Aortic dissection
Epidemiology
Risk factors
Pathophysiology
5-10 per million per year; 2-3x more common than ruptured AAA; 90% fatal within 3/12; 28% fatal in 24hrs; 25%
in hospital mortality; patients who are misdiagnosed and receive thrombolysis have 2x mortality; 65% in males;
86% deaths due to rupture; 70% ruptures occur into pericardial sac
HTN (in 70-90%); atherosclerosis; CT disorders (in younger patients eg. Marfans, Ehlers Danlos); coarctation;
congenital AV disease (eg. AS); prev cardiac OT; arteritis; syphilis; pregnancy; cocaine; GCA
Debakey:
I: ALL begins in ascending and extends into/beyond
arch
II: TOP begins in and limited to ascending
III: BOTTOM descending/distal only
a = stops before diaphragm
b = extends beyond diaphragm
Stanford:
A: involves prox aorta +/- distal aorta; 60-70%
B: BOTTOM involves distal aorta only; 30%
Distal = distal to L subclavian artery
Tear in intimal lining  haemorrhage into false lumen  double lumen aorta
50-65% begin at ascending aorta (within a few cm)
30-35% at arch (at insertion of ligamentum arteriosum)
20% distal
Most re-enter aorta just above bifurcation
Prognosis
Assessment
Investigation
Intramural haematoma: 5-20% cases; haemorrhage in wall but no intimal tear/flap (so no flow on echo, no
contrast enhancement on CT); likely due to bleed from vaso vasorum; can rupture into lumen to create typical
dissection
Penetrating atherosclerotic ulcer: worse outcome; small ruptures of atherosclerotic plaques  penetrate media;
needs early surgical graft
Stanford A: 56-87% 5yr survival with OT
Stanford B: 80% surivival with medical trt; 90% 30/7 survival with aggressive BP mng, 55% 10yr survival
Worse prognosis if: old, tamponade, pleural effusion, ECG changes, anticoagulated
95% pain (75% CP, 50% back pain, 30% AP); 85% sudden onset; max at onset; 65% sharp; 50% tearing/radiation;
10% syncope; 5-15% FND
CP more common in A than B (80% vs 63%); BP more common in B that A (65% vs 47%)
OE: physical signs in <1/3 patients; hypotension in 18%; SBP >150 in 50% (in 35% A, 70% B); <40% have unequal
pulses; BP discrepancy >20mmHg between 2 arms significant (difference of >15 seen in 40-50%); BP discrepancy
between arms and legs; radio-femoral delay; 30% aortic regurg (A>B); LVF; S3 and Austin Flint murmur; pericardial
tamponade in 25% type A; 3% CVA; 3% paraplegia; 16% limb ischaemia
CXR: 81% sens, 85% spec; 90% have an abnormality; 60% widened mediastinum (>8cm at carina; >25%
chest width; 65% sens); 45-50% abnormal aortic contour (blurred aortic knob 70% sens); disparity between size of
descending and ascending aorta (30-60%); double density aorta; separation of aortic intimal calcification by >1cm
(10% sens); cardiomegaly 20%; L pleural effusion 15%; apical capping; loss of aorto-pul window; R tracheal /NG
deviation; depression of L main bronchus; 10% completely normal
ECG: 30% normal; 25% suggestive of ACS (<5% have STE that would be thrombolysed); 41% non-specific T / ST
changes; LVH
D-dimer: 97% sens, 50% spec; may have false –ive with intramural haemorrhage; not safe to use as sole screening
tool
SM myosin heavy chain: 90-97% sens at 12hrs
CT angiography: sens 83-90%, spec 90-100%; shows flap, displacement of calcification, delayed contrast
enhancement of false lumen; need spiral – conventional doesn’t have adequate sens
Pros: quick, readily available; can assess for pleural / pericardial effusion; helical as accurate at TOE and MRI
Cons: can’t look for AR; less accurate than TOE (but equivalent survival);
contrast
TOE: sens 95-100%, spec 70-95%; shows double lumen, flow patterns, intimal tears
Pros: very sens for prox aorta, AR, pericardium, LV, CA’s; can be done at bedside in critically ill
Cons: less sens for distal; CI if oesophageal pathology; operator dependent
Complications
Mng
Angiography: 80-90% sens, 94% spec; can also assess branches and aortic incompetence; requires contrast;
not suitable as only Ix; GOLD STANDARD
TTE: A = sens 78-100%; B = sens 30-55%; spec 63-96%; very poor for distal; OK for prox etc.. as above; limited role
MRI: 100% sens and spec; usually too unstable, not readily available, slow
Dissection (eg. CA (7%, esp R CA), spinal, carotids, mesenteric, limb, renal); rupture (haemothorax, sudden death),
AR (30%), haemopericardium and tamponade (25%), aneurysm, CVA (3%), acute limb ischaemia (16%)
Medical Mng: aim
blockers
1.
SBP 100-110 (aim SBP 90 in AAA) without incr HR; will need life long beta-
Labetalol: 10mg IV bolus  rpt Q10mins to max 300mg
Esmolol: 500mcg/kg over 1min  rpt Q5mins  50mcg/kg/min titrated to effect (max 200mcg/kg/min)
Metoprolol: 5mg IV boluses  2-5mg/hr
Use Ca channel blocker if beta-blocker CI’ed
2.
Nitroprusside: 0.25-10mcg/kg/min; risk of cyanide toxicity; always use with beta-blockers as
3.
risk of reflex incr HR due to vasoD
GTN: 5-20mcg/min (5-50) titrate up every 5-10mins to max 300; always use with beta-blockers as risk
of reflex incr HR due to vasoD
Surgical Mng: in prox dissection; in distal dissection if significant AR / tamponade / leaking / major vessel involved
/ spreading dissection / ischaemic compromise of vital organs / intractable pain or HTN / aortic dilation >5cm /
Marfan syndrome; moving towards using percutaenous mng; operative mortality 5-20%
Notes from: Dunn, Cameron, TinTin