INTRODUCTION: High-voltage electrical injuries are uncommonly reported and may predispose to both immediate and delayed neurologic complications. CASE PRESENTATION: We report the case of a 43-year-old Caucasian man who experienced a high-voltage electrocution injury resulting in ischemic myelopathy and secondary paraparesis. CONCLUSION: High-voltage electrocution injuries are a serious problem with potential for both immediate and delayed neurologic sequelae. The existing literature regarding effective treatment of neurologic complications is limited. Long-term follow-up and multidisciplinary management of these patients is required

Adel Olshansky

Harpreet K Johl

Richard A Rison

Said R Beydoun

Journal of Medical Case Reports

PubMed

Abstract
          
            Introduction
            High-voltage electrical injuries are uncommonly reported and may predispose to both immediate and delayed neurologic complications.
          
          
            Case presentation
            We report the case of a 43-year-old Caucasian man who experienced a high-voltage electrocution injury resulting in ischemic myelopathy and secondary paraparesis.
          
          
            Conclusion
            High-voltage electrocution injuries are a serious problem with potential for both immediate and delayed neurologic sequelae. The existing literature regarding effective treatment of neurologic complications is limited. Long-term follow-up and multidisciplinary management of these patients is required.
          </jats:sec

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Cervicothoracic spinal cord and pontomedullary injury secondary to high-voltage electrocution: a case report

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JOURNAL OF MEDICAL
CASE REPORTS
Johl et al. Journal of Medical Case Reports 2012, 6:296
http://www.jmedicalcasereports.com/content/6/1/296CASE REPORT Open AccessCervicothoracic spinal cord and pontomedullary
injury secondary to high-voltage electrocution:
a case report
Harpreet K Johl1, Adel Olshansky1, Said R Beydoun2 and Richard A Rison3*Abstract
Introduction: High-voltage electrical injuries are uncommonly reported and may predispose to both immediate
and delayed neurologic complications.
Case presentation: We report the case of a 43-year-old Caucasian man who experienced a high-voltage
electrocution injury resulting in ischemic myelopathy and secondary paraparesis.
Conclusion: High-voltage electrocution injuries are a serious problem with potential for both immediate and
delayed neurologic sequelae. The existing literature regarding effective treatment of neurologic complications is
limited. Long-term follow-up and multidisciplinary management of these patients is required.Introduction
High-voltage electrical injuries are uncommonly
reported and may lead to serious neurologic sequelae.
The true incidence and prevalence of these events are
difficult to ascertain. This may be due to the fact that
these cases are underreported in the literature, probably
due to population unawareness and medically under-
served communities. Children and young men are at the
highest risk to receive an accidental electrical injury,
with these subgroups being less likely to report the inci-
dent [1]. The extent of injury may be apparent immedi-
ately or it may take weeks to manifest. Clinicians need
to be aware of the neurological consequences of
electrocution.Case presentation
A 43-year-old right-handed Caucasian man experienced
an electrical burn after contact with a 440 volt line while
working on a roof. Upon standing up from the squatted
position, the right side of our patient’s head came into
contact with an exposed wire, resulting in electrocution
with a loss of consciousness. Witnesses called the emer-
gency medical services, and our patient was intubated at* Correspondence: rison@usc.edu
3Presbyterian Intercommunity Hospital, 12401 Washington Boulevard,
Whittier, CA 90602, USA
Full list of author information is available at the end of the article
© 2012 Johl et al.; licensee BioMed Central Ltd
Commons Attribution License (http://creativec
reproduction in any medium, provided the orthe scene. He was transferred from a local community
hospital to our institution’s burn unit for a higher level
of care. Second and third degree burns covered 21% of
his total body surface area. The entry wound was
through his scalp, traversing through his neck and chest,
into his groin, and exiting from his left foot. No spinal
fractures were identified.
Initially, our patient was alert and able to move all four
limbs. Over the ensuing days, he was observed to move
his legs less than his arms. Two days after our patient
received multiple skin grafts and a calvarial flap, sedation
was held and he was noted to have absent limb move-
ments during routine dressing changes. A neurological
consultation was obtained on his 10th day of
hospitalization because of his evolving weakness. On
examination, our patient was intubated, and his head,
chest, groin and bilateral lower extremities were covered
by dressings. He was awake with eyes open, alert and able
to follow simple commands. A cranial nerve examination
revealed reactive pupils, intact extraocular movements
and symmetrical facial movement to smile, eye closure
and eyebrow elevation. Our patient indicated normal
light touch sensation on his face with nodding. He was
breathing over the ventilator and able to shrug his
shoulders. A motor examination showed normal muscle
bulk with flaccid tone and only intermittent, trace move-
ment in his left fingers. Our patient acknowledged pain. This is an Open Access article distributed under the terms of the Creative
ommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
iginal work is properly cited.
Johl et al. Journal of Medical Case Reports 2012, 6:296 Page 2 of 5
http://www.jmedicalcasereports.com/content/6/1/296with nodding on light pressure to all limbs. His deep ten-
don reflexes were diminished and plantar responses were
equivocal.
On admission, magnetic resonance imaging (MRI) of
his cervical spine demonstrated changes suggestive of
edema from C3 to T2 levels with an intact spinal cord.
Given the changes noted on the neurological examin-
ation, a repeat MRI was suggested. Repeat imaging per-
formed eight days after the first MRI revealed an
interval development of cord swelling and acute ische-
mic infarction (Figure 1 A,B,C). MRI of his brain showed
restricted diffusion in the bilateral medullary pyramids
and pons, indicating infarction of the corticospinal tracts
at the pontomedullary level (Figure 2 A,B).
Our patient was treated with fluid resuscitation, elec-
trolyte replacement and nutritional support as well as
wound care and pain control. Intravenous steroids were
considered however not pursued due to the risk of infec-
tion and imaging findings of ischemia. A tracheostomy
and percutaneous gastrostomy tube were placed. Our
patient’s hospital course was complicated by pneumonia
and the development of pulmonary emboli, requiring
placement of an inferior vena cava filter. Over the next
two months, our patient showed minimal improvement
in motor function. Repeat imaging was obtained. MRI of
his brain revealed near complete resolution of the ische-
mic changes (Figure 2 C,D). A cervical spine MRI sug-
gested a persistent, abnormal signal posteriorly from theIM: 7 SE: 8
BA
Figure 1 Magnetic resonance imaging of the cervical spine repeated
performed on admission. Interval development of cord edema and infarc
(B) Diffusion-weighted image. (C) Apparent diffusion coefficient image. The
do not demonstrate the exact same level of involvement, with the apparen
the cervical spine than the diffusion-weighted image. Also, the diffusion-w
aspect of the cord. This reflects the often diffuse and collateral nature of elcervicomedullary junction to the C6 level with an inter-
val decrease in cord edema (Figure 3 A,B). His course
showed an ability to hold his head up with more move-
ment in his left arm against gravity; some flexion of his
right elbow and wrist was also noted. No improvement
was observed in his lower extremities. Our patient was
subsequently transferred to an inpatient rehabilitation
facility, and unfortunately was lost to follow-up
thereafter.
Discussion
In electrocution injuries, the overall mortality may reach
5%. Electrical injuries have been reported to occur in
low-voltage settings, such as with household use, and
high-voltage exposures from occupational hazards and
lightning strikes [1]. Given the nature of these injuries,
most of the literature has been reported as case studies
with limited data regarding the evaluation and treatment
of neurological complications.
Several pathophysiological mechanisms of injury to
the nervous system have been proposed, including ther-
mal injury, electroporation, and vascular damage
through direct injury as well as indirect injury.
Electrical current flows from an area of low resistance
to high resistance. Low areas of resistance include
muscle, nerve and blood vessels. High-resistance tissue
includes skin, connective tissue and bone, which suffer
greater heat injury, typically at entry and exit sites butC
eight days after the initial magnetic resonance image
tion is seen from the C2 to T2 levels. (A) Sagittal T2 sequence.
diffusion-weighted image and apparent diffusion coefficient image
t diffusion coefficient image showing signal changes slightly lower in
eighted image signal abnormality does affect somewhat the dorsal
ectrical injuries.
IM: 6 SE: 9 I :  :  
Compressed 5:1 :
 cm 
IM: 6 SE: 90 1I :  : 1
Compressed 6:1 :
 cm 
IM: 6 SE: 7I :  :  
Compressed 5:1 :
 cm 
IM: 6 SE: 70 1I :  : 1
Compressed 5:1 :
 cm 
A
B
C
D
Figure 2 Magnetic resonance imaging of the brain demonstrating restricted diffusion in the bilateral medullary pyramids and pons.
(A) Diffusion-weighted image. (B) Apparent diffusion coefficient image. Repeat magnetic resonance imaging of the brain performed two months
later demonstrates resolution of the diffusion restriction: (C) diffusion-weighted image; (D) apparent diffusion coefficient image.
Johl et al. Journal of Medical Case Reports 2012, 6:296 Page 3 of 5
http://www.jmedicalcasereports.com/content/6/1/296damage may be caused in any structure along the path
of the current [2-4]. Nervous tissue provides a low-
resistance route for electrical current. As the electrical
current travels through tissue, neurons with larger sur-
face area are more likely to be damaged by electropor-
ation, in which the increase in cellular permeability and
conductivity caused by permanent conformational
change to membrane proteins ultimately leads to cell
death [5]. The heat loss that occurs as current flows
through tissues of increasing resistance causes damage
to the intima and adventitia of the vasculature, such as
thrombosis, necrosis of the vascular wall, vasospasm and
spread into nearby tissue [3,4]. Most patients survive the
initial insult, limiting the pathological work-up, with few
postmortem studies available for review [1]. Morbidity
of electrocution has been related to electrothermal in-
jury causing direct tissue damage with secondary ische-
mic changes from vascular insult. An accurate prognosis
is challenging given the variations in the duration and
extent of injury, the frequency of current, and theanatomic site. There are relatively few reports that cor-
relate the clinical, electrophysiological and imaging
changes that occur with electrocution injuries [6].
Classification of injuries has been divided by onset of
symptoms. Silversides [7] divided the stages into imme-
diate, secondary and late effects. Immediately after an
electrical current passes through the human body, ther-
mal injury occurs within nerve cells, manifesting effects
such as altered sensorium and/or loss of consciousness,
severe pain, hearing and vision changes, motor signs (in-
cluding paralysis), respiratory compromise, or sensory
complaints. Recovery occurs within 24 hours. Secondary
effects include temporary paralysis and autonomic dis-
turbances. The late effects are noted to start after five
days, manifesting as hemiplegia, movement disorders,
brainstem dysfunction and cranial neuropathies [4,7].
Spinal cord injuries have also been classified into tran-
sient and permanent disability. Motor deficits occur
more often than sensory disturbances [8] and are sec-
ondary to vascular damage incurred by the anterior
IM: 9 SE: 8I :  : 
Compressed 5:1 :
 cm 
A B
Figure 3 Magnetic resonance imaging of the cervical spine two months after the image in Figure 1 was taken. (A) T2 sequence. (B) T1
post-contrast image.
Johl et al. Journal of Medical Case Reports 2012, 6:296 Page 4 of 5
http://www.jmedicalcasereports.com/content/6/1/296spinal artery and its branches [4,8-12], which supply two
thirds of the spinal cord, including the lateral corticosp-
inal tracts, spinothalamic tracts and the anterior horn
cells along with the central gray matter of the spinal
cord. This hypothesis may be supported by the suscepti-
bility of smaller lumen vessels to injury, with less dissi-
pation of heat to surrounding structures compared with
their larger vessel counterparts [7].
Ko et al. carried out a retrospective study of spinal
cord injuries related to electrical burns. They reported
that 11 out of 13 patients with entry wounds in the head
and neck region were found to have quadriplegia with
exit sites located in the upper extremities, and paraplegia
with exit sites located in the lower extremities. Most of
these patients were noted to have hypotonia acutely in
the first two to ten days after injury in an ascending pat-
tern. It was postulated that this pattern of injury was
related to ischemic damage to the arterial blood supply
and vulnerability in the spinal cord. These findings pro-
vided the rationale to administer prostaglandin E1
(10μg/day for three weeks) or steroid therapy to reduce
ischemic injury to the spinal cord [4].
Early discovery of extensive myelopathy of the cervical
spine is aided by neuroimaging. Most of the described
cases used T2 hyperintensities, correlating to clinical
deficits [5]. Initial imaging of our patient did not show
any significant changes to explain his quadriparesis.
However, repeat imaging performed roughly one week
after initial MRI of his brain and cervical spine showed
extensive involvement of the pyramidal tracts as well as
cord edema, which explained our patient’s clinicalfindings. It was felt that the bilateral lesions involving
the corticospinal tracts particularly contributed to our
patient’s paresis. As with our case, serial imaging may
prove essential for identifying delayed sequelae asso-
ciated with electrocution injuries. A differential diagnosis
made with radiology may be wide and includes neo-
plasm, infarction and electrocution injury. Repeat im-
aging may assist in making the correct diagnosis.
Exploring additional neuroimaging modalities may be
beneficial, such as magnetic resonance spectroscopy.
Electrodiagnostic studies, such as evoked potentials,
nerve conduction studies and electromyography may
have prognostic value. The latter two modalities can
help determine the severity of motor axonal loss, stem-
ming from anterograde anterior horn cell degeneration
in the ventral gray matter. Technical aspects limit the
value of these studies secondary to the presence of skin
injury and accessibility.
No established guidelines are available in the literature
regarding the treatment of high-voltage electrical injury.
Each case has been treated with supportive care. Early
treatment of electrical injury starts with initial fluid re-
suscitation, respiratory support and prevention of infec-
tion. The lack of systematic guidelines makes clinical
care for the patient with electrocution injuries challen-
ging. Work-up of the neurological deficit with imaging
or electrodiagnostic studies, treatment, and prognosis
for recovery is dictated by the personal experience of the
physician. There are no randomized double-blinded
trials available on electrocution. The majority of the in-
formation comes from isolated cases, case series and
Johl et al. Journal of Medical Case Reports 2012, 6:296 Page 5 of 5
http://www.jmedicalcasereports.com/content/6/1/296animal experimental models, with fewer articles available
in the radiology and neurological literature.
No consensus exists regarding medication use. High-
dose intravenous steroids and prostaglandin E1 were
cited in the literature as early treatment modalities.
Neurological morbidity has been variable. Some case
studies with delayed findings of severe myelopathy due
to electrocution injury did not show full recovery [4]
while other case reports showed near complete reso-
lution of motor deficits with aggressive physical therapy
[13]. Multidisciplinary management approaches involv-
ing the intensivist, neurologist, plastic surgeon, physical
and occupational therapists, and psychologist, as well as
a nutritionist, is necessary to achieve the best possible
outcomes. Long-term neurological follow-up is justified
by the rich body of evidence of delayed complications
cited in the literature.
Conclusion
High-voltage electrocution injuries are a serious problem
with potential for both immediate and delayed neuro-
logic sequelae. The existing literature regarding effective
treatment is limited. Long-term follow-up and multidis-
ciplinary management of these patients is needed.
Consent
Written informed consent was obtained from the patient
for publication of this case report and accompanying
images. A copy of the written consent is available for re-
view by the Editor-in-Chief of this journal.
Competing interests
HJ, AO, and SRB declare that they have no competing interests. RAR is a
Deputy Editor for the Journal of Medical Case Reports and is an Associate
Neurology Editor for Case Reports in Neurology and Grand Rounds.
Authors’ contributions
HKJ and AO examined the patient and wrote the initial manuscript. SRB
supervised the coordination of clinical care and reviewed the manuscript.
RAR rewrote and edited the manuscript, performed an additional literature
search, and examined and interpreted the magnetic resonance imaging
scans. SRB and RAR were responsible for the intellectual content of the
paper along with critical appraisals, suggestions, and revisions. All authors
significantly contributed to, read and approved the final version of the
manuscript.
Author details
1University of Southern California, Keck School of Medicine, Los Angeles
County Medical Center, 1510 San Pablo Street, Suite 643, Los Angeles, CA
90033, USA. 2University of Southern California, Keck School of Medicine,
Los Angeles County Medical Center, 1520 San Pablo Street, Suite 3000, Los
Angeles, CA 90033, USA. 3Presbyterian Intercommunity Hospital, 12401
Washington Boulevard, Whittier, CA 90602, USA.
Received: 6 February 2012 Accepted: 23 July 2012
Published: 13 September 2012
References
1. Arevalo JM, Lorente JA, Balseiro-Gomez J: Spinal cord injury after electrical
trauma treated in a burn unit. Burns 1999, 25:449–452.
2. Skoog T: Electrical injuries. J Trauma 1970, 10:816–830.3. Baxter CR: Present concepts in the management of major electrical
injury. Surg Clin North Am 1970, 50:1401–1418.
4. Ko SH, Chun W, Kim HC: Delayed spinal cord injury following electrical
burns: a 7-year experience. Burns 2004, 30:691–695.
5. Johansen CK, Welker KM, Lindell EP, Petty GW: Cerebral corticospinal tract
injury resulting from high-voltage electrical shock. AJNR Am J Neuroradiol
2008, 29:1142–1143.
6. Kalita J, Jose M, Misra UK: Myelopathy and amnesia following accidental
electrical injury. Spinal Cord 2002, 40:253–255.
7. Silversides J: The neurological sequelae of electrical injury. Can Med Assoc
J 1964, 91:195–204.
8. Levine NS, Atkins A, McKeel DW Jr, Peck SD, Pruitt BA Jr: Spinal cord injury
following electrical accidents: case reports. J Trauma 1975, 15:459–463.
9. Christensen JA, Herman RT, Balis GA, Wuamett JD: Delayed neurological
injury secondary to high-voltage current, with recovery. J Trauma 1980,
20:166–168.
10. Varghese G, Mani MM, Redford JB: Spinal cord injuries following electrical
accidents. Paraplegia 1986, 24:159–166.
11. Petty PG, Parkin G: Electrical injury to the central nervous system.
Neurosurgery 1986, 19:282–284.
12. Adams RD, Victor M, Ropper AH: Principles of Neurology. 6th edition. New
York: McGraw Hill; 1997:1227.
13. Kingsly PA, Dhanraj P, Gupta A: Recovery after spinal cord injury due to
high tension electrical burns: a 5-year experience. Burns 2008, 34:888–
890.
doi:10.1186/1752-1947-6-296
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A: Recovery after spinal cord injury due to high tension electrical burns: a 5-year experience. Burns

Cite this article as: Johl et al.: Cervicothoracic spinal cord and pontomedullary injury secondary to high-voltage electrocution: a case report.

Electrical injuries.

Electrical injury to the central nervous system. Neurosurgery

HC: Delayed spinal cord injury following electrical burns: a 7-year experience. Burns

Jr: Spinal cord injury following electrical accidents: case reports.

Petty GW: Cerebral corticospinal tract injury resulting from high-voltage electrical shock.

Present concepts in the management of major electrical injury. Surg Clin North Am

Ropper AH: Principles of Neurology. 6th edition.

Spinal cord injuries following electrical accidents. Paraplegia

Spinal cord injury after electrical trauma treated in a burn unit. Burns

The neurological sequelae of electrical injury.

UK: Myelopathy and amnesia following accidental electrical injury. Spinal Cord

Wuamett JD: Delayed neurological injury secondary to high-voltage current, with recovery.

http://dx.doi.org/10.1186/1752-1947-6-296

Cervicothoracic spinal cord and pontomedullary injury secondary to high-voltage electrocution: a case report

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