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Is Serum Creatine Kinase-MB in

Electrically
Injured
Patients Predictive of
Myocardial Injury?
John W.
McBride, MD;
Kingsley
R.
Labrosse, PhD; Harry
G.
McCoy, PharmD;
David H.
Ahrenholz, MD; Lynn
D.
Solem, MD;
Irvin F.
Goldenberg,
MD
We undertook a
retrospective study
of 36 victims of
high-voltage
electrical contact injuries to determine the incidence and
possible
source of
elevated creatine kinase (CK)-MB enzyme in their serum.
Only two sustained
myocardial
infarctions
(one late) according
to
history, electrocardiographic
findings,
and clinical course. Serum lactate
dehydrogenase isoenzyme
levels
were abnormal but revealed no
myocardial infarction
patterns.
Creatine
kinase total
activity, however, reached 1.5 to
1,140
times normal in 92% and
the CK-MB level was abnormal in 50%
despite
the low incidence of
myocardial damage.
Skeletal muscle CK and CK-MB levels in four nonelectri-
cally injured patients
were
comparable
to those in normal muscle while CK
and CK-MB
activity
was elevated in six such electrical
injuries.
There was a
gradient
in CK-MB
activity
with
greatest
CK-MB
activity in "normal" muscle
near the
injury site,
lesser amounts in border
tissue,
and least in the
worst-injured
site. We conclude that
(1) myocardial injury
is uncommon in
high-voltage
electrical
injury
and
(2)
skeletal muscle injured by high
electrical
voltage
is stimulated to
produce,
as well as
release,
CK-MB.
(JAMA 1986;255:764-768)
ELECTRICAL
injuries
result from
conversion of electrical
energy
into
heat
energy
as electrical current
courses
through
tissue.' Heat
gener¬
ated is
proportional
to tissue resist¬
ance,
but
susceptibility
to
injury may
vary.
Vascular tissue with low resist¬
ance
may
be more sensitive to electri¬
cal
injury.
Tissue
damage
is
directly
proportional
to current
density; so,
high voltage
at small entrance sites
causes
deeper
and more severe
inju¬
ries than at
larger
sites.
Cardiac
dysrhythmias
and electro-
cardiographic (ECG)
abnormalities
have been
reported
in
patients
re¬
ceiving
electrical contact
injuries.14
Creatine kinase
(CK)
and lactate
dehydrogenase (LDH)
total
enzyme
activity
and their
respective
isoen-
zymes
have therefore
been
routinely
analyzed
in
such
patients
in the St
Paul-Ramsey
Burn Center since 1975.
We
retrospectively
evaluate our
expe¬
rience to determine the incidence of
myocardial damage
in
high-voltage
electrical contact
injuries.
Elevated
serum CK-MB
activity
in 34 of 36
electrically injured patients
who had
no evidence of
myocardial injury
led
us to prospectively
examine skeletal
muscle as the
possible
source.
METHODS
Between 1976 and
1980, seventy-three
patients
were treated in the St Paul-
Ramsey
Burn Center for electrical
inju¬
ries. Eleven
patients
were excluded from
analysis
because they
sustained thermal
burns rather than direct electrical contact
injury.
Seven
patients were excluded
because
they
contacted
7,200
V or less.
Information
regarding
the
magnitude
of
the power
source was conflicting or not
available in eight patients.
An additional
nine were excluded because data on
enzymes
were not available and two
because of lack of ECGs. The
remaining 36
patients, 35 men and one woman, aged
11
to 59
years (mean
±
SD,
33 ± 12
years),
are
the
subject
of the first part of this
report.
All charts were reviewed for
patient age
and sex, voltage
of the electrical source,
entry and exit
sites,
extent of the
injury,
ECG
abnormalities,
cardiac enzyme activi¬
ty, and the presence
of
cardiopulmonary
disease. The
hospital course was reviewed
for cardiovascular or
neurologic complica¬
tions,
local or other
systemic complica¬
tions,
and the eventual outcome.
Criteria for
myocardial injury or infarc¬
tion included a history compatible
with
ischémie heart
disease,
ECG evidence
including diagnostic Q waves and ischémie
ST-T
abnormalities,
and abnormal cardiac
enzyme levels. The latter included elevated
total CK and LDH enzyme levels,
the
presence
of
CK-MB,
and an abnormally
increased LD, fraction or reversal of the
LDH,/LDH2
ratio:"
Creatine kinase and LDH
isoenzymes
were
separated by electrophoresis on
aga-
rose by using
the Corning ACI
system
(Corning
Medical
Inc, Medfield, Mass).
All
serum
specimens
with total CK levels
greater than 1,000 units/L were diluted to
1,000
units/L before electrophoresis.
En¬
zyme totals
were obtained on an
analyzer
(Abbott VP,
Abbott
Laboratories,
North
Chicago, 111) using
the manufacturer's
reagent.
Six
patients
with electrical injuries
had
muscle
biopsy specimens
taken at the time
of débridement. Specimens were obtained
from
grossly
normal tissue adjacent
to the
entrance or exit site,
from the
margin
between injured
and
apparently
normal
tissue,
and from the center of the most
severely injured
tissue. Muscle
biopsy
specimens
were also obtained from four
patients
with nonelectrical skeletal muscle
injuries:
blunt trauma
(two), penetrating
trauma
(one),
and thermal
injury (one).
The muscle
biopsy specimens
were han¬
dled in the usual manner and stained with
hematoxylin-eosin.
Muscle tissue
specimens (0.5 g)
were
diced and mixed with 3 mL of TRIS-
hydrochloride
buffer
(50mM TRIS, lOOmM
sodium
chloride, pH adjusted
to 7.4 with
5N hydrochloric acid).
The mixture was
From the Section of Cardiology (Drs McBride and
Goldenberg),
the Section of Clinical
Chemistry,
Department
of Pathology (Dr Labrosse), the
Depart-
ments of Clinical
Pharmacology (Dr McCoy) and
Surgery (Drs Ahrenholz and Solem), and the Burn
Center (Drs Solem and Ahrenholz), the St
Paul\x=req-\
Ramsey
Medical
Center;
and the
University of
Minnesota Medical School, Minneapolis.
Drs La-
brosse and
McCoy
are currently with MEDTOX
Laboratories,
New
Brighton,
Minn.
Reprint requests
to Section of
Cardiology,
St
Paul-Ramsey Medical
Center,
640 Jackson
St,
St
Paul, MN 55101 (Dr McBride).
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homogenized using a
polytron (Brinkman
Instruments
Co, Westbury, NY) for two
15-s bursts
separated by
a 30-s
cooling
period. The
homogenate was
centrifuged
at 85,000 g in a
microcentrifuge at room
temperature for two minutes. The super¬
natant was diluted 1:1,000 with TRIS-
hydrochloride buffer before determination
of total CK
activity
in an
analyzer using
the manufacturer's
reagents. The CK
activity was
subsequently adjusted
to
1,000 units/L
prior
to
separation
and
quantitation by electrophoresis on
agarose
using the
Corning
ACI
system.
RESULTS
These 36
patients
received electri¬
cal contact
injuries
from sources of
7,200 to 115,000
V.
Figure
1 shows the
distribution of
voltage.
Current
path¬
way
from exit to entrance sites
involved
upper-to-lower
or lower-to-
upper extremities,
thus
possibly
in¬
cluding
the heart in the
pathway
in 17
patients.
Serum
enzyme
levels were
assayed
as soon as
possible
after
hospitalization
and each
morning
for
the next one to three
days.
Peak
serum CK
activity (Fig 2) ranged
from 97 to
159,960 units/L,
with the
upper
limit of the
reference
range
being
140 units/L for men and 100
units/L for women. Elevations were
seen in 34
(94%)
of 36
patients.
One
patient's peak
serum
activity
was
slightly
elevated at 146 units/L while
all
others exceeded the
upper
limit of
normal
by
1.5 to 1,150
times. One of
two
patients
without CK-total eleva¬
tion nevertheless
reached 137 units/L
of
activity. Figure
2 also
shows
CK-
MB levels in
open
circles. The eleva¬
tions
generally parallel
those of total
CK and
range
from 24 to
2,052
units/
L. The time
course
for the
peak
value
of total CK and CK-MB
activity
roughly paralleled
that seen in acute
myocardial
infarction
4Fig 3). Regres¬
sion
analysis
revealed
poor
correla¬
tions between
voltage
contacted and
total CK
(r=.24),
and between extent
of
burn and
CK-MB
(r=.20). Multiple
regression analysis
was not
per¬
formed because of the
poor
individual
correlations.
Lactate
dehydrogenase total levels
ranged
from 20 to
3,714
units/L
(ref¬
erence
range,
<171
units/L).
No
increased
LDH,
activity was
noted,
nor was an
LDH,/LDH2
reversal
observed. Four
patients
demonstrated
a "shock"
pattern showing decreasing
isoenzyme
from
LDH,
to
LDH,.
Sev-
25
20
15
10
Fig 1.

Distribution of
voltage.
_^_^_^
7,200 8,000 12,000 13,000 13,800 30,000 40,000 47,000 69,000 115,000
Magnitude of the
Energy
Source, V
Fig
2.—Creatine kinase (CK)-total (closed circles) is
portrayed
on left vertical axis of
semilogarithm graph and CK-MB
(open circle) is seen on
right
vertical axis. The horizontal axis
shows the individual
patients.
200,000
r
Patient
No.
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16|-
I
10
II m
1 e
Pi i
ni_m_i_ü_i_h_m i_^_
1 2 3 4 5
Day
Fig
3.—Time course
(day postburn,
horizon¬
tal axis) of
peak
CK total
(open bars) and
peak
CK-MB
activity (hatched bars). The time
course parallels
that of
myocardial
infarction.
enteen
patients, including
all three
with CK-BB
activity,
showed similar
LDH
isoenzyme patterns
that we
have identified as common to these
patients.
The
activity
is
greatest
for
LDH, followed
by nearly equal
LDH,
and
LDH,,
followed in turn
by nearly
equal
LDH,
and
LDH,.
Only
one
among
the 36
patients
fulfilled the criteria for
myocardial
injury.
A
28-year-old
man who con¬
tacted 115,000
V
involving
both hands
and feet had normal ECGs on the
first two
postburn days
followed
by
inferior ST-T
changes
on
day
3. On
day 4,
a classic inferior
myocardial
infarction
pattern
evolved and on
day
5,
a
right
bundle-branch block
ap¬
peared.
Total serum CK
activity
reached
21,396 units/L with 8.3% MB
(1,776 units/L).
Total LDH level
reached 638 units/L.
The LDH isoen-
zymes pattern
showed the shock
pat¬
tern for four
days
without
showing
an
elevation of
LDH, or an LDH,/LDH2
ratio reversal.
Only
one of the 36
patients died,
a
41-year-old
man who
had third-
degree
burns
covering
45% of his
body.
Initial ECGs were
normal,
but
on
day 5,
ischémie T-wave
changes
were seen. Cardiovascular and
respi¬
ratory systems
remained
stable,
with
death from
overwhelming sepsis
oc¬
curring
on the 18th
postburn day.
Autopsy
was not
performed.
Other ECG data are also summa¬
rized in Table 1.
Electrocardiograms
were
initially
normal in 23
patients,
including
the one
patient
who later
manifested the
inferior
myocardial
infarction. Four others were normal
except
for sinus
tachycardia, right-
axis
deviation,
and/or
nonspecific
ST-
T abnormalities.
Right-axis
deviation
without other abnormalities was ob¬
served,
as were
complete
and incom¬
plete right
bundle-branch block. Sev¬
eral
patients
had more than one non-
diagnostic
variation.
Results of the
prospective
histo¬
logie portion
of the
study
are as
follows:
Fig
4 shows the
histologie
findings
of muscle
biopsy specimens
from
apparently
normal tissue
adja¬
cent to the electrical
injury (site A,
top left);
from the area between nor¬
mal and
severely injured
tissue
(site
B, top right);
and from the center of
the
injury
(site
C,
bottom
left).
Mus¬
cle
from
site A shows
apparently
normal tissue with intact cells and
muscle fibers but a
slight
infiltration
of
infammatory
cells. Tissue from site
B shows more fiber
degradation
and
some
necrosis,
but
intact muscle
fibers are
present.
Site C shows loss
of cellular
integrity
with
damaged
cell
membranes,
extensive loss of
muscle fiber
architecture,
and cellu¬
lar necrosis.
The
highest
CK-MB
activity
was
found in
apparently
normal muscle
adjacent
to the
injury site, averaging
23.8% of total CK
(Table 2).
Creatine
kinase-MB
activity
was
progressively
lower as one
approached
the center of
the burn. The lowest levels were
found in
nonelectrically injured
mus¬
cle,
an
average
CK-MB fraction of
4.7%,
nearly
identical to normal mus¬
cle. The
differences in the amounts of
CK-MB
activity present
in the four
tissues were
statistically significant
(one-way analysis
of
variance,
F=35.6, P<.05).
The
CK-MB
activity
of tissue in site A is
significantly
greater
than the
activity
in sites
B, C,
or D
(P<.05,
Scheffe's method of
differences).
Creatine
kinase-MB ac¬
tivity
in site B is
significantly greater
than the
activity
in C or D
(P<.05,
Scheffe's
method).
COMMENT
Reports
of the
frequent
occurrence
of cardiac
dysrhythmias
and ECG
abnormalities in
patients receiving
electrical contact
injuries suggest
the
possibility
of cardiac involvement.'
'
Evidence for
myocardial injury
or
infarction is
usually
confirmed
by
compatible history,
ECG evidence
(in¬
cluding diagnostic Q
waves and ST-T
abnormalities),
and
presence
of ab¬
normal cardiac
isoenzyme
levels
within a
specified
time frame.s"
The
diagnosis
of
myocardial injury
or
infarction, however, may
be
espe¬
cially
difficult to confirm or exclude
in
electrically injured patients.
Histo-
Table 1.

Electrocardiograms
in Electrical Contact
Injury'
Initial/
_Early
Late
Normal 23 23
Sinus
tachycardia 4 2
Right-axis deviation 3 1
Sinus
tachycardia/right-
axis deviation 1
...
Sinus
tachycardia/ST-T 1
...
ST-T
abnormality 2
...
APC/first-degree AVB 1 1
Right
bundle-branch block 1 3t
Ischemia/infarction 0 2
No late
ECG_
4
'ST-T indicates
ST-segment and /or T-wave
abnormalities; APC, atrial
premature complexes; and
AVB, atrioventricular block.
tOne showed transient
incomplete right
bundle-
branch block.
ries are often unobtainable
initially
and
major
muscle trauma results in
elevated CK and LD
enzymes.
Lactate
dehydrogenase isoenzyme
levels
may
also be abnormal because of liver
damage, shock, hemolyzed erythro-
cytes, pulmonary injury,
etc. We
chose
specific
and limited criteria to
diagnose myocardial damage
in these
patients.
While we have not shown
conclusively
that no
myocardial
cells
released
CK-MB,
we believe that the
chances for
underdiagnosis
of
myo¬
cardial
damage
is minimal for the
following
reasons:
(1)
Most of our
patients
were
young
and without
preexisting cardiopulmonary
dis¬
eases. None had a
history suggesting
acute
myocardial
infarction at the
time of
injury. (2)
There were no
supportive laboratory
data with the
exception
of an elevation of levels of
CK and
its
isoenzymes. Specifically,
there were no
diagnostic
ECG abnor¬
malities,
nor
any
LDH,
isoenzyme
increases
suggestive
of
myocardial
damage. (3)
The
patients' hospital
courses did not
suggest myocardial
damage except
for two
patients.
One
patient
manifested an acute
myocar¬
dial infarction
beginning
on the third
postburn days,
and the other suffered
an acute
myocardial
infarction two
months after the initial electrical
injury.
All
except two of the 36
patients
had
elevated total CK values
(Fig 2).
In 15
(42%)
of
36,
serum CK-MB
activity
exceeded that
generally
con¬
sidered
diagnostic
of
myocardial
in¬
farction, greater
than 40 IU.7" Crea¬
tine kinase-MB
activity
exceeded 100
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Fig 4.—Histopathologic findings of electrical contact injury.
Muscle
remote from electrical entrance or exit site but in same
extremity
or
area
(top left). Muscle between worst injured
and more remote
apparently
normal tissue
(top
right). Worst
electrically injured
muscle
(bottom left).
Table 2—Creatine Kinase (CK)-MB Activity
in
Muscle Tissue From Electrical and Nonelectrical
Injuries'
Specimen!
No. A* B* C* D*
1
2
3
4
5
6
7
8
9
Mean± 1 SD
25.9
23.0
25.9
27.9
19.4
23.0
24.4
22.0
22.7
23.8 ±2.5
22.5
11.9
19.6
13.8
18.1
9.0
79
14.7±5.5
10.3
4.9
7.3
5.2
19.4
8.0
7.0
3.9
8.3±4.9
3.1
5.7
8.3
6.3
2.0
2.3
5.0
4.7±2.3
•Activity is
expressed as percentage
of total CK
activity.
tNumber of specimens exceeds six for electrical
injuries
and four for other
forms of trauma because some
patients
returned to the
operating
room for
subsequent
dèbndement and were restudied.
tA indicates muscle remote from the electrical entrance or exit site but in the same
extremity or
area; B,
muscle between worst burned and more remote
apparently
normal
tissue; C, worst electrically injured muscle;
and
D, muscle
damaged by
blunt
trauma, gunshot wound,
or thermal burn.
§Ellipses
indicate
assays not performed.
units/L in 15
patients, 1,000 units/L
in
eight patients,
and reached
45,589
units/L in one
(Fig 2).
We do not believe that the
electro-
phoretic
method
resulted in overload¬
ing
or
spillover
from the MM to the
MB or BB bands for two reasons.
First, specimens containing greater
than
1,000
units/L of total CK were
diluted to a total CK of
1,000
units/L
before
electrophoresis,
a method to
eliminate such bias."
Second,
the
greatest activity
of CK-MB was occa¬
sionally
seen not at the
peak
CK total
but at lesser amounts of CK total
activity.
Our data
suggest
that
myocardial
injury
is uncommon in
electrical con¬
tact
injuries. Nevertheless,
electrical
contact
injury
of muscle
results in
significant
elevations of
plasma
CK-
MB
activity.
Previous
authors have
shown elevated CK-MB
activity
in
predominantly
noncardiac
states, in¬
cluding
alcoholic
rhabdomyolysis,
polymyositis, dermatomyositis,
viral
myositis, ischemia,
and muscular
dys¬
trophy.1518
The levels of
CK-MB in
these various disorders are
reported
to
range
from 10% to 39% of total CK.
Since the
elevated CK-MB levels
occurred in the absence of cardiac
damage,
the
prospective
tissue evalu¬
ation was undertaken to examine
the
source of the CK-MB
elevations. The
marked
elevations of CK-MB detected
in
electrically injured
skeletal muscle
are
significantly larger
than those
found in muscle
injured by blunt,
penetrating,
and thermal
trauma,
or
normal
muscle.""520 These
findings
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suggest
an actual stimulus to
enzyme
production as
well as
release,
which
has characteristics not
yet
defined.
The skeletal
muscle
isoenzyme
data
reported
herein
(Table 2)
demon¬
strated a
gradient
in CK-MB
activity.
Muscle
adjacent
to the
injury,
which
was
judged
to be
grossly
normal at
the time of
surgery, produced
the
greatest proportion
of CK-MB
with
the least variation
(24%
±2.5%
[SD]).
Microscopically,
muscle fibers were
intact but showed an acute inflamma¬
tory response. Marginal
but viable
tissue closer to the
injury (site B)
contained lesser amounts of CK-MB
with
slightly
greater variation.
A
mixture of intact muscle fibers,
a
more severe inflammatory response,
and some necrosis was seen micro¬
scopically.
The center of the
injury
site,
on the other hand,
with
coagula¬
tion
necrosis,
loss of cellular
integri¬
ty, and extensive
loss of muscle fiber
architecture contained the least
amount of CK-MB. There was
signifi¬
cant
overlap
between this
tissue and
that injured by
blunt
trauma, gun¬
shot
wound,
or thermal
burn.
Only
two
specimens
from the former
showed
higher
CK-MB levels than
specimens
from the
latter.
There are several
possible
mecha¬
nisms for this
gradient: (1)
The
elec¬
trical current and resultant
coagula¬
tion necrosis
destroys
or denatures
the
enzymes. (2)
Cell
damage
and
disruption
releases
lysosomal proteo-
lytic enzymes
that
degrade
CK total
activity
and CK-MB.
(3)
Because of
the
injury
to the vascular
supply
to
the
area,
tissue
pH may
be reduced to
levels too low for
enzyme activity. (4)
Activation of the lymphatic system
in
the
presence
of cellular
necrosis
may
occur
(such lymphatic
activation has
been
shown to reduce the measurable
activity
of
CK).21 (5)
The most necrot-
ic cells are incapable
of
synthesizing
CK-MB.
Data on venous effluent from
the
injured
site are not available. Com¬
parison
of venous effluent to
periph¬
eral venous
samples assayed
for CK
total
and
CK-MB levels
would be ideal
for confirmation
of skeletal muscle as
the source
of CK-MB.
Nevertheless,
we believe that the elevated serum
CK total
levels and CK-MB
activity
in
the absence of evidence of
myocardial
injury,
combined with the skeletal
muscle
assay, strongly support
our
hypothesis.
That
hypothesis
is that
electrically injured
skeletal muscle
can be activated to
produce
and
release CK total and CK-MB activity
and is
the source of such
activity
in
electrical contact
injury.
Our recommendation for the care of
these
patients
includes a search
for
the history
of preexisting cardiopul¬
monary
disease or risk factors for
such disease. The
patient
should
undergo
continuous rhythm
monitor¬
ing
for the first three to five
days
with serial 12-lead ECGs.
A
history
suggesting myocardial injury
or ECG
abnormalities suggest
that cardiac
enzymes
and
isoenzymes
should be
obtained and
interpreted
in clinical
context.
Regardless
of the risk
category,
these
patients require early
and
repeated operative
intervention and
general
anesthesia.
When
indicated,
we
routinely perform fasciotomies,
débridement of nonviable
tissue,
and
amputation.
Due to the
apparent pro¬
gressive
nature of muscular necrosis
in
electrical
injuries,
the
patients
are
returned to the
operating room
every
three to five
days
until all necrotic
and nonviable tissue has been re¬
moved. This intervention must con¬
tinue
despite
ECG or
enzymatic
abnormalities.
Early
ambulation and
therapy
to
prevent
contractures in
the acute
phase
will
also dictate close
clinical and ECG
monitoring during
the
early hospital phase.
ADDENDUM
Since this report
was
prepared,
two
additional
patients
have been studied.
Their data were not
included,
even
though
the
muscle
homogenates
were
analyzed
for CK total and CK-MB
levels,
because the
assays
were refer¬
enced
per milligram
of
protein
rather
than
per
0.5
g
of tissue. Their
speci¬
mens showed greatest CK total and
CK-MB
activity
in the
"apparently
normal tissue" as did the other
speci¬
mens. Peak activities
in these two
patients
were as follows: CK
total,
535,000 units/mg
of
protein
with 2.4%
CK-MB,
or
12,840 units/mg;
and CK
total, 35,000 units/mg
of
protein
with
29.6%
CK-MB,
or
10,260 units/mg
of
protein.
This study
was
supported
in part by
the
Medical Education and Research Foundation,
St
Paul-Ramsey
Medical Center.
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