An Extensive Stanford Type A Aortic Dissection Involving Bilateral Carotid and Iliac Arteries

We present a rare case of continuous, extensive aortic dissection (AD) involving the bilateral common carotid arteries, the ascending, thoracic, and abdominal aorta, and bifurcation of the right common iliac artery. A 61-year-old man with history of chronic hypertension presented with a one-day history of chest pain, vertigo, left facial drooping, and left hemiparesis. Despite the presence of bilateral carotid bruits, doppler ultrasound of the neck was postponed, and the patient was treated with thrombolytic therapy for a presumed ischemic stroke. The patient's symptoms began to resolve within an hour of treatment, at which time treatment was withheld. Ultrasound performed the following day showed dissection of bilateral common carotid arteries, and CT angiography demonstrated extensive AD as described earlier. The patient subsequently underwent cardiovascular surgery and has been doing clinically well since then. AD has a myriad of manifestations depending on the involvement of aortic branches. Our paper illustrates the importance of having a high index of suspicion for AD when a patient presents with a picture of ischemic stroke, since overlapping signs and symptoms exist between AD and stroke. Differentiating between the two conditions is central to patient care as thrombolytic therapy can be helpful in stroke, but detrimental in AD. 1. Introduction Aortic dissection is a life-threatening condition that affects 5–30 per 1,000,000 individuals each year [1]. Chronic hypertension is by far the most common risk factor for development of AD and accounts for 62–73% of patients with AD [1]. Other risk factors include diseases of the aorta (e.g., bicuspid valve, coarctation, aneurysm), connective tissue diseases (e.g., Marfan’s, Ehrlo-Danlos), Turner syndrome, trauma, cocaine use (e.g., in normotensive patients), and previous cardiac surgery or catheterization [1]. It typically involves a tear in the intimal layer of the aorta and creation of a “false lumen” between the aortic intima and the media or adventitia. Subsequent propagation of the dissection can occur both proximally and distally, which may lead to severe intravascular volume loss, tissue ischemia, or cardiac tamponade if the ascending aorta is involved. One theory regarding development of AD suggests that the intimal tear, being the initial event, triggers subsequent dissection of the medial layer. Others, however, believe that an expanding hematoma in the medial layer (e.g., from rupture of the vasa vasorum) leads to the ensuing tear of the intima [2]. There exist two classifications of AD. For