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A 53 year old man suffered severe head and blunt chest trauma as a result of a fall (from four metres high). On arrival at the emergency room he was unconscious with hypovolaemic circulatory shock. Following orotracheal intubation and resuscitation with blood, inotropic agents, and crystalloid, he was transferred to the neurosurgical intensive care unit. Analysis of arterial blood gases revealed a Pao2 of 50 mm Hg, Paco 2 35 mm Hg, and pHa 7.47. Increase in FIo2 up to 1.0 did not result in any increase in Pao2. Ventilation with positive end expiratory pressure made the hypoxaemia more severe. Pulmonary embolism was excluded by lung scintigraphy, mild right pulmonary contusion was evident on computed tomography; pneumothorax was not evident using chest radiography. Central venous pressure was 13 mm Hg, mean pulmonary artery pressure 21 mm Hg, pulmonary wedge pressure 15 mm Hg, and cardiac index 2.30 l/min/m2. Cardiac shunting was suspected and transoesophageal echocardiography (TOE) was performed.
TOE showed dilated right atrium and right ventricle. The anterior tricuspid leaflet looked partially avulsed from the annulus; neither valve prolapse nor ruptured chordae were evident. The tricuspid regurgitant jet originated just below the atrioventricular groove and looked relatively narrow at the origin becoming noticeably larger in the right atrium just above the tricuspid leaflets (fig 1). The regurgitant jet was eccentric and directed towards the atrial septum (fig 1). Here a large tear (2.6 cm) was seen in the region of the septum primum (fig 2). The regurgitant jet originating from the tricuspid valve entered the left atrium through the ruptured atrial septum producing a large right-to-left shunting. Surgical repair of the incompetent tricuspid valve and closure of the atrial septal defect led to significant improvement.
Blunt chest trauma may cause severe hypoxaemia by a variety of mechanisms.1 The most common cause of right-to-left shunting is intrapulmonary functional shunt as a consequence of severe parenchymal pulmonary disease such as cardiogenic and non-cardiogenic pulmonary oedema, pneumonia, atelectasis, and pulmonary embolism. In all but the last situation chest radiography usually reveals significant lung abnormalities. In trauma patients the most frequent mechanism of right-to-left intracardiac shunting is increased right atrial pressure following mechanical ventilation with positive end expiratory pressure, forcing the foramen ovale to open.2 3 The magnitude of the shunt in our patient was greater than that usually observed under these circumstances and was the result of three factors: (1) the septal defect was significantly larger than those observed in presence of patent forame ovale; (2) the right atrial pressure was increased because of the severity of the tricuspid valve regurgitation; (3) the tricuspid regurgitant jet was eccentric and directed towards the caudal portion of the atrial septum where the septal tear was located. Colour Doppler TOE demonstrated the regurgitant jet entering the left atrium through the ruptured atrial septum. This streaming effect may have contributed to increase the right-to-left shunting, considering the relatively increased mean right atrial pressure.
We report this case to remind those dealing with the management of patients with blunt chest trauma that there are causes of severe, refractory hypoxaemia outside the lung. In this situation TOE, when performed by skilled operators, is an invaluable diagnostic tool4 because it can provide accurate diagnosis of cardiac injuries in a short time at the bedside.
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