Aortic dissection

• There are three layers to the aorta, the intima, media and adventitia. 
• With aortic dissection, blood enters between the intima and media layers of the aorta. A false lumen full of blood is formed within the wall of the aorta. 
• The right lateral area of the ascending aorta is the most common site of a tear of the intima layer, as this is under the most stress from blood exiting the heart
• The Stanford classification:

  • Type A: dissection involves the ascending aorta with or without involvement of the arch and descending aorta. Accounts for 60-70% of cases.
  • Type B (TBAD): Involves only the descending aorta (distal to the left subclavian artery) and/or abdominal aorta. Accounts for 30-40% of cases
• Aortic dissection shares the same risk factors as peripheral arterial disease, such as age, male sex, smoking, hypertension, poor diet, reduced physical activity and raised cholesterol. 
• Hypertension is a big risk factor. Dissection can be triggered by events that temporarily cause a dramatic increase in blood pressure, such as heavy weightlifting or the use of cocaine.
• Conditions or procedures that affect the aorta increase the risk of a dissection, such as:

  • Bicuspid aortic valve
  • Coarctation of the aorta
  • Aortic valve replacement
  • Coronary artery bypass graft (CABG)
• Conditions that affect the connective tissues can also increase the risk of a dissection, notably:

  • Ehlers-Danlos Syndrome
  • Marfan’s Syndrome
• Typical presentation:

  • Severe ripping or tearing chest pain
  • Pain may be in the chest when the ascending aorta is affected
  • Pain may be in the back if the descending aorta is affected
  • Pain may migrate over time
• Typical clinical findings in AAD include:3,7,9

  • Pulse deficit or asymmetric blood pressure readings: classically associated with type A aortic dissection (secondary to compression/occlusion of the left subclavian artery), but present in only 20% of cases.
  • Hypertension: very common and often extreme. Due to pre-existing hypertensive condition and/or increased sympathetic activation.
  • Hypotension: may be spurious due to branch vessel occlusion or be a sign of cardiac tamponade, aortic regurgitation, hypovolaemia (from aortic rupture), or neurogenic shock.
  • Tachycardia
  • Diastolic murmur: from aortic regurgitation.
  • Pulsus paradoxus, muffled heart sounds, or distended neck veins: suggesting cardiac tamponade.
  • Decreased breath sounds: haemothorax
• An ECG and chest x-ray are often used to exclude other causes (such as myocardial infarction), although they may be normal and falsely reassuring. 
• Relevant laboratory investigations include:

  • FBC, U&Es, LFTs, and coagulation screen
  • Arterial blood gas (including lactate): elevated lactate might indicate potential tissue ischaemia
  • Group and save and crossmatch (if concerns over bleeding)
  • Troponin: may be elevated if dissection causes myocardial ischaemia
  • D-dimer: a negative D-dimer indicates that dissection is very unlikely (however it is not sufficient to exclude aortic dissection).
• most patients will undergo an urgent CT angiogram (CTA) of the whole aorta
• Chest X-ray findings of AAD include:

  • Widened mediastinum (>8cm): classic finding, but only present in approximately 60% of cases
  • Double or irregular aortic contour: occurs in 50% of cases
  • Inward displacement of atherosclerotic calcification
  • Pleural effusion or haemothorax: indicative of dissection rupture
• initial management:

  • ABCDE - high flow oxygen, two wide-bore IV cannulas, continuous observations, invasive monitoring
  • Early senior support and discussion with vascular or cardiothoracic team
  • IV opiate analgesia
  • BP and HR control - IV beta blocker (labetalol)
  • Aim systolic BP 100-120
  • Aim HR 60-80
• Subsequent surgical management depends upon the classification of AAD:

  • Type A dissections require open surgery to prevent aortic rupture and generally carry a worse prognosis than Type B dissections.
  • Type B dissections (TBAD) are usually managed medically, with endovascular intervention indicated for complicated dissections
• Type B may be treated with thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the descending aorta. Complicated cases may require open surgery.
• Complications:

  • Myocardial infarction
  • Stroke
  • Paraplegia (motor or sensory impairment in the legs)
  • Cardiac tamponade 
  • Aortic valve regurgitation
  • Death
• Atypical presentations of acute aortic dissection related to end-organ malperfusion include:

  • Neurological deficits: such as syncope, seizure, limb paraesthesia or paraplegia
  • Limb pain and/or pallor: due to acute limb ischaemia
  • Flank pain and/or reduced urine output: due to renal artery involvement
  • Abdominal pain: due to compromised gut perfusion (e.g. mesenteric ischaemia)
• CT angiogram findings:

  • Double lumen (true and false lumens) thus confirming the diagnosis of AAD
  • The entry tear (where the dissection begins)
  • Any evidence of aortic dilatation (aneurysmal change)
  • Evidence of end-organ malperfusion (for example non-enhancing kidney)
  • Features of acute rupture (including extravasation of contrast or haemothorax)
• Transthoracic echocardiography (TTE) can be used to assess for suspected aortic dissection, but transoesophageal echocardiography (TOE) is more sensitive and specific
• Patients with uncomplicated TBAD are usually managed medically in the initial period, with close blood pressure control and adequate analgesia. Serial imaging with CTA is suggested to monitor for the development of any complications.
• Complicated TBAD is defined by the presence of any of the following complications: aortic rupture, impending rupture or rapidly expanding aortic diameter, malperfusion due to branch vessel occlusion or aortic lumen compression, ongoing pain, and refractory hypertension.
• Type A management:

  • open surgery
  • removal of the ascending aorta with or without the aortic arch and replacement with a synthetic graft.
  •  If the dissection has damaged the aortic valve, this will also require repair or replacement
• Aortic dissection can propagate longitudinally along the aorta either anterograde (towards the iliac arteries) and/or retrograde (back towards the aortic valve).

  Proximal dissections can progress to the aortic valve root and cause cardiac tamponade, acute aortic regurgitation, and/or aortic rupture.