Mythology | Rogue Medic

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

- Rogue Medic

Slaying the Immobilization Dragon – Free JEMS Podcast by Jon Politis

Thu, 18 Apr 2013 18:00:20 +0000 by Rogue Medic

This is an apt metaphor for the way we handle spinal immobilization.

We will do anything, even sacrifice our children, ask us for anything!

Just don’t ask for evidence!

It appears that Jon Politis is going to be describing the abysmal state of evidence (all negative) that looks at the way EMS uses spinal immobilization.

Image credit.

The town had a pond, as large as a lake, where a plague-bearing dragon dwelled that envenomed all the countryside. To appease the dragon, the people of Silene used to feed it two sheep every day, and when the sheep failed, they fed it their children, chosen by lottery. It happened that the lot fell on the king’s daughter, who is in some versions of the story called Sadra.^[8] The king, distraught with grief, told the people they could have all his gold and silver and half of his kingdom if his daughter were spared; the people refused. The daughter was sent out to the lake, dressed as a bride, to be fed to the dragon.^{[citation needed]} ^[1]

George came along and rescued the damsel from the dragon, as Jon will probably be encouraging us to rescue our patients from our backboards.

Jon, not George, but why quibble?

Spinal immobilization is a hot-button topic in the prehospital setting. During this webcast, Jon Politis, MBA, NREMT-P, will delve into the latest science in order to slay the immobilization dragon and provide answers to the following questions:
Is spinal immobilization always necessary?
Are there “high-risk” mechanisms?
How much spinal movement is OK?
Sponsored by Hartwell Medical^[2]

Is this a ploy to defend spinal immobilization?

I come to bury Caesar, not to praise him.

Is this just a way to encourage EMS spinal clearance (limiting spinal immobilization to those most likely to be harmed by spinal immobilization)?

I do not know.

Will this change anything?

Immediately? Probably not.

This may become a part of the evidence used to convince EMS medical directors to ignore the PHTLS (PreHospital Trauma Life Support) dogma.

There is extensive commentary on spinal immobilization, the absence of evidence of benefit, and the abundant evidence of harm.

In the absence of evidence of benefit, we should be limiting treatment to research participants, since these patients are receiving an unexamined treatment.

These patients continue to be test pilots of spinal immobilization.

They are not receiving adequate information to make an informed consent, nor an informed refusal for this guinea pig treatment.

It is reasonable to assume that all treatments cause some harm, and spinal immobilization has well documented harms. We only assume that some benefit actually exists. There probably is no benefit, just as with the rest of our wishful thinking-based medicine.

All quacks seem to uses the same scam – But what if it works and we do not use it?

That kind of fraud would justify using anything that does not have good evidence of benefit – homeopathy or Reiki, but these frauds probably will not directly harm the patient. Spinal immobilization lacks that safety.

Why do we listen to such nonsense?

The stakes are high, and when the stakes are high, a lot of us turn out to be very superstitious.

We don’t know the truth and we do not want to know. We are not protecting our patients. We are harming our patients in order to protect our superstitions.

We are dangerous.

Slaying the Immobilization Dragon – Registration Page.

Footnotes:

^[1] Slaying the Immobilization Dragon
DATE: May 2, 2013
TIME: 1 p.m. Eastern / 10 a.m. Pacific
COST: FREE

Registration Page.

Speaker:
Jon Politis, MPA, NREMT-P, is the retired chief of the Colonie EMS Department in upstate N.Y. An active EMT since 1971, he has been a career firefighter, state EMS training coordinator for Vermont and New York and a paramedic training program coordinator. He has served on the National Registry of EMTs board and on the Committee on Accreditation for the EMS Professions.

To access the live presentation, please click on the following link:
link.

^[2] Saint George and the Dragon
Wikipedia
Article

Filed Under: Heresy, Mythology, Spinal Immobilization

Is Nitroglycerin Bad for Severe Sepsis?

Wed, 17 Apr 2013 16:30:12 +0000 by Rogue Medic

Yesterday at The Paramedic’s Edge, this was the topic of ~~reactive, reflexive, dogmatic, rejection~~ discussion of a possible use of NTG (NiTroGlycerin – GTN GlycerylTriNitrate in Commonwealth countries).

NTG is a vasodilator and sepsis is a vasodialtion problem. There are other problems with sepsis, but vasodilation may be the primary problem.

Nitro for severe septic patients. What are your thoughts?^[1]

Here is a sampling of some of the unfortunately typical responses.

The amateur lawyer who thinks that what we do should be guided by fear of law suits approach.

Oh to put them out of their misery?! Sounds like a lawsuit waiting to happen

The just drive fast, I don’t understand any of this medical mumbo jumbo appraoch.

We’re medics not doctors. Best thing we can do is a diesel infusion

The most common responses seemed to be of this kind.

The I only know one thing about nitro and that scares me approach.

True hemodynamic instability is a contraindication

Hmmmm let’s drop their pressure even more…that’s a thought? So my answer…HE’LL NO!!

We will probably end up using NTG in the treatment of cardiac arrest – the ultimate low blood pressure state, so how far fetched is using NTG for sepsis?^[2],^[3],^[4],^[5],^[6],^[7]

Why?

NTG can lower blood pressure, but it can also increase cardiac output.

To over-simplify things –

If the CO (Cardiac Output) increases by more than the the vasodilation would decrease the BP (Blood Pressure), the BP will actually be expected to increase.

CO = SV (Stroke Volume) x HR (Heart Rate).

CO ≈ MAP (Mean Arterial Pressure)/TPR (Total Peripheral Resistance).

BP = CO x TPR.

Are all cardiac outputs and vascular resistances the same? No, but we simplify things by making that assumption.

Jean-Charles Preiser and colleagues question the routine use of nitroglycerin because of the risk of hypotension and the possible induction of mitochondrial dysfunction.^[8]

Many people question the use of NTG and worry about hypotension.

Although we observed a temporary drop in blood pressure, blood flow was maintained and, in fact, increased in our patients.^[8]

We do ~~worry~~ obsess about things that are brief and insignificant (such as ROSC – Return Of Spontaneous Circulation – in treatment of cardiac arrest), while we ignore the things that are more important (such as living long enough to leave the hospital with a brain that works well enough to recognize family members).

Space constraints meant that we were not able to include specific haemodynamic results in our Research letter, but mean arterial pressure temporarily dropped by an average of 21 mm Hg (range 13—33 mm Hg) in the eight patients we investigated.^[8]

A drop in MAP (Mean Arterial Pressure) of 21 mm/Hg is huge!

Mean arterial pressure returned to baseline level within 1 min in all patients with concomitant fluid infusion.^[8]

Less than 1 minute?

Try using that as a pickup line.

I can rock your world for less than 1 minute.

How much alcohol is going to be required to make that sound significant?

We give adenosine to do what?

To completely stop the heart for usually less than one minute.

We cardiovert to do what?

To completely stop the heart for usually less than one minute.

A short-term worsening of vital signs for a long-term improvement in survival is an excellent trade-off.

Does NTG improve long-term survival?

that is not clear, but this does show that we need to abandon more dogma in our search for the best care of our patients.

The increase in microvascular blood flow as a result of this procedure confirms our clinical experience that resuscitation efforts should be aimed at optimising blood flow not blood pressure.^[8]

NTG does improve blood flow.

Too many of us are afraid to use NTG, or afraid to use large doses of NTG, or afraid to use IV bolus NTG, or afraid to use large doses of IV bolus NTG out of too much concern for blood pressure and not enough concern for blood flow.

This quotes are from a response to a letter about research paper looking at NTG for sepsis. This paper is not something that should be summarily dismissed.^[9]

The EMS drug of choice, dopamine, may be a bad idea for sepsis.^[10],^[11]

Think about that – For sepsis dopamine may make things worse and NTG may make things better.

Is it that simple? Maybe. Maybe not. Dopamine may make things better, but just not do as good a job as norepinephrine. Or all catecholamines may be harmful.

Dr. Mervyn singer makes an excellent case that catecholamines are not helpful, or that they are at least tremendously overused. Go listen to his podcast.^[12]

Footnotes:

^[1] Nitro for severe septic patients. What are your thoughts?
The Paramedic’s Edge
Facebook
Facebook discussion page

^[2] High dose nitroglycerin treatment in a patient with cardiac arrest: a case report.
Guglin M, Postler G.
J Med Case Rep. 2009 Aug 10;3:8782. doi: 10.4076/1752-1947-3-8782.
PMID: 19830240 [PubMed]

Free Full Text from PubMed Central.

A possible explanation for the hemodynamic benefit of NTG in our patients is increased cardiac output produced by rapid vasodilatation in a heart operating at the extreme of the Frank-Starling curve. Vasodilators in heart failure with or without acute myocardial infarction have been proven to decrease left ventricular filling pressure and systemic vascular resistance while increasing cardiac index [7]. The more severe the failure, the more beneficial the effect of vasodilators [13].

^[3] Sodium nitroprusside enhanced cardiopulmonary resuscitation improves survival with good neurological function in a porcine model of prolonged cardiac arrest.
Yannopoulos D, Matsuura T, Schultz J, Rudser K, Halperin HR, Lurie KG.
Crit Care Med. 2011 Jun;39(6):1269-74. doi: 10.1097/CCM.0b013e31820ed8a6.
PMID: 21358401 [PubMed - indexed for MEDLINE]

Free Full Text from acoep.org.

^[4] Sodium nitroprusside-enhanced cardiopulmonary resuscitation improves resuscitation rates after prolonged untreated cardiac arrest in two porcine models.
Schultz JC, Segal N, Caldwell E, Kolbeck J, McKnite S, Lebedoff N, Zviman M, Aufderheide TP, Yannopoulos D.
Crit Care Med. 2011 Dec;39(12):2705-10. doi: 10.1097/CCM.0b013e31822668ba.
PMID: 21725236 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

^[5] Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest.
Schultz J, Segal N, Kolbeck J, McKnite S, Caldwell E, Yannopoulos D.
Resuscitation. 2012 Mar;83(3):374-7. doi: 10.1016/j.resuscitation.2011.07.038. Epub 2011 Aug 22.
PMID: 21864483 [PubMed - indexed for MEDLINE]

Free Full Text from PubMed Central.

^[6] Sodium nitroprusside enhanced cardiopulmonary resuscitation prevents post-resuscitation left ventricular dysfunction and improves 24-hour survival and neurological function in a porcine model of prolonged untreated ventricular fibrillation.
Schultz J, Segal N, Kolbeck J, Caldwell E, Thorsgard M, McKnite S, Aufderheide TP, Lurie KG, Yannopoulos D.
Resuscitation. 2011 Dec;82 Suppl 2:S35-40. doi: 10.1016/S0300-9572(11)70149-6.
PMID: 22208176 [PubMed - indexed for MEDLINE]

^[7] Controlled pauses at the initiation of sodium nitroprusside-enhanced cardiopulmonary resuscitation facilitate neurological and cardiac recovery after 15 mins of untreated ventricular fibrillation.
Yannopoulos D, Segal N, McKnite S, Aufderheide TP, Lurie KG.
Crit Care Med. 2012 May;40(5):1562-9. doi: 10.1097/CCM.0b013e31823e9f78.
PMID: 22430233 [PubMed - indexed for MEDLINE]

^[8] Nitroglycerin for septic shock.
Preiser JC, De Backer D, Vincent JL.
Lancet. 2003 Mar 8;361(9360):880; author reply 880. No abstract available.
PMID: 12642079 [PubMed - indexed for MEDLINE]

Free Full Text from the Lancet.

^[9] Nitroglycerin in septic shock after intravascular volume resuscitation.
Spronk PE, Ince C, Gardien MJ, Mathura KR, Oudemans-van Straaten HM, Zandstra DF.
Lancet. 2002 Nov 2;360(9343):1395-6.
PMID: 12423989 [PubMed - indexed for MEDLINE]

^[10] Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis*.
De Backer D, Aldecoa C, Njimi H, Vincent JL.
Crit Care Med. 2012 Mar;40(3):725-30. doi: 10.1097/CCM.0b013e31823778ee.
PMID: 22036860 [PubMed - indexed for MEDLINE]

CONCLUSIONS:
In patients with septic shock, dopamine administration is associated with greater mortality and a higher incidence of arrhythmic events compared to norepinephrine administration.

^[11] Norepinephrine or dopamine for septic shock: systematic review of randomized clinical trials.
Vasu TS, Cavallazzi R, Hirani A, Kaplan G, Leiby B, Marik PE.
J Intensive Care Med. 2012 May-Jun;27(3):172-8. doi: 10.1177/0885066610396312. Epub 2011 Mar 24. Review.
PMID: 21436167 [PubMed - indexed for MEDLINE]

CONCLUSIONS:
The analysis of the pooled studies that included a critically ill population with shock predominantly secondary to sepsis showed superiority of norepinephrine over dopamine for in-hospital or 28-day mortality.

^[12] Catecholamines Should Be Banned
Mervyn Singer
2009-04-24-1545
6th Annual Critical Care Symposium
Manchester, UK
Page with link to free mp3 download from Free Emergency Medicine Talks.

Guglin, M., & Postler, G. (2009). High dose nitroglycerin treatment in a patient with cardiac arrest: a case report Journal of Medical Case Reports, 3 (1) DOI: 10.4076/1752-1947-3-8782

SPRONK, P., INCE, C., GARDIEN, M., MATHURA, K., & ZANDSTRA, D. (2003). Nitroglycerin for septic shock The Lancet, 361 (9360), 880-880 DOI: 10.1016/S0140-6736(03)12692-X

Spronk, P., Ince, C., Gardien, M., Mathura, K., Straaten, H., & Zandstra, D. (2002). Nitroglycerin in septic shock after intravascular volume resuscitation The Lancet, 360 (9343), 1395-1396 DOI: 10.1016/S0140-6736(02)11393-6

Filed Under: Heresy, Mythology, NTG, Research Blogging

Japanese man dies after 25 hospitals reject him

Sun, 10 Mar 2013 22:00:08 +0000 by Rogue Medic

In January, in Japan, 25 hospitals refused to permit an ambulance to transport a man who was pronounced dead when he finally arrived at a hospital.

Were the patients already in the ED (Emergency Department) less stable than this patient?

Was this patient going to be the straw that breaks the camel’s back and result in the deaths of other patients already in the ED?

What kind of evidence do we have to justify diversion?

Paramedics rushed to his house but were told in turn by all 25 hospitals in the area that they could not accept the man because they did not have enough doctors or any free beds, a local city official said, adding some institutions were contacted more than once.^[1]

We do not know if he would still be alive if he had been transported to the first ED, or to the second, or to the third, . . . . We do not even know the cause of death. However, this is a good way to introduce the topic of diversion.

Diversion is not just a problem in Japan, but also in the US and other countries. It has become more convenient for many people to go to the ED than to wait to see a primary care physician. Until that problem is fixed (assuming that it ever is fixed), is diversion appropriate?

There have been a couple of studies in San Diego of what happens when diversion is minimized, or eliminated.

Even though volume went up, diversion dropped to almost zero.

Click on images to make them larger.

The authors acknowledge that the main limitation of this study was the short time frame of the analysis, comparing one week to another.^[2]

In a longer study, diversion decreased and the need for transfers between hospitals dropped. There did not appear to be any negative consequences of minimizing diversion.

In summary, a community-wide effort to improve getting patients to requested EDs and decreasing ambulance diversion hours can be successful in a large community with an urban, suburban, rural, and remote population distribution. The success of such a process had the additional effect of decreasing the need for ED interfacility transfers for payer request reasons.^[3]

In this month’s Annals of Emergency Medicine is a study looking at what happened when Massachusetts banned diversion.

Figure 1. Changes in ED length of stay by hospital among A, admitted patients and B, discharged patients. C, Changes in ambulance turnaround time by hospital. D, Changes in total hospital volume before and after a ban on ambulance diversion by hospital.^[4]

It seems that the benefits of diversion are just another medical myth.

Research has led to the consensus that crowding is largely due to output factors, particularly the practice of boarding admitted patients in the ED^2,7-10 because of lack of inpatient capacity. Ambulance diversion, in contrast, is an input factor, which has little effect on ED crowding.⁴ ^[2]

Very few of the patients coming in to the ED are arriving by ambulance.

On July 3, 2008, the department released a policy directive ending the practice of ambulance diversion in the state, except in cases of internal hospital disaster.¹⁷ The policy took effect on January 1, 2009, allowing hospitals 6 months to prepare for the changes necessary for its implementation. This policy represented the first statewide ambulance diversion ban in the United States.^[2]

A lot of the bad things were supposed to occur when diversion was banned.

None of them happened.

Preliminary reports from hospitals suggest that the end of ambulance diversion has been a relative success because of operational changes made at individual hospitals in anticipation of the ban.^24,28 Early reports from Boston Emergency Medical Services (EMS) suggest that there has not been an increase in ambulance turnaround time as feared, although this has not been formally studied.²⁹ ^[2]

At the Gathering of Eagles conference, this was one of the topics.

-It negatively impacts EMS operations and could jeopardize our ability to respond to the next critical patient.

-It often results in patients being transported to ED’s other than where their MD’s or medical records are.

-It negatively impacts patient satisfaction and provider morale.

-It does little if anything to reduce ED overcrowding.^[5]

In places that use diversion, when all of the hospitals are on divert, the dispatch center is supposed to notify the hospitals that dispatch will be making destination decisions until things improve. I have not seen any explanation for why that was not the case in Japan.

Diversion does not appear to provide any real benefit to anyone, except that it is consistent with the superstitions of many people, and medical people are as superstitious as gamblers.

Footnotes:

^[1] Saitama man dies after hospitals reject him 36 times
Japan Today
Mar. 06, 2013 – 02:31PM JST
Article

^[2] The effects of minimizing ambulance diversion hours on emergency departments.
Khaleghi M, Loh A, Vroman D, Chan TC, Vilke GM.
J Emerg Med. 2007 Aug;33(2):155-9. Epub 2007 Jun 18.
PMID: 17692767 [PubMed - indexed for MEDLINE]

^[3] Community trial to decrease ambulance diversion hours: the San Diego county patient destination trial.
Vilke GM, Castillo EM, Metz MA, Ray LU, Murrin PA, Lev R, Chan TC.
Ann Emerg Med. 2004 Oct;44(4):295-303.
PMID: 15459611 [PubMed - indexed for MEDLINE]

^[4] The effect of an ambulance diversion ban on emergency department length of stay and ambulance turnaround time.
Burke LG, Joyce N, Baker WE, Biddinger PD, Dyer KS, Friedman FD, Imperato J, King A, Maciejko TM, Pearlmutter MD, Sayah A, Zane RD, Epstein SK.
Ann Emerg Med. 2013 Mar;61(3):303-311.e1. doi: 10.1016/j.annemergmed.2012.09.009. Epub 2013 Jan 24.
PMID: 23352752 [PubMed - in process]

Free Full Text Download in PDF format.

^[5] Taking a Turn For The First: Taking Aim at Diversion Practices
S. Marshal Isaacs, MD, FACEP
Gathering of Eagles XV
February 23, 2010
Presentation slides in PDF format

75-year-old Japanese Man Dies After Hospitals Reject Him 36 Times
By Yue Wang
March 06, 2013
TIME.com
Article

Khaleghi, M., Loh, A., Vroman, D., Chan, T., & Vilke, G. (2007). The Effects of Minimizing Ambulance Diversion Hours on Emergency Departments The Journal of Emergency Medicine, 33 (2), 155-159 DOI: 10.1016/j.jemermed.2007.02.014

Vilke, G., Castillo, E., Metz, M., Upledger Ray, L., Murrin, P., Lev, R., & Chan, T. (2004). Community trial to decrease ambulance diversion hours: The San Diego county patient destination trial Annals of Emergency Medicine, 44 (4), 295-303 DOI: 10.1016/j.annemergmed.2004.05.002

Burke, L., Joyce, N., Baker, W., Biddinger, P., Dyer, K., Friedman, F., Imperato, J., King, A., Maciejko, T., Pearlmutter, M., Sayah, A., Zane, R., & Epstein, S. (2013). The Effect of an Ambulance Diversion Ban on Emergency Department Length of Stay and Ambulance Turnaround Time Annals of Emergency Medicine, 61 (3), 303-3110 DOI: 10.1016/j.annemergmed.2012.09.009

Filed Under: Ethics, Heresy, Management, Mythology, Research Blogging

Destroying a car to pretend to protect against spinal cord injury

Thu, 17 Jan 2013 15:30:40 +0000 by Rogue Medic

This car was not damaged in the original collision.

This car was not even involved in the original collision.

This car was destroyed by fire and EMS in order to pretend to protect the spines of the people who had walked to the car.

Firefighters cut the roof off a woman’s undamaged car to rescue two people she gave shelter to following an accident.^[1]

Yes, the patients did develop neck pain while sitting in the car waiting for police/fire/EMS to arrive, but would getting out of the car, without cutting the roof off, have increased the likelihood of a spinal injury becoming worse?

We don’t know. there is no evidence, but the lawyers tell us that they are afraid of that risk.

Why are we taking medical advice from lawyers?

Because we do not know what we are doing.

Injured people with pain from their injuries probably do a much better job of protecting their own injuries than by allowing a bunch of people playing with various implements of destruction to move them.

A spokesman for the South East Coast Ambulance Service said: “While the pair were sheltering in the car they developed neck pain.

“Paramedics explored every opportunity to get them out of the vehicle. However, in the end they had to get the fire service to cut the roof off and take them out on back boards.

“We can only apologise to Mrs Dunlop for the inconvenience of that.”^[1]

No. You can pay her for the damage you did to her car. This was damage done to protect the agency from liability. They should be held accountable for the damage.

We act as if the patients’ reactions to cutting the car apart around them will not be putting as much strain on any potentially unstable neck injuries as having the patients get out of the car on their own.

People, who have no experience being in cars being cut apart around them, will probably flinch at the sounds of extrication equipment tearing apart a car around them.

People, who do have experience being in cars being cut apart around them, will also probably flinch at the sounds of extrication equipment tearing apart a car around them.

Why pretend that there is reason to believe otherwise?

Why pretend that muscular movement from flinching is any less significant than what the patients would cause by getting out of the car on their own?

Any movement of the car is also going to result in movement of the necks of the occupants.

Is there any evidence that self-extrication causes damage to an unstable spinal cord?

Is there any evidence that we provide any protection to patients by extricating them our way?

This is another example of how far we will go to protect a traditional treatment with no known benefit.

We don’t know and we don’t want to know.

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.

Footnotes:

^[1] Good Samaritan’s car destroyed after pair given shelter
8 January 2013 Last updated at 08:22 ET
BBC News Sussex
Article

Filed Under: Critical Judgment, Heresy, Mythology, Spinal Immobilization

Stop the Madness! Reducing Unnecessary Spinal Immobilizations in the Field – Part I

Thu, 08 Nov 2012 13:30:26 +0000 by Rogue Medic

Picture credit from Voodoo Medicine Man.

Continuing to review the presentations I attended at EMS Expo. Jim Morrissey covers spinal immobilization and the way they are eliminating conventional spinal immobilization (placing a rigid collar on the neck and strapping the patient to a board) in Alameda County.^[1] Alameda County’s medical director, Dr. Sporer, has an article about the reasons for changing the protocol.^[2] Attend his presentations if you have the opportunity.

Oakland is the largest city and they have plenty of experience with trauma, so this will be an important place for EMS to watch to see the rate of spinal disability drop.

Where is the evidence

that spinal immobilization

improves the outcome

of patients?

Even Dr. Dave Ross, who has written some articles critical of spinal clearance protocols, is calling for a study to find out the actual effect of spinal immobilization, because right now there is no good evidence of benefit.^[3]

None.

Yes, there are anecdotes of manipulation leading to worse outcomes.

Spinal immobilization is manipulation – no matter how much we try to pretend otherwise.

Do we sedate combative patients in order to immobilize them without added manipulation?

If we do not, then their movements fighting immobilization are producing much greater stress on any unstable spinal fractures that they have.

Dementia – I transported a patient with altered mental status and a fall, who would not tolerate being placed flat on a board. The smallest size on the C-collar was still too large to not place significant distracting force on the neck of this very little little old lady.

She had a C2 (2nd Cervical vertebra) fracture.

Would she be paralyzed if I had forced immobilization on her?

Maybe. Maybe not.

Would I have been able to get orders for sedation of a change in mental status patient to immobilize her?

Maybe she would have survived immobilization without the immobilization increasing her injury.

Maybe. Maybe not.

We will never know.

What we do know is that she was fine with gentle transport, sitting up on the stretcher, without any forced manipulation of her injury to “immobilize” her.

She was fine when I dropped her off. She was fine hours later when I asked about the cause of her change in mental status and found out about the C2 fracture.

What if somebody sues?

A judge should throw out a law suit for a lack of evidence of harm caused by the lack of manipulation.

We need to stop claiming that manipulating the necks of patients is protecting them from injury.

According to spinal clearance criteria, altered mental status is one of the reasons we must not clear the spine.

If these patients do have spinal injuries, in what way do they benefit from the increased stress on the injury provided by EMS immobilization?

Spinal immobilization does not prevent stress on the injury, but only allows us to pretend it is not happening and that we are not causing the injury.

I will look at what they will be doing in Part II.

Footnotes:

^[1] Stop the Madness! Reducing Unnecessary Spinal Immobilizations in the Field

Nov 2 2012 9:30AM
Room: 206
Category: General
Jim Morrissey, MA, EMT-P
Friday Conference schedule.

A mounting body of evidence shows that the current approach to spine injury assessment and treatment needs to change, and change radically. Several studies show that EMS is immobilizing far too many patients and may be causing more harm than good in some trauma victims. This presentation examines the inaccuracy of using mechanism of injury as a predictor of injury and how EMS textbooks and past guidelines have led us astray. We review several articles and papers showing the detrimental effects of immobilizing victims of penetrating trauma and other patients, and discuss the multitude of problems associated with cervical collars and backboards. We review and validate several models of spine injury assessment protocols, especially ones that can reliably clear patients from the need for spinal protection. Finally, we will evaluate tools appropriate for patients who do require some degree of spinal protection.

^[2] Why We Need to Rethink C-Spine Immobilization
By Karl A. Sporer, MD, FACEP, FACP
Created: November 1, 2012
EMS World
Article

^[3] Confessions of a recovering field spine clearance addict — revisited
November 02, 2012
By Dave Ross
EMS1.com
Article

Revisiting the article below -

Confessions of a recovering field spine clearance addict
September 06, 2012
By Dave Ross
EMS1.com
Article

I commented on that article in the link below -

Confessions of a recovering cervical spine field clearance addict – Part I
Mon, 10 Sep 2012
Rogue Medic
Article

I have not yet written Part II.

Filed Under: EMS Expo, Ethics, Evidence, Heresy, Mythology, Spinal Immobilization

An 85 Mile Per Hour Speed Limit?

Sun, 28 Oct 2012 08:00:09 +0000 by Rogue Medic

An 85 mph speed limit sign is placed on the 41-mile-long toll road in Austin, near the increasingly crowded Interstate between Austin and San Antonio, Texas on Thursday, Sept. 6, 2012. While some drivers will want to test their horsepower and radar detectors, others are asking if safety is taking a backseat to pure speed.
Photo: Statesman.com, Ricardo B. Brazziell / AP^[1]

85 Miles an hour?

In the wide open plains of central Texas, a new addition to State Highway 130 opened for business this week with a compelling marketing hook: Its speed limit of 85 MPH is the highest in America. The 41-mile toll road connects Seguin to Mustang Ridge.^[2]

That’s insane!

Speed kills!

There were 32,310 traffic fatalities in 2011, the fewest there have been since 1949. More importantly, fatality rates per 100 million vehicle miles traveled have dropped substantially over the years, falling from 24.09 in 1921 to 1.09 in 2011.^[2]

Why mess with a good thing.

If we raise the speed limits, the highways will become death traps.

Just listen to common sense.

Everybody knows that speed kills.

In addition, while interstate highway speed limits have risen since Congress repealed all federally imposed speed limits in 1995, fatalities categorized as “speeding-related” by the National Highway Traffic Safety Administration (NHTSA) have declined since then. Specifically, there were 13,414 speeding-related fatalities in 1995 and 10,591 in 2011. Of the 10,591 speeding-related fatalities in 2011, just 964 occurred on interstate highways with speed limits “over 55 MPH.”^[2]

Maybe we should stop listening to the conventional wisdom, the old wives’ tales, and common sense, because the only thing that seems to be reliable about them is that they will be wrong.

Why base traffic laws on mythology?

There are many factors that affect the outcome of a traffic collision. Speed is just one of those factors.

Wouldn’t it be nice to know what the actual speed limit is, rather than seeing many drivers passing a State Trooper parked on the median, monitoring the speed of the passing traffic, with drivers regularly passing by the Trooper at 75 MPH and not being stopped.

Meanwhile there are people driving at what they think is an acceptable speed in the number 1 lane (lane farthest to the left) making the road less safe, because they cause other drivers to change lanes around them. The irony is that many of these drivers are also exceeding the speed limit, but they apparently feel that their level of comfort should be forced on others to make them feel better about whatever.

Then there are those who are just unaware of how to behave on the road. Keep to the right, except to pass. That means that we should only move to the left to pass someone, and only when it can be done safely. That does not mean that passing on the right is a traffic violation.

Driving wherever our whims might motivate us is actually encouraged in Florida –

Governor Bush vetoed 2005 SB732, which would have reserved the left lane for passing, saying that drivers blocking the left lane are “cautious and careful.”^[3]

No. Governor Bush does not understand “cautious and careful.” If these drivers were cautious and careful, they would keep to the right, as I do, rather than go looking for conflict at highway speeds.

A few states permit use of the left lane only for passing or turning left. These have “yes” in the “keep right” column. Six states require drivers to move right if they are blocking traffic in the left lane. Most states follow the Uniform Vehicle Code and require drivers to keep right if they are going slower than the normal speed of traffic (regardless of the speed limit; see below).^[3]

So if you are from a state, such as Florida, that encourages the slowest people to hold everyone else back, you might not want to do your Luddite driving in other states. It probably is not even safe for you to leave your state under any circumstances, after all you can’t be too safe.

Motorists may drive Segments 5 and 6 of SH 130 for free until November 11. Beginning November 11, the toll rate will be set at $0.15 per mile for passenger vehicles using TxTag. Cars and trucks without a TxTag may also use the road and will be billed via TxTag’s Pay-By-Mail service.^[4]

If we don’t want to drive on that toll road, we don’t have to, but there is no good reason to assume that it is any less safe than the roads we would travel on to get to the toll road.

The speed limit is 80 mph on the existing portion of the toll road, which connects Georgetown to south Austin. Open for several years, it’s operated by the Texas Department of Transportation.^[1]

Maybe I should let Huey Lewis explain the irony –

Download | YouTube MP3 Converter

Is it ironic to tell people that 85 MPH is just too darn fast?

What about 88 MPH?

Footnotes:

^[1] Can’t drive 55? On Texas 130, you soon can go at 85 mph
By Vianna Davila
Updated 1:11 a.m., Friday, September 7, 2012
MySanAntonio.com
Article

^[2] Time to Raise the Speed Limit in America?
By Reason Foundation
Thu, October 25, 2012
Article

^[3] State “keep right” laws
MIT.edu
Web page.

^[4] 41-Mile Extension of State Highway 130 Opens Ahead of Schedule in Central Texas – Public-private partnership completed at no cost to the State Highway Fund, more than 150 Texas-based firms employed
130 Toll News
Article

Filed Under: Heresy, Mythology, Traffic

Conspiracy Theory Week – Truthers, Anecdotalists, and Creationists, Oh My!

Sat, 15 Sep 2012 14:00:28 +0000 by Rogue Medic

Conspiracy theorists come in many flavors of self-deception, but they aren’t really that different from the typical true believer in anything else.

I have been writing about myths that we continue to use as standards of care, in spite of a lack of evidence. These are based on the same belief that are behind the myths being pushed by the 9/11 truthers.

The simplest argument against the truthers is that they blame the Bush administration. The same Bush administration that went to war with Iraq, but did not plant any weapons of mass destruction. Are we supposed to believe that thousands of people would murder thousands of Americans based on where they were when the planes hit, but we could not get a much smaller number of people to frame Saddam Hussein – a guy who is easy to hate.

Not just that, but the conspiracy is supposed to have been carried out in the first year of the first term of President Bush, while the absence of a conspiracy of weapons of mass destruction took place years later, after they had much more time to plan.

I know it because of Screwy Idea X.

Screwy Idea X may be true, may be partially true, may be completely false, or may be completely unrelated.

You have to prove that Screwy Idea X is false.

If Screwy Idea X is false, will it be easy to prove it is false? If it is not easy to prove that Screwy Idea X is false, does that mean that anecdote X is true?

Image credit.

The burden of proof should not be on the person who says, Screwy Idea X is ridiculous.

If you can’t prove that Screwy Idea X is false, that proves that Screwy Idea X is true.

Conspiracy theorists and denialists work on the same principle. There is never enough evidence to prove their idea is wrong.

As long as they can claim that there is a tiny possibility that they are right, that is their proof that they are right.

As long as they can claim that there is a tiny possibility that others are wrong, that is their proof that others are wrong.

Vaccines have saved millions of lives and are probably the safest medications we have, but what if your child has an extremely rare adverse reaction? No, autism is not caused by vaccines.

Alternative medicine is better than real medicine, because of _______. There are many problems with real medicine. I write about the problems – I don’t ignore the problems. Alternative medicine pushers ignore their problems and only criticize the problems of real medicine. Alternative medicine is pretending that an unknown treatment has been kept hidden by a conspiracy of Big Pharma and it really works. Except that the evidence consistently shows that alternative medicine does not perform any better than placebo. Alternative medicine is big business and the business is fraud.

We need to get rid of the prescription and over-the-counter medicines that don’t work. We do not need to add more medicines that don’t work.

Creationism is real and evolution is a lie because of conspiracy X. Even though plenty of religions do not see any conflict between their holy books and evolution. Individual preachers will claim that a literal interpretation is essential, but only when it supports what they preach. If the religious do not agree that 6 Day Creationism is real, and there is no evidence that 6 Day Creationism is real, then why should anyone believe that 6 Day Creationism is science?

We accept the crackpot idea because the true believer is charismatic.

Charisma can cover up a lot of flaws, even flaws as ridiculous as what I have already covered.

In medicine, we have our own true believers.

I know it because of Screwy Idea X.

Bleeding to get rid of bad humors.

Oxygen for myocradial infarction.

Antiarrhythmics for myocardial infarction.

Spinal immobilization for mechanism of injury.

Tourniquets mean amputations.

Ventilation for cardiac arrest.

Rotating tourniquets for CHF (because people with heart failure don’t mind a little amputation).

Furosemide (frusemide, brand name Lasix) moves fluid from the lungs to the kidneys.

Furosemide causes vasodilation.

If we give pain medicine, the patient will stop breathing.

Even though epinephrine causes heart failure, it is the best solution to a heart that has stopped.

Not just epinephrine for cardiac arrest – vasopressin, norepinephrine, phenylephrine, amiodarone, lidocaine, and magnesium.

The foundation of successful ACLS is high-quality CPR, and, for VF/pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, early CPR and rapid defibrillation can significantly increase the chance for survival to hospital discharge.^128,–,133 In comparison, other ACLS therapies such as some medications and advanced airways, although associated with an increased rate of ROSC, have not been shown to increase the rate of survival to hospital discharge.^{31,33,134,–,138} ^[1]

Maybe the 2015 ACLS Guidelines will be truly evidence-based and will NOT include any medications.

You have to prove that Screwy Idea X is false.

Some of the treatments mentioned above have been eliminated, but there are many that continue to be used –

Sunday, I wrote about a doctor claiming that there is a ~~screwy~~ compelling idea that demonstrates that oxygen is good, regardless of the lack of evidence. He also claims that since there is not perfect proof that oxygen is harmful, that is PROOF that oxygen is good.

If it helps just one patient, that justifies killing other patients.

Monday, I wrote about a doctor claiming that there is a ~~screwy~~ compelling idea that demonstrates that spinal immobilization is good, regardless of the lack of evidence. He also claims that since there is not perfect proof that spinal immobilization is harmful, that is PROOF that spinal immobilization is good.

If it helps just one patient, that justifies disabling other patients.

Tuesday, I wrote about a bunch of doctors (the AHA – American Heart Association – and others) claiming that there is a ~~screwy~~ compelling idea that demonstrates that ventilation is good, regardless of the lack of evidence. They also claim that since there is not perfect proof that ventilation is harmful, that is PROOF that ventilation is good.

If it helps just one patient, that justifies preventing the resuscitation of other patients.

I didn’t write anything on Wednesday. I was working on something long for Thursday (even the title was long).

Thursday, I wrote about a bunch of doctors (including the AHA) claiming that there is a ~~screwy~~ compelling idea that demonstrates that tPA is good, regardless of the lack of quality of the evidence. They also claim that since there is not perfect proof that tPA is harmful, that is PROOF that tPA is good hours and hours later.

If it helps just one patient, that justifies causing bleeding in the brains of other patients.

Friday, I wrote about the way the standard of care is perceived. All of these people I mentioned are claiming that their pet treatments, about which they are very biased, should not be affected by any negative evidence and why the evidence in favor of their pet therapy is all that we should pay attention to.

Ignore the flaws of the positive research – assuming there is any positive research. Belief.

Only pay attention to the flaws of the negative research. Willful ignorance.

This is not the way to do what is best for our patients.

If it helps just one patient, that justifies all of the harm to the other patients.

Am I exaggerating?

No, I am just simplifying the excuses for the lack of evidence to support their belief.

If you can’t prove that Screwy Idea X is false, that proves that Screwy Idea X is true.

No.

This is just an example of a logical fallacy.

The argument from ignorance.^[2]

Footnotes:

^[1] Overview
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.2: Management of Cardiac Arrest
Free Full Text from Circulation

^[2] Argument from ignorance
Wikipedia
Article

Filed Under: 2010 AHA Guidelines, Creationism, Epinephrine, Ethics, Evidence, Heresy, Lasix, Mythology, Science

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