Subsequently, there was cumulative hyperpigmentation at the burn site, provided that the melanocyte-bearing deep dermis had not been destroyed. Hyperpigmentation correlated significantly with skin color, as quantified by the Fitzpatrick scale (p < 0.01), and with time after injury (p < 0.05).

Burns↗