Acute Aortic Dissection

OVERVIEW

• the most common catastrophe of the aorta (3:100,000); 3 times more common than abdominal aortic aneurysm (AAA) rupture
• aortic dissection is a type of acute aortic syndrome (AAS) characterized by blood entering the medial layer of the wall with the creation of a false lumen.
• AAS is a spectrum of life-threatening thoracic aortic pathologies including intramural haematoma, penetrating atherosclerotic ulcer, and aortic dissection.

CLASSIFICATION

• Stanford (most commonly used)

• Type A — Involves ascending aorta. Can extend distally ad infinitum. Surgery usually indicated.
• Type B — Involves aorta beyond left subclavian artery only. Often managed medically with BP control.
  • DeBakey

A car mechanic said argumentatively to his client, a cardiac surgeon: “So Doc, look at this work. I also take valves out, grind ’em, put in new parts, and when I finish this baby will purr like a kitten. So how come you get the big bucks, when you and me are doing basically the same work?”

The surgeon replied: “Try doing your work with the engine running.”  Michael DeBakey (1908–2008)

PATHOPHYSIOLOGY

• There are 3 possibilities as to how the blood enters the media:
  • Atherosclerotic ulcer leading to intimal tear
  • Disruption of vasa vasorum causing intramural haematoma
  • De novo intimal tear

HISTORY

• Chest pain is classically ripping or tearing in nature, that occurs suddenly and is maximal at onset – however, chest pain is not always present!
• retrosternal chest pain – anterior dissection
• interscapular pain – descending aorta
• severe pain (‘worst ever-pain’) (90%)
• sudden onset (90%)
• sharp (64%) or tearing (50%)
• migrating pain (16%)
• down the back (46%)
• maximal at onset (not crescendo build up, as in an AMI)

• Other features
  • end-organ symptoms: neurological, syncope, seizure, limb paraesthesias, pain or weakness, flank pain, SOB + haemoptysis
  • aortic regurgitation
  • hypertension
  • most have ischaemic heart disease

• Atypical presentations are common
  • consider the diagnosis of acute aortic dissection if there is a combination of chest/ back pain and new or evolving neurological deficit(s)

RISK FACTORS

• Inherited disease (especially younger patients < 40 yrs)
  • Marfan’s syndrome (fibrillin gene mutations)
  • Ehlers-Danlos syndrome type IV (collagen defects)
  • Turner syndrome
  • annulo- aortic ectasia
  • familial aortic dissection
• Aortic wall stress
  • Hypertension (72% (and other CV risk factors: smoker, lipids))
  • previous cardiovascular surgery
  • structural abnormalities (e.g. bicuspid or unicommisural aortic valve, aortic coarctation)
  • iatrogenic (e.g. recent cardiac catheterisation)
  • infection (syphilis)
  • arteritis such as Takayasu’s or giant cell
  • aortic dilatation / aneurysm
  • ‘crack’ cocaine (abrupt catecholamine-induced hypertension)
• Reduced resistance aortic wall: Increasing age

EXAMINATION

• aortic regurgitation is common
• hypertension (if hypotensive ensure it is not due to limb discrepancy caused by an occluded vessel – check BP in the arm with best radial pulse)
• shock – ominous signs: tamponade, hypovolaemia, vagal tone
• heart failure
• neurological deficits: limb weakness, paraesthesiae, Horners syndrome
• SVC syndrome – compression of SVC by aorta
• asymmetrical pulses (carotid, brachial, femoral)
• haemothorax

COMPLICATIONS

• Suspect if hypotensive (check for limb discrepancy!)
  • aortic rupture/regurgitation
  • acute myocardial infarction
  • cardiac tamponade
  • end-organ ischaemia (brain, limbs, spine, renal, gut, liver)
  • death

INVESTIGATIONS

• ECG
  • Normal. inferior ST elevation (right coronary dissection) but can be any STEMI (0.1% of STEMIs are dissections)
  • pericarditis changes, electrical alternans (tamponade)
• Laboratory
  • Cr elevation with renal artery involvement
  • tropnonin elevated if dissection causes myocardial ischaemia
  • D-dimer – if negative dissection is very unlikely, but not sufficient to rule out