Synopsis
Recognise aortic dissection, intramural haematoma and penetrating aortic ulcer early; obtain definitive imaging; begin safe anti-impulse therapy and trigger immediate aortic-team treatment.
- Acute aortic syndromes comprise classic dissection, intramural haematoma and penetrating atherosclerotic ulcer; each may rupture or cause branch-vessel malperfusion.
- Stanford type A involves the ascending aorta; type B does not. The classification predicts the immediate treatment pathway.
- Think of AAS when severe chest, back or abdominal pain is abrupt and maximal at onset, especially with a pulse/BP deficit, focal neurology, syncope, shock or new aortic regurgitation.
- Normal ECG, chest radiograph, troponin or D-dimer does not safely exclude AAS when clinical probability is high.
- Preferred definitive imaging is ECG-gated CTA from neck to pelvis to define the entry tear, full extent, rupture and coronary, cerebral, visceral, renal or limb malperfusion.
- Begin analgesia and anti-impulse therapy in a monitored setting: typical goals are heart rate 60/min or lower and systolic BP below 120 mmHg, or the lowest pressure that maintains organ perfusion.
- Control heart rate with an IV beta-blocker before adding a vasodilator; vasodilation alone may provoke reflex tachycardia and increase aortic shear.
- Type A AAS requires emergency surgical assessment. Complicated type B disease generally requires urgent endovascular repair when anatomy permits; uncomplicated type B begins with optimal medical therapy and close surveillance.
- Survivors need lifelong BP control and aortic imaging, commonly at 1, 6 and 12 months and then annually if stable.