Electricity” comes  

from the Greek

“electron”, the word
for amber. The
ancient Greeks
observed that amber,
when rubbed,
acquired the ability to
attract objects such
as straw. However,
William Gilbert, the
physician to Queen
Elizabeth who wrote
the book, “De
Magnete” in 1600,
was the first to use
the term electricity.
Concepts of
electricity became
well established by
1880. In 1800,
Alessandro Volta
announced that
electricity could be
drawn from a pile of
alternating zinc and
silver disks stacked
one on the other.
Michael Faraday, in
1821, discovered
that a current
carrying conductor
would rotate about a
magnetic pole and
that a magnetised
needle would rotate
about a wire carrying
an electric current.1
In 1879, Edison
introduced the
incandescent electric
light. This single
application fuelled a
tremendous growth
in the use of
electricity and
electrical equipment
and the consequent
inevitable
emergence of
electrical injury from
man made sources.
The first fatality due
to electricity was
recorded in France in
1879, when a stage
carpenter was killed
by an alternating
current of 250 volts.2
Prior to 1880,
electrical injury to
man came primarily
from lightning.3

Comprehensive
literature pertaining
to electric injury
statistics or of the
costs involved is
surprisingly lacking.4
Collection of data
about injury and
death due to
electricity is difficult
due to
inconsistencies in
injury definitions,
data reporting and
record maintenance.

From information
that is available, the
national rates for
fatal electrical
accidents per million
inhabitants in 1967
ranged from 1.3
(Northern Ireland) to
7.6 (Italy).5 The
victims of electrical
injury are most likely
to be workers in the
electric utility and
construction
industries.6
Electrocution is the
fifth leading cause of
fatal occupational
injury in the U.S.7,
where from 1980 to
1992, 5348 workers
died from contact
with electrical energy
(an average of 411
deaths per year).8 3
- 4% of admissions
to a hospital burn
unit are related to
electrical injuries.9,
10 The mortality from
electrical injuries
ranges from 3 –
15%.11

The costs of
electrical injury are
high and continue
long after the initial
injury. Many of those
injured are young
and become
permanently
disabled. Costs can
therefore persist for
decades. In addition
to the direct costs of
the injury, indirect
costs include lost
employment time,
productivity loss,
equipment damage,
replacement
employee hiring and
training, fire loss,
accident
investigation and
overhead costs
associated with
running a self
insurance program. It
is estimated that it
takes fewer than 650
cases worldwide to
cost a billion US
dollars.12

Away from the

workplace, most
injuries are due to
lightning strikes or to
domestic low voltage
(<1000V) electrical
contact. Lightning
strikes account for
several hundred
deaths each year in
the US, with mortality
approaching 30%.13
The rate of disability
is high because of
neurological
effects.14 Domestic
low voltage power
frequency electrical
shocks commonly
involve small
children in and
around the home.15

Physical concepts

Electricity is the
movement of
electrical charge
along a material.

Current (I) is a
measure of the
amount of electrical
charge that is
flowing. It is
measured in
amperes (A).
Electrical current
flow requires the
presence of an
electric potential
difference between
two points. By
convention, electrical
current flow occurs in
the direction
opposite to the flow
of electrons between
the two points.

Voltage (V) is a
measure of the
electrical force that is
driving the flow of
current. It is
measured in volts
(V).

Resistance (R) is the

degree to which a
material opposes the
). If an analogy were
drawn flow of
current through it. It
is measured in ohms
( between an
electrical circuit and
water flowing
through a hose,
current would be the
rate at which water is
flowing through the
hose and voltage
would be the water
pressure driving the
flow of water. There
are also two
equations in the
physics of electricity
that are relevant to
electrical injuries.

Ohm’s law relates

voltage, current and
resistance:

R. V = I

This means that for

any given voltage
level, the amount of
current flow will
increase as
resistance to flow
decreases.

Joule’s law quantities

the amount of heat
generated in a
conductor:
Heat = I2 x R x time
= V2/R x time

The electric field

strength is the rate of
change of potential
difference per unit
distance (V/m) or the
gradient of the
potential difference
with respect to
distance.

The field frequency

is the rate of change
of the field strength.

DC (direct current)
indicates a field
frequency of zero.
AC (alternating
current) indicates
change of polarity of
the field with time.

Capacitative
coupling refers to the
phenomenon
whereby an
alternating electric
field can transfer
energy to charged
molecules in the field
(without actual
physical transfer of
charge) and cause
them to rotate so as
to align with the
direction of the
alternating electric
field. The efficiency
of capacitative
coupling is very
dependent on the
frequency of the
field.11

However, as the
frequency of the field
increases, energy
absorption occurs at
an atomic level. At
frequencies > 1015
Hz, electrons on the
outer orbits may
become unpaired
leading to the
formation of free
radicals. Electric
fields of this
frequency are
termed ionising fields
and mediate cellular
damage via the free
radicals.16

Arc contact or
dielectric breakdown
occurs when the
electric field strength
in a conducting
medium is of such
magnitude that
atoms are pulled
apart and a hot gas
of ions called
“plasma” (a very
good conductor of
electricity) is created.
Consequently, in a
strong electric field
created by a high
voltage power
source, an arc can
mediate direct
electrical contact and
allow passage of
current along its
length before
mechanical contact
is established with
the victim. For
example, the
breakdown strength
of air is
approximately 2
million V/m. Arcing
can occur when the
forearm of a
grounded victim is 3-
4 mm away from a
7500 V power line
source. The
threshold for arc
initiation depends on
the geometry of the
arcing surfaces.
Arcing can occur
across greater
distances when, for
example, an
outstretched finger or
a pointed object held
in the hand
approaches the
power source. The
threshold also
depends on the
weather. Humidity
decreases the
threshold. At < 300V,
arcing cannot be
initiated through
normal air and direct
mechanical contact
must precede
electrical contact.11

A thermo-acoustic
blast arises from the
sudden (sub-second)
thermal expansion of
air due to the high
temperatures (5000
degrees C or higher)
within electric
arcs.17 Such a blast
may propel the victim
away from the
electric source.
Barotrauma from the
blast include
perforated eardrums,
blast lung, abdominal
blast injury and
secondary
acceleration/deceler
ation injuries from
impact and impact
from shrapnel.

Electro-physiologic
interactions

Electrochemical
reactions at the skin

Low frequency
current produces
ions on direct contact
with the body
surface. These alter
the tissue oxygen
 level and pH. Such
electrochemical
reactions at the
interface with the
skin do not occur
when contact is
made through an
aqueous electrolyte
solution or during
capacitative and
magnetic coupling of
electrical power into
the body across the
tissue interface.11

The resistance of the

epidermis

The epidermis forms

a barrier to ion
transport and
contributes 95 to
99% of skin
resistance to
passage of DC
current. On the
palms and soles, the
epidermis is 2 to 3
times thicker and
therefore has 2 to 3
times greater
resistance.18

Epidermal resistance
is dependent on
three factors:

1. Current frequency:
alternating currents
can capacititatively
 couple across
epidermis and
resistance is lower to
AC currents than it is
to DC current.

2. Hydration: resistance
decreases with
increased epidermal
hydration.

3. Voltage: The
resistance of the
epidermis remains
approximately
constant until a
breakdown voltage is
approached and then
it rapidly drops away
with increasing
voltage. The
breakdown voltage is
the voltage at which
the epidermis
undergoes structural
destruction and
electrical conducting
channels in the
epidermis are
formed. The
breakdown voltage is
about 150 V in most
areas and 400 V on
the palms and soles.
Complete epidermal
destruction allows
direct current
passage to the
dermis and
subcutaneous
tissues.18-20
Current

Muscle and nerve

cells use ion currents
for intra and extra
cellular
communication.
Action potentials are
generated by
sufficiently large
transmembrane
electric fields, which
produce neurological
responses and
muscle contraction.
Neuromuscular
responses to electric
currents are
dependent on
frequency.
Alternating currents
at frequencies ≥ 50
Hz pass through
nerve and muscle
membranes
capacititatively
without altering the
transmembrane
potential enough to
generate an action
potential.

The threshold of
human perception for
current passing
through a finger is 1
mA.21 At 16 mA, at
what is known as the
“let-go threshold”,22
the forearm muscles
contract involuntarily,
resulting in a
clenched fist
because the flexor
muscles are stronger
than the extensors.
The fist position
cannot be released
without cessation of
current.

Respiratory muscle
spasm occurs at a
transthoracic current
threshold of 20 mA to
produce respiratory
arrest.23

Atrial or ventricular
fibrillation can result
if there is passage of
non-physiological
current of 60 mA
during the
repolarisation phase
of the cardiac cycle.
The vulnerable
period is at the end
of ventricular systole
and correlates with
the early T wave
component of the
ECG.24

Summary of current
thresholds for
electrophysiologic
responses.21-23
 RESPONSE THRESHOLD CURRENT
Sensation of pain (fingertip contact)1.0 mA (male)
0.5 mA (female)
The ‘let go’ threshold 16 mA (male)
11 mA (female)
Respiratory arrest 20 mA
   
Cardiac: Extrasystole 60 mA
Cardiac: Ventricular fibrillation 100 mA
Permeabilisation of nerve and 1500 mA

muscle membranes

   

The distribution of current within tissues

The current distribution is dependent on the relative conductivity of the various

tissues and the frequency of the current. The tissues behave like a volume conductor
with the conductivity of normal saline solution because the difference in conductivity
of most tissues is small. Current density is highest at contact points.25 26

in the extremities, skeletal muscle carries the bulk of the current because it occupies
a high proportion of the volume of the extremity, despite the higher conductivities and
higher current densities within arteries and nerves. Cortical bone carries the least
amount of current because of its high resistance and small cross sectional
dimensions.25

The orientation of tissue planes also affects the magnitude of the electric field and
current. If current passes parallel to the tissue planes, the electric field strength will
be equal across the tissues but the current will be different in each tissue. If it passes
perpendicular to the tissue planes, then magnitude of the current will be equal in the
different tissues but the electric field will be different in each tissue, being maximal in
the tissue of highest resistance.27
Current mainly travels between cells because cell membranes are good insulators.
Therefore, tissue resistance is proportional to cell density. Furthermore, the
conductivity of muscle cells is higher in a plane parallel to the fibres when compared
to a plane perpendicular to the fibres.

Axial position determines the relative volume fraction occupied by the various tissue
types and therefore, the current distribution and total resistance. The high resistance
of joints is due to the large proportion of the cross sectional area of the extremity
being occupied by skin and bone.
For instance, 25% of total hand foot resistance is in the wrist and 30% arises from the
ankle.20 When the epidermis is intact, the resistance between two points on a body
 surface is 100,000 Ohms. On prolonged contact with a power source of >200 V, the
resistance from one hand to foot falls to 1,000 Ohms, after epidermal breakdown.28
Table - Tissue current density J in mA/cm2 and resistivity r (ohm cm) in cross section
   
versus applied current from experiments using hogs’ hind limbs25
Total Approx Artery Nerve Muscle Fat Bone

Current Applied Cortex

Voltage
mA V J R J r J R r J r J
longit-
trans-
  udinal  
verse
10 6 0.32 147 0.26 201 0.18 296 512 0.12 375 0.03
30 15 1.18 145 0.86 209 0.50 282 525 0.43 360 0.09
100 45 3.1 152 3.0 191 2.0 295 483 1.5 352 0.30
300 135 9.8 140 8.7 197 7.0 287 501 4.9 377 0.85
600 260 21.0 150 15.2 196 12.0 292 492 9.3 366 2.0
1000 415 35.9 155 27.1 200 19.5 290 650 13.4 386 2.8

  Pathogenesis of tissue injury  

Low frequency, high voltage electric fields produce acute tissue injury by:
1. Joule heating of tissue,9
2. permeabilisation of cell membranes by electroporation 29-33 and
3. cell membrane protein denaturation.34, 35

As frequency increases to the optical range and beyond, direct molecular absorption
of electrical energy occurs, with consequent free radical mediated damage.16
Cellular injury translates to tissue and organ dysfunction.

Thermal effects

Joule Heating refers to heat generated from the passage of ionic current.

Dielectric heating refers to the heat generated from rotating molecular dipoles (e.g.
water) in a high frequency AC electric field. Rotation of molecular dipoles is resisted
by viscous drag from interactions with neighbouring molecules. Small molecules like
water can oscillate at the frequency of the applied field up to the gigahertz range.36
However, the frequency of oscillation of larger molecules, such as DNA and proteins,
is highest at the radiofrequency range, giving rise to concern about cellular
telephones.11
 The rate of tissue dielectric heating is dependent on:11
1. The amplitude of the tissue electric field
2. The density of the dipoles
3. The frequency of the field.

Field frequency governs the relative contributions to the heat generated from an AC
electric current.

Electrical effects

Pure electrical injury results from the direct action of electrical forces on electrically
charged or electrically polarised cell components.

Electroporation

Transmembrane potentials of greater than 300 to 400 mV, lead to electroporation.37

This process involve “the punching” of water molecules through molecular sized
pores in the cell membrane,38 until the pore exceeds a critical size, beyond which the
pore is energetically favoured to expand rather than close, disrupting the lipid bilayer
of cell membranes.39 Structural membrane defects result in permeability to ions and
molecules as large as DNA, leading to cellular dysfunction.40, 41 Growth of the
electropores is thought to be restricted by membrane proteins which comprise 30% of
the total membrane mass. Although electropores can seal spontaneously42-44, a cell
ceases to be viable if sufficient numbers of non-sealing pores form.

Electroconformational protein denaturation

Electroconformational protein denaturation refers to the denaturation of membrane

proteins by the direct action of an electric field. Proteins are composed of amino acids
which are electrical dipoles which collectively form a larger electric dipole,34, 35 and
can be influenced by an electric field. Since the function of proteins is dependent on a
precise three-dimensional structure, even minor distortions of configuration lead to
protein dysfunction or even irreversible denaturation. An example of a protein
susceptible to electroconformational damage is the potassium channel, one of the
voltage gated ion channels.45, 46

Effects of AC frequency

Biologic consequences of electrical injury are related to the frequency of the electric
field producing the injury.11 Most of the electrical injuries requiring medical attention
arise from contact with electricity with the frequencies of commercial or domestic
electricity supplies.
  Important frequency ranges of electrical injury  
  Frequency Regimen Applications Harmful effects
 
 DC – 10 kHz Low frequency Commercial Joule heating;

electrical power; Destructive cell

soft tissue membrane

healing; potentials

transcutaneous

electrical

stimulation
100 kHz – 100 Radiofrequency Diathermy; Joule heating;

MHz electrocautery Dielectric heating

of proteins
100 MHz – 100 Microwave Microwave ovens Dielectric heating

GHz of water
1013 – 1014 Hz Infrared Heating; CO2 Dielectric heating

lasers of water
1014 –1015 Hz Visible light Optical lasers Retinal injury;

photochemical

reactions
1015 Hz and Ionising Radiotherapy; x- Generation of

higher ray imaging; UV free radicals

therapy

   

Microwave burns

Microwave frequency electric burns are clinically different to low frequency electric
burns.47-50 The epidermis forms a resistive barrier at low frequencies. In the
microwave range, capacitative coupling permits passage of current with little
dissipation of energy at the epidermis. Unless the epidermis has a high content of
water, it may not even be burnt. Microwave field penetrates to a depth of 1 cm,
characteristically heating up sub epidermal tissue water.

Clinical manifestations
Clinical presentations of electrical injury are variable, ranging from minor to severe
multi-system injury.9, 51-53 The random nature of the circumstances in an accidental
electric shock makes it impossible to formulate empiric guidelines for predicting the
full extent of tissue damage. The variables include duration of contact, points of
contact, frequency of current, electric field strength, magnitude of the thermo-acoustic
blast, radiant heat transport, associated falls and fractures from involuntary muscle
contraction.17, 54, 55

The consequences of contact with high-energy electrical sources are usually major
and the upper extremity is almost always involved, but any or all systems may be
affected. The clinical picture is dominated by primary electrical injuries to the skin,
nerve, skeletal muscle, bone and cardiovascular system.11 Secondary organ
dysfunction often develops in the lung and kidney. An important concept is that there
is no correlation between the size of the contact skin wound and the actual total
extent of all injuries. The total extent of injury in high energy electrical shocks is
almost always more extensive than is apparent at initial triage inspection.

Skin

There are always at least two points of skin contact. In low voltage injuries, the
current path is predictable. However, with high voltages, the current path is
unpredictable as arcing may occur at multiple sites. The size and pattern of the skin
wound is determined by the nature of contact with the power source in terms of area
and topology.11

“Kissing wounds” occur when there is electrical breakdown of skin on opposite sides
of a joint most commonly at the axilla. The breakdown voltage for this occurrence is a
hand foot voltage difference of more than 1000V.11

Electroplating of the skin in high voltage arcing when metal contacts vaporise and
deposit on the skin can manifest as a black metallic coating with sometimes only
superficial thermal skin burns beneath. Thermal burns to the skin can also occur from
ignition of clothing from electrical arcs.11
Skin necrosis may be full thickness or partial thickness.

Cardiac

The cardiac sequelae of electrical injury are often transient, with resolution and
complete recovery being the usual result. However, there is much evidence of
delayed or permanent cardiac dysfunction after electrical injury.56, 57 Ventricular
fibrillation as a result of electrical injury has been reported to recur up to 6 months
after electrical injury.56 Experiments have shown AC to be more dangerous than DC.
The injury produced by AC is dependent on frequency and voltage. Domestic
frequencies carry the highest risk of inducing VF. Very high frequencies (>1 kHz) are
thought to be safe producing only local tissue damage.58 The incidence of VF
following AC injury was inversely proportional to voltage, whereas the incidence of AF
and ventricular tachycardia was directly proportional to voltage.59

Cardiac conducting tissue is primarily affected, particularly the sinoatrial (SA) and
atrioventricular (AV) nodes. The reason for this predilection is unclear but may result
from denaturation of ionic channels in the nodes or from ischaemia or infarction
secondary to spasm of the right coronary artery (RCA), which is the coronary artery
most commonly affected in electrical injury.60

High-energy electrical injury can cause cardiac abnormalities ranging from sinus
node dysfunction, atrial fibrillation (AF), ventricular fibrillation (VF) and asystole to
myocardial infarction. Arrhythmias from electrical contact can be fatal especially if
there is a delay in resuscitation.

In the clinical setting, the incidence of cardiac abnormalities following electrical injury
has been reported to range from 14 to 54%. The majority of these were arrhythmias
and non-specific ECG changes with only five cases of myocardial infarcts from 344
cases in a report.61 Patients who have a normal ECG within the first 24 hours rarely
develop anomalies later.62 Myocardial infarction following electrical injury has been
well described,63 and often diagnosed solely on the basis of transient ST segment
elevations or minor ECG changes. Q wave myocardial infarcts can occur without
thrombus in the lumen or occlusion of the coronary arteries on angiography.
Therefore, prolonged coronary artery spasm is proposed as the mechanism of injury.

Muscle

Injury to skeletal muscle and its sequelae dominate the clinical picture immediately
after electrical trauma. Fixed contracted skeletal muscle and myoglobinuria are
amongst the clinical signs of electrical injury. The escape of intracellular proteins such
as myoglobin and creatine phosphokinase into the circulation is the sine qua non of
membrane permeabilisation. Muscle dysfunction or death is characterised by the
absence of twitching on at surgical exploration. The systemic sequelae of the loss of
these proteins into the circulation include renal failure from obstruction of the
collecting systems by precipitated myoglobin and hyperkalaemia from cell lysis.
Renal failure from myoglobin accumulation can have a mortality rate of 18%.64

The nature of the ‘progressive necrosis’ of muscle seen at serial surgical explorations
for debridement is currently uncertain. Initially after World War II, it was thought that
early surgical manipulation after electrical injury caused progressive necrosis of
muscle. However, it is now postulated that the progressive recognition of initially
already non-viable muscle has been misinterpreted as “progressive necrosis”.65
Electrically injured muscle tissues lack the macroscopic appearances of necrosis at
initial exploration but are already non viable due to damage to their membranes from
electroporation and electro-conformational protein denaturation and only become
visibly necrotic at later explorations.66, 67 However, it is likely that there are
components of both progressive recognition and true progressive necrosis in
electrically injured muscle.11

Skeletal injury

Powerful tetanic skeletal muscle contractions secondary to electrical injury are often
responsible for acute skeletal injuries such as long bone fractures, joint dislocations
and cervical spine fractures.23, 68
Late skeletal complications include heterotopic ossification of soft tissues and
disordered skeletal growth in adolescents. Heterotopic ossification can be found at
joints, bursae, nerve sheaths and ends of amputation stumps.68, 69

Vascular system

Endothelial cells are susceptible to electroporation and electroconformational protein

denaturation, because endothelial cells are electrically coupled through intercellular
gap junctions.30, 70 Injury to endothelial cells can result in activation of the clotting
cascades and platelet adhesion. Platelet activation leading to vascular occlusion,
can also result from thermal injury to blood macromolecules and thermal denaturation
of elastin and collagen. Vessels larger than 2 to 3 mm in diameter are rarely occluded
in the acute post electrical injury.
In addition to intrinsic vascular injury, extrinsic compression from compartment
syndromes due to soft tissue oedema may occlude vessels.

Delayed rupture of arteries is well described, especially in children after oral

commissure injuries (the labial artery often ruptures at 10 – 14 days post injury).

Peripheral nerves

Literature on the clinical effects of electrical injury on peripheral nerves is limited.

Symptoms include anaesthesia, parasthesia and dysesthesia and are usually
transient ("stunning"). Rarely, these may be permanent.71 Paralysis is less common.
Peripheral nerve lesions may develop immediately but sometimes appear several
weeks to 2 years after injury. Entrapment syndromes usually involve compression of
nerves in areas where there is normally little room for swelling e.g. the median (carpal
tunnel) and ulnar nerves (canal of Guyon), the peroneal nerve at the fibula head and
the anterior compartment of the lower leg.72 Transient autonomic disturbances e.g.
reflex sympathetic dystrophy and causalgia may also occur.

Often, neurological symptoms persist without any anomalies in electrophysiological

studies. The degree of vulnerability, theoretically, is determined by a nerve axon's
electrical space constant, which in turn depends on the diameter and degree of
myelination of the axon. Since there are different functional types of axons in a
peripheral nerve, the pattern of damage within a peripheral nerve is likely to be
heterogeneous.11

Autonomic dysfunction associated with peripheral nerve injury is known as causalgia.

Causalgia is not uncommon after high voltage electrical injury with possibly up to
33% of patients with major electrical injuries developing it.64 It typically presents in
three stages; the acute stage, the dystrophic stage and the atrophic stage.73 The
acute stage occurs within hours or days of the injury and has a duration of weeks and
consists of burning pain with hyperpathia, allodynia, hyperalgesia, hyperhydrosis and
oedema.73 The dystrophic stage occurs 3 to 6 months after injury and there is more
oedema. Muscle atrophy, osteoporosis, nail and hair loss emerge.73 The atrophic
stage sets in after 6 to 12 months. Pale and cool skin appears and pain subsides.
Heterotopic calcification leads to stiffness and contractures.73

The significant mechanism of injury to peripheral nerves from electricity is likely to be

direct electrical effects i.e. electroporation and electroconformational protein
deformation because computational simulations suggest it is unlikely for the
peripheral nerve to reach substantially higher temperatures than the surrounding
tissues.11

Central nervous system

A spectrum of transient or permanent central nervous system disabilities may

manifest in victims of electrical shock, even though there may not have been direct
physical contact of the conductor with the head.74

Pathological features of central nervous system injury include reactive gliosis,

demyelinisation, vacuolisation and peri-vascular haemorrhage.71, 75 Alteration of
brain function can be transient or permanent. Permanent changes are possible even
without visible changes at the microscopic level.
There are various time courses of symptom development and regression including
immediate and transient, immediate and prolonged or permanent, delayed and often
progressive.
Memory deficit is the most common neuropsychological complication. Others include
acute and delayed behavioural changes75-79 and psychiatric changes including the
development of phobias, anxiety, irritability, depression, somatoform disorders and
psychosis.80 Symptoms can also result from traumatic brain injury secondary to falls
or hypoxic brain injury secondary to cardiac or respiratory arrest.

Victims of electrical injury who were injured through mere peripheral contacts have
been shown to have more prevalent somatic, cognitive and emotional symptoms, as
determined by a neuropsychological symptom checklist, than control individuals.
They also under-perform in attention and concentration, motor speed and dexterity,
and memory especially visual memory. The symptoms were not related to the
severity of the physical injury. No consistent relationship has been established
between patient or injury-related characteristics and neuropsychological test
performance.81

There is often a delay in the onset of significant central nervous system dysfunction.
Paralysis has been reported up to 5 years post injury without major intervening signs.
Spinal cord nerve lesions are thought to be due to vascular thrombosis,
haemorrhage, and resultant alteration in blood flow. The consequent ischaemia leads
to later fibrosis of perineural structures. Spinal cord medullary lesions can resemble
amyotrophic lateral sclerosis (including progressive development of spastic
paralysis), transverse myelitis or ascending paralysis. Delayed nerve lesions are
usually irreversible.82 The neuropsychological functions of post acute (>3 months)
injury victims were found to be worse than those of the acute victims (<3 months).81

Ocular injury

Cataracts induced by lightning are often bilateral.72 As with the central nervous
system effects, cataracts have been formed in the absence of direct mechanical
contact with the head. However, the patients at greatest risk of forming cataracts are
those who have contact wounds on the head or neck and who have been exposed to
voltages in excess of 1000V.83 The incidence of cataract formation is between 5-
20%. Most patients initially develop visual symptoms within 12 months of the injury.
Whilst the morphological changes within the lenses are well described84, the exact
pathophysiology of electrical cataracts remains obscure.85 Anterior sub-capsular
changes are most common. Most of the affected eyes respond well to surgery.86

Auditory system

Haemorrhage can occur in the tympanic membrane, middle ear, cochlea, cochlear
duct and vestibular apparatus, which may be complicated by infection producing
mastoiditis, sinus thrombosis, meningitis and cerebral abscess.87 The thermo-
 acoustic blast from lightning not uncommonly causes tympanic membrane rupture.
Electrical injuries sustained from lightning though the telephone lines can cause
tympanic membrane perforation, persistent tinnitus, sensori-neural deafness, ataxia,
vertigo and nystagmus.88, 89

Clinical management principles

  SUMMARY  
Field response Separate patient from electrical source
Immobilise cervical spine
Support vital organ systems that may

include cardiopulmonary resuscitation

Fluid volume resuscitation
Transport to trauma centre
Hospital initial Assess other injuries
Correct pH and other electrolyte

imbalances
Control cardiac arrhythmia
Dilute and alkalinise myoglobin in urine
Diagnostic imaging (X-ray, MRI and

radionucleotide)
Tetanus prophylaxis
Early Transport to intensive care unit centre
Decompress muscle and nerve

compartments
Surgical debridement
Evaluate for cardiac muscle damage
Second look procedures (48 hrs):

biologic dressing or primary wound

closure
Intermediate Wound closure
Begin surgical reconstruction
Nutritional support
Musculo-skeletal splinting
Neuro-physiological evaluation
Psychiatric consultation
Coworker evaluation
Late Rehabilitation (physical, psychological

and occupational)
Additional reconstructive measures as
 required
Coworkers and supervisors education

and follow up

   

Field response

Extrication

It is essential to separate the patient from the energised conductor: turn off the power
where possible. Once the victim is separated from the source, any electrical charge
on the victim will dissipate within seconds.

Initial management should be in accordance with the Australian EMST guidelines or

the American ATLS guidelines.

Cervical spine immobilisation

The cervical spine should be immobilised in a hard collar until fractures are excluded.
The patient should be on a resuscitation board should CPR be required.

Resuscitation

Airway, Breathing and Circulation are assessed.

The airway is cleared and oxygen is delivered via a mask in the breathing patient.
The non-breathing patient is intubated. Intravenous access is obtained via an
uninjured extremity. At least 2 Iarge bore IV cannulae should be inserted.

Arrhythmias should then be treated aggressively with appropriate drugs where

possible. Ventricular arrhythmias are the most common and life threatening. Lightning
and high voltage electricity can cause cardiac asystole. The heart may restart
spontaneously, but the associated respiratory arrest may last longer. If adequate
ventilation is not established, a secondary cardiac arrest from hypoxia-induced
ventricular fibrillation will ensue.90

IV fluid resuscitation should be free flowing, with concurrent and continuous

monitoring of blood pressure, heart rate, and sensorium.

Retrieval

Victims of major electrical trauma should be transported to a tertiary trauma centre

with an intensive care unit.

Initial evaluation
Primary survey and resuscitation

The victims of electrical injury often have associated thoracoabdominal and skeletal
injuries due to falls and/or tetanic contractions. Therefore, the patient should be
evaluated as for multi-system blunt trauma before concentrating solely on the
electrical injuries.

Airway, breathing, circulation and neurological status should be rapidly reassessed.

Oxygen is delivered continuously. Venous access is checked and secured. An
indwelling urinary catheter is inserted. Cardiac monitoring is commenced and
arrhythmias are treated with appropriate drugs.

IV fluid resuscitation is continued and titrated against blood pressure, urine output
(UO) and heart rate. UO should be maintained at no less than ½ ml/kg/hr (25-50
ml/hr) unless dark urine suggests myoglobin/ haemoglobin precipitation. Since there
is no relationship between the size of the skin wounds and the extent of the
subcutaneous tissue injury, it is impossible to produce a valid empiric formula for rate
of initial fluid administration. However, despite this principle, various formulae based
on contact wound area have been advocated ranging from 4 - 9 ml/kg/percentage of
body surface area involved.64 91

If the urine is tea-coloured from myoglobin or haemoglobin, the UO should be

increased to 75 –100 ml/hr to avoid acute tubular necrosis. Bicarbonate may be
added to the resuscitation fluids to prevent intrarenal precipitation of myoglobin and
haemoglobin. Arterial pH in preference to urinary pH should guide bicarbonate
therapy. The arterial pH should be maintained above 7.45 92. As soon as the urine
colour clears, the rate of IV fluid administration should be reduced to produce a UO of
30-50 ml/hr (or 1 mg/kg/hr in victims less than 30 kg). Sodium bicarbonate should
also be ceased to reduce the sodium load.

A Swan Ganz catheter should later be inserted if the ECG indicates cardiac injury or if
there is large third space losses or autonomic dysfunction leading to hypo- or
hypertension.

A 12 lead ECG, a cross table cervical spine X-ray and blood assays which include a
full blood count, electrolytes, urea and creatinine, arterial blood gases and CPK levels
should be obtained. Tetanus prophylaxis should be administered.

Secondary survey

A thorough history and examination should be performed, with attention to vascular

and neurological systems. The distribution and extent of injury is determined. Skin
contact points are located.

Peripheral pulses and arterial pressures are determined with a Doppler probe.
Compartment syndrome and compression neuropathies are common manifestations
of an electrical injury. Compartment pressure should be measured and documented,
as clinical examination alone is not reliable. The classical clinical sign of pain on
stretching may not be present due to associated nerve injury. The most common
muscle compartments affected are the forearm and the leg, which have two and four
compartments respectively. Repeat measurements of compartment pressure should
be made at 8 and 24 hours post injury to exclude a compartment syndrome in
evolution.

Monitoring of renal function by UO and serum creatinine is continued

Transfer to an intensive care unit

Patients who are unable to maintain an airway or adequate ventilation (e.g. from
quadriplegia) should be intubated and ventilated. A feeding tube should be inserted in
all patients and enteral alimentation commenced within 6 hours of injury, unless there
is suspicion of concurrent abdominal visceral injury. Electroencephalograms may be
necessary to assess quality of seizure control in a paralysed patient. A 12 lead ECG
should be performed daily for 3 days to detect evolving myocardial injury.

Diagnostic imaging

Cell membrane damage by thermal or electric forces is the hallmark of electrical

injury. MRI (magnetic resonance imaging) can identify the inevitable oedema
associated with cell membrane injury. Early MRI allows rapid localisation of occult
necrotic tissue, facilitating early debridement and wound closure to avoid later
infection. MRI detected oedema should guide attention to potential problem
regions.93, 94 Nerves within oedematous fibro-osseous canals (e.g. carpal and tarsal
tunnels, Guyon’s canal) should be decompressed to prevent compression
neuropathies. If imaging by MRI or CT is negative for oedema, it is unlikely that there
has been significant muscle injury.

Tc99m stannous pyrophosphate can be used as a marker of damaged muscle tissue.

66, 95 It is useful in localising non-viable muscle tissue, which may not become
evident for 5 to 10 days. The isotope is administered intravenously and the scan
performed 2 hours later. Scans are considered indicative of muscle injury by a region
of hyperaemia whilst muscle necrosis is seen as an area of lucency. Radionuclide
scanning with Tc99m stannous pyrophosphate has been reported to have a positive
predictive value of 100% (i.e. if the scan detects necrosis, there is true necrosis) and
a sensitivity of 75% (i.e. the probability that the scan is positive if there is true
necrosis).66 However, use of the Tc99m pyrophosphate scan may not always
translate into a reduction in hospital length of stay or the number of surgical
procedures.66 Newer radioisotopes that may improve localisation of necrosis include
Tc99m methoxy isobutyl isonitrile, Thallium-201 thallous chloride and Tc99m DTPA.
Early surgical treatment

Decompression of muscle and nerve compartments

Compartment pressure in excess of 30 mmHg compromises fluid and gas exchange

between blood and tissue and is an indication for fasciotomy. In smaller
compartments such as the intrinsic muscles of the hand where measurement of
pressure is technically difficult, fasciotomy should be performed empirically when
these areas are involved. Fasciotomy should be performed under direct vision
through adequate skin incisions.

Debridement

Damaged muscle often looks normal at initial exploration unless there has been
severe heat denaturation. Due to the stunning effect of electric shock, intra-operative
pinch and nerve stimulator tests of contractile response are unreliable indicators of
muscle viability. Since the only current practical intra-operative indicators of muscle
viability are colour, contractility and bleeding, non-viable tissue will not be readily
apparent at early surgical exploration.

Early debridement under histological guidance is accurate but protracted in

duration,96 which may increase morbidity due to prolonged general anaesthesia. The
most commonly practised approach is to re-inspect the wound and debride obviously
necrotic tissue every 48 hrs. Between debridements, topical antibiotics such as SSD,
furacin or mafenide should be applied every 8 hours to marginal tissue. Allograft is
applied to decompressed, exposed and viable muscle.

Tertiary survey

Pain and anxiety should be treated pharmacologically initially. Persistent pain should
be treated by transcutaneous electrical stimulation.

A thorough neurological examination to localise and characterise any neuropathology

should be performed. Paralysis and weakness should be managed with
physiotherapy (to ensure that joint and tendon mobility is maintained), which may
involve range of motion exercises in a warm environment. Physiotherapy is also
useful in alleviating pain particularly in cases of causalgia. Non-narcotic analgesia,
anti-inflammatory agents and calcium channel blockers also attenuate any pain.

A spectral technique has been developed, which characterises the conduction deficit
of a nerve in terms of the distribution of the refractory periods of transmission (RPTs)
of its constituent fibers. The RPT is a particularly sensitive index of conduction deficit
and measures the ability of axons to conduct pairs of closely spaced impulses. The
distribution of RPT in the nerve is used to determine the contribution of the various
types of axons to the peripheral nerve; identifying normal from pathologic fibres.97,
98 The refractory transmission spectrum is a measure of the nerve fibre’s ability to
regenerate a transmembrane potential effectively, whereas the conventional
compound action potential in nerve conduction studies describes the conduction
velocity distribution within the nerve.

Investigations that should supplement a thorough sensory and motor neurological

examination of the peripheral nerves include electromyography to assess motor
nerve function, nerve conduction velocity studies and refractory period spectral
neuro-physiological studies are required to completely evaluate the peripheral
nerves.

Since any part of the entire neuraxis may be affected in high energy electrical shock,
an evaluation of the central nervous system, is necessary. A structured psychiatric
interview and a full neuropsychological assessment, (which includes cognitive, fine
motor, sensory recognition, verbal and auditory memory, and the Minnesota
Multiphasic Personality Inventory), should be performed.

Any blast injury (from thermoacoustic blast trauma) to the eyes and eardrums should
be treated early.

Wound closure

The fundamental objective in wound closure is to remove all non viable tissue and
close the wound as soon as possible. Open wounds subject the nerve, muscle and
tendons to desiccation. Whilst it is imperative to remove all non viable tissue before
closure because bacterially contaminated muscle in a closed wound is a great risk for
sepsis, not all the non viable tissue is obvious initially. A second look procedure at 48
to 72 hours should complete the debridement and provide closure in the majority of
cases with skin grafts or fascio-cutaneous local flaps. Management of electrically
damaged bone follows the guidelines for other types of skeletal trauma. The basic
tenets are also debridement and early cover with vascularised soft tissue. Progress in
free micro-vascular tissue transfer has allowed salvage of extremities that would
previously have required amputation and is useful to cover exposed nerve, cortical
bone and tendon.

Rehabilitation

Full functional rehabilitation involves the management of physical and

neuropsychological problems. Neuropsychological evaluation, similar to that for mild
to moderate head trauma, is necessary. Job retraining is also often required if the
injury occurred at work, because the victim is unlikely to return to the same
hazardous job. Residual disability such as impaired sensory and motor functions in
extremities requires extensive physiotherapy, occupational therapy and may require
further reconstructive surgery such as tendon transfers and nerve grafting.

The late development of medical sequelae following electrical injury is not

uncommon, especially with ultra high voltage or lightning injuries. Amongst these are
neuromuscular problems (from muscle fibrosis and peripheral neuropathies coupled
with joint stiffness and loss of tissue on debridements), sensory neuropathies,
paraesthesia, dysaesthesia and reflex sympathetic dystrophy, cold intolerance and
complete spinal cord paralysis.

Growth disturbances can produce skeletal deformities that become long-term

sequelae.

Cataracts tend to be bilateral and can occur in up to 5-20% of victims even when the
current path does not involve the head or neck. However, vision can usually be
improved with surgery e.g. cataract extraction and insertion of intraocular lens.

PTSD and phobias are also common in witnesses and patients.

The future

The major advances in the management of electrical injuries, in the future, will stem
from improved methods of rapidly imaging deep non viable tissue, restoring
membrane integrity, restoring native conformation to damaged proteins, limiting
systemic sequelae and repairing nucleic acids.11

The development of cameras of greater resolution to quantify radio-isotope uptake,

identify and locate tissue with membrane damage more precisely, is currently
underway and will aid early debridement of non viable tissue.

It is known that electropore expansion can be limited by membrane proteins.99

Naturally occurring proteins such as fusigenic proteins already induce sealing of
porated cell membranes after exocytosis or fertilisation. Furthermore, industrial
surfactant polymers, called poloxamers, have been shown to seal electro-
permeabilised100 and heat permeabilised membranes.101 Antioxidants, such as
ascorbate, have been shown to reduce wound oedema.

Lightning injuries

Lightning is the common term for dielectric breakdown. The latter occurs when the
electric field strength in the air between clouds and other objects exceeds 2 million
V/m, producing an enormous current for a short time (10 to 100 msec). The current
can exceed 30,000 A.14, 102 The temperature in the arc can reach 30000K
generating a high pressure thermo-acoustic wave that expands and causes shock
waves known as thunder.

Approximately 400 people are struck by lightning annually in the United States. Of
this number, less than 100 die.

A substantial voltage difference can occur between the feet of a person near a
lightning strike. Voltage drops can reach 7500V and currents up to 2 to 3 A can be
induced to flow through the body between the legs.11

During direct contact with lightning, the body surface potential difference can reach
several thousand volts allowing current of several hundred amperes to flow for up to
10 microseconds, sufficient to produce electroporation without substantial heating.
Fortunately, membranes can spontaneously seal, possibly accounting for high
survival rates amongst victims of lightning strikes.11

Large magnetic fields can be generated from the large currents in lightning. These
magnetic fields can induce a current in conducting objects such as the body. Thermo
acoustic blasts from lightning can be very destructive, strong enough to split trees
and cause physical damage to the eardrums of victims or minor head injury.

Clinical manifestations

Although mortality from lightning accidents is high (30%), significant number of

victims survive. It is paramount to be certain that immediately after a lightning strike,
the victim is electrically discharged prior to providing aid.

The prime clinical feature observed in these patients, is keraunoparalysis or complete

neurological and muscular stunning. The latter can be manifested by
cardiorespiratory arrest. Following this episode, victims can then suffer from amnesia,
confusion, muscle ache and visual disturbances up to 7 days.

The severity of lightning injury is classified into mild, moderate and severe.14

Mild All symptoms are transient and recovery is complete. The clinical features vary
from mild amnesia to temporary blindness and deafness.

Moderate Symptoms of keraunoparalysis and myocardial infarction. They tend to

have superficial cutaneous thermal injury. If the victims survive, they can then suffer
from chronic vascular spasm, permanent neurophysiological disturbances such as
lesions of peripheral motor and sensory nerves.

Severe Central nervous system (CNS) lesions, myocardial infarcts or both103,

secondary to prolonged hypoxia from cardiorespiratory arrest. Their rehabilitation
potential is extremely poor.

Management

Initial resuscitation aims to establish airway, breathing and circulation. Having revived
the victim at scene of the accident, the patient needs to be transferred to a major
trauma and burns unit for further evaluation and treatment.
Obtaining a 12-lead ECG and baseline serum cardiac enzymes is imperative at the
time of initial assessment. The patient will subsequently require continuous cardiac
monitoring either in coronary care or intensive care units. If there is substantial CNS
or cardiac depression, there may be need for ventilatory support, until further
assessment of severity of lightning injury has been made. Seizures, although
uncommon, can occur and should be treated with anticonvulsant medication.

Thermal burns should be addressed early. It is imperative to establish the extent of

cardiac and brain injury prior to surgical management. A coordinated plan should be
constructed between the intensivists and the aesthetic team, for dressings and timing
of any debridement, grafting and reconstruction.

In the long term, lighting-strike patients need special trauma counselling. They may
also suffer from CNS symptoms such as insomnia and regional pain disorders, which
should be referred on to the chronic pain management team. Follow-up visits should
therefore continue for several years.

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