Effects of vitamin C combined with rbFGF on inflammatory factors and oxygen environment in patients with high-voltage electrical burns.

To investigate the effect of vitamin C combined with recombinant basic fibroblast growth factor (rbFGF) on inflammatory factors and oxygen environment in patients with high-voltage electrical burns. A retrospective analysis of 98 patients with high-voltage electrical burns admitted to our hospital from January 2021 to April 2022. A total of 98 patients were divided into research group and control group, including 49 cases treated with vitamin C combined with rbFGF and 49 cases treated with only rbFGF. The disappearance time of clinical symptoms, wound healing rate, area of granulation tissue growth, level of inflammatory factors, oxygen environment were compared between two groups after one and three courses of treatment. After treatment, the disappearance time of erythema, pain, swelling, blisters, exudate symptoms, wound healing time, scab formation time, and hospitalisation time in the research group were significantly better than those in control group (P < .05). There was no significant difference in the wound healing rate and area of granulation tissue growth between the two groups after one course of treatment (P > .05), while it is significantly better than those in control group after three courses of treatment (P < .05). The inflammatory factors, succinate dehydrogenase (SDH), lactate dehydrogenase (LDH) scores in research group were significantly better than that in control group after three courses of treatment (P < .05). Vitamin C combined with rbFGF may be worthy to reduce inflammatory factors, regulate oxygen environment, which can be popularised and applied in clinical practice.

Sociodemographic and culture results of paediatric burns.

Paediatric burn wounds are challenging conditions to manage for both the doctors and patients and can cause several complications entailing a complicated treatment and recovery process. This study aims to evaluate sociodemographic conditions and antibiogram culture results of paediatric burn wounds. Our study retrospectively evaluated 419 paediatric patients with burns regarding age, gender, burn area and degree, total days spent in hospital, surgical history, final condition, additional disease history, previous attempts, and culture results with their antibiotic resistances, haemogram results, C-reactive protein results, sociocultural conditions, burned region of the body, and structure of the burn. The prominent observations were an increased rate of incidence in male patients and patients with low socioeconomic conditions, the highest incidence of burns from scalding and domestic accidents, and the highest incidence of third-degree burns. Furthermore, even though the most encountered burn types were extremity burns, the burn types with the highest culture growth ratio were the perineum burns. The dominant culture growth bacterial group was coagulase-negative staphylococcus, and the ratio of medication resistance was 67.8%. It is imperative to raise awareness regarding domestic accidents to prevent paediatric burn wounds. The mortality risk can be reduced by carefully monitoring multiple organ involvement and providing timely treatment. Moreover, appropriate wound care is warranted to avoid infection from skin flora.

A Histologic Perspective on Electrical and Thermal Burn-Injured Human Skin.

OBJECTIVE: To analyze specific spectroscopic (FT-Raman) and thermal (limiting oxygen index) aspects of skin samples exposed to electrical injury compared with thermal injury. METHODS: An observational case-control study was conducted at the Dr Stanislaw Sakiel Center for Burns Treatment in Siemianowice, Silesia, Poland. A scanning electron microscope was used to diagnose and illustrate the topography of skin samples from electrical and thermal burns and the morphologic effects on damaged versus undamaged skin surfaces. In particular, researchers attempted to detect spectroscopic and thermal changes at the molecular level, namely, specific biomarkers of tissue degeneration and their regeneration under the influence of the applied modifiers (antioxidants and orthosilicic acid solutions). RESULTS: Modification with L-ascorbic acid and hydrogel of orthosilicic acid caused an increase in the intensity of the amide I Raman peaks, whereas modification with sodium ascorbate and orthosilicic acid resulted in the separation of the band protein side chains (1,440-1,448 cm), which is a part of tissue regeneration. The best result was obtained when the skin was treated with 7% orthosilicic acid (limiting oxygen index, 26%). CONCLUSIONS: Antioxidant treatment may be advantageous in minimizing injury in patients with thermal burns but not always in electrical burns.

LL-37-derived peptides eradicate multidrug-resistant Staphylococcus aureus from thermally wounded human skin equivalents.

Burn wound infections are often difficult to treat due to the presence of multidrug-resistant bacterial strains and biofilms. Currently, mupirocin is used to eradicate methicillin-resistant Staphylococcus aureus (MRSA) from colonized persons; however, mupirocin resistance is also emerging. Since we consider antimicrobial peptides to be promising candidates for the development of novel anti-infective agents, we studied the antibacterial activities of a set of synthetic peptides against different strains of S. aureus, including mupirocin-resistant MRSA strains. The peptides were derived from P60.4Ac, a peptide based on the human cathelicidin LL-37. The results showed that peptide 10 (P10) was the only peptide more efficient than P60.4Ac, which is better than LL-37, in killing MRSA strain LUH14616. All three peptides displayed good antibiofilm activities. However, both P10 and P60.4Ac were more efficient than LL-37 in eliminating biofilm-associated bacteria. No toxic effects of these three peptides on human epidermal models were detected, as observed morphologically and by staining for mitochondrial activity. In addition, P60.4Ac and P10, but not LL-37, eradicated MRSA LUH14616 and the mupirocin-resistant MRSA strain LUH15051 from thermally wounded human skin equivalents (HSE). Interestingly, P60.4Ac and P10, but not mupirocin, eradicated LUH15051 from the HSEs. None of the peptides affected the excretion of interleukin 8 (IL-8) by thermally wounded HSEs upon MRSA exposure. In conclusion, the synthetic peptides P60.4Ac and P10 appear to be attractive candidates for the development of novel local therapies to treat patients with burn wounds infected with multidrug-resistant bacteria.

Effect of lidocaine on reducing injury in a rat electrical burn model.

Electrical injuries induce progressive tissue loss. We evaluated the effect of lidocaine on tissue necrosis after electrical burn injuries. Forty-two male Wistar albino rats (250-300 g) were divided into 3 groups [Group A (n=6), control group without an electrical burn injury; and Groups B (n=18) and C (n=18), electrical burn injury groups without and with lidocaine therapy, respectively]. Three separate analyses were performed at different time points on 6 of 18 rats from Groups B and C at each time point. Electrical burns were induced by applying 220 V AC between the left upper and right lower extremities for 10 seconds. Myeloperoxidase and malondialdehyde levels were measured in skin and muscle biopsy specimens after the first hour, fresh and dry weight differences in the amputated extremities were calculated after 24 hours, and live and necrotic tissue areas were measured at 7 days after burn injury. We found that lidocaine reduced edema, the number of neutrophils, and neutrophil damage in tissues. We conclude that lidocaine decreased the amount of necrotic tissue caused by electric injury.

Burn wound angiogenesis is increased by exogenously administered recombinant leptin in rats.

BACKGROUND: Leptin is a potent direct angiogenic factor that stimulates endothelial cell migration and activation in vitro and angiogenesis in vivo. In addition, leptin has been discussed to play an important role in angiogenesis, as it promotes the formation of new blood vessels. PURPOSE: The effect of exogenously administered leptin on the healing process of a full tissue burn wound model. METHODS: Sixty-three Sprague-Dawley male rats were used. Full tissue burn wound was created by electrocautery. The width of the pin was 0.3 cm; its length was 2 cm and was used at the "cut" modulation. Rats were divided into seven groups of nine animals each. Burn wounds were injected with murine recombinant leptin and the rats were sacrificed 3, 7 and 9 days after surgery. Every group had obtained three animals for the three different days of sacrifice. Three different leptin doses of 250 pg/ml, 500 pg/ml and 1000 pg/ml were used in different animal groups (A, B and C). For every one of the three leptin doses used, another animal group was evaluated by using the combined injection of leptin and antileptin (A1, B1, and C1), in order to study the inhibitory effect to the leptin factor. Nine rats were served as controls. These were injected with 0.3 ml water for injection solution and sacrificed at the same time intervals. After sacrifice of the animals, the skin was grossly determined by its appearance, colour and texture. Full thickness burn wounds were dissected for histological examination. A qualitative analysis of angiogenesis in the burn wound was conducted following a standard hematoxylin and eosin stain. The wound tissue samples from each experimental group underwent immunohistochemical evaluation of microvessel density by endothelial cell staining with mouse anti-rat CD 34 monoclonal antibody. RESULTS: The most impressive growth of new blood vessels appeared seven and nine days after treatment with the highest leptin doses. There were no significant differences in microvessel density between the seventh and the ninth postoperative day among different groups treated with leptin. All wounds from the control group, as well as those from animal groups treated with the combined injection of leptin and antileptin did not develop any new vessels. CONCLUSION: Exogenous administration of recombinant leptin increases early tissue angiogenesis in the burn wound level of an experimental animal model.

Targeted release of stromal cell-derived factor-1α by reactive oxygen species-sensitive nanoparticles results in bone marrow stromal cell chemotaxis and homing, and repair of vascular injury caused by electrical burns.

Rapid repair of vascular injury is an important prognostic factor for electrical burns. This repair is achieved mainly via stromal cell-derived factor (SDF)-1α promoting the mobilization, chemotaxis, homing, and targeted differentiation of bone marrow mesenchymal stem cells (BMSCs) into endothelial cells. Forming a concentration gradient from the site of local damage in the circulation is essential to the role of SDF-1α. In a previous study, we developed reactive oxygen species (ROS)-sensitive PPADT nanoparticles containing SDF-1α that could degrade in response to high concentration of ROS in tissue lesions, achieving the goal of targeted SDF-1α release. In the current study, a rat vascular injury model of electrical burns was used to evaluate the effects of targeted release of SDF-1α using PPADT nanoparticles on the chemotaxis of BMSCs and the repair of vascular injury. Continuous exposure to 220 V for 6 s could damage rat vascular endothelial cells, strip off the inner layer, significantly elevate the local level of ROS, and decrease the level of SDF-1α. After injection of Cy5-labeled SDF-1α-PPADT nanoparticles, the distribution of Cy5 fluorescence suggested that SDF-1α was distributed primarily at the injury site, and the local SDF-1α levels increased significantly. Seven days after injury with nanoparticles injection, aggregation of exogenous green fluorescent protein-labeled BMSCs at the injury site was observed. Ten days after injury, the endothelial cell arrangement was better organized and continuous, with relatively intact vascular morphology and more blood vessels. These results showed that SDF-1α-PPADT nanoparticles targeted the SDF-1α release at the site of injury, directing BMSC chemotaxis and homing, thereby promoting vascular repair in response to electrical burns.

Ocular and facial injuries associated with the use of immersion heaters in an inmate population.

PURPOSE: To report ocular and facial injuries caused by the use of electric immersion heaters in an inmate population. DESIGN: Prospective observational case series. METHODS: Data were recorded over a six-month period on age, gender, mechanism of injury, examination, and treatment of Dallas County inmates who experienced ophthalmic injuries from immersion heaters and were referred to a tertiary-care center. RESULTS: Eight male inmates were treated for thermal ocular injuries, which occurred within jail cells as a result of cooking explosions from electric immersion heaters, known by inmates as "stingers." All patients had thermal eyelid burns, either first- or second-degree facial burns, and corneal abrasions with corneal edema. Corneal metallic foreign bodies were removed in one patient, and three patients underwent debridement for corneal sloughing. CONCLUSIONS: Immersion heater-related accidents may cause thermal injuries within the inmate population. Physicians evaluating incarcerated patients with ocular trauma should be aware of immersion heaters as a common cause.

Liposomes as drug carriers for oral ulcers.

The aim of this study was to test the potential of liposomes as drug carriers to the ulcerated oral mucosa. Radioactive triamcinolone acetonide palmitate (3H-TRMAp) was encapsulated in large multilamellar lipid vesicles and served as the test lotion. 3H-TRMAp in solution served as control. Forty-six hamsters were divided into three groups. In group I, multiple confluent ulcers in both cheek pouches were treated by topical application. In group II, single ulcers on the cheeks were treated by intramucosal injection. In group III, multiple confluent ulcers were produced in the cheek pouch on one side, with a single ulcer in the contralateral cheek pouch; no drug was applied, and the tissues were prepared for histology. Hamsters were killed at three and 24 hours, respectively, after treatment. Pouches were divided into ulcerated and intact adjacent mucosa. Cheeks were divided into ulcerated mucosa and distant mucosa. Drug levels in the four mucosal portions as well as in the blood, liver, spleen, brain, and thalamic region were determined by radioactive tracer technique. At three hours, liposomal drug concentrations were lower than in control animals in the brain and the thalamic region. At 24 hours, liposomal drug values were higher than in control animals in the ulcerated mucosa and lower than in control animals in the thalamic region. Mean drug concentrations in the ulcerated mucosa were higher in group II than group I. The results parallel those of Mezei and Gulasekharam (1980, 1982); liposomes increase local and decrease systemic drug concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Citric acid treatment of severe electric burns complicated by multiple antibiotic resistant Pseudomonas aeruginosa.

A case of severe electric burns complicated by multiple antibiotic resistant Pseudomonas aeruginosa not responding to various antibiotics administered systemically is presented. Citric acid (3%) was used successfully to eliminate Pseudomonas aeruginosa from burn wounds and infection was completely controlled in 14 days. Citric acid treatment is evidently of value in the clinical control of burn wound colonization caused by difficult strains of Pseudomonas aeruginosa.

A new explanation for the progressive tissue loss in electrical injuries.

A reproducible electrical injury to the hind limb was produced in rats, an injury characterized by progressive tissue necrosis. Serial histochemical examinations of cross sections with a peroxidase-antiperoxidase method revealed increased production of arachidonic acid metabolites, especially thromboxane, at distal sites near the entrance wound and in periosseous tissues more proximally. Levels of these vasoactive substances remained elevated during the time of progressive necrosis and demarcation of seemingly normal, uninjured tissue. Treatment with agents capable of blocking thromboxane production allowed tissue salvage, as evidenced by a decreased autoamputation rate and an increased total surviving length. From this study it appears that an electrical injury is thermal trauma, producing elevated levels of arachidonic acid metabolites in areas of greatest heat production. Prolonged thromboxane excess, with resultant vasoconstriction and thrombosis in the microcirculation, is seen to play a key role in the progressive tissue loss characteristic of the injury. The use of antithromboxane agents may be of benefit in halting this progression and salvaging tissue in these devastating injuries.

Emergence of a multiply-resistant strain of Acinetobacter in a burns unit.

Multiply-resistant Acinetobacter has emerged as an important organism in the Burns Unit of the Singapore General Hospital. From November 1990 onwards, a strain that was resistant to all antibiotics except Polymyxin B emerged in the Burns Unit. We present two cases where the Acinetobacter isolated was resistant to all antibiotics including Polymyxin B. These cases serve as an important reminder to adhere to strict infection control procedures.

The use of growth hormone in the treatment of extensive burns: a case report.

Growth hormone is an anabolic hormone that causes increased cell growth, positive nitrogen and calcium balance, lipolysis, hyperglycemia, and promotes protein synthesis. Its beneficial effect in burn treatment was proven particularly in children, by Herndon's group. The authors report The case of a 12-year-old boy with an electrical arc burn of 81% of the BSA, 60% of the BSA being full thickness loss. Recombinant human growth hormone (Norditropin, Novo Nordisk) was administered at daily doses of 0.52 i.u./kg starting on day 19 post-burn for 15 consecutive days. The treatment was well tolerated except for mild insulinoresistance, which could be easily corrected by slightly increasing the insulin added to glucose solutions. After 56 days of intensive care treatment and several excision and grafting procedures, the majority of burns were healed.

[Early surgical treatment of injured persons with subfascial electric burn of extremities in combination with preparation Betadine]. / Rannee khirurgicheskoe lechenie postsradavshikh s subfastsial'nym élektroozhogom konechnostei v komplekse s preparatom Betadin.

Basing on the clinical material analysis, on bacteriological investigation data, smear-"prints", the authors recommend application of 10% solution of Betadine for sanatation of the electric wounds with subfascial structures affection, what have permitted to accelerate the wound surface clearance, to reduce exudation, to activate the primary granulation tissue development to prepare the wound for its plastic closure. Application of Betadine in conditions of aseptic inflammation had promoted the secondary necrosis occurrence in the tissue ischemia after deep burn occurrence.

Effects of parecoxib on the prevention of postoperative peritoneal adhesions in rats.

BACKGROUND: No systemic preventive therapy has been successful in inhibiting the development of postoperative peritoneal adhesions (PPAs). OBJECTIVE: The aim of this study was to evaluate the potential effects of 5 day administration of parecoxib, on PPA prevention and on suture or wound healing in rats. METHODS: In a model of PPAs induced by peritoneal electrical burn, 30 rats were randomized into 3 groups according to parecoxib administration route (control; intraperitoneal (IP); intramuscular (IM)). Plasma and peritoneal levels of PAI-1 and tPA were measured at T0, after 90 min of surgery (T90), and on postoperative day 10 (D10). In a cecum resection model, 20 rats were randomized into two groups (control and IP parecoxib), and abdominal wound healing and suture leakage were assessed at D10. In both models, PPAs were evaluated quantitatively and qualitatively on D10. RESULTS: Administration of parecoxib significantly decreased the quantity (p < .05) and the severity (p < .01) of PPAs in both models. In addition, parecoxib administration did not cause healing defects or infectious complications in the two models. In the peritoneal burn model, IP or IM parecoxib administration inhibited the increase of postoperative plasma and peritoneum PAI-1 levels, an increase that was observed in the control group (p < .01). No anastomosis leakage could be demonstrated in both groups in the cecum resection model. CONCLUSION: This study showed that, in these rat models, parecoxib might reduce PPA formation. Confirmation of the safety of parecoxib on intestinal anastomoses is required and should be investigated in further animal models.

Fucoidin, a neutrophil rolling inhibitor, reduces damage in a rat electrical burn injury model.

BACKGROUND: Electrical injuries induce progressive tissue loss caused by free oxygen radicals released from neutrophil aggregates. Fucoidin, a potent inhibitor of L-selectin function, reduces the aggregation of neutrophils. The aim of this study was to evaluate the effect of fucoidin on tissue damage in rat electrical burn injury model. METHODS: Forty-two male Wistar albino rats (250-300 g) were divided into 3 groups (Group A (n=6), control group without electrical burn injury; Groups B (n=18) and C (n=18), electrical burn injury groups without and with fucoidin therapy, respectively). Three separate analyses were performed at different time points on 6 out of 18 mice from Group B and C at each time point. Biochemistry (myeloperoxidase and malondialdehyde levels) and histopathology (number of neutrophils) of the skin and muscle biopsies at 1st hour; tissue edema (ratio of wet weight/dry weight of extremities) at 24th hour; and necrotic areas at 7th day after electrical injury were evaluated. The electrical burn was induced by exposing rats to 220 V AC between their left upper extremity and right lower extremity for 10 s. Fucoidin was administered as 25 mg/kg intravenous bolus injection at 15 min after electrical burn injury. RESULTS: Myeloperoxidase and malondialdehyde levels, number of neutrophils, tissue edema, and necrotic area were significantly less in fucoidin-applied rats than the group without fucoidin therapy. CONCLUSIONS: Fucoidin inhibits tissue damage induced by electrical burn injury in rats by reducing necrotic area, edema and number of neutrophils.

[Alteration in bulbar conjunctiva microcirculation and interventional effect of Pentoxifylline after high-voltage electrical burn in rabbits].

OBJECTIVE: To study the changes in bulbar conjunctiva microcirculation (BCM) and the therapeutic effect of Pentoxifylline on BCM disturbance after high-voltage electrical burn (HEB) in rabbits. METHODS: Forty-five rabbits were divided into control group (C), electrical burn group (EB), and Pentoxifylline treatment group (PT) according to random number table, with 15 rabbits in each group. Model of HEB was reproduced in rabbits from EB and PT groups with voltage regulator and experimental transformer. Rabbits in C group were sham injured with the same devices without electrification. Changes in BCM were observed with microcirculation microscope at 15 minutes before HEB and 5 minutes, 1, 2, 4, 8 hour(s) post HEB (PHM or PHH), including: (1) morphology of microvessels, such as the discernible, diameters of arterioles, venules, and capillaries, the unevenness in caliber, and ischemic area; (2) dynamic changes in microvascular blood flow, such as blood flow speed in arterioles, venules, and capillaries, erythrocyte aggregation, and microthrombi formation; (3) condition of tissues surrounding microvessel, such as bleeding and exudation. Measurement data were processed with t test; enumeration data were processed with Fisher's exact test. RESULTS: (1) Morphology of microvessel: discernible of microvessels in EB and PT groups was decreased, but that of PT group was better than that of EB group. At PHM 5, diameter of arterioles, venules and capillaries was respectively (7.3+/-2.5), (12.3+/-2.4), (3.5+/-0.7) microm in EB group, all narrower than those of the control group [(14.6+/-3.1), (27.2+/-3.5), (9.0+/-1.4) microm, with t value respectively 5.23, 13.66, 14.04, P values all below 0.05]. Diameters of the microvessels in PT group [(10.2+/-3.8), (21.5+/-3.1), (7.1+/-1.2) microm] were larger than those in EB group (with t value respectively 2.21, 8.99, 10.18, P values all below 0.05). Diameters of arterioles, venules and capillaries in EB and PT groups recovered to the before HEB size at PHH 1. From PHH 2 to 8, arterioles and capillaries decreased gradually in caliber, venules dilated gradually in EB and PT groups, but the changes in PT group were not obvious. Thickness of microvessel was observed uneven in EB group at PHM 5, which lasted until PHH 8. Ischemia of the tissue was observed in EB group at PHM 5, which improved at PHH 2. Situation in PT group was better. (2) Dynamic changes in microvascular blood flow: at PHM 5, blood flow speed in arterioles, venules and capillaries was respectively (202+/-53), (198+/-44), (46+/-12) microm/s in EB group, all slower than those of the control group [(544+/-37), (359+/-32), (220+/-19) microm/s, with t value respectively 20.47, 11.51, 30.02, P values all below 0.05], and those of PT group [(335+/-42), (260+/-35), (119+/-23) microm/s] were faster than those of EB group (with t value respectively 7.55, 4.26, 14.85, P values all below 0.05). Blood flow speed in EB and PT groups recovered to the before HEB level at PHH 1. From PHH 2 to 8, blood flow speed decreased gradually in EB and PT groups, but that of PT group was faster than that of EB group. Erythrocyte aggregation in venules and capillaries was observed in EB group at PHM 5, which eased up at PHH 1, but aggregated at PHH 2, lasting until PHH 8. Obvious microthrombi were observed in EB group at PHH 2, which increased gradually. These changes were less obvious in PT group. (3) Condition of surrounding tissues of microvessel: in EB group, exudation was observed around microvessels at PHH 1, bleeding at PHH 2, with a worsening tendency. Changes in those in PT group were less obvious. CONCLUSIONS: HEB causes disturbance in BCM, but it can be ameliorated by Pentoxifylline.