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Spinal injury sequelae

I have seen a run of nasty spinal injuries recently. This has gotten me thinking about the management of the things that go wrong after a serious spinal injury.

SO I thought I would pick a few “spinal conundrums” and look at the current best practice, throw it open to you all and get advice from the ether.  Lots of questions – but the one’s I found toughest-

Spinal (neurogenic) shock: management concepts. [Apologies – this is wordy!]

This is a complex haemodynamic scenario with 3 main problems to consider.  Those of us that regularly give obstetric anaesthesia are familiar with the scenario – a high spinal block, in a dry, haemodiluted, late-3rd trimester woman is a reasonable analogy to a traumatic spinal shock patient.   So what happens?

Initially a lowish lesion will result in loss of sympathetic tone to the vasculature of the lower body – essentially rapidly increasing the capacity of the blood compartment, and decreasing venous return to the heart – so both preload and afterload take a hit at the same time – a double whammy that causes a drop in BP and CO.

It is often said that spinal patient “tolerate” low BP – this is partly true – in a vasodilated state a low BP can mean an intact cardiac output. However, we have all seen the pregnant woman go horribly pale, vomit and pass out despite being supine – not good.  Vomiting in C-spine precautions is just plain ugly.

The 3rd prong to the shock occurs if the lesion is high enough to effect the sympathetic supply to the heart itself – T1-4 level (cardiac plexi).  If this supply is interrupted then the heart loses is sympathetic chronotropic supply and the vagus nerve (X) delivers unopposed parasympathetic input – thus bradycardia and a tendency to fall off the left of the rate/output curve.  In Obs Anaesthesia this is observed when the rate drops below about 35- 40 /min, however it could happen at higher rates in patient with impaired LV function or hypovolemia.

So what to do for shock in spinal trauma – well partly it depends on the level of the lesion and the pulse rate.  All of these patients will have a relative volume depletion, they will need fluid expansion and potentially a lot if they have other injuries.  So first order of business should be to “fill the tank”.

How to measure this?  Not CVP (see this from Paul Marik).  Other options out there include IVC measures / collapsability – easy enough in a non-ventilated, supine patient.  Pulse-volume variation techniques (eg. brachial PVV, Vigileo, Aortic doppler) are OK, they mostly rely on the patient being ventilated (but you have to intubate them first!!)  Passive leg raising techniques are possible, though moving the unstable spine may be impossible depending on the injuries.  All in all – a tough scenario.

Markers of perfusion / O2 supply measured in series – eg. lactate, ScvO2 are probably going to be helpful here if you have the invasive lines in place.  I think these are all part of the puzzle and we need to measure as many as possible to put the picture together.

Once the patient has adequate volume you can start thinking about vasopressors – which ones?  Well initially an α-agonist will help with the loss of peripheral vasc. tone.  Then if bradycardia is an issue you will need something that gives the rate a kick – more Β-agonism.  So what works?

I think phenylepherine (or metaraminol) are OK for the lower lesions with an intact native heart rate.  But once the lesions are higher then probably noradrenaline is your inotrope-of-choice: has good α-effects at lower doses and some β-agonism if required.  Of course you could go for adrenaline – but I still get a bit nervous about running this in the context of trauma through a peripheral IV.  So if you can get a CVC – great, but it can be tricky in a multiply-injured patient, and you really don’t want to prang a lung in this situation.  Maybe the US-guided subclavian is a good option? (Check out Haney Mallemat ultrasoundrounds.com video here)

Respiratory failure and management

Spinal trauma kinda goes backwards – C, B then A. Or at least that is how the problems unfold.

Respiratory failure can occur for a few reasons.  The actual paralysis of the intercostal muscles reduces the patients ability to ventilate – especially in the supine position.  The level of the lesion determines the extent of this effect.  The major problem with breathing occurs if the c3-5 levels are injured as these drive the diaphragm and will result in ventilatory collapse quickly if not supported. Those concepts are reasonably straight forward.

Acute pulmonary oedema can occur in spinal patients.  Why? well there are a few possible causes:  excessive fluid resuscitation, flogging the heart with inotropes might nt help in those with imperfect LV function and then there is the elusive “neurogenic pulmonary oedema” – this is often associated with central brain injury, but can occur in high spinal trauma.

Chest trauma associated with the spinal injury is common – beware the evolving pulmonary contusion etc.  And think about aspiration if there has been a head injury / LOC story. Finding an injury lawyer in the Orlando area can guide you through all aspect of your personal injury claim.

Thanks to Dr Minh le Cong for a set of clinical pearls. He is the guru of the emergency airway in or out of hospital – here is what he has to say:

A. if any sign of hypotension prior to intubation, aggressive treatement with noradrenaline and fluids is warranted. RSI induction agents will drop the BP like a stone, even ketamine.

B. airway positioning will be suboptimal..expect that and use a blind technique like ILMA or RSA to restore oxygenation quickly after induction and paralysis or a VL device if you are slick with one. Bougie has been 100% successful when other techniques have failed in tubing the c spine injured patient. [love this tip Minh – one scenario where accepting an airway over a tube might be a good tactic]

C. Strongly consider a surgical airway primarily if the airway looks tricky from a DL viewpoint. lots of local anaesthetic, cricothyroid puncture with ligoncaine sprayed into the trachea, judicious ketamine IV for analgesia, lots of lignocaine with adrenaline infiltrated over cricothyroid area, vertical incision to get under skin, feel membrane, incise horizontally through membrane, leave blade in position and pass bougie along blade and off tip into trachea. Bit more IV ketamine analgesia, rail road small ETT over bougie, confirm with ETCO2 then fully anaesthetise.

Steroids for acute spinal injury – do they work? Should we do this?

When I started writing this I was a simple country doc, now I am wizened and cynical.  I have been out to the twittersphere and asked everybody I know and I think it is fair to say that sometimes when we “stand on the shoulders of giants” we end up with our “head in the clouds!”

I did a Cochrane search – [here are the results] This was done in Jan 2012 by Dr Bracken.  A read of the abstract and summary left me thinking – OK, methylprednisolone commenced in the first 8 hours seems to be a benefit.  I work at least 12 hours away from a trauma centre –  so I should be doing this? Right??

Then I did the Twitter thing – asked the international brains trust of EM.  And the overwhelming answer was – um, no, we don’t do this.  Then I was pointed at this log post from EM Lit of Note (Dr Radecki).  Suddenly it was all a bit of a conspiracy! Turns out Dr Bracken –  the guy who lead all the big NASCIS studies into steroids for SCI also wrote the Cochrane reviews over the past 12 years.  None of the data was strongly positive, yet there is a definite positive glow to the review. How has David Newman @ SMART EM not done a post on this?

Then @ rfdsdoc pointed me to this summary from Trauma.org in which a blow-by-blow description of the evidence is presented to the ATLS committe to encourage them to remove steroids from the ATLS manual on account of the repeated and negative studies into their efficacy.

After this rollercoaster of evidence I am making the unilateral decision on behalf of myself – NO STEROIDS in SCI.  There are just too many other things to worry about [eg. preventing secondary or iatrogenic injury] in an unstable spinal trauma patient.  I need to have my resus-head on, not be worrying about a small, unproven benefit in this scenario.

OK, that is it from me on this topic.  Bit of a mixed bag.  Really want to hear what you have to say on all of this.  Corrections as always welcome.

Casey

Comments

  1. Michael Toolis says

    Great topic Casey.

  2. Minh Le Cong says

    Hi Casey
    good topic to try to cover!
    we have had a number of unstable c spine injured patients needing intubation over the
    last few years and here are some pearls to be shared.

    1. if any sign of hypotension prior to intubation, aggressive treatement with noradrenaline and fluids is warranted. RSI induction agents will drop the BP like a stone, even ketamine.

    2. airway positioning will be suboptimal..expect that and use a blind technique like ILMA or RSA to restore oxygenation quickly after induction and paralysis or a VL device if you are slick with one.
    Bougie has been 100% successful when other techniques have failed in tubing the c spine injured patient

    3. Strongly consider a surgical airway primarily if the airway looks tricky from a DL viewpoint. lots of local anaesthetic, cricothyroid puncture with ligoncaine sprayed into the trachea, judicious ketamine IV for analgesia, lots of lignocaine with adrenaline infiltrated over cricothyroid area, vertical incision to get under skin, feel membrane, incise horizontally through membrane, leave blade in position and pass bougie along blade and off tip into trachea. Bit more IV ketamine analgesia, rail road small ETT over bougie, confirm with ETCO2 then fully anaesthetise.

  3. Thanks Casey. On IVP U/S assessments of preload– why would this be any better than CVP measures? The echo-enthusiastic docs seem to be the same ones that poo-poo CVPs (fair enough), yet put heaps of faith in IVP measures, which to my logic, are similar?

    • Hi Graeme
      Great question. Lots of new data in recent years, lots of new tricks to assess “fluid responsiveness” – might have to do a whole post to update this area of practice.
      Thanks for the query.
      C

  4. Mike Sherriff says

    “The 3rd prong to the shock occurs if the lesion is high enough…and the vagus nerve (X) delivers unopposed parasympathetic input – thus bradycardia and a tendency to fall off the left of the rate/output curve.”

    With atropine being a parasympatholytic / vagolytic, it should still be effective for bradycardiac resulting from a high spinal cord lesion, because it would act on the vagus nerve. Correct? Would one want to use atropine in this setting?

    • Hi Mike
      Good point, atropine or glycopyrrolate should be useful.
      Not sure if there is any evidence. Thinking of “high spinal cases” we see in c-section anaesthesia as an analogous autonomic imbalance: I have found atropine to be only partially effective, so I tend to use ephedrine it he short term, or push dose adrenaline in homeopathic dilutions.
      Anyone else out there got thoughts on this?
      Casey

Trackbacks

  1. […] Spinal injury sequelae – Casey digs deep into the literature to answer some questions on managing the critically injured spinal patient, and comes up with a post on where the evidence is at, and what is current best practice. […]

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