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Tue Feb 7 11:44:13 GMT 2006

Agreed--this is a classic demonstration of the importance of Ockam's Razor in medicine--if you must make an assumption, you MUST assume the most likely thing to be true--the Razor actually is a philosophic precept saying the simplest explanation is the one always most likely by far to be true.  It is one of the most basic of medical axioms--the more modern version  of this is "when you hear hoofbeats, you think horses, not zebras..." 
And let's all agree without doubt--in hypotension following trauma, BLEEDING is the default assumption of choice (i.e. the horse)--clearly--and assuming vasovagal, and more than that, acting on it, is clearly the zebra, and will be wrong much, much more often than right.
ERF

-----Original Message-----
From: Paul Middleton <paul.middleton at usa.net>
To: Trauma &amp; Critical Care mailing list <trauma-list at trauma.org>
Sent: Tue, 07 Feb 2006 20:58:23 +1100
Subject: Re: Noradrenaline for Severe Traumatic Brain Injury

Nobody is denying that there are certainly pathophysiological neurological dysfunctions which cause hypotension in the setting of acute brain or spinal injury, but the question under discussion is about whether this can be assumed to be the cause of hypotension in the prehospital setting by paramedics or other prehospital staff. 
If there is a mechanism that suggests a spinal injury one could presume that there may indeed be an element of sympathetic dysfunction and unopposed vagal tone, which should present with hypotension and bradycardia as distinct from tachycardia. There are also instances where isolated brain injury may indeed be the cause of hypotension in the absence of bleeding. Neither of these facts are disputed but what is in discussion is should someone in the field, whatever the transfer time, feel that they can safely exclude covert haemorrhage on clinical appearance alone, to the point where they feel justified in commencing therapy with vasopressors? Furthermore, what would one be doing it for? If they are aiming for some ideal systolic blood pressure then they are already making a fundamental error, as what we need is a mean perfusing pressure adequate to deliver oxygenated haemoglobin to vital organs and thereby enable aerobic respiration, not the restoration of some "normal" blood pressure. Although the presurgical management of intracranial space occupying lesions and raised intracranial pressure may involve attempts to maintain CPP and therefore CBF, this is outside the primary trauma role of prehospital trauma clinicians of whatever training. 
None of this is to say that  ambulance staff should not be using vasopressors to maintain CPP/CBF in a retrieval role, but this is an entirely different situation. A hypotensive trauma patient should be transported to hospital ASAP, and in my opinion time spent manipulating blood pressure with vasopressors in primary trauma is time wasted.
Cheers
Paul

Paul Middleton
Sydney

------ Original Message ------
Received: Tue, 07 Feb 2006 02:05:34 PM EST
From: claudia <glamourcv at gmail.com>
To: "Trauma &, Critical Care mailing list" <trauma-list at trauma.org>
Subject: Re: Noradrenaline for Severe Traumatic Brain Injury

I can go even further, neurocardiogenic causes of hypotension are 
common in otherwise healthy people who present with several complaints 
at the ED. If you perform a tilt test in everybody, you can find 
several cases of sympathetic dysfunction or vagotonia among them. 
Why is the brain injured population different from that? 
I think many of the brain injured patients are hypotensive because of 
dysrupted vasovagal tone, for sure. 

claudia 

On 2/3/06, Tom Hurst <tom at veldt.demon.co.uk> wrote: 
> I agree with many of those who have posted regarding the need for rapid 
> evacuation for surgical control of heamorrhage, and of the perils of 
> fluid (+/- vasopressor) therapy to raise the MAP. 
> 
> However, I think it is worth exploring the assumption that all shock in 
> this setting is hypovolaemic. I'm sure that many people will be familiar 
> with the article by Mahoney et al (1) that found that traumatic brain 
> injury may be associted with isolated hypotension i.e. with no later 
> evidence found of haemorrhage. 
> 
> I do not presume to understand the operational setting in which 
> paramedics work in Australia. But, if we factor in a long transfer time, 
> a mechanism of injury consistent with isolated head injury, and a survey 
> that is negative for other injuries (hard to be certain I fully 
> appreciate), might it not be reasonable, to treat the hypotension? 
> 
> 
> On a seperate note: in the north-west UK, I have seen almost exlusively 
> noradrenaline used on neuro-ICU for the management of MAP, both in 
> traumatic and non-traumatic neuro patients (other conditions aside). 
> Per-operatively either noradrenaline or pure pressors such as 
> meteraminol are used. Most of these patients at this stage have quite 
> marked vasodilation, and dobutamine (an ino-dilator) would not be my choice. 
> 
> 
> 1) Isolated brain injury as a cause of hypotension in the blunt trauma 
> patient. Mahoney EJ, Biffl WL, Harrington DT, Cioffi WG. J Trauma. 2003 
> Dec;55(6):1065-9. 
> 
> regards 
> 
> Tom Hurst 
> Anaesthesia SpR, UK 
> 
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