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PubMedDate not supplied

Thermal injury and gastrointestinal function. I. Small intestinal nutrient absorption and DNA synthesis.

The effect of acute burn trauma, produced by scalding hot water, on rat small intestinal nutrient absorption and DNA synthesis has been examined. Burned rats showed decreased small-intestine mucosal weight and altered small-intestine transport of nutrients (calcium, glucose, or amino acid) in vitro. In addition, there was decreased 3H-thymidine incorporation into intestinal DNA in vivo and decreased intestinal thymidine kinase activity in vitro 18 hours after acute burn. These data suggest that after the severe stress produced by acute burn trauma, there is altered small-intestine nutrient absorption and DNA synthesis. These alterations may affect delivery of nutrients by the gut to the burn patient.

Animals↗
PubMedDate not supplied

Thermal injury and gastrointestinal function. II. Evidence for the production of hepatic dysfunction in the rat following acute burn injury.

Following acute thermal injury to rats produced by scalding water, there was marked elevation of a number of plasma enzyme activities, including GOT, GPT, and 5'-nucleotidase, suggesting hepatic dysfunction. Changes in plasma enzyme activities were observed within minutes following application of acute burn trauma, and remained elevated for at least one month. The magnitude of the elevations of the plasma enzyme activities was dependent upon the length of time the acute burn trauma was applied to the skin and/or the percentage of skin surface area burned. These changes in plasma enzyme activity correlated with histologic examination of the hepatic tissue, indicating single cell necrosis. These data suggest that acute burn trauma to rats is associated with altered hepatic function.

5'-Nucleotidase↗
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Burned-and-battered adults.

The existence of a previously unrecognized group of patients, burned-and-battered adults, has been recognized. This retrospective review identifies some of the characteristics of the 41 burned-and-battered adults admitted to a burn center during a two-year period. The typical scenario was a domestic quarrel that included a male victim, a female assailant, and a scald injury involving the victims anterior trunk and upper extremity. The average burn size was 14% of the total body surface area. Four victims died as a result of their injuries. Although these victims represented only 10% of all patients admitted to the burn center, there may be many more undetected burned-and-battered adults. Only when the seriousness and magnitude of the problem are recognized can appropriate medical, legal, and social interventions be made to meet the needs of these burned patients.

Adult↗
PubMedDate not supplied

Skeletal changes after burn injuries in an animal model.

Musculoskeletal deformities can develop after burn injuries. Seventy-five skeletally immature Sprague-Dawley rats were examined after infliction of full-thickness lower extremity scald burns to assess longitudinal growth, joint integrity, and bone composition. Longitudinal bone growth in the immediate postburn period was depressed. However, with the resumption of feeding and activity, normal growth ensued, unless the epiphyseal cartilage had been damaged by septic extension of the wound. Degenerative joint changes occurred in the burned limbs of six animals. Significant soft tissue contractures and collapse of the supporting subchondral bone were present in each of the affected knee joints. There was no evidence of joint sepsis. Large amounts of periosteal new bone consistently formed along the tibia beneath the burn wound. Sequential injections of fluorescent bone markers demonstrated that the stimulus for new bone formation corresponded with the presence of an open granulating burn wound. No further pathologic new bone formed after the wound had healed fully.

Animals↗
PubMedDate not supplied

Effect of topical applications of silver sulfadiazine on the natural killer cell activity in a rat model of thermal injury.

The effect of topical application of silver sulfadiazine cream on the natural killer (NK) cell cytotoxicity was studied in a rat model of thermal injury. The rats were given a 30% total body surface area scald injury and the NK cell cytotoxicity was studied in rats at different days postinjury with or without treatment with silver sulfadiazine. The NK cell activity was observed to be significantly (P less than .0025) suppressed at day 7 postinjury in nontreated burned rats compared with control sham burned animals. Interestingly, in rats treated with silver sulfadiazine twice daily, no suppression in NK cell activity was observed. The application of base cream (without silver sulfadiazine) did not have any significant effect on the NK cell activity in burned rats. The data show that the effect of silver sulfadiazine on NK cell activity may be due to the sulfadiazine component, since the serum levels of sulfadiazine (33.7 +/- 1.9 micrograms/dL) were observed to be maximal at day 7 postinjury.

Administration, Cutaneous↗
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Complications of burn care in patients with neurologic disorders.

Patients with neurologic disorders are frequently burned in mishaps related directly to their diseases. Once burned, these patients face a mortality rate significantly greater than that of the burn population as a whole. To assess the impact of neurologic disease on burn care, we reviewed the records of 37 patients admitted to our burn center with burns and neurologic illness. Thirty-three patients (89%) sustained injuries directly related to their neurologic problems, the most frequent being bathtub scalds (29.8%) and scald/spills (24.3%). We compared 31 of these patients having nonextensive burn injuries (less than or equal to 25% total body surface area) to a control population with similar-sized burns from our burn unit during the study period. This comparison revealed significantly longer length of stay for the neurologically impaired sample. We presume that costs of care are also increased for this sample. The high frequency of burn injury among neurologically impaired persons, coupled with the greater difficulty in caring for them, suggests that this group should receive intensive burn prevention educational efforts.

Accidents, Home↗
PubMedDate not supplied

The role of oxygen-derived free radicals in burn-induced myocardial contractile depression.

The release of oxygen free radicals from ischemic myocardium has been implicated as a causative factor of cardiac dysfunction after thermal injury. In this study, isolated coronary perfused guinea pig hearts were used to determine if free radical scavengers improve left ventricular (LV) intrinsic contractile response to burn shock. Parameters measured included peak isovolumic LV pressure (LVP) and maximal rate of LVP rise (+dP/dtmax) and fall (-dP/dtmax) at a constant preload. Control animals were immersed in body temperature water and divided into four groups: Group 1, untreated N = 10; Group 2, control animals treated with unbound superoxide dismutase (SOD), N = 5; Group 3, control animals treated with ficoll-SOD, N = 5; and Group 4, control animals treated with PEG-SOD, N = 5. Scald burn equivalent to 45% of total body surface area was produced in 64 animals. Fluid resuscitation was initiated immediately after burn in all animals, and animals were then divided into seven burn experimental groups. In Group 5, 10 animals were treated with fluid alone, lactated Ringer's, 4 mL/kg/% burn. Burned animals in Group 6 (N = 10) received a reduced volume of Ringer's 2 mL/kg/% burn plus unbound-SOD, 50 mg/kg; 10 animals in Group 7 received this volume of Ringer's plus ficoll-SOD, 50 mg/kg. In groups 8, 9, and 10 animals were given fluid, lactated Ringer's, 2 mL/kg/% burn plus varying doses of PEG-SOD (Group 8: N = 9, 1,000 U; Group 9: N = 10, 6,000 U; Group 10: N = 5, 12,000 U). In Group 11 (N = 10), animals received SOD-PEG, 6,000 U, plus catalase, CAT-PEG, 6,000 U, given with 4 mL/kg/% burn lactated Ringer's solution. Hypotension, hypothermia, and hemoconcentration were similar in all animals after thermal injury, regardless of treatment regimen. Burn hearts showed significantly lower LVP, +dP/dt max, and -dP/dt max than control hearts (P less than 0.05). Compared to controls, coronary pressure and coronary vascular resistance were significantly higher in all treated burn groups. There was no significant difference in heart rate or time to peak pressure or time to maximal contraction or relaxation among the groups. Left ventricular function curves for burned hearts were shifted downward and to the right of curves obtained from control hearts (P less than 0.01), regardless of scavenger treatment. PEG-SOD, 6,000 U, improved left ventricular contractility (+dP/dt) at maximal levels of end-diastolic pressure but deficits in left ventricular pressure and relaxation persisted.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
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Effect of thermal injury and immunosuppression on the dissemination of Candida albicans from the mouse gastrointestinal tract.

Candida albicans dissemination through the gastrointestinal tract was examined in mice given a thermal injury, immunosuppressive therapy, or both. After gastrointestinal tract colonization with C. albicans, mice were initially subjected to a 20% total body surface area, full-thickness, dorsal scald burn. Only one mouse in the burned group (5%) had evidence of C. albicans in the liver at the time the mice were killed. No dissemination was observed in sham-burned animals. When mice were immunosuppressed with cyclophosphamide, an increased incidence of gastrointestinal tract dissemination was noted in burned (31%) and sham-burned (23%) mice; however, only 3 days after burn was there a significant difference in dissemination between burned and sham-burned mice (p less than 0.02). This corresponded to the day of severest neutropenia in response to cyclophosphamide treatment. The results of the study indicate that C. albicans can disseminate from the gastrointestinal tract in response to thermal injury, but a significant suppression of the immune response must occur for the event to be commonplace.

Animals↗
PubMedDate not supplied

Effect of acute burn trauma on phagocytic activity of the reticuloendothelial system in rats.

The effect of acute burn trauma on phagocytic activity of the reticuloendothelial system measured in vivo with technetium 99m sulfur colloid was examined in rats subjected to acute burn trauma. After the scald injuries (10-second, full-thickness burns) were induced, a reduction in phagocytic activity by the spleen took place with an accompanying increase in the uptake of colloid material by the lungs. Uptake of colloid material by the liver was essentially unchanged. These uptake changes, observed within hours after the inducement of acute burn trauma and apparently continuing for 7 days after burn injury, may explain, in part, the development of septicemia in patients with burns because altered phagocytic activity of the reticuloendothelial system can result in subsequent overabundance of microorganisms and bacteria in the blood.

Animals↗
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Major burns managed without blood or blood products.

Four major burns (two flame, one scald, one electrical) were managed without administration of blood or plasma. Serial changes in hemoglobin, and serum albumin and total protein measurements were compared with those of controlled patients matched in age and total body surface area burned who were treated by standard methods. Hemoglobin values were lower but within one standard deviation, although serum protein and albumin measurements fell more than one standard deviation below mean values observed in control patients at comparable times after burn injury. Important treatment principles that were instrumental to recovery include a high-calorie, high-protein diet, iron supplementation, use of pediatric blood sampling techniques, and monitoring for and prophylaxis against infection while allowing eschar to separate spontaneously rather than performing early debridement. Amputation of mummified electrically burned limbs at more proximal levels, including marginally viable muscle, is recommended to minimize infection and decrease blood loss associated with customary conservative serial debridements.

Adult↗
PubMedDate not supplied

Cytomegalovirus infection promotes bacterial translocation in thermally injured mice.

Thermally injured mice that were given intraperitoneal injections of murine cytomegalovirus (MCMV) appeared to be clinically septic and to have increased mortality rates. To evaluate the possible role of MCMV infection in promoting bacterial translocation in burned mice, mesenteric lymph nodes were cultured from two strains of mice (BALB/c and CBA) that were given thermal injuries alone, MCMV alone, or both. BALB/c mice injected with 5 X 10(5) plaque-forming units MCMV following a 15% to 16% total body surface area scald injury had increased incidence of positive mesenteric lymph node cultures compared with other groups. No intestinal mucosal histologies, mucosal dry weights, or wet-to-dry weight ratios in any animals were abnormal. Differences in cecal bacterial concentrations were not observed. Murine cytomegalovirus infection appears to enhance bacterial translocation in this model.

Animals↗
PubMedDate not supplied

Burns from hot oil and grease: a public health hazard.

We examined the incidence, etiology, and morbidity of burns due to hot oil and grease. Over a 10-year period from 1976 to 1985, of 1818 patients hospitalized for burns, 85 (4.7%) injuries were due to hot grease or oil. The mean age was 20 years; 34% of patients were less than 8 years old. The mean total body surface areas of second- and third-degree burns was 11.5% (range 0.5% to 40%), and the average length of hospital stay was 19.6 days. Fifty-eight percent of patients required split-thickness skin grafting (n = 49), three required intubation, and one required tracheostomy. Seventy-eight percent of oil burns occurred in the home. The most common circumstances consisted of children who grabbed the handle or electric cord of a frying pan and pulled the hot oil down onto themselves. (Nineteen of the 29 children were less than 8 years old (66%).) Burns due to cooking oil and grease are associated with considerable morbidity. The high boiling point, high viscosity, and potential combustibility of oil increase the potential soft-tissue damage when compared with typical scald injuries from hot water. The dangers of children pulling on the appliance, the dangers of transporting hot oil, the importance of supervision while children are cooking, and the importance of knowledge of the management of grease fires is stressed. Public education is needed to underline the potential seriousness of these burns.

Accidents, Home↗
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Enhancement of humoral immunity by heterologous lipid peroxidation products resulting from burn injury.

Lipid peroxidation products (conjugated dienes) extracted from the plasma of scald-burned rats were injected intraperitoneally in mice before immunization of the mice with sheep erythrocytes. Five-day plaque-forming cell assays showed that mice receiving conjugated dienes isolated from the plasma of burned rats had enhanced specific immunoglobulin M antibody production compared to mice receiving dienes from normal rat plasma or sheep erythrocytes alone. These observations suggest that lipid peroxidation products in the plasma of burned animals may modulate the humoral immune response.

Animals↗
PubMedDate not supplied

Reperfusion injury in burned rats after delayed fluid resuscitation.

Organ failure from ischemic injury is common in deaths that are due to burn when fluid resuscitation is not performed. Organ perfusion after a delay in resuscitation, however, may induce or even accelerate ischemic organ damage. To study this phenomenon, 40 rats were classified (n = 10) to serve as normal control, burn with no resuscitation, burn with early fluid resuscitation, and burn with delayed resuscitation groups. A modified Walker burn model was used to inflict 50% total body surface area scald burns on the rats. Cellular energy metabolism and tissue water content of several vital organs were measured at 8 hours after burn injury. Adenosine triphosphate, total adenine nucleotides, and energy charge in liver, heart, and kidney tissues were significantly lower (p less than 0.05) with delayed fluid resuscitation compared with early resuscitation. Furthermore, in heart and kidney tissues adenosine triphosphate, total adenine nucleotides, and energy charge were significantly lower in the delayed resuscitation group compared with the group that received no fluid resuscitation. This indicates that heart and kidney tissue are more viable at 8 hours after burn injury, with no fluid resuscitation compared with delayed resuscitation. Water content of lung and muscle tissue were significantly lower (p less than 0.05) in the burn group that received no fluid resuscitation compared with that in early and delayed resuscitation groups. Water content of muscle was significantly greater with delayed resuscitation compared with the early resuscitation group. Results indicate that delayed fluid resuscitation in cases of burn shock may disrupt the cellular energy metabolism in some vital organs and cause skeletal muscle edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMedDate not supplied

Tumor necrosis factor mediates hypertriglyceridemia during thermal injury in mice genetically susceptible to lipopolysaccharides.

A rise in plasma triglycerides has been noted after thermal injury in a number of animal species including humans. In this study we identified a factor, tumor necrosis factor, which was responsible for increased plasma triglycerides during thermal injury that was induced by scalding. Two strains of mice that differed genetically in susceptibility to lipopolysaccharides were used. These were CH3HEB/HeJ (LPS-) and CH3HEB/FeJ (LPS+). A 15% total body surface area was burned; this resulted in an increase of plasma triglycerides of 126% of preburn levels in the LPS+ strain 24 hours after burn injury. No change in triglycerides was noted in the LPS- mice at any time after burn injury. Sera from LPS+ mice at 1 to 2 hours after burn injury was injected into nonburned animals of the same strain; this caused a 62% +/- 5% increase in plasma triglycerides 24 hours after injection. When thermally injured LPS+ mice were injected with anti-tumor necrosis factor-alpha at 1 hour after injury, they did not show a rise in plasma triglycerides at any time between 24 to 72 hours after injury. Hepatic secretion of triglycerides was also measured 1 day after burn; the average secretion of triglycerides was significantly reduced (2.69 +/- 0.36 mg/kg/hr, compared with 3.83 +/- 0.15 mg/kg/hr for the control). We conclude that tumor necrosis factor, a cytokine that inhibits lipoprotein lipase, causes hypertriglyceridemia during thermal injury in spite of a decreased secretion of triglycerides. This is the first report that demonstrates that hypertriglyceridemia that is secondary to thermal injury is induced by tumor necrosis factor.

Animals↗
PubMedDate not supplied

The effects of burn trauma on adenosine 3':5' cyclic monophosphate, inositol trisphosphate, and contraction in mouse gastrocnemius muscle.

This study examines the nature of skeletal muscle weakness (dysfunction) that is exhibited by patients who have incurred large-size body surface area burns (greater than 30%). It uses the mouse model of scald-burn injury in which groups of mice with varying burn sizes (i.e., 20%, 30%, and 50%) and time-matched controls were evaluated on postburn day 21. The primary purpose of this work was to evaluate secondary messenger cascades in gastrocnemius muscle relative to increasing burn size. Muscles that were distantly located to the actual site of burn injury were used for twitch analyses to measure active tension. The second messengers, adenosine 3':5' cyclic monophosphate (cAMP), inositol, 1,4,5-trisphosphate (IP3) and Ca2+, were measured with radioisotopes. The results of this study indicate that perturbations in the cAMP-IP3 cascade may be responsible for increasing myoplasmic Ca2+, which leads to dysfunction. The long-term goal of this work is to aid in the alleviation of chronic skeletal muscle dysfunction that leads to sustained debilitation and prolonged rehabilitation in patients with burns.

Animals↗
PubMedDate not supplied

Automobile carburetor- and radiator-related burns.

Seventy-nine persons who had sustained automobile engine carburetor- and radiator-related burns were admitted to Grady Memorial Hospital Burn Unit between June 1, 1984 and September 30, 1990. Forty patients with carburetor-priming flame burns had a mean age of 31.5 years, a mean burn size of 13.4% total body surface area, and a mean length of stay of 13.8 days. There were 37 male patients. Four patients had an inhalation injury. Twenty-two surgical procedures were performed on 13 patients. One patient was an innocent bystander, and one patient died. The clothing of 16 patients had ignited, which resulted in larger, deeper burns and in one death. Burns predominantly involved the right sides of the face, head, and torso; the right upper extremity; and the right hand. Thirty-nine patients had scald burns that were associated with uncapping a radiator. These patients had a mean age of 29.6 years, a mean burn size of 8.9% total body surface area, and a mean length of stay of 6.4 days. There were 36 male patients and three innocent bystanders. One autografting procedure was performed, and there were no deaths in this group of patients. The burn-prone person is the young adult male. The circumstances that result in such dangerous behavior are predictable, and resultant burn injuries are preventable.

Accidents, Occupational↗
PubMedDate not supplied

Burns caused by automobile radiators: a continuing problem.

In spite of the fact that injury warning labels have been placed on radiator caps for the last 15 years, automobile radiator scald burns continue to be a burn prevention problem. The temperature of radiator fluid may be as high as 100 degrees F to 250 degrees F in a properly functioning car and higher in an overheated vehicle. From 1974 to 1990, 100 patients with burns that were caused by automobile radiators have been admitted to the Parkland Memorial Hospital Burn Unit (1.5% of acute admissions). Eighty-two percent of the injuries occurred in the summer months, and 93% of the patients were male. Mean age was 31 +/- 17 years (range, 8 months to 79 years), and mean burn size was 11.3% total body surface area (TBSA) (range, 1% to 32%) with a mean full-thickness burn size of 0.6% TBSA. Length of stay was 7 +/- 7.4 days (range, 1 to 38 days). Burns to the face, neck, and trunk necessitated most admissions. Although there were no deaths, five patients required intensive care for airway monitoring; mean length of stay was 6 days. One patient required endotracheal intubation for a total of 11 days. Ten patients required one or more skin grafting procedures, and three patients required burn resuscitation. Four patients sustained minor ocular injuries. A subgroup of patients demands special review: 10 children younger than 10 years of age (mean age, 4.1 years) of which 70% were boys. Mean burn size was 15.5% TBSA; mean full-thickness burn size was 2.4% (four times larger than the mean burn size for the adult population).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗