Just another railway fatality.

We report on a 56-year-old male who was found dead on railroad tracks, equipped with overhead high-voltage power lines (15,000 V AC). Apparently, the body had been hit by a passing train and completely severed at the mid-abdominal level. Based on this apparently unequivocal finding, the police initially assumed a fatal railway accident or suicide. However, close examination of the deceased's clothes revealed heat damage to at least four overlying layers of clothing in different locations. The rubber soles of his heavy leather shoes showed small holes in blackened areas underneath the toes. Furthermore, both socks revealed tears and fabric defects with burnt rims, again most prominent in the area of the toes. Skin burns, consistent with electric burns, and blistering were detected on the deceased's hands and feet. A broken fishing rod was found in the proximity. On autopsy, multiple injuries caused by severe blunt force with subsequent skull fracture and brain laceration as well as multiple injuries to the spinal column and rib fractures were found and visceral organs displayed multiple lacerations. However, the lack of relevant hematomas argues that these injuries were inflicted postmortem. Histological examination confirmed the presence of electric burns from electrocution. Based on the results of the forensic-pathological examination and additional investigations carried out at the scene of death, we could demonstrate that this highly unusual death was caused by an electrocution after contact of the fishing rod with the high-voltage power line and not by overrunning by the train.

Hyperkalemia in electrical burns: A retrospective study in Colombia.

INTRODUCTION: Classically, hyperkalemia has been regarded as a complication in patients with electrical burns. The etiology of hyperkalemia includes metabolic acidosis, destruction of red blood cells, rhabdomyolysis and the development of renal failure. The purpose of this study was to determine the prevalence of hyperkalemia within the first 24h after electrical burn injury and to evaluate the possible association of serum potassium concentration with cutaneous burn size (%TBSA) and serum creatine phosphokinase (CPK) concentration. METHODS: A retrospective, cross-sectional study was conducted, based on review of medical records of adult patients hospitalized in the first 24h post electrical injury. Serum potassium (K+) levels were divided into low, normal, and high groups, with breakpoints at 3.5mmol/L and 5.0mmol/L and normal 3.6-4.9mmol/L. To assess potential differences according to the time elapsed between the time of the injury and the sampling time, data were grouped as follows: t1: samples obtained in the first 6h post-injury; t2: samples taken at 6-12h; t3: samples taken at 12-24h. RESULTS: 336 patients were studied. The median age was 32 years old (IQR: 25-43). 95.2% of patients were men. Low and normal values of K+ were observed in 13.7% and 85.1%, respectively. The prevalence of hyperkalemia was only 1.2%, and was not related to previously-administered medications or to simple blood gas pH value during admission. CPK>10,000IU/L was observed in 22.6%. No association was found between the serum potassium concentration and either %TBSA burned or the highest CPK value. CONCLUSIONS: First, patients admitted to our burn unit with electrical injury accompanied by significant skin and muscle injury rarely exhibit hyperkalemia. Secondly, the presence of hyperkalemia is independent of the severity of rhabdomyolysis or the extent of the burn.

[Changes of platelet rheological behavior and the interventional effects of ulinastatin in rats with high-voltage electrical burns].

Objective: To explore the influence of high-voltage electrical burns on the number of platelet aggregation, ß-thromboglobulin (ß-TG) and platelet factor 4 (PF-4) and the interventional effects of ulinastatin in rats with high-voltage electrical burns. Methods: A total of 240 Sprague-Dawley rats were divided into sham injury (SI) group, simple electrical burn (SEB) group, normal saline (NS) group, and ulinastatin (UTI) group according to the random number table, with 60 rats in each group. The electrical current was applied to the outside proximal part of left forelimb of rats and exited from the outside proximal part of right hind limb of rats. Rats in groups SEB, NS, and UTI were inflicted with high-voltage electrical burn wounds of 1 cm×1 cm at current entrances and exits, with the voltage regulator and experimental transformer. Rats in group SI were sham injured through connecting the same equipments without electricity. At 2 min post injury, rats in group NS were intraperitoneally injected with 2 mL/kg NS, and rats in group UTI were intraperitoneally injected with 2×10(4) U/kg UTI of 10 g/L. At 15 min before injury and 5 min, 1 h, 2 h, 4 h, 8 h post injury, 10 rats in each group were selected to collect 5-7 mL blood of heart respectively. Blood of 0.05 mL were collected to make fresh blood smear for observing the number of platelet aggregation, and serum were separated from the remaining blood to determine content of ß-TG and PF-4 with enzyme-linked immunosorbent assay. Data were processed with analysis of factorial design of variance, student-Newman-Keuls test, Kruskal-Wallis H test, Wilcoxon rank sum test, and Bonferroni correction. Results: (1) At 15 min before injury, the numbers of platelet aggregation of rats were close among groups SI, SEB, NS and UTI (5.9±1.2, 5.8±1.2, 5.9±1.3, 5.9±1.1, respectively, with P values above 0.05). At 5 min, 1 h, 2 h, 4 h, 8 h post injury, the numbers of platelet aggregation of rats in group SEB were 57.2±16.3, 59.1±16.9, 60.8±20.6, 83.6±24.9, and 83.4±30.3, respectively, obviously more than those in group SI (6.0±1.3, 6.0±1.4, 5.9±1.4, 5.7±1.1, and 5.8±1.3, respectively, with P values below 0.001); the numbers of platelet aggregation of rats in group UTI were 29.6±7.4, 31.9±10.1, 35.0±14.2, 43.0±13.6, and 35.2±11.1, respectively, obviously more than those in group NS (58.3±16.1, 63.9±18.0, 60.8±17.7, 74.2±23.0, and 82.3±21.9, respectively, with P values below 0.001). There was no significantly statistical difference in the number of platelet aggregation of rats in group SI between each two time points within the same group (with P values above 0.05), but the number of platelet aggregation of rats in the other 3 groups at each time point post injury was significantly more than that of the same group at 15 min before injury (with P values below 0.001). (2) At 2, 4, and 8 h post injury, ß-TG content of serum of rats in group SEB was significantly higher than that in group SI (with Z values from -3.780 to -3.477, P values below 0.05). At 5 min and 4 h post injury, ß-TG content of serum of rats in group UTI was significantly lower than that in group NS (with Z values respectively -3.477 and -3.780, P values below 0.05). There was no significantly statistical difference in ß-TG content of serum of rats in group SI at all time points of the same group (χ(2)=0.130, P >0.05). At 2, 4, and 8 h post injury, ß-TG content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.553, P values below 0.05). At 5 min, 1 h, and 4 h post injury, ß-TG content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with Z values from -3.780 to -3.477, P values below 0.05). At 1 and 4 h post injury, ß-TG content of serum of rats in group UTI was significantly higher than that of the same group at 15 min before injury (with Z values respectively -3.250 and -3.780, P values below 0.05). (3) At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that in group SI (with P values below 0.05). At 2 h post injury, PF-4 content of serum of rats in group UTI was significantly higher than that in group NS (P<0.05), and at 4 and 8 h post injury, PF-4 content of serum of rats in group UTI was significantly lower than that in group NS (with P values below 0.05). At all time points, PF-4 content of serum of rats in group SI was close (with P values above 0.05). At 2 and 8 h post injury, PF-4 content of serum of rats in group SEB was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). At 1, 4, and 8 h post injury, PF-4 content of serum of rats in group NS was significantly higher than that of the same group at 15 min before injury (with P values below 0.05). There were significantly statistical differences in PF-4 content of serum of rats between all time points except for 5 min post injury and 15 min before injury (with P values below 0.05). Conclusions: Increasing number of platelet aggregation and abnormal secretion of ß-TG and PF-4 of rats with high-voltage electrical burns can lead to microcirculation disturbance. UTI can alleviate microcirculation disturbance caused by high-voltage electrical burns by reducing the number of platelet aggregation and inhibiting secretion of ß-TG and PF-4.

[Influences of high-voltage electrical burns on microcirculation perfusion on serosal surface of small intestine of rats and the interventional effects of pentoxifylline].

Objective: To investigate influences of high-voltage electrical burns on microcirculation perfusion on serosal surface of small intestine of rats and the interventional effects of pentoxifylline (PTX). Methods: Totally 180 SD rats were divided into sham injury group, simple electrical burn group, and treatment group according to the random number table, with 60 rats in each group. The electrical current was applied to the outside proximal part of left forelimb of rats and exited from the outside proximal part of right hind limb of rats. Rats in simple electrical burn group and treatment group were inflicted with high-voltage electrical burn wounds of 1cm×1cm at current entrances and exits, with the voltage regulator and experimental transformer. Rats in sham injury group were sham injured through connecting the same equipments without electricity. At 2 min post injury, rats in sham injury group and simple electrical burn group were intraperitoneally injected with 2 mL normal saline, and rats in treatment group were injected with 2 mL PTX injection (50 mg/mL). At 15 min before injury and 5 min, 1 h, 2 h, 4 h, and 8 h post injury, 10 rats in each group were selected to collect blood of heart respectively. Serum were separated from the blood to determine the level of soluble vascular cell adhesion molecule-1(sVCAM-1) with enzyme-linked immunosorbent assay method. The number of adhesional leukocyte in mesenteric venule of rats was determined with Bradford variable projection microscope system. The microcirculation perfusion on serosal surface of small intestine of rats was detected with laser Doppler perfusion imager. Data were processed with analysis of variance of factorial design and LSD test. Results: (1) At 5 min, 1 h, 2 h, 4 h, 8 h post injury, the serum content of sVCAM-1 in rats of simple electrical burn group were (8 502±1 158), (11 793±3 310), (9 960±2 146), (9 708±1 429), (7 292±1 386) ng/mL respectively, higher than that in sham injury group and treatment group [ (1 897±946), (1 882±940), (1 882±938), (1 888±946), (1 884±942) ng/mL, and (6 840±1 558), (6 742±2 465), (5 625±2 593), (2 373±1 463), (5 187±2 797) ng/mL, respectively, with P values below 0.001]. The serum content of sVCAM-1 in rats of sham injury group and treatment group at all time points post injury, except 4 h post injury of treatment group, was higher than that of the same group at 15 min before injury (with P values below 0.001). (2) At all time points post injury, the number of adhesional leukocyte in mesenteric venule of rats in simple electrical burn group was higher than that in sham injury group and treatment group (with P values below 0.001). The number of adhesional leukocyte in mesenteric venule of rats in simple electrical burn group and treatment group at all time points post injury was higher than that of the same group at 15 min before injury (with P values below 0.001). (3) At all time points post injury, the microcirculation perfusion on serosal surface of small intestine of rats in simple electrical burn group was lower than that in sham injury group and treatment group (with P values below 0.001). The microcirculation perfusion on serosal surface of small intestine of rats in simple electrical burn group and treatment group at all time points post injury was lower than that of the same group at 15 min before injury (with P values below 0.001). Conclusions: High-voltage electrical burns can increase the serum content of sVCAM-1, the number of adhesional leukocyte in mesenteric venule, and reduce microcirculation perfusion on serosal surface of small intestine of rats. PTX can inhibit secretion of serum sVCAM-1, reduce the number of adhensional leukocyte in mesenteric venule to alleviate microcirculation disturbance caused by high-voltage electrical burns.

[Analysis of microRNA expression profile in serum of patients with electrical burn or thermal burn].

Objective: To explore the differential expression of microRNAs in the serum among patients with electrical burn or thermal burn and healthy persons and to explore the significance. Methods: In this study we included three patients with electrical burn and three patients with thermal burn, conforming to the inclusion criteria and hospitalized in our burn ward from June to August 2015, and three healthy adult volunteers. Their serum samples were separated from whole blood and divided into electrical burn group, thermal burn group, and normal control group. Total RNA was extracted from their serum samples using Trizol method. The differentially expressed microRNAs (with differential ratio larger than or equal to 2.000, less than or equal to 0.500) among the three groups were screened by microRNA chip technique. Then cluster and Venn diagram analysis of the differentially expressed microRNAs were performed. Enrichment analysis of Kyoto encyclopedia of genes and genomes (KEGG) signaling pathway was performed on the distinctly changed microRNAs (with differential ratio larger than or equal to 5.000, less than or equal to 0.500). Results: There were 220 differentially expressed microRNAs among serum of the three groups. MicroRNA expression profiles in serum of electrical burn and thermal burn groups were different from that in serum of normal control group. Compared with those in serum of normal control group, the expressions of 59 microRNAs changed more than 2.000 times in serum of electrical burn group, with 50 up-regulated microRNAs and 9 down-regulated microRNAs; the expressions of 40 microRNAs changed more than 2.000 times in serum of thermal burn group, with 21 up-regulated microRNAs and 19 down-regulated microRNAs. Compared with those in serum of thermal burn group, the expressions of 167 microRNAs changed more than 2.000 times in serum of electrical burn group. There were 17 exclusively expressed microRNAs in serum of thermal burn group and 26 exclusively expressed microRNAs in serum of electrical burn group, compared with those in serum of normal control group. Enrichment analysis of KEGG signaling pathway showed that compared with those in serum of normal control group, microRNAs which changed distinctly in serum of electrical burn group took part in the insulin secretion signaling pathway, arrhythmogenic right ventricular cardiomyopathy signaling pathway, hypertrophic cardiomyopathy signaling pathway, glutamatergic synapse signaling pathway, calcium signaling pathway, cyclic adenosine monophosphate signaling pathway, glycerophospholipid metabolism, pyrimidine metabolism, serotonergic synapse signaling pathway, etc, while microRNAs which changed distinctly in serum of thermal burn group took part in the tumor transcription misregulation signaling pathway, proteoglycans in tumor signaling pathway, microRNAs in tumor signaling pathway, long-term potentiation signaling pathway, citrate cycle signaling pathway, tumor necrosis factor signaling pathway, focal adhesion signaling pathway, endocytosis signaling pathway, insulin secretion signaling pathway, p53 signaling pathway, and estrogen signaling pathway, etc. Conclusions: MicroRNA expression profiles in serum of electrical and thermal burn are different from that in serum of healthy adult. The signaling pathways enriched with target genes which are regulated by the differentially expressed microRNAs are related to the pathological changes and clinical manifestations after electrical or thermal burn.

Upon admission coagulation and platelet function in patients with thermal and electrical injuries.

RATIONAL: There has been increased focus on hemostatic potential and function in the initial assessment of the patient with traumatic injuries, that not been extensively studied in patients with burns. We proposed to determine the hemostatic potential of patients with burns upon admission to the emergency department and contrasted their condition with that of healthy controls and patients with other traumatic injuries. In addition we assessed differences due to thermal versus electrical injury and evaluated the effect of burn size. METHODS: This is a patient based prospective observational study conducted with delayed consented. Subjects at the highest level of trauma activation upon admission to the ED had a blood sample collected for research purposes and were subsequently consented. Hemostatic potential was measured by rapid thromelastography (r-TEG®), thrombin generation by calibrated automated thrombogram (CAT) and platelet function by Multiplate® using five activators. Burn subjects were compared to subjects with other traumatic injuries and controls. Within the burn subjects additional analysis compared mechanism (thermal vs. electrical) and burn size. Values are medians (IQR). RESULTS: Two hundred and eighty two trauma patients (with burns n=40, 14%) and 27 controls were enrolled. Upon admission, compared to controls, subjects with burns or trauma were hyper-coagulable based on r-TEG and CAT, with increased rates of clot formation and thrombin generation. There were no differences in burns compared to other traumatic injuries. The presence of hyper-coagulation did not appear to be related to the type of burn or the percentage of total body surface area involved. Employing previous defined cut points for R-TEG driven therapeutic interventions burn patients had similar rates of hyper- and hypo-coagulation noted in patients with traumatic injuries. CONCLUSION: Upon admission patients with burns are in a hyper-coagulable state similar to that of other trauma patients. Employing demonstrated cut points of hemostatic potential in trauma patients associated with increased risk of poor outcomes demonstrated the incidence in burn patients to be similar, suggesting that these values could be used in the early assessment of the patient with burns to guide treatment interventions.

Cardiac troponin T in patients with cardiac implantable electronic devices undergoing magnetic resonance imaging.

PURPOSE: Magnetic resonance imaging (MRI) has been safely performed in many patients with cardiac implantable electronic devices (CIEDs) using institution-specific protocols. A potential risk of MRI is myocardial heating and cardiac injury, which might be detectable with cardiac Troponin (cTn). We evaluated this in patients with CIEDs undergoing MRI. METHODS: Prospective data were collected from 2008 to the present in patients with CIEDs undergoing clinically indicated MRI performed under institutional protocol. Cardiac Troponin T (cTnT) levels were drawn both before and 24­36 h after the procedure. The collective data were retrospectively analyzed. RESULTS: MRI exams (n=512) were performed in 398 patients. Of these, there were 348 unique scans with cTnT recorded before and after MRI (median age 68, IQ 56­78; 62%men). cTnT did not significantly change for the group as a whole (0.00±0.056). There were 22 (6.3 %) exams with cTnT change ≥0.002 ng/mL following MRI (range 0.01­0.09 ng/mL). There were no clinically significant events in these patients directly attributable to MR. There were no significant changes in pacing threshold or impedance in the group with elevated cardiac biomarkers. CONCLUSION: There are very few situations where myocardial injury as detected by cTnT in patients undergoing MRI with CIEDs could be detected. No adverse clinical events or functional changes of the device were noted, even in those with increases in cTnT. Our experience supports that MRI can be performed safely for appropriately selected patients under close clinical observation. Proactive monitoring with the present iteration of cardiac biomarkers appears to be of limited utility, but prospective monitoring with high sensitivity assays may be able to detect subclinical myocardial damage.

Evaluation of children presenting to the emergency room after electrical injury.

BACKGROUND/AIM: To evaluate children who presented to the Pediatric Emergency Department with electrical injury and to discuss the follow-up of these cases and potential precautions that can be taken. MATERIALS AND METHODS: A total of 36 patients presented to the Pediatric Emergency Department with electrical injury between May 2010 and May 2013, and these cases were investigated retrospectively. The patients' age and sex, location and form of exposure to electric current, seasonal distribution, length of hospital stay, musculoskeletal and cardiovascular system complications, renal damage, and treatments were recorded. RESULTS: The majority of the patients were exposed to low-voltage electrical current at home. When the patients were evaluated based on the type of electric current, alanine transaminase, aspartate transaminase, creatine kinase, and creatine kinase-myocardial isoenzyme levels were found to be significantly higher among patients who were exposed to high-voltage electric current. None of the patients died, and the mean length of hospital stay was 2.50 ± 1.06 days. CONCLUSION: Electrical injuries can present with a wide variety of problems, ranging from a simple injury to life-threatening severe multiple organ injury. Even simple precautions can prevent possible morbidity and mortality. We think that the public level of knowledge and awareness should be increased.

[Role of phosphoinositide 3 kinase/protein kinase B signal pathway in monocyte-endothelial adhesion induced by serum of rats with electrical burn].

OBJECTIVE: To observe the change in phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signal pathway in monocytes as induced by serum of rats with electrical burn, and to explore the effects of PI3K/Akt pathway on monocyte-endothelial cell adhesion. METHODS: Sixty-four SD rats of clean grade were inflicted with electrical burn for the collection of serum of rats with electrical burn; another group of twenty-four SD rats were used to obtain normal serum without treatment. (1) Human monocyte line THP-1 was routinely cultured. The THP-1 cells in logarithmic phase were divided into normal serum group (resuspended in RPMI 1640 medium with 20% normal rat serum) and burn serum group (resuspended with RPMI 1640 medium with 20% serum of rats with electrical burn) according to the random number table, with 6 wells in each group. Morphology of THP-1 cells in normal serum group was observed at post culture hour (PCH) 24, and that in burn serum group at PCH 3, 6, 24. The contents of TNF-α in culture supernatant were determined by double-antibody sandwich ELISA at the corresponding time point in each group. The state of Akt activation was determined by Western blotting at PCH 3, 6, 24. (2) Another portion of THP-1 cells were divided into 4 groups according to the random number table, with 6 wells in each group. Cells in normal serum group and burn serum group were given with the same culture condition as above; cells in normal serum+inhibitor group and burn serum+inhibitor group were cultured with the same culture conditions as in the former two groups correspondingly with addition of 100 nmol/L wortmannin in the nutrient solution. At PCH 3 and 6, THP-1 cells were added into the well with a monolayer of endothelial cell line EA.hy926 to observe the monocyte-endothelial cell adhesion. Data were processed with one-way analysis of variance and LSD- t test. RESULTS: (1) In normal serum group, THP-1 cells showed growth in suspension, with uniform shape at PCH 24. In burn serum group, the cell shape became irregular though the membrane was complete at PCH 3; cellular size became irregular and cell membrane and cytoplasm were swollen at PCH 6; cell membrane was disrupted with death of cells at PCH 24. The contents of TNF-α in culture supernatant in normal serum group at PCH 24 and in burn serum group at PCH 3, 6, 24 were respectively (38.5 ± 1.4), (75.1 ± 1.5), (91.5 ± 1.8), (117.0 ± 1.4) pg/mL (F = 1 415.306, P < 0.01). The contents of TNF-α in culture supernatant in burn serum group at PCH 3, 6, 24 were all significantly higher than the content of TNF-α in normal serum group at PCH 24 (with t values respectively 29.614, 42.852, 63.485, P values below 0.01). The ratio values of phosphorylated Akt to Akt in burn serum group at PCH 3, 6, 24 were respectively 2.66, 3.69, 1.17 times of those in normal serum group at the corresponding time point. (2) In normal serum group, normal serum+inhibitor group, burn serum group, and burn serum+inhibitor group at PCH 3 and 6, the numbers of THP-1 cells adherent to endothelial cells were respectively (231 ± 45), (280 ± 47), (703 ± 169), (335 ± 85) per 100-time field; (219 ± 49), (235 ± 21), (562 ± 123), (226 ± 29) per 100-time field (with F values respectively 25.630 and 18.975, P values below 0.01). The number of THP-1 cells adhered to EA.hy926 cells was significantly more in burn serum group than in normal serum group at PCH 3 and 6 (with t values respectively 6.189 and 6.601, P values below 0.01). The number of THP-1 cells adherent to EA.hy926 cells was significantly fewer in burn serum+inhibitor group than in burn serum group at PCH 3 and 6 (with t values respectively 6.821 and 6.465, P values below 0.01). CONCLUSIONS: The serum of rats suffering from electrical burn can induce the monocytes to secrete TNF-α, thus enhancing monocyte-endothelial cell adhesion, but it can be inhibited by blocking PI3K/Akt signal pathway.

[Effects of low molecular weight heparin on the inflammatory response and vascular injury in rat after electric burn].

OBJECTIVE: To observe the effects of low molecular weight heparin (LMWH) on the inflammatory response and vascular injury in rat after electric burn. METHODS: A homemade regulator and transformer apparatus was used to reproduce the model of electric burn (0.5 cm×0.5 cm in size) with depth from full-thickness to full-thickness skin plus muscle and bone on the middle of the inside of right hind limb in 60 Wistar rats. The open wounds were covered with 20 g/L sulfadiazine silver paste immediately after injury. The wound condition was observed every day. The injured rats were divided into group LMWH and control group (C) according to the random number table, with 30 rats in each group. Rats in group LMWH were given subcutaneous injection of LMWH (1 U/g) in abdominal wall, 2 times a day. No other treatment was given in rats in group C. On post burn day (PBD) 3, 5, and 10, 10 rats respectively of two groups were sacrificed. The damaged tissue of wound and that around the wound (1.0 cm×0.5 cm in size) were excised, and heart blood was obtained. The pathological changes and thrombosis in damaged tissue were observed with HE, Masson, and aldehyde fuchsin staining, and the thrombosis rate was calculated. Serum contents of TNF-α and endothelin-1 were determined with ELISA. The mRNA expression of TNF-α in damaged tissue was detected with RT-PCR. Data were processed with Levene homogeneity test, analysis of variance of factorial design, LSD- t test, SNK- q test, and Friedman M nonparametric test. RESULTS: (1) The injured limb of rats was obviously swollen after electric burn, which reached deeply to the muscle and bone. Compared with those of group C, the swelling of rats subsided slightly faster and the inflammatory response was lighter in group LMWH at each time point. (2) The necrosis of damaged tissue and profuse infiltration of inflammatory cells were observed. Dilatation of blood vessels, congestion and thrombosis, and swelling, necrosis, and desquamation of vascular endothelial cells were observed in the damaged tissue. Damaged blood vessel wall, ruptured elastic fiber, loss of internal elastic membrane, and other pathological changes were observed in the damaged tissue of rats in the two groups. Above lesions were improved gradually along with the passage of time, and the improvement was more obvious in rats of group LMWH compared with that of group C on PBD 5 and 10. (3) The thrombosis rates of rats in group LMWH were obviously lower than those of rats in group C (F = 4.921, P < 0.05). The thrombosis rates of rats in group LMWH on PBD 3 and 10 were respectively (0.07 ± 0.11)% and (0.03 ± 0.05)%, which were significantly lower than those of rats in group C [(0.16 ± 0.15)% and (0.13 ± 0.18)%, with t values respectively 2.17 and 2.07, P values below 0.05]. In group LMWH, the thrombosis rate of rats on PBD 10 was obviously lower than that on PBD 3 (t = 3.61, P < 0.05). (4) The serum contents of TNF-α and endothelin-1 of rats in group LMWH were significantly lower than those of rats in group C (F = 47.161, χ(2) = 81.46, P values below 0.01). In group LMWH, TNF-α contents were respectively (71 ± 24), (74 ± 14), (72 ± 20) pg/mL, and endothelin-1 contents were respectively (20.9 ± 3.2), (19.8 ± 5.2), (18.6 ± 1.1) ng/mL on PBD 3, 5, and 10, and they were significantly lower than those of rats in group C [(195 ± 148), (96 ± 20), (159 ± 46) pg/mL and (38.8 ± 15.4), (27.9 ± 3.6), (25.6 ± 7.6) ng/mL, with t values from 3.81 to 8.05, q values from 4.41 to 7.85, P < 0.05 or P < 0.01]. (5) The mRNA expression levels of TNF-α in damaged tissue of rats in group LMWH were significantly lower than those of rats in group C (F = 199.113, P < 0.01). The mRNA expression levels of TNF-α of rats in group LMWH were respectively 0.93 ± 0.10, 1.15 ± 0.12, 1.21 ± 0.11 on PBD 3, 5, and 10, and they were significantly lower than those of group C (1.68 ± 0.15, 1.43 ± 0.12, 1.50 ± 0.13, with t values from 3.75 to 6.12, P < 0.05 or P < 0.01). In group LMWH, the mRNA expression level of TNF-α of rats on PBD 10 was obviously higher than that on PBD 3 (t = 3.61, P < 0.05). CONCLUSIONS: LMWH intervention can ameliorate vascular injury and inflammatory response of electrically burned wounds in rats, and it decreases thrombosis rate in the vessels of injured limb.

[Change in expression of vascular endothelial growth factor in serum and wound tissue of rats with electrical burns].

OBJECTIVE: To observe the change in expression of vascular endothelial growth factor (VEGF) in serum and wound tissue of rats with electrical burn (EB), and to explore its regulation mechanism in the pathological changes of EB. METHODS: Sixty-four SD rats were divided into normal control group (n = 8) and EB group (n = 56) according to the random number table. Eight rats in EB group were sacrificed at post injury hour (PIH) 6 and on post injury day (PID) 1, 3, 7, 14, 21, and 28, to collect wound muscle tissue and serum samples. Histopathological changes in wound tissue were observed with HE staining. The serum content of VEGF was determined with double-antibody sandwich enzyme-linked immunosorbent assay. The expression level of VEGF in wound tissue was determined with Western blotting. VEGF expression intensity in wound tissue was observed with immunohistochemical staining. The microvessel density (MVD) was calculated. The correlation between VEGF expression intensity and MVD was analyzed. Muscle tissue of calf and serum of the rats in normal control group without any treatment were collected for above-mentioned observations and determinations. Data were processed with one-way analysis of variance and Spearman hierarchy correlation analysis, and LSD-t test was applied for paired comparison. RESULTS: (1) In EB group, breakage of muscle fiber, heavy infiltration of inflammatory cells, and obvious tissue edema were observed at PIH 6 and on PID 1; new vessels were observed on PID 3; amount of granulation tissue and number of new vessels were found to be increased on PID 7. (2) In EB group, the serum level of VEGF was (43 ± 11) pg/mL at PIH 6, (44 ± 11) pg/mL on PID 1, and (74 ± 27) pg/mL on PID 14, which were all significantly higher than that in normal control group [(15 ± 9) pg/mL, with t values from 4.001 to 5.724, P values all below 0.01]. (3) The protein expression level of VEGF of wound tissue in EB group was higher than that in normal control group (0.21 ± 0.09) at each time point. The protein expression level of VEGF in EB group peaked on PID 7 (0.63 ± 0.13, t = 4.965, P < 0.05). (4) In EB group, strongly positive expression of VEGF was observed in inflammatory cells at early stage and in new vascular endothelial cells at late stage. (5) The expression intensity of VEGF was positively correlated with MVD in wound tissue on PID 3, 7, 14, 21, and 28 in EB group (r(s) = 0.834, P < 0.01). CONCLUSIONS: Different expression levels of VEGF were observed in serum and wound tissue of rats at various stages after EB, and they were closely correlated with different stages of fluid exudation and wound healing process after EB.

[Influence of high-voltage electrical burn on the rheological property of platelet and leukocyte in rats and the interventional effect of pentoxifylline].

OBJECTIVE: To investigate the influence of high-voltage electrical burn (HEB) on the aggregation and adhesion of platelet and leukocyte in rats and the interventional effect of pentoxifylline (PTX). METHODS: One hundred and eighty SD rats were divided into control, electrical burn (EB), and pentoxifylline treatment (PT) groups according to the random number table, with 60 rats in each group. (1) Ten rats were taken from each group at 15 minutes before injury for the observation of the microcirculatory perfusion of chest skin with Laser Doppler Perfusion Imager (LDPI), and the number of leukocyte adherent to mesenteric venule with Bradford Variable Projection Microscope (BVPM). Serum was collected from heart blood to determine the contents of platelet activating factor (PAF), thromboxane B2 (TXB2), prostacyclin (PGI2), P-selectin, E-selectin and L-selectin by double-antibody sandwich enzyme-linked immunosorbent assay. The ratio of TXB2 to PGI2 was calculated therefrom. (2) Model of HEB was reproduced in the remaining 50 rats of EB group and that of PT group with voltage regulator and experimental transformer (the electrical current applied to the left forelimb and exited from the right hind limb). The remaining 50 rats of control group were sham injured with the same devices without electric current. Within 2 minutes post injury (PIM), rats in control group and EB group were intraperitoneally injected with 2 mL isotonic saline, while rats in PT group were intraperitoneally injected with 2 mL pentoxifylline (50 mg/mL). At PIM 5 and 1, 2, 4, 8 hour(s) post injury (PIH), 10 rats of every group were randomly chosen at each time point for the observation of the microcirculatory perfusion of chest skin and the number of leukocytes adherent to mesenteric venule through the same method as used above, and the levels of the related factors of aggregation and adhesion of platelets and leukocytes were determined, and then the relative ratio was calculated. Data were processed with the analysis of variance of factorial design and LSD test. RESULTS: The contents of PAF, TXB2, PGI2, P-selectin, E-selectin, L-selectin, and the ratio of TXB2 to PGI2, as well as the number of adhered leukocyte in EB group were higher, while the microcirculatory perfusion value was lower than those of control group, with F values from 854.20 to 8156.52, P values all below 0.01. The microcirculatory perfusion value and PGI2 content of PT group were higher, while the contents or number of other indexes were lower than those of EB group, with F values from 33.18 to 1033.99, P values all below 0.01. Only the data within EB group and PT group were comparable. The contents of PAF, TXB2, PGI2, P-selectin, E-selectin, L-selectin, and the ratio of TXB2 to PGI2, as well as the number of adhered leukocyte in EB group and PT group at each time point were significantly higher than those at 15 minutes before injury, while the microcirculation perfusion value was significantly lower than that at 15 minutes before injury (P values all below 0.001), with the exception of the ratio of TXB2 to PGI2 in PT group and E-selectin in EB group and PT group at PIM 5. The contents of PAF, TXB2, and E-selectin and the ratio of TXB2 to PGI2 in EB group peaked at PIH 4, and they were respectively (9.3 ± 0.9) ng/mL, (14.31 ± 0.65) nmol/mL, (271.2 ± 18.4) ng/mL and 4.62 ± 0.26. The contents of PGI2 and P-selectin, and the number of adhered leukocyte in EB group peaked at PIH 8, and they were respectively (3.98 ± 0.24) nmol/mL, (514 ± 24) ng/mL, and (25.50 ± 4.14) per 100 µm venule. The content of L-selectin peaked at PIH 2 [(876 ± 54) ng/mL]. The microcirculatory perfusion value was lowest at PIM 5 [(1.17 ± 0.10) V]. CONCLUSIONS: HEB can increase the contents of PAF, TXB2, PGI2, P-selectin, E-selectin, L-selectin, the ratio of TXB2 to PGI2, and the number of adhered leukocyte, as well as decrease the skin microcirculatory perfusion value. PTX can inhibit the aggregation and adhesion of platelets and leukocytes through increasing the content of PGI2 and decreasing contents of other factors mentioned above, thus alleviating the microcirculatory dysfunction after HEB.

Analysis of factors influencing limb amputation in high-voltage electrically injured patients.

BACKGROUND: Limb amputation is considered one of the most devastating consequences of electrical injury. Any factors that correlate with the degree of muscle damage can be used to predict the necessity of limb amputation. The aim of this study was to determine the factors that can be used to predict limb amputation in high-voltage electrically injured patients. METHODS: Eighty-two high-voltage electrically injured patients were admitted to our hospital during a 17-year period. A retrospective analysis of the possible related risk factors between amputation and non-amputation patients was performed. RESULTS: A total of 68 patients were enrolled for analysis. Thirteen patients underwent limb amputations. Multivariate analysis of the risk factors between amputation and non-amputation groups showed statistical significance for day 1 creatine kinase-isoenzyme MB (CK-MB) level. A serum CK-MB level above 80 ng/ml predicted high risk of limb amputation with high specificity (84%) and sensitivity (77%). Only one patient with a remarkable decrease of creatine kinase (CK) and CK-MB levels after fasciotomy avoided a major limb amputation. CONCLUSION: Our results suggest that CK-MB level is an independent factor for prediction of limb amputation. We suggest that the addition of CK-MB evaluation to clinical symptoms screening may be a valuable method to early detection of muscle damage.

[Dynamic change in microcirculation of pancreas after experimental high-voltage electric burn].

OBJECTIVE: To observe the changes in surface microcirculation of pancreas after high-voltage electric burn (HEB). METHODS: Thirty rabbits were divided into electrical injury (E) group and control (C) group in a simple random method, with 15 rabbits in each group. Rabbit model of HEB was reproduced from E group with TC-30-20KVA type voltage regulator and YDJ-10KVA type experimental transformer. Rabbits in C group were shamly burned with the same equipment as in E group but not electrified. Intravenous blood of rabbits in both groups was drawn 15 mins before HEB and 0, 1, 2, 4, 8 h after to determine the levels of serum amylase and blood glucose. The morphology of the pancreas microvessels and its surrounding tissues, and the dynamic changes in microvascular blood flow were observed with WX-9 microscope and its image analytical system. RESULTS: The level of serum amylase of rabbits in E group increased gradually and peaked (849 +/- 39) U/L at 8 post HEB h (PHH), which decreased gradually reaching the nadir (153 +/- 21) U/L at 8 PHH in C group (P < 0.05). The blood glucose levels of rabbits in E group and C group increased gradually, with the former level obviously higher than the latter (P < 0.05). Arteriole, venule and capillary network on the surface of pancreatic lobules of rabbits in both groups were clearly seen and well-distributed in the natural way before HEB. In E group, arterioles of rabbits contracted at 0 PHH, and increased gradually in caliber size at 1 PHH; venules of rabbits were unevenly thickened at 2 PHH, and dilated at 8 PHH; the capillaries were contracted or with interrupted flow or completely obstructed at 0 PHH, and their thickness were uneven at 2 PHH, showing exudation at 8 PHH. There was no obvious change of microvessels in rabbits in C group at each time point. There was no exudation and bleeding around the microvessels on the pancreas surface of rabbits in both groups before HEB. In E group exudation was observed around microvessels at 1 PHH, bleeding was observed at 2 PHH and became obvious at 4 PHH; exudation and diffuse bleeding from capillaries were observed at 8 PHH. There was no exudation and bleeding in rabbits in C group as observed at each time point. Before HEB, blood flow speed in microvessels of rabbits in 2 groups was similar to each other (P > 0.05), and no erythrocyte aggregation or microthrombus was found in both groups. In E group, blood flow speed slowed down at 0 PHH as compared with that before HEB, it accelerated at 1 h and slowed down later; erythrocyte aggregation in venules and capillaries was found at 0 PHH, and it aggregated gradually. No above-mentioned change was found in C group. CONCLUSIONS: HEB produces microcirculation disturbance and functional disturbance of pancreas.

[Clinical significance of the change of serum CK-MM in electrical injured patients].

OBJECTIVE: To evaluate the diagnostic value of the changes in serum CK and its isozymes in the muscular infection and necrosis in electrical injured patients. METHODS: Seventeen patients were divided into A and B groups according to the causes, i.e. electrical injury as A and electrical arc flame burn as B groups. Obvious muscle necrosis was identified in A but not in B groups. The serum CK-MM concentration was determined after injury, before and after the operations. Simultaneously, the blood and urine routine, the hepatic and renal function and wound bacterial counting were determined and compared with those in 20 healthy people. RESULTS: 1. The serum CK-MM in A group increased evidently after injury and 1 day after wound debridement to the 6 times that in normal control. The enzyme decreased to normal at 3 post-operative days in 15 cases and remained at relative high level in 2 cases due to the wound infection and lowered down to normal level after wound re-debridement. 2. The serum CK-MM in B group increased slightly before and after skin grafting. CONCLUSION: CK-MM could be employed as the index for the infection and necrosis of the muscle in electrical injured patients due to its high specificity and sensitivity.

[Experimental high-voltage electrical burns on limbs of rabbits].

OBJECTIVE: The study was designed to investigate the changes in some rheological parameters and ET-1 in venous blood following electrical burns. METHODS: One of the hind limbs of rabbits was subjected to 3000 V, 2.5 A charge of alternative electric current for 3 seconds. Rheological parameters such as red cell deformability (RED) and platelet aggregation rate (PAR), as well as endothelin-1 (ET-1) in venous blood drained from electrical burn wounds and contents of ATP in damaged muscle were measured at time intervals of 2 h, 24 h, 48 h and 72 h postburn. RESULTS: The changes in the parameters mentioned above were significant following electrical injury. The administration of PGE1 showed an advantageous effect in prevention of thrombosis and muscle "progressive necrosis" through improvement in RCD, reduction of PAR and the content of ET-1 in local circulation. CONCLUSION: RCD, PAR and the content of ET-1 in local circulation changed significantly following electric injury and may play an important role in the process of "progressive necrosis". The potential use of PGE1 in the treatment of electrical injury is proposed.

Procalcitonin--a sepsis parameter in severe burn injuries.

Procalcitonin (PCT) levels increase in patients with systemic infections; the highest levels have been found in sepsis. This study tested whether plasma procalcitonin level was related to sepsis, CRP, burn size, inhalation injury or mortality in severely burned patients over the entire clinical course. In 27 patients with 51 (20-91)% TBSA, PCT was measured three times weekly from admission over the entire course of stay in a single ICU. Daily scoring by the "Baltimore Sepsis Scale" was performed. The patients were assigned to three groups depending on the clinical course and outcome: A = no septic complications, B = septic complications-survivors, C = septic complications non-survivors. PCT levels were elevated slightly at admission (mean 2.1 ng/ml) except in three patients who suffered electrical burns (mean 15.7 ng/ml). PCT peak levels correlated well with the Scoring values (r = 0.84) while CRP did not (r = 0.64). Peak PCT levels were significantly higher (p < 0.005) in septic patients (B and C) who averaged 49.8+/-76.9 ng/ml, than in non-septic patients (A) who averaged peak levels of 2.3+/-3.7 ng/ml. The highest PCT levels were found immediately before death (86.8+/-97 ng/ml). Seven patients had an inhalation injury 3rd degree. In these patients at 24 h postburn, there was no relationship between PCT levels and inhalation injury but during the later days postburn there were significant differences in PCT levels in patients with versus without inhalation injury. All patients with inhalation injury 3rd degree developed septic complications. There was no positive correlation between the PCT-admission-levels and the TBSA, but there was a positive correlation between the TBSA and the mean peak PCT levels during the later days postburn (r = 0.73; p < 0.05). The cut-off value of 3 ng/ ml we found reliable to indicate severe bacterial or fungal infection. PCT values over 10 ng/ml increasing over the following days were found only in life-threatening situations due to systemic infections. The individual course of PCT in one patient is more important than absolute values. PCT presented in this study as a useful diagnostic parameter in severely burned patients.

[Mechanism of changes in coagulation after electric burns in rabbits].

The changes in local lesion after high-voltage electric burns ares dependent on many factors. One of the important factors is the change in coagulation. In this paper, a high-voltage electrical burn model was reproduced in rabbits for the purpose of investigating the coagulation mechanism. It was found that AT-III and PC showed elevation and declination, respectively, at 6h and 12h postburn. PAI:A and t-PA:A also showed obvious changes, while FDP showed continuous elevation at 6h up to 5d postburn. The findings probable provided the explanation of the occurrence of thrombosis at 6h to 12h postburn, and the second episode of thrombosis on the 5th day.