Epidemiology: 5-10 per million per year. Risk factors: untreated HTN, advanced age, disease of the aortic wall, connective tissue disease (Marfan’s), pregnancy.
Pathogenesis: 1) INITIATING EVENT and 2) STRUCTURAL WEAKNESS. Dilatation or high BP tears intima; blood surges into wall, separating layers.
LOCATION: Proximal ascending aorta most susceptible because of large expansion during systole.
1. 60%- convexity of ascending aorta 1-2cm above sinuses
2. 30%- descending aorta (distal to LSC)
3. 10%- arch
In <10% spontaneous rupture of vasa vasorum initiates dissection.
Classification: Standford classification-
1. Type A: ascending
2. Type B: descending
Clinical presentation: 90% present with abrupt, severe retrosternal or interscapular chest pain with migration down back. COMPLICATIONS: pericardial tamponade, L pleural effusion, occlusion of aortic branch/ischemia (20% arms/legs, 15% kidneys, 10% myocardium, 5% brain, 3% mesentery or spinal cord).
1. TTE: diagnostic for 75% Type A, 40% Type B.
2. IF pt unstable( TEE in ER or OR
3. IF pt stable( CT, MRI, or angio
1. Type A( Surgical replacement of ascending aorta. Operative mortality 10-25%.
2. Type B with favorable outlook, or severe comorbidity( Medical reduction of aortic stress- reduce BP, pulse upstroke, HR. (beta-blockers ideal)
3. Type B with less favorable outlook (aortic diameter >5cm, progression of dissection, malperfusion of aortic branch, uncontrollable HTN, persistent pain)( Surgical repair
Lancet. 1997. 349: 1461-64.