Authors: Charlotte Davies / Editor: Nikki Abela, Liz Herrieven /  Codes: CAP7, HAP8, CC7, VC2 / Published: 12/10/2021

As I write this, it’s aortic dissection awareness day. Not another blog on AAD I hear you cry…But we thought you might all like an update and a consolidation on what is happening in the world of this black swan diagnosis. It’s clear that suspicion and diagnosis is difficult, and those best at picking this needle out of the very large haystack are going to be the emergency physicians. The flip side of it is that we will also get blamed when they’re missed.

The new curriculum asks us to all be excellent with quality improvement and a systems based approach so we’ve documented some thoughts and suggestions in a systems based approach that may lead to some QI suggestions. We’ve broadly split our updates into suspect, investigate, treat and transfer. There’s work on going around operating, but no plans for ED vascular repair yet… I’ll try to keep this blog live updated – and I’ll list the updates on #RCEMAAD.


1. Suspect

The NHS pathways algorithm has been adjusted to include some AAD specific questions. JRCALC, the ambulance guidelines, were updated in 2019 to include AAD in the guidelines with a pre-hospital education programme and a paramedic podcast being created.

After the HSIB report, on delayed recognition of AAD, the Manchester triage questions were also changed to include AAD.

Suspicion is the hardest bit to get right as there’s lots of dogma still around dissection. Let’s say it clearly – EQUAL bilateral BPs doesn’t rule out AAD. Nor does a normal CXR. Nor does a normal d-dimer. We often rely on heuristics, and the Canadian risk factor score might go some way into standardising these. The Morello score might be worth looking at – if you discuss this at journal club, send us a summary!

We know patients with Marfan’s are at higher risk of dissection, but they don’t always know, and it is worth signposting to them and making sure they know they are at high risk. Not all patients with Marfan’s or Turner’s syndrome look like they have the syndrome – sometimes it’s only identified on genetic testing. Pregnant patients are also at high risk because of the tachycardia, and hormonal effects on the aortic wall. Labour, including the ergometrine, causes lots of stress on the aorta. These risk factors are true regardless of the age of the patient

The last IRAD data published was a long time ago. More research is happening via the Acute Aortic Dissection ED Diagnosis Research Group chaired by Prof Matt Reed.


2. Investigate

ECG Gated CT scan is essential. RCR & RCEM joint guidelines are nearly out and we’ll add them here when they are. The Think aorta campaign are going to add their voice to us needing more scanners. But if you can’t get a gated CT scan you need a good quality CTA. Not a CTPA – the contrast ends up in the wrong place. Have another listen to the radiology podcast here from 2018.

Arranging the CT scan we know is difficult. Contrast nephropathy probably doesn’t exist yet still we are asked to wait for U&Es.  You need an escort to scan, and maybe a doctor to supervise the contrast – not sure why! And then once you have the scan it needs imaging transfer across to the receiving hospital. Scotland has a pan country service…why can’t the rest of the UK?!?


3. Treat


  • NEWS score as frequently as clinically indicated
  • ECG repeated regularly as long as pain persists
  • Bilateral arm blood pressures initially. Use the highest reading for further monitoring.
  • Consider invasive blood pressure monitoring, preferably right radial.
  • Do not delay transfer to definitive care to obtain IBP – consider early.

If aortic dissection suspected or confirmed:

  • Provide opiate analgesia (eg IV morphine or fentanyl) until pain free.
  • Avoid non-steroidal medications
  • Avoid fluid boluses for hypotension: Discuss with senior. If patient is cerebrating, fluid boluses may dilute clotting factors, dislodge a clot, and worsen outcomes as per NICE guidelines, but judicious fluids may be needed in conjunction with vasoactives if patient hypotensive.

  • Maintain other parameters: oxygenate, tight glycaemic control, normothermia
  • Minimise patient movement: Vigorous movement may precipitate rupture as the aortic root displaces and moves, worsening any dissection. This means PAT sliding even ambulatory patients.

Blood pressure control: whether BP control should start before or after confirmatory imaging is hard to say.

Aim for BP 100 -120mmHg systolic – the lowest tolerated (ie. still perfusing brain)
Aim for HR < 60      (evidence for this is less – the main target is BP control)
Stage one is reducing heart rate.          Stage two is vasodilation
Provide analgesia in conjunction with anti-hypertensives

Give Labetalol:          20 – 50mg bolus (loading dose) over two minutes
Repeat every 10 minutes until systolic <180mmHg
Monitor heart rate, and stop if <60
Max. 4 doses ie 200mg

Labetalol is an 𝛂1 𝛃1 𝛃2 antagonist. If given IV, the hypotensive effect begins within 2-5 minutes, reaching a peak at 5-15 minutes, and lasting for 2-4 hours. The half-life of labetalol is about 5 ½ hours, so further boluses may need to be given. Repeat as needed, up to a maximum of 300mg.

Labetalol Infusion Dilution as per Medusa: make to 1mg / ml: remove 90mL from a 250mL infusion bag and add 200mg (40mL) labetalol 5mg/mL injection, or  remove 100mL from a 500mL bag and add 500mg (100mL) labetalol 5mg/mL injection.

If labetalol is contraindicated, consider diltiazem, nifedipine, or verapamil as rate control before vasodilation is recommended. Verapamil and labetalol should not be used in combination.

Rapid correction of blood pressure can be harmful, and the decision to reduce blood pressure will take into account clinical suspicion.


If BP remains >120mm Hg despite max labetalol, or HR drops to below 60.

  • Start IV GTN infusion at 1mg / hour
  • Titrate every 1-2 minutes by 1mg/hour increments
  • Max rate is 20mg / hour (max 400mcg / min = 24, 000 mcg/hour = 24mg/hour)
  • Alternatives include nifedipine.


4. Transfer

Some transfer services will bring critical care to the patient and iron out the problems caused by makeshift teams working in a different environment. @drsgrier is particularly interested in this. There’s some training resources available from the London teams here.

One systems tool that can be useful to look at a whole system is the Yorkshire Contributory Factors framework. This highlights many things to consider when you think about what goes wrong.

A. Situational Factors
Team factors: in AAD transfers the team is often a new team that hasn’t had a chance to form yet. The paramedics and doctors and nurses may or may not know what the rest of the team is capable of and allowed to do. Team factors certainly influence transfer.

Task Characteristics: in AAD transfers, the task is often unfamiliar to the escorting Clinician who is not used to being in an ambulance with a critically unwell patient.

Patient Factors: in AAD transfers the patient may have unusual physiology making a transfer more complicated.

B. Local working conditions
Workload: in AAD transfers, the escort may not be the most suitable for the job, but the most suitable given the demands and staffing of the transferring unit. This may be due to staff sickness, workload or insufficient staff.

Leadership, Supervision and Roles: in AAD transfers, the escort may not be aware of their responsibilities.

Drugs, Equipment and Supplies: in AAD transfers, escorts may not be aware of how to use the equipment. Drugs they are used to having may be unavailable. Paramedics may be asked to transfer patients with drugs they are not used to having running.

C. Organisational Factors
Physical Environment: in AAD transfers, clinicians are not used to working in an ambulance.

Support: In AAD transfers, local policies for blood transfer need to be adhered to.

Scheduling and Bed Management: bed pressures will influence availability of a transferring ambulance, and potentially acceptance at tertiary unit.

Training: In AAD transfers, not all staff are trained due to inadequate training, no protected time and no updates.

D. External Factors
Equipment: ambulance trolleys are not designed to be vibration absorbent so patients might move a lot.

National Policies: there is no screening for AAD possible. Commissioned resources are under resourced.

E. Communication and Culture
Safety Culture: documenting adverse events on transfer is part of the risk culture.

Verbal and Written Communication: problems with handover and notes are highlighted at a patient transfer.


5. Refer
The number for referrals needs to be easily accessed, and if you’re a specialist aortic service Think aorta will provide some flyers personalised with your service’s number. The vascular guidelines say the aorta service should determine place of care and ED shouldn’t be flitting between services. 

6. Investigate and Educate
There are 81 vascular centres in the UK. We need to encourage them all to submit their own data, and VSQIP are working on this.

Many patients don’t make it to the vascular centre, and a bid for NIHR funding to try to include them in our research has been made. Watch this space.

Paramedic training is also being constantly updated with a module on “ParaPass“.

In summary, in the words of the bot, think aorta.


My questions for further research and learning:What evidence is there for BP control agent?

  • How quickly does an AAD arise? Is a normal scan a year ago enough?
  • What value does clinician escort to CT add?
  • What’s your AAD protocol? Could you share with the RCEM team?

Every department will have their stories of dissection they didn’t miss. Send us your summarised stories or tweet #rcemaad. Here are a few:

  • Collapse + severe headache. All resolved but lactate high. Wanted to self discharge, but stayed for CTA which confirmed dissection.
  • Severe abdominal pain with lactate >8. CTA confirmed thoracic dissection. Died waiting for vascular to accept.
  • <50 year old. Previous AV replacement. Pulsing pain in back and abdomen associated with leg weakness. Pain relieved by codeine.  CTA confirmed AOD.
  • 60ish year old man. Normal vital signs came with left sided chest pain, diagnosed promptly as intramural type A dissection. Triage nurse thought ?AOD. Trigger for thinking ?AOD was recent aorta training, and pain being  sudden onset & maximal intensity pain. Submitted by Farhin Holia. 
  • <40 year old man. Smoker who presented with stabbing chest pain, comes in waves, radiating up to both sides of his neck, does not radiate down left arm. Associated with diaphoresis, SOBOE and one episode of vomiting. Examination unremarkable apart from looking unwell and clammy. Lactate 3.2. SpO2 initially 96%, slowly dropped to 92%. POCUS showed dilated aortic root, pericardial effusion, right ventricle collapse. Immediately urgent CTA performed which suggested Stanford acute Type A dissection extending from aortic root to just proximal of left common carotid plus haemopericardium, 6 cm aortic aneurysm. Successful transfer and operative intervention. Submitted by Farhin Holia. 

Occasionally we miss AAD. Let us learn from the mistakes of others. Send us your summaries or tweet #rcemaad, and let us know about any coroner documents around aortas. 

Coroner Summaries:
Paul Sartori – thinkaorta in chest pain presentations
Andrew Wing – include AAD in radiology requests if it is a differential
Mary Mellor – read scans post op VERY carefully
David Oldfield – AAD affects the young with HTN, and may cause an abnormal ECG.
Chloe Lumb – genetic condition predisposing to AOD not acted on. Not much information in coroner summary.


Sometimes, the diagnosis is made, but the operative intervention is unsuccessful.
Jordan O’Neil – 14 year old
Sajidah Asmat Hussain – orthopaedic surgeon – see BMJ
Dissection identified and patient transferred with BP control. Died on transferring to trolley in tertiary centre. Always PAT slide. 

For education we’re doing the best we can and there’s loads of RCEMLearning resources, and loads of FOAMEd! There’s an excellent set of “tweetorials” here. Send us your aorta resources! If anyone has read the new book on aorta (Springer: Aortic Dissection) send us a review.

RCEMLearning FOAMed

SAQs for members only


Non RCEM Education Resources
Case Report podcast
Resus room acute aortic syndrome podcast.

  1. Gary L A Cumberbatch. Aortic Dissection. RCEMLearning. Published: 17/11/2020
  2. Carsten J. Beller et al. Role of Aortic Root Motion in the Pathogenesis of Aortic Dissection. Circulation 109: 763-769. 17th February 2004.
  3. Miller et al. Labetalol. StatPearls. 16th July 2021.
  4. Ravi Hebballi. Diagnosis and management of aortic dissection. Continuing Education in Anaesthesia Critical Care & Pain, Volume 9, Issue 1, February 2009, Pages 14–18.
  5. Mike Gisondi. Aortic Dissection: Practice Update. NU.EM.
  6. Prateek K. Gipta et al. Hypertensive emergency in aortic dissection and thoracic aortic aneurysm – a review of management. Pharmaceuticals. December 2009.
  7. Chris Nickson. Acute Aortic Dissection. Life in the fast lane. November 3rd 2020.
  8. Unknown. Labetalol Hydrochloride 5mg/ml Solution for Injection. EMC
  9. Toshihiro Fukui. Management of acute aortic dissection and thoracic aortic rupture. Journal of Intensive Care 6. Article 15. 2018.
  10. Duncan Bootland. Emergency Medicine Prompt Card. 2020.
  11. W E Strauss, A F Parisi. Combined use of calcium-channel and beta-adrenergic blockers for the treatment of chronic stable angina. Rationale, efficacy, and adverse effects. Ann Intern Med. 1988 Oct 1;109(7).

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  1. Shawgi MOHAMED says:

    Very good topic

  2. crookd says:

    Absolutely brilliant. A combination of (twitter) open discussion and consensus, dogmalysis, evidenceBM and lessons from coroners is how all future teaching sessions should be. Enjoyable as it is brilliant.

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