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Managing Traumatic bleeding: how can we apply the evidence in smaller hospitals?

OK after Clinical Case 031 I was inspired to go out and slog through the literature and try to discover what is “best practice” for traumatic bleeding, then try and work out what is important, what we can do in small or remote hospitals and what is just too expensive / difficult / marginal or plain impossible to do in the bush.  There was a great review in Critical Care last year by Rossaint et al – Updated European Guidelines – so I have used this as a starting point.  Also a review by Curry et al looked at similar data / trials.

So I spent time going over the evidence, and came up with the post below.  The evidence is there, so you can read it for yourself, however, there is no evidence for my opinions – that you can decide for yourself.  As always – I have tried to keep it simple, my brain being the filter for your reading pleasure!  I have given each “recommendation” a grade from A to F (A = gotta do it,\; C = maybe useful; and F = ‘don’t go there’…)  So here it is….it is big, apologies!

This is an A1 recommendation. In patients who are either unstable or have an identified source of bleeding – they need an operation as soon as possible. Time is vital to outcomes.  Let me repeat – if you know where the blood is leaking from – plug it ASAP – do not resuscitate in lieu of intervening with a procedure.

So for the small centres – this means getting into an OT as soon as you can, less time in ED and less fiddling with resuscitation efforts prior to surgery. If you work in a town without a surgeon – then mobilising retrieval early is important. I have on a few occasions arranged for a surgeon to be flown in with the crew to operate prior to transfer.

If your patient responds well to initial resuscitation measures – then you have time, but it should be clear that they need to get to a place where they can get an urgent operation ASAP

We have all been through ATLS or EMST and learned about primary and secondary surveys. What I will say is that there is not much evidence to suport this strategy, but it is universal and you have to do it. However, doing the classic ABCs doesn’t really help you when it comes to the reality of big bleeding patients – the evidence has moved on a bit.

Your initial clinical assessment should answer the following questions:

  1.  mechanism: is this a significant injury? eg. energy of blunt impact, penetrating abdo or thoracic trauma, head injury with any change in GCS.
  2. Pattern of injury:  is this a cluster of injuries, rather than a single overt lesion.  Along with mechanism, the presence of a cluster of injuries should get you worried.
  3. Patient’s physiology / obs / general presentation:  the obs are helpful, but can be normal despite significant bleeds, especially in fit, young people.  You can use the ATLS guide to shock, but know it can be wrong
  4. Response to initial resuscitation – for me this is more useful than the absolute numbers.  The ATLS folks divide these into: rapid responders, transient responders and minimal / non-responders.  You get the idea – give a bit of fluid and watch closely – are you winning?  A pragmatist’s approach to shock – I love this concept – use it every day in my practice.

If you have a patient presenting in shock after trauma and it is unclear as to where the bleeding is coming from then you have to find it fast. If you find it – then you are in the position to intervene.

Resuscitation without identifying the source can waste valuable time. In reality the resus and investigation happen in parallel ideally.

So what investigations? they are guided by you initial assessment, but empirical CXR, pelvis and FAST scanning are mandatory.  The evidence discusses DPL (diagnostic peritoneal lavage) but in my world this is not done – maybe if you have a surgeon with experience, but a FAST is hard to beat when you look at the numbers.  Image anything else you find on you secondary survey.

Shock is defined as tissue hypoperfusion, and this does not equate to the blood pressure. [There is a whole other post coming up on this concept!]

So what measures tissue hypoperfusion? at this stage, serum lactate is your most evidence-based test.  Base deficit is also used with less evidence to support it – but in my hospital they both spit out on the same gas analysis – so use both.  Beware the youngish, sweating / spewing chap with a normalish BP and high lactate – he is on his way to crashville.  [See this article on ‘Cryptic sepsis’]

I was taught to aim for a low normal ET CO2, but the evidence now suggests this is wrong. The Guidelines recommend normocapnea.

Hyperventilation is associated with poor outcomes (even in brain-injury) including increased mortality, decreased cardiac output and all round badness.

The vent strategy is essentially the same strategy the ARDS Net folks came up with for lung injured patients. The recipe is – low tidal volume (eg. 6 ml/kg IBW), higher RR to keep the minute volume up and clear CO2, and add PEEP to maintain open airways and titrate to oxygenation.  See my case on postop PEEP++ for an example of this strategy.  I now use this on all my intubated patients (even elective gallbags) -unless they have COPD / bad asthma / obstruction.

The evidence shows that using Hct alone is about as good as tossing a coin in the air! It is a poor predictor of volume lost or prognosis. I think you can put Hb in the same basket. It is good to know and use serial assessments, but it is just a part of your more global assessment.

Not a lot of evidence. But it makes sense to try and detect coagulopathy early by testing for it. Of course clinical observation of bleeding and knowing how much fluid / blood has been given can allow you to anticipate ACoTS before the lab can tell you the numbers are bad. The studies did not show much benefit but we should probably check the INR, APTT, platelets and fibrinogen levels. In my practice – I start giving FFP, etc before the labs go bad in the big bleeders – I think this is because – (1) it makes sense to get ahead of the game and (2) the lab can be slow, over an hour to get some results – too late usually.  So if your lab wants confirmation of coagulopathy before the take the FFP out of the freezer – you need to have a ‘meeting’ and change this!

The future includes thromboelastography – this is basically a test of clot strength.  This is used to guide treatment with a variety of coagulation factors – but don’t hold your breath in the regional hospitals – this is still a long way off!

There are some bleeds that need something simple done.

(1) arterial bleeding from and extremity. There is a growing body of evidence from the military showing the safety and improved mortality of torniquet use. See my previous post on Life AND Limb

(2)  Pelvic fracture stabilisation. This depends on where you are and what you have got – but a bed sheet tied around the trochanters is infinitely better than nothin’.  If you have a purpose designed pelvis binder-  then better.  For most small hospitals, that is as good as it gets.  The goal is to make the pelvic volume as small as possible by reducing the injury.

Embolisation seems to be the done thing if you have an angio suite at your disposal.

If you have not heard of this concept before – it basically consists of 3 stages:

(1) Brief ‘resuscitative laparotomy’ – control active bleeding, remove contamination, pack the abdomen and get out

(2) Off to ICU for resuscitation and normalisation of the acidosis, hypothermia and coagulopathy. Optimise fluid status and ventilatory management.

(3) Return to OT for a definitive fix of the injuries / closure of wounds.  This may be hours to days later depending on the injury

There are no RCTs to support this but a lot of retrospective data supports it – it is the new standard of care for the severe end of the trauma spectrum – especially those who have significant acidosis, coagulopathy and low core temp at the outset.

Here we run into some controversy / uncertainty in the literature. What fluid, how much, targets of resus?

Which fluid?  Crystalloids remain the first line.  Most trauma patients now get them en route to the ED.  However, there is evidence showing a direct survival relationship between the volume of crystalloid and mortality.  So if you use them I think it is as a bridge to getting some blood ready.  In my experience too many crystalloids are given in an attempt to get the BP up to unnecessary heights (We are treating our own pulse, rather than the patient’s!)

Which crystalloid – well CSL, Ringer’s etc are good if you patient is acidotic.  See Emcrit’s Acid-base lectures on this.  Saline seems popular – but why? I don’t know, tradition?  It doesn’t make sense in terms of acidosis management – makes it worse not better!

Hypertonic saline (7.5% + dextran) is the new concept here – smaller volumes, and has been used extensively on the Mid-East battlefields.  Watch this space…

Blood products – packed red cells, FFP in my hospital  – these are the mainstay of volume resuscitation in severe trauma.  How to use them – well the Guidelines suggest a target of Hb = 70 – 90 g/L.  However if you are doing a “sympatholytic” resuscitation or “controlled volume / permissive hypotension” then you titrate the fluids to the BP – aiming for a MAP above 65.  Yes, I said 65, which is same as 75/60, or about 80 systolic for round numbers.  This seems low to those of us who trained in Anaesthesia, but that is what the evidence says!

How much?  Well – enough, and just that much – until you can get control of the bleeding source(s).  As above target is MAP > 65.  If you can measure other markers of preload eg. IVC collapse or SVV maybe you can titrate to those as well?  Not sure of the evidence here…

An important caveat to this:  if you have a head-injured or spinal cord patient – then you need a higher target SBP – you probably want to aim for triple figures here [100+]

Ratio of RBCs to FFP (+/- platelets)?  This is a tricky question.  The evidence for RBCs and FFP is much better than adding platelets into the mix, fortunately most small hospitals don’t keep platelets – so the decision to not use them is very easy!  Lots of retrospective, registry analysis of the RBC:FFP ratios has been done.   1:1 is popular, however the dust seems to settle with a ratio somewhere between 1:2 and 1:3 giving the best outcomes.  In the reality of rural practice you have already given at least 4 bags of red before the first FFP is thawed, so I aim for a 1:1 after the FFP is available – the ratio then eventually approaches 1:1 as you give more and more volume, and if you stop early then they probably were not as sick as you thought?  No evidence, just bloody-minded pragmatism.

Calcium has many jobs to do, and in bleeding it has a crucial role in: inotropy, coagulation factors and avoiding citrate toxicity in massive transfusion.

Calcium can be given as CaCl, or Ca-gluconate.  Basically the Ca++ in CaCl is immediately available, but harsh on the veins.  Ca-gluc is cleaved by the liver to release into the plasma ionised Ca++. In severe shock you might want to go with CaCL as hepatic metabolism might be impaired.

The goal is to get the ionised Ca++ level up to around 1.0 mmol/l, acidosis does reduce the available Ca+.

The evidence for the infusion of platelets is not as good as FFP. There are studies showing improved survival if the ratios infused were better than 1:5. In most small hospitals it is a non-argument – they are just too hard to store and not gonna get used frequently enough to justify the expense. If you are giving platelets the recommendation is to aim for a level of 50, or maybe 100 for the brain-injured.

These contain a variety of clotting factors – but importantly they are the only real source of fibrinogen in modern practice. (although FFP has fibrinogen also). This should be used if you show a low fibrinogen level.  This might be viable in small places – though does it add more than just giving more FFP?

PCC is a combo of the vit K dependent factors, protein C and S. It is stored for a good period and doesn’t need cross matching – so it is easy to use. It is expensive, but the in vivo testing(in animal models) shows it is effective for reversing coagulopathy of trauma – better than FFP in ‘mildly hypothermic pigs’.  Not just for those on warfarin. There is a theoretical risk of thrombotic events – so use some mechanical prophylaxis to prevent DVT.  There are a few small trials and reviews: Critical care, and Euro Journ Anaesthesiology.

I think this is viable in the smaller hospitals – easy to store, use and has effects.  I think I might pester the accounting department about this….

This is really controversial. rFVII is super- expensive and hasn’ really passed the evidence-in-practice test from what I can see. It seems to be down the bottom of all the algorithms, and hear this – you need to have all your ducks in a row before using it – make sure the other factors are all replenished, the big vessels are tied and your Ca, fibrinogen and pH are all sweet. For me this is likely not enough bang for my buck in a small centre.

This is not a drug for trauma. Full stop. If you have a bleeder with known vWF problem then you might talk to a Haematologist about it.

CRASH-2 was a huge trial that looked at IV tranexamic acid for trauma. And it showed a mortality benefit – only a small one though – ~ 1.5%.  It was safe though – so not much downside.  Did not reduce the volume of blood required – so may not help you in the instant…

Caveats – you have to use it early.  Get the initial bolus in ASAP then you have a slow 8 hour bag to run in at your leisure.  For me this is now something I do in my hospital – it is cheap and pretty easy.

Watch out for upcoming trials in obstetric bleeding – might be another string to our bow there too!

Sorry folks – it was a marathon of mostly my ramblings and I am asking you to take my word on all of that – but the evidence is not very clear in this field – there are many ways to “resuscitate an exsanguinating cat”.  I would love to hear your questions and comments – so I know if this is total gibberish or if you think it might apply to your place.  Hit me on the comments.

Casey

Comments

  1. Casey Parker says:

    Email comment from Dr Tim L:

    Really useful post, Casey – thanks fro trawling through the evidence and debunking some EMST dogma. I’ve got a couple of Qs for yu and the broader collective:

    – is prothrombinex all that useful, or better reserved for coagulopathy in context of warfarin use or my favourite, the busload of haemophiliacs in a rollover?

    – you mentioned thromboelastography. I think I’ve heard Russell Gruen talk about this, and it’s value in early detection of coagulopathy…bearing in mind that lab turnarounds for ‘coat profile’ may be 30-60 mins and that point-of-care kits are unreliable in context of low Hct/alb etc. So what exactly IS thromboelastography and how applicable is this to use in the resus room? Doesn’t sound as easy as whole blood clotting time using a glass tube for snakebite!”

    Cheers
    tim l

    • Mandie Villis says:

      I’m curious about Tim’s questions (from some time ago!)

      Also curious about IV tranexamic acid – I have just learned this is actually available at my hospital but I hadn’t thought of using it before! How low is your threshold to use it? What doses do you use?

  2. Russell Garnett says:

    Hi Casey,
    was good to see you the other day, hope the obs emergency handbook is still progressing well?
    Just on the Goldie doing the ETM trauma course, Hoods is here too!

    Just a couple of things that we have had drilled into us on the course and pre-reading. They will fail us if we fail to tie the feet in slight internal rotation, in a pelvic fracture once the binder has been applied. This further reduces intrapelvic volume and confers greater stability in synergy with the binder.

    DDAVP- suggested use in trauma (manual) for those who are on anitplatelet agents (APAs) and in haemorrhagic shock. I have not looked at the literature on this but it was something we did in cardiothoracic ICU if patients were “oozy” post op and had been on APAs. Any feed back?

    All the best, love the site, Russ

    • HI Russ
      Hope you are not taking too much heat from Andy & co… he’s a nice chap eh!
      To try and answer your question on DDAVP (desmopressin) in trauma. You are right – there is no great clinical data. The European guidelines from 2013 said this:

      Desmopressin has never been formally investigated in general trauma or TBI [438]. Nevertheless, desmopressin has been recommended in patients treated with platelet inhibitors, suffering from intracerebral bleeding [438,453] and in trauma patients with von Willebrand disease [466]. Interestingly, desmopressin prevents the development of hypothermia-induced impairment of primary haemostasis [467] and significantly increases platelet aggregation dur- ing hypothermia and acidosis.

      The bit about protecting from platelet dysfunction in cold / acidotic blood certainly sounds appealing! But if you are not doing all to fix those bits – then DDAVP isn’t your biggest issue!

      So it was also reviewed from a safety POV and found to not cause clotting as such – so it seems like a reasonable thing do in an old guy on clopidogrel where all else isn’t working. Throw it in I say! Especially if the bleeding is uncontrollable surgically or intracranial.

      Hows that sound.? Casey

      • Thanks Casey,
        it seems to do no harm and there are some encouraging statements in the literature you provided. I’ll make sure its use is not at the expense of more proven haemostatic measures.
        Andy seemed like a good dude indeed. I have yet to benefit form your USS chapter but looking forward to getting some more tips in this fantastic areas of bedside diagnostics, warm regards, Russ

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