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).


Diagnostic modalities:


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.