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 Abstract
A 32 year old male Sri Lankan with acute ST-segment
elevation myocardial infarction presented to the Emergency
Department following a fall from a 3 metre height. He had
multiple skull fractures with an epidural hematoma. He had
two episodes of cardiac arrest which responded to DC shock.
Primary coronary intervention was required and a stent
was placed in the left anterior descending coronary artery.
The procedure was complicated by acute stent thrombosis
which was treated by ballooning and stent overlapping. He
had no sequelae from his head injury and he was discharged
home with outpatient follow-up. In this case, there were no
symptoms or signs of chest trauma, so most probably this
patient had developed acute myocardial infarction leading
to dizziness and a fall causing head injury with epidural
hematoma.
Key words: Acute myocardial infarction, head injury,
epidural hematoma..
Introduction
Acute myocardial infarction (AMI) is one of the most
common diagnoses in hospitalized patients in industrialized
countries (1). It has a wide spectrum of clinical presentation.
The mortality can be decreased significantly with early
thrombolysis or primary angioplasty. One of the challenges
to the emergency medicine physician is the assessment of
a patient with an atypical presentation of AMI. Successful
resuscitation and early restoration of blood flow to the
infarct related vessel influences the outcome and hence the
need to confirm the diagnosis of AMI as soon as possible,
especially in patients with risk factors for coronary heart
disease (2). In up to one-half of cases of ST-segment elevation
myocardial infarction (STEMI), a precipitating factor appears
to be present beforehand, such as vigorous physical exercise,
emotional stress, or a medical or surgical illness (1).
We report a case of acute STEMI, discovered upon
investigation of a patient who presented with a head injury
and epidural hematoma following a fall from a height. This
case is unique because it is the first reported case of AMI
presenting as head injury with epidural hematoma..
Case Report
A 32 year old male Sri Lankan patient, a construction worker,
was brought by ambulance to the emergency department of Hamad General Hospital after falling from a 3 metre height.
He became dizzy, fell, struck his head and had a brief loss
of conscious. Earlier, on the same day, he had suffered from
retrosternal chest pain radiating to the left arm for which he
had consulted a primary health center physician who gave
him an injection that relieved his pain. Further interrogation
revealed that he had suffered from chest pain on and off
for the last three months, which was mostly aggravated by exertion. The patient claimed that he had no chronic illnesses.
However, he smoked 6-7 cigarettes per day for the last ten
years. There was no family history of coronary heart disease,
diabetes or hypertension. Physical examination revealed
Glasgow coma score (GCS) 14/15; pupils were normal in size
and equally reactive to light. His blood pressure was 105/80
mmHg, pulse rate (PR) of 73 beats/min and temperature
was 36.2°C. He had multiple facial abrasions with periorbital
ecchymosis of his left eye and swelling of the left side of his
mouth. Examination of chest, heart and abdomen, as well
as nervous system, was normal. Computerized tomography
(CT) of his head revealed a right frontal epidural hematoma
measuring 0.6 cm with no midline shift (Figure 1). There
were also multiple fractures involving right and left frontal
bones, the walls of the left frontal sinus, ethmoidal air cells
and roof of the sphenoid bone with opacification and airfluid
levels due to hemosinus. Chest and pelvic X-rays were
normal. Electrocardiogram (ECG) showed ST elevation in V1-
6, I, AVL (Figure 2).
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Figure (1): Head CT of the
patient shows right frontal
epidural
hematoma.
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Figure (2): ECG of the
patient
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Troponin T was 0.129 ng/ml (normal value 0.00-0.10 ng/ml),
urea and electrolytes (U/E) were normal. The white blood
cell count (WBC) was 18.1x10^3/ul, hemoglobin (Hb) level
was 15.1 g/dl and platelet count was 299x10^3/ul.
The patient was treated with 100% oxygen by nonrebreather
mask, aspirin 300 mg orally and morphine 5
mg IV stat, clopidogrel 75mg orally qd, propranolol 10 mg
orally q 8hrs, isosorbide dinitrate retard 20 mg orally qd, and
perindopril 2 mg orally qd.
He was admitted to the surgical intensive care unit (SICU)
where a neurosurgeon advised conservative management
with close follow-up. CT head scan was repeated and
revealed similar findings to the previous one. In the SICU
he developed ventricular fibrillation which was converted
to sinus rhythm by DC shock. He was transferred to the
coronary care unit (CCU), where he developed pulseless
Figure (2): ECG of the patient
ventricular tachycardia, which was converted to sinus
rhythm by DC shock. Heparin was started and the patient
was transferred to the catheterization lab. Coronary
angiogram demonstrated an occluded mid-left anterior
descending coronary artery (LAD), so primary coronary
intervention (PCI) and angioplasty for LAD with stent was
done. Upon arrival at the catheterization lab, he developed
sinus bradycardia (PR 37 beats / min), which responded to
atropine IV.
The following day, the patient was fully conscious, GCS 15/15,
had no chest pain, stable vital signs, and normal physical
examination. T was 3.79 ng/dl and creatinie kinase
MB (CK-MB) was 103.3 ng/ml (normal value <5), U/E was
normal, WBC was 14.0x10^3/ul and Hb level was 15.5 g/dl.
For the next two days he remained well. On the fourth post
injury day he had acute stent thrombosis and he was restarted
on heparin and then ballooned with a stent overlap.
On the fifth day Troponin T was 3.22 ng / ml, CK-MB was
10.41 ng/ml and his lipid profile was normal. The patient
was discharged home on aspirin, clopidogrel, perindopril,
atorvastatin, isosorbide dinitrate, with cardiology and
neurosurgery outpatient clinic follow-up appointments.
.
Discussion
Coronary heart disease (CHD) is one of the leading causes
of death worldwide; 3.8 million men and 3.4 million women
die each year due to CHD (3). The presentation of AMI in the
setting of injury is atypical and complications are frequent.
Methods for thorough history-gathering to identify preexisting
conditions, for early hemodynamic monitoring
and intervention for AMI in the setting of trauma should be
defined (4).
The relationship between AMI and trauma has been
investigated by many researchers. Trauma has been
suggested, in case series, as one of the non-atherosclerotic
mechanisms leading to AMI, the leading cause of death in
the USA. AMI following non-penetrating injury has been
shown to carry significant morbidity and mortality. Direct
trauma to the heart following blunt chest injury, was
observed to carry the greatest risk for AMI. Abdominal or
pelvic trauma also increased the risk for AMI (5). Christensen
et al., found 77 cases describing AMI after blunt chest trauma
with atypical age distribution, where 82% of the cases were
less than 45 years old and the most common trauma was
road traffic collisions where LAD was the vessel most often
affected (6). In the same year Zajarias et al., reported a case
of AMI following a blunt chest trauma from automobile
airbag deployment (7). There is also an association between
AMI and spinal epidural hematoma; many cases have been
reported after coronary thrombolysis using either tissue
plasminogen activator (8,9,10,11) or streptokinase (12,13)
but this is the first reported case of AMI and cranial epidural
hematoma.
In the setting of head injury with epidural hematoma, the
use of thrombolytic therapy is absolutely contraindicated in
the two months following intracranial or intraspinal surgery
or trauma. However, in patients who require heparinization
therapy for myocardial ischemia or infarction, the use of
frequent neurological examinations in conjunction with
anticoagulation therapy seems to be the only reasonable
option (14).
There is a single case of anteroseptal AMI and head injury
with multiple fractures involving the skull, right first rib
and left femoral bone with blunt torso trauma due to a
motor cycle accident. Subsequent coronary angiogram
demonstrated laceration at the proximal portion of the LAD
(15). Although this is the second reported case of AMI with
head injury, it is the first reported case of AMI presenting
as head injury with epidural hematoma sustained by a fall.
In this reported case, there were no symptoms or signs of
chest trauma, so most likely the patient presented above
had developed AMI, which presented as dizziness leading
to a fall causing head injury with epidural hematoma.
In conclusion, all cases of trauma should be assessed
thoroughly to identify pre-existing conditions, such as AMI
as in this case, for early monitoring and intervention. Also,
further studies are warranted to better understand the
relationship between trauma and AMI.
References
Other
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Case Report # 5 - Necrotizing fasciitis following tetanus toxoid injection for a young adult male with no risk factors or co-morbidity.
Case Report # 6 - Cesarean Myomectomy of Huge Myoma: A Case Report
Case Report # 7 - Young female with frequent acute uncontrolled asthmatic attacks?
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