ACLS | Rogue Medic

We are there for the good of the patient, not for the good of the protocol, not for the good of the medical director, and not for the good of the company.

- Rogue Medic

Back from the Dead – Rogue Medic Rants 2

Mon, 29 Apr 2013 08:00:27 +0000 by Rogue Medic Leave a Comment

There have been some problems with the Standing Orders site that appear to have been resolved and we have had some hacker attacks at EMS Blogs. Everything seems to be getting back to normal, or close enough for blogging purposes.

Last month on EMS Office Hours, Jim Hoffman, Josh Knapp, and I (with John Broyles and Tom Bouthillet in the chat room) discuss resuscitation.

Then we were jumping to the conclusion that something that sounds too good to be true is real.^[1],^[2]

I did not get to respond to Josh’s comments about how I am killing patients by not automatically adopting this unknown magic treatment that has people walking out of the hospital the next day – after being pulseless for 5 hours. It seems like homeopathy, prayer, acupuncture, Reiki, naturopathy, and chelation therapy rolled into one even bigger scam.

Back from the Dead – Rogue Medic Rants 2.

Image credit.

How should we respond to a demand to rush a treatment to standard of care status based on minimal evidence?

Should we demand evidence?

Should we demand that the approval process be expedited to satisfy our gullibility?

Download | YouTube MP3 Converter

Arise and Walk, My Son!

New and Improved! Standard of Care!

We should implement this right away!

Or we could realize that our patients are real people, who deserve treatments that really work, rather than something that looks good in a newspaper article.

Resuscitation is not about instant gratification.

Resuscitation is not about getting a temporary pulse.

Resuscitation is about long-term survival.

Go listen to the podcast.

Footnotes:

^[1] EMS, CPR, DNR and Hypothermia Treatment
March 20, 2013
EMS Office Hours
Podcast Page.

^[2] Back from the dead – New York researchers are bringing people back to life hours after they pass. And it could change our definition of what ‘dying’ really is
By Maureen Callahan
Last Updated: 12:51 PM, March 10, 2013
Posted: 12:15 AM, March 10, 2013
NY Post
Article

Filed Under: ACLS, Heresy, Unicorn Medicine

Should Merit Badge Organizations Define Standards of Care?

Sun, 07 Apr 2013 08:00:45 +0000 by Rogue Medic

The AHA (American Heart Association), NREMT (National Registry of EMTs), ACS (American College of Surgeons – PHTLS – PreHospital Trauma Life Support), and other organizations end up making standard of care decisions based on superstition.

We need to stop acting as if these organizations are creating good patient care.

They are improving, but they are so busy defending their ancient dogmas that they delay improvements in patient care.

Our patients are their guinea pigs, but we refuse to learn from their failures.

I want to know the real risks and benefits of this treatment.

For example –

AHA guidelines.

Ventilations have never been demonstrated to improve survival to discharge, but we are afraid of removing them because we don’t really understand what we are doing and finding out is even more scary than ignorance.^[1]

Drugs have never been demonstrated to improve survival to discharge, but we are afraid of removing them because we don’t really understand what we are doing and finding out is even more scary than ignorance.^[2]

NREMT guidelines.

Objective examination has never been demonstrated to be better than subjective examination by competent examiners. We are more afraid of people passing their friends and failing their enemies, or getting money to pass people (redundant, since the whole testing process requires a payment), than we are of incompetence.^[3]

Objectivity does not mean competence.

Subjectivity does not mean corruption.

We need to be smart enough to assess competence.

Instead we hide behind a test that is focused on memorization and not understanding.

ACS – PHTLS guidelines.

We still pretend that EMS spinal immobilization is not harmful.^[4]

We have evidence of many kinds of harm from EMS spinal immobilization.^[5],^[6],^[7]

We have only a weak hypothesis of how EMS spinal immobilization might protect the spine of a patient if that patient has an unstable spinal fracture that might get worse during transport.

The evidence shows that this hypothesis is at best misguided.

Manipulating people into EMS spinal immobilization is manipulation of the spine.

We can pretend that it is not, but we can also pretend that we have magical powers. Wishing does not make it so.

We need continuing education that is continual, not sitting in a classroom for 4, or 8, or 16 hours every two years.

We need to keep improving our care of patients, not excuses for the bad care that is in the guidelines.

When will we find time?

At the beginning of every shift, we can work on something.

Intubation practice should be done on a mannequin at a minimum every week. High-quality practice – even if it is on Fred The Head.

The same for medical and trauma megacodes.

We need to demand evidence that the recommendations of these organizations include evidence of improved outcomes that matter.

Any standard of care that does not have evidence of survival benefit needs to have an expiration date.

If nobody can show that it works, then it is just an opinion.

Our patients deserve better than to be treated based on dangerous opinions based on wishful thinking.

Footnotes:

^[1] Nothing

No evidence of improved survival with a thinking brain.

^[2] Nothing

No evidence of improved survival with a thinking brain.

^[3] Nothing

No evidence of competence at assessment of competence.

^[4] Nothing

No evidence of any decrease in disability, although there is evidence of an increase in disability with spinal immobilization. See below.

^[5] The cause of neurologic deterioration after acute cervical spinal cord injury.
Harrop JS, Sharan AD, Vaccaro AR, Przybylski GJ.
Spine (Phila Pa 1976). 2001 Feb 15;26(4):340-6.
PMID: 11224879 [PubMed - indexed for MEDLINE]

All but two patients had complete injuries at admission. One patient with incomplete injury and another that was neurologically intact had early complete cervical cord injuries after cervical immobilization.

Four of the ﬁve patients in the early group (mean age 56 years) developed neurologic worsening during application of cervical immobilization less than 24 hours after injury.

This paper was cited by the ACS as a justification for spinal immobilization for blunt trauma.

^[6] Out-of-hospital spinal immobilization: its effect on neurologic injury.
Hauswald M, Ong G, Tandberg D, Omar Z.
Acad Emerg Med. 1998 Mar;5(3):214-9.
PMID: 9523928 [PubMed - indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

RESULTS:
There was less neurologic disability in the unimmobilized Malaysian patients (OR 2.03; 95% CI 1.03-3.99; p = 0.04). This corresponds to a <2% chance that immobilization has any beneficial effect. Results were similar when the analysis was limited to patients with cervical injuries (OR 1.52; 95% CI 0.64-3.62; p = 0.34).

^[7] Spinal immobilisation for trauma patients.
Kwan I, Bunn F, Roberts I.
Cochrane Database Syst Rev. 2001;(2):CD002803. Review.
PMID: 11406043 [PubMed - indexed for MEDLINE]

The review authors could not find any randomised controlled trials of spinal immobilisation strategies in trauma patients. It is feasible to have trials comparing the different spinal immobilisation strategies. From studies of healthy volunteers it has been suggested that patients who are conscious, might reposition themselves to relieve the discomfort caused by immobilisation, which could theoretically worsen any existing spinal injuries.

REVIEWER’S CONCLUSIONS:
We did not find any randomised controlled trials that met the inclusion criteria. The effect of spinal immobilisation on mortality, neurological injury, spinal stability and adverse effects in trauma patients remains uncertain. Because airway obstruction is a major cause of preventable death in trauma patients, and spinal immobilisation, particularly of the cervical spine, can contribute to airway compromise, the possibility that immobilisation may increase mortality and morbidity cannot be excluded.

^[8] Cervical spine motion during extrication.
Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS.
J Emerg Med. 2013 Jan;44(1):122-7. doi: 10.1016/j.jemermed.2012.02.082. Epub 2012 Oct 15.
PMID: 23079144 [PubMed - in process]

RESULTS:
The results indicated a significant decrease in movement for all motions when the driver exited the vehicle unassisted with CC protection, compared to exiting unassisted and without protection. Decreases in movement were also observed for an event (i.e., Pivot in seat) during extrication with paramedic assistance and protection. However, no movement reduction was observed in another event (i.e., Recline on board) with both paramedic assistance and protection.

CONCLUSION:
In this study, no decrease in neck movement occurred for certain extrication events that included protection and assistance by the paramedics. Future work should further investigate this finding.

There is a detailed evaluation of this paper by Dr. Brooks Walsh at Mill Hill Ave Command.

In order to protect the c-spine, should we stop helping?

Filed Under: ACLS, Ethics, Evidence, Heresy, National Registry, Spinal Immobilization

Does the Goal of a Pulse Lead to Bad Resuscitation Decisions

Tue, 26 Mar 2013 10:30:47 +0000 by Rogue Medic

First, this is a paper that was just added to the Articles In Press for Resuscitation with the editing not yet completed. Do not fault the authors for the lack of polish. The paper does address some interesting aspects of resuscitation.

ROSC (Return Of Spontaneous Circulation) is the goal for many people.

ROSC is a red herring.

Those of us who think ROSC is important do not seem to understand how much long-term damage we can do in our attempts to get ROSC, or to get ROSC quickly.

This study helps to point out some of the inconsistencies with our ROSC fetish.

Here is a table of the results from the study comparing early epinephrine (≤10 minutes) with late epinephrine (>10 minutes).

Click on images to make them larger.

Everything highlighted in blue is favoring early epinephrine and statistically significant.

Overall, things look good for early epinephrine, but VF/VT (Ventricular Fibrillation/Ventricular Tachycardia) is most responsive to resuscitation, yet the results for VF/VT never reach statistical significance. VF/VT may also be most associated with an early response

There is only a trend toward better ROSC for VF/VT, but as with the NINDS study of tPA for ischemic stroke, the healthiest patients are in the intervention group, so they are expected to have better outcomes.

With asystole there are survivors with late epinephrine, but no survivors with early epinephrine. What should we make of that? It is far from statistically significant, but there is not even a trend toward more ROSC with early epinephrine.

PEA (Pulseless Electrical Activity) has not just a trend toward more ROSC with early epinephrine, the results are statistically significant.

One of the reasons may be that PEA is sometimes due to assessment problems. We used to call it EMD (Electro-Mechanical Dissociation) because many of us assumed that if no pulse could be palpated, there was no cardiac output. These were termed pseudo-EMD, since imaging could show that there is heart motion, even though there is no palpable pulse.

I have had a handful of patients who were awake and alert, but did not have any palpable pulses. Clearly, EMD is not a description of reality.

How many of these patients are responding to being shaken up, rather than to the mechanical effects of chest compressions in the circulation? We do not know.

Early Epi may increase blood pressure to allow palpation of a pulse in cases with presumed PEA, but who are actually cases of “pseudo-PEA” which have some cardiac output but not enough to be identified clinically.^[1]

Modified portion of EMS 12 Lead image.

Then there are the expected confounders in this kind of study. Faster response times would be expected to result in earlier epinephrine and less deterioration of the rhythm to asystole.

The faster response times occur in fewer patients, so there should be a much wider confidence interval/standard deviation. That is not the case, because there is an upper limit on the numbers that can be included. The numbers include response time, time to patient contact, time to establish access, and time to epinephrine. All of those have to be less that 11 minutes combined.

Bystander CPR is much more common with early epinephrine. This may be related the higher incidence of arrest in public, but the bystander CPR rate is about twice as high as the rate of arrest in public.

With early epinephrine we have a decrease from the odds of ROSC to the odds of survival.

With witnessed arrest, bystander CPR, and VF/VT the opposite is true.

With VF/VT the difference is dramatic.

Is this an indication of the effect of epinephrine on survival that we have seen in other studies?

Clearly more work is needed to understand the importance of the timing of epi administration and its impact on outcomes from OHCA.^[1]

OHCA is Out of Hospital Cardiac Arrest.

Clearly more work is needed to understand the ~~importance of the timing~~ effects of epi administration and its impact on outcomes from OHCA.

Why should we assume that it is the timing and not the drug?

Maybe the problem is using such a drug that is so dangerous to the heart to treat heart problems.

Samuel Hahnemann would love this use of epinephrine, just at a much lower dose.

Footnotes:

^[1] Rapid Epinephrine Administration Improves Early Outcomes in Out-of-Hospital Cardiac Arrest.
Koscik C, Pinawin A, McGovern H, Allen D, Media D, Ferguson T, Hopkins W, Sawyer K, Boura J, Swor R.
Resuscitation. 2013 Mar 21. doi:pii: S0300-9572(13)00175-5. 10.1016/j.resuscitation.2013.03.023. [Epub ahead of print]
PMID: 23523823 [PubMed - as supplied by publisher]

Koscik, C., Pinawin, A., McGovern, H., Allen, D., Media, D., Ferguson, T., Hopkins, W., Sawyer, K., Boura, J., & Swor, R. (2013). Rapid Epinephrine Administration Improves Early Outcomes in Out-of-Hospital Cardiac Arrest Resuscitation DOI: 10.1016/j.resuscitation.2013.03.023

Filed Under: ACLS, Epinephrine, Heresy, Research Blogging

Another Sinus Tachycardia that F&B Medics Want to Shock

Mon, 11 Feb 2013 08:00:53 +0000 by Rogue Medic

In Worst test question ever! – Maybe, I pointed out some of the problems with the way we “educate” people in EMS. The following question was provided with the rhythm above.

You are dispatched emergency traffic to the scene of a 24 yo F with “palpitations.” You arrive to find her pale, sweaty and lethargic. You palpate a radial pulse with an extreme rate. You hook her up to the monitor and find the following rhythm? You have a 45 minute transport time. Which of the following is the most appropriate initial treatment for this condition?

1.) Nitroglycerin 0.4mg SL
2.) Immediate synchronized cardioversion
3.) Adenosine 12mg Rapid IV push followed by 20cc NS bolus
4.) Epinephrine 1mg 1:10000 q-3-5m IVP

If a test question is so poorly written that there is no justifiable answer, why would anyone competent defend the question?

The answer is that we have dangerous people as “educators” and no really good method of eliminating them from EMS classrooms.

If there are no correct answers, can there be one best answer?

If there are no correct answers, can the most deadly answer possibly be the best answer?

We are supposed to be providing patient care, not making “educators” feel good about being dangerous.

Could the rhythm be atrial flutter?

It is not a bad idea to suspect flutter when the ECG rate is an even fraction of the ≈300 rate that is typical of flutter waves e.g. ≈75, ≈100, and ≈150)?

Is there another wave half way between the P waves seen in this rhythm, which would make both waves F waves?

I do not see any Flutter waves.

That is the same rhythm. Do you see any F waves?

If the rhythm is sinus, then cardioversion/defibrillation is not going to help, but can make things a lot worse.

We can produce anything from pain to death by shocking this rhythm.

Why would we do that to satisfy an incompetent “educator”?

This might be a good question to identify people who should not be trusted to care for patients. If we are willing to make a choice that is the equivalent of harming patients in order to come up with the ~~one best answer~~ right answer in a testing environment, what might we do when faced with a real patient, but a protocol that we think needs to be followed?

Is cardioversion the way to avoid the QA/QI/CYA spanking?

Should we be trying to figure out how to intervene?

Should we be trying to figure out when to intervene?

If the intervention is a heart-stopping dose of electricity (cardioversion), should we be looking for excuses to shock, or should we be trying to figure out if the patient is likely to benefit from that treatment?

What about this 80+ year old patient, who is pale, and lethargic, but is not confused?

Here is a different EMS 12 Lead Facebook post.

More ACLS…
Your pt is a 54 yo male found in bed, with AMS. He looks pale, has BP of 84/52 with the rhythm below. No other hx is available right now. What’s the treatment?

The earlier post looked like a sinus tachycardia from a rhythm generator. With the HeartSim, to get a good fast narrow complex rhythm use atrial tachycardia and hit the faster button once or twice – that produces a rhythm that is not obviously sinus. There were 25 comments choosing from among the choices given, before there was a comment from someone smart enough to recognize that all of the choices were wrong.

Yes, the National Registry does encourage the fraud of one best answer. Why do medics choose a dangerous treatment, when we know it is dangerous?

We have been taught to choose try to figure out what would be most pleasing to the instructor/evaluator – not to do what is best for the patient.

Why aren’t the instructors/evaluators looking for what is best for the patient?

One of the reasons for fewer indefensible answers at EMS 12 Lead is that many of the people following EMS 12 Lead are already medics, nurses, and/or doctors, rather than students looking to please an instructor/evaluator.

This time, there were four good answers before anyone suggested cardioversion, but why are so many of us looking for excuses to use electricity to stop the hearts of patients?

Filed Under: ACLS, Cardiology, Cardioversion, Critical Judgment, Heresy

Advanced Airway vs. BVM During CPR – Which is Worse?

Sun, 10 Feb 2013 11:00:00 +0000 by Rogue Medic

The authors wanted to find out what method is ~~worst~~ best for ventilating patients during out-of-hospital treatment of cardiac arrest.

Endotracheal tube?

Supraglottic airway (laryngeal mask airway, laryngeal tube, and esophageal-tracheal twin-lumen airway device)?

BVM (Bag Valve Mask)?

This assumes that ventilations provide some sort of benefit to the patient. There is no evidence to support this myth.

Their endpoint was neurological outcome at one month for all out-of-hospital cardiac arrest patients treated January 1, 2005, to December 31, 2010.

In addition, we postulated that both advanced airway techniques (endotracheal intubation or use of supraglottic airways) would be similarly associated with favorable neurological outcome after OHCA.^[1]

Intubation training required more intubations in the operating room than is required in the US (zero to ? – 5 are typically given as the minimum requirement, but there is no standard accepted by all agencies), or in the UK.

Beginning in 2004, endotracheal intubation could be performed by specially trained emergency lifesaving technicians who had completed an additional 62 hours of training sessions and performed 30 supervised successful intubations in operating rooms.²⁴ ^[1]

What were the results?

Click on images to make them larger.

Everything underlined in red is worse than BVM and statistically significant. The endotracheal tube numbers underlined in blue are only statistically significant until adjusted for confounding variables and only for ROSC (Return Of Spontaneous Circulation).

ROSC is important – if we do not mind causing long term harm in order to get this short term benefit. This is not a trade off that helps our patients.

A set of potential confounders was chosen a priori based on biological plausibility and a priori knowledge. These selected variables included age, sex, cause of cardiac arrest, first documented rhythm, witnessed status, type of bystander CPR, use of a public access automated external defibrillator, epinephrine administration, and time intervals from receipt of call to CPR by EMS and from receipt of call to hospital arrival.^[1]

Not adjusting for confounders would be wrong.

There is one big confounder that I will get to at the end.

The supraglottic airways did even worse than the endotracheal tubes. There has been research in pigs showing that the inflation of the cuffs of supraglottic airways cause more interruption of carotid circulation than the cuffs of endotracheal tubes and that the cuffs of endotracheal tubes cause more interruption of carotid circulation than BVMs. BVMs have no cuffs to inflate to limit carotid circulation, which is the main source of blood flow to the brain.^[2]

What else does not have a cuff?

A nonrebreather mask doesn’t have a cuff.

A nasal cannula doesn’t have a cuff.

Did failed tubes cause the study to be biased against intubation?

However, we defined advanced airway management as successful endotracheal intubation or supraglottic airway placement only. Thus, in our study, failed advanced airway management cases reverted to and were classified as bag-valve-mask ventilation cases. This would have biased our conclusions toward the null.^[1]

The authors also calculated the results if all of the missing BVM patient data were negative and all of the missing supraglottic airway data were positive. The supraglottic airway data were associated with so much harm, that even this did not make the results look much less harmful for use of supraglottic airways.

Likewise, the authors calculated the results if all of the missing BVM patient data were negative and all of the missing endotracheal tube data were positive. The endotracheal tube data were also associated with so much harm, that even this did not make the results look much less harmful for endotracheal intubation.

Only 6.5% of the patients had endotracheal intubation, so this seems as if we could be dealing with small numbers producing statistical flukes. However, 6.5% of this huge sample is still 41,972. Therefore, this is not a case of statistical manipulation of small numbers with no clinical significance. There are more intubated patients in this study than there are total patients in most studies of airway management.

Assuming the validity of our study, a more secure airway, regardless of its technique, would be detrimental.^[1]

Should we assume the validity of this study?

In addition, multiple studies arrived at similar conclusions despite differing populations, disease groups, and designs.^7-10,12,13 ^[1]

There are two problems.

There is no group with no ventilations. I realize that this was not within the control of the authors, but it would answer a more important question.

We are asking -

What is the best method of ventilation during cardiac arrest?

We have not yet answered –

Should we be ventilating during cardiac arrest?

We have not determined that any ventilation is beneficial during cardiac arrest, but we are spending our time choosing colors and arguing over which brand name is best.

14 minutes to ROSC vs. 6 minutes to ROSC?

This is only mentioned tangentially and I am not satisfied with the explanation.

This presents a lot of different data. They all are similar – right up until the very last one.

This deserves some very specific description.

Unfortunately, the data probably do not include enough information to learn more about these differences.

The difference in time to ROSC is huge.

The IQRs (InterQuartile Ranges) show much more diversity than we should expect when everything else is so similar.

Could this explain the difference in outcomes?

The explanation of the authors (that their subgroup analyses account for this) seems to be unreasonably optimistic.

I want the authors to show that patients who have ROSC in 6 minutes should not be expected to have an outcome that is three times better than patients who take 2 ¹⁄₃ times as long to achieve ROSC.

These numbers are ~~large~~ huge. 281,522 in one group and 367,837 in the other. How can such a heterogeneous variable be given so little attention?

If I tell someone that two groups of patients were resuscitated, but it took over twice as long to resuscitate one group as it took for the patients in another group, should I expect anyone to be surprised that the group resuscitated faster has outcomes that are three times better?

In cardiac arrest, as time increases bad outcomes can be expected to increase at an even greater rate.

There is not even much overlap in the IQRs of the times to ROSC. 8 – 20 minutes vs. 3 – 12. A 12 minute IQR with only 4 minutes of overlap.

Although everything else appears to be well matched, I do not see the subgroup analyses reconciling the differences in ROSC times.

I think that this could adequately explain the differences in outcomes. We do need prospective studies, but we should find out if there is any reason to be providing ventilations in cardiac arrest (except for those that are pediatric and/or respiratory in origin).

See also Advanced Airway Loses to BVM and read the comments.

Footnotes:

^[1] Association of prehospital advanced airway management with neurologic outcome and survival in patients with out-of-hospital cardiac arrest.
Hasegawa K, Hiraide A, Chang Y, Brown DF.
JAMA. 2013 Jan 16;309(3):257-66. doi: 10.1001/jama.2012.187612.
PMID: 23321764 [PubMed - indexed for MEDLINE]

^[2] Impairment of carotid artery blood flow by supraglottic airway use in a swine model of cardiac arrest.
Segal N, Yannopoulos D, Mahoney BD, Frascone RJ, Matsuura T, Cowles CG, McKnite SH, Chase DG.
Resuscitation. 2012 Aug;83(8):1025-30. doi: 10.1016/j.resuscitation.2012.03.025. Epub 2012 Mar 28.
PMID: 22465807 [PubMed - in process]

CONCLUSION:
The use of 3 different SGDs (Supraglottic airway devices) during CPR significantly decreased CBF (carotid blood flow ) in a porcine model of cardiac arrest. While the current study is limited to pigs, the findings suggest that further research on the effects of SGD use in humans and the effects on carotid artery blood flow is warranted.

Hasegawa K, Hiraide A, Chang Y, & Brown DF (2013). Association of prehospital advanced airway management with neurologic outcome and survival in patients with out-of-hospital cardiac arrest. JAMA : the journal of the American Medical Association, 309 (3), 257-66 PMID: 23321764

Segal, N., Yannopoulos, D., Mahoney, B., Frascone, R., Matsuura, T., Cowles, C., McKnite, S., & Chase, D. (2012). Impairment of carotid artery blood flow by supraglottic airway use in a swine model of cardiac arrest Resuscitation, 83 (8), 1025-1030 DOI: 10.1016/j.resuscitation.2012.03.025

Filed Under: ACLS, Airway Management, Correction, Research Blogging

What is the Future for EMS?

Mon, 04 Feb 2013 11:45:55 +0000 by Rogue Medic

Happy Medic has begun a series of looking at how we will look back at EMS from 2066 – a hundred years after the EMS White Paper that much of EMS is based on.

Paramedic – A look back at the first 100 years.

Part 1 looks at Chemical reversal of death. Will we still be using drugs to attempt to resuscitate?

Predictions of the future often focus on technology, technology that rarely develops as we expect. However, medicine is very reliant on technology. In EMS, some people seem to have no idea how to take a pulse. That is what their pulse oximeter is for. While a pulse oximeter can provide information that palpating a pulse cannot, a pulse oximeter cannot provide all of the information that can be obtained by palpating a pulse.

We make a mistake when we assume that all we can see is all there is, and this is a common mistake in medicine.

Will we still be making some of the same mistakes?

Absolutely.

Will we look back on some of what we do now as primitive and ignorant?

Absolutely.

He writes –

It is worrisome that it took something drastic for Paramedics to look at their own practices for efficacy instead of demanding proof before using it that it would do no harm.

I do not think that we will eliminate medications from resuscitation, but I do not expect that we will be using the same medications in 2066 that we are currently using.

Part 2 looks at Cervical Spinal Restriction.

Why on earth would a Paramedic, even an early one, strap a healthy curved spine to a flat board?

That is funny, because I had a trauma specialist explaining to me that the use of spinal immobilization, which has only been demonstrated to be harmful, is something that should not be questioned, because –

1. If a bone is broken, we have to splint it.

2. All bones are to be treated the same – the humerus, which is not articulated and does not contain the spinal cord is identical to the spine.

3. This is too important to find out if it is harmful, because we just know it works.

PHTLS (PreHospital Trauma Life Support) is looking for evidence for possible changes to their next set of guidelines

This is the kind of logic that has been behind abandoned medical procedures for centuries –

Perhaps it has not been demonstrated safe but it has never been demonstrated unsafe either. Better stay with the known than go to the unknown. If you want to develop a research project, please go ahead and do it. But without proof that they are bad, we cannot just assume that they are bad.

Perversely, without any proof that they are good, or even safe, we are strapping millions of people to rigid boards.

When will we be smart enough to limit our interventions to those that really help?

When will we abandon treatment based on weak hypotheses?

Why do we make patients fit our equipment, rather than make equipment that does not harm our patients?

What does it take for an interventionist to put patients ahead of dogma?

At Street Watch: Notes of a Paramedic, there is a description of the continuing fall from grace of “spinal immobilization” – Another Nail in the Board. Go read it.

At Mill Hill Ave Command, there is a review of a recent study of the methods of extrication from vehicles and the amount of movement of the cervical spine – In order to protect the c-spine, should we stop helping?. Go read it.

At First Few Moments, Kyle David Bates, Russell Stine, Bob Lutz, Dr. Laurie Romig, Kelly Grayson and I discuss the lack of evidence of any benefit from spinal immobilization and the evidence of harm in A Change of the Dogma: If it helps only one? Episode 36.

Filed Under: ACLS, Evidence, Heresy, Spinal Immobilization

Should the AHA reintroduce the ‘Indeterminate’ class of ACLS recommendations?

Thu, 06 Dec 2012 23:15:38 +0000 by Rogue Medic

In 2005 the AHA (American Heart Association) used more categories for their drug recommendations. The recent very poor showing of epinephrine in resuscitation studies, and the lack of evidence of benefit in earlier studies, suggest that Class IIb is not an appropriate classification of epinephrine.

Should the AHA reintroduce the Indeterminate class that was in the 2005 guidelines?

Can we justify continuing the Class IIb recommendation?

Where are the people who survived because of epinephrine?

With hundreds of thousands of cardiac arrest patients treated with epinephrine each year, why can’t we find any evidence of improved survival with epinephrine?

All we need is –

Benefit ≥ Risk

Where is the benefit?

Why are we satisfied with such pathetic results?

Table 3.
Applying Classification of Recommendations and Level of Evidence

-

Class I
Benefit >>> Risk
Procedure/treatment or diagnostic test/assessment should be performed/administered.

-

Class IIa
Benefit >> Risk
It is reasonable to perform procedure/administer treatment or perform diagnostic test/ assessment.

-

Class IIb
Benefit ≥ Risk
Procedure/treatment or diagnostic test/assessment may be considered.

-

Class III
Risk ≥ Benefit
Procedure/treatment or diagnostic test/assessment should not be performed/administered. It is not helpful and may be harmful.

-

Class Indeterminate.
• Research just getting started
• Continuing area of research
• No recommendations until further research (eg, cannot recommend for or against)^[1]

Is epinephrine research just getting started?

After over half a century of use, there is only a single prospective randomized, placebo-controlled study of the effects of epinephrine on outcomes. That is from last year and the study was decimated by politicians and the press claiming that it would be unethical to deprive patients of this untested treatment.

Is epinephrine a continuing area of research?

I don’t know, but it should be. We should not continue to use epinephrine without continuing research.

Is epinephrine deserving of any recommendation without further research?

So far, there is only evidence of improvement in surrogate endpoints. surrogate endpoints are things that we measure because a study is too small to show improved survival.

Here is the evidence of of what happens to survival with epinephrine.

I added the two most recent studies to this, since they were not yet published when the review of vasopressors was published.^[2] The quality and outcome of the added studies is my interpretation, but I think that others will rank them similarly.

The Hagihara study is more than 100 times larger than the combined numbers of all of the studies that came before it.

The Hagihara study is not positive.

Why aren’t we demanding evidence that we are not harming patients?

We don’t know enough to know how dangerous epinephrine is.

That is the best that can be stated about epinephrine in cardiac arrest.

Isn’t it time for us to figure out what we are doing?

We should have found out whether epinephrine works before we started using it on everyone dead, but we don’t have to continue that mistake.

Our patients need to know. Does epinephrine improve survival from cardiac arrest?

Footnotes:

^[1] Table 3. Applying Classification of Recommendations and Level of Evidence
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 1: Introduction
Table 3

I have modified this table solely for the purpose of clarity of presentation, by modifying color and font. None of the words have been changed.

^[2] Vasopressors in cardiac arrest: a systematic review.
Larabee TM, Liu KY, Campbell JA, Little CM.
Resuscitation. 2012 Aug;83(8):932-9. Epub 2012 Mar 15.
PMID: 22425731 [PubMed - in process]

CONCLUSION: There are few studies that compare vasopressors to placebo in resuscitation from cardiac arrest. Epinephrine is associated with improvement in short term survival outcomes as compared to placebo, but no long-term survival benefit has been demonstrated. Vasopressin is equivalent for use as an initial vasopressor when compared to epinephrine during resuscitation from cardiac arrest. There is a short-term, but no long-term, survival benefit when using high dose vs. standard dose epinephrine during resuscitation from cardiac arrest. There are no alternative vasopressors that provide a long-term survival benefit when compared to epinephrine. There is limited data on the use of vasopressors in the pediatric population.

Filed Under: ACLS, Cardiology, Heresy, Pharmacology

Is a clot-busting drug safe for 6 hours after stroke symptom onset – or only for an hour and a half? – Part I

Thu, 13 Sep 2012 08:00:25 +0000 by Rogue Medic

The clot-buster tPA (tissue Plasminogen Activator) is given to stroke patients within 3 hours of onset of symptoms (some use 4 1/2 hours), based on a poorly done study. Some doctors are claiming that the benefits from tPA for stroke can be extended even to 6 hours.

Are the authors exhibiting stroke-like symptoms from sipping too much of their own Kool-Aid?

My first experience with a patient being given tPA for stroke was over a decade ago with a patient I brought to the hospital within about 45 minutes of symptom onset. The criteria for treatment were a negative CT (Computerized Tomography) scan for intracranial bleed, ruling out other bleeding risks, and a maximum of 3 hours from witnessed symptom onset.

The biggest delay was supposed to be the time it takes to get the CT scan. The neurologist was there, read the scan – all within an hour and a half of symptom onset, and then waited

and

waited

and

waited

and

- at 2 hours and 55 minutes from the onset of symptoms – the neurologist gave the order to begin treatment.

tPA is not an all-or-nothing drug. This isn’t a movie, where the hero can receive an antidote a few seconds before a poison would kill him, and he is unharmed. Damage is cumulative, and often permanent. The possible benefits decrease with time, while the side effects don’t have much reason to change with time. Damage to the brain does not magically go away.

If I want to take a hot shower, I want to run the water just long enough to get the water hot, but not so long that I run out of hot water. The amount of remaining hot water decreases the longer I wait. There is nothing wrong with cold showers, but if the goal is a hot shower, that is the wrong way to accomplish the goal.

With a stroke, the goal is appropriate treatment as quickly as possible, because the longer the ischemic part of the brain is ischemic, the worse the outcome. The benefit runs out over time.

The NINDS (National Institute of Neurological Disease and Stroke) trial, that led to the original rush to make tPA the standard of care, was the response to smaller studies that showed mixed results with use of tPA.

These results were enough to justify further investigation in the form of a larger, randomized, placebo-controlled trial.^[1]

So, thousands of patients were enrolled in this huge stroke trial was begun. OK, there were 614 patients enrolled. Part 1 only looked at improvement 24 hours later. That may be the ROSC of stroke care – nice, but irrelevant if that is all we get. There were only 333 patients in the part that mattered – Part 2. Only 168 received the study drug in Part 2. But Part 2 was broken down into 0-90 minutes from symptom onset to treatment initiation and 91-180 minutes. There is no real controversy about using tPA within 90 minutes of symptom onset. The controversy is with treatment from 91 to 180 minutes (1 1/2 hours to 3 hours).

Only 82 patients received the study drug in Part 2 that time period. Maybe the Part 1 patients should be included, since their results are included by the authors, but that is still only 168 patients.

We need to be careful of drawing big conclusions from small numbers. These are small numbers representing a diverse patient population.

The primary hypothesis for part 2 was that there would be a consistent and persuasive difference between the t-PA and placebo groups in terms of the proportion of patients who recovered with minimal or no deficit three months after treatment.^[1]

The results reported suggest that this is what happened, but as more information has been released about the study, it has become apparent that the patients in the treatment group were much healthier than patients in the placebo group.

Picture credit.

Some people who want to get rich will trade on the futures market. How do you make a million dollars on the futures market? Start with two million dollars. Your two million dollars will soon become one million dollars.

The authors appear to have a similar philosophy. One way to make a drug look good is to compare it to a drug that is worse. In a placebo trial, that may not be possible, so the way to make an ineffective drug look good is to put the sicker patients in the placebo group. Even a dangerous drug will not look so bad by comparison.

Did the authors hide the difference in stroke severity intentionally? It doesn’t matter. The authors did not make it easy to get the relevant information.

tPA is a treatment that has become standard of care without good evidence.

The AHA (American Heart Association) has also been pushing this poorly studied treatment aggressively with mandatory content in their courses on treating heart problems.

The problems with the study have not gone unnoticed.

Dr. Jerome Hoffman wrote -

Another concern is that, in the 91-180 minute group, patients who received placebo were much sicker at baseline than those treated with tPA. Sicker patients tend to have worse outcomes, and these baseline differences may explain much of the apparent benefit that has been attributed to tPA. These problems make it unclear whether there was any benefit to the use of tPA. If so, it is almost certain that the time limit for benefit is far less than 180 minutes, and perhaps much closer to 90 minutes.^[2]

Dr. Jeffrey Mann wrote -

In summary, the recommendations for the use of tPA in patients with acute ischemic stroke were based on an initial misinterpretation of the results of the NINDS trial and are, therefore, unwarranted.^[3]

In defense of the lack of research, Dr. Patrick D. Lyden, one of the NINDS investigators, writes –

The limitations on this therapy—the only proven stroke treatment—are legendary: patients must be treated promptly after stroke onset, must have no contraindications to thrombolysis, and must be treated by a team skilled in preventing potential complications. Much has been made of these limitations, to the point of considerable nihilism among neurologists. Yet, results similar to the NINDS data are obtained in communities with active stroke teams dedicated to proper use of intravenous thrombolysis.^[4]

Is the study just misunderstood?

Is tPA really a hooker with a heart of gold?

Results Seventy patients (1.8%) admitted with ischemic stroke received IV tPA. Of those, 11 patients (15.7%; 95% confidence interval [CI], 8.1%-26.4%) had a symptomatic ICH (of which 6 were fatal) and 50% (95% CI, 37.8%-62.2%) had deviations from national treatment guidelines. In-hospital mortality was significantly higher among patients treated with tPA (15.7%) compared with patients not receiving tPA (5.1%, P<.001) and compared with the model's prediction (7.9%; P<.006).^[5]

Only half of the patients treated met the treatment criteria for tPA.

The in-hospital death rate was 5.1% without tPA.

The in-hospital death rate was 15.7% with tPA.

This is what Dr. Lyden is defending.

That paper was published before Dr. Lyden’s editorial

Dr. Lyden finishes with an absurd statement –

Perhaps we will find a way to treat patients later than 3 hours, and further studies are needed to push the outer limit of the time window, but within the 3-hour window, no further trials are needed; the drug works. The dictum primum no nocere still applies: we must do no harm, either by actively committing an act or by withholding a proven therapy through inaction.^[4]

We have too many doctors defending too many poorly studied treatments.

Primum non nocere means first, do no harm.

Giving a poorly studied treatment, while claiming that it would be unethical to learn more about the treatment, is dangerous to the patient.

Giving a poorly studied treatment, while claiming that it would be unethical to learn more about the treatment, corrupts our ability to think rationally.

Giving a poorly studied treatment, while claiming that it would be unethical to learn more about the treatment, corrupts our ability to think ethically.

IST-3^[6] is an attempt to extend the treatment window for tPA to 6 hours. I will write about that later. This was just to set the stage and introduce some of the cast of characters.

When treating cardiac arrest, we try to minimize the amount of damage from reperfusion, but with stroke we only seem to be trying to minimize re-examination of a treatment that never should have become the standard of care.

Continued in Part II.

Footnotes:

^[1] Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group.
[No authors listed]
N Engl J Med. 1995 Dec 14;333(24):1581-7.
PMID: 7477192 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

^[2] Thrombolytic therapy for acute ischemic stroke – Tissue plasminogen activator for acute ischemic stroke: Is the CAEP Position Statement too negative?
Hoffman JR.
CJEM. 2001 Jul;3(3):183-5. No abstract available.
PMID: 17610781 [PubMed - in process]

Free Full Text from CJEM.

^[3] Truths about the NINDS study: setting the record straight.
Mann J.
West J Med. 2002 May;176(3):192-4. No abstract available.
PMID: 12016245 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

^[4] Further randomized controlled trials of tPA within 3 hours are required-not!
Lyden PD.
Stroke. 2001 Nov;32(11):2709-10. No abstract available.
PMID: 11692041 [PubMed - indexed for MEDLINE]

Free Full Text from Stroke.

^[5] Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience.
Katzan IL, Furlan AJ, Lloyd LE, Frank JI, Harper DL, Hinchey JA, Hammel JP, Qu A, Sila CA.
JAMA. 2000 Mar 1;283(9):1151-8.
PMID: 10703777 [PubMed - indexed for MEDLINE]

Free Full Text from JAMA.

^[6] The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the third international stroke trial [IST-3]): a randomised controlled trial.
IST-3 collaborative group, Sandercock P, Wardlaw JM, Lindley RI, Dennis M, Cohen G, Murray G, Innes K, Venables G, Czlonkowska A, Kobayashi A, Ricci S, Murray V, Berge E, Slot KB, Hankey GJ, Correia M, Peeters A, Matz K, Lyrer P, Gubitz G, Phillips SJ, Arauz A.
Lancet. 2012 Jun 23;379(9834):2352-63. Epub 2012 May 23. Erratum in: Lancet. 2012 Aug 25;380(9843):730.
PMID: 22632908 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

NINDS researchers (1995). Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. The New England journal of medicine, 333 (24), 1581-7 PMID: 7477192

Hoffman JR (2001). Thrombolytic therapy for acute ischemic stroke – Tissue plasminogen activator for acute ischemic stroke: Is the CAEP Position Statement too negative? CJEM, 3 (3), 183-5 PMID: 17610781

Mann J (2002). Truths about the NINDS study: setting the record straight. The Western journal of medicine, 176 (3), 192-4 PMID: 12016245

Lyden PD (2001). Further randomized controlled trials of tPA within 3 hours are required-not! Stroke; a journal of cerebral circulation, 32 (11), 2709-10 PMID: 11692041

Katzan IL, Furlan AJ, Lloyd LE, Frank JI, Harper DL, Hinchey JA, Hammel JP, Qu A, & Sila CA (2000). Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience. JAMA : the journal of the American Medical Association, 283 (9), 1151-8 PMID: 10703777

IST-3 collaborative group, Sandercock P, Wardlaw JM, Lindley RI, Dennis M, Cohen G, Murray G, Innes K, Venables G, Czlonkowska A, Kobayashi A, Ricci S, Murray V, Berge E, Slot KB, Hankey GJ, Correia M, Peeters A, Matz K, Lyrer P, Gubitz G, Phillips SJ, & Arauz A (2012). The benefits and harms of intravenous thrombolysis with recombinant tissue plasminogen activator within 6 h of acute ischaemic stroke (the third international stroke trial [IST-3]): a randomised controlled trial. Lancet, 379 (9834), 2352-63 PMID: 22632908

Filed Under: ACLS, Ethics, Evidence, Heresy, Mythology, Pharmacology, Research Blogging