Preventing/reducing secondary brain injury in the prehospital setting.

Aidey

Aidey

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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?
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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.
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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?
 
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.
 
...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.
 
JPINFV said:
...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.
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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....
 
JPINFV said:
...and to build on that, hyperoxia is almost as bad as hypoxia since it results in vasoconstriction.
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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.
 
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.
 
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.
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Anyone have any thoughts on ketamine for RSI in head trauma?
 
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.
 
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.
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Care to back that contention (that it causes an ICP spike) with some data? :glare:
 
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.
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"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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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.

Paediatric Critical Care, Meyer Children's Hospital, Rambam Medical Center, Haifa, Israel. g_barjoseph@rambam.health.gov.il

Comment in:

J Neurosurg Pediatr. 2009 Jul;4(1):37-8; discussion 38-9.

Abstract
OBJECT: Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine's use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase-but may rather decrease-ICP.

METHODS: The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1-1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration.

RESULTS: The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 +/- 8.4 to 18.0 +/- 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 +/- 11.7 to 58.3 +/- 13.4 mm Hg (p < 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 +/- 9.1 to 17.5 +/- 9.1 mm Hg) (p < 0.0001) following ketamine administration.

CONCLUSIONS: In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations.
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ffemt8978 said:
Link please
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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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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.
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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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Ooops....misunderstood the request. I assumed that the citation of the article would be sufficient.
 
No worries.
 
usafmedic45 said:
Care to back that contention (that it causes an ICP spike) with some data? :glare:
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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
 
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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