Dr. Ben-Zur, Encino, California

Aortic Dissection

What is it?

– life-threatening condition where blood from the vessel lumen passes through a tear in the intima, into the medial layer of the artery and spreads along the artery

Source: http://www.emdocs.net/core-em-aortic-dissection/

Predisposing Factors:

= any condition that interferes with normal integrity of elastic or muscular components of the medial layer

– Long standing systemic HTN (70%+ of pts)

– cocaine use

– trauma

– connective tissue disease: Marfan, Ehlers-Danlos

– bicuspid aortic valve

– coarctation of the aorta

– 3rd trimester of pregnancy

Demographics:

– more common in men in their 60s and 70s

Classification system

DeBakey anatomic classification: based on site of origin
- type 1 originates in the ascending aorta and propagates to at least the aortic arch
- type 2 originates in the ascending aorta and is confined to the ascending aorta
- type 3 originates in the descending aorta and extends distally or proximally
Stanford anatomic classification
- Type A: involves the ascending aorta (regardless of the site of the primary intimal tear)
  - Type A is more common
  - Right lateral wall is the most common site of aortic dissection
- Type B: descending aorta, all other dissections that do not include the ascending aorta

source:http://www.medbullets.com/step2-3-cardiovascular/20030/aortic-dissection

Most common sites of Dissection:

– ascending thoracic aorta : 65%

– descending thoracic aorta: 20%

– Aortic arch: 10%

– abdominal aorta: 5%

How might a patient present?

Symptoms:

Single most common presenting complaint: sudden onset of sharp pain

– “tearing, ripping” quality (only about 50% have this classic finding)

– Location: anterior chest (type A)

– between the scapula (type B)

– other symptoms relate to the complications that can occur

Signs:

– pulse, bp asymmetry between limbs (15%)

– aortic regurgitation (31%)

– neuro manifestations due to obstruction of carotid artery

– can be hypertensive (49%), normotensive (33%), or hypotensive (18%)

Diagnosis:

– CXR: widened mediastinum (>8mm on AP) – present in 62%

Source: https://www.justintimemedicine.com/CurriculumContent.aspx?NodeID=630#&gid=1&pid=3

– TEE is very specific and sensitive

– CT, MRI

A+B: TEE

C+D: CT

A+ C = acute

B+D = follow up

–> intimal flap forming a true lumen + dilated false lumen

– aortic angiography can determine extent of the dissection for surgery

Treatment:

–> Goal of treatment: stop the progression of the dissecting channel

– immediate medical management: B-blockers (decreases the force of LV contraction, minimizes aortic wall shear stress)

Ex: labetalol, esmolol, propranolol

– IV sodium nitroprusside: rapidly reduce blood pressure –> lower systolic below 120

Type A is most often a surgical emergency: early surgical correction improves outcomes compared to medical therapy alone (early surgery does not improve outcomes in pt’s with type B unless the dissection is propagating, compromises the major branches of the aorta, impending rupture, continued pain)

Surgery: repair the intimal tear, suturing edges of the false lumen, insert a synthetic aortic graft if needed

Why so serious?

Mortality: 25-30%

Causes of death from aortic dissection:

–> rupture of the dissection into pericardium:

– cardiac tamponade

– acute dissection into the aortic valvular annulus (disrupts aortic valve suppor) –> severe aortic regurgitation

– obstruction of the coronary artery ostia (where the left and right mail coronary arteries exit the ascending aorta just above the aortic valve) –> MI

– end organ failure due to aortic branch vessel obstruction

– rupture through the adventitia anywhere along the aorta (often into the left pleural space or pericardium)

– occlusion of major branches of aorta can also cause MI: propagating hematoma compresses the lumen

– stroke from carotid artery involvement

– visceral ischemia, renal failure

Mechanism of Aortic Dissection

–> Tear in the aortic intima

Source: http://www.iradonline.org/about.html

– if non-traumatic, it’s thought that degeneration of the aortic media or cystic medial necrosis (smooth muscle cell necrosis and apoptosis and by degeneration of elastic fibers within the media of the aortic wall. Cystic spaces form in these areas of degeneration) is a prerequisite for the development of nontraumatic aortic dissection

Source: http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/diseases-of-the-aorta/