TBI & 3% NaCl - protocol anyone ?

Sat May 31 14:30:12 BST 2008

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 &amp; 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-

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----- 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 &amp; 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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