Acute Onset Hemoptysis Caused by Mitral Valve Rupture During a Sports Injury

Abstract

INTRODUCTION: While hemoptysis following blunt trauma is typically due to pulmonary injury, we present an unusal cardiovascular cause. CASE PRESENTATION: Case Report: The patient is a 46 year old active duty male who presented to the Walter Reed Army Medical Center Pulmonary Clinic with two days of hemoptysis. He was in his usual state of excellent health until two days prior to presentation when he was involved in a collision during an ice hockey game. Afterwards he noted shortness of breath and cough with blood-streaked sputum. During the subsequent twenty-four hours the patient had 50cc. of hemoptysis. The next day he presented to the Emergency Department where pulmonary contusion, pneumothorax and pulmonary embolism were excluded by CT. He was provided a referral for prompt outpatient pulmonary consultation. At his outpatient appointment the next day his exam was notable for no respiratory distress, normal lung sounds, and a new harsh III/VI holosystolic murmur, that was loudest at the apex with radiation to the left axilla. Because of suspicion for a traumatic papillary muscle rupture, he was admitted to the internal medicine service for expedited evaluation. A transthoracic echocardiogram revealed severe, eccentric, anteriorly directed mitral regurgitation associated with a flail posterior mitral valve leaflet resulting in severe posterior leaflet prolapse. He was diagnosed by cardiology with traumatic rupture of the posterior chordae tendoneae resulting in acute severe mitral regurgitation. Within the first twenty four hours of admission he developed worsening dyspnea and was transferred to the medical intensive care unit, where he received intravenous lasix and nitroglycerin. He responded well to these therapies, and remained clinically stable for the duration of his admission. Prior to definitive mitral valve repair, trans-esophageal echocardiogram demonstrated severe mitral regurgitation due to rupture of the P2 valve chord. Left and right heart catheterization showed no obstructive arterial disease, mitral regurgitation; a hyperdynamic left ventricle, and mild pulmonary hypertension. The patient successfully underwent mitral valve repair without complication and subsequent resolution of hemoptysis. DISCUSSION: Discussion: This case demonstrates an unusual presentation of traumatic posterior mitral valve leaflet rupture with severe regurgitation manifesting as submassive hemoptysis. A recent review of the literature determined that sports injuries are the third most common cause of traumatic mitral valve insufficiency. Overall, mitral valve rupture due to blunt trauma is a rare occurrence with just 82 cases found in the literature since 1964. (1) Of note, hemoptysis as a symptom of acute mitral valve insufficiency appears to be an even rarer, based on our review of the literature. The pathophysiology of traumatic severe mitral valve regurgitation is thought to occur as a result of loss of valve integrity from a sudden increase in intracardiac pressure while the heart is completing diastole and entering systole, with the ventricles dilated and the arterioventricular valves closed. Most frequently damaged is the papillary muscle, followed by the chordae tendineae. (1) Symptoms of acute mitral valve regurgitation are due increased left atrial pressure and decreased left ventricular ejection fraction. Acutely, the patient usually presents with signs of pulmonary edema such as dyspnea, cough and orthopnea. Hemoptysis is most often associated with mitral valvular stenosis, not regurgitation. CONCLUSIONS: Conclusion: Blunt thoracic trauma occurring during contact sports can result in severe injuries such as mitral valve rupture and subsequent hemoptysis. Mitral valve insufficiency should be suspected in a patient with a new murmur and a history of trauma.