Download Dilated cardiomyopathy after electrical injury: report of two cases

CASE REPORT
Dilated Cardiomyopathy After Electrical Injury:
Report of Two Cases
Lee M. Buono, MD
Nicholas L. DePace, MD
David M. Elbaum, DO
The specific etiologic factor and pathogenesis of most
dilated cardiomyopathies have yet to be described definitively. Hypotheses of the etiologic factor of idiopathic
dilated cardiomyopathy (DCM) abound. This report
describes two patients with electrical injury in whom
DCM developed after the electrical insult in the absence
of other precipitating causes. Further histologic examination of myocardial tissue after electrical injury may
reveal clues regarding the pathophysiology behind electrically induced DCM. Because electrical injury may be
associated with myocardial dysfunction, short- and longterm evaluation of left ventricular function may be warranted.
M
any theories have been proposed regarding the etiologic
factors of idiopathic dilated cardiomyopathy (DCM);
however, none has been established.1-5 Physical agents
reported to cause DCM include heat stroke, hypothermia,
radiation, and lightning strike.1,6 Electricity has been documented to cause myocardial necrosis, infarction, dysrhythmia,
and contractile dysfunction, all of which may be delayed as
well as persistent.7,8 We describe DCM in two patients after
electrical injury: in one patient, DCM occurred after highvoltage injury, and in the other, after low-voltage injury. We
believe electrical injury to be an additional physical cause of
DCM.
Case Presentations
Case 1
A 24-year-old black man was brought to the emergency department after receiving an electrical shock. The shock originated
in his left hand from a faulty electrical appliance connected to
a standard wall outlet. During the insult, the patient had to be
pulled away from the electrical device.
The patient was previously in good health and had no hisFrom the Division of Cardiovascular Medicine at the Philadelphia College of
Osteopathic Medicine in Pennsylvania (Dr Elbaum) and the Division of Cardiovascular Medicine (Drs DePace and Elbaum) and the Division of Neurosurgery (Dr Buono) at Thomas Jefferson University Hospital in Philadelphia.
Address correspondence to David M. Elbaum, DO, Jefferson Methodist
Heart Center, 2301 S Broad St, Philadelphia, PA 19148-3542.
E-mail: [email protected]
Buono et al • Case Report
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tory of sustained hypertension, diabetes, substance abuse, or
family history of heart disease. At physical examination, he was
afebrile. His heart rate was 96 beats per minute; respirations
were 20/min; and blood pressure, 130/100 mm Hg. Although
he had no external burn marks or focal neurologic deficits,
he complained of severe pain, decreased range of motion, and
mild edema of the left upper extremity, as well as abdominal
pain. Ketorolac was administered intramuscularly for relief of
pain.
An electrocardiogram (ECG) revealed sinus tachycardia
(108 beats per minute) with premature ectopic complexes and
diffuse ST and T wave abnormalities more prominent anterolaterally.
Laboratory studies revealed a white blood cell (WBC)
count and electrolyte levels within the normal range; the serum
creatine kinase (CK) level was 748 U/L, and serum CK-MB
isozyme, 2.4% of total CK activity. Results of the routine drug
and alcohol screen were negative. Three days after admission, the patient also began complaining of scotoma.
Approximately 5 weeks later, the patient was admitted to
the hospital because of progressive shortness of breath, chest
pain, palpitations, and epigastric pain. At that time, the patient
was afebrile; respirations were 20/min, and blood pressure,
140/110 mm Hg. An ECG revealed sinus tachycardia (101
beats per minute) with ST and T wave abnormalities suggestive of lateral ischemia.
Laboratory studies revealed the complete blood cell count
and electrolyte values to be in the normal range. Findings on
chest x-ray films were consistent with congestive heart failure
(CHF). Two-dimensional echocardiograms showed a dilated,
severely hypokinetic left ventricle. The patient was treated
with furosemide administered intravenously, an angiotensinconverting enzyme inhibitor, and topical nitrates.
Approximately 5 months after the initial electrical insult,
the patient was again admitted to the hospital with CHF and
found to have an ejection fraction of 15%. His blood pressure
was 240/140 mm Hg. An ECG revealed normal sinus rhythm
(94 beats per minute), premature ventricular contractions,
right atrial enlargement, and anterolateral T wave inversions.
Chest x-ray film revealed bilateral interstitial and vascular
prominence with cephalization, bilateral pleural effusions,
and cardiomegaly.
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CASE REPORT
Comment
Cardiac catheterization revealed normal coronary arteries,
elevated left ventricular end-diastolic pressure, a pulmonary
capillary wedge pressure of 32 mm Hg, and severe global
hypokinesis with a cardiac index of 1.4 (calculated as cardiac
output in liters per minute divided by body surface area in
square meters). The findings were consistent with DCM.
Endomyocardial biopsy specimens from the right ventricle revealed myocyte hypertrophy with focal interstitial
fibrosis. No evidence of active inflammation or necrosis was
present.
Eleven months after the initial insult and follow-up neurologic evaluation, the patient was admitted for a second cardiac catheterization and referral for cardiac transplantation.
While awaiting the transplant, the patient was treated pharmacologically for CHF with a persistently depressed ejection
fraction of 15% and a severely dilated left ventricle with diffuse patchy uptake and diaphragmatic attenuation revealed
by thallium-201 myocardial perfusion scintigraphy. Sudden
cardiac death occurred while the patient was being monitored in a transplant program. No autopsy was done.
Electrical injury from lightning strike, direct current cardioversion, and both high-voltage (1000 V) and low-voltage
(350-V standard wall outlet) sources has been well documented in effecting multiple organ injury in muscle (cardiac and
skeletal), nervous tissue, as well as most other soft tissue in its
path.9-20
Cardiac morbidity and mortality associated with electrical injury has been documented to result from cardiac arrest,
tachycardia, arrhythmia, conduction disturbances, myocardial infarction, and contractile dysfunction.8,12,13,21-27 The extent
of cardiac involvement in electrical injuries varies with the
location of the entrance and exit wounds, voltage, magnitude,
current frequency, and duration.10,13,14,19,28-31
Although it is generally appreciated that electrical injuries
can cause fatal arrhythmias,32 it is less appreciated that transient
or permanent myocardial dysfunction with or without CHF can
occur.8,22,23 Our two case presentations describe DCM in association with both high- and low-voltage electrical injuries in the
absence of other precipitating etiologic factors.
Case 2
Conclusion
A 42-year-old man sustained severe first- and second-degree
burns (20%) when he placed a shovel into an electrical line
while digging a hole. Coworkers estimated the line to be
approximately 13,000 V.
The patient was admitted to the burn unit of a local hospital. He denied loss of consciousness, chest pain, dyspnea,
emesis, or loss of bowel and bladder control. On admission,
his blood pressure was 152/90 mm Hg, and his heart rate
was 108 beats per minute and regular. Findings of the physical examination were unremarkable except for burns evident on the chest, arms, abdomen, buttocks, and legs. Urinalysis was negative for myoglobin. The WBC count was
elevated (13,700/L). All other laboratory values were unremarkable.
An ECG showed borderline delay of intraventricular
conduction with no serial changes. Findings on chest and
spine x-ray films were unremarkable. The patient had a 20pack-year history of tobacco use and was a mild social drinker.
He had no history of cardiac disease, hypertension, or diabetes.
The patient was hydrated, and silver sulfadiazine cream
was applied to his wounds. Physical therapy, occupational
therapy, and psychiatric consultation for posttraumatic stress
disorder were initiated. The patient had no telemetry abnormalities while monitored, and he was discharged from the hospital with appropriate follow-up.
Approximately 1.5 years after the initial injury, the patient
had cardiac arrest and died. Autopsy demonstrated DCM
with a markedly dilated left ventricle weighing 540 g. No
coronary atherosclerosis was present. A 1-cm area of bridging
of the left anterior descending coronary artery was noted.
The lungs were congested.
The variability of cardiac injury in survivors of electrical trauma
limits the appearance of cardiac manifestations such as DCM.
The literature is replete with warnings to provide long-term
follow-up of electrically injured patients to monitor for latent
cardiac dysfunction and cardiomyopathy. We believe electrical injury may be associated with myocardial dysfunction and
short- and long-term evaluation of left ventricular function
may be warranted.
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