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< Presentation of Case
>
This 41-year-old male had been in
his usual status of health until 7 days prior to this
admission when he started to have cough, rhinorrhea and a mild
fever. While watching television at about 9 pm one day before
admission, he suddenly developed generalized convulsion. The
symptoms lasted for several minutes. The patient had transient
cyanosis and urinary incontinence. He regained his
consciousness spontaneously without post-ictal confusion. He
was able to get on the ambulance by himself and he was sent to
a regional hospital, where the patient was found to have
hyponatremia (129 mmol/l) and hypokalemia (2.7 mmol/l). A
computed tomography (CT) of the brain did not reveal
intracranial hemorrhage or space-occupying lesions. Potassium
chloride and saline were administered by vein. However, the
patient developed generalized convulsion and cyanosis again at
4 am on the next day. He was found pulseless. The
electrocardiographic monitor showed ventricular tachycardia.
Cardiopulmonary resuscitation was administered immediately,
including direct-current defibrillation, intravenous
vasopressors, cardiac massage, and endotracheal intubation.
Amiodarone was infused. Recovery of spontaneous circulation
was achieved 5 minutes later. CT of the brain was repeated but
failed to reveal intracranial pathology. A lumbar puncture was
performed to show an opening pressure of 105 mm H2O;
cerebrospinal fluid study showed red blood cells, 1 per cubic
milliliter and white blood cell, 0 per cubic milliliter; a
protein level of 3 mg per deciliter; and a glucose level of
110 mg per deciliter. He was transferred to this hospital on
the same day.
The patient was an alcoholic, who
consumed 100-200 ml Kaoliang spirits per day
over the past 2-3 years. He smoked 0.5-1
packs of cigarettes per day for a couple of years.
He denied illicit drugs use. His past medical history was
unremarkable. He denied having other systemic diseases. He did not have syncope,
presyncope, or episodes of seizures before. The patient's family members
all had flu-like symptoms at the same time. His
close relatives did not have a history of heart
disease or sudden death.
On examination, he was moderately
nourished and moderately developed. He was in a confused state
and intubated with the spontaneous respiration of 18 breaths
per minute, the temperature 37.6℃, the pulse rate 102 beats
per minute and blood pressure 123/99 mmHg. The conjunctiva was
pink. The neck was supple. The lungs were clear on
auscultation; the heart sound was regular without murmur or
friction rub. The peripheral pulsation was symmetric and
strong. The other physical examinations were unremarkable.
After
admission, his consciousness became clear and he was
extubated. The electrocardiogram (ECG) showed sinus
tachycardia, PR segments depression and flattened T waves (Figure
1A). However, generalized convulsion recurred,
with ECG monitor leads showing polymorphic ventricular
tachycardia. After receipt of 200-joule direct-current
defibrillation, his heart rhythm returned to normal. The
patient's hyponatremia, hypokalemia and hypomagnesemia were
managed meticulously. Lidocaine was infused, instead of
amiodarone, because of the follow-up ECG showing prolongation
of the QT interval. He later became agitated, and under the
impression of alcohol withdrawal syndrome, lorazepam,
thiamine, and propranolol were administered.
The patient developed desaturation
progressively since the afternoon of 2nd hospital day. A chest
radiograph revealed a pattern of interstitial pneumonia, with
more dominant in the left side (Figure
2). Oseltamivir and moxifloxacin were given for suspected
viral or atypical pneumonia. He was intubated again due to
hypoxemic respiratory failure. His blood pressure dropped
after intubation and inotropic agent (dopamine) was
administered by vein. Follow-up chest radiographs disclosed
frank pulmonary edema. Meanwhile, his ECG showed ST-T
elevation (Figure
1B ). The echocardiography showed regional wall motion abnormality at
the inferior segment of the left ventricle (LV) and impaired LV contractility.
There was no pericardial effusion. Myopericarditis was impressed and supportive
therapy was given. The lung edema improved markedly within
2 days. He was weaned off ventilator successfully on
the 4th hospital day.
The patient
had rhabdomyolysis after admission, which was due to multiple factors, such
as physical restraint, alcoholism and delirium tremens, or virus infection. No more
ventricular tachycardias or convulsions were noted. The
cardiac troponin I data reached it peak on
the admission day (2.64 ng/ml), which declined subsequently. The creatine
kinase (CK)-MB remained less than 5% of the total CK
value. The ST-T elevation normalized a few days later. Oseltamivir and moxifloxacin
were discontinued 5 days and 7 days later, respectively. The
hemodynamics improved and dopamine was tapered off. He was
transferred to ordinary ward after a 9-day stay in
the intensive care unit.
The
patient's ECG evolved to T wave inversion 13 days after this
event (Figure
1C
). He was
subjectively well. Follow-up echocardiography showed good LV
contractility and no pericardial effusion. The patient was
discharged after a six-day hospital stay.
The patient
had been otherwise well and returned to his daily life after
discharge. An ECG 6 weeks later showed normal T wave
morphology and QT interval (Figure 1D ). A thallium scan did not reveal perfusion defect
under adequate stress. He did not experience symptoms of
congestive heart failure or chest tightness during the
follow-up as an outpatient.
< Discussion
>
In the case, we decsribed a case
of acute myopericarditis in a patients presenting with
recurrent convulsion and polymorphic ventricular tachycardia.
His clinical course was complicated by pulmonary edema and
cardiogenic shock. The serology data showed 4-fold increases
of antibody titers against Parainfluenza type I, suggesting
its pathogenic role for this episode of myopericarditis.
In the case, ventricular
tachycardia was manifested as generalized convulsions. Whereas
seizure is often the first impression in a patient suffering
from generalized convulsions, seizure is accompanied by
post-ictal confusion in most cases, which did not develop in
our patient. The ECG/electroencephalography on the scene is
the most important clue to correct diagnosis. Brain
hypoperfusion resulting from either tachycardia or bradycardia
would occasionally induce motor activities of the brain
resulting in generalized tonic-clonic convulsions.
During hospitalization, the
patient's ECG showed PR depression first and then striking ST
elevation. The differential diagnosis of such an ECG change
would include acute pericarditis, myocardial infarction (MI)
involving the antero-septal, lateral, and inferior walls,
subarachnoid hemorrhage, intracranial hemorrhage,
Tako-tsubo-like left ventricular dysfunction, or Osborn wave
of hypothermia. The typical ECG change of pericarditis, though
not necessarily present, would be diffuse concave ST elevation
and, most importantly, PR depression. Both finings were
present in the patient's ECG. The ECG of pericarditis had four
stages of evolutional change, that is: diffuse ST elevation,
normal, T wave inversion, and then normal. It is hard to
differentiate MI from acute pericarditis and the decision
making would be quite different according to the diagnosis.
The ECG of MI often shows convex ST elevation, and it is
mostly confined to a territory. The T wave inversion will
occur while the ST wave remains elevated. PR depression is
rather unique to acute pericarditis. An ECG may provide
further diagnostic clue. Moreover, if the patient had had such
an episode of extensive MI, the clinical presentation would
have been much more catastrophic. The ECG pattern of
subarachnoid hemorrhage or intracranial hemorrhage is mostly
deep inversion of T wave. The findings of patient’s
consciousness, initial normal CT of the brain, and clinical
course make this diagnosis unlikely. Tako-tsubo-like
ventricular dysfunction is a new disease entity that was first
reported in Japan. The etiology was thought to be multiple
coronary artery spasm. The ECG would show transient Q waves in
V leads, besides ST elevation. The ventriculogram showed
hypokinesia-akinesia of the mid- and apical ventricle and
hyperkinesia of the basal ventricular region, that is
Tako-tsubo (octopus pot in Japanese)-like. The findings of ECG
and echocardiography excluded this diagnosis. Hypothermia will
cause Osborn waves, which are morphologically different from
those seen in this patient.
Acute pericarditis is usually not
associated with ventricular arrhythmia. Inflammation of
adjacent tissue, i.e. the myocardium, would be the most
logical consideration. The ECG pattern of myocarditis might be
ST depression, concave ST elevation, convex ST elevation, or T
wave inversion. Bundle branch morphology would be also
present. The rhythm might be sinus tachycardia, atrial
arrhythmia, atrio-ventricular block, or ventricular
arrhythmia, even incessant ventricular tachycardia. In a
patient with acute pericarditis, if the ECG shows localized
changes or atypical evolution, convex ST segment elevation,
conduction block, and significant arrhythmia in the absence of
other heart disease; or the patient has evidence of myocardial
dysfunction in the absence of constrictive pericarditis,
pulmonary edema, cardiomegaly, abnormal hemodynamics, wall
motion abnormality, myopericarditis should be considered.
Myopericarditis is not uncommon,
but frequently under-diagnosed. The presentation is often
vague. However, rapid deterioration and lethal condition may
ensue, often leading to medical-legal issue. If a patient has
chest or epigastric discomfort, fatigue, shortness of breath
while being in recovery from symptoms of upper respiratory
tract infection, a diagnosis of myopericarditis has to be
considered. The treatment of myocarditis is largely supportive
care, and, in fulminant cases, with mechanical life support,
including intraaortic balloon counterpulsation, extracorporeal
membranous oxygenator. Immunosuppressive agents and
intravenous immunoglobulin do not confer benefit in patients
with fulminant myocarditis when compared with supportive care.
The treatment of pericarditis included non-steroid
anti-inflammatory drugs, and use of colchicine may be
considered in recurrent, unresponsive cases.
The patient did not have a
coronary angiogram initially, and we did not perform an
endomyocardial biopsy. The clinical presentations of this
patient on the hospital day 2 and day 3, which showed
elevation of ST segments on the ECG without parallel increases
of cardiac enzymes, exclude the possibility of severe coronary
artery disease. However, it might be better to perform an
endomyocardial biopsy to confirm the diagnosis of myocarditis.
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Case Discussion
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