Aortic dissection
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
- Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome)
- Bicuspid aortic valve (e.g., in Turner syndrome)
Pathophysiology
Characteristic | Abdominal Aortic Aneurysm (AAA) | Aortic Dissection |
---|---|---|
Definition | Localized dilation of abdominal aorta >3cm | Tear in aortic wall creating false lumen |
Risk Factors | Smoking (most important), male, hypertension, age >65, family history | Hypertension (most important), Marfan syndrome, bicuspid valve, pregnancy |
Pathophysiology | Progressive weakening of arterial wall due to elastin degradation and inflammation; atherosclerosis leads to oxidative stress and matrix metalloproteinase activation | Intimal tear allows blood to enter media, creating false lumen; can be triggered by hypertensive crisis or inherited connective tissue disorders |
Onset | Gradual | Sudden, acute |
Pain | Usually asymptomatic; may have dull abdominal/back pain | Severe, tearing chest/back pain; migrating |
Physical Exam | Pulsatile abdominal mass | Unequal pulses, BP differences between arms |
Complications | Rupture with hemorrhagic shock | Organ ischemia, tamponade, aortic rupture |
Imaging | Ultrasound, CT with contrast | CT angiogram, TEE |
Treatment | Endovascular repair (EVAR) or open surgery if >5.5cm | Emergency surgery (Type A), medical management (Type B) |
Mortality | 80% if ruptured; 5% with elective repair | 50% at 48h without treatment (Type A) |
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) (1% to 5%)
- Aortic regurgitation (extension of the dissection into the aortic valve) (70%)
- Cardiac tamponade progressing to cardiogenic shock (30%)
- 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
- Arterial occlusion followed by ischemia of the: