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Page 2 of 6 Lopez-Marco et al. Vessel Plus 2018;2:40 I http://dx.doi.org/10.20517/2574-1209.2018.67
Traumatic ventricular septal defect (VSD) has been reported in 1%-5% of penetrating cardiac injuries.
The diagnosis is usually obscured by the priority of stabilization and treatment of other more obvious and
lethal injuries. It is consequently sometimes missed and diagnosed after the patient is recovered from the
[1-6]
initial trauma .
Mitral and tricuspid insufficiency secondary to cardiac trauma has also been reported, more commonly
after blunt trauma. The trauma can potentially injure the valves at three different levels; papillary muscle,
chordae and leaflet. Their diagnosis is also difficult, requiring an expert echocardiographer available at the
time of the secondary survey. Otherwise, they are commonly missed until a full echocardiographic study is
[4-7]
requested once the patient is more stable. High level of suspicion is key for their diagnosis .
The gold-standard diagnosis for penetrating cardiac trauma is the echocardiography, to confirm
haemopericardium and assess intracardiac structures. The VSD, however, can be missed initially due to
muscle spasm or clot sealing the defect, consequently being commonly diagnosed and treated as a delayed
[1-7]
complication of penetrating injuries .
CASE REPORT
A 28-year-old male presented to the accident and emergency department following a stab injury to the
anterior chest. He sustained a 6 cm stab wound in the subxiphoid area. On arrival, he was fully conscious
and haemodynamically stable, with a heart rate of 90 beats/min, blood pressure 130/80 mmHg and
respiratory rate of 22 breaths/min. He was managed as per advanced trauma life support guidelines and
being described as a “good responder” following commencement of fluid resuscitation.
Physical examination revealed a systolic murmur, multiple bruises to the forehead and sustained soft tissue
swelling of the right orbit and face. Glasgow Comma Scale was 15/15 and his electrocardiogram revealed
sinus tachycardia, with inversion of T wave in the inferior wall leads.
A thoracic and abdominal CT was done to assess the extent of the injuries. There was a mediastinal
haematoma extending to the anterior cardiophrenic recess and moderate to large infero-posterior
haemopericardium. The diaphragm remained intact [Figure 1].
He underwent a bedside transthoracic echocardiography (TTE) that reported preserved left ventricular
function but with infero-posterior wall motion abnormality, causing tethering of the posterior leaflet of
the mitral valve and therefore, moderate mitral regurgitation (MR). There was also moderate tricuspid
regurgitation (TR) with pulmonary hypertension [pulmonary artery systolic pressure (PASP) 40 mmHg +
central venous pressure, normal PASP values 15-25 mmHg]; as well a 1 cm localized pericardial effusion in
the infero-posterior wall, probably clotted. Right ventricular function was preserved.
He was therefore, prepared for emergency cardiac surgery to evacuate the haemopericardium and assess
the extent of cardiac injuries. An intraoperative transoesophageal echocardiography (TOE) confirmed
the infero-posterior pericardial collection as well as the inferior wall dyskinesia. There was severe TR due
to rupture of the head of the posterior papillary muscle and a 2 cm VSD in the muscular interventricular
septum causing a left-right shunt. The MR was mild-moderate and deemed to be secondary to the inferior
wall dyskinesia. At this stage, there was no mitral prolapse [Figure 2A and B].
Surgery was performed through a median sternotomy, extending the stab wound superiorly. A clot was
identified between the inferior wall and the diaphragm. As soon as the clot was dislodged, a profuse bleeding
was identified from a 2 cm full thickness injury on the inferior wall of the right ventricle (RV). Control
of the bleeding was achieved with manual pressure, whilst cardiopulmonary bypass (CPB) with bi-caval