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Kodolitsch et al. Clinical prediction of acute aortic dissection. Arch Int Med 2000;160:2977-2982.
• Consider the diagnosis in any patient with chest or back pain. Clues are unequal pulses/BPs, widened
mediastinum on CXR, and “tearing” quality of pain.
• Complications include MI, cardiac tamponade, acute aortic insufficiency, renal failure, limb ischemia.
• Aggressive BP control in the ICU with beta blocker and nitroprusside.
• Type A dissections require urgent surgery while most Type B dissections are treated medically.
Pathophysiology and nomenclature
• Layers of aorta: intima, media, adventitia
• Tear begins in the intima, allowing blood to
travel through a diseased medial layer. Blood
penetrates the medial layer and cleaves it in two,
forming a false lumen. Dissection extends along
the aortic wall, usually antegrade. The false
lumen can become distended and cause
narrowing of the true lumen thereby impairing
perfusion. The true and false lumens can
communicate in the case of multiple tears.
• Degeneration of medial layer is considered to be chief predisposing factor in nontraumatic
dissections. Classically seen in Marfan’s, Ehlers-Danlos. Less extensive medial necrosis seen in
autopsy of most dissections, thought to be due to longstanding hypertension and aging.
• Risk factors: hypertension (70% of cases), males (2:1 ratio), 6th to 7th decade. Also: Marfan’s
and Ehlers-Danlos, bicuspid aortic valve (7-14% of cases, a/w prox dissection), 3rd trimester of
pregnancy, trauma, IABP placement, cardiac surgery.
• Type A involve the ascending aorta (irrespective of origin of tear), Type B are distal to left
• Abrupt onset of tearing back or chest pain. Severity is at its maximum from the begin