Acute Aortic Syndrome

Photo Credit: Charlotte Astrid

Author: Nathan Haas, MD PGY-1
University of Michigan

Originally Published: Modern Resident, February/March 2015

The acute onset of severe, ripping chest pain radiating to the back quickly brings to mind the diagnosis of aortic dissection. However, dissection is just one potential etiology of Acute Aortic Syndrome (AAS) which includes the acute presentation of aortic dissection, penetrating atherosclerotic ulcer, intramural hematoma, aneurismal leak and traumatic transection. Overlap frequently exists between these processes, and the various etiologies within AAS in some ways represent more of a spectrum of disease than distinct entities.

Aortic dissection results from an intimal tear penetrating the aortic media, with progressive dissection of the media creating a false lumen. Contrarily, a penetrating atherosclerotic ulcer occurs at the site of a preexisting atherosclerotic plaque and is the result of intimal erosion through to the media. Intramural hematoma is defined as a blood collection in the media without the presence of an intimal flap and physiologically is driven by the rupture of vasa vasorum. Aneurismal leaks are related to the acute expansion of a preexisting aortic aneurism. Traumatic transection most frequently occurs secondary to a rapid deceleration injury and classically occurs immediately distal to the left subclavian artery at the ligamentum arteriosum.

Classification of AAS can broadly be dichotomized to Stanford Types A and B. Stanford Type A represents disease involving the ascending aorta and aortic arch (with or without more distal involvement), whereas Stanford Type B represents disease of only the descending aorta (distal to the left subclavian artery) without more proximal involvement.

Initial stabilization of AAS centers on decreasing three metrics, each of which untreated further propagate disease: left ventricular contraction, systemic blood pressure and pain. A beta-blocker (frequently esmolol) is the first agent utilized, and serves the dual purpose of decreasing heart rate (to a goal of less than 60 if tolerated) and blood pressure. If additional anti-hypertensives are required to reach goal (typically a systolic blood pressure of 100-120), vasodilators such as sodium nitroprusside, nicardipine or fenoldopam are added next. It is critical to provide beta-blockade prior to vasodilation to prevent reflex tachycardia, which can further propagate dissection. Morphine is typically the first line analgesic to further minimize catecholamine-driven hypertension and tachycardia.

Stanford Type A dissection is a surgical emergency, and surgical management provides definitive management along with prevention of aortic rupture, pericardial tamponade and aortic regurgitation. Uncomplicated and stable Stanford Type B dissections can be managed medically as above, but can require interventional therapy (stent grafting, fenestration) for aortic expansion, dissection progression, end-organ malperfusion syndromes or recurrent pain.

References:

  1. Ahmad F, et al. Acute aortic syndrome: Pathology and therapeutic strategies. Postgraduate Medical Journal 82.967 (2006): 305-12. Web.
  2. Tsai TT, et al. Acute aortic syndromes. Circulation 112.24 (2005): 3802-813. Web.