The only reason we get away with giving such large doses of epinephrine to these patients is that they are already dead.

- Rogue Medic

The Controversy of Admitting ‘We Do Not Know What Works’

ResearchBlogging.org

 

There are several news articles today criticizing a study because the patients might be deprived of a drug that has not been adequately studied in humans. This criticism is coming from journalists – the people who publicized the fraudulent vaccines research by Andrew Wakefield, who was trying to sell his competing vaccine and was being paid to produce negative research by lawyers suing the vaccine companies.[1]

The real controversy is that this untested drug became the standard of care with no evidence that it improves outcomes that matter.

Is it controversial to give a placebo, rather than a drug not yet adequately tested in humans?

No.

We are not informing patients that there is no evidence that the standard treatment is effective. We are not obtaining consent to give the unproven drug – epinephrine (Adrenaline in Commonwealth countries). How are the ethics different when we substitute a placebo for a mystery medicine?

What is less ethical than continuing the tradition of giving an inadequately studied drug to people who cannot consent to treatment?

Are we depriving patients of effective medicine or are we depriving them of witchcraft?

If you think that epinephrine is effective medicine at improving survival to discharge, provide the evidence and stop this study. The reason the study is being done is that evidence of benefit does not exist.
 

Click on image to make it larger.[2] The studies are in the footnotes.[3],[4],[5],[6],[7],[8],[9],[10]
 

Is Adrenaline beneficial in cardiac arrest?

Probably, but only for some patients and we do not know which patients benefit.

Is Adrenaline harmful in cardiac arrest?

Probably, but only for some patients and we do not know which patients are harmed.

What is the right dose of Adrenaline in cardiac arrest?

Pick a number – any number. We do not know the right dose.
 

 

Even the patients who only received the minimum dose – 1 mg – had worse outcomes.[11]

Wrong timing? Wrong dose? Wrong drug?

We do not know.
 

We have used this untested treatment for half a century and not bothered to find out if it works. A recent study shows that epinephrine produces worse outcomes when given by EMS later,[12] but that does not mean that the outcomes are good when epinephrine is given early. The study had no placebo group, so like a study comparing different doses of cyanide, just because one dose is not as bad as another dose, the results do not suggest that cyanide is beneficial.
 


 

This is comparing three different treatments HDE (High-Dose Epinephrine), SDE (Standard-Dose Epinephrine), and NE (NorEpinephrine). The lines for the HDE and NE are so close to each other, that you may not be able to see the gold line.[13] Other studies produce similar results.[3],[14],[15],[16],[17] Only one study showed better ROSC with standard dose epinephrine.[18]
 

Epinephrine does produce more ROSC (Return Of Spontaneous Circulation – at least a temporary pulse) than placebo, but high dose epinephrine produces even more ROSC than standard dose epinephrine, so why do we give the standard dose that only produces middling ROSC?

Is ROSC the goal? No.

For the guidelines (ACLS and ILCOR), ROSC is the basis for giving standard dose epinephrine, but it would make more sense to give high dose epinephrine if the goal is ROSC. More ROSC, but no more survivors leaving the hospital. If all we want is put the patient in a coma long enough to run up a big hospital bill, then the drugs are great.

If we want people to leave the hospital alive, then We Do Not Know What Works.
 

The guidelines are based on wishful thinking and rationalization. They are not based on improved survival. A lot of research is cited (hundreds of papers), but the research does not show improved survival with any drug(s).

Will the guidelines be revised to remove epinephrine? Maybe.
 

The exciting development is that these data create equipoise about the current standard of resuscitation care. The best available observational evidence indicates that epinephrine may be harmful to patients during cardiac arrest, and there are plausible biological reasons to support this observation. However, observational studies cannot establish causal relationships in the way that randomized trials can.[19]

 

Some cocktails have produced better results than epinephrine in tiny studies. It is too probably too early to tell if these are just statistical aberrations. I will write about them later.

Continued in Does a Placebo vs. Adrenaline Study Deprive Patients of Necessary Care According to the Resuscitation Guidelines?

Footnotes:

[1] “Piltdown medicine” and Andrew Wakefield’s MMR vaccine fraud
Science-Based Medicine
Posted by David Gorski
January 6, 2011
Article
 

In a mere decade and a half, several decades of progress in controlling this scourge had been unravelled like a thread hanging off a cheap dress, all thanks to Andrew Wakefield and scandal mongers in the British press.

[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.

[3] High dose and standard dose adrenaline do not alter survival, compared with placebo, in cardiac arrest.
Woodhouse SP, Cox S, Boyd P, Case C, Weber M.
Resuscitation. 1995 Dec;30(3):243-9.
PMID: 8867714 [PubMed - indexed for MEDLINE]

[4] Adrenaline in out-of-hospital ventricular fibrillation. Does it make any difference?
Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, Holmberg S.
Resuscitation. 1995 Jun;29(3):195-201.
PMID: 7667549 [PubMed - indexed for MEDLINE]

[5] Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest.
Ong ME, Tan EH, Ng FS, Panchalingham A, Lim SH, Manning PG, Ong VY, Lim SH, Yap S, Tham LP, Ng KS, Venkataraman A; Cardiac Arrest and Resuscitation Epidemiology Study Group.
Ann Emerg Med. 2007 Dec;50(6):635-42. Epub 2007 May 23.
PMID: 17509730 [PubMed - indexed for MEDLINE]

Free Full Text Download in PDF format from prdupl02.ynet.co.il

[6] Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L.
JAMA. 2009 Nov 25;302(20):2222-9.
PMID: 19934423 [PubMed - indexed for MEDLINE]

Free Full Text from JAMA

[7] Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial.
Olasveengen TM, Wik L, Sunde K, Steen PA.
Resuscitation. 2011 Nov 22. [Epub ahead of print]
PMID: 22115931 [PubMed - as supplied by publisher]

[8] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed - in process]

Free Full Text PDF Download of In Press Uncorrected Proof from xa.yming.com
 

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.

 

In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.

 

[9] Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest.
Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S.
JAMA. 2012 Mar 21;307(11):1161-8. doi: 10.1001/jama.2012.294.
PMID: 22436956 [PubMed - indexed for MEDLINE]

Free Full Text from JAMA.

[10] Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest.
Hayashi Y, Iwami T, Kitamura T, Nishiuchi T, Kajino K, Sakai T, Nishiyama C, Nitta M, Hiraide A, Kai T.
Circ J. 2012;76(7):1639-45. Epub 2012 Apr 5.
PMID: 22481099 [PubMed - indexed for MEDLINE]

Free Full Text from Circulation Japan.

[11] Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium.
Glover BM, Brown SP, Morrison L, Davis D, Kudenchuk PJ, Van Ottingham L, Vaillancourt C, Cheskes S, Atkins DL, Dorian P; Resuscitation Outcomes Consortium Investigators.
Resuscitation. 2012 Nov;83(11):1324-30. doi: 10.1016/j.resuscitation.2012.07.008. Epub 2012 Jul 31.
PMID: 22858552 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

[12] Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry.
Donnino MW, Salciccioli JD, Howell MD, Cocchi MN, Giberson B, Berg K, Gautam S, Callaway C; American Heart Association’s Get With The Guidelines-Resuscitation Investigators.
BMJ. 2014 May 20;348:g3028. doi: 10.1136/bmj.g3028.
PMID: 24846323 [PubMed - in process]

Free Full Text from BMJ.

[13] A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest.
Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J.
JAMA. 1992 Nov 18;268(19):2667-72.
PMID: 1433686 [PubMed - indexed for MEDLINE]

[14] A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group.
Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, Jastremski M.
N Engl J Med. 1992 Oct 8;327(15):1051-5.
PMID: 1522841 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[15] Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital.
Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, Petit P.
Resuscitation. 1995 Feb;29(1):3-9.
PMID: 7784720 [PubMed - indexed for MEDLINE]

[16] A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group.
Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, Carli P.
N Engl J Med. 1998 Nov 26;339(22):1595-601.
PMID: 9828247 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[17] High dose versus standard dose epinephrine in cardiac arrest – a meta-analysis.
Vandycke C, Martens P.
Resuscitation. 2000 Aug 1;45(3):161-6.
PMID: 10959014 [PubMed - indexed for MEDLINE]

[18] High-dose epinephrine in adult cardiac arrest.
Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, Dickinson GE.
N Engl J Med. 1992 Oct 8;327(15):1045-50.
PMID: 1522840 [PubMed - indexed for MEDLINE]

Free Full Text from NEJM.

[19] Questioning the use of epinephrine to treat cardiac arrest.
Callaway CW.
JAMA. 2012 Mar 21;307(11):1198-200. doi: 10.1001/jama.2012.313. No abstract available.
PMID: 22436961 [PubMed - indexed for MEDLINE]

Link to a free 6 1/2 minute recording of an interview with Dr. Callaway about this paper.

On the right side of the page, to the right of the First Page Preview, is a section with the title Multimedia Related by Topic. Below that is Author Interview. Below that is some information about the edition, . . . , and below that is an embedded recording of the interview. Press on the arrow to play. That has the recording of the interview with Dr. Callaway.

The interview with Dr. Callaway is definitely worth listening to.

Larabee TM, Liu KY, Campbell JA, & Little CM (2012). Vasopressors in cardiac arrest: a systematic review. Resuscitation, 83 (8), 932-9 PMID: 22425731

Woodhouse SP, Cox S, Boyd P, Case C, & Weber M (1995). High dose and standard dose adrenaline do not alter survival, compared with placebo, in cardiac arrest. Resuscitation, 30 (3), 243-9 PMID: 8867714

Herlitz J, Ekström L, Wennerblom B, Axelsson A, Bång A, & Holmberg S (1995). Adrenaline in out-of-hospital ventricular fibrillation. Does it make any difference? Resuscitation, 29 (3), 195-201 PMID: 7667549

Ong ME, Tan EH, Ng FS, Panchalingham A, Lim SH, Manning PG, Ong VY, Lim SH, Yap S, Tham LP, Ng KS, Venkataraman A, & Cardiac Arrest and Resuscitation Epidemiology Study Group (2007). Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest. Annals of emergency medicine, 50 (6), 635-42 PMID: 17509730

Olasveengen, T., Sunde, K., Brunborg, C., Thowsen, J., Steen, P., & Wik, L. (2009). Intravenous Drug Administration During Out-of-Hospital Cardiac Arrest: A Randomized Trial JAMA: The Journal of the American Medical Association, 302 (20), 2222-2229 DOI: 10.1001/jama.2009.1729

Olasveengen TM, Wik L, Sunde K, & Steen PA (2011). Outcome when adrenaline (epinephrine) was actually given vs. not given – post hoc analysis of a randomized clinical trial. Resuscitation PMID: 22115931

Jacobs IG, Finn JC, Jelinek GA, Oxer HF, & Thompson PL (2011). Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation, 82 (9), 1138-43 PMID: 21745533

Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, & Miyazaki S (2012). Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA : the journal of the American Medical Association, 307 (11), 1161-8 PMID: 22436956

Hayashi Y, Iwami T, Kitamura T, Nishiuchi T, Kajino K, Sakai T, Nishiyama C, Nitta M, Hiraide A, & Kai T (2012). Impact of early intravenous epinephrine administration on outcomes following out-of-hospital cardiac arrest. Circulation journal : official journal of the Japanese Circulation Society, 76 (7), 1639-45 PMID: 22481099

Glover BM, Brown SP, Morrison L, Davis D, Kudenchuk PJ, Van Ottingham L, Vaillancourt C, Cheskes S, Atkins DL, Dorian P, & the Resuscitation Outcomes Consortium Investigators (2012). Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium. Resuscitation PMID: 22858552

Donnino, M., Salciccioli, J., Howell, M., Cocchi, M., Giberson, B., Berg, K., Gautam, S., Callaway, C., & , . (2014). Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospital data registry BMJ, 348 (may20 2) DOI: 10.1136/bmj.g3028

Callaham M, Madsen CD, Barton CW, Saunders CE, & Pointer J (1992). A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA : the journal of the American Medical Association, 268 (19), 2667-72 PMID: 1433686

Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, & Jastremski M (1992). A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group. The New England journal of medicine, 327 (15), 1051-5 PMID: 1522841

Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, & Petit P (1995). Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital. Resuscitation, 29 (1), 3-9 PMID: 7784720

Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, & Carli P (1998). A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group. The New England journal of medicine, 339 (22), 1595-601 PMID: 9828247

Vandycke C, & Martens P (2000). High dose versus standard dose epinephrine in cardiac arrest – a meta-analysis. Resuscitation, 45 (3), 161-6 PMID: 10959014

Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, & Dickinson GE (1992). High-dose epinephrine in adult cardiac arrest. The New England journal of medicine, 327 (15), 1045-50 PMID: 1522840

Callaway, C. (2012). Questioning the Use of Epinephrine to Treat Cardiac Arrest JAMA: The Journal of the American Medical Association, 307 (11) DOI: 10.1001/jama.2012.313

.

Since the World is Ending Today, What Should We Do?


 

Oh no! It is the end of the world, again. What should we do?

If the end of the world causes you anxiety, you are probably already prescribed some anti-anxiety medicine. I recommend that you follow the directions on the label and stop annoying less anxious people. Avoid combining your sedatives with other sedatives (alcohol, heroin, propofol, . . . ) and find a way to distract yourself from what you do not understand.
 

Lunar activity is said to mark the END OF TIME, with some religious groups believing it to be a sign of the JUDGEMENT DAY.[1]

 

The end of times has probably been predicted since before writing was first used to record anything. There is one consistent thing about these predictions. They have been completely wrong. Eventually, one will be right, but that will probably be something we learn about from scientists, who will be the first to observe evidence of any problems.

What do scientists predict about the super moon? It will appear a little bit bigger and brighter than most normal full moons. That will be the only noticeable difference from a normal full moon.
 

Lunar activity is said to mark the END OF TIME, with some religious groups believing it to be a sign of the JUDGEMENT DAY.[1]

 

We are still waiting and none of the predictions have come true. None of the predictions are any more likely than any other predictions.
 

But what about he tsunami caused by a super moon?
 

Supermoons have been proven to cause sea levels to rise as the gravitational pull of the Earth’s closest neighbour increases as it gets closer.[1]

 

That is not true.
 

The relative amount of influence is proportional to the object’s mass and distance from the earth.[2]

 

The difference in distance will be tiny.

Here is what the distance will be from our planet to the super moon.
 

Aug 10 5:46 PM         356,922 km         221,796 mi         Closest for this year [3]

 

And here is what the distance was for the full moon on January 1, 2014.
 

Jan 1 9:01 PM         356,945 km         221,811 mi [3]

 

Only 15 miles different.

There is one important thing to understand about a 15 mile difference in the distance between the moon and us. It is not something that humans can notice without machinery to measure the distance.
 

Jul 28 3:39 AM         406,547 km 252,634 mi         Farthest away this year [3]

 

That is a difference of 30,838 miles between the farthest and closest distances. That is a 12% difference. The difference between the 2nd closest full moon and the super moon is 15 miles.

15/221,811

Or 1 our of 14,787. If this is seen by some as prophetic, important, or ominous, it is because those describing the problem lack all sense of perspective.

Some people are claiming that this is important, because they have no idea what they are commenting on, or they are trying to profit from the gullibility of others, or . . . .

But the moon being this close is unprecedented!
 

Jan 30 8:59 AM         356,606 km         221,600 mi         Closest for this year[4]

 

That was the closest distance between the moon and the earth in 2010. 221,600 miles. Today’s end of the world distance – because it is so incredibly close – is 221,796 miles or 196 miles farther than it was in 2010. So much for unprecedented. So much for scary.

If you think that the minuscule difference in distance was enough to cause a disaster, you seem to have the same problem with perspective as the prophets of doom.
 

If this were indeed the case, we would expect to see a correlation between rate at which earthquakes occur and the perturbations to the gravitational field. The dominant perturbation in the earth’s gravitational field generates the semi-diurnal (12 hour) ocean and solid earth tides which are primarily caused by the moon (due to its proximity) and the sun (due to its large mass). No significant correlations have been identified between the rate of earthquake occurrence and the semi-diurnal tides when using large earthquake catalogs.[2]

 

No valid mechanism, no perspective, and no evidence?

The only thing useful out of this is as another example of frauds taking advantage of the vulnerable, but we have no shortage of examples of that. We don’t even have a shortage of people defending the frauds.

Footnotes:

[1] SUPERMOON LIVE: Beautiful lunar event could trigger ‘END OF DAYS’
By: Nathan Rao
Published: Sun, August 10, 2014
Sunday Express
Article

[2] Can the position of the moon or planets affect seismicity?
Earthquake FAQ
Berkeley Seismological Laboratory Outreach Program
Article

[3] Moon distances for UTC
timeanddate.com
Information page

[4] Moon distances for UTC
timeanddate.com
Information page

.

What is the Best Way to Manage Cardiac Arrest According to the Evidence?

ResearchBlogging.org
 
There is an excellent review article by Dr. Bentley Bobrow and Dr. Gordon Ewy on the best management of sudden cardiac arrest from the bystander to the ICU (Intensive Care Unit).

They point out something that we tend to resist learning. Cardiac arrest that is not due to respiratory causes does not need respiratory treatment. A person who is unresponsive and gasping is exhibiting signs of cardiac arrest, not signs of respiratory problems.
 

Except in newborns, gasping or agonal breathing is a common sign of cardiac arrest, occurring in slightly more than 50% of patients with primary cardiac arrest.22-25 [1]

 

Gasping does not mean alive and well. Gasping means dead and having a good chance at resuscitation. Unresponsive and gasping means there is a need for compressions.
 

If adequate chest compressions are promptly initiated, the patient will continue to gasp.23 [1]

 


 

Of interest is that only a minority of individuals with noncardiac arrest received CO-CPR.35 In Arizona, the public was generally capable of recognizing respiratory arrest, where chest compressions and assisted ventilations were recommended.[1]

 


 

It probably has less to do with taking away the ventilation, than with making the compressions continuous and high quality, but ventilations do decrease blood return to the chest and increase the likelihood of vomiting (regardless of what has been eaten), so there are benefits from removing the ventilations.
 


 

Passive oxygen insufflation means just putting a mask over the patient’s mouth and nose and allowing oxygen to be delivered passively. The rise and fall of the chest, due to compressions, and diffusion will allow for all of the oxygenation the patient will need.

Standard CPR (Std CPR) means alternating compressions with two ventilations every 30 compressions. Standard CPR is clearly not what we want to do, unless we want to keep patients from being resuscitated.
 

The problem is that the vast majority of physicians have no idea what the survival rate of patients with OHCA is in their area. This needs to change if major progress is to be made.[1]

 

Many of us do not know the results of what we do, so it is not surprising that a lot of EMS treatment is mythological.

Medicine is a field that encourages superstition. Patients provide intermittent reinforcement, which may be the most effect means of creating superstitions. Intermittent reinforcement?[2]
 

The only way to know the effectiveness of your Emergency Medical System is to know the survival of patients with OHCA and a shockable rhythm. If it is less than 38%,they should be encouraged to institute CCR and reevaluate the results.[1]

 

Maybe you are already doing better than 38% walking out of the hospital, then you are probably already using continuous compressions and passive oxygen insufflation. If you are not, then you need to improve your patient care.

Footnotes:

[1] Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest.
Ewy GA, Bobrow BJ.
J Intensive Care Med. 2014 Jul 30. pii: 0885066614544450. [Epub ahead of print]
PMID: 25077491 [PubMed - as supplied by publisher]

[2] Intermittent reinforcements
Wikipedia
Article
 

Pigeons experimented on in a scientific study were more responsive to intermittent reinforcements, than positive reinforcements.[16] In other words, pigeons were more prone to act when they only sometimes could get what they wanted. This effect was such that behavioral responses were maximized when the reward rate was at 50% (in other words, when the uncertainty was maximized), and would gradually decline toward values on either side of 50%.[17] R.B Sparkman, a journalist specialized on what motivates human behavior, claims this is also true for humans, and may in part explain human tendencies such as gambling addiction.[18]

 

Ewy, G., & Bobrow, B. (2014). Cardiocerebral Resuscitation: An Approach to Improving Survival of Patients With Primary Cardiac Arrest Journal of Intensive Care Medicine DOI: 10.1177/0885066614544450

.

Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest

ResearchBlogging.org
 

This study is interesting for several reasons.

In a system that claims excellence, the most consistent way to identify the study group is by documentation of a protocol violation – but it is not intended as a study of protocol violations.

This may hint at some benefit from epinephrine (Adrenaline in Commonwealth countries), but that would require some study and we just don’t study epinephrine. We only make excuses for not studying epinephrine.

The atropine results suggest that the epinephrine data may be just due to small numbers, or that we may want to consider atropine for drug overdose cardiac arrest patients, or . . . .

The Sodium Bicarbonate (bicarb – NaHCO3) results suggest a flaw in EMS education (probably testing, too). If the patient is acidotic, this is one type of cardiac arrest where hyperventilation may be beneficial. Bicarb is the part of the drug that doesn’t do much, especially if the patient is dead. The sodium is what works, such as when the patient has taken too much of a sodium channel blocker, such as a tricyclic antidepressant or a class I antiarrhythmic. Acidosis is treated by hyperventilation. Use capnography.

Most important – antidotes probably don’t work as expected during cardiac arrest. Not even naloxone (Narcan).
 

Despite clear differences in the etiology of suspected OD [OverDose] and non-OD OHCA [Out of Hospital Cardiac Arrest], the International Liaison Committee on Resuscitation guidelines published in 2010 do not specify different treatments for suspected OD-OHCA patients during resuscitation,and state that there is no evidence promoting the intra-arrest administration of the opioid antagonist naloxone.8 [1]

 

What did they find in the study?

They may have located the highest concentration of heroin overdose in the country. 93% of OD-OHCA patients were treated with naloxone.
 

We relied on either naloxone administration or clear description of circumstantial evidence in the PCR [Patient Care Recod] to identify a suspected OD. Clear descriptions are also rare, and most (93%) of the cases were identified by naloxone administration. Naloxone during cardiac arrest is not part of any regional protocol, and all of these administrations are deviations from recommended practice. There may be other cases in which paramedics suspected OD, but did not deviate from protocol to administer naloxone. Therefore, it is impossible to be certain whether the actual number of OD cases is larger or smaller than the reported number. However, the use of naloxone as a proxy indicator of suspected OD has been supported in the literature.11 [1]

 

The EMS approach to naloxone still appears to be –
 


Image credits – 123
 

These results seem to show better response to the prehospital drugs in the OD-OHCA patients, but that ignores the ROSC (Return Of Spontaneous Circulation) rates.
 


Click on images to make them larger.
 

Why would OD-OHCA patients do better than non-OD-OHCA patients if they get a pulse back?

The average non-OD-OHCA patient is 20+ years older. These older patients may not be as capable of recovery nor as capable of tolerating the toxicity of the drugs they were treated with.

The change after ROSC is dramatic. Is that the important point of this study?

Are they doing anything special for OD patients in the hospital, or is it just a matter of That which does not kill me by anoxic brain damage, may allow me to recover twice as often as a typical cardiac arrest patient.
 

Do drugs (antidotes, antiarrhythmics, . . . ) work the same way in dead people as in living people?
 

Pharmacologic insults are just so massive and normal metabolism and physiology so deranged that no mere mortal can make a meaningful intervention. The seriously poisoned who maintain vital signs in the ED have the best, albeit never guaranteed, chance of rescue from a modicum of antidotes and intensive supportive care.[2]

 

We should understand that normal metabolism is irrelevant to cardiac arrest.

We should understand that we do not need to ventilate adult cardiac arrest patients, when the cause is cardiac. An absence of ventilation would not be appropriate in a living adult, but dead metabolism is not normal. If something as basic as oxygen changes, when the patient is dead, how much less do we understand the behavior of other drugs in dead patients?

Footnotes:

[1] Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest.
Koller AC, Salcido DD, Callaway CW, Menegazzi JJ.
Resuscitation. 2014 Jun 26. pii: S0300-9572(14)00581-4. doi: 10.1016/j.resuscitation.2014.05.036. [Epub ahead of print]
PMID: 24973558 [PubMed - as supplied by publisher]

[2] Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions
Emergency Medicine News:
October 2011 – Volume 33 – Issue 10 – pp 16-18
doi: 10.1097/01.EEM.0000406945.05619.ca
InFocus
Roberts, James R. MD
Article

Roberts, J. (2011). InFocus: Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions Emergency Medicine News, 33 (10), 16-18 DOI: 10.1097/01.EEM.0000406945.05619.ca

Koller, A., Salcido, D., Callaway, C., & Menegazzi, J. (2014). Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest Resuscitation DOI: 10.1016/j.resuscitation.2014.05.036

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Fall With Dementia and No Change from Baseline Mental Status

ResearchBlogging.org
 

This happens many times every day. A patient falls and may have hit her head, but there is no change from her normal mental status. To complicate matter, she takes an anticoagulant.

There are no clear signs of serious trauma. so should we automatically go to the trauma center?

What can help us decide?
 

Patients were not excluded because of dementia, aphasia, or any cognitive or neurologic deficit that was determined by the physician caring for the patient to be the patient’s baseline.[1]

 

The conclusion of the study is useful, but I would reverse the emphasis.
 

Signs of trauma to the head and face or loss of consciousness is predictive of ICI.[1]

 

An absence of Signs of trauma to the head and face or loss of consciousness is predictive of an absence of ICI (IntraCranial Injury).
 

The study is not perfect, for example it is not clear what is included in the signs of trauma to the head, but it does strongly suggest that these patients should not be diverted to a trauma center just for anticoagulants, or for dementia, or for being old.
 

A patient was determined to have no significant acute head injury (1) if he/she had a negative result on head CT performed, (2) if the patient was admitted to the hospital and had no sequelae at discharge, (3) if review of his/her medical record revealed repeat hospital visits unrelated to falls with no sequelae or concerns related to the index visit,or (4) if the patient had no concerns at 30 days postinjury in telephone follow-up.[1]

 

These clearly are not the patients who needed to be trauma alerts.
 


 

Anticoagulants did not matter. While a trend is probably just statistical noise, the trend for anticoagulants other than aspirin was toward less likelihood of ICI.

While Signs of trauma to the head and face increased the likelihood of ICI, History of hitting head had a trend toward less likelihood of ICI.
 

The sensitivity and specificity for signs of trauma to the face/head or loss of consciousness were 92.6% (74.2-98.7) and 40.2% (36.8-43.8), respectively. The positive predictive value in this“low-acuity”cohort was 5.2% (3.4-7.6), and the negative predictive value was 99.4% (97.4-99.9).[1]

 

Should we start to write protocols based on this, or triage patients based on this? We should find out more, but patients with dementia and no change in mental status probably should not be triaged differently from patients with no change in mental status who just happen to not have dementia.

We already knew that, but we did not have evidence to support that bit of common sense.
 

A recent prospective study concluded that 26% of elderly patients presenting to the ED exhibited evidence of cognitive impairment[13].[1]

 

If a quarter of elderly patients have cognitive impairment, this can have a big effect on EMS.
 
 

The following figure that confused me. The percentages in red on the far right are the percentages of each category. That is what I would want to know, when looking at the data. The totals are not explained. Maybe someone will see what I am missing. How did 799 patients become 783, or did they become 783, and what happened to the other 16 patients if the number is now 783?
 


 

Regardless of my confusion with the figure above, this paper is one more reason for me to feel comfortable transporting patients with dementia and no obvious head injury (and no loss of consciousness) to the local hospital.

Footnotes:

[1] Characteristics of elderly fall patients with baseline mental status: high-risk features for intracranial injury.
Hamden K, Agresti D, Jeanmonod R, Woods D, Reiter M, Jeanmonod D.
Am J Emerg Med. 2014 May 12. pii: S0735-6757(14)00318-0. doi: 10.1016/j.ajem.2014.04.051. [Epub ahead of print]
PMID: 24929771 [PubMed - as supplied by publisher]

Hamden K, Agresti D, Jeanmonod R, Woods D, Reiter M, & Jeanmonod D (2014). Characteristics of elderly fall patients with baseline mental status: high-risk features for intracranial injury. The American journal of emergency medicine PMID: 24929771

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Dr. Edward Tobinick Sues Barbara Streisand – or something equally foolish


Dr. Edward Tobinick might not be a quack, but his behavior suggest otherwise.
 

Having a medical degree does not mean not a quack.

Using FDA (Food and Drug Administration) approved drugs does not mean not a quack.

Having a medical web site that does not have the word “quantum” all over the place does not mean not a quack.

Threatening to sue people for writing about the lack of evidence for his treatments does not mean not a quack.
 

Dr. Edward Tobinick is suing Science-Based Medicine for writing about Dr. Edward Tobinick’s dubious medical practices.

That strongly suggests that Dr. Edward Tobinick is a quack.
 

The claims and practice of Dr. Tobinick have many of the red flags of a dubious medical practice, of the sort that we discuss regularly on SBM. It seems that Dr. Tobinick does not appreciate public criticism of his claims and practice,[1]

 

Essentially, what Dr. Edward Tobinick is saying is, Your valid criticism of the way I apparently take advantage of patients might discourage patients from shelling out money for my untested treatment.

or –

Your valid criticism of the way I apparently take advantage of patients might encourage patients to ask reasonable questions about my untested treatment – questions that I cannot honestly answer.
 

Etanercept might work, but so might steroids, or ribavarin, or eye of newt, or a kick in the groin.

All of these treatments are equally valid. Oddly, the patients receiving a kick in the groin will probably report the fewest symptoms after treatment. 90% of the kick in the groin patients claimed to be cured and not in need of any further treatment.

Without evidence, and with his opposition to evidence, Dr. Edward Tobinick is just a quack with a brainstorm. Nothing original there.
 

Dr. Edward Tobinick injects etanercept (Enbrel) around the spine. This is not something he covered in his dermatology residency, so has he injected etanercept into the spine yet?

Why etanercept? Etanercept is an immune suppression/anti-inflammation drug. Inflammation is a problem with everything, so preventing/reversing inflammation is the simplistic cure. If this worked in real people, and not just in the hypotheses of pathophysiologists, steroids would have cured everything decades ago.

Perhaps Dr. Edward Tobinick is imitating Dr. Michael Bracken, who is able to produce improved outcomes with steroids (anti-inflammation drugs) for spinal injury, but only when he is in charge of the data.[2]

At least Dr. Michael Bracken published some research to support his claims. Dr. Edward Tobinick just wants us to believe that his interpretation of pathophysiology is miraculously prescient.
 

Evidence? We ain’t got no evidence. We don’t need no evidence! I don’t have to show you any stinkin’ evidence!
 

Maybe Dr. Edward Tobinick does have some valid evidence.

Maybe Dr. Edward Tobinick is just hiding the valid evidence because it is proprietary. ;-)

Here are a couple of comments by Dr. Novella on science and the importance of evidence. They probably were not directed specifically at Dr. Edward Tobinick, but they do apply to him.
 

What do you think science is? There’s nothing magical about science. It is simply a systematic way for carefully and thoroughly observing nature and using consistent logic to evaluate results. Which part of that exactly do you disagree with? Do you disagree with being thorough? Using careful observation? Being systematic? Or using consistent logic?

 

Science is the way we learn what works.

Dr. Edward Tobinick’s criticism is evidence that he does not understand science.

Is any treatment, that is not based on evidence, likely to provide a benefit to patients?
 

History is strewn with ideas that were intuitive and made sense at the time, but were also hopelessly wrong.

 
Alternative medicine, opposition to EBM (Evidence Based Medicine), and opposition to SBM (Science-Based Medicine) are all the same mistake – evidence denialism.

Evidence denialism is devotion to being hopelessly wrong and remaining ignorant of being wrong.
 

Barbara Streisand?[3]

Footnotes:

[1] Another Lawsuit To Suppress Legitimate Criticism – This Time SBM
Posted by Steven Novella
July 23, 2014
Science-Based Medicine
Article

[2] Cochrane and a Significantly Biased Review of Steroids for acute spinal cord injury
Fri, 25 May 2012
Rogue Medic
Article

[3] Streisand effect
Wikipedia
Article

Maybe there is no such thing as bad publicity for a quack, but the publicity associated with this law suit means that people will associate the name quack with Dr. Edward Tobinick, or vice versa.

Dr. Edward Tobinick is stating I am not a quack.

Reasonable people are hearing –

I, Dr. Edward Tobinick, am a quack.

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Was the In-Custody Death of Eric Garner Due to Police and EMS Abuse? Part I


 

In NYC Medics Restricted By FDNY Pending Investigation Into NYPD Custody Death, The Social Medic writes about the death of Eric Garner during an arrest. Death may have many different causes. Is there any one thing that would have resulted in Eric Garner still being alive – if it had not been done (or if it had been done)?

We do not know.

We probably never will know.

Did Eric Garner deserve to die? No.

Was there a valid reason for an arrest? There is nothing in this video to answer that question.

Should the police have tried to take Eric Garner down the way they did?

Is that a real choke hold, or a movie of the week choke hold?

How much choking was going on?

How much resisting was going on?

The videos only show some of what was going on, but it seems like this was not well thought out.

Eric Garner is a big man and should be approached with a well coordinated plan for the safety of everyone – for the safety of Eric Garner, for the safety of the police, and for the safety of the bystanders. Was ESU (Emergency Services Unit) there? Was a Taser available and is Taser use permitted in that jurisdiction?

A Taser might have saved Eric Garner’s life, but Eric Garner still might have died, even if the police had not arrested him. Sudden death happens hundreds of thousands of times a year in America.

When the police initially take him down, they brush up against/bounce off of a window. If it is glass, what would have happened if it broke? If it is glass, what if they had continued through the glass? If it is not glass, how do they know?

The difference between broken glass and a knife (or a sword) is not in the amount of danger they present, since all can kill you very quickly. This difference is in the perception of that danger.
 

In this video, Eric Garner repeatedly states that he cannot breathe, but this is probably not the first time that police have heard similar statements while wrestling someone into custody. EMS was not there, so no treatment was immediately available, if any treatment had been indicated. We cannot tell. His death later is not proof that he was having trouble breathing, but it does suggest that he was not breathing adequately.
 

The video cannot be shown at the moment. Please try again later.


 

The commentary from the person filming the video is useless. It is just as prejudiced and uninformed as that of any other politically motivated commentary.

All he did was break up a fight?

Unlikely, but how would the person filming this know?

Prejudiced cops on Staten Island, this is what they do?

Does that applied to the non-white cops, too? Or is that just a prejudiced comment? Prejudice does exist. Nobody is immune from it, but what is the critic basing his comments on? He appears to be basing his comments on his prejudice.

Eric Garner was beat up?

He was violently subdued/wrestled to the ground, but I did not see anyone strike him.

Eric Garner was not beat up.

The critic seems to be singing along with the music in the background, which does not really give the impression of someone who thinks he is witnessing someone being killed. He makes a lot of accusations, but his actions do not match his words. If you are singing along with Muzak, you appear to be indicating that there is nothing important distracting you from your singing. Maybe it is someone next to the critic, but that still suggests that there was not a lot of concern among those as close to events as the critic.

Did the police choke Eric Garner into submission or did one officer overestimate the effect he would have on a much larger guy by grabbing him around the neck?

Someone has written, None of the officers knew what to do in this situation on the bottom of the video. What would the film critic like the police to do? Should they put Eric Garner in the back of a police car?

What does the film critic suggest that they do?

They have called for an ambulance and they have Eric Garner in the rescue position.

Did the police use an inappropriate method of arresting Eric Garner?

The prohibition on the use of a choke hold for restraint may have more to do with the way things look to bystanders, than the effect it has on the person being restrained. Choke holds are not prohibited in most combat sport because apparently choke holds can be used safely. Did the choke hold cause death?
 


Image credit – Wikipedia article on choke holds.
 

At about 4:30 of the video, EMS enters.

I have not commented on what The Social Medic wrote about this incident, yet. I will comment on what can be seen of what EMS did (did not do) and whether excited delirium is a part of this in Part II.

.

Does a Medic Need Two Eyes to be Safe?


 

When this story first was reported, there were plenty of social media comments about the lack of safety of having only one eye.

Is there any difference in outcomes for patients treated by two-eyed medics and one-eyed medics? What about medics who wear glasses? Should a three-eyed medic be given preference over two-eyed medics?

Is there any evidence of a difference in job performance?

Is there any evidence of a difference in driving?

Is there any evidence of a difference in anything that is a part of the job?

Provide some valid evidence.

If we are going to make these decisions without evidence, we should admit that we are basing our decisions on prejudice.
 

A Queens woman with a prosthetic eye is suing the FDNY because it won’t hire her as a paramedic.[1]

 

The article lacks information. There may be other reasons she has not been hired, but NYFD is not likely to discuss those directly in the media, because that might also lead to a law suit. If this does go to court there should be more information available.

This topic has generated a lot of righteous indignation from those who insist that two eyes are necessary for the safety of patients. I have not yet seen any evidence to support their attitude.

If there is valid evidence that I am wrong, I am willing to learn from that.
 

See also –

Improving EMS By Hiring Deaf EMTs

Footnotes:

[1] FDNY won’t hire woman with fake eye as paramedic: suit
By Kathianne Boniello and Georgett Roberts
July 6, 2014 | 4:37am
NY Post
Article

.