The Journal of Emergency Medicine, Vol. 43, No. 3, pp.

445e447, 2012
Copyright Ó 2012 Elsevier Inc.
Printed in the USA. All rights reserved
0736-4679/$ - see front matter

doi:10.1016/j.jemermed.2010.05.069

Clinical
Communications: Adults

SEVERE TRICUSPID REGURGITATION AND ATRIOVENTICULAR BLOCK CAUSED BY

BLUNT THORACIC TRAUMA IN AN ELDERLY WOMAN

Hakan Hasdemir, MD, Yücesin Arslan, MD, Ahmet Alper, MD, Damirbek Osmonov, MD, Tolga S. Güvenç, MD,
Esra Poyraz, MD, S‚ükrü Akyüz, MD, and Mustafa Yıldız, MD
Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey
Reprint Address: Hakan Hasdemir, MD, Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and
Research Hospital, Tibbiye Caddesi Haydarpasa, Istanbul, Turkey

, AbstractdBackground: Symptomatic cardiac injury af- INTRODUCTION

ter blunt chest trauma is relatively rare, and valvular injury
is even more rare. The valves most commonly affected are tri-
cuspid. Automobile accidents are mostly responsible for this
type of injury. Objectives: Unlike with the mitral valve,
post-traumatic tricuspid heart valve insufficiency is usually
well tolerated. Indeed, severe tricuspid regurgitation can
resolve spontaneously. Case Report: A 68-year-old woman
with no previous cardiac or medical history was brought to
our Emergency Department after an automobile accident.
She had chest pain and shortness of breath upon admission.
Transthoracic echocardiographic examination revealed
severe tricuspid regurgitation with rupture of the chordae
tendineae and prolapse of the valve cusps into the right
atrium during systole. An electrocardiogram was consistent
with second-degree Mobitz II atrioventricular block on
admission, which subsequently progressed to complete atrio-
ventricular block on day 3. During follow-up with close hemo-
dynamic monitoring, her symptoms disappeared and repeat
echocardiography revealed a regression in the severity of
tricuspid regurgitation. Operative repair of the tricuspid
valve was deemed unnecessary and the patient was discharged
with medical therapy on the eighth day after admission.
Conclusions: It is important to be aware of traumatic tricus-
pid regurgitation after non-penetrating chest trauma. Close
follow-up may suffice in some patients with stable hemody-
namic conditions, and regression of tricuspid regurgitation
can be expected during follow-up. Ó 2012 Elsevier Inc.
, Keywordsdtricuspid valve; blunt thoracic injury;
treatment
Tricuspid insufficiency after blunt thoracic injury is a rare
condition, and diagnosis of this condition is challenging
(1). The onset of symptoms is usually immediate.
However, as the symptoms are usually well tolerated,
the presentation may be delayed for months or even years
after the incident. The severity of symptoms usually
correlates with the severity of regurgitation as assessed
with transthoracic echocardiography (2,3). Here, we
report a 68-year-old woman admitted to our hospital due
to blunt chest trauma, with resultant severe tricuspid
insufficiency, and with remission of symptoms and
regression of regurgitation observed during follow-up.
CASE REPORT
A 68-year-old woman without previous cardiac or medi-
cal history was admitted to our Emergency Department
(ED) with blunt chest trauma that occurred in a traffic
accident. On admission, she suffered from chest pain
and shortness of breath. On physical examination, her
blood pressure was 150/90 mm Hg, heart rate was 56
beats/min, and respiratory rate was 30 breaths/min. An
erythematous lesion was noted on the midsternal area,
with the dimensions of 15 mm  25 mm. Precordial
auscultation revealed a holosystolic murmur at the left
sternal border with a severity of 3/6. When the patient

RECEIVED: 18 December 2009; FINAL SUBMISSION RECEIVED: 19 February 2010;

ACCEPTED: 10 May 2010

445
446
was reclining on the examination table with her head
elevated 45 , increased jugular venous pressure was
noted and the upper border of the internal jugular vein
was clearly visible up to the angle of the jaw. The remain-
der of the examination was unremarkable. A chest X-ray
study of the thorax was normal. An electrocardiogram
(ECG) was consistent with second-degree Mobitz type
II atrioventricular block. A computed tomography scan
of the thorax was obtained to search for possible trau-
matic thoracopulmonary lesions, but the findings were
completely normal. Blood biochemistry demonstrated
increased troponin levels (2.8 ng/dL) upon admission,
and the troponin level was even higher (5.9 ng/dL) in
the sample obtained 6 h after admission. Transthoracic
echocardiographic examination revealed right ventricular
dilatation (4.2 cm), inferior vena cava dilatation (3.0 cm),
minimal pericardial effusion, severe tricuspid regurgita-
tion with rupture of the chordae tendineae, and prolapse
into the right atrium during the systole (Figure 1).
Right heart catheterization was performed using
a Swan-Ganz catheter, and the pulmonary artery, right
Figure 1. (A) Tricuspid valve leaflet prolapsing into the right
atrium (arrow). (B) Four-chamber view showing severe tricus-
pid regurgitation at hospital admission.
H. Hasdemir et al.
ventricle, and right atrium pressures were 25/10, 26/0,
and 11 mm Hg, respectively. However, pulmonary artery
wedge pressure was within normal limits (12 mm Hg),
demonstrating normal left ventricular filling pressure.
As the patient’s hemodynamic status was stable, immedi-
ate operation for tricuspid regurgitation was deemed
unnecessary, and the patient was taken to the coronary in-
tensive care unit for further management and follow-up.
Isotonic fluid infusion was started to keep the right
ventricular filling pressures within high-normal range to
optimize her hemodynamic status. During follow-up,
the patient’s symptoms were considerably improved.
Transthoracic echocardiographic examination repeated
8 h after admission revealed a regression in the right ven-
tricular (3.5) and inferior vena caval (2.5 cm) dimensions,
and mild tricuspid regurgitation. Coronary angiography
with left and right heart catheterization, performed
2 days after admission, was unremarkable. On the third
hospital day, Mobitz type II atrioventricular block pro-
gressed to complete atrioventricular block. During
follow-up, the rhythm reverted back to sinus rhythm.
Transthoracic echocardiographic examination performed
on day 6 demonstrated only mild tricuspid regurgitation
(Figure 2). As the clinical condition of the patient was
stable, she was discharged from hospital on the eighth
day after her admission. After 1 month, the patient had
no complaints, and only mild tricuspid regurgitation
was present on transthoracic echocardiography.
DISCUSSION
Tricuspid insufficiency is a rare complication of non-
penetrating chest trauma (1). This condition is usually
well tolerated. The onset of symptoms may be immediate
or delayed several years after blunt chest trauma, and the
severity of symptoms is associated with the degree of
regurgitation. Chief symptoms of this condition are
dyspnea and chest pain that are usually mild (2,3).
Clinical signs (e.g., increased central venous pressure;
a holosystolic murmur, especially during inspiration)
and echocardiographic findings are generally sufficient
to diagnose this condition (1e3). ECG findings in our
patient, however, were rather unexpected, with Mobitz
type II block on admission progressing to complete
atrioventricular block by day 3. In the follow-up period,
the rhythm reverted back to sinus rhythm. Post-
traumatic cardiac edema occurred at or near the atrioven-
tricular node but resolved over time. No further signs of
decreased atrioventricular conductance were observed
during the follow-up period.
Usually, the catastrophic complication of blunt cardiac
trauma is rupture of a cardiac chamber, although the left
atrium is generally spared (4). The right ventricle is be-
hind the sternum, and this location renders the right
Tricuspid Valve and Blunt Thoracic Injury
Figure 2. Four-chamber view taken 6 days after admission.
Only mild tricuspid regurgitation was present.
ventricle vulnerable to an anteroposterior compression
type of injury, especially during the end diastolic phase
(5). Force on the right ventricle generated during deceler-
ation precipitates rupture of the papillary muscle or chor-
dae tendineae, thereby producing tricuspid regurgitation.
The usual lesion observed at surgery is subvalvular
rupture of the anterior papillary muscle (6e8).
Optimal treatment for tricuspid insufficiency after
blunt, non-penetrating chest trauma is still controversial
(9). Early diagnosis, followed by early treatment, is essen-
tial. The optimal timing for operative repair or replacement
of the valve is still not clearly defined (2,10). In less
symptomatic patients, medical therapy may be attempted
first under close monitoring. If signs and symptoms of
right ventricular failure subsequently appear, operative
repair then should be undertaken. The operative
treatment consists of reinsertion of the ruptured papillary
muscle with or without repair of the valve leaflets with
suturing (2,3). If the valve is not amenable to repair, it
may be replaced (10). Bioprosthetic valves are preferable
in this location, as they are not thrombogenic. Surgical
treatment usually results in complete recovery (10). Our
patient had no previous symptoms associated with tricus-
pid regurgitation, nor any medical record of tricuspid
regurgitation or a cardiopulmonary disease that might
cause tricuspid regurgitation, so we presumed that the
447
insufficiency was caused solely by the automobile acci-
dent. In this patient, right ventricular failure did not persist
after admission, and severe insufficiency reverted back to
mild regurgitation during follow-up, so an emergent surgi-
cal operation to restore the tricuspid valve was deemed
unnecessary. Close follow-up on an outpatient basis is
planned to monitor right ventricular function in this patient.
CONCLUSION
We believe that all patients admitted to the ED who have
sustained serious blunt chest trauma should undergo
echocardiographic examination for emergent diagnosis
of cardiac injury. This is especially so in patients with
hemodynamic instability or any abnormal physical
examination or ECG finding that raises suspicion of
possible cardiac injury. If cardiac injury is not diagnosed
promptly, potential life-threatening conditions may arise.
In mild cases of tricuspid valve injury, only supportive
medical therapy should be administered to defer surgical
repair. Long-term follow-up is mandatory to monitor the
patient’s symptoms and right ventricular function.
REFERENCES
1. Vayre F, Richard P, Ollivier JP. Traumatic tricuspid insufficiency.
Arch Mal Coeur Vaiss 1996;89:459e63.
2. Noera G, Sanguinetti M, Pensa P, et al. Tricuspid valve incompe-
tence caused by nonpenetrating thoracic trauma. Ann Thorac Surg
1991;51:320e2.
3. Pasic M, von Segesser L, Carrel T, Jenni R, Turina M. Severe
tricuspid regurgitation following blunt chest trauma: indication
for emergency surgery. Eur J Cardiothorac Surg 1992;6:455e7.
4. Parmley LF, Manion WC, Mattingly TW. Nonpenetrating traumatic
injury of the heart. Circulation 1953;18:371e96.
5. Krasna MJ, Flancbaum L. Blunt cardiac trauma: clinical manifesta-
tions and management. Semin Thorac Cardiovasc Surg 1992;4:
195e202.
6. Richard P, Vayre F, Sabouret P, Gandjbakhch I, Ollivier JP. Outcome
of traumatic tricuspid insufficiency, treated surgically. Apropos of 9
cases. Arch Mal Coeur Vaiss 1997;90:451e6.
7. dos Santos J Jr, de Marchi CH, Bestetti RB, Corbucci HA,
Pavarino PR Ruptured chordae tendineae of the posterior leaflet
of the tricuspid valve as a cause of tricuspid regurgitation following
blunt chest trauma. Cardiovasc Pathol 2001;10:97e8.
8. Linka A, Ritter M, Turina M, Jenni R. Acute tricuspid papillary
muscle rupture following blunt chest trauma. Am Heart J 1992;
124:799e802.
9. Lin SJ, Chen CW, Chou CJ, et al. Traumatic tricuspid insufficiency
with chordae tendinae rupture: a case report and literature review.
Kaohsiung J Med Sci 2006;22:626e9.
10. Shahidnoorai S, Ameli M. Post traumatic tricuspid insufficiency:
when to intervene? J Cardiovasc Surg (Torino) 1991;32:585e8.