Tag Archive: bleeding


SUSS IT: Secondary UltraSonographic Survey In Trauma

Filed Under: Emergency, Pearls and Pitfalls, Surgery, Useful Evidence by Casey Parker — 7 Comments
January 10, 2012

Definition – To suss: to look into something deeper, and acquire more information; or to solve a problem or puzzle using ingenuity.

This is a concept I have been thinking up for a while.  And it turns out others have also been to the same place.  Dr James Rippey (Ultrasound Village) and colleagues published this paper in 2009 that “brainstormed” all the possible uses of bedside US in trauma patients.

So what the heck is a “SUSS IT” – and why is it any different to what you do now?  It stands for Secondary UltraSonographic Survey In Trauma.  If nothing else it has a cool acronym!  It is not a single scan, or protocol – it is more like a shopping list of all the scans that just might come in handy when dealing with a trauma.

I reckon there is are two types of US-users out there.  There are some true diagnosticians who do scans to a standard that allows them to produce a reportable finding.  Then there are the rest of us: ED docs with a probe and a prayer… we have a varying degree of experience and know our limitations.  I am certainly in the second category – as are most ED docs I know.  For me bedside US is basically an extension of my clinical examination.  Often it provides a  lot more information which allows me to change my management.   My scan will never be comparable to a CT in terms of sensitivity, but it is a whole lot better than me using my eyes, ears and fingers only. Some parts of the ‘SUSS IT’ are clearly validated, have a basis in evidence and are used extensively eg. FAST, lung scans.

Well – same as you currently do a primary and secondary survey, but you use your US probe to sharpen your diagnostic screen. We know that a lot of the clinical examination that we do is insensitive and unlikely to change management (Chris Nickson posted a great example of the inadequacy of rectal examination in trauma this week. Check out LITFL “Adding insult to injury”).

Sure, if you are going to do a panCT you probably will get a lot of the info from that. So why bother?

- Avoid radiation in the lesser trauma patient

- If you work in a CT-free hospital, like many in rural Australia

- If you are in a completely Xray free place – as in many places, at night, or on weekends

- If the patient is too sick to go to CT

- To diagnose those minor injuries that go along with major injuries, without having to go back to radiology dept.

- To get info early in the resus

- The haemodynamic and functional assessments eg. ECHO, IVC, ETTube / line placement – you need this data now – not after the CT.

- Because it is more useful than doing nothing whilst waiting for the flight team.

 

Airway

  • Assessing for intubation difficulty by US might be more accurate than clinical asseesment - small pilot study, suggests it is more accurate than our usual techniques, and can be done in an unconscious  / supine patient.
  • Pre-induction marking of the neck for potential surgical airway has been widely used.
  • US-guided surgical cricothyroidotomy – it might work – see this from the US podcast boys, paper pending – watch this space
  • Verification of ETT placement and bilateral lung ventilation has been shown to be fast and accurate by Pfieffer et al
Breathing   
Circulation
There are a number of applications for US in diagnosing and assessing the circulatory status of trauma patients.  Also good for access in the tough cases
  • IVC diameter / change with respiration – has been used a lot to assess for hypovolemia / fluid responsiveness.  A few studies show it can show subtle loss AJEM published this.  Emcrit has a video showing you how to do it here (IVC collapse). Its not too hard.
  • A focused ECHO looking at the LV for hyperdynamic motion in the context of trauma blood loss is good evidence you need to give red stuff!  Another great clip from Ultrasound Village.
  • Arterial line placement – sure we can do it without an US, but sometimes in the truly shut-down patient it can be tough.  I found this study in Acad. Emerg. Med 2008 which shows it might be quicker, and require less stabs to get it in with the US probe in the other hand.
  • IV access – surely the biggest IVC you can get in the biggest vein is a good thing – but in the world where obese people with deep veins can make you earn your keep – I think having the probe nearby just might come in handy.
  • CVC placement.  For me I always go for an IJ line in trauma if possible.  Check out Sonoguide’s guide to all things US-guided venous access here
Disability / Neuro
This is maybe a bit more controversial.  The use of US measurement of optic nerve sheath diameter (ONSD) to detect raised intracranial pressure has been studied by a few groups in the last 5 years.  Mostly small studies, comparing to CT changes or the readings from an invasive pressure monitor.  Certainly the numbers they come up with look good in terms of sensitivity.  I did a review on this last year (Raised ICP – Can we pick it?).  Not sure if this is ready for “prime time” but it has to be worth a look (it is quick and easy) and add the data to your overall ‘gestalt’ – maybe you will do your RSI a bit differently? Get that CT earlier?
What I want to see is a basic statistical study that looks at 1000+ ONSDs and established a normal curve – there seems to be a wide range of “cut offs” used in the papers I am reading – so I want to know – when is it really 2+ SD outside the norm?  Any takers?  Come on – US Village, US Podcast….
Eyes
When it comes to eye trauma – US is the only way to fly.  You can see it all, even if the brow injury has swollen the lids tight shut!  Lens dislocation, globe rupture, retinal detachment, IO foreign body, bleeds – you can see them all.  Much better than the ophthalmoscope in a patient who cannot follow intructions etc.  Check out Sonoguide’s Ocular section for some good pics.
Picking a hyphema might require you to look with your own eyes – but the rest US is great for!
Chest
Already covered most chest / lung injuries under “Breathing” above – but not the heart injury.
Traumatic pericardial effusion / tamponade – Beck’s triad [low BP, muffled heart sounds and distended neck veins] is the teaching, but it sucks in reality.  So use US / ECHO – as shown at Ultrasound Village here.
Aortic injury – probably outside the scope of the average ED US user.
Pulmonary contusion – Toby Thomas suggested this link – Chest 2006 Soldati e al suggest US is as good as Ct for contusion.
Also this slide set from Ericsoussi has some nice pics of lung pathology.
Abdomen
  • FAST scans are well studied and used all over the planet.  There are well defined clinical algorithms for the use of FAST scans such as this one from the Scand. J of Trauma, Resus and E Med 2009.  I think most of us know and can use the FAST – so I will say no more about it here.
  • Pregnancy assessment – in trauma there are a few questions you need to ask:
    • Is this woman pregnant?
    • Is the fetus alive?
    • What is the gestation?  ie. are we past the point of viability should delivery occur?
    • Are there any obvious injuries.  NB: using US to exclude an abruption is not a good idea, proven to be an insensitive exam (~50%).
Pelvis
Whenever I do a secondary survey I “spring the pelvis” and wonder – what is the sensitivity of this?  My guess not that great,  and we know that PR exam is terrible for detecting pelvic injury.  I recently saw this paper (thanks Cliff Reid @ resus.me) from Journ of EM 2011, which suggests the simple act of scanning down onto the pubic symphysis and measuring the “gap” is prety good for detecting open-book fractures [for me this is a great example of a quick US technique which allows me to make my exam sensitive and objective - thus allowing earlier intervention - get that binder on, arrange transfer to somewhere they can deal with a pelvic injury. ]
So what about other pelvic fractures? well, it is a big bone that you can see on US – I reckon I could pick an iliac wing fracture pretty easily
Boy Bits
Limbs
  • Long bone fractures are usually clinically obvious, but sometimes they can be subtle – especially in the unconscious patient.  It can be easy to miss a radius or fibula fracture when you are busy fixing the chest or head injury.
  • I have often been in the scenario where I finally get around to looking at the littler bones after all the resus is done and find something minor.  Usually we just clean, plaster and tie it up for transit – but why not use the probe to confirm the injury – and avoid another trip to Xray with the ventilator?  At least you can warn the receiving team about it – embarrassing to diagnose it on day 3 when the patient wakes up !
  • Is there a fractured bone in that messy deep wound? Have a look – might need a proper washout sooner rather than later…
  • Need to find some shrapnel, Us is good for this – it would be remiss to not have a link to an article from Dr Blaivas (Journ of US in Med)- so check out this one that looked at gunshot wounds in limbs.  Blaivas is the guru of US in Emergency medicine in case you need to look something up.

IN SUMMARY

 I hope I have convinced you of the following:

  • Ultrasound is a useful extension to clinical examination.  I am not suggesting that you use US in place of X-ray or CT if appropriate – I am saying you can use US as a way of sharpening the clinical exam and finding the pathology etc quicker.
  • We know that our clinical skills are just not that great for much of what we need to achieve early in managing trauma
  • Despite working in a small hospital – you can get a lot of information quickly using US techniques in trauma cases.
  • If you are in the field or on a plane – then the SUSS IT is ideal.  The evidence from disaster scenes shows it does make a difference to disposition and other decisions in the early stages of management.
  • The SUSS IT is a smorgasbord of techniques that you can use as required to get information and modify your management in real-time.
  • Most of these ‘scans’ take seconds to do – in a busy resus, they may be seconds well spent if you have the resources to do it…

I hope this gives you a platform to explore the utility of US in trauma.  This is a rapidly expanding field of evidence, and I know I have missed some great US-tricks.  So please let me know – are there any more morsels we can add to the smorgasbord?

I hope to make this a “Clinical Resource” and update it as new evidence comes to light.

Happy scanning – Casey

 

Twitt
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Clinical case 038: a AAA eh?

Filed Under: Clinical Cases, Emergency, General Practice, Surgery, Useful Evidence by Casey Parker — Leave a comment
December 27, 2011

Todays case – 69 yo woman presents to ED with 3 hour history of sharp, severe left abdominal pain. Pain is colicky, radiating down into groin. Urinalysis shows 2+ blood.
So if you read the “frolic with colic” post and the wise comments from the readers you will be asking for an ultrasound – not to diagnose a stone, but to rule out a AAA rupture.  So off to the dark room, maybe you are a keen US type and you have a look yourself.  So you pick up the probe and identify the aorta, then follow it down and is bulges out just below the renal vessels to a max. diameter of 3.9 cm….

This case got me thinking.  I know there are a lot of ED / Gp docs out there who are keen on bedside sonography.  And looking at the aorta is not the toughest utility for those with a small amount of training.  But, the big problem isn’t finding the pathology – rather knwing what it means and what to do about it.  So here is a quick review on the topic.  Most of the info here is pulled from a nice review article, written by my former boss Mr Paul Norman and Dr Powell in Circulation 2007.  It is worth a read if you have time.  The super simple summary is that:

  •  most of what we know about AAAs comes from data which is heavily skewed towards men.
  • Female AAAs grow faster than those in men
  • Women have a higher rupture rate (~4x) for a similar diameter AAA c/w men
  • Women are technically more tricky to do repairs on, esp. endoluminal.
  • Women tend to be managed “non-surgically” in rupture at higher rates than men.
  • Basically, women seem to get the raw end of the deal in every department when it comes to AAA
  • The rates of AAA are climbing faster in women (?late lag effect of smoking)

 

Q:

Most sources quote 30 mm.  If you want to know how to measure this with an US – check out the Ultrasound Village website lecture on AAAs.   

The guidelines vary from organisation to organisation. But, it is likely that you should consider referring women with smaller diameters than men, as they tend to pop earlier.  So the magic number in men is 5 – 5.5 cm for elective repair, it seems that 4.5 – 5 cm probably confers the same rupture risk in women. 

Of course, the job of the GP is to counsel the patient and do so in the context of other comorbidities and the patient’s own risk beliefs.  After all, this is not trivial surgery.  There are serious comlications and an appreciable surgical mortality.

This paper in Annals of Surgery 2010 looked at the mortality rates for elective repair @ 28 days, 1 year and 5 years.  Being older, female and having comorbidities had a large effect on survival – up to 50% mortality in some groups!

The Circulation paper (above) recommends surveillance “every 6 – 12 months using CT or US”. The goal is to detect expansion and intervene early. So – you should be counselling the patient ahead of this – do they want an elective repair if the risk / size goes up?. In my book this means a long chat and some think time for the family before embarking on surveillance.

Well, in short – probably not. There was a Cochrane review in 2007.  This showed no reduction in all-cause mortality for screening for AAAs.  There was a decreased AAA-related death rate in 65 – 79 yo. men.  There was no mortality benefit shown for women, though they were only allowed in one trial and contributed only about 7% of the trial data used.  So not enough evidence (as Bertrand Russell once said!)

So next time you scan a belly and go looking for an aorta, just recall – you might find something, and if what you are doing amounts to screening you just might be opening a whole can of worms for this patient.  Consider their age, sex and comorbidities. You just might save a life, you also might start the ball rolling on a course of events that the patient never wanted.  This is the downside of widespread bedside US for me – finding stuff that you wished you hadn’t!.

Twitt
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Massive Transfusion Protocol

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Pharmacology, Useful Evidence by Casey Parker — 1 Comment
November 24, 2011

Hi – Apologies for recent sluggish activity- I have been a busy Doc lately and working on what I hope are some good posts / resources for you all.

The first Big project I am wanting your feedback on is my “Massive Transfusion Protocol” which you can click here – or I have added as a permanent resource in the “Clinical Resources” section at the bottom of the blog.

Why have I decided to spend hours on this? 

I have always found the current published Massive Bleeding Protocols to be either too simplistic or not descriptive enough.  There are a few crucial decision points – such as” when to activate” – which are glossed over frequently.

Most protocols deal only with trauma – and in my world, the big bleeding happens on the labour ward, in theatre… etc NOT just in the ED resus bay.

So I have written a protocol for me – one which I can with a click on a page access and remind myself of the steps and “recipes” for resuscitaing in major trauma / bleeding.  I have downgraded the role of platelets – because – we do not use them in smaller hospitals and the evidence is not great for empirical use.

I have tried to include some evidence in a ‘hidden’ way to keep it simple in a crisis – or you can read at your leisure later.

Be aware: this protocol relies heavily on your hospital having in place a system-wide approach to this emergency. Your lab have to have a predefined system, your surgeon should be aware of the protocol and the concepts associated with “damage control” operations. This is not the time to get into a territorial dispute, you need to have your chickens all lined up before it happens!

So please read it- this is my draft, I hope to make it more useful with your feedback.

Let me know what you think.  Casey

Twitt
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Shock: Back to basics, beyond the BP

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Specialist Tips, Useful Evidence by Casey Parker — Leave a comment
November 6, 2011

Apologies to the smart ones reading this – but I have been trying to explain this concept to my students for a while – so I thought I would share.

Shock: this is defined by hypoperfusion of the tissues resulting in insufficient substrates (oxygen, sugar etc) for aerobic cellular respiration.

The good news is that evolution has supplied us with a back up plan in the event of “inadequate substrate for aerobic respiration” – namely anaerobic respiration – neat eh!  But there is a limit to this – you eventually need to get back to Aerobic metabolism, clear the toxic byproducts of anaerobic respiration and repay the oxygen debt.

Ok that is the technical bit done.  Now onto the clinical application of this science.

In order to maintain tissue perfusion (and fuel / oxygen supply) you need to have blood passing through those little terminal arterioles / capillaries at a rate fast enough to keep up with the demands of the tissue – this can vary also.

Here we meet the problem – we (clinicians) have got no good direct way of measuring the flow or demand in those little vessels.  At the bedside we can just guess as to what is going on.  Unfortunately our instincts for this “guess work” are a bit skewed and that is the point of this post – we need to develop better instincts here.  So this is how I do it.

The blood pressure is an important piece of information – very important – but it is not the only player when it comes to working out the perfusion of the important organs.

Problem is – we all cut our teeth on relatively stable, healthy patients who have good physiological reserve and are operating towards the centre of the comfort zone of perfusion.  In these patients the BP is probably a good proxy for “perfusion”.  BUT – in the patient who is sick (ie. the one where you really want to know what is going on ) the physics are not ‘normal’ – you need more info and here the instinct needs to be developed.

Ok, some boring mathematics now :-

Cardiac output (CO) =   HR   x   stroke volume (SV)                  and              BP   =   CO  x   systemic vascular resistance (SVR)  or  CO  = BP  / SVR

So therefore:     HR  x  SV    =     BP  /  SVR.    Yep, I just tried to reduce CV physiology to 4 numbers. Not always so simple – but its a start.

You can read HR and BP off of the monitor, or even do it manually!

The SV  - hard to measure clinically – you can palp the radial pulse and guess its ‘volume’, you can ask the patient if they have some chronic cardiac disease / cardiomyopathy / IHD.  Or you can pick up an ECHO probe and eyeball it, or ask an ECHO tech to give you a number (LVEF).  Knowing that the preload is good certainly helps – so look at the IVC – is it collapsing?

So that just leaves the SVR – and this is tough.  In a sick patient – you cannot interpret the BP or guess the cardiac output without having some idea about the SVR.  So how can we measure this?  Look at the patient – are they red, flushed or pale and white.  Feel the hands and radial pulse – are they cool and thready or bounding and warm?  Urine output – if this is low – there is a good chance the normotensive patient has a high SVR.  Or you can get a fancy monitor which gives you a number – SVV (stroke volume variation) or Oesophageal Doppler etc.  None of these are perfect.

So once you have guessed the patient’s SVR you are in a position to interpret the BP and make an estimate of the perfusing  cardiac output / cardiac index  (NB: the cardiac index sounds impressive, but it is just the CO divided by the patient’s body surface area.  ie. big people need more CO to perfuse their body than little people)

Confused yet?  Lets look at a few common clinical scenarios to illustrate these points.  Also to look at the uses and abuses of inotropic meds in the hypotensive patient.

If you give a decent slug of propofol to anybody over about 60 – they will probably crash their BP. Is this a bad thing? well yes, but not as bad as you might think.

The propofol causes a loss of SVR by relaxing all the peripheral vessels.  So both the BP and SVR have fallen – the CO is proabably not crashing as much as the BP would suggest.  Of course if the propofool renders the heart bradycardic and negative inotropy reduces the ability of the heart to compensate – this is not great.  But any Anaesthetic doc will tell you – if you give them a whiff od metaraminol / phenylepherine  – the BP comes up quick.  And as soon as the surgeon inflicts pain – they settle quickly.  So here is an example of ‘relative’ hypotension – sure it is low – but so is the SVR – so it isn’t so bad.

This is usually a vasoplegic state – all those inflammatory cytokines cause a decrease in SVR,  the vascular bed expands – making the patient “relatively hypovolemic”.  There is a fall in CO due to poor venous return – so the BP drops as does the perfusing pressure – and shock occurs.  In some (maybe 15%) they get myocardial depression form the toxins of sepsis and also therfore suffer from “pump failure as well as the other mechanisms of shock at play.

So – for sepsis the rule of thumb is :-  give a heap of fluids – more than you think.  Give 2 litres and ask questions later.  If they remain hypotensive / acidotic / high lactate then you might need to give inotropes.  BUT you have to “prime the pump first” – check the IVC / SVV (or CVP if you believe in it) to ensure they are fluid loaded adequately.  So which fluid?   The SAFE trial - no difference between saline and albumin, though there was a trend towards benefit in giving albumin in the septic subgroup.  To me, in a small place Hartman’s (Ringer’s) seems to make sense – it is chaep, easy and doesn’t screw with your acidosis too much?

Then, and only then give inotropes…which one?    I think the answer is noradrenaline – it is widely used for sepsis and makes sense as it has good alpha agonism – so combats the low SVR.  You could also use phenylepherine if you cannot get a CVC.  If htere is evidence of myocardial depression – then you might need to get smarter and use adrenaline or call a friend for help! Having said that Myburgh et al (Aussie ICU crew) showed no difference between norad and epi – so it is a bit theoretical.

This is not the same as the septic patient.  In my mind this is the opposite of sepsis in a way.  Consider a 30 yo. motorcyclist with crush chest and pelvic fracture.  The BP is lowish, you guess he is bleeding into his chest, pelvis, ?abdo… and his endogenous adrenaline is surging – so he has a massive SVR.  So here – a lowish BP equals a crappy CO and his perfusion of the terminal vessels is terrible.  This is not a place to use vasopressors – you will make his SVR go higher and kill the perfusion further.

The patient with hypovolemic shock needs volume +++ – see recent post on Massive transfusion in trauma.  Blood, clotting factors, keep them warm and manage acidosis.  And acidosis is the result of the anaerobic metabolism in the O2-starved tissues – muscles, livers etc.

So here what you want to do is open up the vascular bed, get the perfusion happening ASAP – you actually want to drop the SVR – the catch phrase is “sympatholytic resuscitation”.  You do this by filling them up with volume, then giving fentanyl (or your favourite alternative) to reduce the endogenous sympathetic drive and allow the red cells you are pumping in to get to the areas that need the oxygen.

Remember – target MAP is 65 initially – so if your patient has a comfy MAP of 85, yet you know they have bleed a lot – your BP is giving you a seriously false sense of goodness. The best guide here is the pH, or lactate or base deficit or the temp of the hands – these are the markers of poor perfusion – not the BP so much!

This is pretty uncommon… unless you are an Obstetric Anaesthetic doc – then you come across it everytime you do a C-section. So I will use this as an example.

When you do a spinal – the first nerves to go ofline are those little sympathetic fibres – so you lose your peripheral vascular tone and the SVR drops quick – and your patient vomits, looks very grey and sweaty.  If the spinal goes higher, you lose the sympathetic fibres to the cardiac plexus – and your patient gets bradycardic, maybe some aorto-caval compression = a problem (CO = HR x SV), a double whammy – SVR crash, then CO crash – not good at all. {pray there isn’t a big bleed mid-op!}

So how to manage this – well it depends on the level of the cord lesion / block.  Lower levels, without bradycardia – maybe just a phenylepherine infusion.  Higher blocks with slow heart – you might need some chronotropy to help – good old adrenaline is my choice (ephedrine is an option – though a bit weak)  The high-spinal is the one emergency that goes C, B, A  - not A, B, C in real time!

So that is my super-simple and pragmatic approach to SHOCK.  In my experience – the big problem with SHOCK is recognizing it.  Once you have made the diagnosis he management is easier – but just remember – the BP is just part of the story.

If you don’t think about the other players – CO, SVR etc then it is a bit like walking into a movie theatre half way through a good “who-dun-it” murder mystery.  You might never guess who the killer was!

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

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Pharmacology, Useful Evidence by Casey Parker — 1 Comment
October 23, 2011

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

Twitt
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Clinical Case 031: Big transfusion, Little Hospital = big trouble

Filed Under: Anaesthetics, Clinical Cases, Emergency, Pearls and Pitfalls, Surgery, Useful Evidence by Casey Parker — 3 Comments
October 19, 2011

I have been working on a post dealing with massive transfusion – Broome style – for a while now.  So last week we landed in a tricky situation.  My colleague had taken a chap with a splenic rupture to theatre and used a good volume or red cells – depleting our small blood bank, when we received another incoming trauma case!  So I thought this case was a good one to illustrate the “Stripped back” approach to massive transfusion / trauma resuscitation as I see it in smaller hospitals with limited agents.

Here is the Case:

40 yo man with major crush injury. The chap’s abdomen was trapped for about ten minutes until the load could be moved.  Remained conscious throughout this period.  Ambos bundled him into ED within 10 minutes and he arrived… then had a PEA (likely combo of hypovolemia and severe acidosis) arrest.  CPR and IV adrenaline en route to OT.  Regained consciousness as the ETT went down (doh).  Anaesthetised and prepped for laparotomy.  Initial ABG came back showing a lactate of 15! pH = 6.8.

Laparotomy showed a bunch of sub-segmental mesenteric vein ruptures, a big rectus haematoma with a few litres of red in the peritoneum.  The lab called to say – only 4 bags of FFP left, more PRBCs coming in by plane from elsewhere…

So – how to proceed?  Lets keep this big picture – what strategies do we want to use for:

(1)  Anaesthesia / analgesia

(2)  Fluid resuscitation – what type, how much?  targets?

(3) How do we monitor / measure if we are winning?  What is useful?

(4)  Surgeon – what should they do? When?

(5)  This chap developed quite good going “ACoTS” – what agents / strategy should we use to treat this?

I hope to do a post soon looking at the new guidelines released in 2010 and strip them down to make them usable in the smaller hospitals where blood doesn’t grow on trees and budgets are non-existent.  Watch this space….

So all you experts – what gives us bang for our buck, what can we store for a while and what is just hard / expensive for a small hospital.  Better still – what is cheap and easy, available and going to make a difference to patients like this?

Casey

Twitt
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Clinical Case 026: Hangover Haemetemesis

Filed Under: Clinical Cases, Emergency, General Practice, Internal Medicine, Useful Evidence by Casey Parker — 1 Comment
September 9, 2011

10:00 AM, 33 yo man with a history of frequent binge-drinking presents to ED by ambulance after his flat mate found him spewing up blood in the bathroom.  The two had been on a big night out, about a carton each (normal for Broome).  Had a late night kebab and retired around 3 AM.  The flatmate states he has been complaining of stomach aches on and off for weeks.  As you walk into examine the patient he reaches for an Emi-bag and chucks up about a litre of coffee-grounds.  His obs are: pulse 100, BP 110/60, RR 12, SpO2 98% RA, afebrile and has good peripheral perfusion.  HIs belly is soft other than epigastric tenderness ++.  No evidence of chronic liver disease or portal hypertension clinically.   You put in a generous-sized IV and order a litre of saline, some antiemetic and wonder – what to do next?  Here are some options:

  1. IV fluids, analgesia and admit for monitoring
  2. Call the endoscopist immediately – Urgent Scope
  3. Give a high dose PPI (eg esomeprazole or similar)

Here is what I would have done a few months ago – IV fluids, give a big dose of PPIs and admitted to ward to monitor and consider doing an endoscopy if he is not settling or becomes haemodynamically unwell.   Any other plans – let me know on the comments.

After doing a bit of research recently into PPIs in this scenario the waters are far from clear (in my mind).  Damn evidence – always makes things difficult.  I think we all think of treatments such as PPIs as “good” and “harmless”  but this may not be the case….

Well, this is a tougher question to answer than you might think! There are a few good-sized trials, but they were done in such a way that it is difficult to establish risk vs benefit in a meaningful way. The trials I am referring to include: If you want a 90 minute discussion – then go and download Smart EMs podcast on the topic, David and Ashley were not convinced!  The Cochrane Librabry has a few good reviews on PPIs in peptic disease

The big problem with the PPI evidence is that the studies use unusual end points – “stigmata of recent bleeding at endoscopy”, “need for further endoscopic intervention”  rather than the logical ones eg. mortality, need for transfusion or laparotomy.   This is a good example of disease-oriented outcomes vs. patient oriented outcomes.  Most patients care little about the score the Gastro doc gave their ulcer- they just want to get better, avoid an operation and not die!

So the summary of the evidence is basically broken into 2 groups – PPIs for undifferentiated upper GI bleed and PPI for proven peptic ulcers

Proton-pump inhibitors in pre-endoscopy patients have not been shown to be effective for the important patient-oriented outcomes.  If you look at the meta-analysis of 3 trials by Revman you will see:

  • that for mortality, there is a trend towards increased dying in the PPI groups, not significant, but not good either.
  • For Rebleeding – almost a significant benefit, but not quite
  • For need to go to theatre – similar to rebleeding, borderline for benefit.
  • If you just lok at the Daneshmund trial – which is the biggest: mortality was almost statistically significantly worse for the PPI group, rebleed and theatre were basically neutral.  So to compare to Vioxx – this would have almost had the FDA putting a black box label and banning PPIs in this setting, actually there was probably less evidence against Vioxx!

I think the evidence for PPIs is better in the patients whom have had an endoscopy and diagnosed a true ulcer as the cause. Also this allows rapid, accurate, in-vivo testing for H. pylori.   There is good evidence based benefit for patients with ulcers being treated with PPI and eradication therapy (Cochrane review).

So here is how I think I will play it in the future.  Treat the patient on clinical merits – resus as required, monitor for bleeding, check Hb etc, admit and get an endoscopy done when possible – based on clinical urgency.  If I can avoid an urgent GA, wait until the dust is settled and do one under sedation.  Then once you have done the scope – treat the cause – PPI, H. pylori eradication, or inject a variceal bleed etc.  Do nothing except EthOH counselling if he has a Mallory-Weiss tear.

OK, that is my take on PPIs – anybody out there got a different angle?  Casey

 

Twitt
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Clinical Case 018: Life and limb (not life OR limb)

Filed Under: Clinical Cases, Emergency, Pearls and Pitfalls, Pharmacology, Surgery by Casey Parker — 7 Comments
July 25, 2011

Had a tough case this week – 30 odd yo. man came off his motorcycle and suffered a random puncture to the upper thigh, just below the inguinal ligament.  He arrived 20 minutes after the accident with a BP of 70/50.  Interestingly his pulse rate never got much above 100.   The old ATLS classification of shock is far from an ideal tool – sometimes you just gotta look at the whole patient!  This guy was going unconcious due to cerebral hypoperfusion – that is enough for me to say he has big time hypovolemic shock!

There were a lot of great learnings from this case – my first really disciplined attempt at achieving MAP of 65 and titrating drugs / blood products to achieve this end. 

We found no other injury or explanation for the shock – so it was a matter of getting off to the OT for exploration, but we needed to control the loss as it is a good hour until theatre is ready to roll on a weekend.  So we placed a torniquet above the wound and rendered the limb pulseless.  Seemed to work well, and he was “fluid responsive” after this.  Initial ABG showed a lactate of 7.8! pH 7.15…  so we were well behind the 8-ball.  After half an hour of resus, the leg was looking cold and mottled, making the nurses a bit nervous!

This case was timely as I had just finished listening to Dr Jeffery Guy’s Surgery ICU Rounds podcast on the topic: torniquet use in limb trauma.

Check out this study from Iraq  Col. John F. Kragh et al showed that the early application of a good torniquet in limb trauma significantly reduced mortality and did not result in a higher rate of amputation / limb injury secondary to the torniquet use.

To cut a long lecture short – the experience of the US military in Afghanistan / Iraq has shown that with the use of better body armour and IEDs - the limb trauma is now the biggest preventable killer of soldiers in these wars.  The use of field torniquets has now become universal and they have some good data looking at the success and morbidity associated with this practice.  Basically, if you get a torniquet on before shock sets in – the patient does a lot better.  There was little downside – no more amputaitons or permanent disability due to prolonged torniquet time. 

Intuitively this makes sense when you consider the risk associated with the lethal triad of:  acidosis / shock, hypothermia and coagulopathy. 

How does it translate back to our civilian ED / Ambo service?  Well  not entirely the same, but I think I will be applying a torniquet early and getting to the OT ASAP next time this happens!

Oh, they found he had severed his profunda femoris artery in the thigh in case you were interested. Hb never dropped with the blood only resus!

I finally got some IV tranexamic acid (see Massive Transfusion protocol)  in my Resus room – but I didn’t use it on this case – not sure why  – would you have given it based on the CRASH-2 data?

Comments or shared experiences welcome,    Casey

 

 

 

Twitt
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Dabigatran – Clexane you can swallow

Filed Under: Anaesthetics, General Practice, Internal Medicine, Pharmacology by Casey Parker — 5 Comments
July 19, 2011

In case you missed it the newest anticoagulation agent has hit Australia – dabigatran (Pradaxa™).  It is currently on the PBS for just two indications – but watch that space…

  1. Anticoagulation of patients with non-valvular AF – where you would use warfarin usually
  2. For thromboprophylaxis in knee or hip replacement  – where you might use enoxaparin (Clexane™)

When I started trying to incorporate this new drug into my limited brain, I tried to think of it as a warfarin substitute – but apart from being oral admin, it really is not like warfarin.   I have found it far more useful to think of it as “clexane you can swallow”, here is why..

  •  It works way down the clotting cascade – a direct thrombin inhibitor, close to heparin’s antithrombin inhibition in terms of site of action in the Coagulation cascade
  • Relatively short duration of action – you need to take it BD to get 24 hr cover – like BD clexane, and its effects are gone by 12 hours in normal patients
  • It is renally excreted and requires renal dose adjustment – there is no need to adjust for liver disease.
  • You can’t really reverse it, you might be sorta, kinda reduce the effect with factor VIIa ($$$$) or dialysis, but waiting 12 hours might be your best option (actually if it is less than 2 hours since swallowed you can try charcoal)
  • You don’t need to monitor – so easier to get the dose right, you just need to know the patients renal function to dose correctly
  • If you want to know the “effect” you can measure a few obscure clotting times (Thrombin time) but this is not really possible in most centres.  hOwever, if you do an APTT – and the time is low / normal, then you can be assured the patient is not significantly anticoagulated.

All you really need to know about dabigatran in one place – Check out the UNC review. This includes simple guidelines and management of patients in the perioperative period for the Anaesthetic clinic.

You can also check out the eMJA article that accompanied its release in 2010.

For those of us in remote areas I reckon this drug is a bit of a double-edged sword.  Sure it is easier to use than warfarin, no monitoring etc…. but if you get a brain bleed in the middle of nowhere you have no good options to turn it off or even measure the effects,

Comments or questions welcome.

Oh, and I reckon it needs a witty new nickname – so we can all remember it – dabigatran is just too hard.  Suggestions?

Twitt
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Clinical Case 014: “That’s not a knife….”

Filed Under: Anaesthetics, Clinical Cases, Emergency, Surgery, Useful Evidence by Casey Parker — 3 Comments
June 10, 2011

So this is a typical Broome case.  As always – I will not sugar-coat it for you , just a blow by blow description of how it rolled out. Oh, and this one has a happy ending

30 yo. woman presented via ambulance after being stabbed in the left chest (through the axillary tail of her breast).  Seen at 3AM, primary survey all OK, a bit drunk though.  Secondary survey – single stab wound only, explored under local – could not see any penetration through the intercostals, though difficult to say clinically. portable CXR = no pneumothorax, no effusion. No FAST scan done.  Admitted to the ward for observation, IV fluids and surgical RV in AM.  Obs were not normal, but steady overnight.  Hb 134 g/l on gas.

The next AM, complaining of abdo pain, now some shoulder tip pain on the left.  Repeat formal CXR – no PTX, small effusion left costophrenic angle.  I was on for anaesthetics – so called for pre-op review to explore the wound further.  P= 120/min, BP = 110/50, RR = 25/min, feeling sick / vomited.  Hmmm…. not good

I decided to put in a big IV and send bloods for repeat Hb, VBG, cross match etc…the surgeons opted for a CT to look into the cause of the abdo pain – ? occult visceral injury.  So off to the “doughnut of death”

So the VBG comes back: lactate is 4.2 So – something is up, not perfusing her organs as one might hope.  Meanwhile in CT they have found a large amount of blood in the left upper quadrant, a small left chest effusion but no clear source for the bleeding ? spleen.  Clearly she needs some volume resuscitation – the plan is “Haemostatic Resuscitation“, check out the link for an awesome lecture on this topic.  Bottom line – lots of salty water is a bad thing for a bleeding patient, you gotta give some red stuff and products.

So without further ado we whiz her off to OT for a laparotomy, she does pretty well on induction / RSI, art line, central line, IDC and so on.  We now get the formal Hb back – it is 59 g/l (Doh! not good) and we start the packed-cells.  I called for some FFP to give and well – we don’t have platelets.  Of course the lab want us to document ‘coagulaopathy’ before thawing the FFP.  This is one of my pet peeves – in the 60 minutes they take to thaw the FFP, we will likely be in the deep end of ‘coagulopathy’.  Can’t they just trust me, we need some FFP! (See Emcrit podcast on Massive transfusion for details)  My guess was we were dealing with a concurrent blunt trauma to the spleen.

Well, there was a hole in the diaphragm, about an inch lateral to the left ventricle, this wound continued through the following structures: left lobe of liver, lesser omentum (the source of the ongoing bleed), pancreas and just stopped short of the renal vein/artery. The spleen was intact!

At this point I started to get a bit nervous – I had been ventilating the patient for an hour and was starting to think – there must be a lung injury here, is she gonna blow a pneumothorax?  So what to do?  I got out the USS and took some intercostal views to look for a PTX.  None to be seen.

USS has been shown to be more sensitive and specific than supine CXR in trauma – see this review of the literature

So they got control of the bleeding and we got our PRBCs and FFP in and by the time we were closing she had a Hb of 100 and was peeing like a trooper.  We decided to fly her out – the pancreas injury is not one we wanted to “observe” in our little hospital – if she got sick from this we would be in a lot of trouble.  On follow-up all was well – no further surgery required.

The local con’stab’ulary popped in later to say they had found a very long, fishing knife at the scene – my estimate was that it had to be 40cm from the skin wound to the pancreas!

Twitt
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