Roadblocks to return to work after electrical trauma.
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Biomedical subjects
Publications and source records attributed to M Capelli-Schellpfeffer.
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Electrical injuries to the upper extremity are far ranging in extent and vary in magnitude. Proper management requires an appreciation for the pathophysiology, clinical manifestations, and therapeutic options. Persistent neurologic and psychiatric problems further impact the high incidence of disability in the electrical injury patient. Loss is significant for victims, their families, and employers, in part because of the relative youth of those injured.
Electrical arcs commonly occur in electrical injury incidents. Historically, safe work distances from an energized surface along with personal barrier protection have been employee safety strategies used to minimize electrical arc hazard exposures. Here, the two-dimensional computational simulation of an electrical arc explosion is reported using color graphics to depict the temperature and acoustic force propagation across the geometry of a hypothetical workroom during a time from 0 to 50 ms after the arc initiation. The theoretical results are compared to the experimental findings of staged tests involving a mannequin worker monitored for electrical current flow, temperature, and pressure, and reported data regarding neurologic injury thresholds. This report demonstrates a credible link between electrical explosions and the risk for pressure (acoustic) wave trauma. Our ultimate goal is to protect workers through the design and implementation of preventive strategies that properly account for all electrical arc-induced hazards, including electrical, thermal, and acoustic effects.
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The clinical spectrum of electrical injury ranges from the absence of any external physical signs to severe multiple trauma. Reported neuropsychiatric sequelae can vary from vague complaints, which may seem unrelated to the injury in their occurrence over time or by their apparent severity, to sequelae consistent with brain injury accompanying an electrical trauma. In this report, a case study and discussion are presented on the management and coordination of post-acute care of an electrical trauma survivor. Expertise and a multidisciplinary team are essential to cohesive patient care. Patient monitoring for progressive changes and prompt intervention are needed to address the potential difficulties experienced by trauma survivors as they rehabilitate to return to their work and their activities of daily living.
PURPOSE: We review the use of hyperbaric oxygen therapy in urology, and present the mechanisms of hyperoxia action in whole body hyperbaric chamber treatments, patient outcomes and patient selection criteria. MATERIALS AND METHODS: The literature on hyperbaric oxygen use in urology was reviewed. RESULTS: Hyperbaric oxygen is a treatment alternative for patients with an underlying ischemic process unresponsive to conventional therapy. Specific factors which may influence patient selection of hyperbaric oxygen include cancer and absolute contraindications of active viral disease, intercurrent pneumothorax and treatment with doxorubicin or cisplatin. This technique is particularly useful in the treatment of intractable hemorrhagic cystitis secondary to pelvic radiation therapy. Further investigation of the efficacy of hyperbaric oxygen is warranted for patients with necrotizing fasciitis (Fournier's gangrene), posttraumatic ischemic injury and/or impaired wound healing. CONCLUSIONS: Hyperbaric oxygen is a therapeutic alternative which complements the surgical and medical options for select patients.
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Damage to the cell membrane has been implicated as the primary event in the pathogenesis of heat shock, generally resulting in loss of cellular homeostasis and cell death. Thus a promising mode of therapy would involve the restoration of cell membrane integrity. Surfactant molecules, specifically triblock polymers such as Poloxamer 188 (P-188), possess the ability to self-aggregate into membrane-like structures in aqueous solutions and have been shown to restore membrane integrity. The objective of this study was to develop functional and morphological assays to determine whether treatment with P-188 after heat shock enhances the recovery of thermally damaged cells. Human foreskin fibroblasts were placed in sterile vials and heated by immersion in a calibrated water bath for various lengths of time at predefined temperatures. Cell recovery after heat shock was assessed using a functional assay based on the ability of the cells to contract fibroblast populated collagen lattices (FPCLs). Subsequent to heating, collagen lattices were prepared with control (no heat, no P-188) and heat shocked cells (with and without P-188). Our results indicate that treatment with low concentrations of P-188 after heat shock was effective in ameliorating both the morphological integrity and the contractile function of thermally damaged cells. Further, we observed that P-188 was most effective in improving the contractile ability of cells heat shocked at 45 degrees C; however, it had no influence on the contractility of cells exposed to higher temperatures. Our results suggest that there exists a threshold of thermal stress (45 degrees C for 20-60 min) beyond which treatment with low concentrations of P-188 (0.5 mg/ml) is ineffective in minimizing cell damage. Moreover, the results of our morphological assays indicate that cells treated with P-188 after heat shock maintain their cytoskeletal organization, whereas untreated cells exhibit filamentous actin depolymerization.
OBJECTIVE: This study explored the relationship of neuropsychological complaints to accident- and injury-related characteristics, affective state, and work status in a group of electrical injury (EI) patients. METHODS: Sixty-three EI patients and 22 electricians with no history of electrical shock completed the Neuropsychological Symptom Checklist and the Beck Depression Inventory as part of an extensive neuropsychological evaluation. RESULTS: The EI group endorsed significantly more physical, cognitive, and emotional symptoms than did the controls. Symptom complaints were not related to injury parameters or litigation status. Only the time interval between injury and assessment accounted for differences in symptom presentation, with patients in the postacute stages of recovery showing the most cognitive and emotional complaints. CONCLUSION: The neuropsychological syndrome of electrical injury survival includes physical, cognitive, and emotional complaints. Considering that most electrically injured patients are treated within the acute medical setting, greater attention needs to be directed early in the course of treatment toward addressing neuropsychologic and psychiatric issues.
A study of the effects of electrical shock on peripheral nerve fibres is presented. Strength and duration of the applied shocks were similar to those encountered in a typical industrial electrical accident. The purpose of this study is: (i) to identify the electrophysiological and morphological change in nerve fibres after the application of electrical current shocks; (ii) to examine the ability of the peripheral nerve fibres to spontaneously regain function and; (iii) to demonstrate the usefulness of the sensory refractory spectrum as an additional technique in assessing the damage. Three groups of animals received twelve 4-ms electric field pulses of approximately 37 V/cm (n = 5), 75 V/cm (n = 9) and 150 V/cm (n = 6), respectively. Group 4 was a control group and received a direct application of 2 per cent lidocaine over the sciatic nerve for 30 min. Thermal effects of the shocks were negligible. The sensory refractory spectrum shows that electrical shock damage was mainly to the large, fast myelinated fibres and that higher field strengths do more damage. Also in a histological examination it was found that the more heavily shocked myelinated fibres had sustained more damage.
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Joule heating has long been considered the principal component of tissue damage in electrical injury. Recent studies suggest electroporation, a nonthermally mediated mechanism of cell membrane damage, is also a factor. We investigated whether electroporation-mediated muscle necrosis can occur in vivo without significant Joule heating. Pulsed electric fields approximately 150 V/cm were produced in the hind limbs of anesthetized rats. In shocked limbs core muscle temperature rose less than 1.8 degrees C, yet significant damage occurred as determined by technetium-99m pyrophosphate uptake, elevated serum creatine phosphokinase, and prominent hypercontraction band degeneration of myofibers on histopathologic examination. This study is significant because it directly addresses whether nonthermal mechanisms of cell damage can cause tissue necrosis. These results indicate that electroporation effects can mediate skeletal muscle necrosis without visible thermal changes. Thus the phenomenon of "progressive recognition" may be characteristically largely explained by the occurrence of nonthermally mediated tissue damage.