Pathophysiology
Aortic dissection occurs when the there is a rupture in the tunica intima layer, allowing blood foto flow in between it and the tunica media, creating what we call a false lumen.
Acute dissection occurs when diagnosed <14 days and chronic dissection when >14 days.
Peak onset for aortic dissection is 50-70 years old.
⚠️ Risk factors
- Male gender
- Bicuspid aortic valve
- Hypertension and atherosclerosis - especially in older cases
- Connective tissue disorders - especially in younger cases
- Increasing age
- Syphilis
- Pregnancy
- Turner’s syndrome (XO) and Noonan’s syndrome
🔢 Classification
We have 2 types of classification:
- Stanford classification
- DeBakey classification
Stanford classification
2 types: type A and type B.
- Type A - affects ascending aorta and may propagate towards the aortic arch and descending aorta.
- Type B - no ascending aorta involvement at all, only aortic arch and/or descending aorta.
3 types: type I, II and III.
DeBakey classification
- Type I - originates in the ascending aorta and propagates to the aortic arch at least.
- Type II - ascending aorta only.
- Type III - distal to subclavian artery in the descending aorta.
- Extends to diaphragm
- Extends beyond diaphragm into abdominal aorta
😷 Presentation
- ⭐️ Tearing chest pain - that may radiate to the back.
Chest pain is more common in type A dissection. Upper back pain is more common type B dissection.
Signs include:
- Absent/weak carotid, brachial, or femoral pulse. There may be variation in the arm pulses.
- Aortic regurgitation murmur - as blood flows back during diastole. This is accentuated with the handgrip manoeuvre in which one clenches their fist forcefully until they fatigue. The murmur duration directly correlates with severity.
- Tachycardia
- Hypotension (2º to hypovolaemia)
- ST elevation may be seen in the inferior leads (II, III and aVF) but the majority have no ECG signs
The best location to listen to the murmur is at the left parasternal region between the 2nd and 4th ICS. This is where stream of blood may be regurgitating into the left ventricle.
- Coronary arteries → angina
- Spinal arteries → paraplegia
- Distal aorta → lower limb ischaemia
They may also show signs of hypoperfusion: reduced urine output, lower limb ischaemia, abdominal pain (2º to ischaemia).
📝 Differential diagnosis
- MI - but is typically a crushing chest pain with ECG changes
- PE - dyspnoea will be prominent
- Pericarditis - more pleuritic chest pain.
- MSK back pain - no systemic signs and tenderness upon palpation
🔍 Investigations
- Bloods (FBC, U&Es, LFTs, troponin, coagulation, crossmatch of at least 4 units)
- ABG
- ECG to exclude cardiac pathology. ST changes may be seen in the absence of MI.
🧰 Management
Our initial approach is similar to AAA rupture:
- High flow oxygen
- 2 x large bore IV cannulae
Stanford Type B can be managed medically (gold standard) through treatment of hypertension:
→ 🥇 IV labetalol is 1st line → 🥈 CCBs are 2nd line We aim to rapidly reduce the systolic pressure and pulse rate to minimise propagation of the dissection. For type B, only certain complications will warrant surgical repair: rupture, renal, visceral or limb ischaemia, uncontrollable hypertension, refractory pain.
🚨 Complications
- Aortic rupture
- Aortic regurgitation
- Cardiac tamponade
- MI - 2º to coronary artery dissection
- Stroke - 2º to cerebral artery dissection
- Paraplegia - 2º to spinal artery dissection