- 50% of dissections occur in those aged < 60 years (especially if inherited component). Most common in 70s and 80s though.
- 65% occur in men
- Affected women tend to be older, with a lower BMI than affected men, and they are more likely to be diabetic
- Women with dissections are also less likely than men to be smokers, or to have a bicuspid aortic valve
- There’s an increased risk of dissection with larger aneurysms, root phenotype and longer ascending aortic length
- Dissection is twice as common in the winter months, and more common in the morning
- When the aorta dissects blood flows in 2 channels, including a false lumen (layers of aorta peel like an onion). This risks rupture and reduces blood flow to different organs
- The process of dissection can last minutes, hours or days as the tear propagates
- Type A (70%) – Involves ascending aorta. Usually needs surgery
- Type B (30%) – Involves aorta beyond subclavian (descending and posterior). Back pain suggestive. More often medical management
Outcomes
- Around 4000 cases a year in the UK (around 2500 die within 30 days)
- 50% mortality in first 48 hrs
- 50% of type A dissections die before they reach hospital
- In-hospital mortality is 22% of type A dissections and 14% for type B
- Survival rate after surgery is 80%
- More people die of aortic dissection than road traffic accidents
- Most die from tamponade or haemorrhage into the mediastinum
- 7% of out of hospital cardiac arrests thought to be due to aortic dissection
Associations
- 70% due to HTN or atherosclerosis
- 30% have inherited component
- Several important disease associations (all of which require echo surveillance)
- Marfan’s syndrome
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- 5% of all dissections. 0.02% of population have Marfan’s so it confers a significant risk
- Dissections can involve the aortic root, or descending and abdominal aorta (at diameters below usual surgical threshold)
- Often treated with betablockers or ARB to reduce rate of aortic dilatation
- Surgery indicated once aortic root >50mm (or >45mm with additional risk factors)
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- Bicuspid aortic valve
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- Affects 1% of the population, many don’t know their diagnosis
- Highly heritable but not monogenetic (genetic testing not indicated in isolated bicuspid valve)
- Dissection nearly 10x more common
- Surveillance by echo once aorta >40mm
- Consider surgery once aortic root >50mm when risk is around 10-fold higher (nearly 1% in the next 5 years)
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- Turners’ syndrome
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- 50% have cardiac involvement, including aortic dilatation, bicuspid aortic valve and coarctation
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- Noonan’s syndrome
- Vascular Ehlers-Danlos
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- Rare, due to pathogenic variants in COL3A1 gene
- Aortic dissection occurs in up to 10%
- Often treated with long term with celiprolol (vasodilating betablocker)
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- Loeys-diatz syndrome
- ACTA2-related heritable thoracic aortic disease
- Coarctation
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- Associated with bicuspid aortic valve as well as aneurysms, and can occur with Turners
- May present as uncontrolled HTN in a young person, with BP difference between the arms (HTN may persist after successful treatment)
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- Other
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- Aortitis (Bechet’s, Takayasu’s, GCA, syphilis, RA)
- Pregnancy (especially last trimester or postpartum)
- Extreme isometric exertion
- Cocaine
- Previous aortic surgery
- Iatrogenic (cardiac surgery)
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- Notes on genetic causes and screening
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- May be syndromic or non-syndromic
- A generation may be skipped if incomplete penetrance
- The number of genes linked to non-syndromic heritable thoracic aortic diseases (nsHTAD) is growing, including those rarely associated with extra-aortic features such as MYLK, ACTA2, MYH11, and PRKG1
- Refer patients for genetic screen if:
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- Aged < 60 and hx of thoracic aortic dissection
- Aged < 60, aortic dilatation and no hx of HTN
- Aortic dilatation with z score > 3
- Aortic dilatation or dissection, and syndromic features of Marfans, Loeys-Dietz, or vascular Ehlers Danlos
- Aortic dilatation or dissection, and family hx of thoracic aortic disease, peripheral/intracranial aneurysm or unexplained sudden death aged <40
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- Screening family members can involve an echo and genetic testing
- If a patient has thoracic aortic disease, and risk factors for an inherited cause, but no family history or pathogenic variant on genetic testing, family members should still be screened by echo
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Clinical features
- Severe sudden chest pain (maximal at onset) radiating to back
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- Ask about the quality, intensity at onset and radiation of pain. Ask all 3 and your chance of thinking about dissection increases dramatically
- Sudden, tearing pain has high specificity – worst severity is usually at onset
- Can be also described as sharp
- Radiates to the back in 30% (especially if dissection of the descending aorta)
- Can subside, and radiation is common (not having pain when seeing patient does not exclude diagnosis)
- Pain can vanish and recur in epigastrium or elsewhere (migrating pain occurs in 16%)
- ACS is around 150 times more common as a cause of chest pain however
- No pain at all in around 7%
- Chest pain with neurological signs is suggestive (including CVA, paraplegia, syncope).
- Often patients are vomiting, sweating and look sick
- Signs of malperfusion – may be transient neurology, peripheral circulation, MI (usually inferior), bowel ischaemia
- Occasionally abdo pain and hoarseness
- AKI and intestinal ischaemia can occur
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- Examination findings
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- Hypertension, but with asymmetrical pulses and BP – differences in BP useful, but far from confirmatory. 20% normal people have a difference if > 20mmHg.
- Shock – 15%
- Signs of aortic regurgitation (AR murmur not very helpful however)
- Signs of a pericardial effusion
- Focal neurology present in 17%
- Limb ischaemia
- Abdominal tenderness
- Worth checking old echos if diagnosis suspected – is there aortic root dilatation or a bicuspid valve?
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Diagnostic difficulties
- Around 40% don’t present in the typical way that gets picked up in the ED department
- Dissection is correctly picked up clinically in 30% of cases
- 33% are misdiagnosed – usually as ACS or PE, gastritis, musculoskeletal pain, anxiety
- Aortic pain, BP differential and abnormal CxR is present in only 27% but has a high specificity. 96% have one of these findings.
- In branch vessel occlusion symptoms can come and go – collapse, CVA like symptoms, ischemic limbs, ischaemic bowel.
- CT scan is the only reliable way to diagnose
- Some argue that rule out scoring systems probably no better than clinical acumen, however combining the aortic dissection detection risk score with a d-dimer is often used to rule out acute dissection
- Aortic Dissection Risk Score
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- Based upon medical history, pain features, examination findings
- If score 2 or more – proceed to CT aorta
- If score 0 or 1, do d-dimer, ECG to exclude STEMI, POCUS if available and CxR
- If d-dimer positive, or CxR/echo suggestive – CT aorta
- If d-dimer and CxR negative, can r/o dissection
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- Alternatively, some adopt a policy of scanning anyone with chest pain and at least one of:
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- A high-risk condition for dissection – Marfan’s, another associated CTD, aortic valve disease, family hx etc
- High risk pain features – Sudden onset, severe, tearing/ripping, radiating to back
- High risk clinical findings – Pulse deficit, BP differential >20 in both arms, neurology, AR murmur
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Investigations
- ECG can be normal, may see ST changes (especially inferior), or signs consistent with tamponade. Normal ECG in 22%. 0.1% of STEMIs are dissections.
- CxR
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- Probably only normal in 15%
- Widened mediastinum (>8cm on PA film, or about 60%)
- Abnormal aortic contour (50%), ring sign (displacement of aorta >5mm past calcified aortic intima) / calcium sign (in type B)
- Pleural effusion/haemothorax, or left apical opacification
- Deviation of trachea and left main bronchus
- Sensitivity 64%, specificity 86%
- Rules out other causes of chest pain, but if you suspect dissection you need a CT anyway
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- Echo
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- Sensitivity around 90% for diagnosing type A and 40% of type B (may see AR and dilated aortic root, pericardial effusion, dissection flap).
- TOE more sensitive (99%)
- Can identify complications eg AR, tamponade, RWMA
- POC echo might be faster than CT
- TOE can be used in unstable patients who cannot go to CT
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- CT aorta
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- Best test (sensitivity 100%, specificity 98%)
- Best to do gated with ECG synchronisation (prevents motion artefacts which can resemble dissection flaps)
- The non-contrast part of scan is useful to assess for intramural haematoma
- Shows a dissection flap (the ‘tennis ball’ sign) due to appearance of the smaller true and larger false lumen
- In some centres, 3% of CT aorta’s positive for dissection, and 42% pick up other pathologies (in comparison: diagnostic yield of CTPA for PE is 5-30%, and for CT head for neurosurgical lesion is 3%)
- Sometimes advised to do CT neck to pelvis to check extension and complications
- If PE and ACS in differential – can ask for a triple rule out CT
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- Bloods
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- D-Dimer often raised (but if normal does not exclude it)
- Trop can be up
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Management
- Control BP tightly – aim systolic< 120
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- Try IV labetolol first (short half-life), also hydralazine or sodium nitroprusside
- In cases of malperfusion (eg to spine or brain) may tolerate higher BP
- Early arterial line
- Analgesia will also bring down BP – give morphine
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- Aim HR < 60
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- Can use betablockers, or if contraindicated can use IV non-dihydropyridine CCBs
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- Crash blood
- Correct coagulopathy
- Cardiothoracic opinion
- Type A – surgery (or consider palliation if not a candidate. Age should not preclude surgery)
- Type B
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- Surgery if complicated type B dissection (50%) ie. ongoing pain > 12 hrs, limb ischaemia, refractory HTN, progressive aortic enlargement, extending dissection.
- TEVAR vs open repair depending on anatomy
- If uncomplicated but ‘high-risk feature’, and favourable TEVAR anatomy, and life expectancy > 5 years – TEVAR best
- ‘High risk features’ include various radiological criteria (check ESC guidelines), or reappearance of pain/symptoms
- All others (eg low risk and uncomplicated type B dissections, or unfavourable TEVAR anatomy) – treat medically, and do surveillance
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- Chronic type B dissection (ie 3 months after onset of symptoms)
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- Consider intervention if rapid expansion, malperfusion, rupture, descending aorta >60mm
- Control BP
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- In pregnancy
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- Type A – Deliver infant if viable first, then repair aorta
- Uncomplicated type B – conservative medical treatment
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Complications
- Circulatory collapse and death
- Shock could be cardiogenic or hypovolaemic (mortality >50% if present)
- Pericardial tamponade
- Malperfusion – to brain, limbs, gut, kidneys, coronaries (MI). This should be seen as an indication to intervene, not a contraindication
Follow up
- Long term survival good if survives surgery
- Get annual scans afterwards with tight BP control. Avoid isometric / very strenuous exercise.
- Genetic screen if aged < 55 (their 1st degree relatives too)
- For TEVAR, frequent imaging advised (1, 6, 12 months, then annually for first 5 years)
- Medically treated type B dissections also require frequent f/u imaging