A tale of 2 dissections…

Thoracic dissection is a diagnostic challenge to say the least.  Coming from a relatively CT-frugal ED background, it’s not normally in many nature to order CTA’s in people who have pain ‘going through to their back’.  Mostly because I’d order about 9 million a day (that may be a slight overestimate).  However I had a ‘remember that lady’ moment a few months ago from a very good friend on the MAU team.  This good friend is a very able colleague (certainly smarter than me), told me about a case he missed, a case I sent him.  His choice of words was interesting because he didn’t imply I had missed it too (though I feel I had).

It was busy, I was the boss on overnight.  I was trying to make some room in my department, so I was trying to ‘improve flow’ now I don’t care how perfect a doctor you are; we all do this.  In about 30 minutes I’d sent a non-toxic OD’s to the mental health team, and someone with flu home.  Then I went to see this delightful, charming 89 year old lady, who had some chest pain, unfortunately about 3 minutes into the consultation I was grabbed to go and calm down a drunk fat girl with a personality disorder and a cut foot, who had been ‘disrespected’ by the security staff.  I sewed up her ankle while she simulated oral sex on the handle of bay operating light.

After finishing that I went back to my 89 year old.  She had developed chest pain whilst walking up some stairs, the pain had lasted maybe a minute, she told me she nearly blacked out.  The family called her an ambulance.  I noticed from ambulance sheet, her initial BP was 60/40, but it had rapidly improved to a ‘normal figure’ 145/80 while she was with us.  She’d had vasovagals before she told me, and apart from treatment for hypertension, and IHD.  ECG –  flattened lateral T’s, nothing exciting.  The CXR, showed a widened mediastinum, which I noticed, I then looked back at her old CXRs, and I saw one from a month ago that ‘looked the same’ (she had a widened ectatic, unfolded aorta).  So off she went to medicine for a 12 hour troponin, and someone to stop her bendroflumethiazide.  My friend clerked her in, and did the same.  All the way through this she was pain free, and her obs were totally unremarkable.


A CXR with a widened ectatic thoracic aorta.
A CXR with a widened ectatic thoracic aorta. (this is not her CXR, but is close enough for the purposes of this case)

The CXR was reported that morning as showing a widened mediastinum, the medical team arranged urgent CTA and a large type B dissection was noted on the scan.  She went for interventional radiology EVAR, her aorta was perforated, and she died in ICU later that day.

Now I find out about this through my friend, on the grapevine.  The patient was the subject of an M+M meeting which I didn’t attend (as in my current institution we keep the ED M+M and Medicine M+M separate).  I felt awful about this, I’d missed the diagnosis, my colleague had missed the diagnosis, and had we managed to pick it up would she have survived?  It’s difficult to say.  There is evidence that suggests for every hour a diagnosis of AAD is missed the mortality goes up by 1%, however the mainstay of treatment in this group is aggressive BP control, and her BP was normal to low.  Her history was not pathognomonic for AAD, straining at stool (like King George II), chest pain radiating through to back, but I had the CXR which was also abnormal, but not normally abnormal.

On reflection, I made at least 2 cognitive errors; Attribution bias (I saw her old CXR, which showed an ectatic aorta, and I felt her current CXR showed a continuation of that process); and confirmation bias – I felt that the St John low BP finding confirmed my thought that she had had a vasovagal or angina from exertion, neglecting to fit this in with the pain that she very well described to me.

The second case occurred on a busy Saturday evening a few weeks later.  I had picked up a card for a 29 year old gentleman in our monitored bay that said “Leg pain”.  I started looking through his old clinic letters, and scans (a wonderful byproduct of where I work’s beautifully integrated IT system), and I found that he was being treated for idiopathic hypertension.  This letter from a renal physician commented on a normal MRI of renal arteries, drilling down to that report referenced an MRI of his heart which showed a dilated aortic root.  I clicked through a few DNA’s on the computer system, and as I was pondering if his hypertension could be related to his leg pain.  I got grabbed by one of my colleagues who had noticed this guy was being a bit odd.

The guy worked as a woodsman, and had been brought in by his friend.  His friend said he’d come home, complained of pain in his leg, got sweaty and confused, so he’d brought him here.  Now we were all thinking ‘toxins’ at this point but he pointed to his chest, and his belly and said ‘hurts’ then kept trying to sit up, move around and generally make himself more comfortable.  He looked awful.  That was the most history I got from him, after that he had a profound expressive and receptive dysphasia.  The patient’s flatmate, in one of those wonderful moments of honesty, told me he was the only one in the flat that didn’t take synthetic cannabinoids.

This man’s BP was 220/160 he had all of his pulses, no delays, a normal ECG, he got a portable CXR which showed a normal mediastinum, to my eye (and the radiologist the next morning).  His left leg was a little cooler perhaps than his right.


An example of a normal CXR
An example of a normal CXR, (this is not his CXR, but it is close enough for the purposes of this case)

I was pretty worried about this gentleman, and asked for my first ever CTA, then I grabbed one of the ED consultants to have a look at him with me.   She also suggested we start banging in labetalol at this point so we did (it didn’t really work).  I took him up to scan, and after a few attempts to get him to lie flat and stay still we got our diagnostic images (with very very small doses of midazolam).  They showed a type A dissection.

He came back down to ED, and went to theatre about 25 minutes later.  He survived his repair without having to have a valve replacement, but did have some embolic events post op (and probably pre-op), but he’s alive, and independent.

Now I had these cases within about 3 weeks of each other, I’m not sure, but I wonder if my failures with the first, primed me to pick up the second.  I certainly did a fair amount of reading on dissection after I found out about my error.  What has struck me about that is how difficult and nebulous the symptoms can be, but it seems any combination of acute onset pain, and neurology could be a dissection’s only symptoms (and you may not even get that).


About Acute Aortic Dissection

Clinical Features % of cases
Severe/worst ever 90%
‘abrupt’ 84-90%
Sharp 64%
Tearing 50%
Migrating 16%
Down the back 46%
Differential BP >20 mmH in arms or missing pulse 15-30%
Altered or syncope 13%
Hemiplegia 5%
Focal neurology 17%
Abdo pain 43% (descending0 22% (ascending)



CXR: Widened mediastinum in 56-63% of patients.  Abnormal aortic contour 48-71%.

Transthoracic echo 75% diagnostic type A, 40% type B

CT sensitivity is 83-98% (but probably better than this now due to high res scanners).

I think the clinical features make more sense if you imagine the process going on in your patient.  The pain is from the initial tear, the pulse differential, or BP differential is due to the involvement of the arch vessels, and depends entirely on the physical shape of the tear.  It’s the same with neurological symptoms, you might get hemispheric signs if a major vessel is blocked, or you might get random neurology that doesn’t make sense because of embolic phenomena (which is by it’s nature random).  As the tear elongates it will affect lower branches, giving appropriate syndromes (renal failure/infarction, mesenteric ischaemia).


There is some discussion in the literature of using d-dimers has a ‘rule-out’ test for dissection.  As you are forming clot inside the false lumen, in theory the d-dimer should be pretty high.  Certainly a negative d-dimer might rule out a dissection, but I don’t think there are any prospective trials out there to say for definite that this is a safe strategy.   I did find a recent meta-analysis (of observational studies) with approximately 500 participants which suggests it might be sensitive enough to use as a rule out test, (this is quite an interesting topic, and I think I’ll revisit it later).


Type A Vs Type B



Type A dissections need go to theatre, patients need to have either an AVR, and graft, or just a graft to pin the false lumen back.  Other options the cardiothoracic surgeon has is to fenestrate the false lumen (basically cut through it) which allows blood to flow through both lumens.  Type B dissections (which start after the arch) used to be controlled with BP control only, sometimes some centres are using large stents, to push the false lumen closed.  The theory behind controlling the BP is to decrease the pressure flowing through the false lumen and stop the dissection tearing any further.

Management in the ED is mostly around identifying the problem and making the diagnosis, it’s an often missed or delayed diagnosis because the features are so nebulous and changeable, for us you should ask yourself “Could this be a dissection?” for every one of your chest pains.  If you do suspect it, talk to a boss, and consider more investigation.

Once you’ve found one, start lowing the BP, labetalol as a bolus and infusion is recommended in most centres, GTN infusions can also be used (or used together).  Nitroprusside is also still in the textbooks, I’ve never seen this used, but I’m sure other people have.  Aim for a target of <140/90.  Slipping in an arterial line would also be a good idea while the cardiothoracic people are getting ready for theatre.  It will aid your BP management, and make the anaesthetist moderately grateful (as it will make their RSI safer).

Further information

–          Excellent SMACC podcast on dissection from Rob Rogers

–          LIFTL review – here



Useful literature and references

Shimony, Avi, et al. “Meta-analysis of usefulness of d-dimer to diagnose acute aortic dissection.” The American journal of cardiology 107.8 (2011): 1227-1234.

Harris, Kevin M., et al. “Correlates of Delayed Recognition and Treatment of Acute Type A Aortic Dissection The International Registry of Acute Aortic Dissection (IRAD).” Circulation 124.18 (2011): 1911-1918.

Howard, Dominic PJ, et al. “Population-based study of incidence and outcome of acute aortic dissection and pre-morbid risk-factor control: 10-year results from the Oxford vascular study.” Circulation (2013): CIRCULATIONAHA-112.

Howard, Dominic PJ, et al. “Incidence, risk factors, outcome and projected future burden of acute aortic dissection.” Annals of Cardiothoracic Surgery 3.3 (2014): 278-284.

Coyle, Siobhan, et al. “Diagnostic Testing in Acute Aortic Dissection.” Current Emergency and Hospital Medicine Reports 2.2 (2014): 97-103.

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