Aortic Dissection - case report and literature review

1. AORTIC DISSECTION:
TIME IS TICKING!!!
DR MISBAH
REGISTRAR EM ST4
QUEEN ELIZABETH HOSPITAL, WOOLWICH

2. OBJECTIVE
• Case presentation
• Risk Factors
• Clinical Presentation
• Dangerous outliers
• Diagnosis
• Classification
• Management

3. CASE PRESENTATION
• 60 yo lady Bluelight call
• c/o Central CP going to the back
• With SBP difference of 30 mmHg RUL >> LUL
• Hemodynamically stable
• Known to have Aortic Dilatation (4 cm)

4. INVESTIGATIONS
• ECG – unremarkable
• CXR – WNL
• Trop T Negative
• D-dimer Negative
• Bedside Echo – TAA = 4.02 cm (PLAX); no Dissection
in PLAX, SS, AAA

5. WHAT NEXT?
• CT-Aortogram – Unremarkable with TAA 4.3 cm

6. CONCERNS
• Mortality risk
• Repeated CT scans
• Cancer risk

7. THE TELEGRAPH 8:30AM BST 25 SEP 2010
• Cambridge historian dies after junior doctor misses
heart condition
• A Cambridge University historian died after a junior
doctor working his second shift mistook a fatal heart
condition for mild chest pains, an inquest heard.

8. RISK FACTORS
•Inherited disease (especially younger pts < 40 yrs)
•Marfan’s Syndrome, Ehlers-Danlos Syndrome, Turner
Syndrome, annulo-aortic ectasia and familial aortic
dissection.
•Aortic wall stress
•HTN (72%), previous cardiovascular surgery, bicuspid or
unicommisural aortic valve, aortic coarctation,
iatrogenic, infection (syphilis), arteritis such as
Takayasu’s or giant cell, aortic dilatation / aneurysm,
wall thinning, ‘crack’ cocaine or Ecstasy (abrupt
catecholamine-induced HTN).
•Reduced resistance aortic wall

9. CLINICAL PRESENTATION
• Severe or ‘worst ever’ (90%),
• abrupt (84-90%; LR+ 1.6, LR- 0.2),
• sharp (64%) or
• tearing (50%)
• retrosternal or inter-scapular pain,
• migrating (16%), down the back (46%),
• maximal at onset (not crescendo build up, as in an
AMI)

10. PAINLESS AORTIC DISSECTION
• Young J, Herd A M. Painless acute aortic dissection
and rupture presenting as syncope. J Emerg Med.
2002 Feb;22(2):171-4
• C Ayrik, H Cece, O Aslan, O Karcioglu, E Yilmaz.
Seeing the invisible: painless aortic dissection in the
emergency setting. Emerg Med J. 2006 Mar; 23(3):
e24. doi: 10.1136/emj.2004.021790

11. PAINLESS ACUTE AORTIC DISSECTION
• IMAMURA H et al. Circulation Journal Vol.75, January 2011
• 98 pts (53 Males, 45 Females; 66±12 yrs) w/ AAD admitted to hospital
from 2002 to 2007 (OHCA excluded)
• 16 pts (17%) Painless group & 82 pts Painful group
• 81% of the Painless group & 70% of the Painful group - type A
dissection
• Painless group more frequently had a persistent disturbance of
consciousness (44% vs. 6%, P<0.001), syncope (25% vs. 1%, P<0.001) &
NFD (19% vs. 2%, P=0.006) as PC.
• Cerebral ischemia (50% vs. 1%, P<0.001) & cardiac tamponade (38% vs.
13%, P=0.01) were more frequent complications in the Painless group.
• In-hospital mortality was not significantly different (19% vs. 15%).

12. COMPLICATIONS
• Aortic incompetence (32%), cardiac tamponade, myocardial
ischaemia (but only 2-5% of ECG’s mimick AMI + incidence
of AMI is 800 x that of aortic dissection!).
• Different BP >20 mmHg in arms, or missing pulse (15-30%;
LR+ 5.7).
• Pleural rub or effusion, haemothorax.
• Altered consciousness, syncope (13 %), hemiplegia (5%),
paraplegia. Abdominal pain (43% descending, 22%
ascending), intestinal ischaemia, bowel infarct.

13. DIAGNOSIS
• CXR
• Widened mediastinum (56-63%),
• abnormal aortic contour (48-71%),
• aortic knuckle double calcium sign >5mm (9-14%),
• pleural effusion (L>R; 16%),
• tracheal shift,
• left apical cap.
• ‘Normal’ in 11-16%.

14. DIAGNOSIS
• D-dimer
• Limited prospective data suggest D-dimer is useful
to risk stratify and ‘rule out’ if negative (< 0.1
µg/mL has NPV 100%; <500 ng/mL NPV 95% / LR-
0.07 in first 24 hours).
• Perhaps consider particularly if access to imaging is
limited (i.e. in rural / remote areas).
• Also may help ‘rule-in’ if >1600 ng/mL within the
first 6 hours (note: this was only in patients already
with a suspected dissection, NOT in all chest pain

15. DIAGNOSIS
• Echocardiography
• Transthoracic 75% diagnostic Type A (ascending),
40% descending (Type B).
• Transoesophageal (TOE). Much higher sensitivity
(97-99%) / specificity, though operator-dependent,
needs sedation / intubation, & is less readily
available. Useful in ICU / perioperative.

16. DIAGNOSIS
• CT-Aortography
• ‘Gold standard’,
• delineating aortic incompetence and branch vessel
involvement
• but in fact lacks sensitivity.

17. STANFORD CLASSIFICATION
• Type A: A affects ascending aorta and arch
• ~60% of AD
• Surgical Mx
• may result in:
• coronary artery occlusion - MI
• aortic incompetence - AR
• cardiac tamponade
• Type B: B begins beyond Brachiocephalic vessels
• ~40% of AD
• dissection commences distal to Lt Subclavian Artery
• Medical Mx w/ BP control

18. DEBAKEY CLASSIFICATION
• Type I: involves ascending & descending aorta (=
Stanford A)
• Type II: involves ascending aorta only (= Stanford A)
• Type III: involves descending aorta only, commencing
after the origin of Lt subclavian artery (= Stanford B)

19. MANAGEMENT
• Ascending Type A:
• Immediate BP control prior to transfer for OR using
IV beta blocker (propranolol, esmolol or labetalol)
+/- GTN as vasodilators aiming for SBP 100-120
mmHg, & surgery or endovascular stenting.
• Descending Type B:
• Medical control of BP with beta blockers, with
surgery or endovascular stent grafting for selected
pts with an unfavourable outlook.

20. REFERENCES
• www.lifeinthefastlane.com
• https://academic.oup.com/ehjcimaging/article/10/1/i31/2465
433/Echocardiography-in-the-emergency-assessment-of
• https://radiopaedia.org/articles/aortic-dissection
• www.aorticdissection.co.uk

21. THANK YOU