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blunt traumatic arrest pharmacotherapy

htaed_rd at 123mail.org htaed_rd at 123mail.org
Fri Dec 11 20:19:18 GMT 2009



On Fri, 11 Dec 2009 09:37 -0500, "Bjorn, Pret" <pbjorn at emh.org> wrote:
> Okay: first, there is no reason to expect that ACLS will have any effect
> on most traumatic causes of hypotension or pulselessness.  In a vast
> majority of cases, treating the heart with drugs or rhythmic squishing
> is quite literally blaming the victim.  Trauma clinicians should strive
> to discern the differences.

We agree on that much.



> That said, and without going into a lot of detail (lest we follow the
> tangent well beyond the interests of the Trauma-List), I think it's both
> wrong and irresponsible to imply that epinephrine is killing people.  On
> the contrary, there is long and fairly ample evidence to suggest that
> epinephrine has positive effects on resuscitating non-surgical
> pulselessness.  

I didn't state that it is killing people. What I did state is that it is
preventing us from resuscitating people. A subtle difference, but an
important one. As we have decreased the ability of people to excuse
interruptions of CPR, in order to get to the good stuff (the ALS
Witchcraft), we have dramatically improved the rate of resuscitation to
neurologically intact discharge.

Interruptions in cardiopulmonary resuscitation from paramedic
endotracheal intubation.
Wang HE, Simeone SJ, Weaver MD, Callaway CW.
Ann Emerg Med. 2009 Nov;54(5):645-652.e1. Epub 2009 Jul 2.
PMID: 19573949 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19573949


Epinephrine has plenty of evidence to support a return of a pulse, but
high dose epinephrine is more likely to produce ROSC. The spontaneous in
that is kind of amusing, since it is only adrenaline fueled.

High dose epinephrine has been justifiably moved way down on the list of
treatments, because getting a pulse back right away may be good for the
ego of those attempting resuscitation, but it has been shown to lead to
worse long term outcomes. I know you are appropriately interested in the
long term outcome, rather than the short term ROSC, so I am surprised
that you do not seem to grasp this distinction.

Not everything that is good for the short term vital signs (aggressive
prehospital fluid administration with uncontrolled bleeding, MAST, and
others) is good for long term outcome.



> What's true is that long-term outcome in these cases is (unsurprisingly)
> unflattering; but there has been no shortage of recent study selectively
> exploiting epi's alpha2 properties (by pharmacologically blocking beta
> and alpha1 effects) with promising results.  In the near term, we're
> stuck with the whole drug; but it's difficult for any patient to survive
> to discharge without ROSC; and for now, epi's one of the few drugs known
> to get us there.

Why do we presume that we need to give a drug?

All of the improvement in outcomes seems to be due to de-emphasizing ALS
treatment (tubes, IVs, drugs) and emphasizing BLS treatment.



> As for your hypothetical VT patient, your assertion that ACLS recommends
> defibrillation for unstable VT is simply false.  

My apologies. That was my bad editing. I started out writing one thing,
and did not notice  it after I changed it. The recommendation is for
defibrillation of pulseless VT, even if you are familiar enough with
cardiversion to not delay a shock.


> The current
> recommendation remains immediate synchronized cardioversion.  If you're
> purposely confusing unstable VT with pulseless VT (which demands CPR and
> defibrillation) to make a functional argument, then be aware: the
> working indication for boluses of epinephrine -- consistently,
> throughout all of human critical care -- is CPR.  EPINEPHRINE IS NOT
> INDEPENDENTLY INDICATED FOR ANY DISEASES, CONDITIONS OR RHYTHMS; IT'S
> GIVEN TO AMPLIFY THE EFFECTS OF CPR.  In this context, your hypothetical
> loses some of its shock value.

The only difference in whether CPR is indicated is the ability of the
person assessing for a pulse to perceive a pulse.

Epinephrine is probably much more harmful than CPR.

But if the patient would be prohibited from receiving epinephrine or be
required to receive epinephrine just because of the sensitivity of the
fingers palpating a pulse, is that logical?

If a patient with a pulse would be expected to be killed by
administration of epinephrine, why does it suddenly become mandatory
once the patient has no pulse?

If the most common cause of medical arrest is heart attack, is
epinephrine the right drug to use? Is any drug the right treatment
before ROSC?



> 
> Thanks for being provocative; but let's try to be a little more
> circumspect.

Let's try to be a little more circumspect?

Show me any well done research to support epinephrine improving long
term outcome and I will admit that you have a point.

In the absence of any well done research to support epinephrine
improving long term outcome, maybe you are the one who should be
circumspect. You are advocating a treatment that has no basis in
improving meaningful outcome, in spite of abundant research of this use.
How is advocating continuation of this unregistered, uncontrolled,
unauthorized experiment ethical?

The largest trial of outcomes was - 

Advanced cardiac life support in out-of-hospital cardiac arrest.
Stiell IG, Wells GA, Field B, Spaite DW, Nesbitt LP, De Maio VJ, Nichol
G, Cousineau D, Blackburn J, Munkley D, Luinstra-Toohey L, Campeau T,
Dagnone E, Lyver M; Ontario Prehospital Advanced Life Support Study
Group.
N Engl J Med. 2004 Aug 12;351(7):647-56.
PMID: 15306666 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/15306666

Free full text article from NEJM here -
http://content.nejm.org/cgi/content/full/351/7/647

Free full text PDF from NEJM here - 
http://content.nejm.org/cgi/reprint/351/7/647.pdf


This is the OPALS ALS for cardiac arrest study.

In the ALS group, 95.8% received epinephrine.
14.6% were admitted to the hospital, but only 5.1% survived to
discharge.

In the BLS group nobody received epinephrine (no surprise there).
10.9% were admitted to the hospital, yet 5.0% survived to discharge.

Neurological function in those discharged was better in the BLS group,
than in the ALS group. I do not find this surprising, since the biggest
problem with high dose epinephrine was worse neurological outcomes.
Standard dose epinephrine most likely just causes less neurological
damage. Maybe therapeutic hypothermia protocols will affect this, but
why do we keep looking for ways to excuse a treatment that has
continually failed to improve meaningful outcomes.

"Despite the large sample, controlled design, and multiple approaches to
the analysis, we were not able to identify any evidence of a benefit of
advanced life support for any subgroup of patients."

It's almost as if getting a pulse back quickly, by way of medication, is
detrimental to long term outcome. In that case, why are we so focused on
treating the vital signs (rapid ROSC), rather than doing what is best
for long term survival with good neurological function?

"Our study does not address the value of advanced-life-support programs
in urban communities that have high rates of CPR by bystanders or very
rapid advanced-life-support responders. Some cities have had higher
overall survival rates with advanced-life-support systems than the rates
in our study, but those cities typically have a high rate of CPR by
bystanders. Also unknown is the benefit of advanced life support in
rural communities, where transport times to a hospital are longer."

"The numbers in the more recent study (Of 1183 patients for whom
resuscitation was attempted, 851 were included; 418 patients were in the
ACLS with intravenous drug administration group and 433 were in the ACLS
with no access to intravenous drug administration group.) are
significantly lower than in OPALS (1391 were enrolled during the
rapid-defibrillation phase and 4247 during the subsequent
advanced-life-support phase.)"

The OPALS study also required - "To qualify for the
advanced-life-support phase of the OPALS Study, each community had to
meet four criteria: emergency medical services had to achieve a
rapid-defibrillation response interval of 8 minutes or less in 90
percent of patients with cardiac arrest, advanced-life-support
paramedics had to respond to 95 percent of patients, paramedics had to
arrive at the scene within 11 minutes for 80 percent of patients, and
paramedics had to successfully perform an endotracheal intubation in 90
percent of patients. These criteria were monitored regularly, and the
three communities that failed to meet the standards were excluded."

One of the great things about this study is that they excluded systems
that were not able to meet their quality standards. A continual excuse
for the use of epinephrine is that the study's EMS participants were not
of high quality.

If we are to consider the possible benefit of epinephrine in traumatic
arrest of any kind, shouldn't we have an understanding of whether it is
of any benefit in medical arrests? Since there is no evidence of
improved meaningful outcomes in medical arrest, should we assume that
there is something about trauma that is likely to make it more
effective?

As much as the epinephrine is in the ACLS guidelines, there remains no
evidence that it does what it is supposed to do. 


Tim Noonan.



> Pret Bjorn, RN
> Bangor, ME USA
> 
> -----Original Message-----
> From: trauma-list-bounces at trauma.org
> [mailto:trauma-list-bounces at trauma.org] On Behalf Of
> htaed_rd at 123mail.org
> Sent: Friday, December 11, 2009 1:55 AM
> To: Trauma-List [TRAUMA.ORG]
> Subject: Re: blunt traumatic arrest pharmacotherapy
> 
> There is not even good evidence that medical arrests have a good outcome
> with ACLS drugs. In certain specific indications, such as calcium for
> hyperkalemia, there are drugs that work. 
> 
> The "everybody dead gets epinephrine" approach has no evidence to
> support it in medical cardiac arrest, so it is unlikely that this
> decades old hunch improves outcomes in traumatic arrest.
> 
> The question is, will epinephrine be removed in the next revision of the
> guidelines, or will it be the revision after?
> 
> For all of you, who throw hissy fits, when non-trauma treatment is
> mentioned - stop reading here, or you will be scarred for life.Another
> way of looking at epinephrine is to look at the treatment of ventricular
> tachycardia.
> 
> Imagine a medical patient, who is hypotensive, unconscious, and
> unresponsive. The rhythm is ventricular tachycardia. The treatment
> algorithm is ventricular tachycardia with a pulse and an ACLS student
> suggested that epinephrine be given after defibrillation/cardioversion
> (ACLS now recommends defibrillation, not cardioversion for unstable VT).
> 
> How many of you ACLS instructors would claim that the student just
> killed the patient? Perhaps some of you would suggest this in a less
> than subtle fashion. I like to describe epinephrine as a heart attack in
> a syringe. 
> 
> On the other hand, If the fingers of the person assessing the same
> patient are just a little less sensitive, they might not feel a pulse.
> This very same patient is pulseless according to their assessment.
> According to ACLS, that means that the patient should be treated with
> the full 1,000 mcg of epinephrine after defibrillation. The only
> difference is the ability to palpate a pulse by the person treating the
> patient.
> 
> This is the difference between -
> 
> You can't give them that dangerous drug - You'll kill the patient!
> 
> and
> 
> It would be unethical to not give this drug - You'll kill the patient!
> 
> The same patient, just with different people palpating the pulse, but
> the treatments are diametrically opposed.
> 
> 
> Tim Noonan.
> 
>   
> 
> On Thu, 10 Dec 2009 19:08 -1000, "caesar ursic" <cmursic at gmail.com>
> wrote:
> > Who among you treats victims of blunt traumatic cardiac arrest with
> "ACLS
> > protocol" drugs?  I'm referring to the blunt trauma patient brought in
> to
> > ER
> > with closed chest compressions in progress and no palpable pulses with
> > wide-complex bradycardia.  Who gives boluses of
> > epinephrine/atropine/sodium
> > bicarbonate to these patients?  What is the role for these drugs in
> the
> > treatment of obvious blunt traumatic arrest?
> > 
> > CM Ursic, MD
> > g. surg.
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