Acute Aortic Dissection
OVERVIEW
the most common catastrophe of the aorta (3:100,000); 3 times more common than abdominal aortic aneurysm (AAA) rupture
aortic dissection is a type of acute aortic syndrome (AAS) characterized by blood entering the medial layer of the wall with the creation of a false lumen.
AAS is a spectrum of life-threatening thoracic aortic pathologies including intramural haematoma, penetrating atherosclerotic ulcer, and aortic dissection.
CLASSIFICATION
Stanford (most commonly used)
Type A — Involves ascending aorta. Can extend distally ad infinitum. Surgery usually indicated.
Type B — Involves aorta beyond left subclavian artery only. Often managed medically with BP control.
DeBakey
entire aorta affected
confined to the ascending aorta
descending aorta affected distal to subclavian artery
Svensson (defines type of acute aortic syndrome)
classic dissection with true and false lumen
intramural haematoma or haemorrhage
subtle dissection without haematoma
atherosclerotic penetrating ulcer
iatrogenic or traumatic dissection
PATHOPHYSIOLOGY
There are 3 possibilities as to how the blood enters the media:
Atherosclerotic ulcer leading to intimal tear
Disruption of vasa vasorum causing intramural haematoma
De novo intimal tear
Following dissection, blood flow into the media may cause:
extension up or down
rupture
vessel branch occlusion
aortic regurgitation
pericardial effusion / tamponade
HISTORY
Chest pain is classically ripping or tearing in nature, that occurs suddenly and is maximal at onset – however, chest pain is not always present!
retrosternal chest pain – anterior dissection
interscapular pain – descending aorta
severe pain (‘worst ever-pain’) (90%)
sudden onset (90%)
sharp (64%) or tearing (50%)
migrating pain (16%)
down the back (46%)
maximal at onset (not crescendo build up, as in an AMI)
Other features
end-organ symptoms: neurological, syncope, seizure, limb paraesthesias, pain or weakness, flank pain, SOB + haemoptysis
aortic regurgitation
hypertension
most have ischaemic heart disease
Atypical presentations are common
consider the diagnosis of acute aortic dissection if there is a combination of chest/ back pain and new or evolving neurological deficit(s)
RISK FACTORS
Inherited disease (especially younger patients < 40 yrs)
Marfan’s syndrome (fibrillin gene mutations)
Ehlers-Danlos syndrome type IV (collagen defects)
Turner syndrome
annulo- aortic ectasia
familial aortic dissection
Aortic wall stress
Hypertension (72% (and other CV risk factors: smoker, lipids))
previous cardiovascular surgery
structural abnormalities (e.g. bicuspid or unicommisural aortic valve, aortic coarctation)
iatrogenic (e.g. recent cardiac catheterisation)
infection (syphilis)
arteritis such as Takayasu’s or giant cell
aortic dilatation / aneurysm
wall thinning
‘crack’ cocaine (abrupt catecholamine-induced hypertension)
Reduced resistance aortic wall
Increasing age
pregnancy (debatable)
EXAMINATION
Features include:
aortic regurgitation is common
hypertension (if hypotensive ensure it is not due to limb discrepancy caused by an occluded vessel – check BP in the arm with best radial pulse)
shock – ominous signs: tamponade, hypovolaemia, vagal tone
heart failure
neurological deficits: limb weakness, paraesthesiae, Horners syndrome
SVC syndrome – compression of SVC by aorta
asymmetrical pulses (carotid, brachial, femoral)
haemothorax
COMPLICATIONS
Suspect if hypotensive (check for limb discrepancy!)
aortic rupture
aortic regurgitation
acute myocardial infarction
cardiac tamponade
end-organ ischaemia (brain, limbs, spine, renal, gut, liver)
death
INVESTIGATIONS
Bedside
ECG normal
inferior ST elevation (right coronary dissection) but can be any STEMI (0.1% of STEMIs are dissections)
pericarditis changes, electrical alternans (tamponade)
Laboratory
leukocytosis
Cr elevation with renal artery involvement
tropnonin elevated if dissection causes myocardial ischaemia
D-dimer – if negative dissection is very unlikely, but not sufficient to rule out
Cross-match
Various biomarkers being investigated (e.g. elastin fragments, d-dimer, smooth muscle myosin heavy-chain protein)
Imaging
CXR Widened mediastinum (56-63%), abnormal aortic contour (48%), aortic knuckle double calcium sign >5mm (14%), pleural effusion (L>R), tracheal shift, left apical cap, deviated NGT. ‘Normal’ in 11-16%.
Echocardiography Transthoracic 75% diagnostic Type A (ascending), 40% descending (Type B)
can identify complications (e.g. aortic regurgitation, regional wall abnormalities in cardiac ischaemia, cardiac tamponade)
Transoesophageal (TOE) Much higher sensitivity/specificity, though operator-dependent, need sedation, and is less available
Useful in ICU / perioperative
Upper ascending aorta and arch not well visualised
Helical CT Useful screen for widened mediastinum. Newer multiplane/slice scanners may now negate additional need for TOE or aortography to plan operative management.
Aortography – Was the traditional gold standard, delineating aortic incompetence and associated branch vessel involvement as well.
MRI / MRA – Excellent sensitivity and specificity limited by availability.
MANAGEMENT
Emergent priorities
control BP
control bleeding
fluid resuscitation
O2
wide bore IV access (Swan sheath)
invasive monitoring
warn blood bank (x-match 6U + need for other products)
correct coagulopathy
control HR and BP (aim for P 60-80 and BP 100-120 SBP)
IV beta blocker (propranolol, esmolol or labetalol) combined with vasodilators (e.g. GTN, labetalol, SNP)
start b-blocker first to avoid increased aortic wall stress from reflex tachycardia
call cardiothoracic surgeon
Indications for surgery
Persistent pain
Type A
Branch Occlusion
Leak
Continued extension despite optimal medical management
Intra-operative management
avoid hypertension on induction
fast, full and forward
dissection and clamps may interfere with arterial monitoring
TXA2
femoral arterial cannulation used for bypass
anticoagulate before bypass
if aortic root involved then patient may need AVR with coronary artery reimplantation
monitor BP after bypass closely
may have dissected into other organs (monitor function)
Circulatory Arrest
deep hypothermic arrest (DHA) required during arch surgery as it isn’t possible to perfuse cerebral vessels on bypass
safe duration = 45min @ 18 C
other ways of protecting brain; pack head with ice, thiopentone, methylprednisonlone mannitol, GTN (to prevent vasoconstriction)
POCD proportional to DHA time
once circulation arrested -> all infusion and pumps stopped
when warming do not set FAW to >10 C (prevents burns), start propofol and fix coagulopathy with products
Standard post-operative care
References and Links
LITFL
CT scan 006 –
Cardiovascular Curveball 008 —
Trauma Tribulation 034 —
Journal articles and textbooks
Diercks DB et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients With Suspected Acute Nontraumatic Thoracic Aortic Dissection. Annals of Emergency Medicine. 65(1):32–42.e12. PMID
Golledge J, Eagle KA. Acute aortic dissection. Lancet. 2008 Jul 5;372(9632):55-66. Review. PubMed PMID:
.
Holloway BJ, Rosewarne D, Jones RG. Imaging of thoracic aortic disease. Br J Radiol. 2011 Dec;84 Spec No 3:S338-54. doi: 10.1259/bjr/30655825. Review. PubMed PMID:
; PubMed Central PMCID:
.
Lentini S, Perrotta S. Aortic dissection with concomitant acute myocardial infarction: From diagnosis to management. J Emerg Trauma Shock [serial online] 2011 [cited 2013 Apr 21];4:273-8. Available from:
http://www.onlinejets.org/text.asp?2011/4/2/273/82221
Upadhye S, Schiff K. Acute aortic dissection in the emergency department: diagnostic challenges and evidence-based management. Emerg Med Clin North Am. 2012 May;30(2):307-27, viii. Review. PubMed PMID:
.
FOAM and web resources
ALIEM —
Paucis Verbis: International Registry on Aortic Dissection (IRAD)
International registry of Acute Aortic Dissection
EMCrit Podcast 91 –
Treatment of Aortic Dissection
EMLON —
How Do We Miss Aortic Dissection?
EM Updates —
ACC/AHA Aortic Dissection Guideline
NNT —
Radiopaedia —
Critical Care
Compendium
Chris is an Intensivist and ECMO specialist at The Alfred ICU, where he is Deputy Director (Education). He is a Clinical Adjunct Associate Professor at Monash University, the Lead for the
programme, and a CICM First Part Examiner.
He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. He was one of the founders of the
movement (Free Open-Access Medical education)has been recognised for his contributions to education with awards from ANZICS, ANZAHPE, and ACEM.
His one great achievement is being the father of three amazing children.
On Bluesky, he is
and on the site that Elon has screwed up, he is
.
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