At 3 a.m. you’re dispatched to a trailer park for a 26-year-old male with difficulty breathing. Once on scene, the patient’s girlfriend directs you inside. The living conditions are poor, with old trash lining the hallways and drug paraphernalia in the kitchen. The patient is in the tripod position and obviously short of breath with significant accessory muscle use. Your partner immediately assesses the patient’s pulse oximetry and starts the patient on high-flow oxygen via a non-rebreather mask (NRB) as you ascertain a health history from the patient’s girlfriend.
She states the patient has been having worsening dyspnea over the past two hours, but no other symptoms and no recent illness, fever or cough. You learn the patient has an allergy to naloxone and a history of IV drug abuse. The girlfriend says the patient was in a motor vehicle crash (MVC) the day prior, but he left the hospital against medical advice, before any scans were done.
Your partner reports the patient’s initial vital signs: respiratory rate 34 with rales bilaterally up to mid-lung, heart rate 144 bpm, blood pressure 102/68, SpO2 on room air 86%. With a 12-lead ECG he has sinus tachycardia and nasal end-tidal carbon dioxide (EtCO2) level of 26.
You assist your partner in completing a focused physical exam and note intercostal retractions with equal expansion of the chest. There’s a yellow bruise on the anterior chest to the left of the sternum about 3 inches in diameter.
Although you normally don’t assess heart sounds in all your patients, you decide to auscultate the heart on this one. The patient has an S3 gallop and a murmur best heard at the apex that appears to start right after S1 and ends just prior to S2. On 100% oxygen via NRB, the patient’s pulse oximetry only improves to 90%.
Both you and your partner agree the patient needs further intervention, but your local protocols only allow for the treatment of acute pulmonary edema when it’s secondary to congestive heart failure. You make contact with medical control as your partner starts IV access and sets up the stair chair. After discussing the case with medical control, they authorize the use of sublingual nitroglycerin every five minutes and continuous positive airway pressure (CPAP) at 10 cmH2O.
This is a challenging case, with a long list of potential causes. The patient is a previously healthy IV drug abuser who presents with an acute onset of shortness of breath within 24 hours after an MVC. Following trauma, there’s a possibility of pulmonary contusion, myocardial contusion or even acute regurgitation of a heart valve from a ruptured chordae tendinae. Additionally, in a case like this, it’s prudent to consider coronary artery spasm secondary to drug use. Because the patient has a history of IV drug use, he’s likely to be at risk for conditions such as HIV, infective endocarditis or lung abscess. Of the possible traumatic causes, pulmonary contusions can produce localized regions of edema and hemorrhage which would likely manifest as wheezing or rales.
Pulmonary contusions are the most common complication of blunt chest trauma, affecting at least one-third of all patients sustaining major chest injuries. Pulmonary contusions are most commonly scene secondary to MVCs.1 Myocardial contusions can range from minor bruises to complete involvement of the myocardial tissue resulting in signs and symptoms such as chest pain, arrhythmia, cardiac tamponade and even myocardial rupture. Relevant to our case, signs of pulmonary edema aren’t frequently associated with myocardial contusion. Acute regurgitation of a heart valve is a very rare complication of blunt chest trauma, although patients can present with delayed onset of shortness of breath and associated heart failure.
It’s unlikely the patient is suffering from an acute infectious process caused by the immunosuppression-associated HIV infection because he was previously healthy. Additionally, if the patient were suffering from pneumonia or another infection, we’d expect to see other symptoms such as fever or cough. Infective endocarditis (IE) is an infection of the endocardial (innermost) layer of the heart tissue that frequently affects the valves. Numerous bacteria or fungi can cause the disease and it can occur in anyone with exposure to one of the disease-causing organisms, but it’s frequently seen in patients with prosthetic heart valves and IV drug abusers. The most common symptoms of IE are fever, fatigue, appetite loss and dyspnea. On physical exam, signs range from fever and skin lesions to new onset heart murmur.2 The mitral valve is the most commonly affected valve in non-IV drug abusers, but the tricuspid valve is most commonly affected in IV drug abusers.3
Back to the Patient
Upon arrival in the ED, the patient’s respiratory rate has decreased to 22, heart rate has decreased to 114, SpO2 has improved to 98% and EtCO2 increased to 33 mmHg. The ED staff was awaiting your arrival based on your notification via radio, and the doctor is pleased with your assessment and treatment of the patient.
In the ED, the staff perform a focused assessment with sonography in trauma ultrasound exam, which is negative; a chest X-ray, which shows bilateral pulmonary edema; and a CT scan of the chest and abdomen, which reveals minor bleeding around the spleen but no significant intraperitoneal hemorrhage. A transthoracic echocardiogram reveals rupture of the anterior papillary muscle and resultant acute mitral regurgitation (MR).
Acute Traumatic MR
Acute MR is a rare complication of blunt chest trauma, with less than 50 case reports as of 2001.4 In the setting of blunt chest trauma, MR occurs due to a rupture in a papillary muscle. Papillary muscles are located within the ventricular wall and attach to the atrioventricular (AV) valves (tricuspid and mitral) via the tendons and function to prevent the prolapse of the AV valves into the atrium during ventricular systole. The exact mechanism of papillary muscle rupture isn’t clear, but it’s suggested that injury to the papillary muscle causes endocardial ischemia, which is a result of redistributed blood flow due to local edema, myocardial fiber rupture and hematomas. The most vulnerable time for injury occurs during maximal inspiration and during isovolumetric contraction (the point where all heart valves are closed).5
Because the mitral valve is no longer able to stay closed against the pressure of the left ventricle, the valve opens and prolapses into the left atrium. Because the left atrium isn’t designed to handle high volumes of blood, the increased volumes and pressure gets transmitted to the pulmonary circulation, which results in pulmonary edema, much like in left-sided heart failure. It’s worth noting that in rare circumstances of acute MR, there can be localized pulmonary edema in the right upper lobe because the regurgitant blood flow can be directed at the right upper pulmonary vein that returns blood from the right upper lobe.6
Acute MR presents with a rapid onset of dyspnea that’s often accompanied by hypotension. Additionally, auscultation of the heart creates a new holosystolic (between S1 and S2) murmur best heard at the apex and frequently an S3 heart sound. In the setting of trauma, symptoms can develop immediately after the incident, but more commonly are delayed by at least 12 hours and may develop days after the traumatic event.5,7,8
In the Field
Because the diagnosis of acute MR must be confirmed through echocardiography, in the field, an astute provider would need a high index of suspicion for this condition. Treatment will be based upon the patient’s unique presentation, but will entail standard monitoring, CPAP for cases of pulmonary edema not associated with hypotension, and vasopressor support for signs of cardiogenic shock. Intubation and mechanical ventilation should be considered for patients with an altered mental status and signs of cardiogenic shock with respiratory failure.
If you have a high index of suspicion for traumatic MR, consider consultation with medical control as the treatment must take into account the possibility of other injuries. Because the definitive treatment is surgical repair, consider transport to a facility with cardiothoracic surgical capabilities
Traumatic injuries don’t always manifest themselves immediately post-injury. A thorough history and physical examination (including heart sounds) can help narrow the list of possible causes for a patient’s signs and symptoms, especially in complicated patients that may have both medical and traumatic issues. When considering the etiology of a patient’s condition, it’s imperative to be focused, yet maintain a wide scope of possible causes.
1. Chopra PS, Kroncke GM, Berkoff HA, et al. Pulmonary contusion a problem in blunt chest trauma. Wis Med J. 1977;76(1):S1–S3.
2. Sucu M, Davutoğlu V, Özer O, et al. Epidemiological, clinical and microbiological profile of infective endocarditis in a tertiary hospital in the Southeast Anatolia region. Turk Kardiyol Dern Ars. 2010;38(2):107–111.
3. Sousa C, Botelho C, Rodrigues D, et al. Infective endocarditis in intravenous drug abusers: An update. Eur J Clin Microbiol Infect Dis. 2012;31(11):2905–2910.
4. Kumagai H, Hamanaka Y, Hirai S, et al. Mitral valve plasty for mitral regurgitation after blunt chest trauma. Ann Thorac Cardiovasc Surg. 2001;7(3):175–179.
5. Farmery A, Chambers P, Banning A. Delayed rupture of the mitral valve complicating blunt chest trauma. J Accid Emerg Med. 1998;15(6):422–423.
6. Murakami S, Suwa M, Morita H, et al. Localized pulmonary edema after blunt chest trauma. Circulation. 2007;115(8): 206–207.
7. Mazzucco A, Rizzoli G, Faggian G, et al. Acute mitral regurgitation after blunt chest trauma. Arch Intern Med. 1983;143(12):2326–2329.
8. Shammas NW, Kaul S, Stuhlmuller JE, et al. Traumatic mitral insufficiency complicating blunt chest trauma treated medically: A case report and review. Crit Care Med. 1992;20(7):1064–1068.