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[Tap-water scald burns].

OBJECTIVE: To describe the characteristics of patients with tap-water scalds admitted to our hospital and review current knowledge on their prevention. PATIENTS AND METHODS: We performed a retrospective study of admissions for tap-water scalds. The medical records codified as water-tap scalds (MBDS; CIE-9-CM, 940.0-949.5, E.924.0, E.924.2) of patients admitted to our hospital for more than 24 hours from January 1 to December 31, 2003 were reviewed. The following variables were studied: age, sex, mechanism, extent and degree of burn, localization, length of hospital stay, treatment, requirement for skin grafting, mortality, and sequelae. RESULTS: Twenty-nine patients were treated in our hospital. Sixty-two percent were boys. Age ranged from 3 days to 9 years. Six patients (20.6 %) were aged less than 1 year, 19 (63 %) were aged between 1 and 3 years and four (13.8 %) were aged from 3 to 9 years. Body surface area was 10 % or less in 25 patients and more than 20 % in four. Five patients required skin autografting. In two patients, the scald was produced in the neonatal area of our hospital. The mean length of hospital stay was 12 days, ranging from 1 to 38 days. None of the patients died. One patient suffered severe sequelae. CONCLUSIONS: Because of the frequency and severity of the burns reported in this study, pediatricians should increase their efforts in educating families about this type of burn. In addition, effective legislation should be implemented in Spain.

Burns↗

Multivariate analysis of superficial scald susceptibility on Granny Smith apples dipped with different postharvest treatments.

Multivariate methods were used to present the results of different postharvest treatments applied to control superficial scald disorder in Granny Smith apples. In a two-season study, the treatments applied by dips were diphenylamine (DPA), Semperfresh (a sucrose ester coating) formulated alone or with either ascorbyl palmitate or n-propyl gallate, and CaCl(2). DPA correlated negatively with scald, whereas the rest of the treatments showed no clear relationship with the disorder. By means of partial least squares, the incidence of superficial scald after cold storage was shown to correlate with quality parameters (firmness and acidity), measured at the end of storage. In contrast, ethylene production did not appear as a relevant factor in the incidence of scald.

Cold Temperature↗

Temperature-dependent autoxidation of conjugated trienols from apple peel yields 6-methyl-5-hepten-2-one, a volatile implicated in induction of scald.

Conjugated triene (CT) oxidation products of alpha-farnesene have long been thought to be involved in development of superficial scald in apple fruit. Early studies found that CT hydroperoxides and the volatile 6-methyl-5-hepten-2-one (MHO) are major in vitro autoxidation products of alpha-farnesene. However, it was recently shown that > or =99% of the oxidation products of alpha-farnesene that accumulate in apple peel are conjugated trienols (CTols), isomers of 2,6,10-trimethyldodeca-2,7,9,11-tetraene-6-ol. HPLC-purified CTols from fruit of two scald-susceptible cultivars, Granny Smith (GS) and Red Delicious (RD), were used to study autoxidation of these compounds in vitro. Incubation of CTols in sealed glass vials under air resulted in accumulation of MHO. Oxygen enrichment did not increase the amount of MHO produced. Regardless of which cultivar CTols were derived from, at 0 degrees C autoxidation yielding MHO was quite slow and linear, whereas at 20 degrees C MHO production was much more rapid, and after several hours the rate increased abruptly. However, CTols isolated from GS and RD fruit differed in the duration of the initial lag phase and the overall level of MHO generated at 20 degrees C. The sharp increase in MHO production occurred after 3 h with GS CTols and at about 12 h with RD CTols. Also, the yield of MHO from GS CTols after 6 h at 20 degrees C was nearly 6-fold greater than that from RD CTols after 20 h at 20 degrees C. The antioxidants butylated hydroxytoluene and diphenyamine reduced the yield of MHO by about 97%. Recent work has shown that MHO can induce scald-like symptoms in apple peel and that tissue sensitivity increases with time in storage. This may explain the correlation between high CTol levels and scald development, and why symptoms rapidly intensify when fruits are removed from cold storage.

Fatty Acids↗

Mechanisms of biocontrol by Pantoea dispersa of sugar cane leaf scald disease caused by Xanthomonas albilineans.

Albicidins, a family of phytotoxins and antibiotics produced by Xanthomonas albilineans, are important in sugar cane leaf scald disease development. The albicidin detoxifying bacterium Pantoea dispersa (syn. Erwinia herbicola) SB1403 provides very effective biocontrol against leaf scald disease in highly susceptible sugar cane cultivars. The P. dispersa gene (albD) for enzymatic detoxification of albicidin has recently been cloned and sequenced. To test the role of albicidin detoxification in biocontrol of leaf scald disease, albD was inactivated in P. dispersa by site-directed mutagenesis. The mutants, which were unable to detoxify albicidin, were less resistant to the toxin and less effective in biocontrol of leaf scald disease than their parent strain. This indicates that albicidin detoxification contributes to the biocontrol capacity of P. dispersa against X. albilineans. Rapid growth and ability to acidify media are other characteristics likely to contribute to the competitiveness of P. dispersa against X. albilineans at wound sites used to invade sugar cane.

Anti-Bacterial Agents↗

Decontamination of pork carcasses during scalding and the prevention of Salmonella cross-contamination.

AIMS: The objective of this study was to establish critical temperature limits to prevent cross-contamination of pork carcasses during scalding. METHODS AND RESULTS: Mixtures of antibiotic-resistant mutants of Salmonella species were heat treated at 50, 55 and 60 degrees C in samples of commercial scald tank water. Surviving cell numbers were estimated by plating treated suspensions on (i). tryptone soya agar (TSA) and (ii). on TSA, overlaid with brilliant green agar plus nalidixic acid and streptomycin sulphate and used to estimate D-values for the treated mixed cell suspensions. CONCLUSIONS: A time-temperature combination of 1.4 min at 60 degrees C is required to achieve a 1 log reduction in Salmonella in scald tank water. The predicted equivalent at 65 degrees C is 0.18 min. SIGNIFICANCE AND IMPACT OF THE STUDY: This study provides data and a model to enable pork processors to identify and apply processing parameters to limit the risks of transfer of Salmonella between pig carcasses during commercial scalding operations.

Animals↗

Neutrophil recruitment after remote scald injury.

Thermal injury is one trigger for pulmonary neutrophil recruitment. This article describes the time course of neutrophil recruitment after scald injury. Mice aged 8 to 10 weeks were anesthetized and subjected to 15% topical scald injury. Animals were put to death at 6 hours, 24 hours, 3 days, and 7 days after injury, and the pulmonary tissue harvested for staining with hematoxylin and eosin and neutrophil esterase. Cell counts for neutrophil accumulation were obtained. Control animals were handled in a comparable manner apart from the scald injury. Animals killed at 6 hours demonstrated significant neutrophil recruitment relative to the control. This difference had resolved at 24 hours. Animals killed at 3 and 7 days again demonstrated neutrophil accumulation despite normal behavior and absence of weight change from the control. Quantitative cultures of burn wounds failed to disclose infection. Scald injury was associated with significant pulmonary neutrophil recruitment that resolved at 24 hours. The presence of an untreated wound was associated with neutrophil recruitment beyond 24 hours despite outward normal behavior.

Analysis of Variance↗

The effects of U-74389G, a 21-aminosteroid, on pulmonary vascular resistance after a scald.

We tested U-74389G (C37H50N6O2-CH4O4), a 21-aminosteroid, to determine whether it ameliorates the pulmonary vascular effects of a surface scald. We studied 24-anesthetized rabbits mechanically ventilated with 100% and then 13% O2. Twelve rabbits received a scald (75 degrees C water applied to the shaved ventral surface for 90 seconds), and 12 served as control (20 degrees C water). Six control and six scalded animals additionally received U-74389G (5 mg/ kg intravenously). We measured hemodynamics and blood gases prescald, 30 minutes postscald, and 30 minutes after U-74389G or placebo administration. The strength of hypoxic pulmonary vasoconstriction (HPV) was assessed as the difference between pulmonary vascular resistance measured during 13% O2 ventilation and during 100% O2 ventilation. Hemodynamics and gas exchange were similar between groups. The strength of HPV was significantly diminished postscald, but U-74389G treatment restored HPV to baseline values. We conclude that a scald reduces the strength of HPV, and the response to U-74389G suggests this may be mediated by free radicals.

Animals↗

Staphylococcal scalded skin syndrome: potentiation by immunosuppression in mice; toxin-mediated exfoliation in a healthy adult.

Staphylococcal scalded skin syndrome, associated with exfoliative toxin produced by phage group II Staphylococcus aureus, has recently been reported in an adult receiving immunosuppressive therapy. To determine the effect of immunosuppression on the development of the staphylococcal scalded skin syndrome, experimental animals were treated with prednisolone, azathioprine, or a combination of both drugs utilizing the clinical isolate from the adult with scalded skin syndrome. The mean lethal dose and mean exfoliating dose were identical and were 6,000-fold lower in animals receiving both drugs or azathioprine alone. The isolate was not more virulent and did not produce more toxin than other group II phage-type strains. Furthermore, immunosuppressive therapy failed to enhance the susceptibility of experimental animals to a purified preparation of toxin. Finally, purified exfoliative toxin was demonstrated to produce erythema, Nikolsky's sign, bullous formation, and flaking desquamation in a normal human adult. The results demonstrated the enhanced susceptibility of experimental animals receiving immunosuppressive therapy to the development of the staphylococcal scalded skin syndrome. They further showed that human adults are susceptible to the action of exfoliative toxin and suggested that, in the host with compromised defense mechanisms, toxin-producing strains may invade and initiate infection resulting in toxin production and exfoliation.

Adult↗

Effects of nutrition on plasma, liver and muscle amino acids in scalded rats.

This study set out to investigate the effect of three different parenterally administered diets on the free amino acid (AA) levels in the plasma, muscle, and liver of scalded rats. Diet I consisted of AA (1.4 g/100 g weight) and a high glucose dose (6 g/100 g weight), diet II consisted of AA and a low glucose dose (1.4 g/100 g weight) and in diet III only a low glucose dose was infused. Parenteral nutrition was started on the 3rd day posttraumatically. Sampling was performed on the 7th day posttraumatically. Nitrogen balances were significantly different in all three groups, being lowest in group III. Scalded rats fed isonitrogenously, but with different amounts of glucose showed only minor changes in AA concentrations. However scalded rats fed with a nitrogen-free diet exhibited significantly reduced total muscle and liver AA levels. These decreased AA levels were due to a drop of glycine in the muscle tissue (74%) and liver (49%). Contrary to the clinical catabolic situation in scalded and starved rats, it was not intracellular glutamine but glycine which was considerably influenced by catabolism and starvation.

Amino Acids↗

Postburn blood flow, edema, and survival of the hairy mouse ear after scald injury at different temperatures.

In one group (a) one ear of NMRI hairy mice was scalded in water at 36 degrees C, 39 degrees C, 42 degrees C, 45 degrees C, 48 degrees C, 51 degrees C, 52 degrees C, 53 degrees C, 54 degrees C, 57 degrees C, and 60 degrees C for 20 s, using a new dip burn model, for evaluation of edema formation 2 h postburn. In another group of mice (b) one ear was scalded in the 45 degrees C-60 degrees C interval and the ear studied in a vital microscope repeatedly for 4 days. In a third group (c), one ear was scalded in the 36 degrees C-60 degrees C interval and the microcirculatory flow was recorded by a laser Doppler flowmeter (1Df) for a period of 2 h postburn. In a fourth group of animals (d) one ear was scalded at 53 degrees C or 54 degrees C. In some animals the ear was then cooled in 8 degrees C water or saline for 30 min. Others were treated preburn with cimetidine, Ketanserin, indomethacin or methylprednisolone. Edema was determined in group (a) by wet-dry weight measurements of punch biopsies from both the burned and the contralateral unburned ear and expressed as an increase in tissue water content. The long-term effect was determined by observing the survival of the ears (groups b and d); the area of necrosis was expressed as a percentage of the total area of the ear. Significant edema was formed in ears immersed in 48 degrees C to 60 degrees C water with a maximum after 53 degrees C burns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[An experimental study on the change in cardiac sympathetic neuroelectrophysiology in severely scalded rats during early postburn stage].

OBJECTIVE: To investigate the mechanism and the rule of the change in cardiac sympathetic neuroelectrophysiology in severely scalded rats during early postburn stage, so as to explore the relationship between the change and postburn severe cardiac injury. METHODS: Forty-four Sprague-Dawley rats were randomly divided into normal (n = 6), sham injury (n = 8) and scalded (n = 20) groups. The rats in scalded group were inflicted by 30% TBSA III degree burn on the backs. The electric discharge activity of cardiac sympathetic nerve was observed and recorded by neuroelectrophysiological technique. The changes in ECG and myocardial mechanic indices were simultaneously observed. RESULTS: The activity of efferent cardiac sympathetic nerve increased immediately after scalding, but that of the afferent nerve increased obviously after about 90s incubation period. The activity of efferent nerve further increased after the increase of afferent activity, and this increase in both efferent and afferent nerves lasted for about 3 hours and decreased evidently thereafter. The change of afferent nerve was earlier than that of efferent nerve. The average electric discharge activity of cardiac sympathetic nerve increased with obvious fluctuation, which exhibited intermittent burst pattern at 1 PBH in some rats, in which frequent ventricular extrasystole appeared accompanying with the simultaneous increase in electric discharge burst in 4 rats. The postburn LVDP and +/- dp/dtmax in rats decreased significantly. CONCLUSION: The activities of both efferent and afferent cardiac sympathetic nerve increased dramatically in the early postburn stage. The change in efferent nerve activity could be affected to some degree by that of afferent nerve. This implied that the increase of the neuroelectrophysiological activity of cardiac sympathetic nerve might be one of the causes of early severe postburn cardiac injury.

Animals↗

[An experimental study on the apoptosis of PMNs and macrophages during the early postburn stage in severely scalded rats].

OBJECTIVE: To investigate the changes of postburn apoptosis of PMN and the apoptosis of PMN and macrophages after being stimulated by burn sera and the change of the phagocytosis of apoptotic PMNs by macrophages. METHODS: Rats inflicted by 30% TBSA III degree scalding were employed as the model. PMNs were harvested on the 0, 6, 12 and 24 postburn hour (PBH). Burn sera were harvested at 24 PBHs. PMN apoptosis was detected by flow cytometry. Simultaneously, peritoneal macrophages were collected for the study. The apoptotic change of the macrophages (Mphis) after being stimulated by burn sera and the ability of Mphis phagocytizing apoptotic PMNs at 24 PBHs were examined. RESULTS: The PMN apoptosis was obviously inhibited at 6, 12 and 24 PBHs in the scalded rats with no difference between the time spots. Twenty-four hours after being stimulated by burn sera, the apoptotic rate of PMNs on scalded rats was lower than that in normal rats, while the apoptotic rate of Mphis in scalded rats was higher than that in normal rats. The ability of Mphis phagocytizing apoptotic PMNs decreased after severe burn (P < 0.01). CONCLUSION: There exhibited delayed rat PMN apoptosis and decreased ability of the phagocytosis of apoptotic PMNs by the Mphis after severe burn or being stimulated by burn sera. This might lead to the incomplete phagocytosis of apoptotic PMNs by Mphis. As a result, the PMNs would finally come to necrosis and release toxic contents which were important factors in the inducing of SIRS.

Animals↗

[The change in plasma concentration of free amino acids during early postburn stage in severely scalded rats].

OBJECTIVE: To investigate the rule of the change in plasma concentration of free amino acids during early postburn stage in severely scalded rats, so as to provide assistance for the study of postburn abnormal metabolism of skeletal muscle. METHODS: Male Wistar rats inflicted by 30% TBSA III degree scalding were employed as the model and were randomly divided into normal (C), 2 postburn hour (PBH), 6PBH, 12PBH and 24PBH groups, with 8 rats in each group. Plasma concentrations of free amino acids was determined by automatic amino acid analyzer. At the same time, the plasma contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), cortisol, TNF and IL-6 were also assayed. RESULTS: There was adecreasing tendency in varying degrees in plasma concentration of all amino acids at each time points within 24 PBHs although there was no obvious difference in total amino acids content at each time point. The plasma level of BCAA decreased evidently at 2 PBH and increased obviously at 12 PBH, while the plasma levels of aromatic amino acids (AAA) increased evidently at 12 and 24 PBHs. In addition, the BCAA/AAA ratio showed no change. The ratio of phenylalanine to tyrosine increased significantly at all postburn time points except that of 2PBH. The plasma levels of ALT, AST increased obviously at all postburn time points (P < 0.01). Plasma cortisol levels in all scalding groups were markedly higher than that in C group (P < 0.01), and reached peak level at 12 PBH. Plasma contents of TNFalpha and IL-6 increased significantly (P < 0.01). Whereas the changes in IL-6 and cortisol were obviously and positively correlated to the changes in 3 -- mH and Phe/Tyr. CONCLUSION: There were significant changes in plasma contents of free amino acids during early postburn stage in scalded rats, which might be related to the early excessive release of inflammatory mediators and enhanced degradation of skeletal muscle and impairment of hepatic function. The mechanism of the change needs to be further studied.

Alanine Transaminase↗

Effects of shenmai injection on expression of TNF-alpha mRNA in peritoneal macrophages of scald mice.

OBJECTIVE: To explore the effect of shenmai injection (SI) on expression of TNF-alpha mRNA in peritoneal macrophages (pMPhis) of scald mice. METHODS: BALB/c mice were inflicted with 11% of body surface area III degree scald and injected intraperitoneally (ip) with SI daily for 5 days, and expression of TNF-alpha mRNA in pMPhis was determined by semi-quantitative RT-PCR. RESULTS: In scald mice, the expression of TNF-alpha mRNA in pMPhis increased significantly, but it was reduced obviously (P < 0.01) after SI administration, while the livability was increased markedly (P < 0.05). CONCLUSIONS: For scald mice, the cause of death at early stage might be related to the high expression of TNF-alpha mRNA in pMPhis and the use of SI can decrease the death rate.

Animals↗

[Protective effects of Zn-metallothionein on erythrocyte membrane of rats with severe scalding after delayed resuscitation].

OBJECTIVE: To study the antagonism of Zn-metallothionein (Zn-MT) to oxidative stress of rats with severe scalding after delayed resuscitation. METHODS: 27 Wistar rats were randomly divided into three groups: normal control; burn with delayed fluid resuscitation group; and Zn-MT protected group. The rats were scalded with 30% total body surface area (TBSA) third degree burn. Four hours after injury, they were resuscitated, but Zn-MT (1 x 10(-5) mol/L) was given in the third group rats. 24 hours after they were scalded, blood was taken, RBCs were separated and labeled with electron spin resonance (ESR) spin label 3-maleimido-proxy l to detect membrane protein conformation. The serum was collected and added into the reaction system of xanthine, xanthine oxidase and ESR spin trap 5, 5-dimethylpyroline-N-oxide to assay the levels of superoxide dismutase (SOD) by ESR. RESULTS: The ratios of strong solidity and weak solidity of RBC membrane proteins in the three groups were 0.352 +/- 0.043, 0.409 +/- 0.027, and 0.386 +/- 0.062 respectively, and the revolved times of membrane proteins were 1.300 +/- 0.210, 1.576 +/- 0.190 and 1.381 +/- 0.210 seconds respectively. Compared to the first group, the membrane protein conformation in the second group was changed remarkably, and the speed of membrane protein movement decreased significantly. However, those changes were alleviated obviously by Zn-MT. The SOD levels in serum of the three groups rats were 73.2% +/- 1.4%, 48.8% +/- 3.8% and 66.8% +/- 3.2% respectively. Compared to the normal control group, the SOD levels in serum of the second group decreased obviously. However, an excess of oxygen free radicals produced after injury could be scavenged by Zn-MT. CONCLUSION: RBC membrane proteins of rats with severe scalding after delayed resuscitation were injured by oxygen free radicals produced after injury, and Zn-MT could alleviate this injury.

Animals↗

[The changes in the morphology and distribution of substance P and calcitonin-gene related peptide nerves in the anterior pituitary of scalded rats].

OBJECTIVE: To observe the changes in the morphology and distribution of substance SP and calcitonin-gene related peptide nerves in the anterior pituitary of scalded rats. METHODS: The rats inflicted 30% TBSA degree scalding of the back were employed as the model. The SP and CGRP peptide nerve fibres in the anterior pituitary were observed by immunohistochemistry staining during different postburn time points: 1, 2, 6, 10, 12, 24 and 72 postburn hours (PBHs). The areas of coverage of SP and CGRP nerve fibers were determined respectively in the anterior pituitaries by image analysis. RESULTS: The morphology of the two peptide nerve fibers exhibited obvious changes under microscope. The numbers of SP and CGRP nerve fibers increased by 85.7% and 60.5%, respectively at 1 PBH when compared with those in control group. Moreover the varicosities and branches of the nerve fibers in scalded rats increased obviously at 1 PBH and decreased sharply at 2 PBH, bouncing back to near normal level at 24 PBH. reaching image analysis revealed that the changes in the areas of coverage of two peptide nerve fibers were correlated positively with each other. The basic trends of the changes were an increase at 1 PBH, a decrease thereafter, reaching the lowest level at 12 PBH with a rebound later. CONCLUSION: The morphology and distribution of SP and CGRP nerve fibers of anterior pituitary in scalded rats exhibited obvious change after injury. Therefore, they might be involved in the functional modulation of systemic stress.

Animals↗

[The protective effects of small dose of dopamine on the intestinal mucosa of scalded rats in shock stage].

OBJECTIVE: To investigate the protective effects of small dose of dopamine on the intestinal mucosa of scalded rats in shock stage. METHODS: Wistar rats inflicted by 30% TBSA of III degree scalding were employed as the model. The rats were pre-placed with cardiac catheter before and were resuscitated intravenously after injury. The scalded rats were treated by routine (control) and small dose of dopamine (3 micro g.kg(-1).min(-1)), respectively. The changes of rat serum levels of diamine oxidase (DAO), malondialdehyde (MDA) and lactic acid (LA) were observed after treatment. And the pathomorphological changes of the intestine were scored. RESULTS: The general condition of the rats with dopamine treatment in shock stage was better than that in control group. The rat serum levels of MDA, LA and DAO decreased obviously, especially during 3 to 12 postburn hours (PBHs) after treatment by small dose of dopamine. The pathomorphological scoring of ileum in dopamine treating group was better than that in control. CONCLUSION: The intestinal mucosa of severely scalded rats in shock stage could be well protected by small dose of dopamine.

Animals↗

[The relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats].

OBJECTIVE: To investigate relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats. METHODS: Wistar rats inflicted by 40% TBSA III degree scalding were employed as the model. The myocardial tissue was obtained from the left ventricle at different postburn time points. Apoptosis was determined by the determination of myocardial tissue Caspase-3 activity and TUNEL staining (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling). The LVSP (left ventricular systolic pressure), LVEDP (left ventricular end-diastolic pressure) and +dp/dtmax (the rate of the rise of left ventricular pressure) and -dp/dtmax (the rate of the fall of left ventricular pressure) were all monitored by four-channel physiological recorder. In addition, myocardial activities of MPO and SOD were detected. RESULTS: The TUNEL staining of rat myocardial cells was positive at 6 postburn hour (PBH) and reached top level at 12 PBH. The change in Caspase-3 activity was earlier than that of apoptotic morphology and reached peak values at 3 and 6 PBHs. The left ventricular function (systolic and diastolic function) was significantly impaired after the scalding and dropped to the lowest levels at 12 PBHs. The increase in myocardial tissue MPO activity was accompanied by the decrease in SOD activity. CONCLUSION: Myocardial cellular apoptosis was one of the reasons of postburn myocardial injury in scalded rats. Caspase protease cascade pathway might be involved in the process of apoptosis, which suggested that the initiation of apoptosis was closely related to the infiltration of neutrophils and to the release of large amounts of oxygen free radicals in myocardial tissue.

Animals↗