Aortic Dissection
A life-threatening tear in the inner wall of the body's main artery (aorta), causing blood to split the artery layers apart, presenting as sudden, tearing chest pain.
Emergency Management: Administering thrombolytics (TPA) or aggressive antiplatelets for a presumed heart attack in a patient who actually has an aortic dissection is frequently fatal; CTA must rule out dissection if there is suspicion.
Aortic dissection is a catastrophic cardiovascular emergency characterized by a tear in the innermost layer of the aorta (intima). This allows high-pressure pulsatile blood to track into the media, separating the layers and creating a blood-filled false lumen that can occlude major branch vessels or rupture.
Detailed Overview
The condition is highly lethal. As the false lumen extends longitudinally along the aorta, it can compress or tear off branch arteries, causing ischemia to the brain, kidneys, spinal cord, or intestines. Dissections involving the ascending aorta (Stanford Type A) can quickly lead to death via retrograde extension causing aortic valve rupture, acute severe aortic regurgitation, coronary artery occlusion, or rupture into the pericardial space causing fatal cardiac tamponade. Stanford Type B involves only the descending aorta. The primary drivers are chronic hypertension and structural weakness of the aortic media (cystic medial necrosis).
Epidemiology & Demographics
Incidence is roughly 3 per 100,000 person-years. Most commonly affects men in their 60s and 70s. Younger patients are usually affected due to underlying connective tissue disorders.
Etiological Mechanism
The predominant underlying cause is chronic poorly controlled hypertension. Connective tissue disorders (Marfan syndrome, Ehlers-Danlos), bicuspid aortic valve, and prior aortic surgery are significant structural etiologies.
Primary Causes
Chronic Uncontrolled Hypertension (72% of cases)
Marfan Syndrome (fibrillin-1 mutation)
Bicuspid Aortic Valve
Iatrogenic (post-cardiac catheterization or CABG)
1. An initial intimal tear occurs, often at the right lateral wall of the ascending aorta where hydraulic shear stress is highest. 2. Systolic blood pressure forces blood into the diseased tunica media (cystic medial degeneration). 3. The pulsatile force creates and propagates a 'false lumen' alongside the 'true lumen'. 4. The expanding false lumen compresses the true lumen, creating malperfusion syndromes as branch arteries (e.g., renal, mesenteric, spinal) are occluded. 5. Retrograde dissection toward the heart can shear off the coronary arteries (causing STEMI) or rupture into the pericardium (tamponade). Antegrade dissection can rupture through the adventitia into the pleural cavity, causing exsanguination.
Diagnostic Criteria & Guidelines
Diagnosis is confirmed via imaging demonstrating an intimal flap separating two distinct lumens within the aorta.
1. Anti-impulse therapy: Immediate reduction of BP and heart rate to reduce aortic wall shear stress. Target heart rate < 60 bpm and systolic BP 100-120 mmHg. 2. IV Beta-blockers (Esmolol 500 mcg/kg bolus then 50 mcg/kg/min infusion, or Labetalol). 3. If BP remains high, add a vasodilator (Nitroprusside or Nicardipine infusion). 4. Adequate analgesia (Morphine) to decrease sympathetic tone.
Second-Line & Adjunctive Therapy
For Type B dissections with complications (malperfusion, rapid expansion, intractable pain): Thoracic Endovascular Aortic Repair (TEVAR) to stent the true lumen and seal the entry tear.
Surgical & Procedural Management
Stanford Type A is an absolute surgical emergency. Requires median sternotomy, cardiopulmonary bypass, excision of the intimal tear, and replacement of the ascending aorta with a synthetic Dacron graft (often combined with aortic valve replacement).
Patient Counseling & Advice
Type A survivors must understand they require lifelong imaging surveillance to monitor the residual false lumen in the descending aorta, which can form an aneurysm over time.
Follow-Up & Monitoring Schedule
Serial CT angiography at 1, 3, 6, and 12 months, then annually, to monitor for progressive aortic dilation or pseudoaneurysm formation.
Preventive Strategies
Strict management of hypertension. Prophylactic elective aortic root replacement in Marfan syndrome patients when the aortic root reaches 4.5 - 5.0 cm.
Untreated Type A has a mortality rate of 1-2% per hour for the first 48 hours. With surgery, operative mortality is 10-20%. Uncomplicated Type B treated medically has a 30-day mortality of roughly 10%.