Trauma Care Conference UK – March 2017 – Major Trauma in the ED

My second day at Trauma Care this year was mostly spent in the Major Trauma in the ED stream.  I took some notes, which I have expanded on and reported here, on the off-chance that someone might find it useful.  Caution – If I have misrepresented anything, please do let me know and I will update.  My notes on the first day are here.

Epidemiology of trauma

Gareth Davies via @LDNairamb

As an extension of the Ryan Lecture the day before, Dr Gareth Davies extolled the virtues of understanding epidemiology of any disease; how can you begin to become an expert in something without knowing what it is, where it comes from and who is affected?

Sadly, Paediatric trauma is biggest killer of children, yet it is one of the most poorly researched areas of emergency medicine.  Events are seen as just accidents, a fact of life, something which cannot be prevented.  Surely this isn’t right.

The phrase the ‘Golden hour’ was coined because 80% of trauma-related deaths occur in the first hour post-injury.  The importance of getting resuscitation right in the first hour has an effect in the later days, once the cascade of cellular damage and death has started, it will slowly continue until the death of the whole patient.

The Golden Hour, really belongs to pre-hospital practitioners, it used to be thought that clinicians in the ED had an hour to work with, but the clock starts at the time of impact. Average times from call to ED was approx 45mins if not trapped (low transfer times) in one study.

Basic epidemiology

It used to be that 75% of deaths were in 15-45yr olds.  There is a definite increase in older trauma. Deprivation and racial/ethnic variations in distribution.  Despite all the data from TARN, it is still unclear how and exactly when deaths occur in prehospital field.  It is thought that:

  • 40% exsanguination, 40% CNS injury blunt
  • 50-80% exsanguination in penetrating

Brain impact apnoea is an under-recognised process which I think affects a significant proportion of head injured patients.  Many arrive in hospital with a history of having been unconscious and apnoeic, but with no demonstrable lesion on CT and a minor neurological embarrassment.   It only takes a rescuer to provide ventilations for a short period for the patient to resume normal breathing on there own.  There is a definite potential for intervention but only if immediate; it would require training of the public to make the highest impact.  I had a discussion afterwards with a colleague – is compression-only CPR, which is now recommended to the lay-public going to affect outcomes in this scenario,  or is the pulsation of the chest enough to restart respiration?

Gareth also pointed out that we will never get a good handle on the real causes of death at scene due to the treatments we deliver to these patients.  IV fluids will cause more exaggerated brain swelling, and haemorrhage may appear worse at post-mortem if fluid resuscitation has been delivered.

Food for thought.

Ultrasound in trauma

David Gay, Consultant Radiologist, Derriford Hospital

So, the short version – there is no role for ultrasound (US) in the trauma setting.

Unfortunately, that’s not entirely David’s opinion, he managed to think of 4 possible scenarios where it could be of use.

Scenario 1: Normal TU/MTC with CT SCANNER

FAST scanning is fading fast.  Its usefulness has been drowned out by the usefulness of rapidly accessible dual-phase CT imaging.  A FAST scan (or better still a radiologist who performs a whole ultrasonic survey) could be performed if the patient is unstable with a view to going straight to theatre, CT if possible with resuscitation ongoing.  Good sensitivity and specificity in Afghanistan when a consultant radiologist doing FAST.

Caveat: FAST needs training, ongoing practice, governance, and images which are stored in the patient record.

However, NICE say:

“Don’t do FAST” (paraphrased)

And that you shouldn’t use US if going to delay transfer to definitive treatment, something which I heartily agree with.  This is also true of prehospital ultrasound.

Scenario 2: no CT scanner

If no access to CT, then perform plain films, and an ultrasound (not a FAST, more in depth). If managing conservatively, perform serial US for trends. US is remarkably versatile, and can assess solid organs, eyes, brain (via eyes), bowel including appendix.  It can’t assess retro peritoneum, bones (maybe some fractures), adrenals, or bowel trauma.

Lung ultrasound – More accurate than X-ray, less than CT. The problem is it only looks at one part of lung at a time. False positives are common at apex.

Cardiac US – activity, filling, tamponade.

Scenario 3: Mass casualties

A Radiologist embedded in ED (ala Camp Bastion, or Derriford) makes it easier to send a team of SpRs and sonographers to ED in mass casualty events.  There are many potential operators in the hospital, he recommends you shut down outpatient activity.

Use US to triage CT/Theatre/ITU

Scenario 4: Special cases

Pregnancy – more difficult to US; use CT if life at threat. Serial ultrasound is useful.

Paeds- Paeds guidance is to target your imaging based on clinical findings, again though, if serious injury suspected, or life-threatening bleeding, use CT. If stable, plain film and US will give almost all the answers.

Eyes – orbital US useful for injury including foreign bodies and optic nerve sheath diameter for the diagnosis of raised ICP, which is better done as serial measurements.

Permissive hypotension in blunt trauma

Tim Rainer

This presentation’s take home message was that it is particularly difficult to design a study large enough, simple enough and powerful enough to answer the age-old question of how to fluid resuscitate a patient.  It raised more questions than it answered.

Tim wants to perform a multi-centre randomised controlled trial to determine the optimal blood pressure target for patients with major exsanguinating haemorrhage.  There is actually very little evidence out there on what pressure to target, what volumes to infuse.  There is plenty of evidence telling us that patients who present with or develop hypotension do worse, but is that because the wrong target was prescribed, or because lower blood pressure is a result of worse injury score?

Screen Shot 2017-03-23 at 14.44.50The first review to read could be the Cochrane review, “Varying the timing or the volume of intravenous fluids given to people with uncontrolled bleeding due to injury”

Is the doctrine of chasing a cerebral perfusion pressure really a good idea?  It seems a paradox, the pushing up of cerebral blood pressure and intracerebral blood volume in raised ICP.  Wouldn’t it just ultimately push ICP up?

There is only poor quality data to prove that hypotension causes mortality and worse neurological outcome – mainly level 2 evidence, mostly retrospective.

My take on it is similar to the argument of scoop/run v stay/play, this is far more nuanced than BP targets, the process of achieving target must be important – blood products and sympatholysis to achieve flow and hypotension is currently in vogue and seems to be yielding good outcomes.  Any study, particularly multi-centre must take differences in trauma systems into account, the ability to stop bleeding quickly.  I asked this of Tim at the end of the talk – he would much rather study a complex care bundle like this, but NICE have asked the question – what is the best BP target?

The US military have started using altered mental status rather than BP targets, titrating to end-organ perfusion.  This may be possible in the civilian population, but the young, fit and healthy military population is very different.

Traumatic brain injury challenges and recent progress

Fiona Lecky from TARN

90% of CT Head scans done according to NICE guidance are normal, but may have a TBI, there needs to be more work, and more care/engagement in this population.  MRI could be useful in earlier diagnosis, or in the future, brain biomarker screening which could become point-of-care tests.  Out of 1.4m possible head injury attenders, 1-5% have CT proven TBI, not sure how many have CT negative TBI.

The average severity of TBI is increasing, why?

22801a555da18b0db90674093dcf3a_big_galleryA key take home message is that older patients have a higher GCS for the same severity of TBI, they are consistently between 1 and 3 points higher for the same severity.  This is making diagnosis and recognition of injury much more difficult, as neurological signs just aren’t there.  This means that older patients are getting lower access to acute care, less likely to be transferred, less likely to be seen immediately by a consultant – My question is – does this make a difference in outcome?  If an older person compensates better (working theory is more space in the head to tolerate a mass lesion)  and the management of chronic haematoma is safer than the management of acute in the elderly, is there such a rush to diagnose?  I think this question is as yet unanswered.  Luckily, the NICE CT head guidance provides for this discrepancy by recommending all older patients with loss of consciousness or amnesia gets scanned.

Recent studies:

  • late induced hypothermia in TBI caused increased mortality
  • erythropoietin no difference.
  • RESCUEICP – early decompressive craniotomy confers a survival benefit, but no additional survivors with a good neurological outcome

Compassionate governance @civilitysaves

Chris Turner @orangedis

This was one of my favourite talks.  I am so glad I got the opportunity to hear Chris speak. For further information, go to Chris’s Twitter feeds (above) or his Researchgate page.

The whole reason we practice governance is to promote safety and excellence.  Unfortunately, governance is broken.  Current governance processes eg Root Cause Analysis (RCA), etc will often miss potential learning opportunities when selecting a single root cause, especially human factor and communication errors.

We are far from a no-blame culture.  This current environment must result in low incident reporting, for fear of reprisal and blame.

The fascinating part of the presentation was about the evidence that incivility, aggression, and rudeness lead to higher error rates.

In a controlled study, the receiver of rudeness showed a decrease in cognitive ability of 61%, the rude person’s reduced by 50%. A third victim was the next patient the receiver attends to, who receives a negatively loaded care professional. The fourth victim is the family member who witnessed the rudeness, who will shut down and not share information through mistrust.

You may not feel you were rude, but the perception of rudeness is what has the negative impact.  If you were perceived as rude, you need to change.

Governance processes:

  • Safety-1 – only looking at the negative things when things go wrong
  • Safety-2 – looking at both negative and positive experiences and working out what went right

Changes to make in governance:

  • Respect staff decisions, an assumption that staff did things correctly based on information available. Question should be – what made that the right thing to do at the time?
  • Respect the complexity of the situation – atmosphere, environment, aggression.
  • Look at what went well – learning from excellence website (Adrian ?) – safety-2
  • ‘Brilliance box’ – for when things go well. Used to reward people who did things excellently.
  • Accept that error is inevitable, and build systems around that fact. Eg – Never events = bad
  • Facilitate people changing themselves
  • Get a description of what ‘good’ would have looked like

The thing that annoys clinicians is the retrospective analysis of split-second decisions

-Sidney Dekker, pilot and human factors/safety speaker

Also,

People don’t resist change, they resist being changed. (By people who don’t respect or understand them)

-Peter Senge

Top 10 Trauma papers of 2016

Simon Carley @EMManchester

I could never do the man justice in paraphrasing him, and luckily I don’t have to, because he has published the whole thing online himself.

Top 10 Trauma Papers of 2016

What I did learn was that closed CPR was as effective as open heart massage in cardiac arrest, however, there was a spike in ETCO2 when open heart massage was commenced – does this mean that it is more effective, or just that there was CO2 build-up whilst the thoracotomy was performed?

Also, that the anterior-axillary line is the go-to place for needle decompression of the chest, rather than mid-clavicular (knew that bit), or mid-axillary.  Least depth with the least chance of hitting something important.

Endovascular techniques in abdominal trauma

Trevor Cleveland, Endovascular Radiologist, Sheffield

I moved from the Major Trauma in ED stream to the ‘Abdominal Trauma’ stream for this one.

There was a good overview of embolisation; how it works, what substances can be used, etc.  Trevor explained that IR techniques are best suited for areas not easy to access surgically, this may not necessarily hold true for all situations, so long as the IR team can be mobilised quickly enough, sometimes the IR is still better than surgery, for example, IR may reduce need to re-operate after damage control surgery.

Embolism in IR requires optimisation in clotting to work, especially coils and other pro-coag particles, etc; it won’t work if the patient is still coagulopathic – haemostatic resuscitative principles must be employed.

It is possible to embolise temporarily, with the use of gelfoam, or autologous clot (something not really used), so if the body is likely to repair itself, a temporary solution may preserve the greatest amount of tissue.

Everything else is permanent.

Specifics:

  • Gelfoam doesn’t fit through a microcatheter
  • Coils good for smaller arteries
  • Amplatzer plug – expensive but big

Spleen

The indications for IR in splenic trauma:

  • active extravasation
  • pseudoaneurysm
  • AV fistula

Liver

If haemodynamic instability, should go to theatre first, then IR after packing.

Questions:

I asked a question because I’m interested in the processes and sequence of events, how to get to IR in a timely fashion – do you have or do you wish you had a hybrid operating theatre, and how often do you think it makes or would make a difference?  Sheffield haven’t got a hybrid suite, they would like one, but Trevor felt that it would only really be of use if it were co-located with the ED.

They have a great call-in system in Sheffield – when an unstable trauma patient is coming, or is diagnosed in the ED, the IR radiologist comes in and helps report the CT scan.  This helps the registrar learn, and makes the radiologist available at a moment’s notice to go to IR.  The IR suite team are also activated at the same time, reducing delays to a minimum.

Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)

Jim O’Connor, Shock Trauma Center, Baltimore

The traditional treatment of intra-abdominal exsanguinating haemorrhage has been ED thoracotomy and aortic cross clamp – outcomes are poor, whether you clamp with your hand or a clamp.

It is possible that REBOA is better. To be thought of as an aortic cross clamp, just less invasive.  It’s not new! It was first used 1954. It has only been evidenced in small case series.  It has been used in the non-trauma setting too (surgical bleeding).

Its benefits include decreased peripheral flow/pressure to reduce exsanguination, and better myocardial and cerebral flow during CPR (animal study).

There is a time limit for inflation though, after which outcomes get worse, fast. 40mins inflation showed better survival in animals, it is thought to be up to 60mins in humans as an absolute maximum.

Studies

46% survival (n=13) in military pelvic fracture with refractory hypotension J of Trauma 2010.

Brenner J Trauma 2013 – n=6, increase in BP by 55mmHg, no haemorrhage related mortality. Still had mortality of 33%.

DuBose J Trauma 2016. Open thoracotomy n=68, vs REBOA n=46 (50% had cutdown), no difference in time to occlusion.

In Baltimore and most trauma centers in the USA, REBOA is performed by acute care surgeons; REBOA in Japan done by ED physicians, and studies have shown some procedural complications, raising the question – who is the best person to perform REBOA?

The Shock Trauma Center (STC) experience – most REBOA was performed in cardiac arrest, 84% placed by acute care surgeons (n=90), inflation time <60mins;  of those in arrest, 90% died but all 10% survivors were neurologically intact,  took longer to place REBOA in arrested patients. Haemorrhaging patients did better,  5 ended up with lower limb amputation, 8 had fasciotomies as the worst complication, and there were several catheter related complications.

Procedure

STC have reduced the size of their sheath down to 7Fr from 9Fr. It may require a femoral cutdown to femoral artery in arrest, as it is more difficult to identify the anatomy under ultrasound, and more difficult to thread the wires.
reboa-zones-1184x662

  • Aim for Zone 1 (chest) for abdo bleeding Zone 3 for pelvis.
  • The trick could be to place an early femoral line (right side is easier) then switch over a guide wire when changing to REBOA.
  • Use contrast in balloon to check position.
  • Check for distal perfusion.
  • Important to place in common femoral, not SFA.

STC offer the BEST course (Basic Endovascular skills in Trauma).

Jim’s opinion is that REBOA is NOT ready for widespread use, and should still only used by highly trained specialists.

Trauma Induced Coagulopathy: what we know and what we don’t know

Karim Brohi @karimbrohi

The last talk of the day, and another big name.  Once upon a time (ie the 90s), it was all about the shock, treating the pressure, maximising oxygen delivery. Now, it’s no longer about shock, bleeding is where it’s at.

The priority in the exsanguinating patient is coagulation over perfusion

  • stop bleeding
  • permissive hypotension
  • avoid crystalloid
  • target acute coagulopathy of trauma (ACoTs)

Learning point: there are 2 parts to a coagulopathy:

  • traumatic – the bit we are used to thinking about; the consumptive process plus the cellular/endothelial processes that produce a coagulopathic trauma patient
  • iatrogenic – the bit that we as clinicians make worse by not giving the right blood products, giving drugs and fluids that compound the traumatic bit, and dilute clotting factors, and may stimulate the endothelia to make it all worse; all compounded by letting the patient get cold
  • OK, so there’s a third bit; later the patient becomes prothrombotic

Inflammatory response worsens coagulopathy. If bleeding continues, coagulopathy gets worse, 40% of patients are coagulopathic on arrival, 80% coagulopathic after 12U blood products, even at 1:1:1.

Avoiding crystalloid is critical, a hypotensive strategy helps to achieve this.

Key features of traumatic coagulopathy:

  • loss of fibrinogen, consumptive and lysed
  • by 8U transfused, fibrinogen will be gone
  • therefore cryo to be used early

Screen Shot 2017-03-23 at 21.09.19After endothelial activation, factors inhibit clot formation.  The complicated web of factors affecting each other generally reduce clotting and in turn produce hyperfibrinolysis.

Brohi says coagulopathy is the primary problem when looking at the ‘lethal triad of trauma’, the hypothermia and acidaemia are consequences. Acid affects coagulation at ph 7.0 or below, and the effect isn’t significant above this. Neither of those two will improve while bleeding continues.Screen Shot 2017-03-23 at 21.12.01

Getting the basics right is much more important than fancy fringe treatments.

Unknowns, just in question form really:

  • TXA – dosing strategy, demographic who benefits, anti-inflammatory effects, is it the best anti-fibrinolytic? Risk of thromboembolism?
  • Cryo – can we front-load patients with fibrinogen? Cryostat2 trial is running to help answer this.
  • Is fibrinogen concentrate better? Cryo has other beneficial factors.
  • Clotting cascade much more complex than the above picture, and we understand so little.  Lots more research required.
  • Inter-patient variability in clotting profiles, could we tailor care in future?
  • Very little known about platelets except that they don’t work in trauma, platelet transfusion doesn’t help clot formation. Why? How can we fix this?
  • ITACTIC trial – does thromboelastography based treatment algorithm yield better outcome?

The future

Will there be drug based therapies to enhance/repair endothelial injury and minimise coagulopathy?

Blood products – red cells are poor at giving up oxygen once transfused, their storage is been optimised for shelf-life and 2,3-DPG levels are low.  Platelets which are stored at room temp are not as thrombogenic as cold stored platelets.  Could blood banks have two tiers of blood storage, one for emergency haemorrhage use which have better functioning products?

There was a floor question at the end which yielded an interesting answer: the Royal London has stopped giving the TXA second dose, and only gives first dose with activation of MHP, perhaps we should all follow suit if we haven’t already.


Overall, my experience at Trauma Care was brilliant.  Such amazing speakers with such thought provoking talks.  I hope you found my notes useful!

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One thought on “Trauma Care Conference UK – March 2017 – Major Trauma in the ED

  1. Pingback: Trauma Care Conference UK March 2017 – PHEM/HEMS stream – Trauma Resuscitation Anaesthesia

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