Acute aortic dissection is defined as the rapid development of a false, blood-filled channel within the tunica media of the aorta.¹ It has an estimated incidence of 3 per 100,000 persons per year.

Three AADs are ultimately diagnosed out of every 1,000 emergency department patients presenting with acute back, chest, or abdominal pain.^2,3 Mortality in untreated AAD is estimated at more than 1% per hour after onset of symptoms, whereas 30-day survival for appropriately treated patients is greater than 80%. Therefore, timely diagnosis and rapid management of AAD are of paramount importance for the emergency physician.^3,4 Diagnosis is delayed more than 24 hours after initial presentation in almost half of all cases, highlighting the need for emergency physicians to maintain appropriate clinical suspicion for AAD in patients with chest, back, or abdominal pain.⁵

Failure to diagnose AAD carries a significant risk for poor outcomes because of the consequences of progressive disease (e.g., aortic rupture) and the possibility of treating a falsely diagnosed myocardial infarction (MI) or pulmonary embolism (PE) with anticoagulation, a potentially catastrophic error.⁶

Pathophysiology and Risk Factors^2,5

The most common location of a tear is the right lateral ascending aorta.⁷ Tears of the descending aorta usually originate just distal to the left subclavian artery.⁷ Blood may enter the tunica media from the lumen of the aorta via a breech of the intima or from the vasa vasorum, the small vessels that supply nutrients to the aortic wall. Mechanical forces compromise the integrity of the intima by physiologic flexion of the descending aorta with every heartbeat and nonlaminar blood ejection from the left ventricle.⁸

Once blood dissects the tunica media, it forms a false lumen and may stagnate; extend anterograde or retrograde; or rupture into the lumen of the vessel or into the surrounding tissues. Retrograde extension can involve the aortic valve, causing aortic insufficiency and heart failure, and continue into the right coronary artery ostium, causing myocardial infarction.

The mean age of AAD is 62 years, and incidence is extremely low in patients younger than age 40 years in the absence of sympathomimetic drug use, Marfan syndrome, tertiary syphilis, or Ehlers-Danlos syndrome.^6,7,9 Intimal damage is a consequence of normal aging, hypertension, bicuspid aortic valve, cardiac surgery, stimulant use, and insertion of an intra-aortic balloon pump. Atherosclerosis is a common comorbid condition but not often found at the site of dissection.⁸