Traumatic mitral valve rupture

Abstract

A previously healthy 42-year-old man was admitted to our emergency department after a horse had kicked him in his left chest 2 h earlier. At the trauma scene he was conscious but confused and dyspnoeic. A left thoracostomy was performed and he was transferred to our hospital. Upon arrival, he was awake with a heart rate of 120 beats/min, palpable peripheral pulses, normal breath sounds, and bruises across his lower sternum and left ribcage. Shortly after arrival, he became restless with increasing shortness of breath. The systolic blood pressure decreased to 70 mmHg and his heart rate increased to 140 beats/min, while peripheral pulse oximetry indicated significant oxyhaemoglobin desaturation. An endotracheal intubation was performed and the patient developed massive frothy lung oedema fluid. Chest radiography was interpreted as bilateral lung contusion (Fig. 1) and his electrocardiogram showed sinus rhythm, 75 beats/min, with STT depression in inferolateral leads (Fig. 2). Due to progressive hypoxia, mechanical ventilator pressures were increased. His haemodynamic state further deteriorated into pulseless electrical activity requiring high-dose inotropes and two episodes of cardiopulmonary resuscitation. Transthoracic echocardiography was performed but was complicated because of difficulties in obtaining accurate windows and because of the nervous tension in the emergency department resuscitation room. Finally pericardial tamponade was excluded and no other abnormalities were observed, but colour Doppler was not used. The patient was transferred to the ICU with the diagnoses of bilateral lung contusion and possible myocardial contusion. Because of further respiratory deterioration he was placed in a prone position and a transoesophageal echocardiography (TEE) was performed. This time, a massive mitral insufficiency was observed due to a complete avulsion of the anterolateral papillary muscle (Figs. 3 and 4). Mitral valve replacement was readily carried out. Because of massive pulmonary congestion the patient failed to wean from cardiopulmonary bypass and veno-arterial extracorporeal membrane oxygenation (ECMO) was instituted until haemodynamic stabilisation at day 4. Unfortunately, there was no neurological recovery after cessation of sedation and a brain CT scan revealed massive bilateral ischaemic stroke. After excluding other causes for his neurological state, further therapy was withheld and the patient died.