# Preventing/reducing secondary brain injury in the prehospital setting.



## Aidey (Jan 9, 2011)

usalsfyre said:


> If the lower brain is involved, I agree the  outcome is a forgone conclusion. However, if it's not, the only hope for  a future that doesn't involve having the mental capacity of things  planted in a garden (or for that matter death) is rapid control of the  damaged tissue. Whatever damage that has already occured is done, you  have to focus on preventing secondary injury (inflamation, hypoxia,  ect). Is my thinking correct?





Veneficus said:


> I think your thinking is sound.
> 
> My point is with the damage that would likely have happened in such a  scenario, I think that preventing secondary injury is a moot  point.



I created this thread so I wouldn't hijack the other one. 

I know there are a number of things being researched to help TBI patients, what I am curious about is current prehospital practice. Aside from appropriate oxygenation are there any preventative practices that can be done to help reduce the chances of secondary injury? I know mannitol et al can be used to reduce intracranial swelling, but can they be used ahead of time, or only once swelling is suspected?


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## usalsfyre (Jan 9, 2011)

*The deadly twins*

The most important thing you can do is prevent hypotension and hypoxia. A single episode of either has been shown to double mortality in TBI.

This is also why RSI by providers who aren't thoroughly familiar with and skilled at the procedure is so dangerous.


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## JPINFV (Jan 9, 2011)

...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.


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## usalsfyre (Jan 9, 2011)

JPINFV said:


> ...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.



Careful, someone might get the idea a NRB at "shhhh" lpm of O2 is not appropriate for everything, and break a stupid protocol as a result....


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## lightsandsirens5 (Jan 9, 2011)

JPINFV said:


> ...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.



Beat me to it.

So, are any of you all familiar with the new theories of trauma oxygenation? Of maintaining Sats in the mid to high 90s instead of 100? (To be honest I don't know if it is new or not......<_<) But it seems to make sense to me, especially in the case of TBI and/or intercerebral swelling, ^ICP, etc.


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## Smash (Jan 9, 2011)

Early pre-hospital RSI with careful attention to avoiding hypoxia, hypotension, and hypocarbia is beneficial (triplets, not twins).  Maybe hypothermia (for isolated TBI) will prove to be as well, we will have to wait and see.


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## usafmedic45 (Jan 9, 2011)

Smash said:


> Early pre-hospital RSI with careful attention to avoiding hypoxia, hypotension, and hypocarbia is beneficial (triplets, not twins).  Maybe hypothermia (for isolated TBI) will prove to be as well, we will have to wait and see.


Anyone have any thoughts on ketamine for RSI in head trauma?


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## Aidey (Jan 9, 2011)

So really the only thing we can do currently to prevent further injury is to keep the patients vital signs as close to "normal" as possible and let the hospital sort it out from there? 

It wouldn't surprise me if therapeutic hypothermia ends up being found to be beneficial for a number of serious insults, including TBI.


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## Mobey (Jan 9, 2011)

usafmedic45 said:


> Anyone have any thoughts on ketamine for RSI in head trauma?



My first thought is NO!

The rise in ICP (temporary or not) would not be a sought after side effect in these patients.


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## usafmedic45 (Jan 9, 2011)

Mobey said:


> My first thought is NO!
> 
> The rise in ICP (temporary or not) would not be a sought after side effect in these patients.



Care to back that contention (that it causes an ICP spike) with some data?  :glare:


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## medicRob (Jan 9, 2011)

Mobey said:


> My first thought is NO!
> 
> The rise in ICP (temporary or not) would not be a sought after side effect in these patients.



"Our results indicate that S(+)-ketamine does not increase ICP and that  its use in neurosurgical patients should not be discouraged on the basis  of ICP-related concerns."*Effects of fentanyl and S(+)-ketamine on cerebral  hemodynamics, gastrointestinal motility, and need of vasopressors in  patients with intracranial pathologies: a pilot study*

*J Neurosurg Anesthesiol. 2007 Oct;19(4):257-62.*

http://www.ncbi.nlm.nih.gov/pubmed/17893578

See also:

*Racemic, S(+)- and R(-)-ketamine do not increase elevated intracranial pressure.*
Acta Anaesthesiol Scand. 2008 Sep;52(8):1124-30.

http://www.ncbi.nlm.nih.gov/pubmed/18840114


I seem to remember researching the roles N-methyl-D-aspartate receptors played in secondary brain injury and the role of ketamine as a possible neuro-protectant (finding the studies to cite)... 

Also, weren't there some studies into the use of estrogen in TBI as well as certain cardiac events?


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## usafmedic45 (Jan 9, 2011)

I see your that and raise you: 


> J Neurosurg Pediatr. 2009 Jul;4(1):40-6.
> 
> Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension.
> Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN.
> ...


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## ffemt8978 (Jan 10, 2011)

usafmedic45 said:


> I see your that and raise you:



Link please


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## Aidey (Jan 10, 2011)

There - http://www.ncbi.nlm.nih.gov/pubmed/19569909


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## usafmedic45 (Jan 10, 2011)

ffemt8978 said:


> Link please


The abstract as posted on Pubmed is public domain so far as I have been told. The publishers intend for it to be spread around so that more folks will seek out and purchase the full article.


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## ffemt8978 (Jan 10, 2011)

usafmedic45 said:


> The abstract as posted on Pubmed is public domain so far as I have been told.  The publishers intend for it to be spread around so that more folks will seek out and purchase the full article.


We still like to have links so that people may go and view it at the source.  From the Pubmed website Copyright link


> Copyright Status
> 
> Information that is created by or for the US government on this site is within the public domain. Public domain information on the National Library of Medicine (NLM) Web pages may be freely distributed and copied. However, it is requested that in any subsequent use of this work, NLM be given appropriate acknowledgment.


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## usafmedic45 (Jan 10, 2011)

Ooops....misunderstood the request.  I assumed that the citation of the article would be sufficient.


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## ffemt8978 (Jan 10, 2011)

No worries.


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## Mobey (Jan 10, 2011)

usafmedic45 said:


> Care to back that contention (that it causes an ICP spike) with some data?  :glare:




Well, here I am, sitting harmlessly on my high horse, spewing facts that I "know", and you had to ruin it.

This is me surprised :blink:

So to answer your question: NO

As much as I love google scholar, I am exhausted tonight so I am not going to drag out a bunch of studies proving your point. A simple google will bring up many meta-analysis studies with credible references that can be explored if anyone is interested.

http://www.anesthesia-analgesia.org/content/101/2/524.full


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## MrBrown (Jan 10, 2011)

Everybody here gets 1mcg/kg fentanyl.  Patients with neurogenic cause for coma with GCS <10 (eg stroke or TBI) we use 0.1mg/kg midaz and for everybody else we give 1.5mg ketamine.

Midaz and fent are halved for patients with a BP of < 100

Brown thinks there was a study from Israel that said ketamine was safe for head injuries


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## usafmedic45 (Jan 10, 2011)

> Brown thinks there was a study from Israel that said ketamine was safe for head injuries



That would be the one I cited.


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## 18G (Jan 12, 2011)

usalsfyre said:


> The most important thing you can do is prevent hypotension and hypoxia. A single episode of either has been shown to double mortality in TBI.



I agree. This is my main focus with a head injury. Nothing can be done about the primary insult obviously since what's done is done. But death or serious impairment from TBI can largely come from secondary injury. 

It is well recognized that a single instance of hypotension (<90) or a single episode of hypoxia can double mortality. The goal for B/P in the TBI patient is often cited at 110mmhg as to maintain a MAP sufficient to overcome the ICP and to ensure cerebral perfusion. EtCO2 monitoring is useful as to avoid hyperventilation and to target EtCO2 on the low end of normal right around 35. If the patient is not intubated its a good idea to place a EtCO2 nasal line to be able to detect in real time any rise in CO2 and the immediate need to ventilate.


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## Ravemtech (Jan 17, 2011)

In regards to reducing secondary injury in TBI, here is a recent study on RSI with improved outcome for early RSI prehospital for TBI, which showed worse outcome when RSI was delayed to hospital.  It shows a high level of training, appropriate monitoring devices including ETCO2, and a protocol (including pre fluid loading to prevent hypotension, Fentanyl, Midazolam, Sux,  and post RSI, Midaz/Morph infusion and Pancuronium) can have good outcome prehospital ......

*Prehospital Rapid Sequence Intubation Improves Functional Outcome for Patients With Severe Traumatic Brain Injury A Randomized Controlled Trial*

(Ann Surg 2010;252:959–965)

_Objective: To determine whether paramedic rapid sequence intubation in patients with severe traumatic brain injury (TBI) improves neurologic outcomes at 6 months compared with intubation in the hospital.
Background: Severe TBI is associated with a high rate of mortality and longterm morbidity. Comatose patients with TBI routinely undergo endo-tracheal intubation to protect the airway, prevent hypoxia, and control ventilation. In many places, paramedics performintubation prior to hospital arrival. However, it is unknown whether this approach improves outcomes.

Methods: In a prospective, randomized, controlled trial, we assigned adults with severe TBI in an urban setting to either prehospital rapid sequence intubation by paramedics or transport to a hospital emergency department for intubation by physicians. The primary outcome measure was the median extended Glasgow Outcome Scale (GOSe) score at 6 months. Secondary end-points were favorable versus unfavorable outcome at 6 months, length of intensive care and hospital stay, and survival to hospital discharge. 

Results: A total of 312 patients with severe TBI were randomly assigned to paramedic rapid sequence intubation or hospital intubation. The success rate for paramedic intubation was 97%. At 6 months, the median GOSe score was 5 (interquartile range, 1–6) in patients intubated by paramedics compared with 3 (interquartile range, 1–6) in the patients intubated at hospital (P = 0.28). The proportion of patients with favorable outcome (GOSe, 5–8) was 80 of 157 patients (51%) in the paramedic intubation group compared with 56 of 142 patients (39%) in the hospital intubation group (risk ratio, 1.28; 95% confidence interval, 1.00–1.64; P = 0.046). There were no differences in intensive care or hospital length of stay, or in survival to hospital discharge.

Conclusions: In adults with severe TBI, prehospital rapid sequence intubation by paramedics increases the rate of favorable neurologic outcome at 6 months compared with intubation in the hospital._

The full study is attached for those wanting to read the full document.  For those interested in the actual RSI protocol used in the study, here is the link - http://www.rav.vic.gov.au/Media/doc...0906-a04da8a1-e0b5-4b30-8f1d-ce979e76d996.pdf

Victoria is also about to undertake the POLAR trial (prehospital therapeutic coolong) to see if this further improves TBI outcome.


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