Anaesthesiology Intensive Therapy, 2011,XLIII,4; 199-202

Tricuspid valve rupture after blunt chest trauma

Wojciech Dąbrowski1, Andrzej Nestorowicz1, Jarosław Wośko1, Przemysław Zadora1, Andrzej Tomaszewski2, Cezary Jurko3

11st Department of Anaesthesiology and Intensive Therapy, Medical University of Lublin

2Department of Cardiology, Medical University of Lublin

3Department of Cardiac Surgery, Medical University of Lublin

  • Fig. 1. An echocardiogram. 1 – the right ventricle and right atrium in the late diastolic phase, 2 – the right ventricle and right atrium in the systolic phase, 3 – the ventricle and atrium in the diastolic phase with papillary muscle head abrupted (RV – right ventricle, TC – tendinous cord, LV – left ventricle, PMHR – papillary muscle head rupture, RA – right atrium)
  • Fig. 2. Photo of the right ventricle. Anterior papillary muscle damaged (TTCs – tricuspid tendinous cords, PMHR – papillary muscle head abrupted)
  • Fig. 3. Photo of the right ventricle after tricuspid valve reconstruction with the Carpentier-Edwards ring visualized (CE)

Background. Blunt chest trauma is frequently associated with cardiac contusion and structural damage, most cases only being recognized after death. We report a case of multiple organ trauma, where cardiac failure, caused by tricuspid valve rupture, was markedly delayed.

Case report. A 21-yr-old man was admitted to hospital after a car accident. He was suffering from cerebral contusion and oedema, pulmonary contusion, and a left pneumothorax. He also had multiple fractures of the facial bones, orbit, L4 vertebra and left tibia. He was tracheotomised, and a subdural sensor was inserted for continuous monitoring of intracranial pressure. He was sedated and ventilated for two weeks. On the 12th day, his jaw was reconstructed, and immediately after surgery, mild signs of cardiac failure were observed, which were attributed to cardiac contusion. Two weeks after admission, the patient was weaned from the ventilator, and three days later, his facial bones were reconstructed. Four days later, the signs of cardiac failure reappeared. Transoesophageal echocardiography revealed rupture of a head of papillary muscle, with 4th degree tricuspid insufficiency and enlargement of the right ventricle. The ruptured muscle was reconstructed under extracorporeal circulation, and the patient made a satisfactory recovery.

Discussion. Acute tricuspid valve insufficiency, albeit rare, may occur in patients with blunt chest trauma. Sedation and lack of physical activity may delay the definite diagnosis, especially when only transthoracic echocardiography is used. Cardiac arrhythmias, diastolic murmur, or signs of congestive cardiac failure in a chest trauma patient may all suggest some structural damage; therefore, transoesophageal echocardiography should be performed as early as possible in such situations.

Cardiac injuries are an important cause of death amongst patients with multiple organ trauma. They occur in 7-76% of cases after blunt chest trauma, particularly in the sternal region, yet most cases are recognised after death [1, 2, 3]. Depending on the type of trauma, myocardial haemorrhage, partial cardiac rupture (pericardial, myocardial, endocardial) or complete heart rupture, post-traumatic myocarditis, coronary or valvular damage are likely to develop [2, 3]. In the majority of cases, cardiac damage is asymptomatic or its symptoms are non-specific and masked by the symptoms of injuries to other organs. The symptom suggestive of blunt heart trauma is haemodynamic instability accompanied by numerous arrhythmias, among which single premature ventricular contractions (54%) and premature ventricular salvos (16%) predominate. Paroxysmal atrial fibrillation (6%) and ventricular tachycardia (3%) are less common [4]. Moreover, non-specific ST segment and T wave changes are of importance, which are often accompanied by increased concentration of cardiac creatine kinase fraction and both cardiac troponin fractions. The abnormalities occur within the first 24-48 h after trauma [7, 8, 9]. The most sensitive and the quickest diagnostic procedure in such cases is transoesophageal echocardiography [7, 9, 10].

The paper describes the case of remote rupture of the right ventricular papillary muscles complicated with acute tricuspid valve incompetence without haemodynamic dysfunction in a patient after multiple organ trauma.


A 21-year-old patient was admitted to our department due to severe respiratory failure after multiple organ trauma sustained during a car accident. Immediately after admission, the CT was performed and generalized cerebral oedema, pulmonary contusion, left pulmonary parenchymal haematoma and left pneumothorax were found. CT bone imaging showed multiple fractures: the facial bones, orbit, L4 vertebra (without spinal injuries and vertebral canal narrowing) and of the left tibia. An electrocardiogram revealed no pathologic features; persisting tachycardia was attributed to the general condition of the patient. Blood and biochemical tests did not show any significant abnormalities.

Due to multiple fractures of the facial bones and CNS damage, the patient was tracheotomised. Circulation was supported with the infusion of noradrenaline. Left pneumothorax was decompressed by drainage whereas nasal bleeding was stopped by bilateral packing. Due to increasing cerebral oedema, a sensor for monitoring intracranial pressure was inserted; the pressure ranged from 12-18 mm Hg (1.6-2.4 kPa). The anti-oedematous treatment was instituted and cardiovascular parameters controlled by continuous monitoring of ECG action and direct measurements of arterial pressure. Considering damage to CNS, the continuous infusion of the mixture of midazolam and fentanyl was administered and sedation supplemented with the infusion of pentobarbital, followed by propofol. The patient’s general condition improved.

On treatment day 10, CT was repeated, which demonstrated slight, partially haemorrhagic foci of contusion of frontal lobes without features of cerebral oedema. The CNS lesions regressed on treatment day 12 and the fractured maxillary alveolar processes were surgically stabilized. Several hours after surgery, markedly widened superficial veins of the arms, both hands and external jugular vein were noticed. Central venous pressure increased to 15 cm H2O. The X-ray showed the smoothed cardiac waist silhouette and substantial enlargement of the left atrium. Since the defect of the valvular apparatus was suspected, transthoracic echocardiography was performed which visualized the presence of  fluid in the pericardial region, about 1 cm thick. There was no tamponade or systolic dysfunction of the myocardium.  Based on the clinical picture and results of additional tests myocardial contusion was diagnosed.

On day 14 after trauma, the patient was weaned from the ventilator. On day 17, the fractured facial skeleton was surgically stabilised and reconstructed. The surgery and anaesthesia were uneventful. After the  procedure, the patient recovered and was slightly responsive.

On treatment day 18, single premature ventricular contractions were observed without abnormal morphology of electrocardiographic complexes and waves. The changes were accompanied by cough. On auscultation, low systolic murmur in the tricuspid valve projection was detected. Transoesophageal echocardiography showed abruption of a head of papillary muscle of the right ventricle accompanied by acute tricuspid insufficiency (4th degree) and enlargement of the right ventricle without pulmonary hypertension (Fig. 1). There were no symptoms of acute circulatory insufficiency observed. Due to the patient’s clinical condition and short time following ENT intervention, surgical repair of the tricuspid valve was postponed.

General anaesthesia was administered for cardiac surgery. After exposing the right atrium, abruption of the anterior papillary muscle head was confirmed (Fig. 2) with complete tricuspid  valve incompetence. The abrupted fragment of papillary muscle was sutured and the tricuspid valve ring strengthened with the Carpentier-Edwards ring (Fig. 3). The completion of extracorporeal circulation was uneventful – the patient did not require substitution of positive inotropic agents. On postoperative day 1, he regained consciousness, artificial ventilation was discontinued and the endotracheal tube removed. On day 74, the patient was discharged home in general good condition.


Acute tricuspid valve insufficiency is a rare complication following cardiac injury; it occurs in about 1% of cardiac trauma cases and is most commonly caused by the rupture of chordae tendineae [11, 12]. Due to its atypical clinical picture and lack of complaints, the majority of such cases are recognized during autopsy [2, 11]. Traumatic rupture of chordae tendineae is favoured by the location of the right ventricle directly behind the manubrium sterni. The kinetic energy acting during the sternum impact is directly transferred onto the right ventricular muscle producing petechiae in the myocardium or injuring the myocardium. Moreover, the energy increases the blood pressure in the right ventricle. Therefore, valve damage most commonly occurs in the final phase of ventricular diastole and in the majority of cases affects the anterior papillary muscle of the right ventricle [3, 4, 13].

Acute traumatic tricuspid valve insufficiency can develop at any moment of life. In most cases, the rupture of chordae tendineae or papillary muscle occurs in the early posttraumatic period; however, there are cases recognized 25 years after trauma [14, 15]. The major factor hindering the early diagnosis, particularly in young individuals, is the absence of acute circulatory insufficiency and other injuries, e.g. lung contusion. Due to high abilities to compensate for insufficiency and markedly reduced physical activity in the immediate posttraumatic period, the only symptom of the developing cardiac pathology is impaired blood return to the ‘right heart’ [12, 14, 15]. However, this symptom may be completely unnoticeable, especially in patients treated with diuretics due to craniocerebral trauma. In our case, this symptom was detected 6 days before the recognition of acute tricuspid valve insufficiency. Echocardiography performed on that day suggested myocardial contusion without features of valve incompetence yet did not reveal the features of anterior papillary muscle injury. Therefore, it can be assumed that the injury described was of a two-phase nature. However, it is difficult to explain such a course of trauma. In the majority of cases of rupture of chordae tendineae of the tricuspid valve, echocardiography confirmed the existing pathology [6, 10, 11, 13, 14, 15]. The earlier development of symptoms of right ventricular insufficiency might have suggested the developing pathology, yet even significant dysfunction of the right ventricle may be fully compensated by the efficient function of the left ventricle.

At present, echocardiography is considered the standard examination in the diagnosis of myocardial damage. Transthoracic echocardiography, however, carries the risk of high proportion of errors, particularly in patients after pulmonary parenchymal trauma, massive injuries to the thoracic wall or those ventilated mechanically, in whom the probability of overlooking the myocardial injuries reaches even 38% [7, 16, 17].

Transoesophageal echocardiography is considered to be the most sensitive examination [9, 17]. Accurate imaging of the heart structures enables early diagnosis of the pathology whereas multiplanar imaging facilitates visualisation of even slight lesions in the myocardium. The multi-centre study demonstrated that transoesophageal echocardiography is much more sensitive for the diagnosis of cardiac diseases than ECG or cardiac enzymes [9]. Thus, transoesophageal echocardiography performed in our patient during the first examinations might have facilitated proper diagnosis. However, this examination requires high experience and is difficult to perform in patients with craniofacial injuries or after their surgical stabilization. Therefore, transoesophageal examination was abandoned in this case.

Nevertheless, meticulous observation of the patient’s clinical condition is pivotal for the diagnosis of cardiac trauma. Any abnormal heart rhythm, pathological phenomena on auscultation, changes in vascular bed filling, atypical thoracic pain or developing haemodynamic insufficiency may suggest cardiac injury [1, 2, 7]. The additional examinations mentioned, thoracic and cardiac CT or myocardial scintigraphy should be considered helpful for accurate characterisation of the developing pathology.

In the case presented, tricuspid valve insufficiency after posttraumatic rupture of the anterior papillary muscle of the right ventricle was diagnosed based on clinical symptoms, which suggested us to perform echocardiography. Such an examination  should be carried out in all patients after chest trauma suspected of myocardial damage.



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*Wojciech Dąbrowski

Katedra i I Klinika
Anestezjologii i Intensywnej Terapii
Uniwersytet Medyczny w Lublinie
ul. Jaczewskiego 8; 20-954 Lublin
tel.: +48 81 724 43 32

received: 15.05.2011 r.
accepted: 02.10.2011 r.