TBI & HT saline - not fashionable ?
McSwain, Norman E Jr.
nmcswai at tulane.edu
Sun Jun 1 08:14:45 BST 2008
One reason is the FDA has not approved its use
Typed by the thumbs of
Norman on his BlackBerry
Norman McSwain, MD
Tulane Univ Surgery
504 988-5111
----- Original Message -----
From: trauma-list-bounces at trauma.org <trauma-list-bounces at trauma.org>
To: Trauma & Critical Care mailing list <trauma-list at trauma.org>
Sent: Sat May 31 22:05:22 2008
Subject: TBI & HT saline - not fashionable ?
I am all for hypertonic saline on theoretical and safety grounds, however it puzzles me why it never became a "state-of-the-art" fashion such as other non-RCT-proven approaches have and why it still feels experimental after all those years of it being available..anyone knows the answer to that ?
Ivan Hronek MD
SFMC, Los Angeles, CA
http://health.groups.yahoo.com/group/Anesthideas/ Do not fear to be eccentric in opinion, for every opinion now
accepted was once eccentric. - Bertrand Russell-
________________________________
Confidentiality Notice: This transmission and any attached documents may be confidential and contain information protected by State and Federal Medical Privacy statutes and is legally privileged. They are intended for use only by the addressee. If you are not the intended recipient of this transmission, or an agent of the intended recipient, you are prohibited from reading, disclosing, printing, saving, copying, using, or otherwise disseminating any information contained in this transmission. If you received this transmission in error, please accept our apologies and notify me at ivanhronek at yahoo.comand delete the entire message and its attachments. Thank you. Disclaimer: this message contains the personal views of the author. The author will not be responsible in any way for procedures or approaches perfomed in the way suggested in this note.
________________________________
----- Original Message ----
From: MARK FORREST <atacc.doc at btinternet.com>
To: "Trauma & Critical Care mailing list" <trauma-list at trauma.org>
Sent: Saturday, May 31, 2008 5:46:09 PM
Subject: Re: TBI & 3% NaCl - protocol anyone ?
Guy
Oh come on...still waiting for another RCT then...if we are all truly honest and look back over the last years discussions on this list.....how many of the innovative and dynamic practices have already got a firm evidence base? It explains part of the role of the list with the broad depth of experience and knowledge combined with what research we have, we reach a 'balanced opinion'.
Actually, I am a little confused as you disagree with my comments about having to use 'best current opinion' and then go on to describe how we do it every day in ICU?! In addition, if you look at most TBI databases (eg EBIC ) which includes outcome, you will see that any ICP persistently >20 has a worse outcome. However, I did actually state that we obviously use CPP as our primary target. But if you are waiting on the RCT to prove the benefit of this then I guess that you will not be using ICP monitoring or TBI therapeutic goals, as neither have been shown to reduce mortality.....not on your Bandwagon?
Similarly, I assume that based on your desire for proven reduced mortality, that you do not use mannitol, which is known to have adverse effects such as rebound hypertension and has not been shown to reliably improve outcome in countless trials.
I fullly agree with you that a major factor in improving outcome in severe TBI , may well be just good quality intensive care.
Whilst we cannot live in a world of anecdotes and personal views we cannot all simply jump on the bandwagon of not changing anything whilst waiting for someone else to do the RCT to prove things for us. We must look at what options are available and make a balanced judgement that will have the least negative impact on the patient.
Considering HSD/HSS: there is evidence that they MAY improve outcome. They will DEFINITELY help us to achieve our 'therapeutic goals' and 30 years of trials have failed to show any significant side effects, either clinically in survivors or at post mortem. We havent even got this many trials looking at the safety of 'normal' saline!
So in simple terms, HSS/HSD may help but wont make things worse......as for mannitol, at best it may offer a bridge to neuro-surgery, but it does have side effects and is rarely as effective given a second time.
Finally, before you all reach for your keyboards to linch me with the EBM rope can all those who use tourniquets, haemostatic agents, APC, Factor VIIa, ILA devices, 1:1 transfusions, large volume resus, HDF for sepsis, NO, prehospital emergency thoracotomy, pre-hospital RSI, level 1 infusors in the ER etc etc all please not even bother replying.
All that I am saying is that there has to be a role for 'best current opinion' in our current practice.....that is not the same as just working with anecdotes and bandwagon medicine.
Regards
Mark F
UK
----- Original Message ----
From: "r.g.m.jackson at qmul.ac.uk" <r.g.m.jackson at qmul.ac.uk>
To: trauma-list at trauma.org
Sent: Saturday, 31 May, 2008 11:50:44 PM
Subject: Re: TBI & 3% NaCl - protocol anyone ?
Mark,
Ummmm.......No.
The figuue of 20 mmHg (for the first 24 hours) comes from the National
Traumatic Coma Database Study. An observational study. What this did
not show is whether or not controlling ICP made any difference. We
assume that this is useful as the incidence of adverse outcome has
declined over the period of introduction of ICP/CPP management. The
effect of better basic ICU has not been accounted for. Either way we
persist in what seems to work.
The problem here is our desire to do the best for the patient in front
of us. We are motivated to do the best for them. Thus we will try
anything we believe will help. This leads to "bandwagon jumping" (I
admit to being as bad as any). By doing this we prevent the trial that
would tell us.
In the case of hypertonic saline, all the data to date tells us that
it is safe at the time. There is nothing on long term survival, which
is what we are interested in.
Guy
London, UK
Quoting MARK FORREST <atacc.doc at btinternet.com>:
> Norman, you seek the Holy Grail that we all look for in many of our
> 'newer' therapies. Sadly, at present we only have indications of
> improved survival such as the Wade Meta analysis.
>
> What we do know is that if we do not optimise CPP or we leave the
> ICP persistently greater than 20, then the outcome will definitely
> be worse. HSD and HSS are more effective at repeatedly achieving
> these targets, without any apparent adverse effect, than mannitol.
> In addition, we regularly find it effective when mannitol has failed
> to have any effect.
>
> If mannitol was the 'new kid on the block' then it would have little
> chance of achieving such a safety and effectiveness profile, never
> mind and improved 30 day mortality. So let us consider something
> that is effective, with an excellent side effect profile which is at
> the very least as good as mannitol and may well be better. It is
> just like those that hang onto 'cyclic hyper-resuscitation' or
> 'colloid based resuscitation' awaiting the RCT that proves there is
> something better! Just because we have been using something for 20
> years does not make it right.
>
> Until we get these definitive RCTs we must rely on best evidence, be
> it audit, meta-analysis, small trials, SIGN analysis and safety
> profiles to make a balanced decision. Hyeprtonics may not be the
> answer, but in our eyes they seem a safer more effective option than
> mannitol.
>
> Regards
> Mark F
> UK
>
>
>
> ----- Original Message ----
> From: "McSwain, Norman E Jr." <nmcswai at tulane.edu>
> To: trauma-list at trauma.org
> Sent: Saturday, 31 May, 2008 2:40:33 PM
> Subject: Re: TBI & 3% NaCl - protocol anyone ?
>
> You talked about reductions in ICP, what about clinical outcome?
> This is the most important. Randomized studies on outcome?
>
> Typed by the thumbs of
> Norman on his BlackBerry
>
> Norman McSwain, MD
> Tulane Univ Surgery
> 504 988-5111
>
> ----- Original Message -----
> From: trauma-list-bounces at trauma.org <trauma-list-bounces at trauma.org>
> To: Trauma & Critical Care mailing list <trauma-list at trauma.org>
> Sent: Sat May 31 08:30:12 2008
> Subject: Re: TBI & 3% NaCl - protocol anyone ?
>
> Matt, Ivan and list members
>
> We started using hypertonic saline in head injuries over 6 years
> ago. Initially in cases with intractable elevated ICP unresponsive
> to mannitol or other measures.
> At first we used 5% hypertonic saline at doses between 100 and
> 250mls with impressive reductions in ICP without any apparent
> adverse effects (even under the close spotlight of ITU physical and
> biochemical monitoring). The combination of reduced ICP and
> increased MAP would improve CPP and was maximal after ~20mins and
> sustained upto about 4 hours. Hypernatraemia was only a problem
> where the larger volumes were required frequently.
>
> In an attempt to reduce the swings in ICP and to reduce the
> hypernatraemia we tried infusions (5-50mls/hr) as recommended in
> several European papers but we could not achieve the same
> improvement in ICP, although the rises in sodium where less.
>
> A number of years ago we started to use 7.5%Hypertonic saline/6%
> dextran (HSD) and we did see the initial drop in BP that you
> describe Matt (can be upto 20% in our audits, which can be quite
> scary and off-putting). Pre-hospital we would often not see this as
> it is very transient and self-limiting but in ICU using an arterial
> line it is is very obvious. HSD does seem to prolong the improvement
> in ICP but to a variable amount. At the lower volumes that we now
> use for ICP control we do not see the same drop, but we suspect that
> this is a dextran effect (see below)
>
> In the last two years we have been using 7.5% Hypertonic saline/ 6%
> starch and we dont seem to see that initial drop in BP, yet it is at
> least as effective as HSD with an excellent safety record
> (Vasser/Wade and Walter Mauritz have published a considerable amount
> of work on this over the last 20years).
>
> Using HSS or HSD we can often get an effective reduction in ICP
> with as little as 50-100mls. By using smaller volumes we avoid
> dramatic drops in ICP and hypernatraemia but we do not get as much
> rise in MAP. We have currently abandoned infucions for ICP control.
> Our current protocol is:
> - If CPP <70 and ICP >20 then give 50-100ml HSS
> -If CPP <70 and ICP <20 then we drive the MAP (usually with noradreanline)
> Whilst we follow the CPP we also try to keep the ICP <20 in view of
> the poor outcome associated with levels persitently >20.
>
> In our experience we do not see rebound rises in ICP,the response
> can be repeated (unlike mannitol) and we have seen no serious
> adverse effects clinically or at PM (eg pontine demyelination). We
> have had no allergic or adverse drug reactions with the HSS or HSD.
> Regards
> Mark F
>
> Dr Mark Forrest
> Consultant in Anaesthetics & Critical Care
> Medical Director of Cheshire Fire & Rescue Service
> Medical Director of ATACC
>
>
>
> ----- Original Message ----
> From: Matthew Reeds <mgreeds at reeds.uk.com>
> To: "Trauma & Critical Care mailing list" <trauma-list at trauma.org>
> Sent: Saturday, 31 May, 2008 11:30:34 AM
> Subject: TBI & 3% NaCl - protocol anyone ?
>
> Ivan,
>
>
>
> We use it on all head injured patients upon presentation. The preparation
> that we use though is either 7.5% or 7.2% (more commonly) or sometimes 5%.
> We never use 3%.
>
>
>
> On a purely head injured patient - e.g. EDH, SDH etc (without haemorrhage or
> other trauma), then the patient will have an initial bolus to keep up the
> MAP and CPP somewhat, whilst keeping ICP low at the same time (especially in
> the older population who are normally hypertensive and need a higher MAP to
> remain "normotensive" for them.) We do not use regular infusions just
> occasional boluses of 100mls at a time when required. This is usually more
> than adequate and reduces the total volume required. The patient can then
> have maintenance dose of fluids or, more commonly, receive their fluid
> requirements via enteral feeding from the day of injury.
>
>
>
> Infusion of hypertonic saline in such a way does not cause profound
> hypernatraemia, nor have we had any instances of pontine demyelination. The
> only issue to be aware of is that you can get a transient initial
> hypotensive drop in BP but this is always self limiting and resolves
> instantaneously. Because we use the higher strengths of hypertonic saline,
> we find that we use less volume in total and, because of this, we don't
> experience the adverse side effects that have been reported in the
> literature. This also means that we don't get too obsessed with pressure and
> overtreat to too high a CPP as well which can happen with regular infusions.
> Like anything, I think that the point is not to overuse something and
> increase the risks unnecessarily.
>
>
>
> Matthew
>
>
>
>
>
>
>
> -----Original Message-----
> From: Ivan Hronek [mailto:ivanhronek at yahoo.com]
> Sent: 30 May 2008 02:36
> To: Trauma & Critical Care mailing list
> Subject: TBI & 3% NaCl - protocol anyone ?
>
>
>
> Can anyone share a protocol for hypertonic saline use in traumatic brain
> injury ?
>
> Ivan Hronek MD
>
>
> SFMC, Los Angeles, CA
>
> http://health.groups.yahoo.com/group/Anesthideas/
> Do not fear to be eccentric in opinion, for every opinion now
>
> accepted was once eccentric. - Bertrand Russell-
>
> ________________________________
>
>
>
> Confidentiality Notice: This transmission and any attached documents may be
> confidential and contain information protected by State and Federal Medical
> Privacy statutes and is legally privileged. They are intended for use only
> by the addressee. If you are not the intended recipient of this
> transmission, or an agent of the intended recipient, you are prohibited from
> reading, disclosing, printing, saving, copying, using, or otherwise
> disseminating any information contained in this transmission. If you
> received this transmission in error, please accept our apologies and notify
> me at ivanhronek at yahoo.comand delete the entire message and its
> attachments. Thank you. Disclaimer: this message contains the personal views
> of the author. The author will not be responsible in any way for procedures
> or approaches perfomed in the way suggested in this note.
>
> ________________________________
>
>
>
>
>
>
>
>
>
> ----- Original Message ----
>
> From: Matthew Reeds <mgreeds at reeds.uk.com>
>
> To: "Trauma & Critical Care mailing list" <trauma-list at trauma.org>
>
> Sent: Wednesday, May 28, 2008 1:00:25 PM
>
> Subject: Cerebral Perfusion
>
>
>
> As we have discussed at great length on this list, I would not be distracted
>
> by the systolic blood pressure for a number of reasons:-
>
>
>
>
>
>
>
>
>
>
>
> 1) The brain has an excellent in-built mechanism to autoregulate cerebral
>
> perfusion (controlled mainly by pCO2 and, to a lesser extent, pO2).
>
>
>
>
>
>
>
> Increases in pCO2 (e.g. caused by cellular hypo-perfusion secondary to
>
> trauma/haemorrhage) increases cerebral blood flow due to marked cerebral
>
> vasodilatation (CO2 is a vasodilator metabolite which acts on the arteriolar
>
> smooth muscle via myogenic autoregulation.) This is why head injury patients
>
> are ventilated to low-normal pCO2 rather than low pCO2 as low pCO2 causes
>
> vasoconstriction with potential cerebral ischaemia. Too much vasodilatation
>
> on the other hand increases the risk of raised ICP (Monroe-Kellie Doctrine)
>
> which we know is bad as this reduces the cerebral perfusion pressure CPP
>
> (CPP = MAP - ICP). An important balance must therefore be maintained. As you
>
> will see, this mechanism is mainly influence by pCO2 and not pO2 (pO2 only
>
> plays a role at pO2 < 8kPa whereby cerebral blood flow may increase
>
> dramatically below this point.)
>
>
>
>
>
>
>
> The autoregulation works over a wide range (CPP range of between 60-160mmHg)
>
> Indeed we now accept lower CPPs than we used to do as we may have previously
>
> been overly aggressive in treating patients to their own detriment by aiming
>
> for too high CPPs.
>
>
>
>
>
>
>
> These mechanisms are affected to varying degrees by a number of factors
>
> (e.g. neurotrauma).
>
>
>
>
>
>
>
> 2) An excellent crude indicator of cerebral perfusion is conscious level. It
>
> is used daily in neurosurgery and frequently by the military (the crude
>
> correlation of carotid pulse/blood flow present = cerebral perfusion
>
> present.) The military regularly apply the principle that if the patient can
>
> state name, rank and number then they are OK and receive no fluid -
>
> regardless of their other injuries/haemorrhage. Obviously if there is
>
> inadequate cerebral perfusion then this must be addressed expeditiously;
>
>
>
>
>
>
>
> 3) At a systolic BP of 90mmHg in a head injured patient then cerebral
>
> autoregulation may well still be present. It would depend entirely upon the
>
> diastolic BP and ICP as well but many patients with a low BP have still been
>
> able to maintain cerebral perfusion and consciousness;
>
>
>
>
>
>
>
> 4) Aiming for too high a CPP pressure will predispose to cerebral oedema
>
> with raised ICP. This will ultimately have a detriment effect on CPP. This
>
> can be counteracted with hypertonic saline (7.2% or 7.5% which also have an
>
> osmotic diuresis effect and therefore reduce cerebral oedema and ICP as
>
> well.) Hypertonic saline is therefore, in my opinion, the best fluid to give
>
> if you have to give any fluid at all;
>
>
>
>
>
>
>
> 5) A much simpler reason is that C comes before D. If the patient is
>
> haemorrhaging then there is no point trying to continually maintain cerebral
>
> perfusion with fluids if the patient is exsanguinating to death without
>
> correcting the underlying problem. Correct the haemorrhage and you will be
>
> more likely to restore cerebral perfusion to normal physiological levels.
>
> Naturally if the patient has no carotid or vertebral flow then the patient's
>
> autoregulatory mechanisms have failed and fluid boluses (e.g. hypertonic
>
> saline) may be required to increase the cardiac output in order to
>
> re-establish cerebral flow and induce cerebral output!!
>
>
>
>
>
>
>
>
>
>
>
> Although the above regulatory feedback mechanisms work to compensate and
>
> maintain cerebral perfusion in adverse situations, the key is to stop the
>
> haemorrhage and correct the problems rapidly - as these compensatory
>
> mechanisms will eventually fail and the aim is to correct the problems
>
> before this decompensation happens. For the aforementioned reasons, I think
>
> we need to appreciate not to be too over-focused on increasing the cerebral
>
> perfusion pressure, because it will more likely than not be sustained by the
>
> body's autoregulation. This allows you to concentrate on the major
>
> haemorrhage rapidly first and foremost - which is your more immediate
>
> priority.
>
>
>
>
>
>
>
> As you will see, like many others, I therefore don't focus on blood
>
> pressure.
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
> Matthew
>
>
>
>
>
>
>
>
>
>
>
> -----Original Message-----
>
> From: Anthony Caruso [mailto:medic541 at hotmail.com]
>
> Sent: 26 May 2008 19:53
>
> To: Trauma & Critical Care mailing list
>
> Subject: RE: Delayed healing as reason for delaying definitive surgery
>
>
>
>
>
>
>
>
>
>
>
>
>
>
>
> Mike, interesting to say the least. I have a question however. I have done
>
> a bit of reading on this, as well as have seen it on this list from time to
>
> time. What do you do if the pressure drops below 90 systolic with a head
>
> injured patient? I believe that if a pressure drops below 90 systolic that
>
> the patient has a 60% chance of the injury to be fatal. (Keeping in mind
>
> that the near hypotension is related to blood loss and not necessarily a
>
> neurogenic issue). Do we infuse crystalloid's to keep the presure up? We
>
> have discussed on this list that infusing a large amount of crystalloids has
>
> a worse outcome than holding off on giving them. I suppose this would be a
>
> question for one in the pre hospital arena as well as in the EW. Any
>
> thoughts?
>
>
>
>
>
>
>
> Anthony M. Caruso EMT-P
>
>
>
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