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[Intestinal lymphatic circulation is one of the important portals for microbial translocation after thermal injury].

The goal of this study was to determine whether the bacteria and endotoxin from GI tract could pass through the intestinal lymph circulation to the systemic circulation after severe thermal injury. Lymphatic fistula of intestine was created in 46 Wistar rats the rats were then divided randomly in scald and control groups. In scald group, animals were sustained with 30% TBSA full-thickness scald. The items studied were, the dynamic changes in intestinal lymph endotoxin level, the qualitative and quantitative bacterial culture, and pathological alterations in ileal mucosa within 24 hours postburn. Results showed that the levels of intestinal lymph endotoxin and the positive culture rate and counting of bacteria were evidently increased, and ileal mucosal lacteals were dilated and epithelial cells were necrotic and denudated in scald group. These suggested that the intestinal lymph circulation is one of the important portals for endotoxin and microbial translocation after severe thermal injury, and the intestinal mucosal damage is an important factor in pathogenesis.

Animals↗

The mechanisms, intensity of treatment, and outcomes of hospitalized burns: issues for prevention.

The mechanisms, intensity of treatment, and outcomes of fire and burn injuries that result in hospitalizations were investigated to assist in ongoing prevention efforts. All hospital discharge records with a fire or burn diagnosis were extracted from the 1994 Pennsylvania statewide hospital discharge data. Cases were categorized into 4 specific burn mechanisms: conflagrations, controlled fires, clothing ignition, and hot substances and scalds. A total of 3173 cases were reported for a rate of 26.3 per 100,000 people. Hot substances and scalds were the most common mechanism (58%) of fire and burn hospitalizations. While most injuries resulting from clothing ignition, conflagrations, and hot substances and scalds were reported as unintentional, 25% of the cases resulting from controlled fires were reported as self-inflicted. The mean hospital charge per hospitalization day (which reflected the intensity of burn treatment) was 2783 but varied significantly by mechanism (P < .001): $4102 for cases resulting from conflagrations; $3402 for cases resulting from clothing ignition; and $2187 for cases resulting from hot substances and scalds. The overall in-hospital case fatality rate was 2.4%. Prevention strategies for these injuries are outlined for injury control professionals.

Accident Prevention↗

Understanding the mechanism of action of the exfoliative toxins of Staphylococcus aureus.

The exfoliative toxins of Staphylococcus aureus are responsible for the staphylococcal scalded skin syndrome, a blistering skin disorder that particularly affects infants and young children, as well as adults with underlying disease. Their three-dimensional structure is similar to other glutamate-specific trypsin-like serine proteases with two substrate-binding domains and a serine-histidine-aspartate catalytic triad that forms the active site. However, unlike other serine proteases, the exfoliative toxins possess a highly charged N-terminal alpha-helix and a unique orientation of a critical peptide bond, which blocks the active site of the toxins so that, in their native state, they do not possess any significant enzymatic activity. The target for the toxins has recently been identified as desmoglein-1, a desmosomal glycoprotein which plays an important role in maintaining cell-to-cell adhesion in the superficial epidermis. It is speculated that binding of the N-terminal alpha-helix to desmoglein-1 results in a conformation change that opens the active site of the toxin to cleave the extracellular domain of desmoglein-1 between the third and fourth domains, resulting in disruption of intercellular adhesion and formation of superficial blisters. Elucidating the mechanism of action of the toxins and identifying desmoglein-1 as their specific epidermal substrate has not only given us an insight into the pathogenesis of the staphylococcal scalded skin syndrome, but also provided us with useful information on normal skin physiology and the pathogenesis of other toxin-mediated diseases. It is hoped that this knowledge will lead to development of rapid screening and diagnostic tests, and new antitoxin strategies for the treatment and prevention of the staphylococcal scalded skin syndrome in the near future.

Animals↗

Rapid growth of regenerating axons across the segments of sciatic nerve devoid of Schwann cells.

The characteristic response of Schwann cells (SC) accompanies peripheral nerve injury and regeneration. To elucidate their role, the question of whether or not regenerating axons can elongate across the segments of a peripheral nerve devoid of SC was investigated. Rat sciatic nerve was crushed so that the continuity of SC basal laminae was not interrupted. A segment about 15 mm long distal to the crush was either repeatedly frozen/thawed to eliminate SC or scalded by moist heat which, in addition, denatured the proteins in the SC basal laminae, too. Both sensory and motor axons grew rapidly across the frozen/thawed segment of the nerve. Their rate of elongation was reduced by only 30% in comparison to control crushed nerves. SC were not present along the path of growing axons adhering tightly to the bare SC basal laminae. The rate of elongation of regenerating sensory and motor axons in scalded nerve segments was eight times lower than in control crushed nerves. SC were present in that part of the scalded region that had been invaded by the regenerating axons but no further distally. These results suggest that acellular basal laminae of SC provide very good, although not optimal, conditions for elongation of regenerating sensory and motor axons. If biochemical integrity of the basal lamina is destroyed, the regenerating axons must be accompanied or preceded by viable SC. and axon elongation rate is significantly reduced.

Animals↗

Effects of graded thermal injury on microvascular permeability at the site of injury.

To define whether capillary permeability traits at the site of a burn differ according to injury severity, a canine hind leg lymphatic was cannulated to measure macromolecular permeability in response to three different scalding solutions. Leg venous pressure was raised to approximately 40 mm Hg and maintained until a minimal lymph-to-plasma total protein ratio (CL/CP)min and steady-state lymph flow (QL; microliter/min/100 g) was attained. The protein reflection coefficient (1-CL/CP), fluid filtration coefficient (Kf; microliter/min/mm Hg/100 g), and QL were determined before and for 6 hr after a 5-sec hind paw immersion in either 100 degrees C (n = 7), 80 degrees C (n = 7), or 70 degrees C (n = 7) water. A group of five animals served as controls. In the absence of any systemic hemodynamic alterations, the 100 and 80 degrees C scald groups experienced significant (P < 0.05, ANOVA) increases in QL, CL/CP, and Kf as compared to respective preburn values and time-matched unburned control values. Most monitored parameters were significantly higher following 100 degrees C injury vs 80 degrees C injury. Parameters in the 70 degrees C group did change after scald, but were not significantly different from preburn values or from the control group. Alterations in capillary permeability to protein and fluid flux measured at the burn site are graded, not all or none phenomena, being dependent upon the severity of injury.

Analysis of Variance↗

Survival time and prevention of side effects of intraperitoneal hyperthermic perfusion with mitomycin C combined with surgery for patients with advanced gastric cancer.

In an attempt to prevent postoperative intraperitoneal recurrence in patients with advanced gastric cancer and consequently to improve survival time, we treated patients with intraperitoneal hyperthermic perfusion (IPHP) using mitomycin C (MMC) combined with surgery. There were 60 patients with advanced gastric cancer who were treated with IPHP (long-term study) group, and the survival of this group was compared with the outcome in 52 patients with advanced gastric cancer treated with surgery alone (control group). To avoid or diminish side effects derived from scald injury of the peritoneal surface due to IPHP, 50 mg/kg of cimetidine was given intravenously just before administration of IPHP. For prophylaxis of anastomotic leakage, duodenostomy using a Foley catheter was performed. The 60 patients who were treated with IPHP lived longer than the 52 patients in the control group (p = 0.000610). The 3 year survival rate was 45 percent for the former compared with 16 percent for the latter. The intravenous administration of cimetidine just prior to IPHP protected the peritoneoserosal surface from scald injury, even though the heated perfusate exposure was at 44.3-46.3 degrees C for 2 hours. Because the intraabdominal pressure within the duodenum and jejunum was decompressed postoperatively through catheter duodenostomy and the peritoneoserosal surface was protected from scald injury caused by IPHP, anastomotic leakage in the study group was nil. Therefore, IPHP treatment plus aggressive surgery combined with pre-IPHP cimetidine administration are indicated for patients with advanced gastric cancer. The side effects of IPHP and postoperative morbidity can thus be reduced and a favorable outcome obtained.

Adult↗

Effects of metformin on insulin resistance after injury in the rat.

Hyperglycaemia and insulin resistance occur after injury. The effects of the antidiabetic biguanide metformin in injured rats have been studied in order to elucidate the cause of these effects. Metformin (120 mg/kg S. C.) produced a significant hypoglycaemic effect after a 20% dorsal scald but did not affect the blood glucose concentration in non-injured rats. The hypoglycaemic effect did not result from increased insulin secretion. It was associated with a reduction in liver glycogen and an increase in blood lactate concentrations, suggesting that the drug acted by promoting peripheral glucose utilization. This was confirmed by measuring the clearance rate coefficient of [5-3H]glucose. This rate coefficient was significantly increased by metformin treatment (140 mg/kg S. C.) in scalded rats, although it was not affected in non-injured rats. Intravenous glucose tolerance in scalded rats was not improved, probably because of the increased lactate concentration. Metformin (120-160 mg/kg) also produced a hypoglycaemic effect in rats after a 4 hrs period of bilateral hind-limb ischaemia, suggesting that similar metabolic changes occur after these two types of injury.

Animals↗

Studies on the mechanism of insulin resistance after injury in the mouse.

Acute insulin resistance developed after scald injury in the mouse. After 2h plasma glucose and insulin concentrations were each raised about two-fold. Glucose metabolism was studied in vitro in soleus muscles isolated at this time. Glycolysis and glycogen synthesis, and their stimulation by insulin, were unchanged in muscles from scalded mice, and insulin-stimulated transport of 2-deoxyglucose slightly increased, showing that the insulin resistance seen in vivo is not maintained in isolated tissues. Binding of insulin to liver cell membranes prepared from scalded mice was unaltered, whilst that of glucagon was slightly but significantly reduced, showing that changes in polypeptide-hormone receptors can occur within this short time. It was concluded that the acute loss of sensitivity to insulin after injury does not result from a change in insulin receptor sites and presumably reflects an impairment of glucose metabolism in vivo mediated by circulating hormones.

Animals↗

Changes in the microvasculature of skin subjected to thermal injury.

Guinea-pigs were anaesthetized and the caudal 50 per cent of the animal was scalded by immersion in boiling water (100 degrees C) for 3 seconds. Skin samples were obtained from 15 minutes to 24 hours after scalding. The microvascular alterations characteristic of experimentally-induced severe inflammatory responses were studied by electron microscopy. Large intercellular gaps were present in venule endothelium by 15 minutes after injury and in capillary endothelium by 30 minutes after injury. These were detectable for at least 24 hours after the burn. Extensive destruction was observed in peripheral nerves 15 minutes after injury. These were detectable for at least 24 hours after the burn. Extensive destruction was observed in peripheral nerves 15 minutes after injury and in endothelial cells 4 hours after scalding. No morphological evidence of a biphasic pattern of increased vascular permeability was detected in this material. The standardized, reproducible conditions of this study could be used to evaluate the efficacy of anti-inflammatory procedures of burn treatments of skin.

Animals↗

Effects of burns on amino acid levels in rat plasma, liver and muscle.

In this study the influence of a severe catabolic situation (scalding and nitrogen deprivation) on amino acid (AA) metabolism was investigated in an experimental rat model. Scalding of 25 per cent of the total body surface area (TBSA) and hypocaloric alimentation (5.6 kcal per 100 g rat per day, no nitrogen) resulted in mean daily nitrogen losses of -0.27 +/- 0.3 g. Compared to anabolic growing rats this nitrogen catabolism significantly reduced the total free AA content of muscle (-47 per cent, P less than 0.001) and liver (-39 per cent, P less than 0.001). The total plasma AA concentrations were slightly increased in catabolic rats (+10 per cent). In catabolic rats muscle glycine concentrations dropped significantly (-79 per cent, P less than 0.001), while glutamine concentrations decreased by 22 per cent, which was not significant. Branched chain AA and phenylalanine were significantly elevated both in muscle and in plasma. Scalding and nitrogen depletion in rats leads to characteristic changes in plasma, muscle and liver AA concentrations, which are comparable to the results obtained in catabolic patients. However, the low muscle glycine concentrations in burned rats differ from the clinical observations where glutamine rather than glycine concentrations in muscle tissue are reduced. The rat model seems to be well suited for studying the influence of various therapeutic approaches such as different forms of parenteral nutrition or hormonal substitution on nitrogen catabolism.

Amino Acids↗

Burns in young children: a study of the mechanism of burns in children aged 5 years and under in the Hamilton, Ontario Burn Unit.

This paper explores the burn agents involved among children admitted to the Hamilton General Hospital Burn Trauma Unit (BTU), and the severity of their burns. Charts were retrospectively reviewed for all burn cases aged 5 years and under admitted to the BTU between January 1986 and mid-November 1990. Descriptive statistics and one-way analysis of variance were employed. Of the 52 patients aged 5 years and under, two were excluded from the study. The majority (35, 70 per cent) were aged 2 years and under. The mean burn depth for all patients was equivalent to a deep partial thickness burn. Approximately two-thirds of cases resulted from either the preparation or consumption of food or hot liquids, while the remainder suffered from either flame burns or bath-tub scalds. Children burned during food preparation or consumption were younger (mean age 1.8 years) than those sustaining flame burns (mean age 2.7 years) (P = 0.02). Of those burns sustained from either the preparation or consumption of food, 44 per cent were scalds from a cup of hot beverage at the table, 19 per cent were scalds from an electric kettle, and an equal number from a coffee or tea pot sitting at the table. There was a significant difference in both the mean total body surface area of the burn, and the number of days spent in the BTU, according to the agent involved (P = 0.01 and P = 0.004, respectively). Flame and contact injuries were often the most severe. A disproportionate number of burn victims admitted to hospital are infants and toddlers.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Epidemiological survey of burns treated in Ankara, Turkey and desirable burn-prevention strategies.

From 1 January 1979 to 31 December 1993, 1109 patients were admitted to our burn unit located at Hacettepe University. Of the patients, 638 (57.5 per cent) were children (under the age of 16 years). The male to female ratio was 1.4:1 in children, and was approximately 2.6:1 for patients over 16 years of age. Of the 638 paediatric patients, 67 (10.5 per cent) sustained electrical burns. The causes of injury in the remaining 571 cases (89.5 per cent) were hot liquids in 379 (66.4 per cent of the non-electrical burns), flame in 190 (33.3 per cent) and contact burns in two (0.3 per cent). Of the scalds, 296 (78.1 per cent of the scalds), 52 (13.7 per cent), 22 (5.8 per cent) and nine (2.4 per cent) were caused by hot water, milk, meal and oil respectively. Of the flame burns, 21 (11.1 per cent) were due to LPG explosions. Of the 471 adult patients (over 16 years), 159 (33.8 per cent) were injured by electricity. The causes of non-electrical burn injuries were: hot liquid in 25, flame in 274, chemical agents in four, contact in four, and other causes in four. Although our centre is located in Central Anatolia, 41.8 per cent of all patients were referred from the other six regions of Turkey. Of the 1109 inpatients, 645 (58.2 per cent) were injured in Central Anatolia, 279 (25.2 per cent) in the Black Sea Region, 55 (5.0 per cent) in the Mediterranean Region, 18 (1.6 per cent) in the Marmara Region, 34 (3.1 per cent) in the Aegean Region, 52 (4.7 per cent) in Southeastern Anatolia and 26 (2.3 per cent) in Eastern Anatolia. Approximately two-thirds of the patients (419) required one or more surgical interventions, including debridement and grafting, as well as amputation. The most important early complications were acute renal failure (148 patients - 13.3 per cent), sepsis (660 patients - 59.5 per cent) and gastrointestinal haemorrhage (seven patients - 0.6 per cent). The overall mortality rate was 34.4 per cent. The epidemiological pattern of the burns showed that emergency measures should be taken to prevent scalding accidents to children throughout the country, and for electrical burns in adults, particularly those living in the Black Sea Region. In establishing, implementing and directing prevention programmes, regional differences should be taken into consideration.

Acute Kidney Injury↗

Epidemiology of pediatric burn in southern Taiwan.

A 5-year retrospective review of 157 pediatric patients admitted to burn center of Kaohsiung Medical University Hospital (Kaohsiung, Taiwan) was undertaken to identify the incidence, mechanism, and agents of pediatric burn. The highest incidence of pediatric burn was in children aged 1-6 years (57.3%), followed by age group 6-14 years (31.8%). Scald burn (75.2%) made up the major cause of this injury and was dominant in each age group compared to non-scald burn. The kitchen/dining area (57.3%) and living room (29.9%) accounted for the most frequent places where pediatric burns occurred. Among the agents of scald burn, hot drink (49.2%) and soup (32.2%) were the two leading causes. There were more pediatric burns reported in colder seasons (38.2% and 33.1% in winter and fall respectively) and during dining time (19.7% in 11 a.m.-1 p.m. and 35.0% in 5 p.m.-8 p.m.). The results of this report may be closely related to special culinary habits (use of chafing-dish and making hot tea) in the south of Taiwan.

Accidents, Home↗

Analysis of pediatric burns in Nagasaki University from 1983 to 2002.

Pediatric burns are frequently observed: twenty-year burn analysis was performed in a single department, and 354 cases, aged 0-6 years old. The major cause of pediatric burns was scalding (68%) and hot water comprised over half of the scald burns. At 1 year old and younger, the total burn surface area (TBSA) was significantly smaller than from 1 to 6 years old (4.8+/-9.56 versus 10.5+/-18.86%, respectively, p<0.001). TBSA of scald burns was significantly greater than contact burns (8.9+/-15.76 versus 0.9+/-2.0%, respectively, p<0.05). Surgery was performed for 65 patients (18%) and 126 patients were hospitalized (34%). Compared to the first decade of analysis, the second decade had fewer patients (222 versus 142 cases) and lower severity (7.4+/-14.6% versus 6.6+/-13.26%, TBSA). Pediatric burns in younger children should be studied closely as to their causes and with further follow-up.

Body Surface Area↗

Burn injuries in The Netherlands.

The amount and type of burn injuries in The Netherlands are described using Surveillance Systems on treatments at an Accident and Emergency (A&E) department, hospital admissions and fatal injuries and a national survey (to asses treatments by a general practitioner). These data show an estimated 420 persons/year/100,000 inhabitants that are medically treated for burn injuries due to home and leisure accidents in The Netherlands. Fifty percent of all burn injuries concern scalds. But almost all the fatal injuries are caused by fire and flames. From this analysis, three risk groups were identified. Children aged 0-4 and elderly above 84 years have the highest risk of getting admitted to the hospital because of burn injuries. Among the children admitted to hospital, 75% suffer scalds. For injuries treated at an A&E department, people aged 15-24 years appear to have a higher incidence than average. Through a series of surveys among these risk groups, we were able to describe main accident scenarios of burn injuries and their causes. Among young children, 80% of all scald injuries are caused by pushing down or dropping a hot liquid. Parents most frequently reported lack of the supervision (e.g. attention distracted by others) to be one of the causes of the injury. Among the age group 15-29 years and the elderly, most injuries occur during cooking. Clumsiness and inattention are major causes of injuries among young adults. Among the elderly, a quarter of all victims reported health problems or handicaps to be a cause of their injury. Based on the results of our analysis, preventive measures were suggested.

Adolescent↗

Etiology and outcome of pediatric burns.

A 6-year retrospective review of burn victims hospitalized at a major burn center was conducted to determine the etiology and outcome of pediatric burns. Four hundred forty-nine patients under age 16 years were identified and stratified by age, sex, burn size, presence or absence of inhalation injury, cause of burn, and county of residence. The mean patient age was 4.3 +/- 0.2 years, and the male:female ratio was 1.9:1. There were 21 deaths overall (4.7%), the majority of which (18) were among children under 4 years of age. With respect to large burns, defined as > and = 30% total body surface area (TBSA), the mortality rate for children under age 4 was significantly higher than that for older children (46.9% v 12.5%; P < .01), despite the nearly identical mean burn size of the two groups. Except for burn incidence, there were no significant differences between males and females. The mean burn size was 15.1% +/- 0.7%, and was significantly larger for nonsurvivors than survivors (55.3% +/- 5.7 v 13.1% +/- 0.5%; P < .01). Inhalation injuries were strongly associated with large burns and were present in all 15 flame-burn fatalities. Scalds were the most common type of burn among children under 4 years of age; flame burns predominated in older children. There were 6 deaths related to scalds, all of which occurred in children under 4. Burn type, size, and mortality rate did not differ between children from urban and rural counties. Large burn size was the strongest predictor of mortality, followed by (in order) age less than 4 and the presence of inhalation injury. Infants and young children have the highest risk of death from burn injury. Burns smaller than 30% TBSA without an inhalation injury (such as small scald injuries) occasionally are lethal in infants and small children, despite modern therapy.

Adolescent↗

A case of contact dermatitis, erythema multiforme, and toxic epidermal necrolysis.

A young adult female patient, on prolonged corticosteroid therapy for nephrotic syndrome, developed erythema multiforme and toxic epidermal necrolysis following a double exposure to a locally applied perfume. We believe that this route of exposure should be re-emphasized. Toxic epidermal necrolysis, or the scalded skin syndrome, has become a well-recognized entity which may be divided into three distinct subgroups: the staphylococcal scalded skin syndrome, nonstaphylococcal or drug-induced scalded skin syndrome, and idiopathic. We present a patient who developed a dermatitis on her chest and abdomen after using a spray cologne, which resulted in the development of erythema multiforme with progression toxic epidermal necrolysis and, ultimately, her death.

Adrenal Cortex Hormones↗

Distribution of pedal burns by source and depth.

The source and depth relationships of both isolated burns to the feet and pedal burns as part of multifocal thermal trauma are evaluated. Five years of cases at the University of Chicago Burn Center were selected at random and retrospectively reviewed. There were 33 isolated burns of the foot, with a source distribution of 70% scald, 9% grease, 9% hot solid, 6% flame, and 6% other. In patients with multifocal burns that included that foot, there were 89 cases, with a source distribution of 42% scald burns, 5% grease, 2% hot solid, 39% flame, 5% electrical, 1% frostbite, and 6% other. Source versus depth and grafting needs are presented. Admission to hospital which was delayed from the date of burn showed an increased need for grafting and a longer hospitalization than those admitted on the same day. Immediate admission for compliance of proper treatment protocol is advocated. Isolated pedal burns were most commonly sustained at home, indoors, and in the kitchen. A significant number of isolated burns to the feet were from a scald source, partial thickness in depth, and required no grafting. Much of the wound management involved treating elements found in traumatic, dysvascular, and diabetic pedal lesions.

Adolescent↗