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IMBSIR 79-1710

Electrical Injuries - A Literature

Review

Yung-Chi Wu

Product Safety Technology Division

Center for Consumer Product Technology

February 1979

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NBSIR 79-1710

ELECTRICAL INJURIES - A LITERATURE

REVIEW

( 3,

Yung-Chi Wu

Product Safety Technology Division

Center for Consumer Product Technology

February 1979

Report to: Consumer Product Safety Commission

5401 Westbard Avenue

Bethesda, Maryland 20016

U.S. DEPARTMENT OF COMMERCE. Juanita M. Kreps, Secretary

Jordan J. Baruch, Assistant Secretary tor Science and Technology

NATIONAL BUREAU OF STANDARDS, Ernest Ambler, Director

INTRODUCTION

Ever since electricity was first put into commercial use, electrical

injuries have occurred. During the hundred years since the first recorded

accident in 1879 (1), both the number and variety of electrical injuries

have increased with the advancement of technology and the utilization of

electricity. In the first quarter of this century, the number of fatal

electrical accidents in the U.S. averaged about 750 annually (1), and

currently are only slightly more frequent, around 1110 per year (2,3).

Today "there are more than 4000 extension and appliance cord injuries (in '

1 974 alone) serious enough to require hospital emergency room treatment."

Of these, approximately 20% involved burns to the mouths of children (4).

Electrical injuries have become a significant concern for consumer safety,

hence this study was initiated and sponsored by the Consumer Product Safety

Commission.

Humans frequently sustain traumatic injuries from the interaction with

electricity. It is generally believed that the effect is due to the

magnitude of electric current flowing through the body (1,2, 5-8). However,

for a given condition, the electric current is a function of electromotive

force (E.M.F.), or voltage. Moreover, after an accident, the current cannot

be reconstructively determined: only the voltage can be assessed. For this

reason, electrical injuries are generally classified in terms of high or low

voltage, depending upon the voltage involved in the accident. "Low voltage"

has been conventionally defined as a voltage of 1000 volts or less. Unless

otherwise indicated, this definition is used throughout this report. With

respect to consumer products and their safety, the low voltage injuries are of particular interest and will be discussed here. However, because

electrical injuries are not delineated by specific categories, it is

important to attempt to assess the relative frequency and severity of low

voltage and high voltage injuries.

The basic principles of electricity are applicable to both high and low

voltage electrical injuries, whereas the physiological reactions are different and manifest different injurious phenomena. The causation and

severity of an injury depend in part upon the physical parameters of the

electrical source, and in part on the physiological parameters of the human

body as it reacts to the electricity supplied by the source. These

parameters will be reviewed and discussed in conjunction with the mechanism

of injuries.

Since that first reported electrical accident in 1879, a voluminous

body of literature has been produced by both life and physical scientists.

The older literature has been thoroughly reviewed and critically analyzed by

Jellinek (9) in the first part of this century; by Jaffe (1) in the

twenties, and by Alexander (5) in the thirties. Over the past 'forty years,

the increased frequency and alarming effects of injury have led to more

studies of electrical injuries and more reports in the literature. Many of

these are case studies dealing with clinical treatments, and only a few have

provided a different approach to the problem. Among the latter, reports of
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Dale (10), Lewis (11), Artz (12), Ugland (13), Skoog (14), DiVincenti (15), • Hunt (16) and their coworkers are noteworthy.

The so called "mouth burn" type of electrical injury was not

specifically addressed until about forty years ago, after which the number

of injuries reported annually has been increasing. This problem was not

discussed in the earlier literature and has been reviewed only recently

(4,17-23).

In the vast body of literature there are some consensus interpretations

of the causation of the injurious phenomena. However, the exact nature of

how electricity affects the physiological entity remains unresolved. It is

the purpose of this study to review the current state-of-the-art knowledge

of the phenomenon, especially the non-fatal (but serious) low voltage

electrical burns.

The term "electrical burn" is not clearly defined in the literature.

In a narrow sense, the term may be interpreted to mean an injury resembling

a burn, that is caused by electricity; in a broader interpretation, the term

simply refers to an injury caused by electricity. Thus, Artz (12) observed

that "many physicians refer to the injury caused by electricity as electrical burn" and that "It is not uncommon to see an electrical injury of

an extremity resemble a burn and be so treated, only to find that

clostridial myositis* has developed (deep within the injured part, author’s

note) in two or three days." Dale (10) noted that "All workers are agreed

that the electrical injury, as Jellinek names it, is unique, and that

whether it is caused by heat coagulation or by specific electrical effects,

its clinical appearance and characteristics are the same." In the

literature, it is apparent that the terms "electrical burn" and "electrical

injury" are often used in referring to the same injury. In this report,

therefore, no attempt is made to define or interdistinguish the

terminologies, and the terms "electrical burn" and "electrical injury" are loosely employed in referring to injuries caused by electricity.

*For this and similar terms see Glossary at the end of this report.
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STATISTICS OF HIGH AMD LOW VOLTAGE ELECTRICAL BURN INJURIES

Statistics on the severity of electrical trauma (which may range from a non-injurious, tingling shock to fatality), the frequency of occurrence of

electrical accidents, and their origins appear to be only partially reported

in the literature. In 1958, Lewis (11) observed that "In most cases these

data (frequency of non-fatal electrical burns) are included in the

statistics relative to burns per se, and are not classified under initial

causes." Only recently, the National Center for Health Statistics (3) has

compiled the annual statistics for hospitalized electrical injuries in which

both high and low voltage injuries are lumped together and no initial causes

are given. These statistics show the annual rate for electrical burns in

the United States is about 4% of the total number of burns (thermal,

chemical and electrical inclusive). This figure compares favorably with

estimations reported in the literature for different periods and for

different nations (3, 14, 15, 24). All these data are summarized in table

1. There is no further detail given in these statistics.

. In 1977, Butler (25) reported on a group of electrical injuries,

summarized in table 2. This table provides somewhat more detailed

information than is evident in table 1; however, the causes of the 2%

domestic injuries (low voltage) are not specified. In the interest of

consumer safety it is necessary to know the frequency of low voltage

electrical injuries related to consumer products. Since this type of

statistic does not seem to be directly available, an effort was made to

obtain such data through a few randomly selected hospitals. The results,

listed in table 3, only confirm the general lack of detailed information.

This is probably due io the infrequent incidence of electrical burn injuries

in comparison with other hospitalized injuries or diseases (3), so that

relative little effort has been exercised in keeping detailed records.

However, special effort has been made by the "Project Burn Prevention" in

Boston, Massachusetts (26), to collect data from 18 hospitals in the Boston

and Springfield areas. A total of 171 electrical injuries from 1974 to 1976 were reported. Half of these were treated in the emergency room and

released; the other half required hospitalization. About 41 % of the

released cases and 53% of the in-patient cases involved indoor, low voltage

electrical sources. The National Electronic Injury Surveillance System data

show a total of 2644 extension and appliance cord cases treated in emergency

rooms in 1977, of which 548 were mouth injuries*. From the data cited

above, it is difficult to reach any definite conclusions. However, the

limited information appears to indicate that low voltage injuries,

especially those that are related to consumer products, are relatively small

in number. Among these, the number of mouth burns is relatively high.

*These data are product-oriented and do not provide detailed information on physical causation. The numbers cited here may not all be electrical

injuries.
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THE MATURE OF ELECTRICAL INJURY

Two fundamental factors directly govern the electrical injury. One is

the physical parameters of the electrical source which transmits

electricity to the human body when the latter comes into contact with it.

The other is the set of biophysical parameters of the physiological

entities (such as organs, tissue, nerve fibers, and bio-fluids) which react

to the electricity. These parameters are listed as follows:

Electrical Source

1. c Electromotive force, or voltage

2. Direct or alternating current

3. Frequency of alternating current

4. Physical properties of the contact surfaces (entrance and exit)

Physiological Entity

1 . Contact surface conditions (wet or dry) -

2. Contact area • v

3. Contact duration

4. Resistivity (more generally, electrical

organs, tissue, nerve fibers and fluids

characteristics) of

(see tables 4 and 5)

It should be noted that the data given in table 4 were measured in

vitro; they may be very different in vivo, hence, they can be used only as reference values. Thus, Kouwenhoven (8) showed that the resistance of the

skin is not constant, but varies with the amount of moisture content, the

temperature and the applied voltage (76). Jaffe (1) suggested that dry

skin could have a resistance of 50,000 to IMP (megohm), whereas wet skin

may have a resistance of only 2500 ft . Further, during the passage of

current, the resistance can decrease from 260KP to 3800. Kouwenhoven

measured the skin resistance of cadavers at 60 Hz and gave the following

results: at 50 V, 5000-18,000 ohms; 500 V, 800-1800 ohms; and 1000 V, 800-

1800 ohms. He noted further that, in vivo^ "dry epidermis has a high

resistance which may reach 1,000,000 P/cm (ohms per square centimeter).”

Since the epidermis is the surface most likely to contact an electrical

source in an electrical accident, the condition and area of contacting skin

will affect the distribution and density of current flow, hence the

severity of injury. Furthermore, the basic principles of electricity

reveal that the current flow, for a given circuit, is a function of applied

voltage, and takes the least resistant path. According to table 4, the

bio-fluids, nerve fibers and blood have the least resistances among the
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physiological entities. It may be inferred, then, that the bio-fluids,

nerve fibers and blood stream conduct most of the current which flows

through the body. Various current and current density thresholds are shown

in table 6.

High frequency alternating current (A.C.) is relatively harmless (1,

32). Thus, D'Arsonval (33) and others (34,35) found that, for a short

duration, currents up to 3 amperes at frequencies from 400 kHz to 1 MHz

have no effect on the human body. Kennelly (36) observed that "An

alternating current of sufficient strength to light up an ordinary 0.5 amp

incandescent lamp can be tolerated at high frequency when the human body is

in the circuit," and maintained that "the skin effect in the human body is

practically negligible hnd that. up to the highest frequency (100 kHz) here

considered the current diffuses throughout the cross-sections of the body

in substantially the same manner as a continuous current." He further

suggested that "The nerve stimulation of one alternation does not have time

to register an effect before it is annulled by the next succeeding

alternation." Kouwenhoven, et. al. (37) demonstrated that the current

required for fibrillation at 1200 Hz is about 12 times that required at 60

Hz. The domestic current most commonly used today is 50-60 Hz, which is in

the most dangerous range of frequencies.

In general, 50-60 Hz alternating current is more dangerous to life than

direct current (1, 5, 10, 38). Dale (10) reasoned that this is "because

the rapid electrical impulses produced by the alternations throw the

muscles into tetanic spasm, causing the victim to close a vise-like grip on

the electrodes, from which he can be removed only with difficulty. Direct

current, while' perhaps less lethal, is more liable to cause severe local

injuries.
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THE PHENOMENA OF ELECTRICAL BURN INJURIES

There are two types of electrical burn injuries. One is caused by

flame, flash, or spark of external electrical energy, in situations where

the body is not directly involved in the electrical network. This type of

injury is a pure thermal burn and will not be examined in this discussion.

The other type of injury is caused by contact with, or arcing over of,

electricity, in which the body is a part of the electrical network. The

phenomena of this type of injury may be listed as follows:

1 . Mild shock

2. « Involuntary muscle contraction

3. Neuro-system damage

4. Ventricular fibrillation

5. Respiratory paralysis

6. Tissue damage

7. Instantaneous death

The extremes in this listing, jnild shock and fatality, are outside the scope

of this investigation, which reviews only non-fatal electrical injuries.

Specific cases will be discussed after a review of general observations

appearing in the literature.

General

As discussed above, electric current flows through the human body when

it contacts an electric source and becomes part of the circuit. If the

current is above the threshold values listed in table 6, injurious events

occur. A person who suffers a tingling shock or mild involuntary muscle

contraction is likely to recover almost immediately if the contact duration

is short. However, if the contact duration is long or the current is

sufficiently high (see table 6), damage to the nervous system and other

tissue may result. A current on the order of 100 mA (1, 5, 10-14) flowing

from hand to feet will cause heart fibrillation, respiratory paralysis and,

usually, unconsciousness. Often, resuscitation efforts must be continued

for as long as 12-18 hours in order to save the victim (1, 5). It should be

noted that the quantity of current and the duration of time involved in an electrical injury can never be reconstructively determined. At best these

can only be described qualitatively as above.

If the current penetrates muscles (12), follows the path of blood

vessels leading to the head, and/or follows the nerve fibers leading to the nerve centers controlling vital functions, the resulting injury is usually

severe. The higher the current, the more severe the injury. If only the
- 7

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peripheral blood vessels and nerve fibers are involved, the accident may

cause thrombosis and sensory disturbance at the. site of, or even some distance from, the original injury (1,5,10-14,24,25). This led Brinn (39)

to believe that "there may be progressive central nervous system or peripheral nerve damage leading to paralysis, sensory disturbances or vasomotor phenomena. There may also be vascular disturbances with

progressive vessel thrombosis as well as weakness and fragility of blood

vessel walls. Tissue repair is often poor." In general, a patient

surviving an electrical injury will usually have more tissue damage than

might be expected on initial examination (1,5,10-15,24,25).

Arc burns are very destructive (1, 5, 10-15). Jaffe (1) described that

"when permanent damage occurs, it is usually due to the multilating effect

of the electric arc which necessitates the amputation of extremities." Dale

(10) observed that when the local lesion of electrical injury is caused by

arcing, "the effect on the tissue is immediate and profound. . .Small

electrical injury presents as a clear circumscribed area of yellowish grey

skin surrounded’ by a sharp line of hyperemia. In the center there may be

charring, in which case it is probable that an electrical arc has occurred.

The lesion is bloodless, cold and painless. The destruction of tissue is

deep and often involves muscles, tendons and bones."

Local injuries caused by electric current from contact or arcing are apparently due to "prolonged vasoconstriction, followed by vasoparalysis

leading to formation of parietal and occluding thrombi and to necroses of

vessel walls which are followed by immediate, insidious or delayed necrosis

of tissue, usually preceded by edema" (5). Thus, "The separation of dead

tissues is extremely slow. After the slough has eventually separated, a process which may take several weeks, a slow healing ulcer is left" (10).

Because of vascular alterations, which are initiated by the passage of

current through the blood vessel walls., especially the intima (5), it may be

assumed that the circulatory disturbance has produced numerous perivascular

necroses (1, 5, 10). This may lead to massive gangrene (10) and delayed

occurrence of nervous system damage (5,10,11,13).

High Voltage Injuries

According to the statistics cited earlier, high voltage injuries

account for 2/3 of the total electrical injuries, or more than 2500

annually. The severity of burns may be classified into three groups,

according to Barnes (40):

Severity Group Body Surface Burn (%)

1st-2nd degree 3rd degree

I < 15% < 5%

II 15-30% 5-15%

III > 30% > 15%
- 8 -

This led Ugland to classify his observations of 64 cases of high voltage**

burn as follows:

Severity Group '

I II III

High voltage burn 40 16 7 j

The statistics given by DiVincen'ti, et. al. (15), for a set of 65 cases

show that "The total area of burn ranged from 1% to 87% of the body, with

an average of 20%. . . The hospital days for electrical injury averaged 85

days, wliich was 20 days longer than for non-electrical burns, thus

indicating a more severe injury." Skoog (14) summarizes that "thrombi are

apt to form within the damaged vessels and ischemic necrosis is common in

high voltage burns." The involvement is deep and extensive. Amputation of

extremities is sometimes required (11, 13). Cases reported are numerous (5,

10-15, 24-25, 39, 41-56). No further detail will be given here. Additional

information may be found in the references cited above.

Low Voltage Injuries

For low voltage injuries (5, 11, 13-14, 38, 55, 56, 58-63) other than

mouth burns, Muir (62) has described that "the majority of burns involved

the hands. . . They are generally small in size and of relatively minor

severity. . Skin is dead wliite and surrounded by a bright red margin. . . The limit of injury shortly after electrical burns is clearly defined. . . Later this skin becomes black and mummified for many days and weeks without

changes occurring." However, in some cases, "tissue previously thought to

be viable sloughs, and tendons, joints, or bones thought to be out of danger

are exposed and at hazard." Skoog has summarized that "low tension burns

were almost exclusively of the contact type; but burning did not occur where

one contact point was large," and asserted that "the small lesion of the so- called current mark heals spontaneously, leaving insignificant scar."

(11,13,14,39).

O'Flannagan (63) reported the following case of 240 V, A.C. injury.

"The victim was unplugging an electrical drill from an extension cord and

apparently came in contact with the live terminals. He didn't fall or loose

consciousness. After a 10-15 sec delay his wife disconnected the extension

lead. He had no apparent burn marks on his hand. . . He was tender over

the upper half of the humerus. Movement of shoulder was severely

restricted. . . X-rays showed an incomplete fracture of the surgical neck

below the greater tuberosity and crack fracture of the greater tuberosity."

For low voltage direct current injury, Alexander (5) reported an incident involving 115 V, 25 mA that occurred to a healthy male of 46 who

was changing a light bulb in a hanging lamp with a pullchain. He suddenly

felt an electric shock in his left hand with which he held the socket. He was able to remove his left hand immediately from the socket and noticed

**High voltage, in this case, is defined by the author as the voltage of the

electric source at or above 380V.

This value was given by the author without mention of how it was determined
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that he had received a burn on the end of the fourth finger of his left

hand; otherwise everything was normal. However, the next morning he noticed

pain and weakness, almost paralysis, of his left arm. Three weeks later the

pain and weakness became definitely worse and quivering of his left upper

arm was also noticed. Six weeks later, examination revealed muscular

atrophy. The circumference of the upper left arm measured 4 cm smaller than

that of the right arm. Panse (64) has collected and described a number of

similar cases.

Mouth Burns

When a child’s mouth or lips come in contact, by chewing or sucking,

with exposed live elements of an extension cord, a mouth burn injury usually

results. The saliva and the wet tissues of the mouth provide a highly

conductive environment, and current flows through the mucosa, taking a path

along the peripheral blood vessels and nerve fibers. In most cases, the

wound is found to be much deeper than it initially appears. Usually,

variable expanses of both lips, laterally, plus the corners of the mouth

will be found coagulated or charred. Detailed descriptions of the phenomena

have been given by Pitts (17) and others (4,17-23,65), and also reviewed by

Oglesby of NBS (66). Specific case histories can be found in those reports.
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THE RELATIVE MAGNITUDE AND SEVERITY

OF LOW VOLTAGE ELECTRICAL BURNS

In view of the preceding discussions, it appears that the annual rate

of non-fatal, low-voltage injuries requiring hospitalization (mouth burns

are included) is about one third of the total of 4000 electrically injured

patients (25). This annual rate is about 1.5% of all burns and is about

0.04% of all injuries (3.5 million in' 1975) requiring hospitalization (3).

This amounts to about one low-voltage injury in every 2500 injured patients.

The rank is relatively low. If mouth burns are excluded, the severity of

low voltage electrical injuries is relatively minor compared to those caused

by high voltage.
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ELECTRICAL BURN MECHANISM

Since electrical injury results from human interaction with electricity

when the body is involved in an electrical network, both the electrical and

physiological parameters listed in the preceding section require

examination. As described above, electric current flows through the body,

taking the least resistant paths. The resulting physiological reaction to

the electricity is the essential cause of injury. The quantity of current

through those paths depends upon the EMF of the source, the contact area of

the conducting surface, the resistance of each path, and the physiological

distribution and structure of the paths. Furthermore, the distribution and

structure of physiological entities differ .at the micro level among

individuals and within an individual body. Therefore, it is very difficult,

if not impossible, to quantitatively evaluate the current distribution for

any typical path. In addition, individual responses differ and there are no identical electrical injuries (11, 12). The physiological reaction to

electricity is current dependent, and may result in only a tingling

sensation from low current, but almost instantaneous death from high current

flow. For nonfatal electrical injury, the apparent results of physiological

reaction to electric current are disturbance or destruction of the natural

functions of the entities in the current paths.

Since knowledge of the distribution and structure of physiological

entities in the electrical network involved in an electrical accident is

limited, there can be no quantitative interpretation and assessment of the

injurious phenomena and mechanisms. Qualitatively, however, there are two

contemporary theories of interpretation and assessment, viz., the traumatic

effect is due to (1) the Joulean heat effect I R, and (2) the specific

electrical effect.

The theory of heat effect derives from- the generation of heat as a current flows through a resistive path, with the amount of heat„proportional

to the square of the current and to the amount of resistance (Ik). This

theory was initiated by Jaffe and his coworkers (67) in a controlled

experiment where current was passed through a section of the femoral artery

of a dog, in situ, for a duration of 2 minutes. During the experiment, the

flow of blood through the artery could be stopped or allowed to continue

normally. When the flow was stopped, damage to the vessel wall occurred;

during normal flow, no change in the arterial wall was observed. In another

experiment, the same artery was touched with a heated 3 rnm steel wire. In

the latter experiment, damage to the vessel wall closely resembled that

caused by the electric current. They concluded that for the electrical

experiment "it was the heat liberated in the obstructed vessel that was detrimental to the tissue of the vascular wall." Hunt and his coworkers

(16), in 1976, reported on a series of experiments with animals. Two

electrodes were taped to the distal end of one fore and one hind paw of

rats. The animals were shocked with constant sources of 125, 250, 500, and

1000 volts, A.C. until arcing occurred, at which time "the amperage falls to

zero." The durations of the shock (before arcing occurred) were found to be

inversely proportional to the applied voltage, and ranged from 20 seconds at
- 12 -

125 V to 2.5 seconds at 1000 V. Currents from 1 to 8 amperes were recorded.

The tissue temperature was measured proximal and distal to the contact

sites. Adjacent to the contact sites, tissue temperatures of from 60-95°C

were observed during current flow. This was associated with significant

damage to deep muscles and other tissues. They concluded that "an

electrical burn is simply a thermal injury." Many investigators adopt this

theory to interpret the phenomena of electrical injuries (13-

15,21 ,24,25,41

,

2 13 ,

, 46, 51-53, 55-61 ) . Even though some authors

(1 3, 14,24,25,45,68,69) have noted clinical distinctions between the

electrical burn and thermal burn, they believe that Joulean heat -is

generated during the passage of current and that this heat destroys cells.

Ugland (13) has reviewed 122 clinical cases and much of the available

literature up to 1967. . He concludes that "the transformation of electrical

energy into heat is therefore maximal in the skin at the contact site and in

the adjacent tissues. . . The voltage drop and the resultant release of

heat along a pathway of varying resistance is directly proportional to the

latter at any one point." He provided a simplified circuit diagram of

current pathways through the human body, and suggested that "the most severe local lesions would be expected with current flow through the pathway of

greatest resistance." However, as regards peripheral nerves, he

distinguished between thermal and pure electrical effects (70-72). He

performed a series of elaborate experiments on the sciatic nerve of rabbits,

using various electrical shocks from 250 to 1700 rnA, at 200 to 500 V, for 5 sec. He observed that "following electrical injury there was a decrease in

conduction velocity. . . It seems feasible that derangement of the myelin

(70) should be associated with changes in conduction velocity." He

concluded that "Electrical current shocks of strength sufficient to cause serious injury^ in man, produce changes’ in the function of peripheral nerves

in acute test animals. . . These changes are most likely caused by direct

neuronal damage induced by the current itself. Heat plays a minor role, if

any."

The theory of specific electrical effect was first suggested by

Jellinek (73), recapitulated by Alexander (5,70) and followed by some of

their contemporaries (71,72) in the twenties and thirties. This theory, in

a broad sense, suggests that electric current interacts with a physiological

entity to alter its natural function, hence injury results. Dale (10) and

Buris (7^) observed histological differences between thermal and electrical

burns in that (10) elastic fibers remain in the tissue after electrical

burns, but are not seen after thermal burns. This led Dale (10) to believe

that cells are destroyed not by heat, but by electrical action which causes

an imbalance of ionic exchange. In explaining the syndrome of electrical

injury, Spitzka (75), as early as 1912, postulated that the process of

electrolysis occurs, and Mills (51) has recounted recently that "The

phenomenon of electrolysis undoubtedly occurs, and it has been postulated

that the syndrome of electric shock may be partially .explained by

electrolysis and changes in cellular composition." Chasmar (45) has

suggested an alteration in chemical balance, and Brinn (39) has described

electrical injury to bones and joints (non-mechanical) as due to

decalcification. These effects are quite distinct from thermal effects.
- 13 -

The validity of the Joulean heat and specific electrical effect

theories may be examined by comparison with the interpretations of injurious

phenomena as described in the preceding section. The better theory should

be able to explain, at least qualitatively, all types of electrical injuries

from minor shock to fatality.

Physical Aspects

• When the human body completes an electrical circuit, a current flows

from higher to lower potential through the contact areas and the body. The'

size of the entrance and exit sites on the body affects the current density

and depends on the effective contact area and the amount of moisture on the

body surface. Variations in these factors lead to different injurious

phenomena.

When the contact surface of the human body is wet, its surface

resistance is substantially reduced, from approximately 100,000 to 300 ohms.

In this case, the flow of current through the contact area is similar to

that through an electrolyte solution (76). The solution, in turn, connects

to the tissue fluids and the ends of blood vessels and nerve fibers through

capillary diffusion. These ends are membranes, with a resistance of about

1,000 ft (28,77). While the membranes of blood vessels are resistive, the

membranes of nerve fibers permit free ion mobility, hence a conductive path

is formed. The current will, therefore, have a greater tendency to perfuse

through the tissue fluids and flow along the nerve fibers (77), giving rise

to high current density in these specific pathways of the network flow.

On the other hand, if the surface is dry, the high resistivity of the

epidermal layer* of skin will act as a dielectric. Immediately on contact,

but before the start of current flow, an electric charge will begin to

accumulate at the contact point and the dipoles will line up along the

field. The higher the voltage, the higher the charge concentration becomes,

until the phenomenon of arcing occurs (78). The arcing may involve an area of pinpoint size, a small circle, or a treelike branching which may spread

over an extensive area. The epidermal layer of that area will be destroyed,

and the underlying tissue will be exposed. The current will pass through

the exposed surface, taking the least resistant path, and flow through the

fluids in the perivascular spaces and the vascular channels (79), the nerve fibers and the cerebrospinal fluid (80), and the blood stream (11, 79).

The exit sites (through which the current leaves the body to complete

the circuit) also depend on the contact surface condition and the potential

difference. The phenomena at these sites are similar to those described for

entrance sites.

Jaffe (1) found that electric current spreads radially from the point

of entrance and is collected again at the exit point of the body involved.

This led Lewis (11) to believe that the greatest density of current is to be

found at the sites of entrance and exit.'
- 14 -

In the human body, the tissue fluids, the cerebrospinal fluid and the

blood stream are electrolyte solutions in equilibrium with different kinds

of proteins and biomolecules. The nerve fibers are also filled internally

with an electrolyte solution, and are bathed in a similar electrolyte

solution separated by a membrane, across which a delicate balance of ionic

concentration is maintained (see table 7) (81-82). The membrane permits

ion movement under the influence of an action potential (83-86). Thus, the

nerve fibers may be considered as electrolyte solutions for conducting

current.

According to the theory of heat effect, Joulean heat develops and

causes cell damage when an electric current traverses body paths. On the

other hand, the theory of specific electrical effect provides no detailed

explanation of injury mechanisms, hence requires further examination.

When current passes through electrolyte solutions, the ions carry the

charges from higher to lower potential under the applied voltage. If it is

direct current, an electrolysis phenomenon results wherein the processes of

charging and discharging, ionic association and dissociation, and the

forming and reforming of molecules continue until the circuit is broken

(87). If the current is alternating, the processes of electrolysis are the same except that they periodically reverse direction because of the applied

alternating EMF. At 50 Hz, the direction of current flow and the processes

reverse every 1/100 of a second.. However, this period of 1/100 sec provides sufficient time for ions to move a long distance in terms of

molecular ^dimension. For example, the mobility of a sodium ion (Na+

) n is

5.2 X 10 cm/sec (88); thus in 1/100 sec it will traverse 520 X 10 m

The. thickness of the membrane of a nerve fiber is in the -order of 100 X

10 m (77) and the crystal radius of Na

+

is 0.95 X 10 m (89). It can be seen that the distance the Na ion traverses in 1/100 sec. is about 250

times its own diameter and five times the thickness of a nerve fiber

membrane. The other ions commonly contained in physiological fluids are potassium (K ), calcium (Ca '

)

L and chloride (Cl ). There are also

hydrogen (H ) and hydroxyl (OH ) ions from the dissociation of water, in

addition to many minute quantities of other inorganic and organic ions.

When a positive ion meets a negative ion, a neutral molecule may be formed

and this molecule may or may not redissociate when the polarity of the

applied EMF reverses. This process of molecular formation and reformation

depends upon the chemical affinity and bonding energy of the involved ions,

and is beyond the scope of this study. It is. not known whether or not the

processes which take place in a given half cycle' of current flow are reversible during the following half cycle.- However, judging from the

injurious phenomena some of those processes are irreversible. If this is

the case, the constituents of the electrolyte solutions will be altered and

their natural functions will be disturbed, changed, or even destroyed.

Physiological Aspects

In the human body, every physiologic.al entity has a specific function.

If the entity is changed constitutionally by an external agent, such as
15 -

Joulean heat or specific electrical effect, its natural function will be

disturbed, changed or destroyed, and injury results.

Joulean heat is strongly time dependent, whereas electric current flow

is essentially instantaneous. In an electrical accident it is commonly

observed (10, 11) that a strong muscular contraction may fling the body away

from the contact and break the current, or the victim may be unable to

release the conductor until the current is broken. Lewis (11) has observed

that when electric current traverses the body, strong tetanic contractions

of the entire musculature are produced. These could lead to extreme

opisthotonos (i.e., extreme arching of the back), with torn muscles,

dislocated joints and fractured bones (11, 90). This muscular reaction may

take place instantly as a result of a severe disturbance to the nervous

system. Joulean heat could not induce such a spasmodic effect, but specific

electrical action could. Since the nerve system is controlled under a delicate ionic balance (81, 82), the disturbance must be caused by unnatural

ion transfer. This could only be induced by current, not by heat.

The ionic unbalance in the nerve system induced by electricity (77, 83-

86) could also explain other phenomena of shock, such as ventricular

fibrillation and respiratory paralysis, for the latter are also controlled

by the nervous system. Urquhart (91) demonstrated that the heart beat was inhibited with the passage of electric current through the vagus nerve centers of animals. When the vagus nerve centers were controlled by the

administration of atropine, the heart beat was not affected by passage of

current. Obviously, the minute amount of atropine could not diminish the

I R effect, were it to occur, but the chemical might readily alter the ionic

activity in the nerve fiber. It therefore appears that ventricular

fibrillation is caused by the specific electrical effect, rather than from

the heat effect.

In the case of non-arcing contact injury, the theory of specific

electrical effect again appears to offer a better explanation. An

experiment conducted by Hooker, et. al. (92) serves as evidence. In this

experiment, the diagonally opposite fore and hind leg of a dog were shaved

and immersed in separate containers of a 1% saline solution. Through

electrodes in the solutions, a current of 5 amperes from a 2000 V, 60 Hz source was passed for 5 seconds through the body of the dog. Breathing and

heart action both stopped during current flow, but recovered normally soon after the circuit was broken. No tissue or organ damage was immediately

apparent, nor was observed £or the following six years. This experiment

appears to contradict the I R effect since the current was high and time

duration was long. Under these conditions, the Joulean heat effect would

have been deemed to be sufficient to cause damage comparable with many other

low voltage electrical injuries. This experiment also yields further

evidence to support the observations of Skoog (14) that for large and wet

surface contacts, no burn occurs. Bathtub type electrocution accidents

which result in heart fibrillation or respiratory paralysis are comparable

to the experiment cited above.
- 16 -

If arcing occurs at the contact site, temperatures on the order of

2000»3000°C could be developed. The arcing phenomenon generally occurs in

high voltage accidents. Because of the high current density at the entrance

and exit sites, electrical energy transformed into heat is very high and

local damages are severe. Delayed effects of tissue damage often occur.

The theory of heat effect could explain the local damages but the delayed

effect does not conform to the phenomena usually observed with thermal burns

(10-12). However, when the epidermal layer is destroyed by intense

electrical energy, the dermis and adjacent tissues will be exposed. The

current will flow through the tissue fluids, blood stream and nerves. The

process of electrolysis could take place; electrolytes could shift and the

natural functions of the entities involved in the process could be

disturbed. Hence, the delayed effect of tissue damage could result. The

theory of specific electrical effect seems to provide a better explanation

of observed phenomena.

For low voltage injury and mouth burn, commonly encountered with 1 1Q220 V, 60 Hz A.C., current marks (9) generally appear at the site of

contact. The lesion is bloodless, cold and painless (10), and delayed

tissue necrosis commonly occurs (1, 5, 10, 11). For mouth burns, the injury

is usually localized, for the current enters and exits in the same general

vicinity. In the general assessment, the current involved is small (5, 10,

11, 17), on the order of 100 ma (5). At low current levels the heat

developed should be very small.

In view of the foregoing arguments, the theory of specific electrical

effect appears to better explain the mechanism of low voltage electrical

injuries than does the theory of Joulean heat. Both theories are qualitative. A quantitative description of the mechanism requires further

experimental determinations of the functional relationship of the

physiological interaction with electricity.
17 -

CONCLUSIONS AND RECOMMENDATIONS

The non-fatal electrical injury is a complex phenomenon, both

clinically and physiologically. It may range from a minor lesion,

resulting in an insignificant scar, to severe damage requiring amputation.

Clinically these injuries may be treated in emergency rooms, by plastic

surgery or in special burn units, hence hospital records for electrical

injuries may be scattered over several departments. It is a difficult, if

not impossible, task to obtain detailed national statistics for electrical

injury. The statistical data presented in the preceding sections are cited

for reference only, and are not necessarily to be considered

representative. The discussion of the mechanism of electrical injury is

only a qualitative assessment of the current- state-of-the-art, and it

leaves many open questions. The major problem is that our knowledge of the

structure, distribution and properties of the physiological entities in the

current pathway is limited. The electrical characteristics of their

biochemical constituents are far from quantitatively determined, hence

neither the I R effect nor the specific electrical effect can be

quantitatively assessed at this time.

In order to understand this type of trauma more fully, a systematic

experimental examination of both the physical and phy-siological parameters

discussed in the preceding sections is necessary. This will require a carefully planned, long-range program involving cooperative investigations

by physicians, physiologists, physical scientists and other experts using

sophisticated, state-of-the-art techniques, equipment, and facilities.

Specific recommendations on the approach and nature of these investigations

is beyond the scope of this report and should be developed by a multidisciplinary team of experts familiar with the many aspects of the

problem.
TABLE 1. Annual Rate of Non-Fatal Electrical Injuries

State Period Total // of

Burns

Total // of

E.I. Annual

Rate of

E.I. 'Burns

Source

U.S.A. 1974-1976 100,000/yr 4,000/yr 4% National Center

for Health Stat.

U.S. Army

Hospital, Texas

1951-1967 2,477 • 65 3% DiVincenti (14)

Birmingham,

England

1951-1955 1,893 70 4% Davis (24)

Sweden 1955-1970 2,000 141 7% Skoog (13)

TABLE 2. Electrical Injuries (25)

182 cases in 20 years

3 female

5 deaths

95% utility worker

3% industrial

2% domestic

of which

67% high tension

33% low tension
TABLE 3- Burn Cases Treated in Selected Hospitals

Hospital/years Total Burns Total Electric High Low Mouth

All Types Burns (all) Voltage Voltage Burn

U. of Virginia Hospital

Charlottesville, VA

73-6/78

San Francisco General

Hospital, San Francisco

CA

70-77

Shriners Children

Hospital, Cincinnatti

OF! . 70-6/78

Massachusetts General

Hospital, Boston, MA 7^-76

461 30

1,182 ' 28

784 56

11 ;

17 - 13

25-3

18 - 38

8 3

-

Shriners Burn Institute - 20 12 8

Boston, MA

74-76

King’s County Hospital 1,690 96 - Center, Brooklyn, NY

70-78
TABLE 4. Resistivities of the Human Body (27)

Body Segment freq. (Hz) temp. (°C) Resistivity(ohm-cm) Remarks

Blood D.C. 40 150 Normal subjects

20-5k 40 155

Ik 37 165 avg.

Body fluid 1 k- 30k 2^4 .5 64.6

*

Physiological - 38 50

solution saline

Cardiac muscle 1M room. 132 2-3 hours after death

Skeletal muscle D.C. 37 245 longitudinal

100-1k 37 240 longitudinal

100-1k 37 675 transverse

Lung 200M-900M 27 161 avg. autopsy

Kidney 1M room 126 2-3 hours after death

Liver 1M room 298 2-3 hours after death

Spleen 1M room* 256 2-3 hours after death

Fat 1M room-body 2,180 freshly excised

Bone low — 16,000 freshly excised

1M

** room-body 1,800

Skin 1M room-body 289 freshly excised

'Arm D.C. pulses 37 (body) 160 corrected for bone

and fat

Forearm D.C. 37 330 geometrical mean

Finger & hand D.C. 37 280

Finger D.C. 37 235

Neck D.C. 37 280

Trunk D.C. 37 .415 along axis of body

Head D.C. 37 840 trans-temporal

Head (scalp) D.C. 37 230

Thorax D.C. 37 463
TABLE 5. Resistance and Resistivity of the Human Body

Segment Resistance (ohms) Resistivity

(ohm-cm)

Reference*

Total body

(criminal electrocution)

218 Kennelly

Hand to hand 550-1,970

610-1 ,870

Bullard

Jelliffe

Bone 900,000 Jellinek

Brain 2,000 Jellinek

Liver 900 Jellinek

Muscle 1,500 Jellinek

Skin (dt;y)

(per cm ) p

100,000 Brandon

50,000

M0, 000

* Galinary & Kratter

Chapuis

(per 100 cm ) 500

V Jaffe

Skin (wet) 2,500-3,000 Cardieu

(in water) 1,200-1 ,500 Jaffe

Skin (current passing

for 1 min)

380 Jolly & Gaertner

Cell protoplasm

(mammalian)

• 300 Cole (28)

Surface membrane

(most probable range)

1 ,000(ohm/cm^) Cole (28)

Medium for mammalian

cells • 100 Cole (28)

^References for resistances are given in reference 1.
TABLE 6. Electric Current (60 Hz) and Current Density Thresholds

Event Current Current Density External Field Reference

(mA) (mA/cm ) Strength (60 Hz)

Sensation 1 0.1-1 1 MV/cm

2

(29)

Let go 10 0.1-1 1 MV/cm2

Fibrillation 100 1 10 MV/cm2

Air breakdown 30 kV/cm

Perception 1 (6)

Pain 5

Tetanic muscle

contraction

15

Respiratory muscle

tetanically contracted

30

Cardiac fibrillation 60-5,000 . Respiratory failure, ' 10,000

0. 1-0.5 (3D

5-9

Perception

Let go

Fibrillation >10
TABLE 7. Ionic Equilibria in Human Body Fluids

A. Human

Cation

Plasma (81)

mEq/1* Anion mEq/1*

Na 138 Cl 105.0

K 4.5 HCCL 25

Ca 5.2 Pr 5 16

Mg 2.0 POn 2.2

so; . 0.5

Other anions 1.0

B. Human Erythrocytes (81)

Na 16 Cl 55

K 96 HC0-, 15

Ca 0.5 Other anions

Mg 4.6 Other anions 47

C. Nerve Cell (82)

Ion Outside (mEq/1) Inside (mEq/1)

Na 150 15

K 5.5 150

Cl 125 9

D. Muscle of Dog (1 kg of fa't free muscle) (81)

Na 146 12

K 3.8 137.4

Ca 3.2 . 3.2

Mg 1.3 38.5

Cl 124.4

P 2.6 117.3
E. Sweat Constituents (81)

Cl ion, NHjj ion, urea, uric acid

*mEq/l means one thousandth of the molar

solution which can react or replace the

corresponding amount of hydrogen ion in

1/1000 of 1 normal solution.
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GLOSSARY

Action potential - when an excitation impulse propagates through the nerve

system, there accompanies this action a potential difference which is called

action potential.

Atropine - a poisonous, white, crystalline alkaloid, used to increase heart

rate by blocking the vagus nerve.

Atrophy - arrested development of a part or organ of an animal.

Biofluid - a fluid contained in living matter.

Bond energy - the energy required to break a chemical bond which holds atoms

together to form a molecule.

Cardiac muscle - heart muscle.

Cerebrospinal fluid - the fluid in the brain and spinal cord system.

Chemical affinity - the tendency for a chemical reaction to occur.

Clostridial myositis - an inflammation of a voluntary muscle caused by some kinds of bacteria.

Conduction velocity - the velocity of the conduction of excitation along a nerve fiber.

\ Decalcification - the action of the removal of calcium ion from a calcium

containing chemical substance.

Dermis - the layer of skin beneath the epidermis.

Edema - an abnormal accumulation of fluid in the intercellular tissue spaces

of the body.

Epidermis - the outermost layer of the skin.

Erythrocytes - red blood corpuscles.

Femoral artery the artery in the thigh.

Histology - tissue study.

Humerus - the bone that extends from the shoulder to the elbow.

Hyperemia - an excess of blood in a part,

in situ - in its natural position.

Intima - innermost.
in vitro - within a glass; observable in a test tube,

in vivo - within the living body.

Ionic association - the formation of an ionic aggregate from free ions in a solution of electrolyte.

Ionic dissociation - molecules of an electrolyte in a solution dissociate

into free ions.

Ischemic - pertaining to the deficiency of blood in a part.

Muscosa - a mucous membrane.

Myelin - a fatlike substance forming a sheath around certain nerve fibers.

Opisthotonos - a form of tetanic spasm.

Parietal thrombi - the formation of clot in walls of cavity.

Peripheral nerve - external nerve; away from the central nervous system.

Perivascular - situated around a vessel.

Redissociate - to dissociate into free ions from a previously formed ionic

aggregate or neutral molecule in an electrolyte solution.

Respiratory paralysis - the loss or impairment of the function of

breathing.

Sciatic nerve - the nerve in the region of the hip.

Tetanic - tending to produce a state of a muscle when undergoing continued

contraction.

Thrombosis - the formation of clot.

Tuberosity - an obtuse prominence on bones for the attachment of ligaments.

Vagus nerve - the tenth cranial nerve.

Vascular - pertaining to vessels.

Vasoconstriction - the diminution of the vessels leading to decreased blood

flow.

Vasomotor - affecting the caliber of a blood vessel.

Vasoparalysis - partial paralysis of vasomotor nerves.
Ventricular fibrillation - a condition characterized by fibrillary

twitching of the ventricular muscles; the impulses traversing the

ventricles so rapidly that coordinated contraction cannot occur.

135- 1 I 4 A (REV. P-78)

I

U.S. DEPT. OF COMM.

BIBLIOGRAPHIC DATA

SHEET

1. PUBLICATION OR REPORT NO. NBSIR79-1 710

2 .C-jv’L Act c-ssion K! o.| 3. Recipient's Accession No.

4. TITLE AND SUBTITLE

I Electrical Injuries - A Literature Review

5. Publication Date February 1979

6. Performing Organization Code

I

AUTHOR(S)

Yunn -Chi Wu

8. Performing Organ. Report No.

PERFORMING ORGANIZATION NAME AND ADDRESS

NATIONAL BUREAU OF STANDARDS

DEPARTMENT OF COMMERCE

WASHINGTON, DC 20234

30. Pfoject/Task/Work Unit No.

11. Contract/Grant No.

l2. SPONSORING ORGANIZATION NAME AND COMPLETE ADDRESS (Street, City, State, ZIP)

t

Consumer Product Safety Commission

5401 Westbard Avenue

Be the s da , MD 20016

13. Type of Report & Period Covered

14. Sponsoring Agency Cods

. SUPPLEMENTARY NOTES

|

I Document describes a computer program; SF-185, FIPS Software Summary, is attached.

lil. ABSTRACT (A 200-word or les3 factual summary of most si gni ficant information. If document includes a s i gni ficant bibliography or

literature survey, mention it here.) This reoort reviews and discusses the frequency, .severity and mechanisms of the

electrical injury as reported in the literature. Detailed national statistics on the frequency and severity of specific types of electrical injury are not available,

however, limited data from t

! :e literature and from a survey of a few randomly

selected hosoitals are summarized and presented. The mechanisms of injury involve

the ohysical and physiological parameters of. the electrical source and the human

body. These parameters are discussed according to known principles.

Injury to the human body, initiated by the flow of electrical current, is the

consequence of disturbance, change or destruction of physiological entities such as nerves, blood vessels, o^aans, muscles and bones. For interpreting the electrical

injury phenomena two theories exist in the literature. One theory suggests^that

electrical injury is thermal in nature and is cuased by the Joulean heat (I R)_

resulting from current flow through the body. The other theory suggests that injury

is caused by specific electrical effects such as electrolyte shifts thac are induced

by the current flow. Evidence to support or dispute both theories was found in the

literature. Due to the lack of quantitative data, however, the validity of these

theories can only be assessed qualitatively.

L7 . KEY WORDS (six to twelve entries; alphabetical order; capitalize only the first letter of the first key word unless a proper name;

separa ted by semicolons) , _ , t j i _• r • . Arc burn; contact burn; current threshold; electrical injury; eleccrolyte shiti,

heat effect; injury mechanism; mouth burn: specific electrical effect; injury

statistics.

18. AVAILABILITY XXKUnlimited

I | For Official Distribution. Do Not Release to NTIS

EU Order From Sup. of Doc., U.S. Government Printing Office, Washington, DC

20402, SD Stock No. SN003-003-

Order From National Technical Information Service (NTIS), Springfield, VA. 22161

19. SECURITY CLASS 21. NO. OF

(THIS REPORT) PRINTED PAGES

UNCLASSIFIED

20. SECURITY CLASS 22. Price (THIS PAGE)

UNCLASSIFIED

USCOMM-DC •



3 UteratUre

^

QC 100.U56 no. 79-1710 1979

NIST Research Library

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