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At least 19 recordsLinked to original sources
PubMedDate not supplied

Determination of tissue viability in experimental electrical injuries.

Electrical burns or ischemia (induced by vascular ligation) were produced in the legs of 15 anesthetized dogs to study evolution of tissue changes compared with impedance alterations. After the application of 1-ampere currents at 60 Hz, animals were monitored from 1 to 4 days. Muscle impendance was measured with frequency sweeping to determine tissue destruction. Nuclear magnetic resonance spectroscopy (phosphorus 31) was used to assess metabolic activity, and results were compared to impedance measurements. In burned limbs, 70% reduction in muscle impedance was seen, which corresponds to decreased metabolic activity (absent organic phosphates) and suggests necrosis. Visually viable tissue had impedance decreases of 25% and levels of organic phosphates slightly lower than normal. Relaxation frequencies in dogs with severe burns exceeded 80 kHz; in viable tissue, 30 to 40 kHz (normal: 30 kHz). In ischemic muscle, organic phosphates decreased rapidly (1 to 2 hours); impedance changes evolved more slowly (1 day), but they ultimately reached the same degree of severity. Measurement of impedance may be a valuable adjunct in the evaluation of electrical burns, since significant changes strongly suggest nonviability.

Animals↗
PubMed1977

The natural history of electrical injury.

The natural history of electrical injury, exclusive of electrical flash burns, was determined in 64 patients. These patients sustained relatively small burns (x=11%); only nine patients (14%) had burns greater than 25%. Forty-six patients suffered 114 major complications. EKG abnormalities occurred in 36%, including major cardiac arrhythmias in ten patients. One-fourth of the patients developed neurologic sequelae (CNS-8, peripheral-8). Electrical vascular injury with subsequent arterial occlusion was responsible for many of the major amputations. Nineteen patients required 32 amputations (digits-17, hand-1, foot-2, leg-3, arm-9). Early patient referral and vigorous fluid resuscitation minimized renal failure (1.5%) and mortality (3.1%). Early fasciotomy and vigorous debridement appeared to decrease wound sepsis (8%), but apparently had little if any effect on major limb salvage. The unsolved problems of electrical injury, namely neurological and vascular sequelae, are major contributors to the high morbidity of electrical injury.

Adolescent↗
PubMed1992

Lightning and electrical injuries.

Lightning and electrical injuries are similar in that both produce immediate tissue injury from burn and trauma induced by fall and both can arrest the heart and respiratory center. Immediate support of circulation and respiration is life-saving. Subsequently the nervous system may show signs of injury, and seizures, cerebral edema, and muscle and nerve lesions should be handled as the indications arise. Prevention of the injury is more effective than any postinjury treatment. Outdoors hikers and campers must take shelter to minimize their exposure; indoors properly installed equipment and attention to the relation of the equipment user to the electrical ground are the key elements in avoiding electrocution.

Electric Injuries↗
PubMed1991

[Heart damage after electric injury].

Death from electrical accident due to low voltage (220 Volt/380 Volt) is usually caused by ventricular fibrillation. In humans who sustain non fatal electrical injury abnormal ECG findings due to myocardial damage are rare. 243 (76%) of 320 ECGs of survivors of an electrical accident were diagnosed as normal. In 42 patients (13%) unspecific electrographic changes were seen and in 35 (11%) abnormal ECGs were found. In comparison to findings in normal populations no significant accumulation of ECG changes was observed. A causal relationship between abnormal ECG findings and electrical accident is only then probable if ECG abnormalities are documented immediately after injury and serial ECG controls demonstrate significant changes in comparison to the initial abnormality.

Adolescent↗
PubMedDate not supplied

[Diagnostic and therapeutic difficulties in a case of severe craniocerebral injury caused by an electric injury and a fall].

The authors describe a 37-year-old man suffering electric shock caused by high-voltage current 3 000 Volt. The shock caused a fall with severe craniocerebral injury with fracture of occipital squama and subacute epidural haematoma in the posterior cerebral fossa. The injury was associated with vascular disturbances of the brain and brain stem which caused difficulties in disclosing typical signs of epidural heaematoma. Good therapeutic effects were obtained not only by surgical intervention and also by intensive treatment with antioedematous agents and drugs improving cerebral circulation.

Adult↗
PubMed1991

Fatal occupational electrical injuries in Virginia.

Work-related electrical injuries and fatalities in Virginia were reviewed for the period 1977 to 1985. Of 196 workers electrocuted (0.9/100,000/year), 65% (127) died between May and September. Death rates were highest for male workers in utility companies (10.0/100,000), mining (5.9/100,000), and construction industries (3.9/100,000), but these high risk groups accounted for only 50% of the deaths. Most accidental electrocutions resulted from power line contact (53%) and machine or tool usage or repair (22%). Only 1.5% (2/101) of the workers who died within 6 hours of injury and had blood alcohol concentration tested were legally intoxicated. All workers need safety education on active measures to prevent hazardous electrical exposures, not just those at high risk for electrical injury. Every work-related electrical injury represents a sentinel health event--an opportunity for preventive intervention in the workplace.

Accidents, Occupational↗
PubMed1976

[Intracerebral measurement of electric tensions following peripheral electric injury].

The present research has originated from observing a 25-year-old man who - after an electrotrauma-- showed a hydrocephalus internus in the pneumoencephalogram. The review of the literature available at that time resulted in obtaining only one information concerning this nexus of related problems; thus the search of patients suffering from this trauma began, but as well experiments on animals. Most of the cats being injured by A.C. actually showed a dilatation of the lateral ventricles. Further experiments on dogs have shown that not only in case of transcerebral but also of peripheral injuries by electric currents of certain strength, distinct states of paling on the brain surface could be observed occurring in consequences of the extreme vasosoconstriction of the meningeal vessels. By a further series of experiments on dogs, there was finally demonstrated that also after peripheral electric irritations resp. injuries of different variations, electric tensions in the brain can be measured by intracerebrally installed electrodes at varying irritatnt voltages; up to now, this possibility has been in contest. Neuropathological investigations showed intracerebral and subarachnoid haemorrhages of different size in all injured animals.

Animals↗
PubMed1979

Induced ischemia: means of prediction of demarcation line of necrosis after electrical injury. An experimental study on rabbit ear.

Necrosis due to an electrical injury extends by progressive obstruction of blood vessels. Means of inhibiting expansion of necrosis and predicting early the demarcation line after an electric injury were studied in the local electric injury of a rabbit ear produced by application of an electric current of 50 Hz, 1800 V for 1 sec between the right ear and the right posterior leg. Although no effective method of inhibiting expansion of necrosis was obtained, a method of predicting a demarcation line of necrosis was obtained by inducing ischemia of the ear early after the application of an electric current. From three hours to three days after the application of the electric current, ischemia of the ear was induced by compressing it between a pair of blood pressure cuffs at a pressure of 300 mmHg. As a result, the area proximal to the expected demarcation line of necrosis became white by ischemia, while the peripheral part remained dark red because of thrombi, and the expected demarcation line was clearly observed. Two to three weeks after the application of the electric current, the ear almost invariably fell off at this expected line. Therefore, in the electric injury of the hand, it can be distinguished clinically whether or not the area will become necrotic by inducing ischemia from the tips of the fingers to the upper arm early after the electric injury.

Animals↗
PubMed1990

Clinical predictors of myocardial damage after high voltage electrical injury.

Myocardial damage after high voltage electrical body injury is a serious and often life-threatening situation. The purpose of this pilot study was to identify early clinical predictors of myocardial damage in patients with high voltage electrical injury. Twenty-four patients with high voltage electrical injuries and no evidence of arc burns were evaluated. In 13/24 patients the diagnosis of myocardial damage was confirmed by total creatine kinase (CK) and creatine kinase MB (CK-MB) isoenzyme elevation (group A). In these patients the total CK range was 1373 to 52,544 mU/ml. In 11/24 patients CK-MB was negative (group B) indicating absence of myocardial damage. ECG changes occurred in 10/13 group A and 4/11 group B patients (p less than .095). No patient in either group gave a history suggestive of myocardial ischemia after the electrical injury. The pathways of electricity through the body, as mapped by a line drawn between the wound(s) of entrance and exit, were vertical in all group A patients, i.e., from upper to lower body segment, vs. 5/11 group B patients with evidence of a vertical pathway (p less than .003). Group A patients also had greater body surface burns (16.0 +/- 2.7%) vs. group B patients (4.0 +/- 1.6%, p less than .001). The presence of a vertical pathway and the magnitude of percent surface burns were found to be the most significant clinical predictors of myocardial damage in multiple logistic regression analysis (p less than .0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Repair of experimental high voltage electrical injuries.

Repair methods for high voltage electrical injury were studied in 46 rats submitted to symmetrical bilateral hind limb electrical injuries using 1,600 V AC. Out of 40 hind limbs of the 40 rats which were treated with conservative debridement and flap coverage, 20 limbs repaired prior to the 48th post-injury hour obtained a good appearance and functions, the rest operated after the 4th post-injury day showed partial or complete disability. Forty contralateral limbs served as controls, including 20 hind limbs grafted with mesh-grafts which recently necrotized and 20 of them debrided thoroughly resulting in substantial loss of tissue, showed disabling effects. The investigation suggested that a better appearance and functions in such injuries would be obtained if using the technique of immediate conservative debridement and flap coverage.

Animals↗
PubMedDate not supplied

Electrical injuries to peripheral nerves.

As people come frequently into contact with electrical power sources, electrical injuries to peripheral nerves are commonly seen. The authors first review the parameters determining the severity and distribution of electrical injury to nerve tissue. These include tissue resistance, tissue susceptibility, current pathway, type of current, current density, duration and size of electrical contact. Subsequently, the pathophysiology of electrical injuries to nerve tissue is reviewed. Such injuries can be the result of thermal damage, vascular impairment, histological or electrophysiological changes in peripheral nerves, or direct mechanical trauma. Each of these types of injuries causes, specific lesions. As these lesions, especially delayed peripheral neurologic injury, can cause medico-legal problems, it is important to emphasize that electroneuromyography must be performed as early as possible.

Burns, Electric↗
PubMed1986

Homonymous hemianopia following electrical injury.

The clinical spectrum of electrical injuries is complex and diverse. Despite the high annual incidence of electrical accidents, little has been reported recently regarding the neurological deficits associated with this form of trauma. The most frequently cited reviews are those of Critchley, Langworthy, Naville and De Morsier, and Silversides. These authors have divided the neurological complications into three groups based on the temporal relationship between the shock and the manifestation of clinical signs: immediate, secondary, and delayed. The present case developed a dense homonymous hemianopia 4 days following an electrical accident. The details of the above mentioned classification, as well as a review of the pathophysiology, will be presented.

Accidents, Occupational↗
PubMed1977

Xenon-133 determination of muscle blood flow in electrical injury.

Xe-133 washout determination of muscle blood flow (MBF) was used to detect muscle ischemia in electrical injury of an experimental animal model and three patients. The control MBF of rabbit hindlimbs, which averaged 11.29 +/- 1.07 cc/min/100 gm, was significantly reduced by electrical injury, to 5.82 +/- 1.49 cc/min/100 gm (p less than 0.001). An electrical injury of 4,000 watt-seconds or greater was associated with uniform MBF less than 1.00 cc/min/100 gm and with histopathologic alterations of muscle necrosis. Thenar MBF less than 1.00 cc/min/100 gm in two patients was associated with muscle necrosis requiring distal arm amputation. The remaining patient with sequential muscle blood flows above this level had uneventful healing of hand electrical injuries. Xe-133 determination of MBF may be a useful objective technique to determine the extent of electrical injury in muscle.

Adult↗
PubMed1989

Preservation of devitalized calvarium following high-voltage electrical injury: case reports.

Three victims of electrical injury with necrosis of a portion of the skull had excision of overlying necrotic soft tissue soon after injury with immediate coverage of the devitalized bone with soft-tissue flaps. In two instances, the flap was from adjacent scalp; in the other a free myocutaneous flap was used. All wounds healed without sequestration of bone. Necrosis of the calvarium was substantiated by evidence of nonperfusion on a radionucleotide bone scan. In each instance, a followup bone scan showed evidence of regeneration of bone. This experience supports an earlier observation which suggested that devitalized but intact calvarium following electrical injury does not need to be removed and is the perfect in situ bone graft.

Adolescent↗
PubMed1975

[Electrical injuries in childhood (author's transl)].

11 children were admitted with electrical injuries to the Department of Paediatrics, University of Graz, over the 10-year period 1965 to 1974. The electricity was of low voltage in the case of 9 of these children, who were injured whilst playing with plug sockets of defective cables and of high voltage in 4 case. 1 child was stuck by lightning. Cessation of respiration occurred in 4 of the patients and was successfully counteracted in all cases by prompt mouth-to-mouth breathing. 7 children were still shocked on admission. All children showed the characteristic skin lesions of electrical injury (current marks of linear, round or spidery form). The boy injured by high voltage electricity received extensive burns, in addition. The modes of electrical injury in childhood, the various forms of the resultant lesions, especially of the skin and the treatment of electrical burns are discussed.

Adolescent↗
PubMed1991

Myoglobinuric acute renal failure following electrical injury.

Eight patients with acute renal failure (ARF) following electrical injury were studied. The mean area of cutaneous burns was 23 +/- 16% (range 6-60%) and extensive tissue necrosis with gangrene was uniformly present. Oliguria developed 9.3 +/- 7 h (range 3-24 h) after the injury in 7 patients (88%). Urinalysis revealed presence of myoglobin in 75% of the patients. The mean duration of oliguria among those who recovered was 16 +/- 6 days (range 11-23 days) and the mean interval between the onset of oliguria and recovery of renal function was 25 +/- 6 days (range 21-34 days). Four patients died. The cause of death was Klebsiella septicemia in 1, hyperkalemia associated with extensive myonecrosis in 2 patients, and uncertain in 1 patient. Our observations showed that myoglobinuric acute renal failure associated with electrical injury carries a high mortality. Early detection and aggressive management of hyperkalemia and sepsis are necessary to reduce mortality among these patients.

Acute Kidney Injury↗