Tag Archive: resuscitation


Course Review: Advanced Paediatric Life Support (APLS)

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Paediatrics, Uncategorized by Casey Parker — 7 Comments
April 9, 2012

Last week I completed the APLS course over 3 days.  I am an impartial educator and thought I would give my review – so what did I think?

APLS is a well organised and run course.  It covers a lot of material over 3 days.  The level is pitched at the post-graduate trainee – ideally PGY 2 -4 I think.  The days were long – 11 hours of material in a day… this is probably counterproductive.  The course could be streamlined I think without losing too much.

At ~$1900 – it is a reasonably expensive course.  For that money you get a lot of theory, manikin-based scenario training, but no animal / cadaveric models to improve your clinical skills.

The learning is largely based around lectures – not everybody’s preferred format!  I found the lectures a bit long and repetitive, especially if you had done the required pre-course reading of the manual.  The teachers were friendly and well-informed, and an effort to remain entertaining was evident.

The scenarios and skills stations were OK.  As a more experienced participant I found being put on the spot in simulation to be a strong learning tool and allowed me to identify my weaknesses and cognitive errors.  I was aware that some of the more junior participants found the live simulation a bit confronting.

The material presented is largely up-to-date, though there are some areas where there is a lack of evidence base.  For a ‘resus course’ the absence of ultrasound strategy was striking.  The preference for ETT over LMAs in resus seemed odd given recent changes in most major guidelines

The testing and scenarios were OK, but did lack some flexibility to allow more experienced clinicians to make judgement calls rather than blindly follow protocol – ie. there is some ‘lowest common denominator’ effect – I guess this is a function of running such a broad ranging course.  Good for jnior staff, but a bit frustrating if you are 10+ years into your career.

Summary:

APLS is a well run course that covers an ambitious amount of material in 3 days.  The educators are entertaining and well-versed.  I recommend it to junior doctors, and staff who are unfamiliar with Paeds patients and wanting to extend their knowledge from adult care.  For the office GP who wants to brush up their resus skills – it is OK.

If you already do a lot of Paeds, especially in ED or anaesthesia environments than this course might e aiming a bit below your educational needs.

Any one out there got experinces of the APLS to share?    Casey

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 020: the ABC of APO

Filed Under: Clinical Cases, Emergency, Internal Medicine, Pearls and Pitfalls, Pharmacology, Useful Evidence by Casey Parker — 4 Comments
August 6, 2011

53 yo man with a history of hypertensive cardiomyopathy presents to ED at midnight with severe dyspnoea.  No chest pain, no oedema, no fever, cough or signs of infection. On examination he has bilateral creps up to his scapulae, invisible JVP due to big neck / beard.  ECG shows an old LBBB, same as previous.  Obs – pulse 100 sinus tachy, BP 200/120, RR is 30, Spo2 = 90% RA – he looks sick, sweaty and scared.  So what is the diagnosis?  Well most of us would have no problem saying this chap has acute pulmonary oedema.  But is it all that  clear, and how should one treat APO?  I have done a bit of research and come up with my own personal APO approach.

In my mind “APO” is usually one of 4 different clinical entities…

  1. SCAPE (Sympathetic Crashing Acute Pulmonary (O)Edema).  Scott Weingart has a great podcast on this group at Emcrit.  You diagnose this by looking at the BP – does this look like a patient who is running his own endogenous Adrenaline infusion?  The case above fits into this group nicely.  Often there is no history of CCF, no oedema, no clear ‘trigger’, normal LV function.  This process is largely neuro-hormonal in aetiology and comes on pretty quickly – over hours.
  2. Acute-on-chronic (Acute decompensated HF).  This group have a history of CCF, chronic poor LV function and likely are already on treatment (which hey have often missed!).  They have low BP, poor urine output and borderline renal perfusion / function, they might have worsening peripheral oedema, and they tend to come on a bit slower – over days.
  3. The “Acute Cause” APO group.  These are the folks who have a clear new cause for their APO – common causes: ACS / STEMI, rapid AF / arrhythmia, PE , acute valve rupture, high output state – sepsis, anaemia… These people might have a reversible cause or at least something you can try and fix / get to definitive care.
  4. Iatrogenic APO – uniquely occurs on surgical wards!!  The old duck who has had a few too many litres of saline for her chronic low BP,  This one is easier to pick, and might be a subset of group 2.

Probably not as good as we think. There are a lot of confounders – classically it can be tough to differentiaite APO from COPD clinically – large studies have shown this. So I just admit my shortfallings and get a CXR, it either looks like APO, or you find another cause for the SOB (pneumonia etc).  Get a few ECGs, troponins and make sure you have thought about the other “reversible” causes.  Oh and BNP – it is only helpful if negative – if the BNP is low – it is probably not APO!

 The Oxford Handbook of Medicine lists the treatment of APO using the LMNOP mnemonic.  So lets look at the evidence for these interventions.

No good evidence. Never been shown to improve short or longer term outcomes. Based on the flawed assumption that the patient is “fluid overloaded” which is usually not true – especially for the SCAPE patient. I almost never use Lasix in the acute setting, unless there is clear overload, and the patient is on it long term.

Morphine is bad! The ADHERE registry of APO patients showed that morphine was independently associated with increased mortality. Sure it might make the patient feel better – and that is fine if your goal is palliation, but not if you want to fix them! I don’t ever use morphine in APO. There are better options for sedation if you need that.

Nitrates are good. especially in the SCAPe with BP up high. The problem with GTN infusions is that we have all been trained to use homeopathic doses. If you really want to get the patient better quick, use GTN in a proper dose – 400mcg/min to start (see Emcrit for references). I put 50 mg of GTN in 100 ml, and start it at 48 ml/hr for a few minutes and tirate back by 6 -12 ml/hr until I have a MAP around 80. If you do this well, the true SCAPE will be better in an hour.  An art line is great – makes titration so much easier.

Oxygen is good – but we can do better. All the recent studies show that NIV is superior to oxygen. So if your patient can tolerate it – go with CPAP, if not, then O2 is good.

 

Along with GTN, CPAP is the thing that will get your patient better quickly and mean you don’t even have to consider an ETT. I start with 10 cm and titrate to RR and effort.  Beware the low BP / floppy heart / super dry patient – they might crash with the combo of GTM and CPAP. If so – they are probably a type 2 patient – tough scenario. Oh, and the studies show no difference between CPAP and BiPAP – so I only use BiPAP if I think there is a ventilation / COPD component or hypercapnea.

Well ACE inhibitors are probably useful, they get at the neuro-hormonal axis that can be the cause of the SCAPE syndrome.

Magnesium – often low in CCF /AHF and can lead to arrythmia – so I like to load with Mag

Good Palliation: APO is sometimes the end of the line for a patient with severe heart disease.  It is analogous to the COPD presenting in extremis in some cases.  So before you embark on invasive manouvres you might want to have “the talk” with the patient and the family if it is clear that the underlying disease process is not remediable.

I aplogise for saying “studies show” but there is a lot of good data out there and a few great reviews – too many to go into in a quick blog.  If you are keen to see them go to Crashing Patient and see the links.

The summary is: get them on the NIV ASAP, and hit em with a proper dose of GTN – they will get better quicker and you will intubate less people!

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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Clinical case 016: Toddler vs. TV

Filed Under: Clinical Cases, Emergency, Paediatrics, Pearls and Pitfalls, Surgery by Casey Parker — 5 Comments
June 29, 2011

This is an older case that sticks in my mind.  A great example of the subtle signs and compensation kids can show despite being very sick!

3 yo boy carried into the ED of a small, peripheral metro hospital by mother – screaming.  She is crying, and between sobs says:  ”I was in the kitchen when I heard a crash.  I rushed into the living room to find him lying on the floor, on a bean bag, with the new TV face down on the floor beside him.  He must have tried to climb the TV cabinet and pulled the TV down!”  [CP: this was a while back when TVs were boxy and v. heavy in the front.  Pre-plasma / baby bonus era!]

The boy is screaming unconsolably, undressed and there is not a mark on him, no graze, no haematoma, nothing.  Scalp all looks normal, no haematoma etc.

Obs: pulse 180, RR – 30 (screaming), Spo2 98% RA, BP – hard to record, not perfusing his hands or feet well, cap refill slow @ 4 -5 secs.  Belly is scaphoid, soft.  Chest looks and feels normal – no obvious fractures, HS normal, air entry equal, trachea midline.

IV access pronto x 2 and 20 ml/kg of N/saline bolus given by hand.

10 minutes later the kid is settling, sobbing quietly.  Obs have improved = pulse 160, RR = 16, cap refill now 2 – 3 secs, hands a bit pinker.

So what is going on?  We start thinking:  ?occult belly bleed eg. spleen, concealed haemothorax, maybe an intracranial bleed…

Normal CXR, no fractures, pneumothorax or effusion seen…

This was the bad old days, before bedside US in the ED was widely available.  So we were scratching our heads for a minute or two when Mum noted he had become very quiet – too quiet for a 3 yo. in an ED.  Recheck of his Obs:  responds to name and gentle prodding, seems sleepy.  Pulse now 190/min, BP done = 50/20, cap refill once again – sluggish, pale hands.  Hmmmm…. not good.   Another bolus of 20 ml/kg of N/saline given over the next 10 minutes and urgent transfer to the tertiary hospital arranged – “we need to get him to a Paeds surgeon / CT” is the thinking.

Ambulance with lights/sirens up the freeway 30 minutes.  A third 20ml/kg saline bolus en route.  Obs remain bad, peripheral pulse is weak @ 190 – 200.  On arrival the plan is to go to CT if he is stable or OT if not – ?laparotomy.

This boy had a ruptured right atrium with cardiac tamponade. Fortunately a cardiothoracic team had just completed a case and he went into their theatre. Urgent ECHO showed the tamponade, so he had a sternotomy and decompression which revealed the ruptured atrium! The surgeon suspected hat his heart was crushed between the sternum and the thoracic spine – like in zealous CPR – and pop went the atrium!

This was one tricky case.  What would you have done differently?     I think the bedside US / RUSH protocol would have made the diagnosis in quick time.

Check out these ECHO images and discussion from Ultrasound Village

OK, there has been a bit of debate about emergency thoracotomy after this post.  So I will direct you to Scott Weingart’s podcast on the topic.

Thoracotomy for trauma thanks to EmCrit

Twitt
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Are you an Occasional Intubator?

Filed Under: Anaesthetics, Emergency, General Practice, Pearls and Pitfalls, Pharmacology, Specialist Tips, Useful Evidence by Casey Parker — 3 Comments
June 14, 2011

If you are a reader of our comments sectio, you will know about Dr Minh Le Cong – RFDS Doc from Cairns who is one of the most enthusiastic teachers I have come across in the ether.  If you want a sample of his pearls of wisdom – go to my post on Preoxygenation Pearls and check out the comments section.

One of his passions is teaching airway skills to GPs / occasional intubators.  He also loves debunking medical mythology and dogma – and he has taken aim at the classical Rapid Sequence Intubation (RSI) and cricoid pressure.

So if you are an occasional intubator, or just would like to know what all the controversy is about – Minh has allowed us to put up his lecture on the topic.

The Occasional Intubator for Broome Docs blog

Check it out  – let me, and Minh know what you think.  I am sure there are some Anaesthetists out there who have something to say?   Casey

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Can’t Intubate, Can’t Ventilate! The low down on code brown

Filed Under: Anaesthetics, Critical care / ICU, Emergency, Pearls and Pitfalls, Specialist Tips, Useful Evidence by Casey Parker — 2 Comments
June 7, 2011

Now this is a huge post, apologies in advance – goes a bit over the usual 2 minute read I aspire to!  But… this is gold.

Ever been in a “Can’t Intubate, Can’t ventilate” scenario  - if you said ‘no’ then lucky you.  It is a rare occurrence in Airway management but one which has a very high mortality – and sadly often the harm is iatrogenic, ie. our fault.

In my career I have witnessed one true CICV scenario when in training and it scared the pants off of me.  If you want the details they are a matter of public record in the Coroner’s Findings into the death of Rachael RASMUSSEN. (FYI the Dr Casey in this report is not me)    I was a “fly-on-the-wall” trainee that day and saw some great Anaesthetists struggle with a CICV scenario which was entirely avoidable.

Since then I have been involved in 2 emergency surgical airways and which have gone well, mainly as a result of the training my colleagues and I have undertaken after having our pants scared off.  In my opinion, this the ‘Elephant in the Airway’ that nobody is talking about.  We all know that surgical airway is down the bottom of the difficult intubation algorithm – but how many of us are confident enough in our training and decision-making to make the best of such a disastrous situation?

Here in WA we have a wonderful training facility based at Royal Perth Hospital which has done a lot of research into the CICV scenario using wet-lab simulations on sheep.  Dr Heard and his team have published their CICV Algorithm based on the experience derived from hundreds of trials using anaesthetic trainees (the sheep were the ‘guinea pigs’, not the trainees – excuse my Irish logic).

Anyway after spending a bit of time debating my preferred Surgical airway technique with my colleagues I decided to get the low down straight from the horse’s mouth (way to many animal puns in this post) and do an interview with Dr Andy Heard.  Here is the proposed algorithm from Dr Heard’s paper from Anaesthesia, 2009 for your reference.

To answer this question in full would require two pages, but I will be brief. My algorithm has been developed primarily as a plan for airway specialist trained in anaesthesia. Ultimately the skill mix of other groups may well mean that they would be better attempting a different path. E.g. an ENT surgeon should use a scalpel blade. Which approach is appropriate would be a decision for the individual. Note that NAP4 surgical techniques were often performed by specialised airway surgeons with all the theatre backup they would be used to. No technique is infallible; our algorithm encourages a systematic progression through techniques, with the pathway moving from cannula to a scalpel technique if required. I would recommend that you are prepared for all eventualities i.e. familiar with both cannula and scalpel to allow you a better chance of success. If this is appropriate, then a cannula technique performed along our guidelines does not cause major difficulties with scalpel techniques but a scalpel technique that fails but causes intra-tracheal bleeding unfortunately makes aspiration of air as an end point very difficult and leads to cannula failures which would have been successful. Ultimately there are a lot of requirements for successful management of this scenario: teaching, training, equipment availability etc. which can also affect your choice. I can add that we have regular E.D physicians coming through the wet lab, at least 2 of whom have successfully saved a patients life with a cannula technique and then secured the airway with a Melker.

(2)

This is actually a similar question to number one. An (our) observational study on success is no guarantee of success. These were all on easy necks with easy to palpate anatomy. Performing a scalpel technique with no identifiable anterior neck anatomy is inherently far more difficult and not appropriate for the scalpel bougie. I occasionally have people attend the wet lab and say that the scalpel bougie is their “take home” choice. I point out that if that is their plan, probably in 1/3 of patients they will not be able to proceed due to difficult anatomy. You can proceed with a cannula no matter what the anterior neck airway anatomy. Part of the problem, in anaesthesia at least, is that speciailists struggle to make the decision to go round the front of the neck. Giving a simple choice, with no decision process required of a cannula first every time encouraged people to attempt rescues oxygenation through the front of the neck. This reluctance is well documented in critical events (e.g. Elaine Bromiley). They can still move onto a scalpel technique if required.

(3)

Again requires a long answer. But put simply we have pointed out for many years now that most of the anterior neck airway equipment “designed for purpose” is unreliable and often unsuccessful in the emergency situation. Hence we have rewritten the plan, techniques and changed the equipment to suit the requirements of the CICO scenario. NAP4 has often very nicely validated our points in regards to this. Also many (if not all) of the surgical airways using a scalpel were completed by surgeons (in particular head and neck surgeons), not anaesthetists. They also point out that they may have missed many events, including successful cannula that were not reported. There were no recorded details of operator experience or training. Emergency airway management through the anterior neck is not something we do every day. To try and use an analogy – If we were to advise all surgeons to use a laryngeal mask (which they had never used before) and asked them to use them for the first time in anger in the worst airway scenario of their life, the results would not be reassuring; in a NAP4 equivalent study looking at airway disaster for surgeons. If interpreted as NAP4 seems to be interpreted against cannulas, it would convince surgeons to never use a laryngeal mask in an airway emergency. If they also audited anaesthetists who used laryngoscopes then they would say that laryngoscopes worked very well and hence all surgeons should just switch to using laryngoscopes. This would not improve their outcomes, but would end in disastrous results. Even with some training you do not gain satisfactory laryngoscopy skills easily on a manikin. What they would need is training in the technique which suited them, using appropriate equipment. Looking at the surgical “High success rate” that they compare against the cannula low success rate. Only 11 of the scalpel surgical airways were true emergencies in NAP4, and of these 2 patients died. This is with surgeons who know how to hold and manipulate a scalpel blade, have diathermy ready and know how to use it, are in their relative “comfort zone” i.e. using a scalpel not a cannula and in many are airway surgeons who do incise the neck every day of their working life. If this is to become the gold standard for all airway specialists how are we ever going to teach everyone to manage this situation? I suggest the only way would be for all airway specialists to have to undertake at least 1 year of ENT training. We purposely moved away from standard scalpel techniques in our plan for a variety of reasons, one as stated to allow a direct path onto the algorithm to avoid decisions and fixation errors, and secondly because our, now quite extensive, experience of scalpels held in anger by anaesthetists and other specialists in the wet lab showed very poor results. This has been addressed in some way by the scalpel bougie technique which minimises scalpel manipulation and hence scalpel skills, but this technique is only appropriate if the airway anatomy is palpable. Trying to give anaesthetists or other specialists the skills to manipulate a scalpel in anger in a stressful environment is a virtually insurmountable task. One final comment is training also needs to switch from the ongoing plan of ventilating through the cannula to accepting oxygenation is the priority and ventilation is secondary. The cannula is only a temporising measure to prevent death from hypoxia whilst working out your next step (See algorithm). NAP4 lists cannula failures, but some of them are surely jetting failures due to poor jetting plans and technique. Having a safe plan for this is essential, and we are currently publishing our latest on this.

(4)

There is some evidence regarding recall and hence requirements for ongoing training, one that comes to mind is Wong et al from Canada published that study showing that on a manikin it requires 5 practices at cannulae to get the technique correct… and that they recommend retraining every 6-9 months since this is the time period for deskilling.. All airway specialist do not need to attend a wet lab for training. Attending a training program that teaches a plan and techniques that are well thought out and logical is the first step. The algorithm and techniques I have developed are now taught around Australia, on NATCAT, at Airway SIG meetings, AAMRC in Melbourne, WAAG meeting and wet and dry labs here in WA, Also in Brisbane on Keith Greenland’s course and in Adelaide on Chris Acott’s courses. Also To encourage and help with ongoing refresher training we have put a set of videos on yotube to allow people to refresh their plan. Look for drambheardairway on youtube.

(5)

This is a scenario that was faced by a G.P. anaesthetist who had attended our wet lab training to return to the Kimberley region in WA and end up having to perform a surgical airway on a colleague for just this reason 3 days later. He initially (successfully) put a cannula in and then was going to convert to a melker but realised his hospital at that point did not stock the melker kit. He, having had experience of the EMST technique in the past which had not been altogether positive, went on to do a scalpel bougie, after removing the cannula and secured the airway with a 6.5 CETT. Having performed many ICU transfers in the UK, admittedly mainly by road but often very prolonged, I am of the opinion that securing a cuffed airway is of major benefit to the patient. It will always be scenario specific, but either cannula or scalpel technique can be attemped. Looking at complications, one of the major issues with cannulas, I accept, is the attaching of high pressure oxygen to the cannula to oxygenate the patient. In this scenario there is no requirement for this and you can just perform a control melker insertion without jetting or time pressure. This is the ideal scenario for inserting a melker as there is no time pressure for success and you don’t have to jet down the cannula hence avoiding barotraumas issues.

(6)

I just had a paper published recently in the European Journal of Anesthesiology on this topic. If U/S is available and you are having difficulty identifying the anterior neck airway anatomy then definitely it is worthwhile We showed that in a time pressured environment, if the trachea was not midline, U/S significantly improved performance. In this day and age of U/S becoming ubiquitous in many critical care areas this is certainly going to become more used. If nothing else ensuring the trachea is midline prior to induction, or an X marks the spot, is worthwhile if you have time.

 

In the 14th century, French philosopher Jean Buridan was satirised for his philosophy using the paradox of “Buridan’s Ass”.  The paradox involves a donkey who is standing exactly midway between a bale of hay and a bucket of water.  The donkey dies of both starvation and thirst whilst inconclusively trying to decide on a logical course of action.

How is this relevant?  Well I think that the real problem with surgical airways is the “option paralysis” that takes hold when one finds oneself in a CICV scenario.  If you have not thought it through or practiced a solid, reliable (in your hands) technique. Then your patient may go the way of the aforementioned donkey.  I am sure there is no single, perfect surgical airway technique, but you have just gotta have a “go to” technique for when the situation arises.

Twitt
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