A 59-year-old woman involved in a motor vehicle crash presented to the ED via emergency medical services. The patient had been the front-seat passenger and was wearing a seat belt. She complained of chest wall pain, but denied head injury, loss of consciousness, neck pain, abdominal pain, or shortness of breath. Her past medical history was unremarkable.
A chest X-ray was performed and interpreted as normal by the attending radiologist. Laboratory studies were normal except for mild anemia. The patient was discharged from the hospital with a diagnosis of chest wall contusion. She died 36 hours later from a ruptured thoracic aorta. The family of the patient brought a malpractice suit against the emergency physician (EP) for failing to diagnose and treat acute aortic rupture. At trial, a defense verdict was returned.
Aortic rupture from blunt trauma is a devastating injury. More than 90% of patients who have sustained this type of injury in a motor vehicle crash die at the scene.1 For the remaining 10%, 50% die within the following 24 hours.1 The injury occurs in the proximal descending aorta, secondary to the fixation of the vessels between the left subclavian artery and the ligamentum arteriosum; the cause in approximately 80% to 90% of cases is due to blunt trauma. Involvement of the ascending aorta is much less common. Many patients, such as the one in this case, exhibit no external physical findings of injury. Chest pain is the most frequent complaint, followed by dyspnea—both fairly nonspecific symptoms. Physical findings that should raise a suspicion for a thoracic aortic injury include hypotension, hypertension in the upper extremity and hypotension in the lower extremity, unequal BPs in the extremities, external evidence of chest wall trauma, and palpable fractures of the sternum and ribs.2 While it is unclear if this patient had unequal extremity BPs, she did not have any of the other classic findings of aortic rupture. Associated neurological, abdominal, or orthopedic injuries are frequently present as well, and can mask the subtle signs of aortic rupture.
A chest radiograph is often the initial screening test used to evaluate for possible thoracic aortic injury. Suspicious findings include a widened mediastinum (greater than 8 cm), right-sided deviation of the esophagus, depression of the left mainstem bronchus, loss of the aortic knob, and an apical pleural cap. Unfortunately, chest X-ray can be normal, and a normal mediastinum on the radiograph does not exclude the diagnosis.
For patients with suspected thoracic aortic injury, helical computed tomography with angiography is the study of choice. It can accurately identify operative and nonoperative lesions, as well as associated injuries (eg, small pneumothorax, rib fractures). Magnetic resonance angiography provides similar sensitivity and specificity, but is not practical for the majority of trauma patients. Occasionally, aortography can be considered when the CT scan results are indeterminate and when thought to be needed to plan operative intervention. Finally, transesophageal echocardiography can be considered in hemodynamically unstable patients unable to be transferred to the radiology suite.
For most patients, immediate operative intervention is the definitive treatment. For patients with suspected thoracic aortic injury and hypertension, shear forces need to be decreased just as they are for patients with aortic dissection. A short-acting β-blocker like intravenous (IV) esmolol can be used initially to slow HR. Then, an IV arterial vasodilator can be given to decrease BP. To prevent rebound tachycardia and increased shear forces, the β-blocker should always be initiated before the vasodilator is given. Vital-sign targets include an HR of 60 beats/minute and a systolic BP in the range of 100 to 120 mm Hg.
This was a very atypical presentation of a devastating injury. Given the benign presentation, lack of associated injuries, and the normal chest X-ray, a defense verdict appears to be the correct one in this very unfortunate case.