Electrical burns, although less common compared with other burn types (comprising about 5% of all admissions to burn treatment centers1), constitute a serious problem because of high patient mortality. Patients with burns caused by high electrical voltage are more likely to develop deep tissue damage and compartment syndrome.2,3 High-voltage burns more closely resemble crush injury than standard burns because of progressive tissue necrosis that can penetrate deep inside bone.4,5 Histologically, however, the damaged skin reveals features similar to thermal burns.6,7
Electrical injuries are unique because of the pathophysiologic mechanism of the electric field, which can cause additional injury independent of increased tissue temperature. Electrical injury causes thrombotic vascular insult (both micro and macro).6,7 Of patients with electrical injury, 90% have mononeuropathy,8,9 which can be caused by vascular occlusion of the vasa nervorum and direct destruction of nerves.5,10
Electrical injuries can occur after contact with both high (>1,000 V) and low voltage (usually 220 or 360 V).4,7–14 In the case of exposure to high-voltage currents, the range of organ damage can be very broad and cause more serious tissue damage.6,14–16 Temperature is a critical factor deciding the degree of tissue damage.2,3 Electric arcs can reach temperatures up to 2,000° C and cause thermal and electrical burns of varying depth and resulting damage to internal organs.2,3
The main cause of death after electrical injury is cardiac arrest or respiratory function impairment. In addition, electrical burns can lead to deep tissue necrosis and organ damage as well as to secondary systemic disorders.11,17 Unlike in thermal burns, the extent of the damage after an electrical burn may be difficult to estimate in the short term.16,18 Over time, patients with electrical burns may demonstrate necrotic changes to the skin and subcutaneous tissue, cardiac necrosis, damage to the central nervous system, and secondary multiple organ failure.17,19 The most common complication of an electrical burn is sepsis, which occurs in approximately 24% of patients.12,13
Clinical outcomes depend on the burn's pathway through the victim’s body and the length of contact with the power source.17,19 A vertical pathway (parallel to the body axis) is the most dangerous because it has the potential to affect all of an individual’s organs. Horizontal paths through the chest can also be fatal if the electrical current travels through the heart, lungs, and/or central nervous system. A pathway through lower body parts is associated with a lower risk of death.
Although electrical burns are quite different from thermal and chemical burns,20,21 there are no treatment guidelines specific to electrical burns.22,23 In general, early debridement is a good treatment option; however, deep muscle injury may not be apparent during early debridement.19,24 Multiple operations should not be viewed as a failure.19,24
Current clinical procedure treats both thermal and electrical burns the same way. The aim of this study was to analyze specific spectroscopic (FT-Raman) and thermal (limiting oxygen index [LOI]) aspects of electrical injury compared with thermal injury. In particular, researchers attempted to detect spectroscopic 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) to discover better treatments for electrical burns specifically.
This study was approved by the Bioethics Committee in Bielsko-Biała (no. 2015/12/03/01), and conducted in accordance with the Declaration of Helsinki. All patients gave their informed consent after an explanation of the facts, implications, and outcomes of the proposed study was provided; participation was voluntary, and the anonymity of participants was preserved.
Data and Skin Samples
Data were collected from a database of 583 patients with thermal and electrical burns who were hospitalized at the Dr Stanislaw Sakiel Center for Burns Treatment in Siemianowice, Silesia, Poland, in 2016. Patient age and sex, percent of the total body surface area (TBSA) burned, length of hospitalization, the need for amputation, the need for rehabilitation, and patient mortality were all assessed.
The test group comprised skin samples acquired from patients included in the database; the selection criterion was the type of burn: high- or low-voltage electric burn. Skin samples from two patients were included (Table 1), a 48-year-old man (10S) and a 22-year-old man (11S).
Human Skin Sampling Procedure
The exact procedure of biopsy material extraction from patients with burn injuries is as follows.
Biopsy material was obtained as a result of necrosis resection and placed in 0.9% saline and was stored in a freezer for further studies. Active antioxidants (7% L-ascorbic acid or sodium ascorbate) and 20% lauric acid and 7% H4SiO4 × nH2O hydrogels and 80% dimethyl sulfoxide (DMSO) solutions were applied to biopsied skin.
The samples were prepared for FT-Raman spectroscopic and scanning electron microscopy (SEM) analysis by drying them in a laboratory dryer at 35° C for 3 days. Allogeneic unburned full-thickness skin was added as a control to complement basic research.
The surface of the skin samples was examined using a JSM 5500LV scanning electron microscope (JEOL Ltd, Akishima, Tokyo, Japan) to diagnose and illustrate the morphologic effects of damaged and undamaged allogeneic skin. The samples were placed on aluminum stubs and coated with gold (JFC 1200; JEOL Ltd). Secondary electrons and back-scattered electrons were observed using an accelerating voltage of 10 kV. Microphotographs were taken at magnifications between ×35 and ×500.
FT-Raman Spectroscopic Analysis
FT-Raman spectrometry was used to assess collagen molecular structure changes in electrical injuries compared with thermal injuries. The FT-Raman spectra of the samples were recorded on an FTS 6000 spectrometer equipped with a MAGNA-IR 860, NICOLET, with FT-Raman accessory. The solid samples were then irradiated with a 1,064-nm line YAG laser, and scattered radiation was collected with 4-cm−1 resolution.
Limiting Oxygen Index Method
The obtained flame-retardant effect of skins was evaluated using the LOI method. The selection of the LOI method for examining skin flammability was based on similar research for protein fibers, collagen fibrous protein (eg, wool, bovine leather),23–32 and flame-retardant leathers produced from pigskin by adding nanocomposite.33,34 The parameter that characterizes the method is the lowest percentage of oxygen in the mixture with nitrogen, at which the test specimen ignites and burns on its own. The measurements were performed in accordance with PN-ISO 4589 standard.
Statistical analysis was performed with the STATISTICA 12 software (StatSoft, Krakow, Poland). The normal distribution assumptions were tested with the Shapiro-Wilk test. Statistical hypothesis testing for two independent samples was determined by the Mann-Whitney U test. The significance level was P = .05. The data were collected in the Solmed software (SPIN, Katowice, Poland).
Among patients with electrical burns, mortality was 8%, whereas in the group with thermal injuries it was 5%. The majority of people admitted to the burn ward were male: 95% of electrical injuries and 66% of thermal injuries, a significant difference (P = .009). Patients admitted because of electrical burns were significantly younger (P = .015), by an average of 10 years, compared with patients with thermal burns.
The average age of patients with electrical burns was 37 ± 13 years. This is generally older than the findings presented by Kurt et al,16 who conducted their study on 94 patients whose average age was 26.4 ± 13.2 years. Aguilera-Sáez et al15 confirm that electric shock injuries affect mainly young males and are the leading cause of amputations in this population. In this study, 16% of patients with electrical injuries underwent amputation, whereas only 12% of the group with thermal injuries did (P < .001).
The TBSA was not significantly different in either group; 91% of all studied thermal burns covered less than 20% of TBSA, compared with 100% of all studied electrical burns.
Electrical burns differ visually from the surrounding skin; these burns are much deeper, the damage affects the whole thickness of the skin, and cracks and charring can be visible. Burn depth translates in a statistically significant way into the length of hospitalization, which was significantly longer for patients with electrical burns (P = .016) by an average of 11 days.
Figures 1 and 2 present skin surface topography and the cross section of an electrically degraded human epidermal necrotic scab sample. In contrast, Figure 3 presents the surfaces of allogeneic undamaged human skin samples. Figure 1 shows atrophy of natural corrugation and epidermal damage in the form of electrical cracking of the surface. After electrical burns, characteristic electric marks occur on the skin. The burns are much deeper there, the damage affects the whole thickness of the skin, and deep cracks (even holes) or melting of collagen fibers is visible. Electrical injury is relatively uncommon, but it is a devastating form of thermal injury, and the incident can lead to coagulation necrosis in a few seconds.
Samples of burned human skin are characterized by altered surface morphology. Figure 4 shows the influence of modifiers (the solution of L-ascorbic acid and lauric acid and H4SiO4 × nH2O) minimizing the effects of electrical burns. Generally speaking, the topography of the surface of skin samples incubated in the solution of the antioxidant and orthosilicic acid demonstrates the development of a structure resembling a coherent solid composite. In particular, by comparing Figures 1 and 2 (electrically damaged human skin) and Figure 3 (allogeneic undamaged human skin) with Figure 4, it can be noted how the substances selected for the surface modification of the samples cover the damaged tissue.
FT-Raman Spectroscopic Analysis
Analyses of bands in FT-Raman spectra in the region of the amide I band (~1,665 cm−1), the CH2 scissoring band (~1,445 cm−1), structural proteins, amide III, phospholipid membranes (1,240-1,304 cm−1), protein side chains (1,440-1,448 cm−1), phenylalanine (1,030 cm−1), and proline and hydroxyproline (930 and 860 cm-1) bands in burned human skin are shown in Figures 5 and 6. A decrease in intensity of the above Raman bands for samples 11S (with a 6 kV electrical burn) was observed in comparison with sample 10S (1-kV electrical burn). Figure 5, in particular, shows a decrease in the intensity of the amide I Raman peaks and other bands mentioned above, which proves that high-voltage electrical burns (11S) cause more serious tissue damage than 1-kV electrical burns (10S) and thermal burns.
An increase in the intensity of the same Raman peaks (1,746, 1,664, and 1,542 cm−1; Figure 6) for 10S samples shows the healing process observed during modification of the degraded skin by antioxidant solutions. The lipid band 1,245 cm−1 is exposed during electrical damage of the skin, although its intensity decreases after treatment with modifying solutions.
Limiting Oxygen Index Method
Results of initial LOI measurements of studied skin are presented in Table 2. In the case of skin burned by electric current (6 kV), application of antioxidants (11S2, 11S3 in Table 2) does not bring intended results. The LOI is in this case significantly reduced in relation to the LOI of the burned skin that was not treated with antioxidants. In the case of skin burned by a lower-voltage electric current (1 kV), the situation seems a bit better (10S2 in Table 2). This is most likely attributable to the depth of skin damage caused by electrical burn (ie, in the case of burns caused by lower-voltage currents, the skin is less damaged).
This study began with a comparison of the skin samples (topography of the necrotic scab; Figures 1 and 2) using FT-Raman and LOI studies. In particular, SEM was used to diagnose and illustrate the morphologic effects of damaged (Figures 1 and 2) and undamaged skin surfaces (Figure 3). In other studies, the effects of thermal damage to demarcated epidermis of both animal33,35,36 and human26,27,36–38 have been presented; the skin samples are morphologically different. The degree of tissue damage depends on the type of burn (I–III) and burn cause, TBSA burned, location of sample extraction (on the patient's body), and patient sex.
The mechanism of modification of the surface and the influence of the modification on the process of skin regeneration are the subject of earlier research.26,27,33,35–38 Generally speaking, the topography of the surface of skin samples incubated in antioxidant and orthosilicic acid solutions demonstrates the development of a structure resembling a coherent solid composite. It is worth noting that antioxidant solutions (L-ascorbic acid or sodium ascorbate) smooth the damaged surface of human skin and animal skin in a different way.33 Vitamin C, in particular, seems to be important; apart from functioning as an antioxidant and protecting against oxidative stress, vitamin C participates in collagen synthesis, which is critical in wound healing, and applied locally to the skin stimulates collagen production in human skin in vivo.39
Whereas SEM was used to illustrate skin surface changes, FT-Raman spectrometry was used to assess molecular structure changes in electrical injury compared with thermal injury. Figure 5 shows a decrease in the intensity of the amide I Raman peaks and other bands, which proves that high-voltage electrical burns (11S) cause more serious tissue damage than 1-kV electrical burns (10S) and thermal burns (S). The observations that high-voltage electrical burns cause more serious tissue damage because of high amounts of energy are confirmed in other reports.3,6,16 An increase in the intensity of the same Raman peaks (1,746, 1,664, and 1,542 cm−1; Figure 6) for 10S samples shows the healing process observed during modification of the degraded skin by antioxidants. In particular, the emergence of 1,245-cm−1 band, characteristic of intact allogeneic skin (Figure 6), is the sign of epidermal lipids modification by DMSO solution.38
Although the exact mechanism of modification of burned skin with active antioxidants has been the subject of earlier research,26,27,33,35–38 it is worth noting in this study that modification with L-ascorbic acid and orthosilicic acid hydrogel causes an increase in the intensity of the amide I Raman peaks (samples 10S in Figure 6) and results in separation of the band protein side chains (1,440-1,448 cm−1, sample 11S3 in Figure 6), which is a sign of tissue regeneration.37
Observed differences in the values of thermogravimetric analysis and small-angle X-ray diffraction presenting changes in the supramolecular structure of protein were analyzed in detail in an earlier study,37 allowing the authors of the current study to better understand the mechanism of modification of the surface of the burned skin and the influence of the modifying substances on the process of skin regeneration. It is worth noting, on the basis of the results presented in Figure 6, that tissue damaged by high-voltage electricity (6 kV; sample 11S) does not show regeneration characteristics in the region of the amide I band. The interpretation of changes within an intense 706- and 671-cm–1 band from DMSO was the subject of a subsequent study.38
Spectroscopic studies were complemented with the LOI method, used in macroscopic evaluation of the effectiveness of modification with antioxidants and orthosilicic acid solutions. It is worth adding that although the test is always performed on an artifact (burned) tissue, it is an indirect source of useful information about polymer structure.28–32,34,38
The objective of the earlier detailed studies40 was ex vivo examination of injured human skin with DMSO, a chemical compound that easily penetrates biologic membranes to modify the structure of the tissue. In particular, the DMSO changes the scope of penetration of chemical compounds in biologic membranes, including human skin, affecting the nature of interactions in protein-lipid membranes.
Thermal injury is associated with the appearance of lipid peroxidation products in burned skin. Correlation of the abilities of DMSO and other agents to enhance membrane permeability of solutes through rat skin and fluidity of liposomal membranes modeling stratum corneum has also been reported.34 The DMSO accelerates fixation and enhances stabilization of cellular ultrastructure via its interaction with remnant interfacial water in fixed cells.40 Lipid fusogens could induce a conformational change in the bilayer-forming lipids at physiologic and probably also at pathologic temperatures (eg, in burns).
These reasons are at the root of the researchers’ choice of this study’s modifiers, that is, L-ascorbic acid, an orthosilicic acid hydrogel, sodium ascorbate, DMSO, and lauric acid. In analyzing these results, one should ask whether external treatment with antioxidants on skin that is so damaged is justifiable and whether the addition of DMSO, a solvent that easily penetrates necrotic eschar, has sufficient impact on the LOI to reverse the damage. These results show an increase in the LOI for thermal burn injury samples treated with a mixture of antioxidants38 (Table 3) and a decrease in the LOI (Table 2) for electrical burn injury samples treated with a mixture of antioxidants and DMSO. The latter observations confirm an earlier thesis proved by the spectral tests; in general, tissue damaged as a result of an electrical burn appears to lose its regenerative properties.
Although electrical burns, which are severe burns, are less common compared with other burn types, they constitute a serious problem because they their higher mortality. Despite the differences between electrical and thermal burns, the criterion standard of treatment is the same. The aim of this study was to draw attention to specific aspects of electrical injuries in comparison with thermal injuries. It was observed that antioxidant treatment may be advantageous in minimizing injury in patients with thermal burns but not always in electrical burns. Because regenerative reactions in wounds are dynamic and complex, these results may help inform clinical practice.
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Keywords:Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
antioxidant; burn treatment; electrical burns; limiting oxygen index; orthosilicic acid; spectroscopy; thermal burns