Epidemiology
Etiology
Acquired
Hypertension (most common risk factor) Trauma, e.g., deceleration injury in a motor vehicle collision, or iatrogenic injury during valve replacements or graft surgery (traumatic aortic dissection)
Vasculitis with aortic involvement (e.g., syphilis, Takayasu arteritis)
Congenital
Pathophysiology
Clinical features
Diagnostics
Pathology
Cystic medial degeneration: a degeneration (necrosis) of large blood vessels such as the aorta.
Seen in disorders that cause increased arterial wall stress (e.g., hypertension, coarctation of the aorta ) as well as connective tissue disorders (especially Ehlers-Danlos syndrome and Marfan syndrome )
Can lead to aortic aneurysm and aortic dissection
Histopathology
Loss, thinning, disorganization, and fragmentation of elastic tissue in the media
Accumulation of mucoid extracellular matrix
Loss of smooth muscle nuclei
Treatment
Complications
Aortic rupture and acute blood loss: acute back and flank pain (tearing pain), symptoms of shock → indication for emergency surgery
Complications of Stanford type A dissections
Myocardial infarction (coronary artery occlusion) Aortic regurgitation (extension of the dissection into the aortic valve) Cardiac tamponade progressing to cardiogenic shock
Stroke (extension of the dissection into the carotids)
Complications of both Stanford type A dissection and Stanford type B dissections
Arterial occlusion followed by ischemia of the:
Celiac trunk, superior/inferior mesenteric artery → acute abdomen, ischemic colitis
Renal arteries → acute renal failure (oliguria, anuria)
Spinal arteries → weakness of lower extremities or acute paraplegia
