Aortic Dissection

So what is an aortic dissection? Before we discuss this, let’s quickly revise the layers of a blood vessel. Our innermost layer is the tunica intima, superficial to this is our tunica media (which in arteries is the thickest layer through extensive elastic fibers), and our outermost layer is our tunica adventitia. So, an aortic dissection occurs through a transverse tear forming in the tunica intima of the aorta. This causes blood to enter the tunica media, creating a false lumen between the intima and media. A hematoma forms and propagates downwards, leading to pressure to rise within the aortic wall. Rupture occurs, occluding branching vessels and causing ischemia.

Now the aorta is an enormous artery, so where do these mostly occur? 65% of aortic dissections occur in the ascending aorta, 20% in the descending arch, 10% in the arch, and 5% in the abdominal aorta. This leads us to classification. The go-to classification for aortic dissection is the Stanford Classification, and it is separated into type A and type B.

Type A: involves the ascending aorta (defined as proximal to the brachiocephalic artery). These require surgery and complications involve aortic regurgitation + cardiac tamponade. Type B: does not involve the ascending aorta and is defined as distal to the left subclavian artery. It can be managed with beta-blockers and vasodilators.

In terms of the clinical features of aortic dissection, many were described in the clinical case. It involves sudden severe tearing/ripping pain (chest, back, interscapular, neck/jaw), hypertension, asymmetrical BP and pulse readings, wide pulse pressure, syncope.

From this, some important differentials to rule out quickly involve aortic embolism, ST-elevation myocardial infarction (STEMI), cardiac tamponade, pericarditis, heart failure exacerbation, and tension pneumothorax.

Risk factors of aortic dissection can be divided into acquired and congenital causes. Acquired involves hypertension, trauma (deceleration injury), vasculitis (such as syphilis and Takayasu arteritis), and cocaine use (through rapidly increasing BP). Congenital causes involve connective tissue diseases such as Marfan syndrome, bicuspid aortic valve (seen in Turner syndrome), and aortic coarctation (which means aortic narrowing).

Now, how on earth do we approach one of these? Firstly, the gold standard for diagnosis of an aortic dissection is CT angiography. However, this is only done for stable patients. This shows the intimal dissection flap and double lumen. A transesophageal echocardiography is done for unstable patients, showing a dissection flap + double lumen and thrombosis in the false lumen. Also, a chest X-ray will show a widened mediastinum >8 cm at the level of the aortic knuckle.

Now to treatment. Let’s go back to our Stanford classification of aortic dissection. For Stanford classification type A (involving the ascending aorta), open surgery should be performed, replacing the dissection with a polyester graft implantation (surgical emergency). For Stanford B, care is usually supportive, and treatment is conservative through watchful waiting – we can use beta-blockers and vasodilators as we previously discussed.